's flying acupuncture for acute cerebral infarction hemiplegia: a randomized controlled trial / 中国针灸

<p><b>OBJECTIVE</b>To compare the efficacy difference between's flying acupuncture combined with conventional treatment and conventional treatment alone on acute cerebral infarction hemiplegia.</p><p><b>METHODS</b>A total of 120 patients were randomly divided into an observation group and a control group, 60 cases in each one. The control group was treated with conventional treatment, including anti-platelet aggregation, lipid-lowering, formula of traditional Chinese medicine which could promote circulation and remove stasis, neurotrophic medication and symptomatic treatment; mannitol was used for cerebral infarction with large area or increased intracranial pressure. Based on the conventional treatment applied in the control group, the observation group was treated with flying acupuncture at the affected Jianyu (LI 15), Quchi (LI 11), Shousanli (LI 10), Waiguan (TE 5), Hegu (LI 4), Huantiao (GB 30), Biguan (ST 31), Futu (ST 32), Zusanli (ST 36), etc. The treatment was given once a day, six days per week, for totally 2 weeks. The simplified Fugl-Meyer score, National Institute of Health Stroke Scale (NIHSS) and ADL-Bathel index (BI) score were evaluated before and after treatment in the two groups.</p><p><b>RESULTS</b>After the treatment, the simplified Fugl-Meyer and BI were significantly increased in both groups (all<0.05), which was significantly higher in the observation group (both<0.05); after the treatment, the NIHSS was significantly lowered in both groups (both<0.05), which was significantly lower in the observation group (<0.05).</p><p><b>CONCLUSION</b> 's flying acupuncture combined with conventional treatment were effective for acute cerebral infarction hemiplegia, which have better efficacy than conventional treatment on improving motor function, neurological deficit and daily living ability, and the pain is mild.</p>

Changes in levels of apoptosis in the walls of different segments of great saphenous varicose veins.

OBJECTIVE: Disordered programmed cell death may play a role in the development of superficial venous incompetence. We have determined the number of cells undergoing apoptosis and the alterations in the apoptotic level in the wall of different segments of the great saphenous varicose vein. METHODS: Twenty-one varicose great saphenous veins (VGSVs) (varicose group) and 12 normal great saphenous veins (GSVs) (control group) were collected, and the apoptosis level in the upper, middle, and lower segments were immunohistochemically stained with antibodies (anti-Bax and anti-Bcl-xl). Apoptosis was evaluated by the TUNEL assay and immunofluorescence staining. The morphology of apoptotic cells was observed with an electron microscope. RESULTS: Quantitative analysis showed that the apoptotic ratios in venous walls (intima and media) of the varicose group were significantly lower than the corresponding regions in the control group (all P < 0.05). A significantly higher apoptotic rates of the venous walls was observed in control group within the upper compared with the lower segment (P < 0.05). Significantly higher positive proteins expression rates of Bcl-xl/Bax were also detected in the VGSVs compared with the GSVs within the three segments, respectively (P < 0.01). Electron microscopic observations confirmed that endothelial and smooth muscle cells in varicose and normal vein walls exhibited apoptotic morphologic features, such as fuzzy mitochondrial cristae, medullary changes, and margination of the nuclear chromatin. CONCLUSION: VGSV walls were found to have a significant decrease in apoptotic rate compared with that of GSVs. The rate of apoptosis in the intima and media within the upper segment was increased more than the middle and lower segments in the GSVs. Our findings confirm that programmed cell death is down-regulated in primary varicose veins.

Dysregulated apoptosis of the venous wall in chronic venous disease and portal hypertension.

