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Koffey recommended former best online viagra WellCare Health Plans CEO Kenneth Burdick and past Anthem chief financial officer Wayne DeVeydt join the insurer as board directors, WSJ said. An opportunity to update the company's board will open later this month. Centene paid $17 billion for Medicare Advantage insurer Wellcare in 2020. Koffey did not immediately best online viagra respond to interview requests.

Over the past two years, Centene said it has added four new directors to its board, three of whom are independent. The most recent addition came in September when Sarah London, who serves as president of the company's best online viagra non-insurance health care enterprises division and executive vice president of advanced technology business line, was appointed vice chairman of the board. A month after the announcement, David Steward retired from Centene's board after 14 years of service. He said he wanted to spend more time with his best online viagra family and pursue other business interests.

"The company intends to make further changes to the composition of the board and diversity will continue to be a strong consideration," the insurer said. The insurer has made other recent, and abrupt changes, to best online viagra its personnel. In September, Brent Layton was also named chief operating officer of Centene and the office of the president changed its name to the office of the chairman and CEO. Centene is best online viagra headed by long-time CEO Michael Neidorff.

Later that month, Centene and long-time executive Jeffrey Schwaneke "mutually agreed" that he should resign, after 13 years of work at the insurer. Schwaneke had more recently served as executive vice president of healthcare enterprises, where he was transferred to six months before as part of the insurer's professional development program. The transfer moved him from reporting to the insurer's top office to best online viagra Sarah London. No further details were disclosed.

At the end of October, Centene and former executive vice president and chief strategy officer Jesse best online viagra Hunter also agreed to part ways, with Hunter's last day being Nov. 5 rather than at the end of 2021, according to a filing with the U.S. Securities and Exchange Commission best online viagra. The insurer did not disclose why Hunter was ending his 19-year stretch at the company early.At the end of the company's most recent third quarter on September 30, Centene reported $32.4 billion in revenue, up 11% from the $29.1 billion reported during the same time last year.

The company reported net income of $584 million, up 4% from $561 million reported during the same time last year.Walmart has hired Ochsner Health executive best online viagra Dr. David Carmouche to lead its omnichannel care organization.Carmouche had been the president of Ochsner Health Network, where he oversaw 2,700 physicians across 34 hospitals, as well as vice president of the New Orleans-based health system's value-based care and network operations. Carmouche will best online viagra join Walmart as the retailer restructures its healthcare offerings. Business Insider first reported the hire.Carmouche helped coordinate a direct contracting agreement between Ochsner Health and Walmart in 2018 that covers about 6,600 Walmart and Sam's Club associates in Louisiana.

Walmart has been steadily expanding its direct contracts with hospitals and physician groups to steer employees to select providers.The retail giant has also been best online viagra opening more comprehensive primary care centers inside its stores. These clinics provide chronic disease management, urgent care, mental health counseling, and dental, vision and hearing services. The locations also offer lab services, x-rays and diagnostics via a joint venture with Quest Diagnostics.Walmart recently partnered with Transcarent, which offers second opinions, medication reviews and referrals to surgery sites and centers of excellence to more than 100 self-insured employers.In May, the retailer acquired telehealth provider MeMD, which will be featured in Walmart Health centers as a supplement to in-person care..

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How to hop over to this website cite this female viagra article:Singh O P. Aftermath of celebrity suicide – Media coverage and role of psychiatrists. Indian J Psychiatry 2020;62:337-8Celebrity suicide is one of female viagra the highly publicized events in our country. Indians got a glimpse of this following an unfortunate incident where a popular Hindi film actor died of suicide. As expected, the media went into a female viagra frenzy as newspapers, news channels, and social media were full of stories providing minute details of the suicidal act.

Some even going as far as highlighting the color of the cloth used in the suicide as well as showing the lifeless body of the actor. All kinds of personal details were dug up, and speculations and hypotheses became the order of the day in the next few days that followed. In the process, reputations of many people associated with the actor were besmirched and their private and personal female viagra details were freely and blatantly broadcast and discussed on electronic, print, and social media. We understand that media houses have their own need and duty to report and sensationalize news for increasing their visibility (aka TRP), but such reporting has huge impacts on the mental health of the vulnerable population.The impact of this was soon realized when many incidents of copycat suicide were reported from all over the country within a few days of the incident. Psychiatrists suddenly started getting distress calls from their patients in despair female viagra with increased suicidal ideation.

This has become a major area of concern for the psychiatry community.The Indian Psychiatric Society has been consistently trying to engage with media to promote ethical reporting of suicide. Section 24 (1) of Mental Health Care Act, 2017, forbids publication of photograph of mentally ill person without female viagra his consent.[1] The Press Council of India has adopted the guidelines of World Health Organization report on Preventing Suicide. A resource for media professionals, which came out with an advisory to be followed by media in reporting cases of suicide. It includes points forbidding them from putting stories in prominent positions and unduly repeating them, explicitly describing the method used, providing details about the site/location, using sensational headlines, or using photographs and video footage of the incident.[2] Unfortunately, the advisory seems to have little effect in the aftermath of celebrity suicides. Channels were full of speculations about the person's female viagra mental condition and illness and also his relationships and finances.

Many fictional accounts of his symptoms and illness were touted, which is not only against the ethics but is also contrary to MHCA, 2017.[1]It went to the extent that the name of his psychiatrist was mentioned and quotes were attributed to him without taking any account from him. The Indian Psychiatric Society has written to the Press Council of India underlining this concern and asking for measures to ensure ethics in reporting suicide.While there is a need for engagement with media to make them aware of the female viagra grave impact of negative suicide reporting on the lives of many vulnerable persons, there is even a more urgent need for training of psychiatrists regarding the proper way of interaction with media. This has been amply brought out in the aftermath of this incident. Many psychiatrists and mental health professionals were called by media houses to comment on the episode female viagra. Many psychiatrists were quoted, or “misquoted,” or “quoted out of context,” commenting on the life of a person whom they had never examined and had no “professional authority” to do so.

There were even stories with byline of a psychiatrist where the content provided was not only unscientific but also way beyond the expertise of a psychiatrist. These types of viewpoints perpetuate stigma, myths, and “misleading concepts” about psychiatry and are detrimental to the image of psychiatry in addition female viagra to doing harm and injustice to our patients. Hence, the need to formulate a guideline for interaction of psychiatrists with the media is imperative.In the infamous Goldwater episode, 12,356 psychiatrists were asked to cast opinion about the fitness of Barry Goldwater for presidential candidature. Out of 2417 respondents, 1189 psychiatrists reported him to be mentally unfit while none had actually examined him.[3] This led to the formulation of “The Goldwater Rule” by the American Psychiatric Association in 1973,[4] but we have witnessed the same phenomenon at the time of presidential candidature of Donald Trump.Psychiatrists should be encouraged to interact with media to provide scientific information about mental illnesses and reduction of stigma, but “statements to the media” can be a double-edged female viagra sword, and we should know about the rules of engagements and boundaries of interactions. Methods and principles of interaction with media should form a part of our training curriculum.

Many professional societies female viagra have guidelines and resource books for interacting with media, and psychiatrists should familiarize themselves with these documents. The Press Council guideline is likely to prompt reporters to seek psychiatrists for their expert opinion. It is useful for them to have a template ready with suicide rates, emphasizing multicausality of suicide, role of mental disorders, as well as help available.[5]It is about time that the Indian Psychiatric Society formulated its own guidelines laying down the broad principles and boundaries governing the interaction of Indian psychiatrists with the media. Till then, it is desirable to be guided female viagra by the following broad principles:It should be assumed that no statement goes “off the record” as the media person is most likely recording the interview, and we should also record any such conversation from our endIt should be clarified in which capacity comments are being made – professional, personal, or as a representative of an organizationOne should not comment on any person whom he has not examinedPsychiatrists should take any such opportunity to educate the public about mental health issuesThe comments should be justified and limited by the boundaries of scientific knowledge available at the moment. References Correspondence Address:Dr.

O P SinghAA 304, Ashabari Apartments, O/31, Baishnabghata, Patuli Township, Kolkata - female viagra 700 094, West Bengal IndiaSource of Support. None, Conflict of Interest. NoneDOI. 10.4103/psychiatry.IndianJPsychiatry_816_20Abstract Electroconvulsive therapy (ECT) is an effective modality of treatment for a variety of psychiatric disorders. However, it has always been accused of being a coercive, unethical, and dangerous modality of treatment.

The dangerousness of ECT has been mainly attributed to its claimed ability to cause brain damage. This narrative review aims to provide an update of the evidence with regard to whether the practice of ECT is associated with damage to the brain. An accepted definition of brain damage remains elusive. There are also ethical and technical problems in designing studies that look at this question specifically. Thus, even though there are newer technological tools and innovations, any review attempting to answer this question would have to take recourse to indirect methods.

These include structural, functional, and metabolic neuroimaging. Body fluid biochemical marker studies. And follow-up studies of cognitive impairment and incidence of dementia in people who have received ECT among others. The review of literature and present evidence suggests that ECT has a demonstrable impact on the structure and function of the brain. However, there is a lack of evidence at present to suggest that ECT causes brain damage.Keywords.

Adverse effect, brain damage, electroconvulsive therapyHow to cite this article:Jolly AJ, Singh SM. Does electroconvulsive therapy cause brain damage. An update. Indian J Psychiatry 2020;62:339-53 Introduction Electroconvulsive therapy (ECT) as a modality of treatment for psychiatric disorders has existed at least since 1938.[1] ECT is an effective modality of treatment for various psychiatric disorders. However, from the very beginning, the practice of ECT has also faced resistance from various groups who claim that it is coercive and harmful.[2] While the ethical aspects of the practice of ECT have been dealt with elsewhere, the question of harmfulness or brain damage consequent upon the passage of electric current needs to be examined afresh in light of technological advances and new knowledge.[3]The question whether ECT causes brain damage was reviewed in a holistic fashion by Devanand et al.

In the mid-1990s.[4],[5] The authors had attempted to answer this question by reviewing the effect of ECT on the brain in various areas – cognitive side effects, structural neuroimaging studies, neuropathologic studies of patients who had received ECT, autopsy studies of epileptic patients, and finally animal ECS studies. The authors had concluded that ECT does not produce brain damage.This narrative review aims to update the evidence with regard to whether ECT causes brain damage by reviewing relevant literature from 1994 to the present time. Framing the Question The Oxford Dictionary defines damage as physical harm that impairs the value, usefulness, or normal function of something.[6] Among medical dictionaries, the Peter Collins Dictionary defines damage as harm done to things (noun) or to harm something (verb).[7] Brain damage is defined by the British Medical Association Medical Dictionary as degeneration or death of nerve cells and tracts within the brain that may be localized to a particular area of the brain or diffuse.[8] Going by such a definition, brain damage in the context of ECT should refer to death or degeneration of brain tissue, which results in the impairment of functioning of the brain. The importance of precisely defining brain damage shall become evident subsequently in this review.There are now many more tools available to investigate the structure and function of brain in health and illness. However, there are obvious ethical issues in designing human studies that are designed to answer this specific question.

Therefore, one must necessarily take recourse to indirect evidences available through studies that have been designed to answer other research questions. These studies have employed the following methods:Structural neuroimaging studiesFunctional neuroimaging studiesMetabolic neuroimaging studiesBody fluid biochemical marker studiesCognitive impairment studies.While the early studies tended to focus more on establishing the safety of ECT and finding out whether ECT causes gross microscopic brain damage, the later studies especially since the advent of advanced neuroimaging techniques have been focusing more on a mechanistic understanding of ECT. Hence, the primary objective of the later neuroimaging studies has been to look for structural and functional brain changes which might explain how ECT acts rather than evidence of gross structural damage per se. However, put together, all these studies would enable us to answer our titular question to some satisfaction. [Table 1] and [Table 2] provide an overview of the evidence base in this area.

Structural and Functional Neuroimaging Studies Devanand et al. Reviewed 16 structural neuroimaging studies on the effect of ECT on the brain.[4] Of these, two were pneumoencephalography studies, nine were computed tomography (CT) scan studies, and five were magnetic resonance imaging (MRI) studies. However, most of these studies were retrospective in design, with neuroimaging being done in patients who had received ECT in the past. In the absence of baseline neuroimaging, it would be very difficult to attribute any structural brain changes to ECT. In addition, pneumoencephalography, CT scan, and even early 0.3 T MRI provided images with much lower spatial resolution than what is available today.

The authors concluded that there was no evidence to show that ECT caused any structural damage to the brain.[4] Since then, at least twenty more MRI-based structural neuroimaging studies have studied the effect of ECT on the brain. The earliest MRI studies in the early 1990s focused on detecting structural damage following ECT. All of these studies were prospective in design, with the first MRI scan done at baseline and a second MRI scan performed post ECT.[9],[11],[12],[13],[41] While most of the studies imaged the patient once around 24 h after receiving ECT, some studies performed multiple post ECT neuroimaging in the first 24 h after ECT to better capture the acute changes. A single study by Coffey et al. Followed up the patients for a duration of 6 months and repeated neuroimaging again at 6 months in order to capture any long-term changes following ECT.[10]The most important conclusion which emerged from this early series of studies was that there was no evidence of cortical atrophy, change in ventricle size, or increase in white matter hyperintensities.[4] The next major conclusion was that there appeared to be an increase in the T1 and T2 relaxation time immediately following ECT, which returned to normal within 24 h.

This supported the theory that immediately following ECT, there appears to be a temporary breakdown of the blood–brain barrier, leading to water influx into the brain tissue.[11] The last significant observation by Coffey et al. In 1991 was that there was no significant temporal changes in the total volumes of the frontal lobes, temporal lobes, or amygdala–hippocampal complex.[10] This was, however, something which would later be refuted by high-resolution MRI studies. Nonetheless, one inescapable conclusion of these early studies was that there was no evidence of any gross structural brain changes following administration of ECT. Much later in 2007, Szabo et al. Used diffusion-weighted MRI to image patients in the immediate post ECT period and failed to observe any obvious brain tissue changes following ECT.[17]The next major breakthrough came in 2010 when Nordanskog et al.

