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Additional file 1: Appendix 1. PRISMAChecklist. Appendix 2. Studies included at full-text review. Supplementary Figure 1. Funnel plot summarising publication bias for studies with data regarding effect of age on depressive symptoms after stoma surgery. Supplementary Figure 2. Funnel plot summarising publication bias for studies with data regarding mean age and standard deviations in studies with data regarding effect of age on depressive symptoms after stoma surgery. Supplementary Figure 3. Funnel plot summarising publication bias for studies with data regarding effect of sex on depressive symptoms after stoma surgery. Supplementary Figure 4. Forest plot summarising prevalence of male sex in studies with data regarding effect of sex on depressive symptoms after stoma surgery. Supplementary Figure 5. Funnel plot summarising publication bias for studies with data regarding prevalence of male sex and data regarding effect of sex on depressive symptoms after stoma surgery. Supplementary Figure 6. Forest plot showing prevalence of depressive symptoms after stoma surgery in studies reporting by region. Supplementary Figure 7. Funnel plot summarising publication bias for studies with data regarding effect of region on depressive symptoms after stoma surgery. Supplementary Figure 8. Forest plot summarising the odds of experiencing depressive symptoms before versus after stoma surgery. Supplementary Figure 9. Funnel plot summarising publication bias in studies reporting odds of experiencing depressive symptoms before versus after stoma surgery. Supplementary Figure 10. Forest plot summarising the odds of experiencing depressive symptoms after surgery in stoma versus non-stoma populations. Supplementary Figure 11. Funnel plot summarising publication bias in studies reporting data regarding the odds of experiencing depressive symptoms after surgery in stoma versus non-stoma populations. Supplementary Figure 12. Forest plot summarising mean differences in experiencing depressive symptoms after surgery in stoma versus non-stoma populations. Supplementary Figure 13. Funnel plot summarising publication bias in studies reporting data regarding mean differences in experiencing depressive symptoms after surgery in stoma versus non-stoma populations. Supplementary Figure 14. Forest plot summarising the mean differences in experiencing depressive symptoms after surgery in colostomy versus ileostomy patients. Supplementary Figure 15. Funnel plot summarising publication bias in studies reporting data regarding the mean differences in experiencing depressive symptoms after surgery in colostomy versus ileostomy patients. Supplementary Table 1. Risk of bias assessment using the Downs and Black Checklist for 65 non-randomised studies of interventions included in the present systematic review. Supplementary Table 2. Overall risk of bias assessment using the Cochrane RoB 2.0 checklist for three randomised controlled trials included in the present systematic review.

Existing assembly programming simulator tools used for educational instruction are stand-alone programs with aged user-interfaces. These tools are antiquated for modern programmers who are accustomed to powerful IDE environments. VSCode has emerged as the go-to in an academic and industry setting. Dashmips is a MIPS Interpreter and Debugger which adds MIPS assembly programming support to VSCode. The interpreter, developed in Python, has a functional design that is easily customizable and extensible for academic instruction specific to a course. Inline Python documentation automatically generates program usage and help documentation for student support. Additionally, the MIPS interpreter is stand-alone from the debugger and can be utilized on the command-line and programmatically via scripting or a Python program allowing integration into auto-grading frameworks. This demo will provide a brief introduction to the features of Dashmips as an educational tool, including simple setup, one-click debugging, clear visualization of register and memory data, and framework for instructor customizations. A step-by-step tutorial for creating a new program and interacting with the debugging environment will illustrate the accessibility of the environment for modern programmers. Information about Dashmips and the Dashmips Debugger can be found at https://github.com/nbbeeken/dashmips and https://github.com/nbbeeken/dashmips-debugger, respectively.

