Objective To study the clinical and immunologic features of 67 cases of patients with scrub typhus.Methods Epidemiological data,clinical manifestations,laboratory and image examination results and treatment of 67 cases of patients with scrub typhus hospitalized from January 2010 to December 2013 at the First Affiliated Hospital of Nanjing Medical University were retrospectively analyzed.Results Autumn-winter type scrub typhus was predominant in the 67 patents.The main clinical manifestations included hyperpyrexia (100％,67/ 67),eschar or ulcer (91.0％,61/67),rash (52.2％,35/67),lymphadenopathy (46.3％,31/67) and other non-specific symptoms.Laboratory test results:①80.6％ (54/67) of the patients had normal or decreased white blood cell count,62.7％ (42/67) of them with elevated lymphocytes (＞ 40％),thrombocytopenia was detected in 34.3％ (23/67) of the patients,the lowest platelets count was 14 × 109/L.②14 of 17 cases (82.4％) had normal percentage of CD3+ T lymphocytes,CD8+ T lymphocytes increased in 16 of 17 cases (94.1％),while the percentage of CD4+ T lymphocytes (14 of 17,82.4％) and B lymphocytes (15 of 17,88.2％) decreased in most of the patients.③C reactive protein (CRP),ferritin and erythrocyte sedimentation rate (ESR) were elevated in 95.2％ (59/62),93.8％ (45/48) and 89.1％ (49/55) of the patients,respectively.④Elevated alanine aminotransferase (77.6％,52/67) and aspartate aminotransferase (80.6％,54/67) were frequent findings.⑤94.6％ (35/37) of the patients had increased adenosine deaminase.⑥ Antinuclear antibody was positive in 31.0％ (13/42) patients.⑦Epstein-barr virus DNA was detected in 15.6％ (7/ 45) cases,77.6％ (38/49) was accompanied with chest radiographic abnormalities.Two cases had tuberculosis.All the patients recovered after therapy with doxycycline,levofloxacin or moxifloxacin.Conclusion Autumn-winter scrub typhus has typical clinical manifestations in the 67 patients,and it can cause patients' immune disorders.

Objective: To investigate the role of piperine on the transformation of endothelial cells into fibroblasts. Methods: Cultured human umbilical vein endothelial cells (HUVECs, 4-6 passage) were used for the main experiments. The transformation models of endothelial cells into fibroblasts were induced by transforming growth factor β (TGF-β) stimulation. HUVECs were divided into 6 groups: control group, TGF-β group and 4 groups treated with various concentrations of piperine (1, 5, 10, 20 μmol/L). CKK-8 was used to detect cell proliferation. The CD31/α-smooth muscle actin (α-SMA) expression level was detected by fluorescent staining. The vascular endothelial cadherin (VE-cadherin)/vimentin expression was detected by immunofluorescence staining. RT-PCR was used detect the mRNA expressions of transformation markers. Western blot was used to detect the protein expression of snail and twist. Results: TGF-β increased HUVECs proliferation (P<0.05), which could be significantly inhibited by 10 and 20 μmol/L of piperine, but not by 1 and 5 μmol/L of piperine. Immunofluorescence results demonstrated that TGF-β increased HUVECs transformation to fibroblasts as shown by downregulated expression of endothelial markers CD31, VE-cadherin, and upregulated expression of α-SMA and vimentin, again, these effects could be attenuated by 10 and 20 μmol/L piperine. The expression levels of collagen type Ⅰ and type Ⅲ were significantly higher in TGF-β group than in control group (P<0.05), significantly lower in TGF-β+10 μmol/L piperine group and TGF-β+20 μmol/L piperine group than in TGF-β group (P<0.05).In addition, RT-PCR results showed that TGF-β increased mRNA expression of transformation markers (snail1, snail2, twist1, twist2), while 10 and 20 μmol/L of piperine could significantly downregulated the mRNA expressions of these markers. The protein expression levels of snail and twist were significantly higher in TGF-β group than in control group (both P<0.05), which was significantly lower in TGF-β+20 μmol/L piperine group than in TGF-β group (both P<0.05). Conclusions Piperine can inhibit the transformation of endothelial cells into fibroblasts. This effect might be viewed as one of the potential mechanisms of reduced myocardial fibrosis post piperine treatment.

Multiple sclerosis is a severe autoimmune inflammatory disease mainly involving the central nervous system. In recent years, the exploration of the mechanism of nerve injury in multiple sclerosis has made great progress. At the same time, disease-modifying therapeutic drugs with different targets are also emerging. Understanding of the mechanisms of nerve injury in multiple sclerosis can help clinicians comprehensively understand the evolution of disease-modifying therapeutic targets of this disorder. Here, the mechanisms of nerve injury in multiple sclerosis and the relationship with the evolution of disease-modifying therapeutic targets are reviewed.