Demonstrated that there was a significant increase in the volume of the hippocampus bilaterally following a course of ECT in a cohort of patients with depressive illness.[18] This contradicted the earlier observations by Coffey et al. That there was no volume increase in any part of the brain following ECT.[10] This was quite an exciting finding and was followed by several similar studies. However, the perspective of these studies was quite different from the early studies. In contrast to the early studies looking for the evidence of ECT-related brain damage, the newer studies were focused more on elucidating the mechanism of action of ECT. Further on in 2014, Nordanskog et al.

In a follow-up study showed that though there was a significant increase in the volume of the hippocampus 1 week after a course of ECT, the hippocampal volume returned to the baseline after 6 months.[19] Two other studies in 2013 showed that in addition to the hippocampus, the amygdala also showed significant volume increase following ECT.[20],[21] A series of structural neuroimaging studies after that have expanded on these findings and as of now, gray matter volume increase following ECT has been demonstrated in the hippocampus, amygdala, anterior temporal pole, subgenual cortex,[21] right caudate nucleus, and the whole of the medial temporal lobe (MTL) consisting of the hippocampus, amygdala, insula, and the posterosuperior temporal cortex,[24] para hippocampi, right subgenual anterior cingulate gyrus, and right anterior cingulate gyrus,[25] left cerebellar area VIIa crus I,[29] putamen, caudate nucleus, and nucleus acumbens [31] and clusters of increased cortical thickness involving the temporal pole, middle and superior temporal cortex, insula, and inferior temporal cortex.[27] However, the most consistently reported and replicated finding has been the bilateral increase in the volume of the hippocampus and amygdala. In light of these findings, it has been tentatively suggested that ECT acts by inducing neuronal regeneration in the hippocampus – amygdala complex.[42],[43] However, there are certain inconsistencies to this hypothesis. Till date, only one study – Nordanskog et al., 2014 – has followed study patients for a long term – 6 months in their case. And significantly, the authors found out that after increasing immediately following ECT, the hippocampal volume returns back to baseline by 6 months.[19] This, however, was not associated with the relapse of depressive symptoms. Another area of significant confusion has been the correlation of hippocampal volume increase with improvement of depressive symptoms.

Though almost all studies demonstrate a significant increase in hippocampal volume following ECT, a majority of studies failed to demonstrate a correlation between symptom improvement and hippocampal volume increase.[19],[20],[22],[24],[28] However, a significant minority of volumetric studies have demonstrated correlation between increase in hippocampal and/or amygdala volume and improvement of symptoms.[21],[25],[30]Another set of studies have used diffusion tensor imaging, functional MRI (fMRI), anatomical connectome, and structural network analysis to study the effect of ECT on the brain. The first of these studies by Abbott et al. In 2014 demonstrated that on fMRI, the connectivity between right and left hippocampus was significantly reduced in patients with severe depression. It was also shown that the connectivity was normalized following ECT, and symptom improvement was correlated with an increase in connectivity.[22] In a first of its kind DTI study, Lyden et al. In 2014 demonstrated that fractional anisotropy which is a measure of white matter tract or fiber density is increased post ECT in patients with severe depression in the anterior cingulum, forceps minor, and the dorsal aspect of the left superior longitudinal fasciculus.

The authors suggested that ECT acts to normalize major depressive disorder-related abnormalities in the structural connectivity of the dorsal fronto-limbic pathways.[23] Another DTI study in 2015 constructed large-scale anatomical networks of the human brain – connectomes, based on white matter fiber tractography. The authors found significant reorganization in the anatomical connections involving the limbic structure, temporal lobe, and frontal lobe. It was also found that connection changes between amygdala and para hippocampus correlated with reduction in depressive symptoms.[26] In 2016, Wolf et al. Used a source-based morphometry approach to study the structural networks in patients with depression and schizophrenia and the effect of ECT on the same. It was found that the medial prefrontal cortex/anterior cingulate cortex (ACC/MPFC) network, MTL network, bilateral thalamus, and left cerebellar regions/precuneus exhibited significant difference between healthy controls and the patient population.

It was also demonstrated that administration of ECT leads to significant increase in the network strength of the ACC/MPFC network and the MTL network though the increase in network strength and symptom amelioration were not correlated.[32]Building on these studies, a recently published meta-analysis has attempted a quantitative synthesis of brain volume changes – focusing on hippocampal volume increase following ECT in patients with major depressive disorder and bipolar disorder. The authors initially selected 32 original articles from which six articles met the criteria for quantitative synthesis. The results showed significant increase in the volume of the right and left hippocampus following ECT. For the rest of the brain regions, the heterogeneity in protocols and imaging techniques did not permit a quantitative analysis, and the authors have resorted to a narrative review similar to the present one with similar conclusions.[44] Focusing exclusively on hippocampal volume change in ECT, Oltedal et al. In 2018 conducted a mega-analysis of 281 patients with major depressive disorder treated with ECT enrolled at ten different global sites of the Global ECT-MRI Research Collaboration.[45] Similar to previous studies, there was a significant increase in hippocampal volume bilaterally with a dose–response relationship with the number of ECTs administered.

Furthermore, bilateral (B/L) ECT was associated with an equal increase in volume in both right and left hippocampus, whereas right unilateral ECT was associated with greater volume increase in the right hippocampus. Finally, contrary to expectation, clinical improvement was found to be negatively correlated with hippocampal volume.Thus, a review of the current evidence amply demonstrates that from looking for ECT-related brain damage – and finding none, we have now moved ahead to looking for a mechanistic understanding of the effect of ECT. In this regard, it has been found that ECT does induce structural changes in the brain – a fact which has been seized upon by some to claim that ECT causes brain damage.[46] Such statements should, however, be weighed against the definition of damage as understood by the scientific medical community and patient population. Neuroanatomical changes associated with effective ECT can be better described as ECT-induced brain neuroplasticity or ECT-induced brain neuromodulation rather than ECT-induced brain damage. Metabolic Neuroimaging Studies.

Magnetic Resonance Spectroscopic Imaging Magnetic resonance spectroscopic imaging (MRSI) uses a phase-encoding procedure to map the spatial distribution of magnetic resonance (MR) signals of different molecules. The crucial difference, however, is that while MRI maps the MR signals of water molecules, MRSI maps the MR signals generated by different metabolites – such as N-acetyl aspartate (NAA) and choline-containing compounds. However, the concentration of these metabolites is at least 10,000 times lower than water molecules and hence the signal strength generated would also be correspondingly lower. However, MRSI offers us the unique advantage of studying in vivo the change in the concentration of brain metabolites, which has been of great significance in fields such as psychiatry, neurology, and basic neuroscience research.[47]MRSI studies on ECT in patients with depression have focused largely on four metabolites in the human brain – NAA, choline-containing compounds (Cho) which include majorly cell membrane compounds such as glycerophosphocholine, phosphocholine and a miniscule contribution from acetylcholine, creatinine (Cr) and glutamine and glutamate together (Glx). NAA is located exclusively in the neurons, and is suggested to be a marker of neuronal viability and functionality.[48] Choline-containing compounds (Cho) mainly include the membrane compounds, and an increase in Cho would be suggestive of increased membrane turnover.

Cr serves as a marker of cellular energy metabolism, and its levels are usually expected to remain stable. The regions which have been most widely studied in MRSI studies include the bilateral hippocampus and amygdala, dorsolateral prefrontal cortex (DLPFC), and ACC.Till date, five MRSI studies have measured NAA concentration in the hippocampus before and after ECT. Of these, three studies showed that there is no significant change in the NAA concentration in the hippocampus following ECT.[33],[38],[49] On the other hand, two recent studies have demonstrated a statistically significant reduction in NAA concentration in the hippocampus following ECT.[39],[40] The implications of these results are of significant interest to us in answering our titular question. A normal level of NAA following ECT could signify that there is no significant neuronal death or damage following ECT, while a reduction would signal the opposite. However, a direct comparison between these studies is complicated chiefly due to the different ECT protocols, which has been used in these studies.

It must, however, be acknowledged that the three older studies used 1.5 T MRI, whereas the two newer studies used a higher 3 T MRI which offers betters signal-to-noise ratio and hence lesser risk of errors in the measurement of metabolite concentrations. The authors of a study by Njau et al.[39] argue that a change in NAA levels might reflect reversible changes in neural metabolism rather than a permanent change in the number or density of neurons and also that reduced NAA might point to a change in the ratio of mature to immature neurons, which, in fact, might reflect enhanced adult neurogenesis. Thus, the authors warn that to conclude whether a reduction in NAA concentration is beneficial or harmful would take a simultaneous measurement of cognitive functioning, which was lacking in their study. In 2017, Cano et al. Also demonstrated a significant reduction in NAA/Cr ratio in the hippocampus post ECT.

More significantly, the authors also showed a significant increase in Glx levels in the hippocampus following ECT, which was also associated with an increase in hippocampal volume.[40] To explain these three findings, the authors proposed that ECT produces a neuroinflammatory response in the hippocampus – likely mediated by Glx, which has been known to cause inflammation at higher concentrations, thereby accounting for the increase in hippocampal volume with a reduction in NAA concentration. The cause for the volume increase remains unclear – with the authors speculating that it might be due to neuronal swelling or due to angiogenesis. However, the same study and multiple other past studies [21],[25],[30] have demonstrated that hippocampal volume increase was correlated with clinical improvement following ECT. Thus, we are led to the hypothesis that the same mechanism which drives clinical improvement with ECT is also responsible for the cognitive impairment following ECT. Whether this is a purely neuroinflammatory response or a neuroplastic response or a neuroinflammatory response leading to some form of neuroplasticity is a critical question, which remains to be answered.[40]Studies which have analyzed NAA concentration change in other brain areas have also produced conflicting results.

The ACC is another area which has been studied in some detail utilizing the MRSI technique. In 2003, Pfleiderer et al. Demonstrated that there was no significant change in the NAA and Cho levels in the ACC following ECT. This would seem to suggest that there was no neurogenesis or membrane turnover in the ACC post ECT.[36] However, this finding was contested by Merkl et al. In 2011, who demonstrated that NAA levels were significantly reduced in the left ACC in patients with depression and that these levels were significantly elevated following ECT.[37] This again is contested by Njau et al.

Who showed that NAA levels are significantly reduced following ECT in the left dorsal ACC.[39] A direct comparison of these three studies is complicated by the different ECT and imaging parameters used and hence, no firm conclusion can be made on this point at this stage. In addition to this, one study had demonstrated increased NAA levels in the amygdala following administration of ECT,[34] with a trend level increase in Cho levels, which again is suggestive of neurogenesis and/or neuroplasticity. A review of studies on the DLPFC reveals a similarly confusing picture with one study, each showing no change, reduction, and elevation of concentration of NAA following ECT.[35],[37],[39] Here, again, a direct comparison of the three studies is made difficult by the heterogeneous imaging and ECT protocols followed by them.A total of five studies have analyzed the concentration of choline-containing compounds (Cho) in patients undergoing ECT. Conceptually, an increase in Cho signals is indicative of increased membrane turnover, which is postulated to be associated with synaptogenesis, neurogenesis, and maturation of neurons.[31] Of these, two studies measured Cho concentration in the B/L hippocampus, with contrasting results. Ende et al.

In 2000 demonstrated a significant elevation in Cho levels in B/L hippocampus after ECT, while Jorgensen et al. In 2015 failed to replicate the same finding.[33],[38] Cho levels have also been studied in the amygdala, ACC, and the DLPFC. However, none of these studies showed a significant increase or decrease in Cho levels before and after ECT in the respective brain regions studied. In addition, no significant difference was seen in the pre-ECT Cho levels of patients compared to healthy controls.[34],[36],[37]In review, we must admit that MRSI studies are still at a preliminary stage with significant heterogeneity in ECT protocols, patient population, and regions of the brain studied. At this stage, it is difficult to draw any firm conclusions except to acknowledge the fact that the more recent studies – Njau et al., 2017, Cano, 2017, and Jorgensen et al., 2015 – have shown decrease in NAA concentration and no increase in Cho levels [38],[39],[40] – as opposed to the earlier studies by Ende et al.[33] The view offered by the more recent studies is one of a neuroinflammatory models of action of ECT, probably driving neuroplasticity in the hippocampus.

This would offer a mechanistic understanding of both clinical response and the phenomenon of cognitive impairment associated with ECT. However, this conclusion is based on conjecture, and more work needs to be done in this area. Body Fluid Biochemical Marker Studies Another line of evidence for analyzing the effect of ECT on the human brain is the study of concentration of neurotrophins in the plasma or serum. Neurotrophins are small protein molecules which mediate neuronal survival and development. The most prominent among these is brain-derived neurotrophic factor (BDNF) which plays an important role in neuronal survival, plasticity, and migration.[50] A neurotrophic theory of mood disorders was suggested which hypothesized that depressive disorders are associated with a decreased expression of BDNF in the limbic structures, resulting in the atrophy of these structures.[51] It was also postulated that antidepressant treatment has a neurotrophic effect which reverses the neuronal cell loss, thereby producing a therapeutic effect.

It has been well established that BDNF is decreased in mood disorders.[52] It has also been shown that clinical improvement of depression is associated with increase in BDNF levels.[53] Thus, serum BDNF levels have been tentatively proposed as a biomarker for treatment response in depression. Recent meta-analytic evidence has shown that ECT is associated with significant increase in serum BDNF levels in patients with major depressive disorder.[54] Considering that BDNF is a potent stimulator of neurogenesis, the elevation of serum BDNF levels following ECT lends further credence to the theory that ECT leads to neurogenesis in the hippocampus and other limbic structures, which, in turn, mediates the therapeutic action of ECT. Cognitive Impairment Studies Cognitive impairment has always been the single-most important side effect associated with ECT.[55] Concerns regarding long-term cognitive impairment surfaced soon after the introduction of ECT and since then has grown to become one of the most controversial aspects of ECT.[56] Anti-ECT groups have frequently pointed out to cognitive impairment following ECT as evidence of ECT causing brain damage.[56] A meta-analysis by Semkovska and McLoughlin in 2010 is one of the most detailed studies which had attempted to settle this long-standing debate.[57] The authors reviewed 84 studies (2981 participants), which had used a combined total of 22 standardized neuropsychological tests assessing various cognitive functions before and after ECT in patients diagnosed with major depressive disorder. The different cognitive domains reviewed included processing speed, attention/working memory, verbal episodic memory, visual episodic memory, spatial problem-solving, executive functioning, and intellectual ability. The authors concluded that administration of ECT for depression is associated with significant cognitive impairment in the first few days after ECT administration.