Variations in anxiety-related behavior are associated with individual allostatic set-points in chronically stressed rats. Actively offensive rats with the externalizing indicators of sniffling and climbing the stimulus and material tearing during 10 days of predator scent stress had reduced plasma corticosterone, increased striatal glutamate metabolites, and increased adrenal 11-dehydrocorticosterone content compared to passively defensive rats with the internalizing indicators of freezing and grooming, as well as to controls without any behavioral changes. These findings suggest that rats that display active offensive activity in response to stress develop anxiety associated with decreased allostatic set-points and increased resistance to stress.

Variations in anxiety-related behavior are associated with individual allostatic set-points in chronically stressed rats. Actively offensive rats with the externalizing indicators of sniffling and climbing the stimulus and material tearing during 10 days of predator scent stress had reduced plasma corticosterone, increased striatal glutamate metabolites, and increased adrenal 11-dehydrocorticosterone content compared to passively defensive rats with the internalizing indicators of freezing and grooming, as well as to controls without any behavioral changes. These findings suggest that rats that display active offensive activity in response to stress develop anxiety associated with decreased allostatic set-points and increased resistance to stress. © 2020 by the authors. Licensee MDPI, Basel, Switzerland. The Russian Science Foundation (grant № 17-15-013418) supported this study. This was supported in part by the contracts of the Ministry of Education and Science of the Russian Federation with South Ural State University (17.7255.2017/8.9) and Institute of Immunology and Physiology (AAAA-A18-118020690020-1). The work was furthermore supported by institutional funds from the State University of New York (SUNY) Upstate Medical University. This work is part of the TransCampus project between TU Dresden and King’s College London and was partially supported by the U.S. Department of Veterans Affairs (5101CX001219) and the U.S. Department of Defense (W81XWH-16-1-0773).

Additional file 1.

Studies have demonstrated students’ resistance to active learning, despite evidence illustrating that their learning is improved relative to students in lectures. Specifically, while active learning and group work are effective at engaging students in their learning process, studies report that students’ perceptions of active learning approaches are not always positive. What remains underexplored is whether students’ perceptions of active learning improve with effective instructor facilitation and whether there exists differential perceptions between racially minoritized students and represented students. Here, we estimate students’ perceptions of effective instructor facilitation as the mediator in the relationship between active learning and perceptions of learning and perceived utility for class activities (task value). Then, we examine differences by racial identification. We collected classroom observation data to empirically categorize courses as active learning or lecture-based and surveyed 4,257 college students across 25 STEM classrooms at a research-intensive university. We first examined the relationship between active learning on student perceptions and found a negative relationship between active learning and perceptions of learning and task value for both racially minoritized students and represented students. Next, we assessed whether students’ perceptions of instructor effectiveness in facilitating group activities mediate these negative relationships. We found that, on average, students of all races were more likely to positively perceive instructor facilitation in active learning classes relative to lectures. In turn, the positive perceptions of instructor facilitation partially suppressed the negative relationship between active learning and perceptions of learning and task value. These results demonstrate that effective instructor facilitation can influence both students’ self-assessment of learning and perceived utility of the learning activities, and underscores the importance of developing pedagogical competence among college instructors.

We respond to Dr. Acierno's concerns about the measurement of elder mistreatment and social support in the National Social Life, Health, and Aging Project. We made our analytic decisions carefully and conducted systematic robustness checks and believe our findings are theoretically important.

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Tesis de Maestría

We have had the honor and pleasure to have worked and shared a sincere and unique friendship with Dr. S.M. McCann. Dr. McCann was a unique person: enthusiastic, inspiring and a terrific scientist whose passion for science and knowledge were limitless. His scientific achievements as a pioneer of the two interrelated fields of neuroendocrinology and neuroimmunomodulation included more than 1,000 publications and a number of outstanding scientific prizes. Above all, Don was a generous, talented mentor and fostered the career of several young scientists, who have become world-renowned academic leaders in leading universities and research centers. This mini-review focuses on our collaborative work with Dr. McCann, providing evidence for a bidirectional communication between the neuroendocrine and -immune systems. Interestingly, it is believed that chronic stress can alter the balance between this bidirectional interaction and eventually cause psychiatric disorders (20)., Sociedad Argentina de Fisiología

