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How to cite this article:Singh O buy real zithromax online P. Aftermath of celebrity suicide – Media coverage and role of psychiatrists. Indian J Psychiatry 2020;62:337-8Celebrity buy real zithromax online 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 buy real zithromax online 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 buy real zithromax online 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 buy real zithromax online calls 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 guidelines of World Health Organization report buy real zithromax online 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 illness and buy real zithromax online 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 buy real zithromax online 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 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 buy real zithromax online 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 buy real zithromax online 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, buy real zithromax online 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 buy real zithromax online 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 buy real zithromax online 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 - 700 094, West Bengal buy real zithromax online 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.

Part I. A perspective on the evolution and current practice of ECT. J Psychiatr Pract 2009;15:346-68. 2.Lauber C, Nordt C, Falcato L, Rössler W. Can a seizure help?.

The public's attitude toward electroconvulsive therapy. Psychiatry Res 2005;134:205-9. 3.Stefanazzi M. Is electroconvulsive therapy (ECT) ever ethically justified?. If so, under what circumstances.

HEC Forum 2013;25:79-94. 4.Devanand DP, Dwork AJ, Hutchinson ER, Bolwig TG, Sackeim HA. Does ECT alter brain structure?. Am J Psychiatry 1994;151:957-70. 5.Devanand DP.

Does electroconvulsive therapy damage brain cells?. Semin Neurol 1995;15:351-7. 6.Pearsall J, Trumble B, editors. The Oxford English Reference Dictionary. 2nd ed.

Oxford, England. New York. Oxford University Press. 1996. 7.Collin PH.

Dictionary of Medical Terms. 4th ed. London. Bloomsbury. 2004.

8.Hajdu SI. Entries on laboratory medicine in the first illustrated medical dictionary. Ann Clin Lab Sci 2005;35:465-8. 9.Mander AJ, Whitfield A, Kean DM, Smith MA, Douglas RH, Kendell RE. Cerebral and brain stem changes after ECT revealed by nuclear magnetic resonance imaging.

Br J Psychiatry 1987;151:69-71. 10.Coffey CE, Weiner RD, Djang WT, Figiel GS, Soady SA, Patterson LJ, et al. Brain anatomic effects of electroconvulsive therapy. A prospective magnetic resonance imaging study. Arch Gen Psychiatry 1991;48:1013-21.

11.Scott AI, Douglas RH, Whitfield A, Kendell RE. Time course of cerebral magnetic resonance changes after electroconvulsive therapy. Br J Psychiatry 1990;156:551-3. 12.Pande AC, Grunhaus LJ, Aisen AM, Haskett RF. A preliminary magnetic resonance imaging study of ECT-treated depressed patients.

Biol Psychiatry 1990;27:102-4. 13.Coffey CE, Figiel GS, Djang WT, Sullivan DC, Herfkens RJ, Weiner RD. Effects of ECT on brain structure. A pilot prospective magnetic resonance imaging study. Am J Psychiatry 1988;145:701-6.

14.Qiu H, Li X, Zhao W, Du L, Huang P, Fu Y, et al. Electroconvulsive therapy-Induced brain structural and functional changes in major depressive disorders. A longitudinal study. Med Sci Monit 2016;22:4577-86. 15.Kunigiri G, Jayakumar PN, Janakiramaiah N, Gangadhar BN.

MRI T2 relaxometry of brain regions and cognitive dysfunction following electroconvulsive therapy. Indian J Psychiatry 2007;49:195-9. [PUBMED] [Full text] 16.Pirnia T, Joshi SH, Leaver AM, Vasavada M, Njau S, Woods RP, et al. Electroconvulsive therapy and structural neuroplasticity in neocortical, limbic and paralimbic cortex. Transl Psychiatry 2016;6:e832.

17.Szabo K, Hirsch JG, Krause M, Ende G, Henn FA, Sartorius A, et al. Diffusion weighted MRI in the early phase after electroconvulsive therapy. Neurol Res 2007;29:256-9. 18.Nordanskog P, Dahlstrand U, Larsson MR, Larsson EM, Knutsson L, Johanson A. Increase in hippocampal volume after electroconvulsive therapy in patients with depression.

A volumetric magnetic resonance imaging study. J ECT 2010;26:62-7. 19.Nordanskog P, Larsson MR, Larsson EM, Johanson A. Hippocampal volume in relation to clinical and cognitive outcome after electroconvulsive therapy in depression. Acta Psychiatr Scand 2014;129:303-11.

20.Tendolkar I, van Beek M, van Oostrom I, Mulder M, Janzing J, Voshaar RO, et al. Electroconvulsive therapy increases hippocampal and amygdala volume in therapy refractory depression. A longitudinal pilot study. Psychiatry Res 2013;214:197-203. 21.Dukart J, Regen F, Kherif F, Colla M, Bajbouj M, Heuser I, et al.

Electroconvulsive therapy-induced brain plasticity determines therapeutic outcome in mood disorders. Proc Natl Acad Sci U S A 2014;111:1156-61. 22.Abbott CC, Jones T, Lemke NT, Gallegos P, McClintock SM, Mayer AR, et al. Hippocampal structural and functional changes associated with electroconvulsive therapy response. Transl Psychiatry 2014;4:e483.

23.Lyden H, Espinoza RT, Pirnia T, Clark K, Joshi SH, Leaver AM, et al. Electroconvulsive therapy mediates neuroplasticity of white matter microstructure in major depression. Transl Psychiatry 2014;4:e380. 24.Bouckaert F, De Winter FL, Emsell L, Dols A, Rhebergen D, Wampers M, et al. Grey matter volume increase following electroconvulsive therapy in patients with late life depression.

A longitudinal MRI study. J Psychiatry Neurosci 2016;41:105-14. 25.Ota M, Noda T, Sato N, Okazaki M, Ishikawa M, Hattori K, et al. Effect of electroconvulsive therapy on gray matter volume in major depressive disorder. J Affect Disord 2015;186:186-91.

26.Zeng J, Luo Q, Du L, Liao W, Li Y, Liu H, et al. Reorganization of anatomical connectome following electroconvulsive therapy in major depressive disorder. Neural Plast 2015;2015:271674. 27.van Eijndhoven P, Mulders P, Kwekkeboom L, van Oostrom I, van Beek M, Janzing J, et al. Bilateral ECT induces bilateral increases in regional cortical thickness.