However, it was also seen that impairment in cognitive functioning resolved within a span of 2 weeks and thereafter, a majority of cognitive domains even showed mild improvement compared to the baseline performance. It was also demonstrated that not a single cognitive domain showed persistence of impairment beyond 15 days after ECT.Memory impairment following ECT can be analyzed broadly under two conceptual schemes – one that classifies memory impairment as objective memory impairment and subjective memory impairment and the other that classifies it as impairment in anterograde memory versus impairment in retrograde memory. Objective memory can be roughly defined as the ability to retrieve stored information and can be measured by various standardized neuropsychological tests. Subjective memory or meta-memory, on the other hand, refers to the ability to make judgments about one's ability to retrieve stored information.[58] As described previously, it has been conclusively demonstrated that anterograde memory impairment does not persist beyond 2 weeks after ECT.[57] However, one of the major limitations of this meta-analysis was the lack of evidence on retrograde amnesia following ECT. This is particularly unfortunate considering that it is memory impairment – particularly retrograde amnesia which has received the most attention.[59] In addition, reports of catastrophic retrograde amnesia have been repeatedly held up as sensational evidence of the lasting brain damage produced by ECT.[59] Admittedly, studies on retrograde amnesia are fewer and less conclusive than on anterograde amnesia.[60],[61] At present, the results are conflicting, with some studies finding some impairment in retrograde memory – particularly autobiographical retrograde memory up to 6 months after ECT.[62],[63],[64],[65] However, more recent studies have failed to support this finding.[66],[67] While they do demonstrate an impairment in retrograde memory immediately after ECT, it was seen that this deficit returned to pre-ECT levels within a span of 1–2 months and improved beyond baseline performance at 6 months post ECT.[66] Adding to the confusion are numerous factors which confound the assessment of retrograde amnesia.

It has been shown that depressive symptoms can produce significant impairment of retrograde memory.[68],[69] It has also been demonstrated that sine-wave ECT produces significantly more impairment of retrograde memory as compared to brief-pulse ECT.[70] However, from the 1990s onward, sine-wave ECT has been completely replaced by brief-pulse ECT, and it is unclear as to the implications of cognitive impairment from the sine-wave era in contemporary ECT practice.Another area of concern are reports of subjective memory impairment following ECT. One of the pioneers of research into subjective memory impairment were Squire and Chace who published a series of studies in the 1970s demonstrating the adverse effect of bilateral ECT on subjective assessment of memory.[62],[63],[64],[65] However, most of the studies conducted post 1980 – from when sine-wave ECT was replaced by brief-pulse ECT report a general improvement in subjective memory assessments following ECT.[71] In addition, most of the recent studies have failed to find a significant association between measures of subjective and objective memory.[63],[66],[70],[72],[73],[74] It has also been shown that subjective memory impairment is strongly associated with the severity of depressive symptoms.[75] In light of these facts, the validity and value of measures of subjective memory impairment as a marker of cognitive impairment and brain damage following ECT have been questioned. However, concerns regarding subjective memory impairment and catastrophic retrograde amnesia continue to persist, with significant dissonance between the findings of different research groups and patient self-reports in various media.[57]Some studies reported the possibility of ECT being associated with the development of subsequent dementia.[76],[77] However, a recent large, well-controlled prospective Danish study found that the use of ECT was not associated with elevated incidence of dementia.[78] Conclusion Our titular question is whether ECT leads to brain damage, where damage indicates destruction or degeneration of nerves or nerve tracts in the brain, which leads to loss of function. This issue was last addressed by Devanand et al. In 1994 since which time our understanding of ECT has grown substantially, helped particularly by the advent of modern-day neuroimaging techniques which we have reviewed in detail.

And, what these studies reveal is rather than damaging the brain, ECT has a neuromodulatory effect on the brain. The various lines of evidence – structural neuroimaging studies, functional neuroimaging studies, neurochemical and metabolic studies, and serum BDNF studies all point toward this. These neuromodulatory changes have been localized to the hippocampus, amygdala, and certain other parts of the limbic system. How exactly these changes mediate the improvement of depressive symptoms is a question that remains unanswered. However, there is little by way of evidence from neuroimaging studies which indicates that ECT causes destruction or degeneration of neurons.

Though cognitive impairment studies do show that there is objective impairment of certain functions – particularly memory immediately after ECT, these impairments are transient with full recovery within a span of 2 weeks. Perhaps, the single-most important unaddressed concern is retrograde amnesia, which has been shown to persist for up to 2 months post ECT. In this regard, the recent neurometabolic studies have offered a tentative mechanism of action of ECT, producing a transient inflammation in the limbic cortex, which, in turn, drives neurogenesis, thereby exerting a neuromodulatory effect. This hypothesis would explain both the cognitive adverse effects of ECT – due to the transient inflammation – and the long-term improvement in mood – neurogenesis in the hippocampus. Although unproven at present, such a hypothesis would imply that cognitive impairment is tied in with the mechanism of action of ECT and not an indicator of damage to the brain produced by ECT.The review of literature suggests that ECT does cause at least structural and functional changes in the brain, and these are in all probability related to the effects of the ECT.

However, these cannot be construed as brain damage as is usually understood. Due to the relative scarcity of data that directly examines the question of whether ECT causes brain damage, it is not possible to conclusively answer this question. However, in light of enduring ECT survivor accounts, there is a need to design studies that specifically answer this question.Financial support and sponsorshipNil.Conflicts of interestThere are no conflicts of interest. References 1.Payne NA, Prudic J. Electroconvulsive therapy.

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A cohort study. Lancet Psychiatry 2018;5:348-56. Correspondence Address:Dr. Shubh Mohan SinghDepartment of Psychiatry, Postgraduate Institute of Medical Education and Research, Chandigarh IndiaSource of Support. None, Conflict of Interest.

NoneDOI. 10.4103/psychiatry.IndianJPsychiatry_239_19 Tables [Table 1], [Table 2].

How to cite this best online viagra article:Singh http://subwaycaterstampa.com/one-page/ O P. Aftermath of celebrity suicide – Media coverage and role of psychiatrists. Indian J best online viagra Psychiatry 2020;62:337-8Celebrity suicide is one of the highly publicized events in our country. Indians got a glimpse of this following an unfortunate incident where a popular Hindi film actor died of suicide. As expected, the media went into a frenzy as newspapers, news best online viagra channels, and social media were full of stories providing minute details of the suicidal act.

Some even going as far as highlighting the color of the cloth used in the suicide as well as showing the lifeless body of the actor. All kinds of personal details were dug up, and speculations and hypotheses became the order of the day in the next few days that followed. In the process, reputations of many people associated with the best online viagra actor were besmirched and their private and personal details were freely and blatantly broadcast and discussed on electronic, print, and social media. We understand that media houses have their own need and duty to report and sensationalize news for increasing their visibility (aka TRP), but such reporting has huge impacts on the mental health of the vulnerable population.The impact of this was soon realized when many incidents of copycat suicide were reported from all over the country within a few days of the incident. Psychiatrists suddenly started getting distress calls best online viagra from their patients in despair with increased suicidal ideation.

This has become a major area of concern for the psychiatry community.The Indian Psychiatric Society has been consistently trying to engage with media to promote ethical reporting of suicide. Section 24 (1) of Mental Health Care Act, 2017, forbids publication of photograph of mentally ill person without his consent.[1] The Press Council of India has adopted the best online viagra guidelines of World Health Organization report on Preventing Suicide. A resource for media professionals, which came out with an advisory to be followed by media in reporting cases of suicide. It includes points forbidding them from putting stories in prominent positions and unduly repeating them, explicitly describing the method used, providing details about the site/location, using sensational headlines, or using photographs and video footage of the incident.[2] Unfortunately, the advisory seems to have little effect in the aftermath of celebrity suicides. Channels were full of speculations about the person's mental condition and best online viagra illness and also his relationships and finances.

Many fictional accounts of his symptoms and illness were touted, which is not only against the ethics but is also contrary to MHCA, 2017.[1]It went to the extent that the name of his psychiatrist was mentioned and quotes were attributed to him without taking any account from him. The Indian Psychiatric Society has written to the Press Council of India underlining this concern and asking for measures to ensure ethics in reporting suicide.While there is a need for engagement with media to make them aware of the best online viagra grave impact of negative suicide reporting on the lives of many vulnerable persons, there is even a more urgent need for training of psychiatrists regarding the proper way of interaction with media. This has been amply brought out in the aftermath of this incident. Many psychiatrists best online viagra and mental health professionals were called by media houses to comment on the episode. Many psychiatrists were quoted, or “misquoted,” or “quoted out of context,” commenting on the life of a person whom they had never examined and had no “professional authority” to do so.

There were even stories with byline of a psychiatrist where the content provided was not only unscientific but also way beyond the expertise of a psychiatrist. These types of viewpoints perpetuate stigma, myths, and “misleading concepts” about psychiatry and are detrimental to the image of psychiatry in addition to doing harm and injustice to our patients best online viagra. Hence, the need to formulate a guideline for interaction of psychiatrists with the media is imperative.In the infamous Goldwater episode, 12,356 psychiatrists were asked to cast opinion about the fitness of Barry Goldwater for presidential candidature. Out of 2417 respondents, 1189 psychiatrists reported him to be mentally unfit while none had actually examined him.[3] This led to the formulation of “The Goldwater Rule” by the American Psychiatric Association in 1973,[4] but we have witnessed the same phenomenon at the time of presidential candidature of Donald Trump.Psychiatrists should be encouraged to interact with media to provide best online viagra scientific information about mental illnesses and reduction of stigma, but “statements to the media” can be a double-edged sword, and we should know about the rules of engagements and boundaries of interactions. Methods and principles of interaction with media should form a part of our training curriculum.

Many professional societies have guidelines and resource best online viagra books for interacting with media, and psychiatrists should familiarize themselves with these documents. The Press Council guideline is likely to prompt reporters to seek psychiatrists for their expert opinion. It is useful for them to have a template ready with suicide rates, emphasizing multicausality of suicide, role of mental disorders, as well as help available.[5]It is about time that the Indian Psychiatric Society formulated its own guidelines laying down the broad principles and boundaries governing the interaction of Indian psychiatrists with the media. Till then, it is desirable to be guided by the following broad principles:It should be assumed that no statement goes “off the record” as the media person is most likely best online viagra recording the interview, and we should also record any such conversation from our endIt should be clarified in which capacity comments are being made – professional, personal, or as a representative of an organizationOne should not comment on any person whom he has not examinedPsychiatrists should take any such opportunity to educate the public about mental health issuesThe comments should be justified and limited by the boundaries of scientific knowledge available at the moment. References Correspondence Address:Dr.

O P SinghAA 304, Ashabari Apartments, O/31, Baishnabghata, Patuli Township, Kolkata - 700 094, best online viagra West Bengal IndiaSource of Support. None, Conflict of Interest. NoneDOI. 10.4103/psychiatry.IndianJPsychiatry_816_20Abstract Electroconvulsive therapy (ECT) is an effective modality of treatment for a variety of psychiatric disorders. However, it has always been accused of being a coercive, unethical, and dangerous modality of treatment.

The dangerousness of ECT has been mainly attributed to its claimed ability to cause brain damage. This narrative review aims to provide an update of the evidence with regard to whether the practice of ECT is associated with damage to the brain. An accepted definition of brain damage remains elusive. There are also ethical and technical problems in designing studies that look at this question specifically. Thus, even though there are newer technological tools and innovations, any review attempting to answer this question would have to take recourse to indirect methods.

These include structural, functional, and metabolic neuroimaging. Body fluid biochemical marker studies. And follow-up studies of cognitive impairment and incidence of dementia in people who have received ECT among others. The review of literature and present evidence suggests that ECT has a demonstrable impact on the structure and function of the brain. However, there is a lack of evidence at present to suggest that ECT causes brain damage.Keywords.

Adverse effect, brain damage, electroconvulsive therapyHow to cite this article:Jolly AJ, Singh SM. Does electroconvulsive therapy cause brain damage. An update. Indian J Psychiatry 2020;62:339-53 Introduction Electroconvulsive therapy (ECT) as a modality of treatment for psychiatric disorders has existed at least since 1938.[1] ECT is an effective modality of treatment for various psychiatric disorders. However, from the very beginning, the practice of ECT has also faced resistance from various groups who claim that it is coercive and harmful.[2] While the ethical aspects of the practice of ECT have been dealt with elsewhere, the question of harmfulness or brain damage consequent upon the passage of electric current needs to be examined afresh in light of technological advances and new knowledge.[3]The question whether ECT causes brain damage was reviewed in a holistic fashion by Devanand et al.

In the mid-1990s.[4],[5] The authors had attempted to answer this question by reviewing the effect of ECT on the brain in various areas – cognitive side effects, structural neuroimaging studies, neuropathologic studies of patients who had received ECT, autopsy studies of epileptic patients, and finally animal ECS studies. The authors had concluded that ECT does not produce brain damage.This narrative review aims to update the evidence with regard to whether ECT causes brain damage by reviewing relevant literature from 1994 to the present time. Framing the Question The Oxford Dictionary defines damage as physical harm that impairs the value, usefulness, or normal function of something.[6] Among medical dictionaries, the Peter Collins Dictionary defines damage as harm done to things (noun) or to harm something (verb).[7] Brain damage is defined by the British Medical Association Medical Dictionary as degeneration or death of nerve cells and tracts within the brain that may be localized to a particular area of the brain or diffuse.[8] Going by such a definition, brain damage in the context of ECT should refer to death or degeneration of brain tissue, which results in the impairment of functioning of the brain. The importance of precisely defining brain damage shall become evident subsequently in this review.There are now many more tools available to investigate the structure and function of brain in health and illness. However, there are obvious ethical issues in designing human studies that are designed to answer this specific question.