Background To study the potential association of antidepressant use and suicide at a population level, we analyzed the associations between suicide rates and dispensing of the prototypic SSRI antidepressant fluoxetine in the United States during the period 1960–2002. Methods and Findings Sources of data included Centers of Disease Control and US Census Bureau age-adjusted suicide rates since 1960 and numbers of fluoxetine sales in the US, since its introduction in 1988. We conducted statistical analysis of age-adjusted population data and prescription numbers. Suicide rates fluctuated between 12.2 and 13.7 per 100,000 for the entire population from the early 1960s until 1988. Since then, suicide rates have gradually declined, with the lowest value of 10.4 per 100,000 in 2000. This steady decline is significantly associated with increased numbers of fluoxetine prescriptions dispensed from 2,469,000 in 1988 to 33,320,000 in 2002 (rs = −0.92; p < 0.001). Mathematical modeling of what suicide rates would have been during the 1988–2002 period based on pre-1988 data indicates that since the introduction of fluoxetine in 1988 through 2002 there has been a cumulative decrease in expected suicide mortality of 33,600 individuals (posterior median, 95% Bayesian credible interval 22,400–45,000). Conclusions The introduction of SSRIs in 1988 has been temporally associated with a substantial reduction in the number of suicides. This effect may have been more apparent in the female population, whom we postulate might have particularly benefited from SSRI treatment. While these types of data cannot lead to conclusions on causality, we suggest here that in the context of untreated depression being the major cause of suicide, antidepressant treatment could have had a contributory role in the reduction of suicide rates in the period 1988–2002., An association has been shown between the introduction of the antidepressant fluoxetine in the USA in 1988 and a reduction in the number of suicides., Editors' Summary Background. Depression is very common. For example, in the US, an estimated 10% of men and 20% of women will suffer from major depression at some stage in their lives. One way of treating the condition is with drugs. Several types of antidepressant drugs are available, and in many countries they are among the most commonly prescribed medicines. However, all antidepressants have side effects. One family of antidepressants, called selective serotonin uptake inhibitors (SSRIs), was introduced in the late 1980s. The name of these drugs comes from their effect, which is to prevent the removal (reuptake) from the nerve endings of one type of chemical (serotonin) that is important for transmitting nerve impulses between brain cells. SSRIs are claimed to be more effective and to have fewer side effects than older antidepressants, and many brands of SSRI are now on the market. However, in recent years there have been claims that some people taking SSRIs have committed suicide as a result of the drugs. Whether the SSRIs are the cause of the suicide is hard to know, because people who are depressed do sometimes feel like killing themselves; so if a depressed person taking an SSRI commits suicide, it is hard to tell whether this is a result of the depression or a side effect of the treatment (the SSRI). The drug regulatory authorities in some countries are now carefully studying the issue of suicides and antidepressant use, both in adults and in children. The US Federal Drug Administration has issued what it calls a “black box warning” on the use of these drugs. Why Was This Study Done? The researchers wanted to discover whether the number of suicides in the US had increased or decreased since treatment with the first widely used SSRI (fluoxetine, also known as Prozac) began in 1988. Any difference in the number of suicides found before and after that date would not necessarily be the result of the introduction of this antidepressant, or other SSRIs, but the information would provide helpful information about the effects of these drugs. What Did the Researchers Do and Find? They looked at annual suicide rates between 1960 and 1988 and compared them with annual rates in the period 1988 to 2002. They used several sources of data, including the Centers of Disease Control and the US Census Bureau. The researchers found that from the early 1960s until 1988, in the entire US population, between 12.2 and 13.7 people in every 100,000 committed suicide each year. After that time, the numbers of suicides gradually declined, with the lowest figure (10.4 people per 100,000) reached in 2000. The researchers did mathematical tests, which demonstrated that the steady decline was statistically associated with the increased number of fluoxetine prescriptions—that is, the more prescriptions there were, the fewer suicides there were. (There were around two-and-a-half million prescriptions of the drug in 1988, increasing to over 33 million in 2002.) What Do These Findings Mean? In all scientific research, it is an important principle that finding an association between two events does not prove that one caused the other to occur. However, the authors of this paper suggest that the use of this drug could have contributed to the reduction of suicide rates in the US in the period 1988 to 2002. Several other SSRIs are also now in common use, but they were not considered in this study, nor were other antidepressants, or other treatments for depression. Additional Information. As depression is such a common condition—and because there are so many ways of treating it, including counseling and psychotherapy—there are many Web sites devoted to the subject. We have given a small selection below. Please access these Web sites via the online version of this summary at http://dx.doi.org/10.1371/journal.pmed.0030190. • From the American Academy of Family Physicians (AAFP), general advice on depression • Also from the AAFP, advice specifically about antidepressant drugs • MedlinePlus brings together authoritative information about depression from the US National Library of Medicine, National Institutes of Health, and other government agencies and health-related organizations • Health pages of the BBC on depression • Information about depression from other UK health advice sites: Patient UK and NetDoctor.co.uk

