Body mass index and migraine: a survey of the Chinese adult population

The objective of this study is to evaluate the association between body mass index (BMI) and migraine in general population Chinese cohort. This was a cross-sectional secondary analysis from a general population Chinese cohort of men and women of reproductive and post-reproductive age ranging between 18 and 65 years. Migraine was defined utilizing ICHD criteria. Body mass indices were calculated using measured height and weight and categorized based on the World Health Organizations criteria. The 1-year period prevalence of migraine was 9.3 %. No association was identified between migraine and those with a BMI < 30.0. Compared to those with normal BMI (18.5–23.0), those with BMI ≥ 30 (morbid obesity) had a greater prevalence of migraine (8.6 vs. 13.8 %, p = 0.000). Multivariate-adjusted odds ratio demonstrated that those with morbid obesity had a greater than twofold increased odds of migraine [OR 2.10 (1.39–3.12)] as compared to those with a BMI between 18.5 and 23.0. No association was found between obesity and migraine severity, frequency, or disability. Morbid obesity was associated with twofold increased odds of migraine in this Chinese men and women cohort of predominantly reproductive age.     

Qushi Huayu Decoction (祛湿化瘀方) Inhibits Protein and Gene Expression of Cathepsin B in HepG2 Cells Induced by Free Fatty Acids

Objective: To study the experimental efficacy of Qushi Huayu Decoction (祛湿化瘀方,QHD) on protein and gene expression of cathepsin B (ctsb) in HepG2 cells induced by free fatty acids (FFAs).Methods: The model of HepG2 steatosis and tumor necrosis factor-α (TNF-α) secretion was induced by long-chain FFAs.HepG2 cells were divided into 4 groups: control group (group C),model group (group M),low-dose QHD group (group L) and high-dose QHD group (group H ).Long-chain FFAs were added to groups M,L and H.The 10% blank-control serum was added to group C and M,while 5% and 10% QHD-containing sera were added to group L and H,respectively.The levels of serum TNF-α and cellular triglyceride (TG) were detected.Cellular p-IκB and ctsb expression were detected using Western blot and PCR.The expression and distribution of ctsb were observed by immunofluorescence.Results: After incubating with FFA for 24 h,TG deposition in HepG2,TNF-α content in cell supernatant,the protein expression of cellular ctsb and P-IκB,as well as mRNA expression of ctsb increased markedly in group M compared with group C (P0.05,P0.01).Compared with group M,TG deposition,the expression of cellular ctsb,P-IκB and ctsb mRNA in groups L and H,as well as TNF-α content in group H,decreased significantly (P0.05).Cell immunochemical fluorescence studies showed that ctsb was released from lysosomes and distributed in the cytoplasm extensively and diffusedly after being stimulated with FFA.In this study,these above-mentioned changes were inhibited markedly in groups L and H.Conclusion: QHD might have a direct inhibitory effect on the ctsb target in the FFA-ctsb-TNFα pathway of hepatic lipotoxicity.     

养鸡场工人革螨皮炎病例报道

患者 ,女性 ,4 2岁 ,养鸡场工人。因全身皮肤出现丘疹、瘙痒 1周来我所临床部就医。 1周前患者与数人一起从事清理、运输鸡粪工作 ,第二天双耳廓、颈部、四肢末端时感瘙痒 ,之后数天发展至双腋部、胸背及双侧腹股沟皮肤亦瘙痒难忍 ,直至以手抓破皮肤 ,以疼代痒为止。有时在抓痒处可见红色小虫 ,针尖大小 ,有足数对 ,可活动 ,虫体被挤破后出血。至此 ,被迫停工就医。曾去村卫生室诊治 ,给予四环素、肤炎康软膏、扑而敏治疗 ,疗效不明显。目前 ,患者携带从自己床单、内衣上捕获的小红虫来所就诊。体检 :患者颈部、双侧乳房下、腹股沟、四肢末…     

Construction and analysis of cDNA library of Necator americanus third stage larvae.

OBJECTIVE: To obtain the genetic information on Necator americanus and to search for the purpose genes. METHODS: mRNA was isolated from the third stage larvae of Necator americanus maintained in hamsters. Double strand cDNA was synthesized and ligated to lambda ZAPII vector to construct the cDNA library. Expressed sequence tages (ESTs) were obtained by single pass sequencing of randomly isolated cDNA clones from the established library. RESULTS: A cDNA library of N. americanus was successfully constructed with high recombinant efficiency. The titer of unamplified library was 1 x 10(7). The insert size was about 750-3,000 bp. Of 11 ESTs obtained from the library, 7 have a significant homology with certain functional genes. CONCLUSION: A high quality and high representative cDNA library of N. americanus was constructed at the first time and some functional genes were identified from the library by ESTs.     

Serological prevalence and risk factor analysis of hepatitis G virus infection in Hubei Province of China

Hepatitis G virus (HGV),also known as GB virus C, is a recently cloned virus which may be associated with human non A-E hepatitis[1,2] It is parenterally transmitted and usually coinfected or superinfected with hepatitis B or hepatitis C virus[3-5]. Some investigations have been reported on the seroprevalence and molecular prevalence of HGV infection in different areas and different population[6-15]. Current infection of HGV is diagnosed by detection of HGV RNA, and past infection with HGV is detectable by testing anti-HGV envelope protein (E2)[16-17]. To investigate the prevalence of HGV in Hubei Province, a central area of the People's Republic of China, ELISA and RT-PCR were employed to detect serum anti-HGV and HGV RNA in 1516 patients who were divided into 16 groups.     

