Effect of Tai Chi exercise for hypertension: a meta-analysis of randomized controlled trials

Objectives: We designed this study to evaluate the effect of Tai Chi exercise for hypertension patients. Methods: RCTs designed to evaluate the effect of Tai Chi exercise for hypertension patients were searched from Science Direct, EBSCO, Pub Med, CNKI and Wanfang databases. Results: The meta-analysis found that (ATC) the SBP (WMD = 13.19 mmHg; 95%CI: 11.52 to 14.87; P < 0.0001) and DBP (WMD = 8.92 mmHg; 95% CI: 7.94 to 9.90; P< 0.0001) can be significantly reduced after Tai Chi exercise compared to before Tai Chi exercise (BTC). ATC significantly improved the content of NO (WMD =−7.98mmol/L; 95%CI: −10.63 to −5.33; P < 0.0001), and decreased the content of TG (WMD =0.22mmol/ml; 95%CI: 0.06 to 0.38; P =0.006) and LDL-C (WMD =0.20mmol/ml; 95%CI: 0.13 to 0.26; P < 0.0001). There was no obvious difference between ATC and BTC on HR (WMD = 1.64; 95%CI: −0.51 to 3.97; P =0.14), TC (WMD = −0.03mmol/ml; 95%CI: −0.22 to 0.17; P =0.80) and HDL-C (WMD =−0.04 mmol/ml; 95%CI: −0.09 to 0.01; P =0.13). Conclusions: As a valid treatment for hypertension patients, Tai Chi exercise can decrease SBP, DBP, TG, LDL-C and increase NO

Effect of Free Treatment and Surveillance on HIV-Infected Persons Who Have Tuberculosis, Taiwan, 1993–2006

In 1997, Taiwan made highly active antiretroviral therapy (HAART) available without cost to HIV-infected persons; in 2001, a national web-based surveillance system was implemented. Healthcare workers use the system to monitor patients' conditions and can intervene when necessary. Free HAART, coupled with the surveillance system, appears to have increased survival rates of HIV-infected persons with tuberculosis in Taiwan

The pathological effects of CCR2+ inflammatory monocytes are amplified by an IFNAR1-triggered chemokine feedback loop in highly pathogenic influenza infection

Background: Highly pathogenic influenza viruses cause high levels of morbidity, including excessive infiltration of leukocytes into the lungs, high viral loads and a cytokine storm. However, the details of how these pathological features unfold in severe influenza infections remain unclear. Accumulation of Gr1 + CD11b + myeloid cells has been observed in highly pathogenic influenza infections but it is not clear how and why they accumulate in the severely inflamed lung. In this study, we selected this cell population as a target to investigate the extreme inflammatory response during severe influenza infection. Results: We established H1N1 IAV-infected mouse models using three viruses of varying pathogenicity and noted the accumulation of a defined Gr1 + CD11b + myeloid population correlating with the pathogenicity. Herein, we reported that CCR2+ inflammatory monocytes are the major cell compartments in this population. Of note, impaired clearance of the high pathogenicity virus prolonged IFN expression, leading to CCR2+ inflammatory monocytes amplifying their own recruitment via an interferon-alpha/beta receptor 1 (IFNAR1)-triggered chemokine loop. Blockage of IFNAR1-triggered signaling or inhibition of viral replication by Oseltamivir significantly suppresses the expression of CCR2 ligands and reduced the influx of CCR2+ inflammatory monocytes. Furthermore, trafficking of CCR2+ inflammatory monocytes from the bone marrow to the lung was evidenced by a CCR2-dependent chemotaxis. Importantly, leukocyte infiltration, cytokine storm and expression of iNOS were significantly reduced in CCR2-/- mice lacking infiltrating CCR2+ inflammatory monocytes, enhancing the survival of the infected mice. Conclusions: Our results indicated that uncontrolled viral replication leads to excessive production of inflammatory innate immune responses by accumulating CCR2+ inflammatory monocytes, which contribute to the fatal outcomes of high pathogenicity virus infections

5-Fluorouracil Induced Intestinal Mucositis via Nuclear Factor-κB Activation by Transcriptomic Analysis and In Vivo Bioluminescence Imaging

5-Fluorouracil (5-FU) is a commonly used drug for the treatment of malignant cancers. However, approximately 80% of patients undergoing 5-FU treatment suffer from gastrointestinal mucositis. The aim of this report was to identify the drug target for the 5-FU-induced intestinal mucositis. 5-FU-induced intestinal mucositis was established by intraperitoneally administering mice with 100 mg/kg 5-FU. Network analysis of gene expression profile and bioluminescent imaging were applied to identify the critical molecule associated with 5-FU-induced mucositis. Our data showed that 5-FU induced inflammation in the small intestine, characterized by the increased intestinal wall thickness and crypt length, the decreased villus height, and the increased myeloperoxidase activity in tissues and proinflammatory cytokine production in sera. Network analysis of 5-FU-affected genes by transcriptomic tool showed that the expression of genes was regulated by nuclear factor-κB (NF-κB), and NF-κB was the central molecule in the 5-FU-regulated biological network. NF-κB activity was activated by 5-FU in the intestine, which was judged by in vivo bioluminescence imaging and immunohistochemical staining. However, 5-aminosalicylic acid (5-ASA) inhibited 5-FU-induced NF-κB activation and proinflammatory cytokine production. Moreover, 5-FU-induced histological changes were improved by 5-ASA. In conclusion, our findings suggested that NF-κB was the critical molecule associated with the pathogenesis of 5-FU-induced mucositis, and inhibition of NF-κB activity ameliorated the mucosal damage caused by 5-FU

Comparison of Human and Soil Candida tropicalis Isolates with Reduced Susceptibility to Fluconazole

Infections caused by treatment-resistant non-albicans Candida species, such as C. tropicalis, has increased, which is an emerging challenge in the management of fungal infections. Genetically related diploid sequence type (DST) strains of C. tropicalis exhibiting reduced susceptibility to fluconazole circulated widely in Taiwan. To identify the potential source of these wildly distributed DST strains, we investigated the possibility of the presence in soil of such C. tropicalis strains by pulsed field gel electrophoresis (PFGE) and DST typing methods. A total of 56 C. tropicalis isolates were recovered from 26 out of 477 soil samples. Among the 18 isolates with reduced susceptibility to fluconazole, 9 belonged to DST149 and 3 belonged to DST140. Both DSTs have been recovered from our previous studies on clinical isolates from the Taiwan Surveillance of Antimicrobial Resistance of Yeasts (TSARY) program. Furthermore, these isolates were more resistant to agricultural azoles. We have found genetically related C. tropicalis exhibiting reduced susceptibility to fluconazole from the human hosts and environmental samples. Therefore, to prevent patients from acquiring C. tropicalis with reduced susceptibility to azoles, prudent use of azoles in both clinical and agricultural settings is advocated