Objective The objective of the review is to evaluate circulating levels of leptin in people diagnosed with myalgic encephalomyelitis chronic fatigue syndrome or fibromyalgia syndrome and to investigate the differences compared with healthy controls. Introduction Myalgic encephalomyelitis chronic fatigue syndrome is a condition that has major symptoms, including self-reported fatigue, post-exertional malaise, and unexplained pain across the body. The widespread pain is measured in a systematic way and is often referred to as fibromyalgia. The two disorders have many similarities, but their association with leptin has indicated that leptin may affect the role of pro-inflammatory cytokines and symptom severity. Inclusion criteria This review will consider observational studies of varying study designs including prospective and retrospective cohort studies, case-control studies, time-series, and analytical cross-sectional studies that include both cases and healthy comparators. Cases will include a diagnosis of myalgic encephalomyelitis, chronic fatigue syndrome, and/or fibromyalgia. Controls are people without this diagnosis, usually healthy participants. Only studies published in English will be included due to limited resources for translation. Methods This protocol will be reported based on the Preferred Reporting Items for Systematic Reviews and Meta-analysis (PRISMA) checklist and will follow the JBI methodology for systematic reviews of etiology and risk. A comprehensive search strategy will include PubMed, Embase, Scopus, Science Direct, and PsycINFO. Two reviewers will screen, critically appraise eligible articles, and extract data using a standardized data extraction tool informed by JBI SUMARI. The authors will complete a quantitative analysis that synthesizes findings across studies using pooled effect sizes and confidence intervals of the measures provided. Systematic review registration number PROSPERO [CRD42020169903].

Background Depression and obesity are significant global health concerns that commonly occur together. An integrated group cognitive behavioural therapy program was therefore developed to simultaneously address comorbid depression and obesity. Methods Twenty-four participants (63% women, mean age 46 years) who screened positively for depression with a body mass index ≥25 were recruited from a self-referred general population sample. The group therapy program (10 two-hour weekly sessions) was examined in a single-arm, before-after pilot trial, conducted in a behavioural health clinic in Adelaide, Australia. Primary outcomes included survey and assessment-based analyses of depression, anxiety, body image, self-esteem, and weight (kg), assessed at four time-points: baseline, post-intervention, three-months and 12-months post program. Eighteen participants (75%) completed the program and all assessments. Results Significant improvements in depression, anxiety, self-esteem and body shape concern scores, several quality of life domains, eating behaviours and total physical activity (among others) – but not weight – were observed over the course of the trial. Conclusions Results from this pilot trial suggest that combining interventions for depression and obesity may be useful. Further development of the program, particularly regarding the potential for physical health benefits, and a randomised controlled trial, are warranted. Trial registration Trial registration: ANZCTR, ACTRN12617001079336, 13 July 2017. Retrospectively registered after date of the first consent (6 July 2017), but before the date of the first intervention session (20 July 2017).

