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"Busch, M"
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What We Have Learned from Two Decades of Epidemics and Pandemics: A Systematic Review and Meta-Analysis of the Psychological Burden of Frontline Healthcare Workers
In light of the current coronavirus disease 2019 (COVID-19) pandemic and potential future infectious disease outbreaks, a comprehensive understanding of the negative effects of epidemics and pandemics on healthcare workers’ mental health could inform appropriate support interventions. Thus, we aimed to synthesize and quantify the psychological and psychosomatic symptoms among frontline medical staff. We searched four databases up to March 19, 2020 and additional literature, with daily search alerts set up until October 26, 2020. Studies reporting psychological and/or psychosomatic symptoms of healthcare workers caring for patients with severe acute respiratory syndrome, H1N1, Ebola, Middle East respiratory syndrome, or COVID-19 were eligible for inclusion. Two reviewers independently conducted the search, study selection, quality appraisal, data extraction, and synthesis and involved a third reviewer in case of disagreement. We used random effects modeling to estimate the overall prevalence rates of psychological/psychosomatic symptoms and the I 2 statistic. We included 86 studies, reporting data from 75,991 participants. Frontline staff showed a wide range of symptoms, including concern about transmitting the virus to the family (60.39%, 95% CI 42.53–76.96), perceived stress (56.77%, 95% CI 34.21–77.95), concerns about own health (45.97%, 95% CI 31.08–61.23), sleeping difficulties (39.88%, 95% CI 27.70–52.72), burnout (31.81%, 95% CI 13.32–53.89), symptoms of depression (25.72%, 95% CI 18.34–33.86), symptoms of anxiety (25.36%, 95% CI 17.90–33.64), symptoms of posttraumatic stress disorder (24.51%, 95% CI 18.16–31.46), mental health issues (23.11%, 95% CI 15.98–31.10), and symptoms of somatization (14.68%, 95% CI 10.67–19.18). We found consistent evidence for the pervasive and profound impact of large-scale outbreaks on the mental health of frontline healthcare workers. As the COVID-19 crisis continues to unfold, guaranteeing easy access to support structures for the entire healthcare workforce is vitally important.
Journal Article
The gut microbiome’s role in the development, maintenance, and outcomes of sepsis
The gut microbiome regulates a number of homeostatic mechanisms in the healthy host including immune function and gut barrier protection. Loss of normal gut microbial structure and function has been associated with diseases as diverse as
Clostridioides difficile
infection, asthma, and epilepsy. Recent evidence has also demonstrated a link between the gut microbiome and sepsis. In this review, we focus on three key areas of the interaction between the gut microbiome and sepsis. First, prior to sepsis onset, gut microbiome alteration increases sepsis susceptibility through several mechanisms, including (a) allowing for expansion of pathogenic intestinal bacteria, (b) priming the immune system for a robust pro-inflammatory response, and (c) decreasing production of beneficial microbial products such as short-chain fatty acids. Second, once sepsis is established, gut microbiome disruption worsens and increases susceptibility to end-organ dysfunction. Third, there is limited evidence that microbiome-based therapeutics, including probiotics and selective digestive decontamination, may decrease sepsis risk and improve sepsis outcomes in select patient populations, but concerns about safety have limited uptake. Case reports of a different microbiome-based therapy, fecal microbiota transplantation, have shown correlation with gut microbial structure restoration and decreased inflammatory response, but these results require further validation. While much of the evidence linking the gut microbiome and sepsis has been established in pre-clinical studies, clinical evidence is lacking in many areas. To address this, we outline a potential research agenda for further investigating the interaction between the gut microbiome and sepsis.
Journal Article
Psychological and Psychosomatic Symptoms of Second Victims of Adverse Events: a Systematic Review and Meta-Analysis
Despite growing interest in the second-victim phenomenon and greater awareness of its consequences, there has not been a meta-analysis quantifying the negative impact of adverse events on providers involved in adverse events. This study systematically reviewed the types and prevalence of psychological and psychosomatic symptoms among second victims.