Therefore, one must necessarily take recourse to indirect evidences available through studies that have been designed to answer other research questions. These studies have employed the following methods:Structural neuroimaging studiesFunctional neuroimaging studiesMetabolic neuroimaging studiesBody fluid biochemical marker studiesCognitive impairment studies.While the early studies tended to focus more on establishing the safety of ECT and finding out whether ECT causes gross microscopic brain damage, the later studies especially since the advent of advanced neuroimaging techniques have been focusing more on a mechanistic understanding of ECT. Hence, the primary objective of the later neuroimaging studies has been to look for structural and functional brain changes which might explain how ECT acts rather than evidence of gross structural damage per se. However, put together, all these studies would enable us to answer our titular question to some satisfaction. [Table 1] and [Table 2] provide an overview of the evidence base in this area.

Structural and Functional Neuroimaging Studies Devanand et al. Reviewed 16 structural neuroimaging studies on the effect of ECT on the brain.[4] Of these, two were pneumoencephalography studies, nine were computed tomography (CT) scan studies, and five were magnetic resonance imaging (MRI) studies. However, most of these studies were retrospective in design, with neuroimaging being done in patients who had received ECT in the past. In the absence of baseline neuroimaging, it would be very difficult to attribute any structural brain changes to ECT. In addition, pneumoencephalography, CT scan, and even early 0.3 T MRI provided images with much lower spatial resolution than what is available today.

The authors concluded that there was no evidence to show that ECT caused any structural damage to the brain.[4] Since then, at least twenty more MRI-based structural neuroimaging studies have studied the effect of ECT on the brain. The earliest MRI studies in the early 1990s focused on detecting structural damage following ECT. All of these studies were prospective in design, with the first MRI scan done at baseline and a second MRI scan performed post ECT.[9],[11],[12],[13],[41] While most of the studies imaged the patient once around 24 h after receiving ECT, some studies performed multiple post ECT neuroimaging in the first 24 h after ECT to better capture the acute changes. A single study by Coffey et al. Followed up the patients for a duration of 6 months and repeated neuroimaging again at 6 months in order to capture any long-term changes following ECT.[10]The most important conclusion which emerged from this early series of studies was that there was no evidence of cortical atrophy, change in ventricle size, or increase in white matter hyperintensities.[4] The next major conclusion was that there appeared to be an increase in the T1 and T2 relaxation time immediately following ECT, which returned to normal within 24 h.

This supported the theory that immediately following ECT, there appears to be a temporary breakdown of the blood–brain barrier, leading to water influx into the brain tissue.[11] The last significant observation by Coffey et al. In 1991 was that there was no significant temporal changes in the total volumes of the frontal lobes, temporal lobes, or amygdala–hippocampal complex.[10] This was, however, something which would later be refuted by high-resolution MRI studies. Nonetheless, one inescapable conclusion of these early studies was that there was no evidence of any gross structural brain changes following administration of ECT. Much later in 2007, Szabo et al. Used diffusion-weighted MRI to image patients in the immediate post ECT period and failed to observe any obvious brain tissue changes following ECT.[17]The next major breakthrough came in 2010 when Nordanskog et al.

Demonstrated that there was a significant increase in the volume of the hippocampus bilaterally following a course of ECT in a cohort of patients with depressive illness.[18] This contradicted the earlier observations by Coffey et al. That there was no volume increase in any part of the brain following ECT.[10] This was quite an exciting finding and was followed by several similar studies. However, the perspective of these studies was quite different from the early studies. In contrast to the early studies looking for the evidence of ECT-related brain damage, the newer studies were focused more on elucidating the mechanism of action of ECT. Further on in 2014, Nordanskog et al.

In a follow-up study showed that though there was a significant increase in the volume of the hippocampus 1 week after a course of ECT, the hippocampal volume returned to the baseline after 6 months.[19] Two other studies in 2013 showed that in addition to the hippocampus, the amygdala also showed significant volume increase following ECT.[20],[21] A series of structural neuroimaging studies after that have expanded on these findings and as of now, gray matter volume increase following ECT has been demonstrated in the hippocampus, amygdala, anterior temporal pole, subgenual cortex,[21] right caudate nucleus, and the whole of the medial temporal lobe (MTL) consisting of the hippocampus, amygdala, insula, and the posterosuperior temporal cortex,[24] para hippocampi, right subgenual anterior cingulate gyrus, and right anterior cingulate gyrus,[25] left cerebellar area VIIa crus I,[29] putamen, caudate nucleus, and nucleus acumbens [31] and clusters of increased cortical thickness involving the temporal pole, middle and superior temporal cortex, insula, and inferior temporal cortex.[27] However, the most consistently reported and replicated finding has been the bilateral increase in the volume of the hippocampus and amygdala. In light of these findings, it has been tentatively suggested that ECT acts by inducing neuronal regeneration in the hippocampus – amygdala complex.[42],[43] However, there are certain inconsistencies to this hypothesis. Till date, only one study – Nordanskog et al., 2014 – has followed study patients for a long term – 6 months in their case. And significantly, the authors found out that after increasing immediately following ECT, the hippocampal volume returns back to baseline by 6 months.[19] This, however, was not associated with the relapse of depressive symptoms. Another area of significant confusion has been the correlation of hippocampal volume increase with improvement of depressive symptoms.

Though almost all studies demonstrate a significant increase in hippocampal volume following ECT, a majority of studies failed to demonstrate a correlation between symptom improvement and hippocampal volume increase.[19],[20],[22],[24],[28] However, a significant minority of volumetric studies have demonstrated correlation between increase in hippocampal and/or amygdala volume and improvement of symptoms.[21],[25],[30]Another set of studies have used diffusion tensor imaging, functional MRI (fMRI), anatomical connectome, and structural network analysis to study the effect of ECT on the brain. The first of these studies by Abbott et al. In 2014 demonstrated that on fMRI, the connectivity between right and left hippocampus was significantly reduced in patients with severe depression. It was also shown that the connectivity was normalized following ECT, and symptom improvement was correlated with an increase in connectivity.[22] In a first of its kind DTI study, Lyden et al. In 2014 demonstrated that fractional anisotropy which is a measure of white matter tract or fiber density is increased post ECT in patients with severe depression in the anterior cingulum, forceps minor, and the dorsal aspect of the left superior longitudinal fasciculus.

The authors suggested that ECT acts to normalize major depressive disorder-related abnormalities in the structural connectivity of the dorsal fronto-limbic pathways.[23] Another DTI study in 2015 constructed large-scale anatomical networks of the human brain – connectomes, based on white matter fiber tractography. The authors found significant reorganization in the anatomical connections involving the limbic structure, temporal lobe, and frontal lobe. It was also found that connection changes between amygdala and para hippocampus correlated with reduction in depressive symptoms.[26] In 2016, Wolf et al. Used a source-based morphometry approach to study the structural networks in patients with depression and schizophrenia and the effect of ECT on the same. It was found that the medial prefrontal cortex/anterior cingulate cortex (ACC/MPFC) network, MTL network, bilateral thalamus, and left cerebellar regions/precuneus exhibited significant difference between healthy controls and the patient population.

It was also demonstrated that administration of ECT leads to significant increase in the network strength of the ACC/MPFC network and the MTL network though the increase in network strength and symptom amelioration were not correlated.[32]Building on these studies, a recently published meta-analysis has attempted a quantitative synthesis of brain volume changes – focusing on hippocampal volume increase following ECT in patients with major depressive disorder and bipolar disorder. The authors initially selected 32 original articles from which six articles met the criteria for quantitative synthesis. The results showed significant increase in the volume of the right and left hippocampus following ECT. For the rest of the brain regions, the heterogeneity in protocols and imaging techniques did not permit a quantitative analysis, and the authors have resorted to a narrative review similar to the present one with similar conclusions.[44] Focusing exclusively on hippocampal volume change in ECT, Oltedal et al. In 2018 conducted a mega-analysis of 281 patients with major depressive disorder treated with ECT enrolled at ten different global sites of the Global ECT-MRI Research Collaboration.[45] Similar to previous studies, there was a significant increase in hippocampal volume bilaterally with a dose–response relationship with the number of ECTs administered.

Furthermore, bilateral (B/L) ECT was associated with an equal increase in volume in both right and left hippocampus, whereas right unilateral ECT was associated with greater volume increase in the right hippocampus. Finally, contrary to expectation, clinical improvement was found to be negatively correlated with hippocampal volume.Thus, a review of the current evidence amply demonstrates that from looking for ECT-related brain damage – and finding none, we have now moved ahead to looking for a mechanistic understanding of the effect of ECT. In this regard, it has been found that ECT does induce structural changes in the brain – a fact which has been seized upon by some to claim that ECT causes brain damage.[46] Such statements should, however, be weighed against the definition of damage as understood by the scientific medical community and patient population. Neuroanatomical changes associated with effective ECT can be better described as ECT-induced brain neuroplasticity or ECT-induced brain neuromodulation rather than ECT-induced brain damage. Metabolic Neuroimaging Studies.

Magnetic Resonance Spectroscopic Imaging Magnetic resonance spectroscopic imaging (MRSI) uses a phase-encoding procedure to map the spatial distribution of magnetic resonance (MR) signals of different molecules. The crucial difference, however, is that while MRI maps the MR signals of water molecules, MRSI maps the MR signals generated by different metabolites – such as N-acetyl aspartate (NAA) and choline-containing compounds. However, the concentration of these metabolites is at least 10,000 times lower than water molecules and hence the signal strength generated would also be correspondingly lower. However, MRSI offers us the unique advantage of studying in vivo the change in the concentration of brain metabolites, which has been of great significance in fields such as psychiatry, neurology, and basic neuroscience research.[47]MRSI studies on ECT in patients with depression have focused largely on four metabolites in the human brain – NAA, choline-containing compounds (Cho) which include majorly cell membrane compounds such as glycerophosphocholine, phosphocholine and a miniscule contribution from acetylcholine, creatinine (Cr) and glutamine and glutamate together (Glx). NAA is located exclusively in the neurons, and is suggested to be a marker of neuronal viability and functionality.[48] Choline-containing compounds (Cho) mainly include the membrane compounds, and an increase in Cho would be suggestive of increased membrane turnover.

Cr serves as a marker of cellular energy metabolism, and its levels are usually expected to remain stable. The regions which have been most widely studied in MRSI studies include the bilateral hippocampus and amygdala, dorsolateral prefrontal cortex (DLPFC), and ACC.Till date, five MRSI studies have measured NAA concentration in the hippocampus before and after ECT. Of these, three studies showed that there is no significant change in the NAA concentration in the hippocampus following ECT.[33],[38],[49] On the other hand, two recent studies have demonstrated a statistically significant reduction in NAA concentration in the hippocampus following ECT.[39],[40] The implications of these results are of significant interest to us in answering our titular question. A normal level of NAA following ECT could signify that there is no significant neuronal death or damage following ECT, while a reduction would signal the opposite. However, a direct comparison between these studies is complicated chiefly due to the different ECT protocols, which has been used in these studies.

It must, however, be acknowledged that the three older studies used 1.5 T MRI, whereas the two newer studies used a higher 3 T MRI which offers betters signal-to-noise ratio and hence lesser risk of errors in the measurement of metabolite concentrations. The authors of a study by Njau et al.[39] argue that a change in NAA levels might reflect reversible changes in neural metabolism rather than a permanent change in the number or density of neurons and also that reduced NAA might point to a change in the ratio of mature to immature neurons, which, in fact, might reflect enhanced adult neurogenesis. Thus, the authors warn that to conclude whether a reduction in NAA concentration is beneficial or harmful would take a simultaneous measurement of cognitive functioning, which was lacking in their study. In 2017, Cano et al. Also demonstrated a significant reduction in NAA/Cr ratio in the hippocampus post ECT.

More significantly, the authors also showed a significant increase in Glx levels in the hippocampus following ECT, which was also associated with an increase in hippocampal volume.[40] To explain these three findings, the authors proposed that ECT produces a neuroinflammatory response in the hippocampus – likely mediated by Glx, which has been known to cause inflammation at higher concentrations, thereby accounting for the increase in hippocampal volume with a reduction in NAA concentration. The cause for the volume increase remains unclear – with the authors speculating that it might be due to neuronal swelling or due to angiogenesis. However, the same study and multiple other past studies [21],[25],[30] have demonstrated that hippocampal volume increase was correlated with clinical improvement following ECT. Thus, we are led to the hypothesis that the same mechanism which drives clinical improvement with ECT is also responsible for the cognitive impairment following ECT. Whether this is a purely neuroinflammatory response or a neuroplastic response or a neuroinflammatory response leading to some form of neuroplasticity is a critical question, which remains to be answered.[40]Studies which have analyzed NAA concentration change in other brain areas have also produced conflicting results.

The ACC is another area which has been studied in some detail utilizing the MRSI technique. In 2003, Pfleiderer et al. Demonstrated that there was no significant change in the NAA and Cho levels in the ACC following ECT. This would seem to suggest that there was no neurogenesis or membrane turnover in the ACC post ECT.[36] However, this finding was contested by Merkl et al. In 2011, who demonstrated that NAA levels were significantly reduced in the left ACC in patients with depression and that these levels were significantly elevated following ECT.[37] This again is contested by Njau et al.

Who showed that NAA levels are significantly reduced following ECT in the left dorsal ACC.[39] A direct comparison of these three studies is complicated by the different ECT and imaging parameters used and hence, no firm conclusion can be made on this point at this stage. In addition to this, one study had demonstrated increased NAA levels in the amygdala following administration of ECT,[34] with a trend level increase in Cho levels, which again is suggestive of neurogenesis and/or neuroplasticity. A review of studies on the DLPFC reveals a similarly confusing picture with one study, each showing no change, reduction, and elevation of concentration of NAA following ECT.[35],[37],[39] Here, again, a direct comparison of the three studies is made difficult by the heterogeneous imaging and ECT protocols followed by them.A total of five studies have analyzed the concentration of choline-containing compounds (Cho) in patients undergoing ECT. Conceptually, an increase in Cho signals is indicative of increased membrane turnover, which is postulated to be associated with synaptogenesis, neurogenesis, and maturation of neurons.[31] Of these, two studies measured Cho concentration in the B/L hippocampus, with contrasting results. Ende et al.