Transl Psychiatry 2016;6:e874. 28.Bouckaert F, Dols A, Emsell L, De Winter FL, Vansteelandt K, Claes L, et al. Relationship between hippocampal volume, serum BDNF, and depression severity following electroconvulsive therapy in late-life depression. Neuropsychopharmacology 2016;41:2741-8. 29.Depping MS, Nolte HM, Hirjak D, Palm E, Hofer S, Stieltjes B, et al.

Cerebellar volume change in response to electroconvulsive therapy in patients with major depression. Prog Neuropsychopharmacol Biol Psychiatry 2017;73:31-5. 30.Joshi SH, Espinoza RT, Pirnia T, Shi J, Wang Y, Ayers B, et al. Structural plasticity of the hippocampus and amygdala induced by electroconvulsive therapy in major depression. Biol Psychiatry 2016;79:282-92.

31.Wade BS, Joshi SH, Njau S, Leaver AM, Vasavada M, Woods RP, et al. Effect of electroconvulsive therapy on striatal morphometry in major depressive disorder. Neuropsychopharmacology 2016;41:2481-91. 32.Wolf RC, Nolte HM, Hirjak D, Hofer S, Seidl U, Depping MS, et al. Structural network changes in patients with major depression and schizophrenia treated with electroconvulsive therapy.

Eur Neuropsychopharmacol 2016;26:1465-74. 33.Ende G, Braus DF, Walter S, Weber-Fahr W, Henn FA. The hippocampus in patients treated with electroconvulsive therapy. A proton magnetic resonance spectroscopic imaging study. Arch Gen Psychiatry 2000;57:937-43.

34.Michael N, Erfurth A, Ohrmann P, Arolt V, Heindel W, Pfleiderer B. Metabolic changes within the left dorsolateral prefrontal cortex occurring with electroconvulsive therapy in patients with treatment resistant unipolar depression. Psychol Med 2003;33:1277-84. 35.Michael N, Erfurth A, Ohrmann P, Arolt V, Heindel W, Pfleiderer B. Neurotrophic effects of electroconvulsive therapy.

A proton magnetic resonance study of the left amygdalar region in patients with treatment-resistant depression. Neuropsychopharmacology 2003;28:720-5. 36.Pfleiderer B, Michael N, Erfurth A, Ohrmann P, Hohmann U, Wolgast M, et al. Effective electroconvulsive therapy reverses glutamate/glutamine deficit in the left anterior cingulum of unipolar depressed patients. Psychiatry Res 2003;122:185-92.

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.

Acta Psychiatr Scand 2016;133:154-64. 39.Njau S, Joshi SH, Espinoza R, Leaver AM, Vasavada M, Marquina A, et al. Neurochemical correlates of rapid treatment response to electroconvulsive therapy in patients with major depression. J Psychiatry Neurosci 2017;42:6-16. 40.Cano M, Martínez-Zalacaín I, Bernabéu-Sanz Á, Contreras-Rodríguez O, Hernández-Ribas R, Via E, et al.

Brain volumetric and metabolic correlates of electroconvulsive therapy for treatment-resistant depression. A longitudinal neuroimaging study. Transl Psychiatry 2017;7:e1023. 41.Figiel GS, Krishnan KR, Doraiswamy PM. Subcortical structural changes in ECT-induced delirium.

J Geriatr Psychiatry Neurol 1990;3:172-6. 42.Rotheneichner P, Lange S, O'Sullivan A, Marschallinger J, Zaunmair P, Geretsegger C, et al. Hippocampal neurogenesis and antidepressive therapy. Shocking relations. Neural Plast 2014;2014:723915.

43.Singh A, Kar SK. How electroconvulsive therapy works?. Understanding the neurobiological mechanisms. Clin Psychopharmacol Neurosci 2017;15:210-21. 44.Gbyl K, Videbech P.

Electroconvulsive therapy increases brain volume in major depression. A systematic review and meta-analysis. Acta Psychiatr Scand 2018;138:180-95. 45.Oltedal L, Narr KL, Abbott C, Anand A, Argyelan M, Bartsch H, et al. Volume of the human hippocampus and clinical response following electroconvulsive therapy.

Biol Psychiatry 2018;84:574-81. 46.Breggin PR. Brain-Disabling Treatments in Psychiatry. Drugs, Electroshock, and the Role of the FDA. New York.

Springer Pub. Co.. 1997. 47.Posse S, Otazo R, Dager SR, Alger J. MR spectroscopic imaging.

Principles and recent advances. J Magn Reson Imaging 2013;37:1301-25. 48.Simmons ML, Frondoza CG, Coyle JT. Immunocytochemical localization of N-acetyl-aspartate with monoclonal antibodies. Neuroscience 1991;45:37-45.

49.Obergriesser T, Ende G, Braus DF, Henn FA. Long-term follow-up of magnetic resonance-detectable choline signal changes in the hippocampus of patients treated with electroconvulsive therapy. J Clin Psychiatry 2003;64:775-80. 50.Bramham CR, Messaoudi E. BDNF function in adult synaptic plasticity.

The synaptic consolidation hypothesis. Prog Neurobiol 2005;76:99-125. 51.Duman RS, Monteggia LM. A neurotrophic model for stress-related mood disorders. Biol Psychiatry 2006;59:1116-27.

52.Bocchio-Chiavetto L, Bagnardi V, Zanardini R, Molteni R, Nielsen MG, Placentino A, et al. Serum and plasma BDNF levels in major depression. A replication study and meta-analyses. World J Biol Psychiatry 2010;11:763-73. 53.Brunoni AR, Lopes M, Fregni F.

A systematic review and meta-analysis of clinical studies on major depression and BDNF levels. Implications for the role of neuroplasticity in depression. Int J Neuropsychopharmacol 2008;11:1169-80. 54.Rocha RB, Dondossola ER, Grande AJ, Colonetti T, Ceretta LB, Passos IC, et al. Increased BDNF levels after electroconvulsive therapy in patients with major depressive disorder.

A meta-analysis study. J Psychiatr Res 2016;83:47-53. 55.UK ECT Review Group. Efficacy and safety of electroconvulsive therapy in depressive disorders. A systematic review and meta-analysis.