We conducted a systematic review of nine electronic databases up to February 2017, without restrictions to publication date or language, examining also additional sources (e.g., gray literature, volumes of journals). Two reviewers performed the search, selection process, quality assessment, data extraction, and synthesis. We resolved disagreements by consensus and/or involving a third reviewer. Quantitative studies on the prevalence of psychological and psychosomatic symptoms of second victims were eligible for inclusion. We used random effects modeling to calculate the overall prevalence rates and the I statistic.
Of 7210 records retrieved, 98 potentially relevant studies were identified. Full-text evaluation led to a final selection of 18 studies, based on the reports of 11,649 healthcare providers involved in adverse events. The most prevalent symptoms were troubling memories (81%, 95% confidence interval [CI] = 46-95), anxiety/concern (76%, 95% CI = 33-95), anger toward themselves (75%, 95% CI = 59-86), regret/remorse (72%, 95% CI = 62-81), distress (70%, 95% CI = 60-79), fear of future errors (56%, 95% CI = 34-75), embarrassment (52%, 95% CI = 31-72), guilt (51%, 95% CI = 41-62), and sleeping difficulties (35%, 95% CI = 22-51).
Second victims report a high prevalence and wide range of psychological symptoms. More than two-thirds of providers reported troubling memories, anxiety, anger, remorse, and distress. Preventive and therapeutic programs should aim to decrease second victims' emotional distress.
Journal Article
Activity-dependent regulation of mitochondrial motility in developing cortical dendrites
Developing neurons form synapses at a high rate. Synaptic transmission is very energy-demanding and likely requires ATP production by mitochondria nearby. Mitochondria might be targeted to active synapses in young dendrites, but whether such motility regulation mechanisms exist is unclear. We investigated the relationship between mitochondrial motility and neuronal activity in the primary visual cortex of young mice in vivo and in slice cultures. During the first 2 postnatal weeks, mitochondrial motility decreases while the frequency of neuronal activity increases. Global calcium transients do not affect mitochondrial motility. However, individual synaptic transmission events precede local mitochondrial arrest. Pharmacological stimulation of synaptic vesicle release, but not focal glutamate application alone, stops mitochondria, suggesting that an unidentified factor co-released with glutamate is required for mitochondrial arrest. A computational model of synaptic transmission-mediated mitochondrial arrest shows that the developmental increase in synapse number and transmission frequency can contribute substantially to the age-dependent decrease of mitochondrial motility.
Journal Article
Comparison of FLASH Proton Entrance and the Spread-Out Bragg Peak Dose Regions in the Sparing of Mouse Intestinal Crypts and in a Pancreatic Tumor Model
Ultra-high dose rate FLASH proton radiotherapy (F-PRT) has been shown to reduce normal tissue toxicity compared to standard dose rate proton radiotherapy (S-PRT) in experiments using the entrance portion of the proton depth dose profile, while proton therapy uses a spread-out Bragg peak (SOBP) with unknown effects on FLASH toxicity sparing. To investigate, the biological effects of F-PRT using an SOBP and the entrance region were compared to S-PRT in mouse intestine. In this study, 8–10-week-old C57BL/6J mice underwent 15 Gy (absorbed dose) whole abdomen irradiation in four groups: (1) SOBP F-PRT, (2) SOBP S-PRT, (3) entrance F-PRT, and (4) entrance S-PRT. Mice were injected with EdU 3.5 days after irradiation, and jejunum segments were harvested and preserved. EdU-positive proliferating cells and regenerated intestinal crypts were quantified. The SOBP had a modulation (width) of 2.5 cm from the proximal to distal 90%. Dose rates with a SOBP for F-PRT or S-PRT were 108.2 ± 8.3 Gy/s or 0.82 ± 0.14 Gy/s, respectively. In the entrance region, dose rates were 107.1 ± 15.2 Gy/s and 0.83 ± 0.19 Gy/s, respectively. Both entrance and SOBP F-PRT preserved a significantly higher number of EdU + /crypt cells and percentage of regenerated crypts compared to S-PRT. Moreover, tumor growth studies showed no difference between SOBP and entrance for either of the treatment modalities.
