Publisher Health

A combined analysis of results from 149 earlier studies finds that treatment rates for major depressive disorder remain low worldwide, particularly for people living in low and lower-middle income countries. Alize Ferrari of the University of Queensland, Australia, Modhurima Moitra of the University of Washington, U.S., and colleagues present these findings in the open-access journal PLOS Medicine.
In recent years, national and global initiatives have made increasing efforts to address the tremendous burden posed by major depressive disorder. However, treatment rates remain low. Analyses that combine results from studies on depression treatment from different regions can help identify opportunities for improvement. However, many such analyses do not adequately account for variations in study methods that make results from different studies difficult to compare.
To provide further clarity, Ferrari and colleagues conducted an updated analysis of 149 studies on treatment for major depressive disorder conducted in 84 countries between 2000 and 2021. Applying a statistical method known as Bayesian meta-regression analysis, they combined the studies to examine treatment rates around the world.
The findings of this meta-analysis suggest that treatment rates remain low worldwide, and it highlights disparities in treatment between countries with different resource levels. In particular, use of mental health services by people with major depressive disorder is estimated to be 33 percent in high-income countries and just eight percent in low and lower-middle income countries.
Rates of treatment considered to be minimally sufficient for treating major depressive disorder are lower, estimated at 23 percent for high-income countries and 3 percent in low and lower-middle income countries.
The authors note a lack of high-quality data on depression treatment for low and lower-middle income countries, mostly in Sub-Saharan Africa and South Asia; further research could attempt to address that gap and thereby improve the accuracy of the treatment rates reported in this study. Future research could also examine how to best improve treatment access in different regions.
Overall, the researchers say, their findings could help inform efforts by governments and policymakers to more effectively address depression treatment worldwide.
Ferrari adds, “Treatment coverage for major depressive disorder continues to be low globally, with many individuals failing to receive a level of care consistent with practice guideline recommendations. This highlights the need to reconsider the availability of appropriate care and facilitators of treatment as we respond to the large burden imposed by this disorder.”
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New studies emerge daily on the effect of the human microbiome on human health: colon cancer, ulcers, and cognitive conditions such as Alzheimer’s disease have been associated with the communities of microbes that live in our bodies. However, global research into the human microbiome is heavily biased in favor of wealthy countries such as the United States and United Kingdom, according to a study publishing February 15th in the open-access journal PLOS Biology by Richard Abdill, Elizabeth Adamowicz and Ran Blekhman at the University of Minnesota.
The authors evaluated global repositories of DNA sequencing data used to measure microbiome content and found that almost half of all publicly available samples come from subjects in the U.S., even though that country represents only 4.3 percent of the global population. These findings raise questions about whether advances in the field will be applicable to countries that have fewer resources and populations that don’t receive as much attention in the literature.
The “human microbiome” refers to the communities of microorganisms living on and in the human body — estimates suggest a person’s human cells are greatly outnumbered by the trillions of bacteria making up their microbiome, living everywhere from the small intestine to the surface of the eyeball.
Research shows that these microbes have extensive interactions with their human hosts and have wide-ranging effects, both positive and negative. Some gut microbes, for example, help break down food into nutrients that humans cannot naturally access, while others have been linked to conditions such as inflammatory bowel disease, stomach cancer, and diabetes. Accordingly, billions of dollars have been invested in researching these relationships since the early 2000s. To understand where this funding was being used, the Minnesota researchers inventoried more than 440,000 samples of human microbiome data shared in international repositories maintained by organizations such as the National Institutes of Health in the United States and Japan’s National Institute of Genetics.
“Interest in the human microbiome has been growing worldwide,” said Richard Abdill, the study’s lead author. “When we look at how the field is developing, who is being included, and where resources have been allocated, it is clear that our understanding of the ‘human’ microbiome does not include most humans. Our study is a step towards quantifying this disparity.”
There are many reasons for these disparities, such as economic and political factors that impact scientific research, and logistical difficulties with performing research in countries with less infrastructure. However, the microbiome is in turn influenced by factors such as genetics, geography, diet, and lifestyle, making it important to study many populations to find links to human health. Because of this, the authors maintain that the exclusion of the developing world from microbiome research threatens to create a situation in which future microbiome-based medical treatments may only be effective for people in some countries or populations.
