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61.
Victoria Garland Anita B. Kumar Marie L. Borum 《Journal of the National Medical Association》2021,113(2):142-146
The novel coronavirus, SARS-CoV-2, has caused a global pandemic with high morbidity and mortality. It was first observed to cause a severe acute respiratory syndrome. However, gastrointestinal and hepatic manifestations have been increasingly recognized.Gastrointestinal symptoms include diarrhea, epigastric pain, nausea, and vomiting. Diarrhea is the most common GI manifestation of SARS-CoV-2 and can present without or without respiratory symptoms. Patients with GI symptoms have been associated with longer duration of illness and may be associated with more severe illness. Mechanism of diarrhea is thought to be related to direct viral cytotoxicity occurring when the SARS-CoV-3 enters GI cells via the ACE-2 receptor. Inflammatory response and cytokine release likely contributes to symptoms.SARS-CoV-2 can cause hepatic injury. Studies have shown mild to moderate elevation of liver enzymes. The pattern of liver abnormalities can be hepatocellular, cholestatic or mixed. Patients with severe infection have significantly higher rates of liver injury and worse outcomes. Proposed mechanisms for injury include immune mediated systemic inflammatory response, direct cytotoxicity from viral replication and hypoxia-reperfusion dysfunction.Recent data suggests that GI and hepatic injury may be under-recognized manifestation of SARS-CoV-2 infection. Patients with diarrhea and liver disease may have a worse prognosis. The rapidly evolving literature continues to reveal a growing body of information which enables updated guidance for management. More investigation is needed which focuses on vulnerable patients, including the elderly, those with underlying illness, as well as, racial and ethnic minorities. 相似文献
62.
63.
G Jancso MT Jaberansari B Gasz Z Szanto B Cserepes E Rth 《Experimental & Clinical Cardiology》2004,9(1):21-25
OBJECTIVES:
To show that angiotensin-converting enzyme (ACE) inhibition potentiates subthreshold ischemic preconditioning (IPC) via the elevation of bradykinin activity, leading to a fully delayed cardioprotective response.METHODS:
On day 1 of the experiment, pigs were subjected to sham (group 1, controls) or IPC protocols. In groups 2 and 3, 4×5 min and 2×2 min of IPC, respectively, were elicited by occluding the left anterior descending coronary artery with percutaneous transluminal coronary angioplasty inflatable balloon catheter. Group 4 was subjected to the ACE inhibitor perindoprilate only. In group 5, the pigs were pretreated with perindoprilate (0.06 mg/kg) and then subjected to 2×2 min IPC. In group 6, intracoronary HOE 140 (a selective bradykinin B2 receptor antagonist) was added before the perindoprilateaugmented subthreshold (2×2 min) PC stimulus. On the second day, all animals underwent 40 min left anterior descending coronary artery ligation and 3 h reperfusion, followed by infarct size analysis using triphenyl tetrazolium chloride staining.RESULTS:
The rates of infarct size and risk zone were the following in the experimental groups: group 1, 42.8%; group 2,19.5% (P<0.05); group 3, ischemia/reperfusion (I/R) 33.4%; group 4, I/R 18.4% (P<0.05); group 5, I/R 31.2%; and group 6, I/R 36.3%. A significant increase of nuclear factor kappa B activation in groups 2 and 4 was seen.CONCLUSIONS:
Results confirm that ACE inhibitors do not give total pharmacological IPC, but they enhance the induction effect of small ischemic insults, which raises the ischemic tolerance of myocardium. It was determined that enhanced bradykinin activity leads to downstream nuclear factor kappa B activation in this model. 相似文献64.
65.
66.