Journal Article
A high-resolution mRNA expression time course of embryonic development in zebrafish
We have produced an mRNA expression time course of zebrafish development across 18 time points from 1 cell to 5 days post-fertilisation sampling individual and pools of embryos. Using poly(A) pulldown stranded RNA-seq and a 3′ end transcript counting method we characterise temporal expression profiles of 23,642 genes. We identify temporal and functional transcript co-variance that associates 5024 unnamed genes with distinct developmental time points. Specifically, a class of over 100 previously uncharacterised zinc finger domain containing genes, located on the long arm of chromosome 4, is expressed in a sharp peak during zygotic genome activation. In addition, the data reveal new genes and transcripts, differential use of exons and previously unidentified 3′ ends across development, new primary microRNAs and temporal divergence of gene paralogues generated in the teleost genome duplication. To make this dataset a useful baseline reference, the data can be browsed and downloaded at Expression Atlas and Ensembl.
Journal Article
Randomized controlled trial of behavioral treatment for comorbid obesity and depression in women: the Be Active Trial
Objective:
Depression is associated with increased risk for obesity and worse weight loss treatment outcomes. The purpose of the present study was to test the hypothesis that delivering evidence-based behavior therapy for depression before a lifestyle weight loss intervention improves both weight loss and depression.
Design:
In a randomized controlled trial, obese women with major depressive disorder (
N
=161, mean age=45.9 (s.d.: 10.8) years) were randomized to brief behavior therapy for depression treatment followed by a lifestyle intervention (BA) or a lifestyle intervention only (LI). Follow-up occurred at 6 and 12 months. Main outcome measures included weight loss and depression symptoms.
Results:
Intention-to-treat analyses revealed both conditions lost significant weight, but no differences between conditions in weight change at 6 months (BA=−3.0%, s.e.=−0.65%; LI=−3.7%, s.e.=0.63%;
P
=0.48) or 12 months (BA=−2.6%, s.e.=0.77%; LI=−3.1%, s.e.=0.74%;
P
=0.72). However, the BA condition evidenced significantly greater improvement in Beck Depression Inventory-II scores relative to the LI condition at both 6 months (BA mean change=−12.5, s.d.=0.85; LI mean change=−9.2, s.d.=0.80,
P
=0.005) and 12 months (BA mean change=−12.6, s.d.=0.97; LI mean change=−9.9, s.d.=0.93;
P
=0.045). Participants who experienced depression remission by 6 months (61.2%) lost greater weight (mean=−4.31%; s.e.=0.052) than those who did not (39.7%; mean=−2.47%, s.e.=0.53;
P
=.001).
Conclusion:
Adding behavior therapy to a lifestyle intervention results in greater depression remission but does not improve weight loss within 1 year. Improvement in depression is associated with greater weight loss.
Journal Article
Placentation defects are highly prevalent in embryonic lethal mouse mutants
Large-scale phenotyping efforts have demonstrated that approximately 25–30% of mouse gene knockouts cause intrauterine lethality. Analysis of these mutants has largely focused on the embryo and not the placenta, despite the crucial role of this extraembryonic organ for developmental progression. Here we screened 103 embryonic lethal and sub-viable mouse knockout lines from the Deciphering the Mechanisms of Developmental Disorders program for placental phenotypes. We found that 68% of knockout lines that are lethal at or after mid-gestation exhibited placental dysmorphologies. Early lethality (embryonic days 9.5–14.5) is almost always associated with severe placental malformations. Placental defects correlate strongly with abnormal brain, heart and vascular development. Analysis of mutant trophoblast stem cells and conditional knockouts suggests that a considerable number of factors that cause embryonic lethality when ablated have primary gene function in trophoblast cells. Our data highlight the hugely under-appreciated importance of placental defects in contributing to abnormal embryo development and suggest key molecular nodes that govern placenta formation.
Analysis of embryonic lethal and sub-viable mouse knockout lines reveals that ablation of many genes affects placental development, and that the occurrence of placental defects is co-associated with abnormal brain, heart and vascular system development.
Womb woes increased in mutant mice
Large-scale analysis of mouse gene knockouts have demonstrated the prevalence of deleterious defects that arise in the mutant's offspring during development in the womb, thought to reflect defects during the development of the embryo itself. By analysing mouse knockouts from the Deciphering the Mechanisms of Developmental Disorders program, Myriam Hemberger and colleagues have found that knockout of many genes affects placental development and subsequently the development of the brain, heart and vasculature in the embryo. The studies highlight the importance of considering the role of the placenta when analysing developmental disorders.
Journal Article