Lancet 2003;361:799-808. 56.57.Semkovska M, McLoughlin DM. Objective cognitive performance associated with electroconvulsive therapy for depression. A systematic review and meta-analysis. Biol Psychiatry 2010;68:568-77.

58.Tulving E, Madigan SA. Memory and verbal learning. Annu Rev Psychol 1970;21:437-84. 59.Rose D, Fleischmann P, Wykes T, Leese M, Bindman J. Patients' perspectives on electroconvulsive therapy.

Systematic review. BMJ 2003;326:1363. 60.Semkovska M, McLoughlin DM. Measuring retrograde autobiographical amnesia following electroconvulsive therapy. Historical perspective and current issues.

J ECT 2013;29:127-33. 61.Fraser LM, O'Carroll RE, Ebmeier KP. The effect of electroconvulsive therapy on autobiographical memory. A systematic review. J ECT 2008;24:10-7.

62.Squire LR, Chace PM. Memory functions six to nine months after electroconvulsive therapy. Arch Gen Psychiatry 1975;32:1557-64. 63.Squire LR, Slater PC. Electroconvulsive therapy and complaints of memory dysfunction.

A prospective three-year follow-up study. Br J Psychiatry 1983;142:1-8. 64.Squire LR, Slater PC, Miller PL. Retrograde amnesia and bilateral electroconvulsive therapy. Long-term follow-up.

Arch Gen Psychiatry 1981;38:89-95. 65.Squire LR, Wetzel CD, Slater PC. Memory complaint after electroconvulsive therapy. Assessment with a new self-rating instrument. Biol Psychiatry 1979;14:791-801.

66.Calev A, Nigal D, Shapira B, Tubi N, Chazan S, Ben-Yehuda Y, et al. Early and long-term effects of electroconvulsive therapy and depression on memory and other cognitive functions. J Nerv Ment Dis 1991;179:526-33. 67.Sackeim HA, Prudic J, Devanand DP, Nobler MS, Lisanby SH, Peyser S, et al. A prospective, randomized, double-blind comparison of bilateral and right unilateral electroconvulsive therapy at different stimulus intensities.

Arch Gen Psychiatry 2000;57:425-34. 68.Abrams R. Does brief-pulse ECT cause persistent or permanent memory impairment?. J ECT 2002;18:71-3. 69.Peretti CS, Danion JM, Grangé D, Mobarek N.

Bilateral ECT and autobiographical memory of subjective experiences related to melancholia. A pilot study. J Affect Disord 1996;41:9-15. 70.Weiner RD, Rogers HJ, Davidson JR, Squire LR. Effects of stimulus parameters on cognitive side effects.

Ann N Y Acad Sci 1986;462:315-25. 71.Prudic J, Peyser S, Sackeim HA. Subjective memory complaints. A review of patient self-assessment of memory after electroconvulsive therapy. J ECT 2000;16:121-32.

72.Sackeim HA, Prudic J, Devanand DP, Kiersky JE, Fitzsimons L, Moody BJ, et al. Effects of stimulus intensity and electrode placement on the efficacy and cognitive effects of electroconvulsive therapy. N Engl J Med 1993;328:839-46. 73.Frith CD, Stevens M, Johnstone EC, Deakin JF, Lawler P, Crow TJ. Effects of ECT and depression on various aspects of memory.

Br J Psychiatry 1983;142:610-7. 74.Ng C, Schweitzer I, Alexopoulos P, Celi E, Wong L, Tuckwell V, et al. Efficacy and cognitive effects of right unilateral electroconvulsive therapy. J ECT 2000;16:370-9. 75.Coleman EA, Sackeim HA, Prudic J, Devanand DP, McElhiney MC, Moody BJ.

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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As the next wave began in early March, through an imported case from the UK, the government knew that it was crucial to contain virus transmission as fast as possible, in order also to safeguard its economy.Viet Nam therefore closed its borders and suspended international flights from mainland China in February, extending this to UK, Europe, the US and then the rest of the world progressively in March, whilst requiring all travelers entering the country, including its nationals, to undergo 14-day mandatory buy real zithromax online quarantine on arrival.This helped the authorities keep track of imported cases of COVID-19 and prevent further local transmission which could have then led to wider community transmission. Both the military and local governments were mobilized to provide testing, meals and amenity services to all quarantine facilities which remained free during this period.No lockdown requiredWhile there was never a nationwide lockdown, some restrictive physical distancing measures were implemented throughout the country. On 1 April 2020, the Prime Minister issued a nationwide two week physical distancing directive, which buy real zithromax online was extended by a week in major cities and hotspots.

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The committee will also interact with two other entities, exchanging information and sharing findings. They are the Independent Panel for Pandemic Preparedness and Response, established last month to evaluate global response buy real zithromax online to the COVID-19 pandemic, and the Independent Oversight Advisory Committee for the WHO Health Emergencies Programme. It is expected that the committee will present a progress report to the World Health Assembly, WHO’s decision-making body, at its resumed session in November.

The Assembly comprises delegations from WHO’s 194 member States who meet annually in May buy real zithromax online. A truncated virtual session was held this year due to the pandemic. The committee will present its full report to the Assembly in 2021.

Committed to ending COVID-19 The IHR was first adopted in 1969 and is legally-binding on buy real zithromax online 196 countries, including all WHO Member States. It was last revised in 2005. The treaty outlines rights and obligations buy real zithromax online for countries, including the requirement to report public health events, as well as the criteria to determine whether or not a particular event constitutes a “public health emergency of international concern”.

Mr. Tedros underscored WHO’s commitment to ending the pandemic, “and to working with all countries to learn from it, and to ensure that together we build the healthier, safer, fairer world that we want.” Invest in mental health buy real zithromax online WHO is also shining light on the pandemic’s impact on mental health at a time when services have suffered disruptions. For example, Mr.

Tedros said lack of social interaction has affected many people, while others have experienced anxiety and fear. Meanwhile, some mental health facilities buy real zithromax online have been closed and converted to COVID-19 treatment facilities. Globally, close to one billion people are living with a mental disorder.

In low- and middle-income countries, more than three-quarters buy real zithromax online of people with mental, neurological and substance use disorders do not receive treatment. World Mental Health Day is observed annually on 10 October, and WHO and partners are calling for a massive scale-up in investments. The UN agency also will host its first-ever global online advocacy event on mental buy real zithromax online health where experts, musicians and sports figures will discuss action to improve mental health, in addition to sharing their stories.

