Advances of research on mechanisms of acupuncture underlying improvement of ischemic stroke by regulating neuronal mitochondria. / é’ˆåˆºè°ƒæŽ§ç¼ºè¡€æ€§å’ä¸­åŽç¥žç»å ƒçº¿ç²’ä½“çš„ä½œç”¨æœºåˆ¶ç ”ç©¶è¿›å±•.

Acupuncture has a positive effect in the treatment of ischemic stroke (IS). A number of studies have confirmed that the role of acupuncture in the treatment of IS, which is closely related to its functions of regulating mitochondrial functions. In the present article, we review the mechanisms of acupuncture underlying improvement of mitochondria in the treatment of IS from 4 aspects： 1) protecting mitochondrial structure integrity, 2) regulative effect on mitochondrial functional activities, including regulating energy metabolism, reducing oxidative stress, suppressing calcium overload, and regulating mitochondrial membrane potential changes, 3) regulating mitochondrial quality control system, including promoting mitochondrial biosynthesis, regulating mitochondrial dynamics and apoptosis, and 4) regula-ting mitochondria-related apoptosis pathways. All of these may provide a theoretical basis for acupuncture in the treatment of IS and a reference for further research.

Hydrogen-rich saline attenuates skin ischemia/reperfusion induced apoptosis via regulating Bax/Bcl-2 ratio and ASK-1/JNK pathway.

INTRODUCTION: Many pathways have been reported involving the effect of hydrogen-rich saline on protecting skin flap partial necrosis induced by the inflammation of ischemia/reperfusion injury. This study focused on the influence of hydrogen-rich saline treatment on apoptosis pathway of ASK-1/JNK and Bcl-2/Bax radio in I/R injury of skin flaps. METHODS: Adult male Sprague-Dawley rats were divided into three groups. Group 1 was sham surgery group, Group 2 and 3 were ischemia/reperfusion surgery treated with physiological saline and hydrogen-rich saline respectively. Blood perfusion of flap was measured by Laser doppler flowmeters. Hematoxylin and eosin staining was used to observe morphological changes. Early apoptosis in skin flap was observed through TUNEL staining and presented as the percentage of TUNEL-positive cells of total cells. pASK-1, pJNK, Bcl-2 and Bax were examined by immunodetection. In addition Bcl-2, Bax and caspase-3 were detected by qPCR. Caspase-3 activity was also measured. RESULTS: Compared to the Group 2, tissues from the group 3 were observed with a high expression of Bcl-2 and a low expression of pASK-1, pJNK, and Bax, a larger survival area and a high level of blood perfusion. Hydrogen-rich saline ameliorated inflammatory infiltration and decreased cell apoptosis. CONCLUSION: The results indicate that hydrogen-rich saline could ameliorate ischemia/reperfusion injury and improve flap survival rate by inhibiting the apoptosis factor and, at the same time, promoting the expression of anti-apoptosis factor.

Quantitative anatomic basis of antegrade lag screw placement in posterior column of acetabulum.

BACKGROUND: Lag screw fixation has been recommended for treatment of acetabular and pelvic fracture for several years. The aim of the present study was to determine the projection of the axis of the posterior column on the inner table of the iliac wing in the supra-acetabular region. METHODS: Thirty adult dried bony hemipelves specimens and other five intact adult dried pelvic specimens were included in this study. The projection point of the axis of the posterior column of the acetabulum was determined on the inner table of the iliac wing of the hemipelves specimens. The perpendicular distance from the optimal entry point to the linea terminalis of pelvis was measured and recorded as the lateral distance. The same measurement along the linea terminalis from the optimal entry point to the junction between the anterior border of iliosacral articulation and the linea terminalis of pelvis was made and recorded as the posterior distance. The depth of the anchor path and the corresponding average retroversion angulation and extraversion angulation were also measured. According to the results acquired from this study, a series of 6.5 mm lag screws were inserted into the posterior column of each side of the other five intact specimens, respectively, to evaluate the position of the screws. The data were expressed as mean +/- SD and analyzed by using the descriptive methods with SPSS 10.0. RESULTS: The average length of lag screw was 104.8 +/- 4.2 mm. The average lateral distance was 16.8 +/- 2.1 mm. The average posterior distance was 23.5 +/- 3.4 mm. The corresponding average retroversion angulation and extraversion angulation were 57 degrees 36' +/- 4 degrees 28' and 119 degrees 18' +/- 2 degrees 32', respectively. The insertion of the single 6.5 mm lag screw of adequate length was possible in the posterior column along its anchor path and no accidental extraosseous or intraarticular screw placement had occurred. CONCLUSIONS: The present study describes a safe anchor path of antegrade lag screw fixation in the posterior column. Insertion of the lag screws of adequate length is possible in the posterior column along its functional axis.

Expression of PDCD5, a novel apoptosis related protein, in human osteoarthritic cartilage.

AIM: To investigate the expression features of PDCD5 (programmed cell death 5 protein) in osteoarthritic and normal human cartilage, and speculate on its potential functions in the pathogenesis of osteoarthritis (OA). METHODS: Articular cartilage specimens were obtained from 30 patients with OA and 16 healthy patients at the time of arthroplasty. Expression of PDCD5 was detected by flow cytometry, immunofluorescence, RT-PCR and immunohistochemical analysis. RESULTS: Enhanced expression and nuclear accumulation of PDCD5 in OA chondrocytes were found. PDCD5-positive chondrocytes were mainly distributed in the superficial and deep zones of OA tissue sections, as opposed to, in the superficial and middle regions of normal healthy tissue sections. CONCLUSION: Since apoptotic chondrocyte death occurs more frequently in OA cartilage than in normal healthy cartilage and PDCD5 is an apoptosis-related protein, the different expression patterns of PDCD5 in OA cartilage from that in normal healthy cartilage indicate that PDCD5 is involved in the pathogenesis of OA.