ObjectiveTo evaluate the clinical therapeutic effect of biceps tendon tenotomy and fixation versus biceps tendon repair for shoulder superior labrum anterior posterior (SLAP) lesions with Meta-analysis. MethodsThe databases such as PubMed, EMbase, the Cochrane Library (Issue 3, 2014), CBM, VIP and CJFD (from the establishment time of databases to December 2014) were searched to collect all randomized controlled trials (RCT) on the clinical effectiveness of biceps tendon tenotomy and fixation versus biceps tendon repair for shoulder SLAP lesions. Two reviewers independently screened the literature according to the inclusive and exclusive criteria, extracted the data, and assessed the methodological quality of included studies. After the data extraction and methodological quality evaluation, meta-analysis was conducted with RevMan 5.0 software. ResultsThree RCT were included. Among the total 137 patients involved, Meta-analysis showed that, compared with the biceps tendon repair group, the biceps tenotomy group had superior amount in the UCLA score [WMD=3.43, 95%CI (2.29, 4.56), P<0.000 01], the shoulder pain [WMD=1.18, 95%CI (0.30, 2.05), P=0.009], function [WMD=0.96, 95%CI (0.51, 1.41), P<0.000 1] and satisfaction [WMD=1.16, 95%CI (0.31, 2.01), P=0.007] with significant differences. But there were no significant differences between the two groups in the shoulder flextion [WMD=0.10, 95%CI (-0.87, 1.06), P=0.84] and strength [WMD=0.13, 95%CI (-0.09, 0.35), P=0.25]. ConclusionBased on the current studies, the biceps tenotomy and fixation is superior to the biceps tendon repair in treating shoulder SLAP lesions. For the quality restrictions and possible publication bias of the included studies, more double blind, high quality RCT are required to further evaluate the effects.
ObjectiveTo observe the effect of integrin β8 on the neuronal apoptosis after hypoxia ischemia (HI) in astrocyte/neuron co-culture system. MethodsAstrocytes and neurons were cultured in vitro from cerebral cortex of the P1-3 days Sprague Dawley rats and E16 days fetal rats, respectively. Immunocytochemistry staining was used to identify the purity of cells. Integrin β8 mRNA expression was qualified in the astrocytes at 12 hours, 1 day, and 2 days after HI and reoxygenation (experimental group) and in normal astrocytes (control group) by RT-PCR. Integrin β8 small interering RNA (siRNA) system was established to specifically block astrocyte β8 expression, the efficiency of integrin β8 inhibition was detected by real-time fluorescent PCR. The astrocytes and neurons were co-cultured to established the astrocyte/neuron co-culture system. The neuronal apoptosis was detected with TUNEL in the normal neurons/astrocytes group (co-cultured HI group), the astrocytes infected by integrin β8 siRNA for 2 days/normal neurons group (β8 RNA interference group), and normal neurons in vitro with HI treatment group (HI group) at 1 day after HI and reoxygenation. The normal neurons without treatment as control (control group). ResultsGlial fibrillary acidic protein and neuronal nuclei staining suggested a purity of more than 90% in cultured cells. HI resulted in an increase of integrin β8 mRNA expression at 12 hours after reoxygenation in astrocytes, which peaked at 1 day after reoxygenation, then slowly decreased and remained higher at 2 days, showing significant differences between control group and experimental group and among different time points in experimental group (P<0.05). RNA interference efficiency was most significant at 2 days after astrocytes infected with integrin β8 siRNA (P<0.05). The neuronal apoptosis was significantly increased in HI group, co-cultured HI group, and β8 RNA interference group when compared with control group (P<0.05). But neuronal apoptosis index (AI) was significantly decreased in co-cultured HI group and β8 RNA interference group when compared with HI group (P<0.05). The significant difference of AI was found between co-cultured HI group and β8 RNA interference group (P<0.05). ConclusionIntegrin β8 expression can be induced with hypoxic-ischemic brain damage, leading to decreased AI of neurons and obvious protective effect.