Global fight against polio continues The milestone eradication of wild poliovirus in Africa does not mean the disease has been defeated globally, Mr. Tedros reminded journalists. WHO announced on Tuesday that the continent has been declared free of the virus, which can cause paralysis, after no cases were reported for four years “We buy real zithromax online still have a lot of work to do to eradicate polio from the last two countries where it exists.

Afghanistan and Pakistan,” he said. Mr. Tedros also congratulated Togo, which on Wednesday celebrated the end of sleeping sickness as a public health problem.

The disease, officially known as human African Trypanosomiasis, is spread by tsetse flies and is fatal without treatment..

What if I miss a dose?

If you miss a dose, take it as soon as you can. If it is almost time for your next dose, take only that dose. Do not take double or extra doses. There should be an interval of at least 12 hours between doses.

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A strict permit system is in place for all flights arriving in NSW zithromax and dairy products from Victoria and passengers undergo comprehensive police and health checks upon does zithromax contain sulfa arrival. Health Minister Brad Hazzard said all flights are met by NSW Health staff and police officers to ensure anyone entering NSW complies with the current health orders. “There are only limited reasons anyone from Victoria should be entering NSW and people have been turned back despite being allowed on the plane in Melbourne,” does zithromax contain sulfa Mr Hazzard said.

€œVictorian residents are not permitted into NSW at all unless they are needed for specific purposes and even then have to apply for and get a permit. €œWe are constantly reviewing the situation in Victoria and will adjust the does zithromax contain sulfa health orders as necessary to protect the people of NSW.” Anyone who flies into NSW from Victoria must either be a NSW resident or have a relevant permit that allows entry into NSW – that can include:defence officialsdoctors and nursescritical workers in energy, mining and constructionchild protection workersdisability workers.All travellers are provided with a pack of two masks and hand sanitiser by the airlines. Upon arrival into NSW all passengers from Victoria are.

given masks if they left them on the planetemperature checkedasked relevant questions about their health. And their does zithromax contain sulfa permit is checked to ensure it complies with the strict permit system.Anyone without a valid permit is referred to NSW Police and taken to the Special Health Accommodation to complete 14 days of quarantine. Strict instructions and rules are in place for those going into ‘Home Isolation’ including.

Recommended they be collected in a private car by family or friendsnot to use public transport to get hometo only sit in the back seat of a car with the windows open and air conditioning not does zithromax contain sulfa on recirculationtold to wear their face masks and observe hand hygiene recommendations, andcalled to make sure they arrive home.NSW Health is provided the contact details of everyone who enters NSW from Victoria. NSW Police is conducting regular compliance checks for people told to go into ‘Home Isolation’ as well as responding to reports from the community in relation to suspected breaches. Over the weekend, NSW Police visited almost 600 homes to check that those that were meant to does zithromax contain sulfa be self-isolating were doing so.

In addition to that, over the same period NSW Police received 374 calls to Crime Stoppers reporting suspected breaches of the health orders, the majority of which were for people suspected of not following self-isolation rules. ​Seven cutting-edge NSW research projects have been awarded almost $15 million in NSW Government grants to improve the health of people with spinal cord injuries (SCI).Treasurer Dominic Perrottet and Minister for Health and Medical Research Brad Hazzard today announced the grants at the opening of the Neuroscience Research Australia (NeuRA) Spinal Cord Injury Research Centre at Randwick where three of the projects will be carried out. €œThe investment of close to $15 million over four years was a centrepiece of our last does zithromax contain sulfa Budget and it’s exciting to see the range of research projects now underway,” Mr Perrottet said.

€œThis is about improving the health and wellbeing of people with spinal cord injuries, and these projects could help people not just in NSW but right around the world.” Minister Hazzard said every one of the innovative projects holds tremendous promise to improve treatment for people living with spinal cord injuries, giving back muscle function, sense of touch and other abilities that most of us take for granted. €œA spinal injury brings very substantial life challenges, but advances in research now mean survivors can have a better quality of life – and even the hope of a cure,” does zithromax contain sulfa Mr Hazzard said. €œThese projects have great scope, from investigating ways to restore touch sensation through immersive virtual reality through to using electrical stimulation to improve breathing for people affected by the most severe form of paralysis.” The following grant recipients will conduct their research at the new NeuRA centre.

Associate Professor Sylvia Gustin, The University of NSW, does zithromax contain sulfa Neuroscience Research Australia – received $2.5 million for her research project on using virtual reality training to restore touch sensation. Professor Jane Butler – Neuroscience Research Australia, The University of NSW, received $1.5 million to develop a treatment to restore voluntary function after spinal cord injury. And Dr Euan McCaughey, Neuroscience Research Australia, The University of NSW, received $2.4 million for his research into using muscle stimulation to improve respiratory function for people with tetraplegia.

The projects have been awarded through the NSW Government’s Spinal Cord Injury Research Grants program, launched in November 2019, with guidance does zithromax contain sulfa from an advisory committee of spinal cord injury experts. NeuRA CEO, Professor Peter Schofield, said the range and scope of the funded research projects held exciting promise for health related outcomes. €œNeuroscience Research Australia is at the forefront of spinal cord injury research does zithromax contain sulfa in Australia.

Our new Spinal Cord Injury Research Centre and these research projects will dramatically improve Australia’s understanding of how to best treat people with these life-long injuries,” Professor Schofield said. €œNeuRA thanks the NSW Government for funding the Spinal Cord Injury Research Grants Program, and SpinalCure Australia for its tireless efforts in campaigning for more research funding to improve the quality of life for people with a spinal cord injury.” Information on grant recipients and their research projects is available on the OHMR Funded Research Directory​​.​​​.

A strict permit system buy zithromax online with free samples is in place for all flights arriving in NSW from Victoria and passengers undergo comprehensive police and health buy real zithromax online checks upon arrival. Health Minister Brad Hazzard said all flights are met by NSW Health staff and police officers to ensure anyone entering NSW complies with the current health orders. “There are only limited reasons anyone from Victoria should be entering NSW and people have been turned back despite being buy real zithromax online allowed on the plane in Melbourne,” Mr Hazzard said. €œVictorian residents are not permitted into NSW at all unless they are needed for specific purposes and even then have to apply for and get a permit.