E. D. Gorham C. F. Garland A. A. Burgi S. B. Mohr K. Zeng H. Hofflich J. J. Kim C. Ricordi 《Diabetologia》2012,55(12):3224-3227
Aims/hypothesis
Low serum 25-hydroxyvitamin D [25(OH)D] concentration may increase risk of insulin-requiring diabetes.Methods
A nested case–control study was performed using serum collected during 2002–2008 from military service members. One thousand subjects subsequently developed insulin-requiring diabetes. A healthy control was individually matched to each case on blood-draw date (±2?days), age (±3?months), length of service (±30?days) and sex. The median elapsed time between serum collection and first diagnosis of diabetes was 1?year (range 1?month to 10?years). Statistical analysis used matched pairs and conditional logistic regression.Results
ORs for insulin-requiring diabetes by quintile of serum 25(OH)D, from lowest to highest, were 3.5 (95% CI 2.0, 6.0), 2.5 (1.5, 4.2), 0.8 (0.4, 1.4), 1.1 (0.6, 2.8) and 1.0 (reference) (p trend <0.001). The quintiles (based on fifths using serum 25(OH)D concentration in the controls) of serum 25(OH)D in nmol/l, were <43 (median 28), 43–59 (median 52), 60–77 (median 70), 78–99 (median 88) and ≥100 (median 128).Conclusions/interpretation
Individuals with lower serum 25(OH)D concentrations had higher risk of insulin-requiring diabetes than those with higher concentrations. A 3.5-fold lower risk was associated with a serum 25(OH)D concentration ≥60?nmol/l. 相似文献67.
68.
69.
Nilana MT Barros Raquel L Neves William N Addison Diego M Assis Monzur Murshed Adriana K Carmona Marc D McKee 《Journal of bone and mineral research》2013,28(3):688-699
X‐linked hypophosphatemia (XLH/HYP)—with renal phosphate wasting, hypophosphatemia, osteomalacia, and tooth abscesses—is caused by mutations in the zinc‐metallopeptidase PHEX gene (phosphate‐regulating gene with homologies to endopeptidase on the X chromosome). PHEX is highly expressed by mineralized tissue cells. Inactivating mutations in PHEX lead to distal renal effects (implying accumulation of a secreted, circulating phosphaturic factor) and accumulation in bone and teeth of mineralization‐inhibiting, acidic serine‐ and aspartate‐rich motif (ASARM)‐containing peptides, which are proteolytically derived from the mineral‐binding matrix proteins of the SIBLING family (small, integrin‐binding ligand N‐linked glycoproteins). Although the latter observation suggests a local, direct matrix effect for PHEX, its physiologically relevant substrate protein(s) have not been identified. Here, we investigated two SIBLING proteins containing the ASARM motif—osteopontin (OPN) and bone sialoprotein (BSP)—as potential substrates for PHEX. Using cleavage assays, gel electrophoresis, and mass spectrometry, we report that OPN is a full‐length protein substrate for PHEX. Degradation of OPN was essentially complete, including hydrolysis of the ASARM motif, resulting in only very small residual fragments. Western blotting of Hyp (the murine homolog of human XLH) mouse bone extracts having no PHEX activity clearly showed accumulation of an ~35 kDa OPN fragment that was not present in wild‐type mouse bone. Immunohistochemistry and immunogold labeling (electron microscopy) for OPN in Hyp bone likewise showed an accumulation of OPN and/or its fragments compared with normal wild‐type bone. Incubation of Hyp mouse bone extracts with PHEX resulted in the complete degradation of these fragments. In conclusion, these results identify full‐length OPN and its fragments as novel, physiologically relevant substrates for PHEX, suggesting that accumulation of mineralization‐inhibiting OPN fragments may contribute to the mineralization defect seen in the osteomalacic bone characteristic of XLH/HYP. © 2013 American Society for Bone and Mineral Research. 相似文献
70.
Gina Shetty BS Georgia M. Beasley MD Sara Sparks BS MT ASCP Michael Barfield MD Melanie Masoud BS Paul J. Mosca MD PhD Scott K. Pruitt MD PhD April K. S. Salama MD Cliburn Chan MD PhD Douglas S. Tyler MD Kent J. Weinhold PhD 《Annals of surgical oncology》2013,20(4):1128-1135