Adult ; Aged ; Female ; Humans ; Male ; Middle Aged ; Otorhinolaryngologic Surgical Procedures ; adverse effects ; methods ; Postoperative Complications ; prevention & control ; Sleep Apnea, Obstructive ; surgery ; Treatment Outcome ; Uvula ; surgery ; Young Adult

Adhesives ; Adolescent ; Adult ; Aged ; Aged, 80 and over ; Child ; Endoscopy ; Epistaxis ; therapy ; Female ; Humans ; Male ; Middle Aged ; Treatment Outcome ; Young Adult

Animals ; Cytokines ; blood ; Humans ; Peripheral Vascular Diseases ; etiology ; physiopathology ; Rabbits ; Vibration ; adverse effects

Endothelial Cells ; metabolism ; pathology ; Humans ; Sepsis ; metabolism ; physiopathology

Limb-shaking transient ischemic attack (TIA), a rare manifestation, is commonly caused by severe stenosis or occlusion of an extracranial internal carotid artery. Such patients are usually treated with surgical revascularization or anti-platelet therapy. We present a 56-year-old woman with 6 months’ episodic attacks starting with mouth skewed to the right and a sensation of ‘weakness’ involving predominantly her left arm, and at times, also involved the left leg. This was immediately followed by rhythmic jerky movements of the left arm and at times, also involved the left leg. Magnetic resonance angiography revealed severe stenosis of M1 segment of the right middle cerebral artery. The patient’s symptoms were signifi cantly improved by treatment with anti-platelet drugs and nimodipine.

The acute and chronic respiratory tract inflammation models were made to investigate the effect and mechanism of sterol extracts from Begonia Sinensis Rhizome (BSR). The first model of acute lung injury was made with Kunming mice by inhaling cigarette smoke, then the mice were treated with different concentrations of BSR sterol extracts. Lung tissue morphology was detected by HE staining, TNF-alpha/MPO were detected by Elisa, and cPLA2 protein were, detected by Western blotting respectively. Results showed that in model group, lung sheet became real, alveolar space shrank or disappeared, alveolar septum was thickened, plenty of inflammatory cells were infiltrated, capillary blood vessels were congestive and the expression of TNF-α, MPO, cPLA2 increased; after administration, a small amount of inflammatory cells were infiltrated, alveolar septum became obvious, capillary congestion status was significantly relieved and the expression of TNF-α, MPO, cPLA2 decreased (P < 0.05). The second model of chronic respiratory tract inflammation in BALB/c mice with bronchial asthma was induced by OVA, then the mice were treated with different concentrations of BSR sterol extracts. Lung tissue morphology was detected by HE staining, indexes such as IL-4, IL-5, IL-13 were detected by Elisa, and the cPLA2 protein expression was detected by Western blotting respectively. Results showed that in model group, a lot of inflammatory cells around lung vessels and bronchi exuded, bronchial goblet cells proliferated and the expression of IL-4, IL-5, IL-13, cPLA2 increased; after administration, inflammatory and goblet cell hyperplasia reduced, the expression of IL-4, IL-5, IL-13, cPLA2 also decreased (P < 0.05). The above results showed BSR sterol extracts could resist against respiratory inflammation by inhibiting cPLA2 in a dose-dependent manner.
Animals ; Asthma ; drug therapy ; genetics ; immunology ; Begoniaceae ; chemistry ; Cytokines ; genetics ; immunology ; Disease Models, Animal ; Drugs, Chinese Herbal ; administration & dosage ; Female ; Humans ; Interleukin-13 ; genetics ; immunology ; Interleukin-4 ; genetics ; immunology ; Interleukin-5 ; genetics ; immunology ; Lung ; immunology ; Male ; Mice ; Mice, Inbred BALB C ; Rhizome ; chemistry ; Sterols ; administration & dosage

Adolescent ; Adult ; CD36 Antigens ; blood ; Diagnosis, Differential ; Female ; Humans ; Male ; Medicine, Chinese Traditional ; Middle Aged ; Platelet Activation ; Psoriasis ; blood ; diagnosis ; Thrombin ; metabolism ; Thrombospondins ; blood

The hemoglobin A1c(HbA1c) results can reflect the average level of blood glucose over the past 2-3 months,its clinical application value is transforming from evaluation indicator to diagnosis indicator.The application of HbA1c as a diagnostic indicator of diabetes is limited by many factors,such as multi-factor influence on measurement and its late start on standardization process in our country,optimal cut-point and the defect of HbA1c existing in the molecular level,etc.Therefore,clarifying the limitations of HbA1c in the practical application is of great significance for its clinical application.