双侧听神经瘤的治疗

目的：探讨双侧听神经瘤的显微外科手术和伽玛刀治疗方法，及如何保留神经功能和长期的肿瘤控制率。方法：分为两组治疗，A组12例病人直接采用伽玛刀治疗；B组14例病人采用单侧手术而对侧和术后残余肿瘤伽玛刀治疗。结果：A组病人全部保留至少一侧有用的听力，听力保留率为87．5％(2l／24，24耳中有21耳保留听力)，肿瘤控制有效率为91．7％。B组14例病人除2例病人双侧听力丧失外，12例病人均至少保留一侧有用的听力。听力保留率为46．4％(13／28，28耳中13耳听力保留)，肿瘤控制有效率为100％。结论：双侧听神经瘤的治疗应该根据病人的双侧听力情况、双侧肿瘤的大小以及颅高压及解除脑干压迫的必要性等情况，以伽玛刀为主要治疗手段配合显微外科手术切除的综合治疗，并尽力至少保留病人一侧有用的听力。     

食品中铬元素的含量分析

目的：了解常见食品中铬的含量，指导人群合理摄取铬元素，对糖尿病、动脉粥样硬化、冠心病患者的合理膳食提供理论依据。方法：用石墨炉原子吸收分光光度法测定25种食品中铬含量。选用357．9μm波长，采用二步干燥。测定回收率为92．6％--98．1％，相关系数r＝0．9987，回归方程Y＝0．0l19C 0．0766。结果：肉、蛋类中铬含量在102—532μg/kg之间，谷、豆和坚果类铬含量在104．1—355μg/kg之间，蔬菜、水果类铬合量在35．8—214．7μg/kg之间。结论：铬含量以动物性食品最高，谷类食物居中，蔬菜、水果较低。     

Involvement of reactive oxygen intermediates in cyclooxygenase-2 expression induced by interleukin-1, tumor necrosis factor-alpha, and lipopolysaccharide.

Reactive oxygen intermediates (ROIs) play an important role in inflammatory processes as mediators of injury and potentially in signal transduction leading to gene expression. Cyclooxygenase (COX) is a rate-limiting enzyme in prostanoid biosynthesis, and its recently cloned inducible form, COX-2, is induced by proinflammatory cytokines. This study linked ROIs to the signaling pathways that induce COX-2 expression. The hydroxyl radical scavengers DMSO (1%), as well as di- and tetramethylthiourea, inhibited IL-1-, TNF alpha-, and LPS-induced COX-2 expression in rat mesangial cells. The suppression of COX-2 mRNA expression correlated with the COX-2 protein level. In comparison with the prolonged induction of the inducible gene encoding protein-tyrosine phosphatase by hydrogen peroxide, the COX-2 gene was only transiently induced. Protein-tyrosine phosphatase is also induced by heat shock and chemical stress, whereas COX-2 is not. Superoxide was a more potent inducer for COX-2 than hydrogen peroxide. In addition, NADPH stimulated COX-2 expression, and an inhibitor of NADPH oxidase blocked COX-2 expression induced by TNF alpha. COX-2 and KC gene expression costimulated by IL-1 were inhibited differentially by the scavengers. These studies demonstrate that oxidant stress is a specific and important inducer of COX-2 gene expression. This induction may contribute to the deleterious amplification of prostanoids in inflammation and compound the direct effects of ROI production.     

Heparanase overexpression impairs inflammatory response and macrophage-mediated clearance of amyloid-β in murine brain

Neuroinflammation is typically observed in neurodegenerative diseases such as Alzheimer's disease, as well as after traumatic injury and pathogen infection. Resident immune cells, microglia and astrocytes, are activated and joined by blood-borne monocytes that traverse the blood-brain barrier and convert into activated macrophages. The activated cells express various cytokines, chemokines and proteolytic enzymes. To study the role of heparan sulfate proteoglycans in neuroinflammation, we employed a transgenic mouse overexpressing heparanase, an endoglucuronidase that specifically degrades heparan sulfate side chains. Neuroinflammation was induced by systemic challenge with lipopolysaccharide, or by localized cerebral microinjection of aggregated amyloid-β peptide, implicated in Alzheimer's disease. Lipopolysaccharide-treated control mice showed massive activation of resident microglia as well as recruitment of monocyte-derived macrophages into the brain parenchyma. Microinjection of aggregated amyloid-β elicited a similar inflammatory response, albeit restricted to the injection site, which led to dispersion and clearance of the amyloid. In the heparanase-overexpressing mice, all aspects of immune cell recruitment and activation were significantly attenuated in both inflammation models, as was amyloid dispersion. Accordingly, an in vitro blood-brain barrier model constructed from heparanase-overexpressing cerebral vascular cells showed impaired transmigration of monocytes compared to a corresponding assembly of control cells. Our data indicate that intact heparan sulfate chains are required at multiple sites to mediate neuroinflammatory responses, and further point to heparanase as a modulator of this process, with potential implications for Alzheimer's disease.