Recruitment in mental health research is challenging, as some disorders such as depression or schizophrenia may involve vulnerable participants that lack motivation as part of their illness. A mental health diagnosis can be stigmatising, so privacy and access to hospital-based patient cohorts is carefully controlled. Our team describe a pragmatic portal recruitment process for facilitating timely recruitment into multiple research studies focusing on mental health. Three factors were analysed; evaluating the success and impact of this novel recruitment process; identification of patterns in recruitment to better target participants; and provision of metrics of the different media formats engaged. A web-based recruitment portal was developed by the research team in collaboration with the South Australian Health and Medical Research Institute (SAHMRI) Consumer & Carer Research Advisory Group. A comprehensive marketing campaign was then undertaken to direct participants towards the portal. Recruitment insights from the dates and times of registration across a two-year period is provided. In total, 933 potential participants registered with the recruitment portal across a two-year period at a cost of approximately $10,000. The advertisement campaign linked to the portal page enabled 506 participants to register in just one week. The area of research was self-selected by the potential participants, then eligibility was followed up with telephone and face to face interviews. Of the total 933 people who registered 706 (76%) expressed an interest in the target clinical depression study, 119 (13%) opted to be clinical controls, and the remainder chose one of the alternative studies. 240 (26%) of those who registered were excluded through telephone interviews because they fell outside of the strict eligibility criterion. We learnt that 77% (n = 723/933) of participants were recruited within seven days of promotional events, providing an interesting pattern of recruitment that may assist future recruitment design. Refereed/Peer-reviewed

Major depressive disorder (MDD) is a common but serious psychiatric disorder with significant levels of morbidity and mortality. Recent genome-wide association studies (GWAS) on common variants increase our understanding of MDD; however, the underlying genetic basis remains largely unknown. Many studies have been proposed to explore the genetics of complex diseases from a viewpoint of the “missing heritability” by considering low-frequency and rare variants, copy-number variations, and other types of genetic variants. Here we developed a novel computational and statistical strategy to investigate the “missing heritability” of MDD. We applied Hamming distance on common, low-frequency, and rare single-nucleotide polymorphism (SNP) sets to measure genetic distance between two individuals, and then built the multi-dimensional scaling (MDS) pictures. Whole-exome genotyping data from a Los Angeles Mexican-American cohort (203 MDD and 196 controls) and a European-ancestry cohort (473 MDD and 497 controls) were examined using our proposed methodology. MDS plots showed very significant separations between MDD cases and healthy controls for low-frequency SNP set (P value P value = 7.681e−12). Our results suggested that low-frequency and rare variants may play more significant roles in the genetics of MDD.

We are at the dawn of a new era of treatment for major depressive disorder involving precision medicine. Research is using big data, genome-wide association studies, and pharmacogenomics to create a combinatorial biological and environmental model of depression. Biomarkers have already been used to indicate causative pathways and the effectiveness of treatment responses in other areas of medicine. As technology advances, psychiatric practice will be able to use new tools and technology to assist with diagnosis and drug treatment options. The complex interaction of the inherited genome, epigenetic responses, pharmacokinetics, and environmental factors combine to produce endophenotypic outcomes that are predictable. The prevalence and cost burden of depression are so great that improved diagnostic tools are needed. The role of pharmacogenomics and related sciences pharmacokinetics and pharmacodynamics are discussed. Refereed/Peer-reviewed

Evidence indicates that inflammatory mediators play a role in the development of major depressive disorder (MDD). MDD is thought to be a multigenic disorder in that many genes are implicated in its development. Genetics has enabled researchers to identify the effects of single-nucleotide polymorphisms in specific inflammatory pathways. The link between these genes and biochemical expression of inflammatory mediators is explored. The advance in genomics is rapidly growing as technology enables us to examine large sections of the human genome in a short period of time. At the same time, laboratories across the world are creating genetic databases, mapping samples on a grand scale, and providing the opportunity to access anonymized MDD clinical and genetic data with relative ease. In the last decade, a combination of candidate gene studies, linkage studies, and genome-wide association studies have started to reveal the inheritance of MDD and the genes responsible. Refereed/Peer-reviewed

