Objective To analyze the nerve electrophysiological characteristics of stroke occurrence shoulder hand syndrome patients.Methods A total of 70 stroke patients hospitalized in the Department of Neurology of Ruian City Red Cross Hospital were selected.According to whether the occurrence of shoulder hand syndrome,the patients were defined as the observation group (32 cases) and the control group (38 cases).All patients during hospitalization received the median nerve needle electromyography and nerve conduction determination.The needle pole electromyo-gram examination results, sensory nerve action potential changes were observed and compared in the two groups. Results (1) After needle electromyography,all patients in the observation group showed abnormal potential ( such as fibrillation potentials was sharp waves).Among them,fibrillation potential observed in 2 cases(5.26%) in the control group,which was significantly lower than 21 cases (65.63%) in the observation group (χ2 =6.954,P=0.026).Positive sharp wave observed in 1 case(2.63%) in the control group,which was significantly lower than 11 cases (34.38%) in the observation group (χ2 =8.323, P =0.014 ) .Nerve conduction measurement results showed that the sensory nerve action potential amplitude of the observation group was significantly lower than that of the control group, and amplitude of sensory nerve in the observation group decreased more significantly than the control group.The average sensory nerve action potential of the observation group was (7.48 ±4.12) ms,which was significantly lower than (12.53 ±1.61)ms of the control group,amplitude of wave in the observation group decreased more significantly than the control group ( t =12.064, P =0.017 ) .Conclusion Shoulder hand syndrome nerve electrophysiological parameters changed significantly after stroke occurrence.Therefore,it can be used further for the early found brain after stroke shoulder hand syndrome and provide a theoretical basis.

Objective To explore the clinical effect of phalangeal fractures with self-made mini external fixator. Methods From June, 2014 to June, 2017, 16 cases of phalangeal fracture were treated with self-made mini external fixator. In the followed-up periods, the regulating rechecks of X-ray and measurement of interpha-langeal joint activity were determined. The total active movement (TAM), numerical pain ranting scale (NPRS) and morning stiffness was used to estimate the fracture healing and the hand function recovery. Results Pain and ab-normal movement around fracture was found 6 weeks after the operation in 1 case, which had been healed by re-moving the external fixation, open reduction and internal fixation with kirschner wire. The other 15 cases were fol-lowed-up of 48-72 (average, 58) weeks. The fracture has healed. And there was no osteomyelitis, no breakage and loosening of steel needles. The clinical healing time of the fracture was 14 to 16 weeks, with an average of 15.5 weeks. According to the TAM, NPRS and morning stiffness, there was excellent in 11 cases, and good in 4 cases. Conclusion The self-made mini external fixator can maintain the stability after fracture reduction, provide the tension required for the healing of collateral ligament and joint capsule, and meet the need of early functional exer-cise. It is an ideal treatment option for phalangeal fractures.

SIRT6 belongs to the conserved NAD⁺-dependent deacetylase superfamily and mediates multiple biological and pathological processes. Targeting SIRT6 by allosteric modulators represents a novel direction for therapeutics, which can overcome the selectivity problem caused by the structural similarity of orthosteric sites among deacetylases. Here, developing a reversed allosteric strategy AlloReverse, we identified a cryptic allosteric site, Pocket Z, which was only induced by the bi-directional allosteric signal triggered upon orthosteric binding of NAD⁺. Based on Pocket Z, we discovered an SIRT6 allosteric inhibitor named JYQ-42. JYQ-42 selectively targets SIRT6 among other histone deacetylases and effectively inhibits SIRT6 deacetylation, with an IC₅₀ of 2.33 μmol/L. JYQ-42 significantly suppresses SIRT6-mediated cancer cell migration and pro-inflammatory cytokine production. JYQ-42, to our knowledge, is the most potent and selective allosteric SIRT6 inhibitor. This study provides a novel strategy for allosteric drug design and will help in the challenging development of therapeutic agents that can selectively bind SIRT6.