Dexamethasone weakens the respiratory effects of pro-inflammatory cytokine TNF-α in rat.

The goal of the current study was to identify the role of the glucocorticoids in the respiratory effects of proinflammatory cytokines. For this purpose intravenous injections of TNF-α were used in anesthetized spontaneously breathing rats before and after pretreatment of dexamethasone, a synthetic steroid with predominant glucocorticoid activity. Dexamethasone was injected intraperitoneally at a dose of 1 mg/kg.

Battle of the sections: Student outcomes and course feedback support combined prosection and dissection laboratory formats to maximize student success.

Gross anatomy laboratories frequently utilize dissection or prosection formats within medical curricula. Practical examination scores are consistent across the formats, yet these examinations assessed larger anatomical structures. In contrast, a single report noted improved scores when prosection was used in the hand and foot regions, areas that are more difficult to dissect.

Innovations Through Virtual Reality Simulation.

The need to augment standardized learner outcomes related to performance and clinical competency led to creating curricular elements that would provide instruction and assessment from multiple perspectives. The COVID-19 pandemic brought about needs for re-imagination of standardized simulated clinical experiences given the need for increased distance-learning and asynchronous formats. Our goal was to identify activities that would engage pre-clinical simulation through asynchronous virtual reality (VR) case scenarios.

Cyclooxygenase and nitric oxide synthase pathways mediate the respiratory effects of TNF-α in rats.

TNF-α is the key inflammatory cytokine. TNF-α receptors are expressed in brain stem regions involved in respiratory control and also in the carotid bodies, which are the sensory organs monitoring arterial blood O. We hypothesised that the circulating tumour necrosis factor (TNF)-α may affect the lung ventilation and modulate the hypoxic ventilatory response via activation of cyclooxygenase (COX) and nitric oxide synthase (NOS) pathways.

Interleukin-1beta suppresses the ventilatory hypoxic response in rats via prostaglandin-dependent pathways.

We investigated the effect of the major inflammatory cytokine interleukin-1beta (IL-1β) on the ventilatory response to hypoxia. The goal was to test the hypothesis that IL-1β impairs the hypoxic ventilatory response in vivo by indirectly inhibiting respiratory neurons in the brainstem via prostaglandins. Thus, IL-1β was delivered by cerebroventricular injection, and the ventilatory hypoxic response was assessed in anesthetized, spontaneously breathing rats pretreated with or without diclofenac, a nonspecific inhibitor of prostaglandin synthesis.