Of the samples for which a country of origin could be determined, the researchers found more than 71 percent came from Europe and North America, almost five times as many as would be expected given their population. Central and Southern Asia was the most underrepresented region: Though more than 2 billion people live in countries such as India, Pakistan, and Bangladesh, only 13,620 microbiome samples were available from that region, or 1.5 percent of samples from almost 26 percent of the world’s population. No samples at all were found from countries such as Algeria, Yemen, Afghanistan, and Kazakhstan.
Blekhman adds, “Interest in the human microbiome has been growing quickly, but there are conspicuous gaps in where that interest is being directed. Our study investigated all publicly available human microbiome samples — almost half a million samples — to quantify these gaps. We found that our understanding of the ‘human’ microbiome leaves out a lot of the humans.”
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The impact of the COVID-19 pandemic hit hardest in deprived areas of England and Wales, with excess years of life lost more than three times as high in the North West than the South West of England. The research, publishing February 15th in the open access journal PLOS Medicine, also finds 11 times as many excess deaths in 15-44 year olds in the most deprived areas compared to the most affluent ones, and suggests that measuring years of life lost can be more informative for assessing inequalities resulting from the pandemic than looking at excess deaths alone.
Comparing the number of deaths during the pandemic with statistics from previous years can shed light on its impact, but looking at excess deaths alone underestimates years of life lost and does not account for the differences in ages at which people die in different social groups. Evangelos Kontopantelis at the University of Manchester and colleagues looked at mortality registers and estimated expected years of life lost during 2020, by sex, geographical region, and deprivation quintile, using data from Jan 2015 to December 2020.
The team finds striking socioeconomic and geographical health inequalities, with 1,645 years of life lost per 100,000 of the population in the most deprived areas and 916 years per 100,000 people in the most affluent. London and the North West had the highest years of life lost with South Central and the South West lowest. These inequalities were also seen when examining excess deaths, especially in younger age groups: there were 11 times as many excess deaths in deprived compared to affluent areas in 15-44 year olds, three times as many in 45-64 year olds, almost twice as many in 65-74 year olds, 1.4 times more in 75-84 year olds and no significant difference in people over 85.
Looking at years of life lost is an effective way of determining unmet needs and the authors suggest this could be used for prioritising vaccine delivery and providing targeted financial and social support as part of immediate and longer-term recovery plans. Public health measures and wider socioeconomic interventions are needed to support communities that have been disproportionately affected by the pandemic.
Kontopantelis adds, “The impact of the pandemic, when quantified using years of life lost, was higher than previously thought, on the most deprived areas of England and Wales, widening pre-existing health inequalities.”
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It happens in the first hours after fertilization: The cells of the early embryo begin to independently produce proteins, the building blocks for cells and organs. Their own, uniquely composed genetic material serves as the blueprint. In vertebrates, the starting signal for this process comes from three maternal proteins that bind to the DNA of the offspring. New findings from Dr. Meijiang Gao from a research team led by Dr. Daria Onichtchouk in the University of Freiburg’s Institute of Biology I now show, using a zebrafish model, how two of these three start proteins of the egg cell elicit their roles and how they act in further development. The findings were published in a study in the journal Nature Communications.
“We have shown how the proteins Pou5f3 and Sox19b function at different time points in embryonic development and in different areas of the embryo,” says the biologist of the study’s integrative approach. She conducts her research at the University of Freiburg’s Cluster of Excellence CIBSS — Centre for Integrative Biological Signalling Studies, whose scientists are pursuing the goal of understanding signaling processes across scales. Prof. Dr. Jens Timmer und Markus Rosenblatt from the University of Freiburg’s Institute of Physics also participated in the study.
Important molecules for stem cell research
Similar human proteins, so-called homologues of Pou5f3 and Sox19b, are used in research to artificially produce stem cells from human skin cells. “The precise role of these factors in development is highly interesting for research and medicine for this reason as well,” says Onichtchouk.
To determine precisely what genes are controlled in what way by these two proteins and how they interact, the biologist and her team studied the development of zebrafish embryos. They induced mutations in the genes for Pou5f3 and Sox19b so that the fish would no longer produce these regulatory proteins. In this way, they succeeded in demonstrating that the two proteins have independent tasks. However, they both act on the DNA by binding to gene regulatory regions and making the genes freely accessible to the cellular machinery.