Introduction The etiology of varicose veins remains elusive. We hypothesized that abnormal cell cycle events in the vein wall may contribute to changes in the structural integrity, thus predisposing to the development of varicosities. The present study was designed to determine whether or not the same molecular apoptotic pathway exists between great saphenous and splenic veins. Methods Thirty-six samples of diseased splenic veins and varicose great saphenous veins were collected. Twenty-five samples of control splenic and great saphenous veins were also collected. The apoptotic cell proteins expression was immunohistochemically stained with antibodies (anti-Bax and anti-Bcl-xl). Apoptosis was evaluated by the terminal deoxynucleotidyl transferase-mediated nick-end labeling (TUNEL) assay and immunofluorescence staining. The morphology of apoptotic cells was observed with an electron microscope. Results The apoptotic ratio in walls (intima and media) of diseased splenic vein and varicose great saphenous vein groups were significantly lower than the corresponding regions in the splenic vein and great saphenous vein groups ( p < 0.01), respectively. A significant difference was not noted in the ratio change of apoptotic cells between the diseased splenic vein and varicose great saphenous vein groups ( p > 0.05). The high positive expression of Bcl-xl proteins was detected in the diseased splenic vein and varicose great saphenous vein groups, respectively. While the high positive expression of Bax proteins was also observed in the splenic vein and great saphenous vein groups, respectively. Electron microscopic observations confirmed that endothelial and smooth muscle cells in diseased splenic vein, varicose great saphenous vein, splenic vein, and great saphenous vein walls exhibited apoptotic morphologic features, such as fuzzy mitochondrial cristae, medullary changes, and margination of the nuclear chromatin. Conclusions Our results showed the same dysregulation of apoptosis via the intrinsic pathway in diseased splenic veins and varicose great saphenous veins. This observational study suggests that apoptotic down-regulation in the veins wall is a cause of diseased splenic veins and varicose great saphenous veins, but does not exclude the possibility that other mechanisms are involved.

Mechanism underlying acute lung injury due to sulfur mustard exposure in rats.

Sulfur mustard (SM), a bifunctional alkylating agent that causes severe lung damage, is a significant threat to both military and civilian populations. The mechanisms mediating the cytotoxic effects of SM are unknown and were investigated in this study. The purpose of this study was to establish a rat model of SM-induced lung injury to observe the resulting changes in the lungs. Male rats (Sprague Dawley) were anesthetized, intratracheally intubated, and exposed to 2 mg/kg of SM by intratracheal instillation. Animals were euthanized 6, 24, 48, and 72 h post-exposure, and bronchoalveolar lavage fluid (BALF) and lung tissues were collected. Exposure of rats to SM resulted in rapid pulmonary toxicity, including partial bronchiolar epithelium cell shedding, focal ulceration, and an increased amount of inflammatory exudate and number of cells in the alveoli. There was also evidence that the protein content and cell count of BALF peaked at 48 h, and the alveolar septum was widened and filled with lymphocytes. SM exposure also resulted in partial loss of type I alveolar epithelial cell membranes, fuzzy mitochondrial cristae, detachment and dissociation of ribosomes attached to the surface of rough endoplasmic reticulum, cracked, missing, and disorganized microvilli of type II alveolar epithelial cells, and increased apoptotic cells in the alveolar septum. The propylene glycol control group, however, was the same as the normal group. These data demonstrate that the mechanism of a high concentration of SM (2 mg/kg) induced acute lung injury include histologic changes, inflammatory reactions, apoptosis, oxidative stress, and nuclear DNA damage; the degree of injury is time dependent.

Pathologic changes of corneal lesions in rabbits after ocular exposure to mustard gas / 中华创伤杂志

Objective To observe the pathologic changes of corneal lesions in rabbits induced by mustard gas and changes of lymphocytes in the pathologic development so as to discuss the role of lymphocytes in the pathogenic process.Methods Thirty-five New Zealand white rabbits were randomly divided into experiment group and control group according to the random number table.In experiment group,rabbits were exposed to 0.2 ml of mustard gas liquid (400 μl/L) for a period of 4 minutes and were divided into 6 subgroups at 15 min,2 h,1 w,3 w,4 w,and 8 w after injury.Corneal tissue from each group was collected to detect changes of lymphocytes with aid of HE and immunohistochemical stainings.Results In experiment group,corneal epithelium was dropped totally,basement membrane was exposed,swelling was thickened,matrix layer was loosened and swelled,and collagen fibre was ranged loosely at 15 minutes and two hours ; corneal epithelium appeared multi-layer hyperplastic change in acute restoration period at 1 week; basal corneal epithelium cells appeared irregular column arrangement in chronic inflammation period at 3 and 4 weeks; around 10％ of toxic corneas had delayed reaction with partial corneal epithelium resloughed,fundus membrane appeared,edema thickened,and stroma collagens loosened and swelled at eight weeks.Immunohistochemical Envision staining showed positive expression of plymphomonocytes (CD20,CD45RO,and LCA) inside matrix layer at corneoscleral junction.Conclusions Ocular exposure to 400 μ/L mustard gas for a period of four minutes leads to direct and delayed lesions to cornea,which presents at one week and eight weeks respectively.The lymphocyte-mediated cellular and humoral immunity responses may be involved in the pathogenic process.