In 2000 demonstrated a significant elevation in Cho levels in B/L hippocampus after ECT, while Jorgensen et al. In 2015 failed to replicate the same finding.[33],[38] Cho levels have also been studied in the amygdala, ACC, and the DLPFC. However, none of these studies showed a significant increase or decrease in Cho levels before and after ECT in the respective brain regions studied. In addition, no significant difference was seen in the pre-ECT Cho levels of patients compared to healthy controls.[34],[36],[37]In review, we must admit that MRSI studies are still at a preliminary stage with significant heterogeneity in ECT protocols, patient population, and regions of the brain studied. At this stage, it is difficult to draw any firm conclusions except to acknowledge the fact that the more recent studies – Njau et al., 2017, Cano, 2017, and Jorgensen et al., 2015 – have shown decrease in NAA concentration and no increase in Cho levels [38],[39],[40] – as opposed to the earlier studies by Ende et al.[33] The view offered by the more recent studies is one of a neuroinflammatory models of action of ECT, probably driving neuroplasticity in the hippocampus.

This would offer a mechanistic understanding of both clinical response and the phenomenon of cognitive impairment associated with ECT. However, this conclusion is based on conjecture, and more work needs to be done in this area. Body Fluid Biochemical Marker Studies Another line of evidence for analyzing the effect of ECT on the human brain is the study of concentration of neurotrophins in the plasma or serum. Neurotrophins are small protein molecules which mediate neuronal survival and development. The most prominent among these is brain-derived neurotrophic factor (BDNF) which plays an important role in neuronal survival, plasticity, and migration.[50] A neurotrophic theory of mood disorders was suggested which hypothesized that depressive disorders are associated with a decreased expression of BDNF in the limbic structures, resulting in the atrophy of these structures.[51] It was also postulated that antidepressant treatment has a neurotrophic effect which reverses the neuronal cell loss, thereby producing a therapeutic effect.

It has been well established that BDNF is decreased in mood disorders.[52] It has also been shown that clinical improvement of depression is associated with increase in BDNF levels.[53] Thus, serum BDNF levels have been tentatively proposed as a biomarker for treatment response in depression. Recent meta-analytic evidence has shown that ECT is associated with significant increase in serum BDNF levels in patients with major depressive disorder.[54] Considering that BDNF is a potent stimulator of neurogenesis, the elevation of serum BDNF levels following ECT lends further credence to the theory that ECT leads to neurogenesis in the hippocampus and other limbic structures, which, in turn, mediates the therapeutic action of ECT. Cognitive Impairment Studies Cognitive impairment has always been the single-most important side effect associated with ECT.[55] Concerns regarding long-term cognitive impairment surfaced soon after the introduction of ECT and since then has grown to become one of the most controversial aspects of ECT.[56] Anti-ECT groups have frequently pointed out to cognitive impairment following ECT as evidence of ECT causing brain damage.[56] A meta-analysis by Semkovska and McLoughlin in 2010 is one of the most detailed studies which had attempted to settle this long-standing debate.[57] The authors reviewed 84 studies (2981 participants), which had used a combined total of 22 standardized neuropsychological tests assessing various cognitive functions before and after ECT in patients diagnosed with major depressive disorder. The different cognitive domains reviewed included processing speed, attention/working memory, verbal episodic memory, visual episodic memory, spatial problem-solving, executive functioning, and intellectual ability. The authors concluded that administration of ECT for depression is associated with significant cognitive impairment in the first few days after ECT administration.

However, it was also seen that impairment in cognitive functioning resolved within a span of 2 weeks and thereafter, a majority of cognitive domains even showed mild improvement compared to the baseline performance. It was also demonstrated that not a single cognitive domain showed persistence of impairment beyond 15 days after ECT.Memory impairment following ECT can be analyzed broadly under two conceptual schemes – one that classifies memory impairment as objective memory impairment and subjective memory impairment and the other that classifies it as impairment in anterograde memory versus impairment in retrograde memory. Objective memory can be roughly defined as the ability to retrieve stored information and can be measured by various standardized neuropsychological tests. Subjective memory or meta-memory, on the other hand, refers to the ability to make judgments about one's ability to retrieve stored information.[58] As described previously, it has been conclusively demonstrated that anterograde memory impairment does not persist beyond 2 weeks after ECT.[57] However, one of the major limitations of this meta-analysis was the lack of evidence on retrograde amnesia following ECT. This is particularly unfortunate considering that it is memory impairment – particularly retrograde amnesia which has received the most attention.[59] In addition, reports of catastrophic retrograde amnesia have been repeatedly held up as sensational evidence of the lasting brain damage produced by ECT.[59] Admittedly, studies on retrograde amnesia are fewer and less conclusive than on anterograde amnesia.[60],[61] At present, the results are conflicting, with some studies finding some impairment in retrograde memory – particularly autobiographical retrograde memory up to 6 months after ECT.[62],[63],[64],[65] However, more recent studies have failed to support this finding.[66],[67] While they do demonstrate an impairment in retrograde memory immediately after ECT, it was seen that this deficit returned to pre-ECT levels within a span of 1–2 months and improved beyond baseline performance at 6 months post ECT.[66] Adding to the confusion are numerous factors which confound the assessment of retrograde amnesia.

It has been shown that depressive symptoms can produce significant impairment of retrograde memory.[68],[69] It has also been demonstrated that sine-wave ECT produces significantly more impairment of retrograde memory as compared to brief-pulse ECT.[70] However, from the 1990s onward, sine-wave ECT has been completely replaced by brief-pulse ECT, and it is unclear as to the implications of cognitive impairment from the sine-wave era in contemporary ECT practice.Another area of concern are reports of subjective memory impairment following ECT. One of the pioneers of research into subjective memory impairment were Squire and Chace who published a series of studies in the 1970s demonstrating the adverse effect of bilateral ECT on subjective assessment of memory.[62],[63],[64],[65] However, most of the studies conducted post 1980 – from when sine-wave ECT was replaced by brief-pulse ECT report a general improvement in subjective memory assessments following ECT.[71] In addition, most of the recent studies have failed to find a significant association between measures of subjective and objective memory.[63],[66],[70],[72],[73],[74] It has also been shown that subjective memory impairment is strongly associated with the severity of depressive symptoms.[75] In light of these facts, the validity and value of measures of subjective memory impairment as a marker of cognitive impairment and brain damage following ECT have been questioned. However, concerns regarding subjective memory impairment and catastrophic retrograde amnesia continue to persist, with significant dissonance between the findings of different research groups and patient self-reports in various media.[57]Some studies reported the possibility of ECT being associated with the development of subsequent dementia.[76],[77] However, a recent large, well-controlled prospective Danish study found that the use of ECT was not associated with elevated incidence of dementia.[78] Conclusion Our titular question is whether ECT leads to brain damage, where damage indicates destruction or degeneration of nerves or nerve tracts in the brain, which leads to loss of function. This issue was last addressed by Devanand et al. In 1994 since which time our understanding of ECT has grown substantially, helped particularly by the advent of modern-day neuroimaging techniques which we have reviewed in detail.

And, what these studies reveal is rather than damaging the brain, ECT has a neuromodulatory effect on the brain. The various lines of evidence – structural neuroimaging studies, functional neuroimaging studies, neurochemical and metabolic studies, and serum BDNF studies all point toward this. These neuromodulatory changes have been localized to the hippocampus, amygdala, and certain other parts of the limbic system. How exactly these changes mediate the improvement of depressive symptoms is a question that remains unanswered. However, there is little by way of evidence from neuroimaging studies which indicates that ECT causes destruction or degeneration of neurons.

Though cognitive impairment studies do show that there is objective impairment of certain functions – particularly memory immediately after ECT, these impairments are transient with full recovery within a span of 2 weeks. Perhaps, the single-most important unaddressed concern is retrograde amnesia, which has been shown to persist for up to 2 months post ECT. In this regard, the recent neurometabolic studies have offered a tentative mechanism of action of ECT, producing a transient inflammation in the limbic cortex, which, in turn, drives neurogenesis, thereby exerting a neuromodulatory effect. This hypothesis would explain both the cognitive adverse effects of ECT – due to the transient inflammation – and the long-term improvement in mood – neurogenesis in the hippocampus. Although unproven at present, such a hypothesis would imply that cognitive impairment is tied in with the mechanism of action of ECT and not an indicator of damage to the brain produced by ECT.The review of literature suggests that ECT does cause at least structural and functional changes in the brain, and these are in all probability related to the effects of the ECT.

However, these cannot be construed as brain damage as is usually understood. Due to the relative scarcity of data that directly examines the question of whether ECT causes brain damage, it is not possible to conclusively answer this question. However, in light of enduring ECT survivor accounts, there is a need to design studies that specifically answer this question.Financial support and sponsorshipNil.Conflicts of interestThere are no conflicts of interest. References 1.Payne NA, Prudic J. Electroconvulsive therapy.

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37.Merkl A, Schubert F, Quante A, Luborzewski A, Brakemeier EL, Grimm S, et al. Abnormal cingulate and prefrontal cortical neurochemistry in major depression after electroconvulsive therapy. Biol Psychiatry 2011;69:772-9. 38.Jorgensen A, Magnusson P, Hanson LG, Kirkegaard T, Benveniste H, Lee H, et al. Regional brain volumes, diffusivity, and metabolite changes after electroconvulsive therapy for severe depression.

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Subjective memory complaints prior to and following electroconvulsive therapy. Biol Psychiatry 1996;39:346-56. 76.Berggren Š, Gustafson L, Höglund P, Johanson A. A long-term longitudinal follow-up of depressed patients treated with ECT with special focus on development of dementia. J Affect Disord 2016;200:15-24.

77.Brodaty H, Hickie I, Mason C, Prenter L. A prospective follow-up study of ECT outcome in older depressed patients. J Affect Disord 2000;60:101-11. 78.Osler M, Rozing MP, Christensen GT, Andersen PK, Jørgensen MB. Electroconvulsive therapy and risk of dementia in patients with affective disorders.

A cohort study. Lancet Psychiatry 2018;5:348-56. Correspondence Address:Dr. Shubh Mohan SinghDepartment of Psychiatry, Postgraduate Institute of Medical Education and Research, Chandigarh IndiaSource of Support. None, Conflict of Interest.

NoneDOI. 10.4103/psychiatry.IndianJPsychiatry_239_19 Tables [Table 1], [Table 2].

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Peru Scientists declared a Liolaemus lizard the discount viagra world's highest-altitude reptile after a population was spotted at site here 5,400 meters in the Andes. These lizards must endure frigid temperatures, a particular challenge for cold-blooded animals, as well as reduced oxygen and increased ultraviolet radiation. Algeria Analysis suggests a meteorite from the Sahara Desert contains discount viagra material as old as, or older than, Earth itself.

The meteorite holds the oldest-known sample of magma from space and most likely came from a protoplanet forming in the early solar system. Egypt An excavation on the Red Sea coast revealed what seems to be a pet cemetery from nearly 2,000 years ago, the earliest yet identified. Nearly 600 cats, dogs and monkeys—mostly cats—were carefully buried, many with textiles, pottery or ornate collars discount viagra.

China Researchers tested a new soft-body swimming robot first in a lake, next in the South China Sea, and finally in the Mariana Trench—almost 11,000 meters down—to prove it can flap its fins in extreme pressure as it explores the depths. Borneo Scientists captured dung beetles in a forest in Sabah, dissected them, then sequenced the DNA in their guts to find matches with nearby wildlife. Because dung lasts within the beetles for about 48 hours, this method can reveal discount viagra a location's recent visitors and inhabitants.

New Zealand Conservation rangers worked with hundreds of volunteers to “refloat” 40 stranded long-finned pilot whales, returning them to open water. Nine more of the discount viagra beached whales died.Picture the scene. A small drone the size of a suitcase descends into a dark Martian crevasse—perhaps a lava tube that was formed billions of years ago by volcanic activity on the Red Planet.

The drone illuminates its surroundings, recording views never seen before by human eyes as its suite of instruments seeks out signs of past or present alien biology. Finally, its reconnaissance complete, the drone flies back discount viagra to a landing zone on the surface to transmit invaluable data back to Earth. After soaking up the Martian sunlight to recharge its batteries, it continues its explorations of terrain inaccessible to any other machine.

Far from being some starry-eyed flight of fancy, such a mission could soon become a reality thanks to the resounding success of NASA’s Ingenuity rotorcraft, sometimes referred to as a helicopter or drone—a technology demonstration that has taken place on Mars over the past few weeks. Carried to the planet by NASA’s Perseverance rover, which touched discount viagra down on February 18, this small machine, weighing a paltry 1.8 kilograms, was the first attempt at controlled aerial flight on another world—more than a century after that same feat was mastered on Earth by the Wright brothers. €œWe can now say that human beings have flown a rover craft on another planet,” said MiMi Aung, project manager of Ingenuity at NASA’s Jet Propulsion Laboratory (JPL), in a speech to her team from mission control following the successful first flight on April 19.

€œWe together now have our Wright brothers moment.” With Ingenuity’s success, space scientists are contemplating the roles that aerial vehicles might play in our exploration of the discount viagra solar system. Few worlds possess the necessary conditions for powered aerodynamic flight, namely an atmosphere and rocky surface like that of Mars or Earth, but there are two others of note. €œThe general technique of aerial flight is applicable to places like [Saturn’s moon] Titan and Venus,” said Bob Balaram, chief engineer of the Ingenuity team, in a press briefing following the first flight.