€œWe are constantly reviewing the situation in Victoria and will adjust the health orders as necessary to protect the people of NSW.” Anyone who flies into NSW from Victoria must either be a NSW resident or have a relevant permit that allows entry into NSW – that can include:defence officialsdoctors and nursescritical workers in energy, mining and constructionchild protection workersdisability workers.All travellers are provided with a pack of buy real zithromax online two masks and hand sanitiser by the airlines. Upon arrival into NSW all passengers from Victoria are. given masks if they left them on the planetemperature checkedasked relevant questions about their health. And their permit is checked to ensure it complies with the strict permit system.Anyone without a valid permit is referred to buy real zithromax online NSW Police and taken to the Special Health Accommodation to complete 14 days of quarantine.

Strict instructions and rules are in place for those going into ‘Home Isolation’ including. Recommended they be collected in a private car by family or friendsnot to use public transport to get hometo only sit in the back seat of a car with the windows open and air conditioning not on recirculationtold to wear their face masks and observe hand buy real zithromax online hygiene recommendations, andcalled to make sure they arrive home.NSW Health is provided the contact details of everyone who enters NSW from Victoria. NSW Police is conducting regular compliance checks for people told to go into ‘Home Isolation’ as well as responding to reports from the community in relation to suspected breaches. Over the buy real zithromax online weekend, NSW Police visited almost 600 homes to check that those that were meant to be self-isolating were doing so.

In addition to that, over the same period NSW Police received 374 calls to Crime Stoppers reporting suspected breaches of the health orders, the majority of which were for people suspected of not following self-isolation rules. ​Seven cutting-edge NSW research projects have been awarded almost $15 million in NSW Government grants to improve the health of people with spinal cord injuries (SCI).Treasurer Dominic Perrottet and Minister for Health and Medical Research Brad Hazzard today announced the grants at the opening of the Neuroscience Research Australia (NeuRA) Spinal Cord Injury Research Centre at Randwick where three of the projects will be carried out. €œThe investment of close to $15 million over four years was a centrepiece of our last Budget and it’s exciting to buy real zithromax online see the range of research projects now underway,” Mr Perrottet said. €œThis is about improving the health and wellbeing of people with spinal cord injuries, and these projects could help people not just in NSW but right around the world.” Minister Hazzard said every one of the innovative projects holds tremendous promise to improve treatment for people living with spinal cord injuries, giving back muscle function, sense of touch and other abilities that most of us take for granted.

€œA spinal injury brings very substantial life challenges, but advances in research now mean survivors buy real zithromax online can have a better quality of life – and even the hope of a cure,” Mr Hazzard said. €œThese projects have great scope, from investigating ways to restore touch sensation through immersive virtual reality through to using electrical stimulation to improve breathing for people affected by the most severe form of paralysis.” The following grant recipients will conduct their research at the new NeuRA centre. Associate Professor Sylvia Gustin, The University of NSW, Neuroscience Research Australia – received $2.5 million for her research project on using virtual reality training to restore buy real zithromax online touch sensation. Professor Jane Butler – Neuroscience Research Australia, The University of NSW, received $1.5 million to develop a treatment to restore voluntary function after spinal cord injury.

And Dr Euan McCaughey, Neuroscience Research Australia, The University of NSW, received $2.4 million for his research into using muscle stimulation to improve respiratory function for people with tetraplegia. The projects have been awarded through the NSW Government’s Spinal Cord Injury Research Grants program, launched in November 2019, with guidance buy real zithromax online from an advisory committee of spinal cord injury experts. NeuRA CEO, Professor Peter Schofield, said the range and scope of the funded research projects held exciting promise for health related outcomes. €œNeuroscience Research Australia is at the forefront buy real zithromax online of spinal cord injury research in Australia.

Our new Spinal Cord Injury Research Centre and these research projects will dramatically improve Australia’s understanding of how to best treat people with these life-long injuries,” Professor Schofield said. €œNeuRA thanks the NSW Government for funding the Spinal Cord Injury Research Grants Program, and SpinalCure Australia for its tireless efforts in campaigning for more research funding to improve the quality of life for people with a spinal cord injury.” Information on grant recipients and their research projects is available on the OHMR Funded Research Directory​​.​​​.

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Patients Figure free zithromax antibiotics 1 find out this here. Figure 1 free zithromax antibiotics. Enrollment and Randomization. Of the 1107 patients who were assessed for eligibility, 1063 free zithromax antibiotics underwent randomization. 541 were assigned to the remdesivir group and 522 to the placebo group (Figure 1).

Of those free zithromax antibiotics assigned to receive remdesivir, 531 patients (98.2%) received the treatment as assigned. Forty-nine patients had remdesivir treatment discontinued before day 10 because of an adverse event or a serious adverse event other than death (36 patients) or because the patient withdrew consent (13). Of those assigned to receive placebo, 518 patients (99.2%) received free zithromax antibiotics placebo as assigned. Fifty-three patients discontinued placebo before day 10 because of an adverse event or a serious adverse event other than death (36 patients), because the patient withdrew consent (15), or because the patient was found to be ineligible for trial enrollment (2). As of April 28, 2020, a total of 391 patients in the remdesivir group and 340 in the placebo group had completed free zithromax antibiotics the trial through day 29, recovered, or died.

Eight patients who received remdesivir and 9 who received placebo terminated their participation in the trial before day 29. There were 132 patients in the free zithromax antibiotics remdesivir group and 169 in the placebo group who had not recovered and had not completed the day 29 follow-up visit. The analysis population included 1059 patients for whom we have at least some postbaseline data available (538 in the remdesivir group and 521 in the placebo group). Four of the 1063 patients were not included in the primary analysis because no free zithromax antibiotics postbaseline data were available at the time of the database freeze. Table 1.

Table 1 free zithromax antibiotics. Demographic and Clinical Characteristics at Baseline. The mean age of free zithromax antibiotics patients was 58.9 years, and 64.3% were male (Table 1). On the basis of the evolving epidemiology of Covid-19 during the trial, 79.8% of patients were enrolled at sites in North America, 15.3% in Europe, and 4.9% in Asia (Table S1). Overall, 53.2% of the free zithromax antibiotics patients were white, 20.6% were black, 12.6% were Asian, and 13.6% were designated as other or not reported.

