ABSTRACT
ObjectiveTo investigate the effects of Fangji Fulingtang on macrophage polarization and oxidative stress in the mouse model of myocardial fibrosis. MethodThe mouse model of myocardial fibrosis was established by subcutaneous injection of isoproterenol （ISO， 5 mg·kg-1·d-1）. Fifty C57BL/6J mice were randomly assigned into control （0.9% NaCl）， model （0.9% NaCl）， low- and high-dose （3.315 g·kg-1·d-1 and 13.26 g·kg-1·d-1， respectively） Fangji Fulingtang （FFD-L and FFD-H， respectively）， and metoprolol tartrate （Meto， 15 mg·kg-1·d-1） groups， with 10 mice each group. After 2 weeks of treatment， the heart appearance， cardiac weight index （CWI）， heart weight （HW）/tibia length （TL） ratio， and myocardial histopathological alterations were observed. Meanwhile， the serum levels of creatine kinase-MB （CK-MB）， transforming growth factor-β1 （TGF-β1）， tumor necrosis factor-α （TNF-α）， interleukin （IL）-1β， IL-6， IL-10， malondialdehyde （MDA）， superoxide dismutase （SOD）， and glutathione （GSH） were measured by enzyme-linked immunosorbent assay （ELISA）. The expression levels of CD86 and CD206 were observed by immunohistochemical staining. ResultCompared with the model group， the FFD-L， FFD-H， and Meto groups showed improved heart appearance， decreased CWI and HW/TL ratio （P<0.01）， lowered serum levels of CK-MB， TGF-β1， TNF-α， IL-1β， and IL-6 （P<0.05， P<0.01）， and elevated IL-10 level （P<0.05）. Furthermore， the three groups showed reduced infiltration of inflammatory cells， myocardial injury， collagen deposition， and myocardial fibrosis， decreased CD86， SOD， and GSH （P<0.01）， and increased CD206 and MDA （P<0.01）. ConclusionFangji Fulingtang can mitigate ISO-induced myocardial fibrosis by regulating macrophage polarization and oxidative stress.
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Objective@#To investigate the etiology, clinical features, treatment and outcome of nephrotic syndrome associated with chronic mercury poisoning.@*Methods@#From June 2013 to April 2018, Beijing Chaoyang Hospital, Capital Medical University received 33 patients with chronic mercury-neutral nephrotic syndrome. The clinical manifestations, laboratory tests, treatment methods, and outcomes were analyzed.@*Results@#Among the 33 patients, 27 patients had mercury exposure due to daily-life contact and the other 6 patients were caused by iatrogenic mercury. The symptom was characterized by typical nephrotic syndrome such as lower extremity edema and proteinuria at first onset. The treatment was based on mercury-removing treatment, 19 cases were treated with mercury removal alone, 16 cases were completely relieved; 10 cases were treated with mercury removal and glucocorticoids, all of which were completely relieved; 4 cases were treated with mercury removal, glucocorticoids and immunosuppressive agents, all complete remission; clinical complete remission rate is about 90.9% (30 cases in total) . Urinary mercury levels decreased the fastest between the first and second courses of mercury treatment, but the total amount of urine protein increased. As the amount of urinary mercury excreted increased, the total amount of urine protein decreased gradually (Z=2.86, P<0.01) .@*Conclusion@#The clinical features of chronic mercury-induced nephrotic syndrome are non-specific, easy to be misdiagnosed and missed. The treatment is mainly treated with mercury removal treatment. The prognosis is good. In severe cases, glucocorticoid therapy can be supplemented.
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<p><b>OBJECTIVE</b>To carry out genetic testing for a family affected with pulmonary hypertension (PH) as the initial sign of hereditary hemorrhagic telangiectasia (HHT).</p><p><b>METHODS</b>High throughput sequencing was performed to detect potential mutation in the coding regions of endoglin (ENG), activin receptor-like kinase 1 (ACVRL1) and mothers against decapentaplegic homolog 4 (SMAD4) genes.</p><p><b>RESULTS</b>A pathogenic heterozygous c.814C>T (p.Gln272Ter) mutation of the ACVRL1 gene was identified in the proband. Her mother and two sons have carried the same mutation.</p><p><b>CONCLUSION</b>The c.814C>T (p.Gln272Ter) mutation of the ACVRL1 gene probably underlies the disease in this family. Genetic testing should be recommended to HHT patient, in particular those with pulmonary hypertension.</p>
Subject(s)
Child , Female , Humans , Male , Middle Aged , Activin Receptors, Type II , Genetics , Endoglin , Genetics , Genetic Testing , High-Throughput Nucleotide Sequencing , Hypertension, Pulmonary , Genetics , Mutation , Telangiectasia, Hereditary HemorrhagicABSTRACT
Recent studies have shown that changes in the form and color of sublingual collaterals were related to diabetes. And the changes of sublingual collaterals have certain clinical value in judging the condition, stage, treatment and prognosis of diabetes. This article summarized the research progress of sublingual collaterals from two aspects: the relationship between sublingual collaterals and diabetes mellitus and laboratory indexes, and the modern science and technology.