The latter’s exceedingly high temperatures and pressures pose discount viagra some unique challenges. €œNear the surface it’s closer to swimming,” says Paul Byrne, a planetary scientist at North Carolina State University. Yet flight there is not impossible, which was proved by the Soviet Union’s Vega balloons in 1985.

With a rotorcraft called Dragonfly already being developed to visit Titan in discount viagra the next decade and work continuing on a conceptual successor to Ingenuity, the future looks bright for aerial exploration of alien worlds. €œThis could be the start of a new era,” Byrne says. Ingenuity’s first flight, from a strip of land on Mars’s Jezero Crater that is discount viagra now dubbed “Wright Brothers Field,” was modest but impressive.

The planet’s atmosphere is incredibly thin, just 1 percent that of Earth, so generating lift is exceedingly difficult. €œIt’s similar to Earth at about 100,000 feet above the ground,” says Ben Pipenberg, an engineer at defense contractor AeroVironment, who helped build Ingenuity. With Perseverance watching from a safe discount viagra distance, Ingenuity spun its blades at 2,500 revolutions per minute (rpm) to rise to an altitude of three meters, where it hovered for 30 seconds and performed a 96-degree rotation.

Then it descended back to the ground, landing on its four legs, with a total flight time of 39.1 seconds. From there, things got more complex. The second flight lasted 51.9 seconds, reaching discount viagra a height of five meters.

And it included a lateral movement of about two meters—something not attempted in the confines of the test chamber on Earth where Ingenuity first flew in simulated Mars conditions. Flight three saw Ingenuity travel half the length of a football field, some 50 meters, reaching a top discount viagra speed of just more than two meters per second. The fourth flight on April 30 pushed the envelope once again, with Ingenuity remaining airborne for nearly two minutes—117 seconds—and reaching an impressive speed of 3.5 meters per second as it scouted a potential future landing zone over a round trip of more than 260 meters.

Ingenuity’s fifth flight—completed on May 7 and initially planned to be its last—sent it on a one-way trip to the new landing zone to await the arrival of Perseverance, its mothership. Now, this wildly successful technology demonstration drone is entering a new phase of its mission—a second discount viagra month-long set of more ambitious operational tests. These tests are meant to show how airborne drones “could play an active role in a future rover science mission,” says Dave Lavery, the program executive for Ingenuity at NASA headquarters in Washington, DC.

Although Ingenuity will not directly support the science objectives of Perseverance, namely looking for signs of past life on Mars, it will help scout out the rover’s potential route ahead as the team plans their optimal path through Jezero Crater’s riches, or even photograph nearby locations not in the rover’s planned path. There is even a slim chance Ingenuity could support discount viagra the rover’s later mission too, if it survives. €œWe might see about potentially looking over the rim of the crater,” Lavery says.

Much has been made of how these vehicles might one day support human missions, acting as reconnaissance drones for humans to scout out regions of interest near a landing site or carrying tools between locations. In the near-term, prospects of more exciting robotic science are on the horizon—perhaps in the same way that the Sojourner discount viagra rover in 1997, itself a prototype of wheeled exploration and part of NASA’s Pathfinder mission, paved the way for its successors Spirit, Opportunity, Curiosity and now Perseverance. €œI do think we’re going to see some flying vehicles in the future,” says Michael Meyer, lead scientist of NASA’s Mars Exploration Program at the agency’s headquarters in Washington, D.C.

€œIt will now be part of our portfolio of methods that we discount viagra use for exploration. There are things you can do with a helicopter that you can’t do with other platforms.” Examples could include exploring the aforementioned lava tubes or perhaps approaching crater walls—too high and steep for a rover to scale—where a helicopter could take images and perform some up-close analysis as well. Another example could be studying recurring slope lineae, dark flows on Mars that have arguably been linked to liquid water flowing on the surface.

Perversely, it is this possibility of water—and the accompanying risk of contamination with bacteria imported from Earth—that essentially prohibits anyone or anything from setting discount viagra foot (or wheel) there to seek out signs of native Martian life. But a hovering drone could look without touching, offering a novel route of exploration. €œA rotorcraft would give us the ability to go and look up close at something that we would otherwise deem not suitable for a rover,” Byrne says, “either because of planetary protection issues or because it’s too dangerous.” One concept for a possible aerial vehicle beyond Ingenuity is already being investigated.

Known as the Mars discount viagra Science Helicopter, this six-bladed hexacopter would weigh nearly 30 kilograms. And it would be equipped with several kilograms worth of instruments to analyze different regions of the Martian surface and would have the ability to fly for minutes at a time over several kilometers. €œWe’re trying to learn from Ingenuity and ask ourselves, ‘What could we accomplish discount viagra if we push it further?.

€™â€ says Theodore Tzanetos of JPL, who is part of the Mars Science Helicopter concept team. The science such traits would afford would be tremendous, bringing large swathes of the Martian surface suddenly within reach. The current distance record on Mars is discount viagra held by NASA’s Opportunity rover, which traveled more than 42 kilometers in a little more than 11 years.

A helicopter could achieve the same feat in weeks. Other ideas involve using rotorcraft to perform surveys of exposed water ice on regions of the Martian surface inaccessible to rovers. Drones could dive into Martian valleys like the two-kilometer-deep Mawrth Vallis, looking for evidence of clays linked to discount viagra astrobiology, or perhaps use instruments to probe the lower reaches of the Martian atmosphere says Shannah Withrow-Maser, the Mars Science Helicopter vehicle systems lead at NASA’s Ames Research Center in California.

And this could all be done either alongside a bigger rover mission or as more cost-effective and much lighter standalone missions, enabling more widespread exploration of a variety of Martian locales. €œI personally would love that,” says Withrow-Maser discount viagra. Elsewhere in the solar system, flight options are more limited.

One could imagine a rotorcraft in the atmosphere of one of the gas giants such as Jupiter or Saturn, where theoretically flight would be possible. But actually getting discount viagra there would be an issue. €œThe problem, of course, is slowing down and the amount of energy that would take” on arrival at the planet, Byrne says.

But Titan, Saturn’s intriguing moon with an incredibly thick atmosphere and lakes of hydrocarbons on its surface, is a very tantalizing prospect. In 2019 NASA selected a mission that would attempt to discount viagra deploy the rotorcraft Dragonfly on the moon. Dragonfly is intended to launch as early as 2026 and arrive in 2034, and its team has been watching Ingenuity’s successes very closely.

€œWe’ve been following with great interest,” says Elizabeth Turtle, lead of discount viagra the Dragonfly mission at the Johns Hopkins University Applied Physics Laboratory. €œWe’re very anxious to see what lessons we can take forward to Dragonfly.” Like Ingenuity, Dragonfly will be flying autonomously, so it will make use of similar onboard image processing capabilities to decide where to land on the Titanian surface. (Ingenuity performs terrain mapping by taking 30 images of the ground per second.) But Dragonfly is a mammoth compared to Ingenuity, weighing nearly half a metric ton and powered by plutonium.

And it is a discount viagra standalone mission rather than a ride along like Ingenuity. €œIt’s like Perseverance [in scale], except we fly instead of drive across the surface,” Turtle says. Despite Titan being a much more distant alien world than Mars—with a light travel time from Earth of about an hour, compared with up to about 20 minutes for the Red Planet—flight is relatively easier there.

Titan’s gravity is only 14 percent that of Earth and much discount viagra less than that of Mars, while the moon’s much thicker atmosphere makes generating lift a comparative breeze. €œA person could put wings on and soar over Titan’s surface,” Turtle says. Winds on discount viagra Titan are also much slower, barely more than a kilometer an hour versus tens of kilometers an hour on Mars.

And whereas Ingenuity’s blades require 2,500 rpm to lift its fragile 1.8-kg body off the surface, Dragonfly’s half-metric-ton bulk can be lofted just by its rotors spinning at 800 rpm. Titan’s major challenge is its temperature, which averages only about –180 degrees Celsius—hence the need for a long-lived, heat-generating plutonium power source. €œIt’s certainly cold,” Turtle says discount viagra.

€œIt’s a nontrivial challenge.” With Dragonfly on the horizon, and perhaps future missions such as the Mars Science Helicopter in the works, there is plenty to be excited about beyond Ingenuity. This little machine has, for the first time, proved flight on alien worlds is possible—from both a physical and logistical point of view. Now this exciting new era of discovery discount viagra awaits, and while only a handful of worlds afford the right conditions for this method of exploration, the sky is very much the limit for the science that could be performed by aerial vehicles in these alien skies.

€œThere are things to be sorted out,” Meyer says. €œThen I think we’re going to start seeing some new and improved helicopter platforms that can actually carry tempting payloads.”.

Peru Scientists declared a Liolaemus lizard the world's highest-altitude best online viagra reptile after a population was spotted at 5,400 meters in the Andes. These lizards must endure frigid temperatures, a particular challenge for cold-blooded animals, as well as reduced oxygen and increased ultraviolet radiation. Algeria Analysis suggests a meteorite from the Sahara Desert best online viagra contains material as old as, or older than, Earth itself. The meteorite holds the oldest-known sample of magma from space and most likely came from a protoplanet forming in the early solar system.

Egypt An excavation on the Red Sea coast revealed what seems to be a pet cemetery from nearly 2,000 years ago, the earliest yet identified. Nearly 600 cats, dogs and monkeys—mostly cats—were carefully buried, many with textiles, best online viagra pottery or ornate collars. China Researchers tested a new soft-body swimming robot first in a lake, next in the South China Sea, and finally in the Mariana Trench—almost 11,000 meters down—to prove it can flap its fins in extreme pressure as it explores the depths. Borneo Scientists captured dung beetles in a forest in Sabah, dissected them, then sequenced the DNA in their guts to find matches with nearby wildlife.

Because dung lasts within the beetles for about 48 hours, this method can reveal a best online viagra location's recent visitors and inhabitants. New Zealand Conservation rangers worked with hundreds of volunteers to “refloat” 40 stranded long-finned pilot whales, returning them to open water. Nine more of the beached whales died.Picture best online viagra the scene. A small drone the size of a suitcase descends into a dark Martian crevasse—perhaps a lava tube that was formed billions of years ago by volcanic activity on the Red Planet.

The drone illuminates its surroundings, recording views never seen before by human eyes as its suite of instruments seeks out signs of past or present alien biology. Finally, its reconnaissance complete, the drone flies back to a landing zone on the surface best online viagra to transmit invaluable data back to Earth. After soaking up the Martian sunlight to recharge its batteries, it continues its explorations of terrain inaccessible to any other machine. Far from being some starry-eyed flight of fancy, such a mission could soon become a reality thanks to the resounding success of NASA’s Ingenuity rotorcraft, sometimes referred to as a helicopter or drone—a technology demonstration that has taken place on Mars over the past few weeks.

Carried to the planet by NASA’s Perseverance rover, which touched down on February 18, this small machine, weighing a paltry 1.8 kilograms, was the first attempt at controlled aerial flight on another world—more than a century after that same feat was mastered on Earth by the best online viagra Wright brothers. €œWe can now say that human beings have flown a rover craft on another planet,” said MiMi Aung, project manager of Ingenuity at NASA’s Jet Propulsion Laboratory (JPL), in a speech to her team from mission control following the successful first flight on April 19. €œWe together now have our Wright brothers moment.” With Ingenuity’s success, space scientists are contemplating the roles that aerial vehicles might play in our exploration of the best online viagra solar system. Few worlds possess the necessary conditions for powered aerodynamic flight, namely an atmosphere and rocky surface like that of Mars or Earth, but there are two others of note.

€œThe general technique of aerial flight is applicable to places like [Saturn’s moon] Titan and Venus,” said Bob Balaram, chief engineer of the Ingenuity team, in a press briefing following the first flight. The latter’s best online viagra exceedingly high temperatures and pressures pose some unique challenges. €œNear the surface it’s closer to swimming,” says Paul Byrne, a planetary scientist at North Carolina State University. Yet flight there is not impossible, which was proved by the Soviet Union’s Vega balloons in 1985.

With a rotorcraft called Dragonfly already being developed to visit Titan in the next decade and work continuing on a conceptual successor to Ingenuity, the future looks bright for aerial exploration of alien worlds best online viagra. €œThis could be the start of a new era,” Byrne says. Ingenuity’s first flight, from a strip of land on Mars’s Jezero Crater that is now dubbed “Wright best online viagra Brothers Field,” was modest but impressive. The planet’s atmosphere is incredibly thin, just 1 percent that of Earth, so generating lift is exceedingly difficult.

€œIt’s similar to Earth at about 100,000 feet above the ground,” says Ben Pipenberg, an engineer at defense contractor AeroVironment, who helped build Ingenuity. With Perseverance watching from a safe distance, Ingenuity spun its blades at 2,500 revolutions per minute (rpm) to rise to an altitude of three meters, where it hovered for 30 seconds and performed a 96-degree rotation best online viagra. Then it descended back to the ground, landing on its four legs, with a total flight time of 39.1 seconds. From there, things got more complex.

The second best online viagra flight lasted 51.9 seconds, reaching a height of five meters. And it included a lateral movement of about two meters—something not attempted in the confines of the test chamber on Earth where Ingenuity first flew in simulated Mars conditions. Flight three saw Ingenuity travel half the length of a football field, some 50 meters, best online viagra reaching a top speed of just more than two meters per second. The fourth flight on April 30 pushed the envelope once again, with Ingenuity remaining airborne for nearly two minutes—117 seconds—and reaching an impressive speed of 3.5 meters per second as it scouted a potential future landing zone over a round trip of more than 260 meters.

Ingenuity’s fifth flight—completed on May 7 and initially planned to be its last—sent it on a one-way trip to the new landing zone to await the arrival of Perseverance, its mothership. Now, this wildly successful technology demonstration drone is entering a best online viagra new phase of its mission—a second month-long set of more ambitious operational tests. These tests are meant to show how airborne drones “could play an active role in a future rover science mission,” says Dave Lavery, the program executive for Ingenuity at NASA headquarters in Washington, DC. Although Ingenuity will not directly support the science objectives of Perseverance, namely looking for signs of past life on Mars, it will help scout out the rover’s potential route ahead as the team plans their optimal path through Jezero Crater’s riches, or even photograph nearby locations not in the rover’s planned path.

