The American journal of the medical sciences
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Heterogeneity of clinical presentation of chronic obstructive pulmonary disease (COPD) attributes to different pathological basis. High-resolution computed tomography (HRCT) phenotypes of COPD may reflex the pathological basis of COPD indirectly by evaluating the small airway inflammation and emphysema. How the pulmonary function related with different HRCT phenotypes has not been well known. The aim was to explore the features of pulmonary function parameters in the 3 phenotypes. ⋯ The different features of pulmonary function parameters were found in various HRCT phenotypes; MEF50/MEF25 ratio could imply phenotype A, whereas RV/TLC% may be the indicator of phenotype E.
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One previous study has shown that patients with end-stage renal disease (ESRD) with higher blood lead levels (BLLs) have shorter survival, in a cohort without occupational exposure where follow-up began an average of 5 years after dialysis (a survivor population). ⋯ The authors found no association between BLL and survival after ESRD diagnosis. The authors' finding differs from earlier findings, possibly because the cohort had higher blood leads (25 versus 10 μg/dL), follow-up began at the time of ESRD diagnosis, and BLLs were measured before ESRD incidence.
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The mechanisms responsible for the development of acute pancreatitis (AP) and its complications are not fully understood. ⋯ Patients with hypertriglyceridemia-induced AP were more likely to develop persistent SIRS.
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Proteinuria is not only a sign of kidney damage but is also involved in the progression of renal disease as an independent pathologic factor. Although patients with mutated type 1 cannabinoid receptors (CB1) polymorphism are associated with renal microvascular damage, the biologic role of CB1 signaling in proteinuria remains uncharacterized till now. Herein, we investigate whether CB1 participates in glomerular proteinuria in CB1 transgenic mice and treatment with CB1 agonist WIN55212-2 rat, neither of which are diabetic models. ⋯ Taken together, CB1 transgenic mice and rats treated with CB1 agonist WIN55212-2 induced proteinuria with upregulation of CB1 resulting in impaired nephrin expression, by inducing excess VEGF reaction in the renal glomeruli. Genetic and pharmacological manipulation of CB1 signaling revealed VEGF-dependent nephrin depression of glomerulopathy. Controlling CB1 activity can be used an alternative strategy for sustaining renal function in the presence of CB1 activation.