Background Genetic components play important roles in the susceptibility to major depressive disorder (MDD). The rapid development of sequencing technologies is allowing scientists to contribute new ideas for personalized medicine; thus, it is essential to design non-invasive genetic tests on sequencing data, which can help physicians diagnose and differentiate depressed patients and healthy individuals. Methods We have recently proposed a genetic concept involving single-nucleotide variant proportion (SNVP) in genes to study MDD. Using this approach, we investigated combinations of distance metrics and hierarchical clustering criteria for genetic clustering of depressed patients and ethnically matched controls. Results We analysed clustering results of 25 human subjects based on their SNVPs in 46 newly discovered candidate genes. Conclusions According to our findings, we recommend Canberra metric with Ward's method to be used in hierarchical clustering of depressed and normal individuals. Futures studies are needed to advance this line of research validating our approach in larger datasets, those may also be allow the investigation of MDD subtypes. Limitations High quality sequencing costs limited our ability to obtain larger datasets.

Background: Major depressive disorder (MDD) is a leading contributor to global disease burden. Recent studies have shown that genetic factors play significant roles in the susceptibility to this condition; however, the underlying genetic basis currently remains largely unknown. Short tandem repeat (STR) has been proposed as an explanatory factor in the “missing heritability” of complex diseases or traits. Methods: We investigated STR variations from 15 MDD patients and 10 ethnically matched healthy controls based on their deep whole-genome sequencing (WGS) data. The lobSTR software was used to computationally determine STRs. Results: The results of the Mexican-American sample showed that STRs are significantly richer in healthy controls than in MDD cases on each of the 23 chromosomes (all false discovery rates, FDR P-values < 0.0062); while for the Australian of European-ancestry sample, there was no statistically significant STRs difference between MDD cases and controls. Limitations: High quality WGS costs limited obtaining larger datasets. Conclusions: This preliminary work is the first study that STR variations are applied to investigate MDD based on WGS data. The results on Mexican-American population may imply that within the same ancestry, targeted sequencing on a specific chromosome or region of genome would be sufficient for examining the relationship between STR and MDD. Further studies should examine larger sequencing datasets on other ethnic groups. Refereed/Peer-reviewed

Major depressive disorder (MDD) is highly prevalent, resulting in an exceedingly high disease burden. The identification of generic risk factors could lead to advance prevention and therapeutics. Current approaches examine genotyping data to identify specific variations between cases and controls. Compared to genotyping, whole-genome sequencing (WGS) allows for the detection of private mutations. In this proof-of-concept study, we establish a conceptually novel computational approach that clusters subjects based on the entirety of their WGS. Those clusters predicted MDD diagnosis. This strategy yielded encouraging results, showing that depressed Mexican-American participants were grouped closer; in contrast ethnically-matched controls grouped away from MDD patients. This implies that within the same ancestry, the WGS data of an individual can be used to check whether this individual is within or closer to MDD subjects or to controls. We propose a novel strategy to apply WGS data to clinical medicine by facilitating diagnosis through genetic clustering. Further studies utilising our method should examine larger WGS datasets on other ethnical groups.

Recent advances in DNA technologies have provided unprecedented opportunities for biological and medical research. In contrast to current popular genotyping platforms which identify specific variations, whole-genome sequencing (WGS) allows for the detection of all private mutations within an individual. Major depressive disorder (MDD) is a chronic condition with enormous medical, social and economic impacts. Genetic analysis, by identifying risk variants and thereby increasing our understanding of how MDD arises, could lead to improved prevention and the development of new and more effective treatments. Here we investigated the distributions of whole-genome single nucleotide variants (SNVs) on 12 different genomic regions for 25 human subjects using the symmetrised Kullback-Leibler divergence to measure the similarity between their SNV distributions. We performed cluster analysis for MDD patients and ethnically matched healthy controls. The results showed that Mexican-American controls grouped closer; in contrast depressed Mexican-American participants grouped away from their ethnically matched controls. This implies that whole-genome SNV distribution on the genomic regions may be related to major depression. Refereed/Peer-reviewed