249 (23.4%) were Hispanic or Latino. Most patients had either one (27.0%) or two or more (52.1%) of the prespecified coexisting conditions at enrollment, most commonly hypertension (49.6%), obesity free zithromax antibiotics (37.0%), and type 2 diabetes mellitus (29.7%). The median number of days between symptom onset and randomization was free zithromax antibiotics 9 (interquartile range, 6 to 12). Nine hundred forty-three (88.7%) patients had severe disease at enrollment as defined in the Supplementary Appendix. 272 (25.6%) patients met category 7 criteria on the ordinal scale, 197 (18.5%) category free zithromax antibiotics 6, 421 (39.6%) category 5, and 127 (11.9%) category 4.

There were 46 (4.3%) patients who had missing ordinal scale data at enrollment. No substantial free zithromax antibiotics imbalances in baseline characteristics were observed between the remdesivir group and the placebo group. Primary Outcome Figure 2. Figure 2 free zithromax antibiotics. Kaplan–Meier Estimates of Cumulative Recoveries.

Cumulative recovery estimates are shown in the free zithromax antibiotics overall population (Panel A), in patients with a baseline score of 4 on the ordinal scale (not receiving oxygen. Panel B), in those with a baseline score of 5 (receiving oxygen. Panel C), free zithromax antibiotics in those with a baseline score of 6 (receiving high-flow oxygen or noninvasive mechanical ventilation. Panel D), and in those with a baseline score of 7 (receiving mechanical ventilation or ECMO. Panel E) free zithromax antibiotics.

Table 2. Table 2 free zithromax antibiotics. Outcomes Overall and According to Score on the Ordinal Scale in the Intention-to-Treat Population. Figure free zithromax antibiotics 3. Figure 3.

Time to free zithromax antibiotics Recovery According to Subgroup. The widths of the confidence intervals have not been adjusted for multiplicity and therefore cannot be used to infer treatment effects. Race and ethnic group were zithromax wiki reported free zithromax antibiotics by the patients. Patients in the remdesivir group had a shorter time to recovery than patients in the placebo group (median, free zithromax antibiotics 11 days, as compared with 15 days. Rate ratio for recovery, 1.32.

95% confidence interval [CI], 1.12 to free zithromax antibiotics 1.55. P<0.001. 1059 patients (Figure free zithromax antibiotics 2 and Table 2). Among patients with a baseline ordinal score of 5 (421 patients), the rate ratio for recovery was 1.47 (95% CI, 1.17 to 1.84). Among patients with a baseline score of 4 (127 patients) and those with a baseline score of 6 (197 patients), the rate ratio estimates for recovery were 1.38 (95% free zithromax antibiotics CI, 0.94 to 2.03) and 1.20 (95% CI, 0.79 to 1.81), respectively.

For those receiving mechanical ventilation or ECMO at enrollment (baseline ordinal scores of 7. 272 patients), the rate free zithromax antibiotics ratio for recovery was 0.95 (95% CI, 0.64 to 1.42). A test of interaction of treatment with baseline score on the ordinal scale was not significant. An analysis adjusting for baseline ordinal score as a stratification variable was conducted to evaluate the overall effect free zithromax antibiotics (of the percentage of patients in each ordinal score category at baseline) on the primary outcome. This adjusted analysis produced a similar treatment-effect estimate (rate ratio for recovery, 1.31.

95% CI, 1.12 free zithromax antibiotics to 1.54. 1017 patients). Table S2 in the Supplementary Appendix shows results according to the baseline severity stratum of mild-to-moderate as compared with severe free zithromax antibiotics. Patients who underwent randomization during the first 10 days after the onset of symptoms had a rate ratio for recovery of 1.28 (95% CI, 1.05 to 1.57. 664 patients), whereas patients who underwent randomization more than 10 free zithromax antibiotics days after the onset of symptoms had a rate ratio for recovery of 1.38 (95% CI, 1.05 to 1.81.

380 patients) (Figure 3). Key Secondary Outcome The free zithromax antibiotics odds of improvement in the ordinal scale score were higher in the remdesivir group, as determined by a proportional odds model at the day 15 visit, than in the placebo group (odds ratio for improvement, 1.50. 95% CI, free zithromax antibiotics 1.18 to 1.91. P=0.001. 844 patients) free zithromax antibiotics (Table 2 and Fig.

S5). Mortality was numerically lower in the free zithromax antibiotics remdesivir group than in the placebo group, but the difference was not significant (hazard ratio for death, 0.70. 95% CI, 0.47 to 1.04. 1059 patients) free zithromax antibiotics. The Kaplan–Meier estimates of mortality by 14 days were 7.1% and 11.9% in the remdesivir and placebo groups, respectively (Table 2).

The Kaplan–Meier estimates of mortality by 28 days are not reported in this preliminary analysis, given the large number of free zithromax antibiotics patients that had yet to complete day 29 visits. An analysis with adjustment for baseline ordinal score as a stratification variable showed a hazard ratio for death of 0.74 (95% CI, 0.50 to 1.10). Safety Outcomes Serious adverse events occurred in 114 patients (21.1%) in the remdesivir group and 141 patients (27.0%) in the placebo group (Table free zithromax antibiotics S3). 4 events (2 in each group) were judged by site investigators to be related to remdesivir or placebo. There were 28 serious respiratory failure adverse events in the remdesivir group (5.2% free zithromax antibiotics of patients) and 42 in the placebo group (8.0% of patients).

Acute respiratory failure, hypotension, viral pneumonia, and acute kidney injury were slightly more common among patients in the placebo group. No deaths were considered to be related to treatment assignment, as judged by the site investigators free zithromax antibiotics. Grade 3 or 4 adverse events occurred in 156 patients (28.8%) in the remdesivir group and in 172 in the placebo group (33.0%) (Table S4). The most common free zithromax antibiotics adverse events in the remdesivir group were anemia or decreased hemoglobin (43 events [7.9%], as compared with 47 [9.0%] in the placebo group). Acute kidney injury, decreased estimated glomerular filtration rate or creatinine clearance, or increased blood creatinine (40 events [7.4%], as compared with 38 [7.3%]).