Gene control in sleep mode
In addition, the team discovered that Pou5f3 and Sox19b suppress late genetic programs. “They keep important processes in sleep mode so that they do not start until later, when the appropriate step in development approaches,” describes Onichtchouk. “This concerns the genes responsible for the development of the organs.” However, Pou5f3 and Sox19b appear to be the determining factors for the activation of the genes only on the ventral side of the embryo. On the dorsal side, they are ineffective. Onichtchouk wants to determine the reason for this: “We are curious to find out what takes over this function here and whether these proteins also originate from the mother.”
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Scientists have developed mathematical models that act as patient ‘surrogates’ for evaluating potential prostate cancer treatments.
The research, published today in eLife, could ultimately help clinicians choose the most effective drug combination before they start to treat a patient, potentially improving their response and avoiding drug resistance.
Researchers used an approach called Boolean modelling, which is already used to describe dynamics of complex cell signalling processes. But existing models have been generic and have not accounted for the differences between individual patients’ diseases or how they respond to treatment.
“The dream has always been to use more and more complex models and data until we can have digital twins, or virtual humans or surrogates — a simulation that helps select the proper clinical treatment for a given patient with high degrees of specificity or sensitivity,” explains Arnau Montagud, who was a researcher at Institut Curie, Paris, France, at the time the study was carried out, and is now at the Barcelona Supercomputing Center (BSC), Spain. “We wanted to know if our method of tailoring Boolean models of cell signalling was accurate enough to discriminate between different patients, and whether the models could be used as testbeds to rank personalised drug treatments.”
To begin, the team used data from The Cancer Genome Atlas (TCGA) and other databases to create a network of all relevant pathways involved in prostate cell signalling. Then they converted this into a generic Boolean model where all the nodes in the network can be assigned one of two values — 0 (inactivated or absent) or 1 (activated or present). Data from 488 prostate cancer patients from TCGA were used to create 488 patient-specific Boolean models. For example, where a patient’s tumour had a mutation in a specific gene, this meant the node in the network was inactivated, and assigned a value of 0.
Having built these models, the team looked in each patient model for genes that, when inhibited, would block growth or encourage death of cancer cells. They narrowed these genes down to a list of targets of existing drugs, and ran simulations to predict what would happen if the drugs were combined. This allowed them to compare the effects of individual drugs on each patient, and to propose certain drugs that would work for specific patients or for groups of patients. Inactivation of some of the genes had a greater effect in some patients compared with others, highlighting opportunities for personalised drug treatments. The simulations also spotted patterns linked to the grade of patients’ tumours as measured by the Gleason score, suggesting it might be possible to tailor drug treatments to prostate cancer patients according to their score in the future.
Testing whether these treatment predictions hold true in patients would require a clinical trial, so the team instead built eight different personalised prostate cancer cell line models from publicly available data. As with the patient models, they looked for commonly occurring mutations in the cell lines that influenced cancer cell growth or death. This resulted in the identification of 17 proteins that could be targeted with drugs.
Next, to investigate if drugs targeting these proteins would have the anticipated effects, they mimicked the effect of different drug dosages in the model by switching off each node from 100% active to 0% active and looking at the effects on growth, death and spread of the cancer cells. When they carried out the same experiment in real cell lines, it confirmed that blocking the identified nodes in the model had differential effects on cell growth and survival. Moreover, the model could predict synergistic effects of treatments that work against different nodes in the network, which could help to identify promising drug combinations for future investigation.
“Our personalised models suggest single and combined drug treatments for individual prostate cancer patients,” concludes Laurence Calzone, a researcher at Institut Curie, and a co-senior author of the study alongside Julio Saez-Rodriguez from Heidelberg University, Germany. “These advances are incremental steps towards having digital twins that will help clinicians before they go to the patient’s bedside, allowing them to capture patient individualities and test and rank different drug treatments.”
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A potential new treatment approach for complications relating to diabetes has been described today in the open-access eLife journal. Findings shed new light on how diabetes causes tissue damage when oxygen levels drop, and point to the repression of a protein complex as a possible treatment target.