Background Despite recent intensive research using genome-wide association studies, the underlying biological basis of major depressive disorder (MDD) still remains unknown. In contrast to genotyping platforms which identify specific variations, whole-genome sequencing (WGS) allows us to detect all private genetic variations within an individual. So far there have been no studies investigating copy number variations (CNVs) in subjects with MDD using WGS data. Methods We obtained complete WGS paired-end reads data of 15 MDD patients and 10 ethnically matched healthy controls. We performed alignments for the sequencing reads and used GASV package to call CNVs including deletion, inversion, translocation and divergence for those subjects. Results Our results show that, in the Mexican-American sample, deletion CNVs were significantly richer in MDD cases than healthy controls on each of 23 chromosomes. However, other types of CNVs failed to reach any significance. In the Australian sample, there was no statistically significant difference of CNVs between MDD cases and controls. Furthermore, we found that the Australian group had significantly more deletion CNVs than the Mexican-American group. Limitations High quality WGS costs limited obtaining larger datasets. The GASV package does not currently support duplication or insertion CNVs. Conclusions To our knowledge this is the first time that CNVs detected by WGS data are used to study major depression. The conclusion that deletion CNVs are significantly richer in MDD cases than healthy controls is consistent with the previous finding about recurrent depressive disorder by genome-wide association analysis of CNVs on a large genotyping microarray data.

Major depressive disorder (MDD) is a common psychiatric illness with significant medical and socioeconomic impact. Genetic factors are likely to play important roles in the development of this condition. DNA sequencing technology has the ability to identify all private genetic mutations and provides new channels for studying the biology of MDD. In this proof-of-concept study we proposed a novel concept, single-nucleotide variant proportion (SNVP), to investigate MDD based on whole-genome sequencing (WGS) data. Our SNVP-based approach can be used to test newly found candidate genes as a complement to genome-wide genotyping analysis. Furthermore, we performed cluster analysis for MDD patients and ethnically matched healthy controls, and found that clusters based on SNVP may predict MDD diagnosis. Our results suggest that SNVP may be used as a potential biomarker associated with major depression. Our methodology could be a valuable predictive/diagnostic tool as one can test whether a new subject falls within or close to an existing MDD cluster. Advances in this study design have the potential to personalized treatments and could include the ability to diagnose patients based on their full or part DNA sequencing data. Refereed/Peer-reviewed

ObjectiveTo examine the association between antidepressant use and weight gain, as well as the interaction with lifestyle factors.DesignLongitudinal study.Setting and participantsWe used data from 2334 adults from two stages (4.4 years apart) of the North West Adelaide Health Study, including validated diet and lifestyle questionnaires, measured body weight and linked pharmaceutical prescription data.Main outcome measuresBody weight change.Results188 (8.1%) participants had a mean annual number of 1–2 antidepressant prescriptions, and 212 (9.1%) had over two prescriptions. The mean annual weight gain was 0.12, 0.18 and 0.28 kg in non-users, low (1–2 prescriptions/year) and high (>2 prescriptions/year) antidepressant users, respectively. In multivariable regression models, antidepressant use was positively associated with weight gain: high antidepressant users gained an extra 0.22 (95% CI 0.00 to 0.44) kg per year. This association was mainly due to selective serotonin reuptake inhibitor (SSRI) use. High SSRI users gained 0.48 (95% CI 0.20 to 0.76) kg more than non-users. There was no association between tricyclic or other antidepressant use and weight gain. The association between SSRI use and weight gain was stronger among those with high intake of Western diet, greater sedentary activity, and who smoked.ConclusionsSSRIs use was associated with weight gain in the presence of unhealthy behaviours including Western diet, sedentarism and smoking.