Pyrexia (27 events free zithromax antibiotics [5.0%], as compared with 17 [3.3%]). Hyperglycemia or increased blood glucose level (22 events [4.1%], as compared with 17 [3.3%]). And increased aminotransferase levels including alanine aminotransferase, aspartate aminotransferase, or both (22 free zithromax antibiotics events [4.1%], as compared with 31 [5.9%]). Otherwise, the incidence of adverse events was not found to be significantly different between the remdesivir group and the placebo group..

Patients Figure http://sw.keimfarben.de/how-much-does-zithromax-cost/ 1 buy real zithromax online. Figure 1 buy real zithromax online. Enrollment and Randomization.

Of the 1107 patients who were assessed for eligibility, 1063 underwent buy real zithromax online randomization. 541 were assigned to the remdesivir group and 522 to the placebo group (Figure 1). Of those assigned to receive remdesivir, 531 patients (98.2%) buy real zithromax online received the treatment as assigned.

Forty-nine patients had remdesivir treatment discontinued before day 10 because of an adverse event or a serious adverse event other than death (36 patients) or because the patient withdrew consent (13). Of those assigned to receive placebo, 518 patients (99.2%) buy real zithromax online received placebo as assigned. Fifty-three patients discontinued placebo before day 10 because of an adverse event or a serious adverse event other than death (36 patients), because the patient withdrew consent (15), or because the patient was found to be ineligible for trial enrollment (2).

As of April 28, 2020, a total of 391 patients in the remdesivir buy real zithromax online group and 340 in the placebo group had completed the trial through day 29, recovered, or died. Eight patients who received remdesivir and 9 who received placebo terminated their participation in the trial before day 29. There were 132 patients in the remdesivir group and 169 in the placebo group who had not recovered and had not completed the day buy real zithromax online 29 follow-up visit.

The analysis population included 1059 patients for whom we have at least some postbaseline data available (538 in the remdesivir group and 521 in the placebo group). Four of the 1063 patients were not included in the primary analysis because no postbaseline data were available at the buy real zithromax online time of the database freeze. Table 1.

Table 1 buy real zithromax online. Demographic and Clinical Characteristics at Baseline. The mean age of buy real zithromax online patients was 58.9 years, and 64.3% were male (Table 1).

On the basis of the evolving epidemiology of Covid-19 during the trial, 79.8% of patients were enrolled at sites in North America, 15.3% in Europe, and 4.9% in Asia (Table S1). Overall, 53.2% of the patients were white, 20.6% were black, 12.6% were buy real zithromax online Asian, and 13.6% were designated as other or not reported. 249 (23.4%) were Hispanic or Latino.

Most patients had either one (27.0%) or two buy real zithromax online or more (52.1%) of the prespecified coexisting conditions at enrollment, most commonly hypertension (49.6%), obesity (37.0%), and type 2 diabetes mellitus (29.7%). The median number of days between symptom onset and randomization was 9 buy real zithromax online (interquartile range, 6 to 12). Nine hundred forty-three (88.7%) patients had severe disease at enrollment as defined in the Supplementary Appendix.

272 (25.6%) patients met category 7 criteria on the ordinal scale, 197 (18.5%) category 6, buy real zithromax online 421 (39.6%) category 5, and 127 (11.9%) category 4. There were 46 (4.3%) patients who had missing ordinal scale data at enrollment. No substantial imbalances in baseline characteristics were buy real zithromax online observed between the remdesivir group and the placebo group.

Primary Outcome Figure 2. Figure 2 buy real zithromax online. Kaplan–Meier Estimates of Cumulative Recoveries.

Cumulative recovery estimates are shown in the overall buy real zithromax online population (Panel A), in patients with a baseline score of 4 on the ordinal scale (not receiving oxygen. Panel B), in those with a baseline score of 5 (receiving oxygen. Panel C), in those with a baseline score of 6 (receiving high-flow buy real zithromax online oxygen or noninvasive mechanical ventilation.

Panel D), and in those with a baseline score of 7 (receiving mechanical ventilation or ECMO. Panel E) buy real zithromax online. Table 2.

Table 2 buy real zithromax online. Outcomes Overall and According to Score on the Ordinal Scale in the Intention-to-Treat Population. Figure 3 buy real zithromax online.

Figure 3. Time to buy real zithromax online Recovery According to Subgroup. The widths of the confidence intervals have not been adjusted for multiplicity and therefore cannot be used to infer treatment effects.

Race and buy real zithromax online ethnic group were reported by the patients. Patients in buy real zithromax online the remdesivir group had a shorter time to recovery than patients in the placebo group (median, 11 days, as compared with 15 days. Rate ratio for recovery, 1.32.

95% confidence interval [CI], 1.12 to buy real zithromax online 1.55. P<0.001. 1059 patients (Figure buy real zithromax online 2 and Table 2).

Among patients with a baseline ordinal score of 5 (421 patients), the rate ratio for recovery was 1.47 (95% CI, 1.17 to 1.84). Among patients with a baseline score of 4 (127 patients) and those with a buy real zithromax online baseline score of 6 (197 patients), the rate ratio estimates for recovery were 1.38 (95% CI, 0.94 to 2.03) and 1.20 (95% CI, 0.79 to 1.81), respectively. For those receiving mechanical ventilation or ECMO at enrollment (baseline ordinal scores of 7.

272 patients), the rate ratio for recovery buy real zithromax online was 0.95 (95% CI, 0.64 to 1.42). A test of interaction of treatment with baseline score on the ordinal scale was not significant. An analysis adjusting for baseline ordinal score as a stratification variable was conducted to evaluate the overall effect (of the percentage of patients in each ordinal score buy real zithromax online category at baseline) on the primary outcome.

This adjusted analysis produced a similar treatment-effect estimate (rate ratio for recovery, 1.31. 95% CI, buy real zithromax online 1.12 to 1.54. 1017 patients).

Table S2 in the Supplementary buy real zithromax online Appendix shows results according to the baseline severity stratum of mild-to-moderate as compared with severe. Patients who underwent randomization during the first 10 days after the onset of symptoms had a rate ratio for recovery of 1.28 (95% CI, 1.05 to 1.57. 664 patients), whereas patients who underwent randomization more than 10 days after the onset of symptoms had a rate buy real zithromax online ratio for recovery of 1.38 (95% CI, 1.05 to 1.81.

380 patients) (Figure 3). Key Secondary Outcome The odds buy real zithromax online of improvement in the ordinal scale score were higher in the remdesivir group, as determined by a proportional odds model at the day 15 visit, than in the placebo group (odds ratio for improvement, 1.50. 95% CI, 1.18 to 1.91 buy real zithromax online.

