-
Bowden Leach posted an update 6 months, 4 weeks ago
MDD patients with anhedonia showed different inflammatory characteristics compared to patients without anhedonia. Our results provide novel evidence suggesting that increased plasma CFH levels may be a potential biomarker of anhedonia of subtyping MDD.
MDD patients with anhedonia showed different inflammatory characteristics compared to patients without anhedonia. Our results provide novel evidence suggesting that increased plasma CFH levels may be a potential biomarker of anhedonia of subtyping MDD.
About every fourth patient with major depressive disorder (MDD) shows evidence of systemic inflammation. Previous studies have shown inflammation-depression associations of multiple serum inflammatory markers and multiple specific depressive symptoms. It remains unclear, however, if these associations extend to genetic/lifetime predisposition to higher inflammatory marker levels and what role metabolic factors such as Body Mass Index (BMI) play. It is also unclear whether inflammation-symptom associations reflect direct or indirect associations, which can be disentangled using network analysis.
This study examined associations of polygenic risk scores (PRSs) for immuno-metabolic markers (C-reactive protein , interleukin -6, IL-10, tumour necrosis factor -α, BMI) with seven depressive symptoms in one general population sample, the UK Biobank study (n=110,010), and two patient samples, the Munich Antidepressant Response Signature (MARS, n=1058) and Sequenced Treatment Alternatives to Relieve Dystemic inflammatory markers are primarily associated with somatic/neurovegetative symptoms of depression such as changes in appetite and fatigue, consistent with previous studies based on circulating levels of inflammatory markers. We extend these findings by providing evidence that associations are direct (using network analysis) and extend to genetic predisposition to immuno-metabolic markers (using PRSs). Our findings can inform selection of patients with inflammation-related symptoms into clinical trials of immune-modulating drugs for MDD.Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a debilitating condition characterized by fatigue and post-exertional malaise, accompanied by various signs of neurological and autonomic dysfunction. ME/CFS is often triggered by an infectious episode and associated with an aberrant immune system. Here we report that ME/CFS is a disorder characterized by skewed B cell receptor gene usage. By applying a next-generation sequencing to determine the clone-based IGHV/IGHD/IGHJ repertoires, we revealed a biased usage of several IGHV genes in peripheral blood B cells from ME/CFS patients. #link# Results of receiver operating characteristic (ROC) analysis further indicated a possibility of distinguishing patients from healthy controls, based on the skewed B cell repertoire. Meanwhile, B cell clones using IGHV3-30 and IGHV3-30-3 genes were more frequent in patients with an obvious infection-related episode at onset, and correlated to expression levels of interferon response genes in plasmablasts. Collectively, these results imply that B cell responses in ME/CFS are directed against an infectious agents or priming antigens induced before disease onset.
Nursing home (NH) populations have borne the brunt of morbidity and mortality of COVID-19. We surveyed Michigan NHs to evaluate preparedness, staffing, testing, and adaptations to these challenges.
Interpandemic survey responses were collected May 1-12, 2020. We used Pearson’s Chi-squared test, Fisher’s exact test, and logistic regression to evaluate relationships.
Of 452 Michigan NHs contacted via e-mail, 145 (32.1%) opened the survey and of these, 143 (98.6%) responded. Sixty-eight percent of respondents indicated their response plan addressed most issues. NHs reported receiving rapidly changing guidance from many sources. Two-thirds reported shortages of personal protective equipment and other supplies. Half (50%) lacked sufficient testing resources with only 36% able to test residents and staff with suspected COVID-19. A majority (55%) experienced staffing shortages. Sixty-three percent experienced resignations, with front-line clinical staff more likely to resign, particularly in facilities caring for COVID-19 patients (P < .001). Facilities adapted quickly, creating COVID-19 units (78%) to care for patients on site. To reduce isolation, NHs facilitated communication via phone calls (98%), videoconferencing (96%), and window visits (81%). A majority continued to provide requisite therapies (90%).
NHs experienced shortages of resources, testing supplies, and staffing challenges. COVID-19 in the facility was a key predictor of staff resignations. Facilities relied on rapidly changing, often conflicting advice from multiple sources, suggesting high-yield areas of improvement.
NHs experienced shortages of resources, testing supplies, and staffing challenges. COVID-19 in the facility was a key predictor of staff resignations. Facilities relied on rapidly changing, often conflicting advice from multiple sources, suggesting high-yield areas of improvement.The transcription factor nuclear factor erythroid-derived 2-like 2 (NRF2) participates in the activation of the antioxidant cytoprotective pathway and other important physiological processes to maintain cellular homeostasis. The dysregulation of NRF2 activity plays a role in various diseases, such as cardiovascular diseases, neurodegenerative diseases, and cancer. Thus, NRF2 activity is tightly regulated through multiple mechanisms, among which phosphorylation by kinases is critical in the posttranslational regulation of NRF2. For instance, PKC, casein kinase 2, and AMP-activated kinase positively, while GSK-3 negatively regulates NRF2 activity through phosphorylation of different sites. Here, we provide an overview of the phosphorylation regulation pattern of NRF2 and discuss the therapeutic potential of interventions targeting NRF2 phosphorylation.Early treatment can prevent the occurrence of diabetes; however, there are few pharmacological treatment strategies to date. The liver is a major metabolic organ, and hepatic glucose homeostasis is dysregulated in type 1 and type 2 diabetes mellitus. However, the potential of specifically targeting the liver to prevent diabetes has not been fully exploited. In this study, we found that compartmentally inhibiting hepatic oxidants by nano-MitoPBN, a liver mitochondrial-targeting ROS scavenger, could effectively prevent diabetes. click here demonstrated that nano-MitoPBN reversed the downregulation of PGC-1α and the enhanced gluconeogenesis in the livers of diabetic mice. PGC-1α, through an AMPK- and SIRT3-mediated mechanism, promoted mitochondrial biogenesis, increased the number of mitochondria, and enhanced the rate of aerobic oxidation, leading to decreased glucose levels in the blood by increasing glucose uptake and catabolism in the liver. Moreover, the increase in PGC-1α activity did not promote the activation of gluconeogenesis.
Please follow & like us :)
All content contained on CatsWannaBeCats.Com, unless otherwise acknowledged,is the property of CatsWannaBeCats.Com and subject to copyright.