[Arthroscopic glenoid labrum repair by anchor fixation for recurrent anterior shoulder dislocation].

OBJECTIVE: To investigate the curative effect of arthroscopic glenoid labrum repair by biodegradable anchor fixation for recurrent anterior shoulder dislocation. METHODS: Twenty-one patients of recurrent anterior shoulder dislocation with the average UCLA function score of 22.3 ± 4.1 were treated with arthroscopic glenoid labrum repair by biodegradable anchor fixation. The shoulder was fixed by shoulder-elbow elastic band for 4-6 weeks and canonical exercise of shoulder joint was taken postoperatively. RESULTS: The patients were followed up for 3-18(mean 8) months; and the average UCLA score was 32.3 ± 2.6 postoperatively. The excellent results (34-35) were obtained in 11 patients, good (28-33) in 7 patients and fair (21-27) in 3 patients. The activity of shoulder joint was normal in all patients with an excellent subjective degree of satisfaction. CONCLUSION: Arthroscopic glenoid labrum repair by anchor fixation for recurrent anterior shoulder dislocation has the advantages of less invasiveness, simpler procedure, reliable fixation, less complications and rapid functional recovery.

The apoptosis of grass carp (Ctenopharyngodon idella) muscle during postmortem condition regulated by the cytokines via TOR and NF-κB signaling pathways.

Postmortem alteration by apoptosis has significant effects on flesh quality. Currently, the information necessary to understand the apoptotic behavior and the molecular mechanisms during postmortem alteration in fish muscle is still lacking. Activation of apoptosis and the cytokines involved in regulating apoptosis in fish muscle were evaluated during postmortem condition at 4 °C for 5 days in terms of apoptotic morphology changes, nucleus DNA fragmentation, caspases activation and related gene expressions. The triggering apoptotic mechanisms associated with multiple cytokines transcriptional levels showed that the up-regulated pro-apoptotic mediators [IFN-γ2, TNF-α, IL-6, IL-1ß, IL-17D, IL-12p35 and IL-10 (except IL-15)] and the down-regulated anti-apoptotic mediators of [IL-8 and IL-11 (except TGF-ß and IL-4)] both regulated apoptosis at early stage, which were regulated by NF-κB and TOR, respectively. Results suggested that transcriptional regulation of multiple cytokines produce a positive outcome on triggering apoptosis.

The effects of selenium supplementation on antibody titres in patients with Hashimoto's thyroiditis.

INTRODUCTION: The objective of this study was to evaluate the effect of selenium supplementation on autoantibody titres, thyroid ultrasonography, and thyroid function in patients with Hashimoto's thyroiditis (autoimmune thyroiditis) and normal thyroid reference range. MATERIAL AND METHODS: A total of 100 patients were given 200 ug/d selenium yeast orally, their thyroid function, levels of serum selenium, thyroid peroxidase antibodies (TPOAb), thyroglobulin antibodies (TGAb), and urine iodine were measured, and thyroid ultrasonography was performed before administration and three and six months afterwards, and the data were statistically analysed. RESULTS: The subjects exhibited a selenium deficiency before the administration of selenium, and the serum levels increased to moderate levels three and six months after the selenium supplementation (p < 0.05). The titres of TGAb decreased significantly in patients after six months of selenium supplementation (p < 0.05). In the high antibody group, TgAb decreased after 6 months compared with baseline (p = p < 0.05), and TPOAb decreased after 3 and 6 months of selenium supplementation compared with baseline (p < 0.05). CONCLUSION: In patients with autoimmune thyroiditis and normal thyroid reference range, there was a general selenium deficiency, but after six months of treatment it was shown that selenium supplementation may be effective in reducing the titres of TGAb and TPOAb.

Fighting Type-2 Diabetes: Present and Future Perspectives.

BACKGROUND: Type-2 diabetes mellitus accounts for 80-90% of diabetic patients. So far, the treatment of diabetes mainly aims at elevating insulin level and lowering glucose level in the peripheral blood and mitigating insulin resistance. Physiologically, insulin secretion from pancreatic ß cells is delicately regulated. Thus, how insulin-related therapies could titrate blood glucose appropriately and avoid the occurrence of hypoglycemia remains an important issue for decades. Similar question is addressed on how to attenuate vascular complication in diabetic subjects. METHODS: We overviewed the evolution of each class of anti-diabetic drugs that have been used in clinical practice, focusing on their mechanisms, clinical results and cautions. RESULTS: Glucagon-like peptide-1 receptor agonists stimulate ß cells for insulin secretion in response to diet but not in fasting stage, which make them superior than conventional insulinsecretion stimulators. DPP-4 inhibitors suppress glucagon-like peptide-1 degradation. Sodium/ glucose co-transporter 2 inhibitors enhance glucose clearance through urine excretion. The appearance of these new drugs provides new information about glycemic control. We update the clinical findings of Glucagon-like peptide-1 receptor agonists, DPP-4 inhibitors and Sodium/glucose cotransporter 2 inhibitors in glycemic control and the risk or progression of cardiovascular disease in diabetic patients. Stem cell therapy might be an alternative tool for diabetic patients to improve ß cell regeneration and peripheral ischemia. We summarize the clinical results of mesenchymal stem cells transplanted into patients with diabetic limb and foot. CONCLUSION: A stepwise intensification of dual and triple therapy for individual diabetic patient is required to achieve therapeutic target.

MiR-499a-5p suppresses apoptosis of human nucleus pulposus cells and degradation of their extracellular matrix by targeting SOX4.

Emerging evidence suggests that microRNAs (miRNAs, miRs) play important roles in the development of intervertebral disc degeneration (IVDD). Nonetheless, the expression level and biological function of miR-499a-5p in IVDD are still unclear. In this study, we found that miR-499a-5p was significantly downregulated in degenerative tissues of the human nucleus pulposus (NP) compared with healthy tissues. Knockdown of miR-499a-5p promoted NP cell (NPC) apoptosis, stimulated caspase activation, enhanced MMP3 and MMP13 expression, and downregulated aggrecan and type II collagen. Furthermore, TNF-α-treated NPCs showed increased apoptosis and induced an imbalance between anabolism and catabolism of the extracellular matrix (ECM); these changes were attenuated by miR-499a-5p overexpression. Research into possible mechanisms revealed that miR-499a-5p suppressed the expression of SOX4 both at mRNA and protein levels and directly bound to the 3' untranslated region of SOX4 mRNA. Ectopic expression of SOX4 attenuated the negative effect of miR-499a-5p on NPC apoptosis and the positive effect on ECM synthesis. Taken together, these results indicate that miR-499a-5p may attenuate TNF-α-induced NPC apoptosis and an imbalance between anabolism and catabolism of the ECM by downregulating SOX4.