Journal of internal medicine
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Persistent symptoms of SARS-CoV-2 are prevalent weeks to months following the infection. To date, it is difficult to disentangle the direct from the indirect effects of SARS-CoV-2, including lockdown, social, and economic factors. ⋯ SARS-CoV-2 infection leads to persistent symptoms over several months, including in young healthy individuals, in addition to the pandemic effects, and potentially more than other common respiratory infections. Symptoms impact functional capacity up to 12 months post infection.
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Diabetic ketoacidosis (DKA) patients present with low serum bicarbonate ( HCO 3 - ${\rm{HCO}}_{3}^{-} $ ), and an increase in its level to ≥15 mEq/L is considered one of the criteria for DKA resolution. Both proton pump inhibitors and histamine-2 receptor antagonists inhibit downstream functioning of H+ /K+ ATPase in the gastric parietal cells, which results in the decreased secretion of HCO 3 - ${\rm{HCO}}_{3}^{-} $ into the bloodstream. ⋯ We found that Clostridium difficile and pneumonia predicted longer LOS in DKA patients with concomitant PUD, hinting at the possible role of acid suppression in prolonging the LOS in such patients. However, further studies are needed to examine the effect of lesser HCO 3 - ${\rm{HCO}}_{3}^{-} $ generation on LOS.
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The central nervous system (CNS) coordinates all our body functions. Neurons in the CNS parenchyma achieve this computational task by high speed communication via electrical and chemical signals and thus rely on a strictly regulated homeostatic environment, which does not tolerate uncontrolled entry of blood components including immune cells. The CNS thus has a unique relationship with the immune system known as CNS immune privilege. ⋯ Built for protection and defense this two-walled rampart at the outer perimeter of the CNS parenchyma allows for accommodation of different immune cell subsets and efficient monitoring of potential danger signals derived from inside or outside of the CNS parenchyma. It enables effective mounting of immune responses within the subarachnoid or perivascular spaces, while leaving the CNS parenchyma relatively undisturbed. In this study, we propose that CNS immune privilege rests on the proper function of the brain barriers, which allow for CNS immune surveillance but prohibit activation of immune responses from the CNS parenchyma unless it is directly injured.