There is even a slim chance Ingenuity best online viagra could support the rover’s later mission too, if it survives. €œWe might see about potentially looking over the rim of the crater,” Lavery says. Much has been made of how these vehicles might one day support human missions, acting as reconnaissance drones for humans to scout out regions of interest near a landing site or carrying tools between locations. In the near-term, prospects of more exciting robotic science are on the horizon—perhaps in the same way that the Sojourner rover in 1997, itself a prototype of wheeled exploration and part of NASA’s Pathfinder mission, paved the way for its successors Spirit, Opportunity, best online viagra Curiosity and now Perseverance.

€œI do think we’re going to see some flying vehicles in the future,” says Michael Meyer, lead scientist of NASA’s Mars Exploration Program at the agency’s headquarters in Washington, D.C. €œIt will now be part of our portfolio of methods that we use for exploration best online viagra. There are things you can do with a helicopter that you can’t do with other platforms.” Examples could include exploring the aforementioned lava tubes or perhaps approaching crater walls—too high and steep for a rover to scale—where a helicopter could take images and perform some up-close analysis as well. Another example could be studying recurring slope lineae, dark flows on Mars that have arguably been linked to liquid water flowing on the surface.

Perversely, it is this possibility of water—and the accompanying risk of best online viagra contamination with bacteria imported from Earth—that essentially prohibits anyone or anything from setting foot (or wheel) there to seek out signs of native Martian life. But a hovering drone could look without touching, offering a novel route of exploration. €œA rotorcraft would give us the ability to go and look up close at something that we would otherwise deem not suitable for a rover,” Byrne says, “either because of planetary protection issues or because it’s too dangerous.” One concept for a possible aerial vehicle beyond Ingenuity is already being investigated. Known as the Mars Science Helicopter, this six-bladed hexacopter would weigh nearly 30 kilograms best online viagra.

And it would be equipped with several kilograms worth of instruments to analyze different regions of the Martian surface and would have the ability to fly for minutes at a time over several kilometers. €œWe’re trying to learn best online viagra from Ingenuity and ask ourselves, ‘What could we accomplish if we push it further?. €™â€ says Theodore Tzanetos of JPL, who is part of the Mars Science Helicopter concept team. The science such traits would afford would be tremendous, bringing large swathes of the Martian surface suddenly within reach.

The current distance record on Mars is held by NASA’s Opportunity rover, which traveled more than 42 kilometers best online viagra in a little more than 11 years. A helicopter could achieve the same feat in weeks. Other ideas involve using rotorcraft to perform surveys of exposed water ice on regions of the Martian surface inaccessible to rovers. Drones could dive into Martian valleys like the two-kilometer-deep Mawrth Vallis, looking for evidence of clays linked to astrobiology, or best online viagra perhaps use instruments to probe the lower reaches of the Martian atmosphere says Shannah Withrow-Maser, the Mars Science Helicopter vehicle systems lead at NASA’s Ames Research Center in California.

And this could all be done either alongside a bigger rover mission or as more cost-effective and much lighter standalone missions, enabling more widespread exploration of a variety of Martian locales. €œI personally best online viagra would love that,” says Withrow-Maser. Elsewhere in the solar system, flight options are more limited. One could imagine a rotorcraft in the atmosphere of one of the gas giants such as Jupiter or Saturn, where theoretically flight would be possible.

But actually getting there would be an best online viagra issue. €œThe problem, of course, is slowing down and the amount of energy that would take” on arrival at the planet, Byrne says. But Titan, Saturn’s intriguing moon with an incredibly thick atmosphere and lakes of hydrocarbons on its surface, is a very tantalizing prospect. In 2019 NASA best online viagra selected a mission that would attempt to deploy the rotorcraft Dragonfly on the moon.

Dragonfly is intended to launch as early as 2026 and arrive in 2034, and its team has been watching Ingenuity’s successes very closely. €œWe’ve been following with great interest,” says Elizabeth Turtle, lead of the Dragonfly mission at the Johns Hopkins University Applied Physics best online viagra Laboratory. €œWe’re very anxious to see what lessons we can take forward to Dragonfly.” Like Ingenuity, Dragonfly will be flying autonomously, so it will make use of similar onboard image processing capabilities to decide where to land on the Titanian surface. (Ingenuity performs terrain mapping by taking 30 images of the ground per second.) But Dragonfly is a mammoth compared to Ingenuity, weighing nearly half a metric ton and powered by plutonium.

And it best online viagra is a standalone mission rather than a ride along like Ingenuity. €œIt’s like Perseverance [in scale], except we fly instead of drive across the surface,” Turtle says. Despite Titan being a much more distant alien world than Mars—with a light travel time from Earth of about an hour, compared with up to about 20 minutes for the Red Planet—flight is relatively easier there. Titan’s gravity is only 14 percent that best online viagra of Earth and much less than that of Mars, while the moon’s much thicker atmosphere makes generating lift a comparative breeze.

€œA person could put wings on and soar over Titan’s surface,” Turtle says. Winds on Titan are also much slower, barely more than a kilometer an hour best online viagra versus tens of kilometers an hour on Mars. And whereas Ingenuity’s blades require 2,500 rpm to lift its fragile 1.8-kg body off the surface, Dragonfly’s half-metric-ton bulk can be lofted just by its rotors spinning at 800 rpm. Titan’s major challenge is its temperature, which averages only about –180 degrees Celsius—hence the need for a long-lived, heat-generating plutonium power source.

€œIt’s certainly cold,” Turtle best online viagra says. €œIt’s a nontrivial challenge.” With Dragonfly on the horizon, and perhaps future missions such as the Mars Science Helicopter in the works, there is plenty to be excited about beyond Ingenuity. This little machine has, for the first time, proved flight on alien worlds is possible—from both a physical and logistical point of view. Now this exciting new era of discovery awaits, and while only a handful of worlds afford the right conditions for this method of exploration, the sky is very much the limit for the science that could be performed by aerial best online viagra vehicles in these alien skies.

€œThere are things to be sorted out,” Meyer says. €œThen I think we’re going to start seeing some new and improved helicopter platforms that can actually carry tempting payloads.”.

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August 28, where can i buy viagra over the counter usa 2020Contact Purchase viagra. Office of CommunicationsPhone. 202-693-1999U.S.

Department of Labor Issues Revised Final Beryllium StandardsFor Construction and Shipyards WASHINGTON, DC - The U.S. Department of Labor's Occupational Safety and Health Administration (OSHA) today published a final rule revising the beryllium standards for construction and shipyards. The final rule includes changes designed to clarify the standards and simplify or improve compliance.

These changes maintain protection for workers while ensuring that the standard is well understood and compliance is simple and straightforward. The final rule amends the following paragraphs in the beryllium standards for construction and shipyards. Definitions, Methods of Compliance, Respiratory Protection, Personal Protective Clothing and Equipment, Housekeeping, Hazard Communication, Medical Surveillance, and Recordkeeping.

OSHA has removed the Hygiene Areas and Practices paragraph from the final standards because the necessary protections are provided by existing OSHA standards for sanitation. The effective date of the revisions in this final rule is September 30, 2020. OSHA began enforcing the new permissible exposure limits in the 2017 beryllium standards for construction and shipyards in May 2018.

OSHA will begin enforcing the remaining provisions of the standards on September 30, 2020. The final standard will affect approximately 12,000 workers employed in nearly 2,800 establishments in the construction and shipyard industries. The final standards are estimated to yield $2.5 million in total annualized cost savings to employers.

Under the Occupational Safety and Health Act of 1970, employers are responsible for providing safe and healthful workplaces for their employees. OSHA's role is to help ensure these conditions for America's working men and women by setting and enforcing standards, and providing training, education, and assistance. For more information, visit www.osha.gov.

The mission of the Department of Labor is to foster, promote, and develop the welfare of the wage earners, job seekers, and retirees of the United States. Improve working conditions. Advance opportunities for profitable employment.

And assure work-related benefits and rights. # # # U.S. Department of Labor news materials are accessible at http://www.dol.gov.

The Department's Reasonable Accommodation Resource Center converts departmental information and documents into alternative formats, which include Braille and large print. For alternative format requests, please contact the Department at (202) 693-7828 (voice) or (800) 877-8339 (federal relay).August 27, 2020U.S. Department of Labor Announces ActionsTo Assist Americans Impacted By Hurricane Laura WASHINGTON, DC – The U.S.

Department of Labor today announced actions it is taking to assist Americans in states affected by Hurricane Laura. In response to the anticipated needs of those living in states in the path of Hurricane Laura, the Department and its agencies are taking the following actions. The Occupational Safety and Health Administration (OSHA) has actively engaged with the U.S.

Department of Homeland Security, the Federal Emergency Management Administration, the Environmental Protection Agency, and other federal agencies and is prepared to provide assistance. The Wage and Hour Division (WHD) will be prioritizing all calls in the affected areas to continue to provide uninterrupted service to workers and employers. The Employment and Training Administration (ETA) is prepared to provide Disaster Dislocated Worker Grants to help affected states address workforce needs.

The disbursement of funds will be determined as needs are assessed by state and local partners. ETA is also prepared to assist in administering Disaster Unemployment Assistance. The Employee Benefits Security Administration (EBSA) will coordinate with other federal agencies, including the U.S.

Department of Treasury, the IRS and the Pension Benefit Guaranty Corp. On the release of compliance guidance for employee benefit plans, and plan participants and beneficiaries in response to Hurricane Laura. General information on disaster relief under the Employee Retirement Income Security Act (ERISA) is available on EBSA's website at Disaster Relief Information for Employers and Advisers and Disaster Relief Information for Workers and Families, or by contacting EBSA online or by calling 1-866-444-3272.

The Office of Federal Contract Compliance Programs (OFCCP) issued a Temporary Exemption from certain federal contracting requirements. For a period of three months, from August 27, 2020, to November 27, 2020, new federal contracts to provide relief, clean-up or rebuilding efforts will be exempt from having to develop written affirmative action programs as required by Executive Order 11246. The Mine Safety and Health Administration (MSHA) is responding to Hurricane Laura's impact on mines, and stands ready to respond more generally with specialized equipment and personnel.

And The Veterans' Employment and Training Service (VETS) is working with its grantees to identify further flexibilities and additional funding needs for its programs. VETS staff is prepared to assist employers, members of the National Guard and Reserves and members of the National Disaster Medical System and Urban Search and Rescue who deploy in support of rescue and recovery operations. The Department will continue to monitor developments regarding Hurricane Laura and take additional actions as necessary.

For additional information, please visit the Department's Severe Storm and Flood Recovery Assistance webpage. The mission of the Department of Labor is to foster, promote and develop the welfare of the wage earners, job seekers and retirees of the United States. Improve working conditions.

Advance opportunities for profitable employment. And assure work-related benefits and rights. # # # Media Contact.

Eric Holland, 202-693-4676, holland.eric.w@dol.gov Release Number. 20-1654-NAT U.S. Department of Labor news materials are accessible at http://www.dol.gov.

The Department's Reasonable Accommodation Resource Center converts departmental information and documents into alternative formats, which include Braille and large print. For alternative format requests, please contact the Department at (202) 693-7828 (voice) or (800) 877-8339 (federal relay)..

August 28, best online viagra 2020Contact. Office of CommunicationsPhone. 202-693-1999U.S.

Department of Labor Issues Revised Final Beryllium StandardsFor Construction and Shipyards WASHINGTON, DC - The U.S. Department of Labor's Occupational Safety and Health Administration (OSHA) today published a final rule revising the beryllium standards for construction and shipyards. The final rule includes changes designed to clarify the standards and simplify or improve compliance.

These changes maintain protection for workers while ensuring that the standard is well understood and compliance is simple and straightforward. The final rule amends the following paragraphs in the beryllium standards for construction and shipyards. Definitions, Methods of Compliance, Respiratory Protection, Personal Protective Clothing and Equipment, Housekeeping, Hazard Communication, Medical Surveillance, and Recordkeeping.

OSHA has removed the Hygiene Areas and Practices paragraph from the final standards because the necessary protections are provided by existing OSHA standards for sanitation. The effective date of the revisions in this final rule is September 30, 2020. OSHA began enforcing the new permissible exposure limits in the 2017 beryllium standards for construction and shipyards in May 2018.

OSHA will begin enforcing the remaining provisions of the standards on September 30, 2020. The final standard will affect approximately 12,000 workers employed in nearly 2,800 establishments in the construction and shipyard industries. The final standards are estimated to yield $2.5 million in total annualized cost savings to employers.

Under the Occupational Safety and Health Act of 1970, employers are responsible for providing safe and healthful workplaces for their employees. OSHA's role is to help ensure these conditions for America's working men and women by setting and enforcing standards, and providing training, education, and assistance. For more information, visit www.osha.gov.

The mission of the Department of Labor is to foster, promote, and develop the welfare of the wage earners, job seekers, and retirees of the United States. Improve working conditions. Advance opportunities for profitable employment.

And assure work-related benefits and rights. # # # U.S. Department of Labor news materials are accessible at http://www.dol.gov.

The Department's Reasonable Accommodation Resource Center converts departmental information and documents into alternative formats, which include Braille and large print. For alternative format requests, please contact the Department at (202) 693-7828 (voice) or (800) 877-8339 (federal relay).August 27, 2020U.S. Department of Labor Announces ActionsTo Assist Americans Impacted By Hurricane Laura WASHINGTON, DC – The U.S.

Department of Labor today announced actions it is taking to assist Americans in states affected by Hurricane Laura. In response to the anticipated needs of those living in states in the path of Hurricane Laura, the Department and its agencies are taking the following actions. The Occupational Safety and Health Administration (OSHA) has actively engaged with the U.S.

Department of Homeland Security, the Federal Emergency Management Administration, the Environmental Protection Agency, and other federal agencies and is prepared to provide assistance. The Wage and Hour Division (WHD) will be prioritizing all calls in the affected areas to continue to provide uninterrupted service to workers and employers. The Employment and Training Administration (ETA) is prepared to provide Disaster Dislocated Worker Grants to help affected states address workforce needs.

