Congenital lobar emphysema (CLE) is a clinico-radiological diagnosis, seen usually by four-six weeks of age (50% of patients) and rarely (<5% of patients) after the age of six months. Here, we report a young male with gradual onset of mild exertional breathlessness and physical examination revealing the features of right sided pneumothorax. X-ray of chest, with subsequent CT of chest, leads to the diagnosis of CLE. The pulmonary function tests, bronchoscopic examination and α1-antitrypsin level are normal. Patient is managed conservatively.
Experimental Autoimmune Encephalomyelitis (EAE) is a well-established animal model of human multiple sclerosis (MS). The effect of this inflammatory disease on hippocampus has not been addressed. Keeping in view the above consideration an attempt was made to delineate the effect of EAE on the hippocampus of Wistar rats. The assessment of the damage to the hippocampus was done 16 days post induction by the immunolocalization of ChAT (choline acetyl transferase). ChAT decreased remarkably after induction that revealed cholinergic neuronal degeneration in the hippocampus. Subsequently, many biochemical parameters were assessed to ascertain inflammatory activation of nitric oxide and associated oxidative damage as a putative mechanism of the cholinergic degeneration. Nitric oxide metabolites increased significantly (P < 0.05) with enhancement of MPO (Myeloperoxidase activity) (P < 0.001) in the MOG (myelin oligodendrocyte protein) group as compared to the controls. Peroxidation of biomembranes increased (P < 0.001), while reduced glutathione depleted (P < 0.001) with parallel decrease in catalase (P < 0.01) and superoxide dismutase enzyme activity (P < 0.001) in the MOG group. Our results show a strong role of peroxidase dependent oxidation of nitrite and oxidative stress in cholinergic degeneration in EAE.
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the novel coronavirus that causes coronavirus disease 2019 (COVID-19), was first reported in Wuhan, China, in December 2019 and has spread worldwide. SARS-CoV-2 is a positivestranded RNA virus that is enclosed by a protein containing lipid bilayer with a single-stranded RNA genome; SARS-CoV-2 has 82% homology with human SARS-CoV, which causes severe acute respiratory syndrome.SARS-CoV-2, virus binds to angiotensinconverting enzyme 2 (ACE2) receptors, which are expressed in key metabolic organs and tissues, including pancreatic beta cells, adipose tissue, the small intestine, and the kidneys. Thus, it is believed that SARS-CoV-2 may cause pleiotropic alterations of glucose metabolism that could complicate the pathophysiology of pre-existing diabetes or lead to new mechanisms of disease. Many studies have made observations that provide support for the hypothesis of a potential diabetogenic effect of Covid-19; in addition it is well-recognized that stress response associated with severe illness have diabetogenic effect. However, whether the alterations of glucose metabolism that occur with a sudden onset in severe COVIOD-19 persist or remit when the infection resolves is unclear. How frequent is the phenomenon of newonset diabetes, and is it classic type 1 or type 2 diabetes or a new type of diabetes. Key words: COVID 19; Prediabetes; Diabetes; Pneumonia.
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