Diabetes is a serious condition that causes the blood sugar level to become too high. In patients with diabetes, the overproduction of cellular reactive oxygen species (ROS) — highly reactive chemicals formed from oxygen — can lead to severe tissue damage. The new study suggests that the repression of a protein complex called hypoxia-inducible factor-1 (HIF-1) contributes to this overproduction of ROS, and is therefore an attractive therapeutic target.
“Hypoxia, a condition where oxygen levels drop in our tissues, has also recently been identified as a harmful player in diabetes,” explains Xiao-Wei Zheng, Senior Lab Manager at Karolinska Institutet, Stockholm, Sweden, and a co-first author of the study alongside Sampath Narayanan and Cheng Xu, also from Karolinska Institutet. “In our study, we wanted to find out if the overproduction of cellular ROS in diabetes is caused by impaired responses to hypoxia due to the inhibition of HIF-1 by high blood sugar levels.”
To answer this question, Zheng, Narayanan, Xu and colleagues recruited 13 non-smoking volunteers with type 1 diabetes and 11 healthy volunteers. They exposed the participants to mild and intermittent hypoxia five times in total for one hour. They took blood samples from the participants before and immediately after exposure to hypoxia, and analysed the changes in their ROS levels. The results showed that hypoxia led to increased ROS levels in the volunteers with diabetes, while those without the condition were unaffected.
As hypoxia increases cellular ROS levels in diabetes, and HIF-1 helps cells to respond to hypoxia, the team hypothesised that repressing HIF-1 would contribute to the overproduction of ROS. To test this, they analysed the relation between HIF-1, glucose levels, and ROS production and its functional consequences, in cells taken from mouse kidneys and directly in the kidneys of mouse models of diabetes. They found that high glucose levels repressed HIF-1 both in hypoxic cells and in the mouse kidneys through a mechanism that relied on enzymes called HIF prolyl-hydroxylases (PHDs). This repression of HIF-1 contributed in turn to the excess production of ROS.
Finally, the team demonstrated that restoring HIF-1 function in the mice reduced the overproduction of ROS in their tissue cells and protected the animals’ kidneys against cell death and injury.
“We’ve shown that the repression of HIF-1 plays a central role in ROS overproduction and tissue damage in diabetes, and is therefore a potential treatment target for these complications,” concludes Sergiu Catrina, Lecturer/Senior Physician at Karolinska Institutet, and a co-senior author of the study alongside Fredrik Palm, from Uppsala University, Sweden. “These results are timely, since the first PHD inhibitor that can activate HIF-1 has recently been approved for clinical use in patients with chronic kidney diseases. If our findings are verified by future studies, then similar inhibitors could be tested as potential new therapies for diabetes.”
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While neurons and glial cells are by far the most numerous cells in the brain, many other types of cells play important roles. Among those are cerebrovascular cells, which form the blood vessels that deliver oxygen and other nutrients to the brain.
Those cells, which comprise only 0.3 percent of the brain’s cells, also make up the blood-brain barrier, a critical interface that prevents pathogens and toxins from entering the brain, while allowing critical nutrients and signals through. Researchers from MIT have now performed an extensive analysis of these difficult-to-find cells in human brain tissue, creating a comprehensive atlas of cerebrovascular cell types and their functions.
Their study also revealed differences between cerebrovascular cells from healthy people and people suffering from Huntington’s disease, which could offer new targets for potential ways to treat Huntington’s disease. Breakdown of the blood-brain barrier is associated with Huntington’s and many other neurodegenerative diseases, and often occurs years before any other symptoms appear.
“We think this might be a very promising route because the cerebrovasculature is much more accessible for therapeutics than the cells that lie inside the blood-brain barrier of the brain,” says Myriam Heiman, an associate professor in MIT’s Department of Brain and Cognitive Sciences and a member of the Picower Institute for Learning and Memory.
Heiman and Manolis Kellis, a professor of computer science in MIT’s Computer Science and Artificial Intelligence Laboratory (CSAIL) and a member of the Broad Institute of MIT and Harvard, are the senior authors of the study, which appears today in Nature. MIT graduate students Francisco Garcia in the Department of Brain and Cognitive Sciences, and Na Sun in the Department of Electrical Engineering and Computer Science, are the lead authors of the paper.
