Rossmead3692

Dry eye disease (DED) is a common ocular surface condition causing symptoms of significant discomfort, visual disturbance, and pain. With recent advancements, DED has become recognized as a chronic self-perpetuating inflammatory condition triggered by various internal and environmental factors. DED has been shown to arise from the activation of both the innate and adaptive immune systems, leading to corneal epithelium and lacrimal gland dysfunction. While the cornea is normally avascular and thus imbued with angiogenic and lymphangiogenic privilege, various DED models have revealed activated corneal antigen-presenting cells in regional lymph nodes, suggesting the formation of new corneal lymphatic vessels in DED. The recent availability of reliable lymphatic cell surface markers such as LYVE-1 has made it possible to study lymphangiogenesis. Accordingly, numerous studies have been published within the last decade discussing the role of lymphangiogenesis in DED pathology. We systematically review the literature to identify and evaluate studies presenting data on corneal lymphangiogenesis in DED. There is considerable evidence supporting corneal lymphangiogenesis as a central mediator of DED pathogenesis. These findings suggest that anti-lymphangiogenic therapeutic strategies may be a viable option for the treatment of DED, a conclusion supported by the limited number of reported clinical trials examining anti-lymphangiogenic modalities in DED.Survivors of COVID-19 are a vulnerable population, with complex needs because of lingering symptoms and complications across multiple organ systems. Those who required hospitalization or intensive care are also at risk for post-hospital syndrome and post-ICU syndromes, with attendant cognitive, psychological, and physical impairments, and high levels of health-care utilization. Effective ambulatory care for COVID-19 survivors requires coordination across multiple subspecialties, which can be burdensome if not well coordinated. With growing recognition of these needs, post-COVID-19 clinics are being created across the country. We describe the design and implementation of multidisciplinary post-COVID-19 clinics at two academic health systems, Johns Hopkins and the University of California-San Francisco. We highlight components of the model which should be replicated across sites, while acknowledging opportunities to tailor offerings to the local institutional context. Our goal is to provide a replicable framework for others to create these much-needed care delivery models for survivors of COVID-19.

To study the impact of 48h of simulated military operational stress (SMOS) on executive function, in addition to the role of trait resilience (RES) and aerobic fitness (FIT) on executive function performance. Associations between executive function and neuropeptide-Y (NPY), brain-derived neurotropic factor (BDNF), insulin-like growth factor-I (IGF-I), oxytocin, and α-klotho (klotho) were assessed to elucidate potential biomarkers that may contribute to cognitive performance during a multi-factorial stress scenario.

Fifty-four service members (SM) (26.4±5.4 years, 178.0±6.5cm, 85.2±14.0kg) completed the 5-day protocol, including daily physical exertion and 48h of restricted sleep and caloric intake. Each morning subjects completed a fasted blood draw followed by Cognition, a 10-part cognitive test battery assessing executive function. SMs were grouped into tertiles [low (L-), moderate (M-), high (H-)] based on Connor Davidson Resilience Score (RES) and V˙O

(FIT). Repeated measures ANOVA were run to analy/or selection processes targeting at augmenting trait resilience and aerobic fitness for increased readiness.Saccharomyces boulardii, a probiotic yeast is well prescribed for various gastrointestinal disorders accompanied by gut dysbiosis such as inflammatory bowel disease, bacterial diarrhea and antibiotic associated diarrhea. Gut dysbiosis has been associated with central nervous system via gut brain axis primarily implied in the modulation of psychiatric conditions. In the current study we use Saccharomyces boulardii as a therapeutic agent against gut dysbiosis associated cognitive decline. In mice, gut dysbiosis was induced by oral Ampicillin Na (250 mg/kg twice-daily) for 14 days. While in the treatment group S. boulardii (90 mg/kg once a day) was administered orally for 21 days along with 14 days of antibiotic treatment. Gene expression studies revealed antibiotic mediated decrease in the Lactobacillus, Bifidobacterium, Firmicutes and Clostridium which were restored by S. boulardii treatment. Cognitive behavioral studies showed a parallel reduction in fear conditioning, spatial as well as recognition memory which were reversed upon S. AZD6094 boulardii treatment in these animals. S. boulardii treatment reduced myeloperoxidase enzyme, an inflammatory marker, in colon as well as brain which was increased after antibiotic administration. Similarly, S. boulardii reduced the brain acetylcholine esterase, oxidative stress and inflammatory cytokines and chemokines which were altered due to antibiotic treatment. S. boulardii treatment also protected hippocampal neuronal damage and restored villus length and crypt depth thus normalizing gut permeability in antibiotic treated animals. Hence, we conclude that S. boulardii prevented antibiotic associated gut dysbiosis leading to reduced intestinal and brain inflammation and oxidative stress thus preventing hippocampal neuronal damage and eventually reversing gut dysbiosis associate cognitive decline in mice.Mitochondria are a major source of ATP provision as well as cellular suicidal weapon store. Accumulating evidences demonstrate that mitochondrial bioenergetics, biosynthesis and signaling are important mediators of tumorigenesis. Metabolic plasticity enables cancer cell reprogramming to cope with cellular and environmental alterations, a process requires mitochondria biology. Mitochondrial metabolism emerges to be a promising arena for cancer therapeutic targets. The permeability transition pore (PTP) participates in physiological Ca2+ and ROS homeostasis as well as cell death depending on the open state. The hypothesis that PTP forms from F-ATP synthase provides clues to the potential collaborative role of mitochondrial respiration and PTP in regulating cancer cell fate and metabolic reprogramming.