P=0.001. 844 patients) buy real zithromax online (Table 2 and Fig. S5).

Mortality was numerically lower in the remdesivir group than in the placebo group, but buy real zithromax online the difference was not significant (hazard ratio for death, 0.70. 95% CI, 0.47 to 1.04. 1059 patients) buy real zithromax online.

The Kaplan–Meier estimates of mortality by 14 days were 7.1% and 11.9% in the remdesivir and placebo groups, respectively (Table 2). The Kaplan–Meier estimates of buy real zithromax online mortality by 28 days are not reported in this preliminary analysis, given the large number of patients that had yet to complete day 29 visits. An analysis with adjustment for baseline ordinal score as a stratification variable showed a hazard ratio for death of 0.74 (95% CI, 0.50 to 1.10).

Safety Outcomes Serious adverse events occurred in 114 patients (21.1%) in the remdesivir group and 141 patients (27.0%) in the placebo group buy real zithromax online (Table S3). 4 events (2 in each group) were judged by site investigators to be related to remdesivir or placebo. There were 28 serious respiratory failure adverse events in the remdesivir group (5.2% of patients) and 42 buy real zithromax online in the placebo group (8.0% of patients).

Acute respiratory failure, hypotension, viral pneumonia, and acute kidney injury were slightly more common among patients in the placebo group. No deaths were considered to be related buy real zithromax online to treatment assignment, as judged by the site investigators. Grade 3 or 4 adverse events occurred in 156 patients (28.8%) in the remdesivir group and in 172 in the placebo group (33.0%) (Table S4).

The most common adverse events in the remdesivir group were anemia or decreased hemoglobin (43 events buy real zithromax online [7.9%], as compared with 47 [9.0%] in the placebo group). Acute kidney injury, decreased estimated glomerular filtration rate or creatinine clearance, or increased blood creatinine (40 events [7.4%], as compared with 38 [7.3%]). Pyrexia (27 events [5.0%], as compared with 17 [3.3%]).

Hyperglycemia or increased blood glucose level (22 events [4.1%], as compared with 17 [3.3%]). And increased aminotransferase levels including alanine aminotransferase, aspartate aminotransferase, or both (22 events [4.1%], as compared with 31 [5.9%]). Otherwise, the incidence of adverse events was not found to be significantly different between the remdesivir group and the placebo group..

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Protecting the safety and health of essential workers who support America’s food security—including the meat, poultry, and pork processing industries—is a top priority for the Occupational Safety and Health Administration (OSHA).OSHA and the Centers for Disease Control and Prevention issued additional guidance to reduce the risk of exposure to the coronavirus where can i buy zithromax z pak and keep workers safe and healthy in the meatpacking and meat processing industries —including those involved in beef, pork, and poultry operations. This new guidance provides specific recommendations for employers to meet their obligations to protect workers in these facilities, where people normally work closely together and share workspaces and equipment. Here are eight where can i buy zithromax z pak ways to help minimize meat processing workers’ exposure to the coronavirus.

Screen workers before they enter the workplace. If a worker becomes sick, send them home and disinfect their workstation and any tools they used. Move workstations where can i buy zithromax z pak farther apart.

Install partitions between workstations using strip curtains, plexiglass, or similar materials. To limit spread between groups, assign the same workers to the same shifts with the same coworkers. Prevent workers from where can i buy zithromax z pak using other workers’ equipment.

Allow workers to wear face coverings when entering, inside, and exiting the facility. Encourage workers to report any safety and health concerns to their supervisors.OSHA is committed to ensuring that workers and employers in essential industries have clear guidance to keep workers safe and healthy from the coronavirus—including guidance for essential workers in construction, manufacturing, package delivery, and retail. Workers and employers who have questions or concerns about where can i buy zithromax z pak workplace safety can contact OSHA online or by phone at 1-800-321-6742 (OSHA).

You can find additional resources and learn more about OSHA’s response to the coronavirus at www.osha.gov/coronavirus. Loren Sweatt is the Principal Deputy Assistant Secretary for the U.S. Department of Labor’s Occupation Safety and Health Administration where can i buy zithromax z pak Editor’s Note.

It is important to note that information and guidance about COVID-19 continually evolve as conditions change. Workers and employers are encouraged to regularly refer to the resources below for updates:.

Protecting the safety and health of essential workers who support America’s food security—including the meat, poultry, and pork processing industries—is a top priority for the Occupational Safety and Health Administration (OSHA).OSHA and the Centers for Disease Control and Prevention issued how long do the side effects of zithromax last additional guidance to reduce the risk of exposure to the coronavirus and keep workers safe and healthy in the meatpacking and meat processing industries —including those buy real zithromax online involved in beef, pork, and poultry operations. This new guidance provides specific recommendations for employers to meet their obligations to protect workers in these facilities, where people normally work closely together and share workspaces and equipment. Here are buy real zithromax online eight ways to help minimize meat processing workers’ exposure to the coronavirus. Screen workers before they enter the workplace.

If a worker becomes sick, send them home and disinfect their workstation and any tools they used. Move workstations buy real zithromax online farther apart. Install partitions between workstations using strip curtains, plexiglass, or similar materials. To limit spread between groups, assign the same workers to the same shifts with the same coworkers.

Prevent workers from using other workers’ buy real zithromax online equipment. Allow workers to wear face coverings when entering, inside, and exiting the facility. Encourage workers to report any safety and health concerns to their supervisors.OSHA is committed to ensuring that workers and employers in essential industries have clear guidance to keep workers safe and healthy from the coronavirus—including guidance for essential workers in construction, manufacturing, package delivery, and retail. Workers and employers who have questions or concerns buy real zithromax online about workplace safety can contact OSHA online or by phone at 1-800-321-6742 (OSHA).

You can find additional resources and learn more about OSHA’s response to the coronavirus at www.osha.gov/coronavirus. Loren Sweatt is the Principal Deputy Assistant Secretary for the U.S. Department of Labor’s Occupation Safety and buy real zithromax online Health Administration Editor’s Note. It is important to note that information and guidance about COVID-19 continually evolve as conditions change.

Workers and employers are encouraged to regularly refer to the resources below for updates:.