A comprehensive atlas
Cerebrovascular cells make up the network of blood vessels that deliver oxygen and nutrients to the brain, and they also help to clear out debris and metabolites. Dysfunction of this irrigation system is believed to contribute to the buildup of harmful effects seen in Huntington’s disease, Alzheimer’s, and other neurodegenerative diseases.

African children and adolescents hospitalized with COVID-19 experience much higher mortality rates than Europeans or North Americans of the same age, according to a recently published study conducted by researchers from the Institute of Human Virology (IHV) at the University of Maryland School of Medicine (UMSOM) and the Institute of Human Virology Nigeria (IHVN). Both organizations are members of the Global Virus Network (GVN).
The study, titled,”Assessment of Clinical Outcomes Among Children and Adolescents Hospitalized with COVID-19 in six Sub-Saharan African Countries,” was conducted by a collaboration under AFREhealth (the African Forum for Research and Education in Health), a consortium of cross-disciplinary health personnel across Africa. The research was published on January 19 in JAMA Pediatrics, the highest-ranked pediatrics journal in the world.
“This study provides important information about COVID-19 among African children, which was not previously available at this scale. We now have evidence from multiple countries to show that African children also experience severe COVID-19; they experience multisystem inflammatory syndrome; some require intensive care; some also die, and at much higher rates than outside Africa,” said Nadia Sam-Agudu, MD, Associate Professor of Pediatrics at the UMSOM’s Institute of Human Virology, and Senior Technical Advisor for Pediatric and Adolescent HIV, Institute of Human Virology Nigeria. Dr. Sam-Agudu is a co-first author along with Principal Investigator Dr. Jean Nachega of the University of Pittsburgh and Stellenbosch University in Cape Town, South Africa.
The AFREhealth study collected data from 25 health facilities across Nigeria, Ghana, Democratic Republic of the Congo, Kenya, South Africa, and Uganda. The study included 469 African children and adolescents aged three months to 19 years hospitalized with COVID-19 between March and December 2020. The team reported a high overall mortality rate of 8.3%, compared with 1% or less totaled from Europe and North America. Furthermore, African children less than a year old and with pre-existing, non-communicable diseases were more likely to have poorer outcomes, such as requiring intensive care, and death.
Eighteen participants had suspected or confirmed multisystem inflammatory syndrome (also known as MIS-C), and four of these children died.
Dr. Sam-Agudu, who led the West Africa team for the study, urged health authorities and policymakers in Nigeria and other African countries to act upon the study findings “to protect children by expanding vaccine approvals and procurements for children specifically, as the variants emerging since our study’s completion have either caused more severe disease and/or more cases overall. We cannot leave children behind in the pandemic response.”
Dr. Sam-Agudu was recently awarded a 2022 Dr. Thomas Hall-Dr. Nelson Sewankambo Mid-Career Leadership Award from The Consortium of Universities for Global Health. The award acknowledges outstanding individuals for accomplishments and commitment to contributing to the advancement of global health worldwide.

Mayo Clinic researchers have developed a new scoring system to help health care professionals predict the 30-day mortality risk for patients with alcohol-associated hepatitis, and the tool appears to more accurately identify patients at highest risk of death and those likely to survive.
The new scoring system, called the Mortality Index for Alcohol-Associated Hepatitis (MIAAH), is at least as accurate as existing models in identifying patients with alcohol-associated hepatis who are at high risk of death, according to results of a study published in Mayo Clinic Proceedings.
“While we believe the MIAAH will be refined over time, possibly in conjunction with an existing model, our study finds that it’s a useful tool in assessing mortality risk,” says Douglas Simonetto, M.D., a Mayo Clinic gastroenterologist and the study’s senior author. “Given the significant mortality seen in patients with alcohol-associated hepatitis, assessing disease severity and prognosis is critical.”
Alcohol-associated hepatitis is an acute inflammatory process in the liver that occurs in patients who consume excessive amounts of alcohol. Patients with milder forms of the disease often improve with limited treatment, but severe disease is associated with significant short-term mortality. No pharmacologic treatments have been found to reduce 90-day mortality in severe cases. Accurate prognostic tools are essential for clinicians to identify patients at high risk of death and determine appropriate treatment.