Objective To detect the expression of CRF and CRF receptors in colonic mucosa of DSS induced colitis in mice model and to study the effect of CRF and CRF receptors on the development.Methods Six to eight weeks healthy female BALB/c mice were divided into control group and DSS group.Setting up DSS colitis model and colitis was evaluated by the disease activity index(DAI) and histological score.The immunofluorescence technique was used to assay the CRF1 and CRF2 receptors expression in colonic mucosa.The expression of CRF and CRF receptors protein were analyzed by western blotting.Results DSS colitis was set up successfully with significant inflammation in colonic mucosa by the disease activity index (DAI) and histological score.Immunofluorescenee staining evidenced that expression of CRF1 receptor in DSS colitis group has no significant deviation compared to control group(P ＞ 0.05),while the expression of CRF2 receptor was elevated in DSS colitis group compared to control group (P ＜ 0.05).CRF2 receptor was localized in epithelial cells and mononuclear cells in the lamina propria.The levels of CRF and CRF2 receptor protein by western blotting were higher in in DSS colitis group compared to control group (P ＜ 0.05).The level of CRF1 receptor protein in DSS colitis group had no significant deviation compared to control group(P ＞ 0.05).Conclusion The higher expression of CRF and CRF2 in colonic mucosa of DSS colitis may participate in the development of colitis.

Objective To investigate the role of mitochondrial KATP channel in the mechanism of the protective effect of ischemic preconditioning (IP) against ischemia-reperfusion (I/R) injury.Methods Forty-eight Wistar rats of both sexs weighing 250-350 g were used in this study. Forty rats were randomly divided into 5 groups ( n = 8 each): group A I/R; group B IP+ I/R; group C diazoxide (DZ mito-KATP channel activator) + I/R; group D 5-HD (mito-KATP channel blocker) + IP + I/R and group E 5-HD + DZ + I/R. Another 8 animals were used for electron microscopic examination of normal mitochondria as control. The animals were anesthetized with intraperitoneal pentobarbital 30 mg?kg-1. The hearts were immediately excised and passively perfused in a Langendorff apparatus with K-H solution at 5.8 kPa perfusion pressure and 36.5-37.5℃ via aortic cannulation. A fluid-filled latex balloon was via left atrium in left ventricle for the measurement of left ventricular function. I/R was induced after 30 min stabilization by clamping aortic cannula for 40 min followed by 30 min reperfusion. In group B and D the isolated hearts underwent 2 episodes of 5 min ischemia followed by 5 min reperfusion before I/R. In group C and E DZ 50 ?mol?L-1 was infused for 10 min and in group D and E 5-HD 100 ?mol?L-1 was infused for 10 min before I/R. HR, LVSP, LVEDP and coronary flow (CF) were measured at the end of stabilization (T0 , baseline), immediately before I/R (T1 ) and at 10, 20 and 30 min of reperfusion (T2.3.4.), and left ventricular developed pressure (LVDP= LVSP- LVEDP) was calculated. Myocardial tissue was obtained at the end of 30 min reperfusion for electron microscopic examination of mitochondria. Mitochondrial ultrastructure was assessed by Flameng scoring system (0 = normal, 4 = severely damaged) .Results Ischemic and DZ preconditioning significantly increased LVDP and decreased LVEDP and Flameng score. 5-HD pretreatment partly antagonized the protective effect of IP and completely antagonized that of DZ against I/R injury. Conclusion Ischemic preconditioning protects the heart against I/R injury mainly by activating mitochondrial KATP channel.