The disbursement of funds will be determined as needs are assessed by state and local partners. ETA is also prepared to assist in administering Disaster Unemployment Assistance. The Employee Benefits Security Administration (EBSA) will coordinate with other federal agencies, including the U.S.

Department of Treasury, the IRS and the Pension Benefit Guaranty Corp. On the release of compliance guidance for employee benefit plans, and plan participants and beneficiaries in response to Hurricane Laura. General information on disaster relief under the Employee Retirement Income Security Act (ERISA) is available on EBSA's website at Disaster Relief Information for Employers and Advisers and Disaster Relief Information for Workers and Families, or by contacting EBSA online or by calling 1-866-444-3272.

The Office of Federal Contract Compliance Programs (OFCCP) issued a Temporary Exemption from certain federal contracting requirements. For a period of three months, from August 27, 2020, to November 27, 2020, new federal contracts to provide relief, clean-up or rebuilding efforts will be exempt from having to develop written affirmative action programs as required by Executive Order 11246. The Mine Safety and Health Administration (MSHA) is responding to Hurricane Laura's impact on mines, and stands ready to respond more generally with specialized equipment and personnel.

And The Veterans' Employment and Training Service (VETS) is working with its grantees to identify further flexibilities and additional funding needs for its programs. VETS staff is prepared to assist employers, members of the National Guard and Reserves and members of the National Disaster Medical System and Urban Search and Rescue who deploy in support of rescue and recovery operations. The Department will continue to monitor developments regarding Hurricane Laura and take additional actions as necessary.

For additional information, please visit the Department's Severe Storm and Flood Recovery Assistance webpage. The mission of the Department of Labor is to foster, promote and develop the welfare of the wage earners, job seekers and retirees of the United States. Improve working conditions.

Advance opportunities for profitable employment. And assure work-related benefits and rights. # # # Media Contact.

Eric Holland, 202-693-4676, holland.eric.w@dol.gov Release Number. 20-1654-NAT U.S. Department of Labor news materials are accessible at http://www.dol.gov.

The Department's Reasonable Accommodation Resource Center converts departmental information and documents into alternative formats, which include Braille and large print. For alternative format requests, please contact the Department at (202) 693-7828 (voice) or (800) 877-8339 (federal relay)..

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President Trump may be just another of the 7 girl viagra effects million Continue Reading Americans infected with erectile dysfunction treatment. But he is also the most powerful person in the world — which means that more than any other patient, he could use extraordinary measures to treat the viagra with unapproved therapies.Will he?. Should girl viagra effects he?. From the start of his administration, Trump has argued that patients suffering from potentially deadly diseases should have earlier access to experimental drugs. In May, Trump veered outside the bounds of normal medical practice girl viagra effects by taking hydroxychloroquine in hopes the malaria drug would prevent erectile dysfunction treatment , based not on solid scientific evidence but on letters sent to him by supporters who told him the drug worked to ward off the viagra.advertisement There is also a difficult reality.

The few drugs that have been proven to have an effect on erectile dysfunction treatment are not for patients who are just starting to show symptoms, but for those who need to be hospitalized.“When the president calls, it’s hard to say no, but it’s also important to stay within the process. Just as girl viagra effects the president is not above the law, he is not above any type of regulatory oversight and protection when it comes to experimental medicines,” said Peter Pitts, former associate commissioner of the Food and Drug Administration and president of the Center for Medicine in the Public Interest.advertisement Still, experts told STAT that at least one drug, remdesivir, made by Gilead Sciences and granted an emergency use authorization by the FDA, is a likely candidate to offer the president, based on medical practice. Scott Gottlieb, who served as the commissioner of the FDA earlier in Trump’s term, said he thinks it would be “reasonable to consider” giving him remdesivir.“If the reports are true that the president is symptomatic, I think it would be reasonable to consider giving him remdesivir, given that we have good information about that drug’s profile, and this is the president of the United States, so we want to lean forward on getting him the best possible care,” Gottlieb said.Gottlieb acknowledged that remdesivir, technically, is cleared only for patients who are in the hospital, so this would be “off-label,” but he said that its safety profile is well understood and it’s “reasonable” to believe that it could help patients earlier in their illness. How remdesivir works girl viagra effects. What if Trump’s medical team wants to go further?.

Another option would be the experimental monoclonal antibodies being developed by Eli Lilly and Regeneron, which are considered among the more promising girl viagra effects experimental therapies. Both companies have said they plan to discuss the possibility of an emergency use authorization with the FDA. But many experts see these as too early to give in this situation.Eli Lilly said girl viagra effects Sept. 16 that some doses of its monoclonal antibody seemed to speed the reduction of levels of the viagra in patients’ erectile dysfunction treatment tests, and might be helping prevent hospitalization. On Sept girl viagra effects.

29, Regeneron said that its monoclonal antibody cocktail also lowered viagra levels, especially in patients who were not producing their own natural antibodies. But large-scale tests of the drugs are ongoing, and many experts have said it is too early to grant them emergency use authorization.“I think the antibody drugs are too early along in their development to consider them at this point, Gottlieb said, “especially since there are drugs like remdesivir where we have much more information about its application in this setting.” Other drugs that have been proven to have a benefit in treating the erectile dysfunction — including steroids, which have had the most dramatic effect, and baricitinib, an Eli Lilly arthritis drug — would be used only much further along in the disease.Dexamethasone, a widely available steroid, has proved to improve the odds of survival for patients girl viagra effects hospitalized with erectile dysfunction treatment. But there are no data to support using the drug for patients with mild, early-stage disease like Trump, said Nahid Bhadelia, an infectious disease physician and medical director of the Special Pathogens Unit at the Boston University School of Medicine. And it girl viagra effects may do more harm than good.“You don’t want to give it to a patient too early,” Bhadelia said. €œIt’s a blunt instrument, so it may suppress a good immune response as well as a bad one.”If Trump’s medical team did want to push for a drug that was more experimental and was not on the market, they could likely do so through a single-patient investigational new drug application, or IND.

In the case of a president, the FDA might grant such girl viagra effects an application in a matter of hours, and it is likely that a manufacturer would make a drug available.But the effort to get access could also become political. €œThey could contact the company and work on right-to-try access,” Pitts said, referring to legislation that permits patients easier access to experimental medicines. €œThe president talks a lot about right to try, so maybe this is girl viagra effects an opportunity to see how that works on the executive level.”It’s not simply a question of whether the president should have access to medicines that are not approved for other people, though. It’s a question of whether taking an unproven treatment is wise. Doctor’s call this “the therapeutic misconception” — the idea that a patient should have a treatment, even when girl viagra effects sometimes it is better to do nothing.“There are a host of unproven therapies for erectile dysfunction treatment 19 that are recommended by various clinicians and researchers,” said Robert Califf, who served as the FDA commissioner during the final years of the Obama administration.“It’s important to remember that the vast majority of drugs that enter testing have unexpected toxicity or turn out to be ineffective or have higher risk than benefit,” said Califf, who is now the head of clinical policy and strategy for Verily and Google Health.

€œIn addition, any of the proposed therapies that are not being developed under FDA oversight are modern snake oils.” Even medicines that work for some people can be detrimental for other patients. The antibodies, he said, “are not definitively beneficial,” especially if someone is producing antibodies against their disease.There are other ways that the decision of how to treat the president girl viagra effects could become political. Members of the administration, including economic advisor Peter Navarro, have continued to push for the benefit of hydroxychloroquine in treating erectile dysfunction treatment. President Trump called convalescent plasma, a treatment made from the blood of girl viagra effects recovered patients, a “very historic breakthrough in our fight against the China viagra” when it received a controversial emergency use authorization in August. But studies showed its benefits were underwhelming.

In addition, supplies of the plasma are limited, and it’s recommended mainly for hospitalized patients.It’s possible that the president could want access to either, or to a cocktail of hydroxychloroquine, the antibiotic azithromycin, and the mineral zinc, which has been much talked about on the internet despite limited evidence of efficacy and side effects including diarrhea and potential heart risks.In May, explaining his daily regimen of hydroxychloroquine plus zinc, Trump told reporters during a meeting in the White House State Dining Room. €œI’ve taken it for a week-and-a-half now and I’m still here. What do you have to lose?. €Throughout the erectile dysfunction viagra, the president has, through his comments, made many decisions political. The question is whether that will happen with his own treatment decisions.Damian Garde contributed to this story..

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In May, Trump veered outside the bounds of normal medical best online viagra practice by taking hydroxychloroquine in hopes the malaria drug would prevent erectile dysfunction treatment , based not on solid scientific evidence but on letters sent to him by supporters who told him the drug worked to ward off the viagra.advertisement There is also a difficult reality. The few drugs that have been proven to have an effect on erectile dysfunction treatment are not for patients who are just starting to show symptoms, but for those who need to be hospitalized.“When the president calls, it’s hard to say no, but it’s also important to stay within the process. Just as the president is not above the law, he is not above any type of regulatory oversight and protection when it comes to experimental medicines,” said Peter Pitts, former associate commissioner of the Food and Drug Administration best online viagra and president of the Center for Medicine in the Public Interest.advertisement Still, experts told STAT that at least one drug, remdesivir, made by Gilead Sciences and granted an emergency use authorization by the FDA, is a likely candidate to offer the president, based on medical practice. Scott Gottlieb, who served as the commissioner of the FDA earlier in Trump’s term, said he thinks it would be “reasonable to consider” giving him remdesivir.“If the reports are true that the president is symptomatic, I think it would be reasonable to consider giving him remdesivir, given that we have good information about that drug’s profile, and this is the president of the United States, so we want to lean forward on getting him the best possible care,” Gottlieb said.Gottlieb acknowledged that remdesivir, technically, is cleared only for patients who are in the hospital, so this would be “off-label,” but he said that its safety profile is well understood and it’s “reasonable” to believe that it could help patients earlier in their illness.

How remdesivir best online viagra works. What if Trump’s medical team wants to go further?. Another option would be the experimental monoclonal antibodies being developed best online viagra by Eli Lilly and Regeneron, which are considered among the more promising experimental therapies. Both companies have said they plan to discuss the possibility of an emergency use authorization with the FDA.

But many experts see these as too early to give best online viagra in this situation.Eli Lilly said Sept. 16 that some doses of its monoclonal antibody seemed to speed the reduction of levels of the viagra in patients’ erectile dysfunction treatment tests, and might be helping prevent hospitalization. On Sept best online viagra. 29, Regeneron said that its monoclonal antibody cocktail also lowered viagra levels, especially in patients who were not producing their own natural antibodies.

But large-scale tests of the drugs are ongoing, and many experts have said it is too early to grant them emergency use authorization.“I think the antibody drugs are too early along in their development to consider them at this point, Gottlieb said, “especially since there are drugs like remdesivir where we have much more information about its application in this setting.” Other drugs that have been proven to have a benefit in treating the erectile dysfunction — including steroids, which have had the most dramatic effect, and baricitinib, an Eli Lilly arthritis drug — would be used only much further along in the disease.Dexamethasone, a widely available steroid, has proved to improve the odds of best online viagra survival for patients hospitalized with erectile dysfunction treatment. But there are no data to support using the drug for patients with mild, early-stage disease like Trump, said Nahid Bhadelia, an infectious disease physician and medical director of the Special Pathogens Unit at the Boston University School of Medicine. And it may do more harm than good.“You don’t want to give it best online viagra to a patient too early,” Bhadelia said. €œIt’s a blunt instrument, so it may suppress a good immune response as well as a bad one.”If Trump’s medical team did want to push for a drug that was more experimental and was not on the market, they could likely do so through a single-patient investigational new drug application, or IND.

In the case of a best online viagra president, the FDA might grant such an application in a matter of hours, and it is likely that a manufacturer would make a drug available.But the effort to get access could also become political. €œThey could contact the company and work on right-to-try access,” Pitts said, referring to legislation that permits patients easier access to experimental medicines. €œThe president talks a lot about right to try, best online viagra so maybe this is an opportunity to see how that works on the executive level.”It’s not simply a question of whether the president should have access to medicines that are not approved for other people, though. It’s a question of whether taking an unproven treatment is wise.

Doctor’s call this “the therapeutic misconception” — the idea that a patient should have a treatment, even when sometimes it is better to do nothing.“There are a host of unproven therapies for erectile dysfunction treatment 19 that are recommended by various clinicians and best online viagra researchers,” said Robert Califf, who served as the FDA commissioner during the final years of the Obama administration.“It’s important to remember that the vast majority of drugs that enter testing have unexpected toxicity or turn out to be ineffective or have higher risk than benefit,” said Califf, who is now the head of clinical policy and strategy for Verily and Google Health. €œIn addition, any of the proposed therapies that are not being developed under FDA oversight are modern snake oils.” Even medicines that work for some people can be detrimental for other patients. The antibodies, he said, “are not definitively beneficial,” especially if best online viagra someone is producing antibodies against their disease.There are other ways that the decision of how to treat the president could become political. Members of the administration, including economic advisor Peter Navarro, have continued to push for the benefit of hydroxychloroquine in treating erectile dysfunction treatment.

President Trump called convalescent plasma, a treatment made from the blood of recovered patients, a “very historic breakthrough best online viagra in our fight against the China viagra” when it received a controversial emergency use authorization in August. But studies showed its benefits were underwhelming. In addition, best online viagra supplies of the plasma are limited, and it’s recommended mainly for hospitalized patients.It’s possible that the president could want access to either, or to a cocktail of hydroxychloroquine, the antibiotic azithromycin, and the mineral zinc, which has been much talked about on the internet despite limited evidence of efficacy and side effects including diarrhea and potential heart risks.In May, explaining his daily regimen of hydroxychloroquine plus zinc, Trump told reporters during a meeting in the White House State Dining Room. €œI’ve taken it for a week-and-a-half now and I’m still here.

What do best online viagra you have to lose?. €Throughout the erectile dysfunction viagra, the president has, through his comments, made many decisions political. The question is whether that will happen with his own treatment decisions.Damian Garde contributed to this story..