著者
Yanli Wang Baocheng Deng Jie Zhang Wei Cui Wenqing Yao Pei Liu
出版者
一般社団法人 日本内科学会
雑誌
Internal Medicine (ISSN:09182918)
巻号頁・発行日
vol.53, no.8, pp.903-906, 2014 (Released:2014-04-15)
参考文献数
6
被引用文献数
11 16

Severe fever with thrombocytopenia syndrome (SFTS) is an emerging infectious disease recently discovered in northeastern and central China that is caused by a novel bunyavirus, severe fever with thrombocytopenia syndrome virus (SFTSV). Humans are primarily infected through tick bites. Four previous reports have discussed SFTS infection from person to person, all cases of which were symptomatic. In this report, we analysed the epidemiological and clinical data for a cluster of cases, including one case of secondary-asymptomatic infection, and review the literature regarding SFTSV transmission from person to person. We conclude that SFTSV caused the asymptomatic infections via person-to-person contact with infected blood.
著者
Ying Wen Ying Zhou Wen Wang Yu Wang Xu Lu Cui Ming Sun Wei Cui Jing Liu Wen Qing Geng Hong Shang Pei Liu
出版者
一般社団法人 日本内科学会
雑誌
Internal Medicine (ISSN:09182918)
巻号頁・発行日
vol.53, no.21, pp.2455-2461, 2014 (Released:2014-11-01)
参考文献数
29
被引用文献数
2 4

Objective Short-term mortality rates remain high among critically ill human immunodeficiency virus-1 (HIV-1) patients though long-term mortality rates have dropped. Baseline risk factors for short-term mortality have not yet been determined in China. In this paper, we herein describe clinical characteristics, laboratory findings, causes of clinical deterioration, and risk factors associated with mortality among HIV-1 patients within six months after hospital admission. Methods We carried out a prospective study of hospitalized patients in advanced stages of HIV infection. These patients started antiretroviral therapy three or four weeks after admission. Follow-up was conducted for a period of six months. We used a multivariate logistic-regression analysis to identify risk factors associated with mortality. Results A total of 141 patients met our inclusion criteria. The mean age was 41 years. Fever and weight loss were the most common clinical manifestations of advanced HIV disease. Oral candidiasis, tuberculosis, cytomegaloviremia, and pneumocystis pneumonia were the most common opportunistic infections. Significantly decreased CD4+ T-cell counts, hypoalbuminemia, anemia, hyponatremia, as well as elevated C-reactive protein (CRP) and glutamic alanine transaminase levels were common laboratory test abnormalities. The mortality rate was 21.3%. The patients who died were more likely than the survivors to have low CD4+ T-cell counts as well as low creatinine, hemoglobin, albumin, and serum sodium levels while also having longer intervals of fever and higher CRP levels. A multivariate analysis demonstrated that the independent risk factors for mortality were active tuberculosis [odds ratio (OR): 2.681; 95% confidence interval (CI), 1.006-7.142; p=0.049], hyponatremia (OR: 3.027; 95% CI, 1.238-7.401; p=0.015), and being at clinical stage 4 (as defined by the World Health Organization) (OR: 9.492; 95% CI, 1.200-75.065; p=0.033) within the first six months of admission. Conclusion Special consideration should be given to patients who have active tuberculosis, are at clinical stage 4, and present with hyponatremia upon admission as these were found to be important factors associated with mortality within six months of hospital admission in HIV-1 patients.
著者
Jie Hao Wei-Wei Li Hong Du Zhi-Fang Zhao Fan Liu Jing-Chao Lu Xiu-Chun Yang Wei Cui
出版者
The Pharmaceutical Society of Japan
雑誌
Chemical and Pharmaceutical Bulletin (ISSN:00092363)
巻号頁・発行日
vol.64, no.6, pp.548-557, 2016-06-01 (Released:2016-06-01)
参考文献数
27
被引用文献数
5 6

How to provide effective prevention and treatment of myocardial ischemia/reperfusion (I/R) injury and study of the mechanism underlying I/R injury are hotspots of current research. This study aimed to elucidate the effect and cardioprotective mechanism of vitamin C (VC) on myocardial I/R injury. Our study introduced two different I/R models: I/R in vitro and oxygen–glucose deprivation/recovery (OGD/R) in primary neonatal rat cardiac myocytes. We used the mitochondrial permeability transition pore (mPTP) opener lonidamine (LND) and the mitochondrial KATP (mitoKATP) channel inhibitor 5-hydroxydecanoate (5-HD) to analyze the underlying mechanisms. We found that post-treatment with VC decreased I/R injury in our models. Post-treatment with VC significantly decreased I/R-induced injury, attenuated apoptosis, and maintained the functional integrity of mitochondria via alleviation of Ca2+ overload, reactive oxygen species burst, inhibition of the opening of mPTP, and prevention of mitochondrial membrane potential (ΔΨm) depolarization. VC post-treatment increased the phosphorylation of Akt and glycogen synthase kinase (GSK)-3β. The present results demonstrate that VC might protect the myocardium from I/R-induced injury by inhibiting the mPTP opening via activation of mitoKATP channels. VC mediates cardioprotection via activation of the phosphatidyl inositol 3-kinase (PI3K)-Akt signaling pathway. These findings may contribute toward the development of novel strategies for clinical cardioprotection against I/R injury.