At least four prognostic models are available, but the Mayo research team set out to develop a new system that more accurately predicts 30-day mortality. Using deidentified patient health records from Mayo Clinic in Rochester from 1998 to 2018, researchers identified 266 adult patients with a diagnosis of alcohol-associated hepatitis. Of those patients, the 30-day mortality rate was 19.2%. The study derived several variables, such as blood urea nitrogen and bilirubin, and developed a model scoring system that incorporated the variables.
The MIAAH model then was used to predict outcomes for an external validation cohort of 249 patients from health care centers at the University of South Dakota and the University of Kansas. The model was found to be at last as accurate as existing tools in identifying patients at high risk of short-term mortality.
“The MIAAH also showed advantageous performance characteristics in its ability to increasingly accurately identify patients at highest risk of death versus those who are more likely to survive,” says Camille Kezer, M.D., a Mayo Clinic resident physician and the study’s first author. “It also has the advantage of performing well in patients, regardless of whether they’ve been treated with steroids, which makes it generalizable.”
Despite decades of research, treatment options for patients with alcohol-associated hepatitis remain limited, with questionable efficacy. Prognostic models are important for determining which treatments may have value and whether patients are responding to treatment. Modeling is also integral in determining whether patients are candidates for a liver transplant.
“This is why a prognostic model that accurately identifies short-term mortality risk has such value,” says Dr. Simonetto. “With this study, we set out to create a novel model with more consistent and reliable accuracy, based on laboratory variables and demographic data that’s routinely obtained at the time of admission. While the optimal process may include a combination of models, the MIAAH can be an important tool in helping our patients.”
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The COVID-19 pandemic upended many aspects of daily life, particularly in the first months and year. Not least among the changes: decreased use of ordinary health care, such as routine medical exams and screenings.
New findings, published in JAMA Network Open on February 15, 2022, bear that out. Researchers at Moores Cancer Center at UC San Diego Health surveyed and compared early- and late-stage breast and colorectal cancer diagnoses in patients in pre-pandemic 2019 and 2020, the first full year of the ongoing COVID-19 pandemic.
While total numbers of diagnoses were roughly similar in 2019 and 2020, there were significant differences in the percentages of stage I diagnoses for breast cancer compared to stage IV diagnoses.
In 2019, for example, 63.9 percent of diagnosed patients presented with stage I disease compared to 51.3 percent in 2020. Conversely, 1.9 percent of patients were diagnosed with stage IV breast cancer in 2019 compared to 6.2 percent in 2020.
(Most cancers are given a stage designation at time of diagnosis, from stage I when the malignancy is limited to its originating location to stage IV, when the cancer has spread to other organs or parts of the body. Each stage indicates progressive difficulty of treatment and cure, from good to worse.)
Among colorectal cancer patients studied, similar trends were seen, though the magnitude was somewhat less than with patients with breast cancer.
“For breast cancer, at least, these data demonstrate a continuing trend,” said first author Jade Zifei Zhou, MD, PhD, a clinical fellow in hematology and oncology at UC San Diego School of Medicine. “They suggest that concerns and consequences caused by the pandemic have prompted at least some patients to delay routine health care, such as screenings or doctor visits, that might have revealed early stage diagnoses.”
The researchers noted several limitations of the study. First, it reflects data from a single center, and does not assess disease causality. Second, the number of patients with colorectal cancer were relatively small. Third, the study included individuals seeking second opinions, who may or may not have undergone any previous treatment.
“Cancer screening is crucial to the early detection of cancer, particularly in colorectal and breast cancers where many early stage cancers can be treated and cured,” said senior author Kathryn Ann Gold, MD, a medical oncologist at Moores Cancer Center and professor of medicine at UC San Diego School of Medicine.
“There is increasing concern that one effect of the pandemic is the growing number of patients who are being diagnosed for the first time with late, incurable stages. Patients who have delayed preventative care during the pandemic should be encouraged to discuss age appropriate cancer screening with their primary care providers as soon as possible.”
Co-authors include: Shelly Kane, Celia Ramsey, Melody Akhondzadeh, Ananya Banerjee and Rebecca Shatsky, all at UC San Diego.
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