Objective To observe the expression of IGF-1 in the peri-hematomal brain region of Intracerebral Hemorrhage(ICH) patients,and to investigate the relationship among IGF-1,excessive and depletion syndrome of stroke.Methods 28 patients were evenly and randomly recruited into 3groups:Yin excessive group,Yang excessive group and depletion group.Additional 6 persons of normal death within 3 hours were taken their brain tissue.The IGF-1 expression was detected with Western blotting method.The correlation among the expression of IGF-1,excessive and depletion syndromes were observed.Results The expression of IGF-1 in the peri-hematomal brain region of ICH patients significantly increased in comparison with the normal control group (P=0.00).The expression of IGF-1 was significantly different among Yang excessive,Yin excessive and the depletion syndromes [ (0.696±0.111)、(1.151 ±0.185)、(1.697±0.108),P＜0.01],with the expression of IGF-1 of depletion syndrome ranked the highest,followed by Yin excessive and Yang excessive syndrome.Conclusion The expression of IGF-1 could reflect the degree of brain impairment.

The peak of the brain edema after intracerebral hemorrhage usually begins after 3 to 4 days.A large quantity of hemoglobin releases and degrades during this process,and its degradation products iron ion,bilirubin and carbon monoxide,etc play important roles in the process of cerebral edema.They all involve in the formation Of delayed brain edema after intracerebral hemorrhage.The research of hemoglobin and its degradation products is expected to find out a new way for the treatment of intracerebral hemorrhage.

Autophagy is a vital phenomena which widely exists in eukaryotic cells.It runs through the cellular normal growth,development,and physiological pathology processes.Studies in recent years have shown that autophagy involves in the pathological process after stroke,and affects the survival and death of nerve cells,This article reviews the classification,formation process,molecular mechanism and detection of autophagy as well as its relation with stroke.Our purpose is to provide a new direction for clinical treatment of stroke.

Background: Unstable distal clavicles experience high non-union rates, prompting surgeons to recommend surgery for more predictable outcomes. There is a lack of consensus on the optimal method of surgical fixation, with an array of techniques described in the literature. We describe an alternative method of fixation involving the use of a distal clavicular anatomical locking plate with Fibertape cerclage augmentation in our series of patients. Methods: Nine patients (8 males and 1 female), with a mean age of 36 years, who sustained unstable fracture of the distal clavicle in our institution were treated with our described technique. Postoperative range of motion, functional and pain scores, and time to radiographic union were measured over a mean follow-up period of 10 months. Incidences of postoperative complications were also recorded. Results: At the last patient consult, the mean visual analog scale score was 0.88±0.35, with a mean Disabilities of the Arm, Shoulder, and Hand (DASH) score of 1.46±0.87 and American Shoulder and Elbow Surgeons (ASES) score of 94.1±3.57. The mean range of motion achieved was forward flexion at 173°±10.6°, abduction at 173°±10.6°, and external rotation at 74.4°±10.5°. All patients achieved internal rotation at a vertebral height of at least L2 with radiographical union at a mean of 10 weeks. No removal of implants was required. Conclusions Our described technique of augmented fixation of the distal clavicle is effective, produces good clinical outcomes, and has minimal complications.

Background::While type 2 diabetes mellitus (T2DM) is considered a putative causal risk factor for coronary artery disease (CAD), the intrinsic link underlying T2DM and CAD is not fully understood. We aimed to highlight the importance of integrated care targeting both diseases by investigating the phenotypic and genetic relationships between T2DM and CAD.Methods::We evaluated phenotypic associations using data from the United Kingdom Biobank ( N = 472,050). We investigated genetic relationships by leveraging genomic data conducted in European ancestry for T2DM, with and without adjustment for body mass index (BMI) (T2DM: Ncase/ Ncontrol = 74,124/824,006; T2DM adjusted for BMI [T2DM adjBMI]: Ncase/ Ncontrol = 50,409/523,897) and for CAD ( Ncase/ Ncontrol = 181,522/984,168). We performed additional analyses using genomic data conducted in multiancestry individuals for T2DM ( Ncase/ Ncontrol = 180,834/1,159,055). Results::Observational analysis suggested a bidirectional relationship between T2DM and CAD (T2DM→CAD: hazard ratio [HR] = 2.12, 95% confidence interval [CI]: 2.01–2.24; CAD→T2DM: HR = 1.72, 95% CI: 1.63–1.81). A positive overall genetic correlation between T2DM and CAD was observed ( rg = 0.39, P = 1.43 × 10 -75), which was largely independent of BMI (T2DM adjBMI–CAD: rg = 0.31, P = 1.20 × 10 –36). This was corroborated by six local signals, among which 9p21.3 showed the strongest genetic correlation. Cross-trait meta-analysis replicated 101 previously reported loci and discovered six novel pleiotropic loci. Mendelian randomization analysis supported a bidirectional causal relationship (T2DM→CAD: odds ratio [OR] = 1.13, 95% CI: 1.11-1.16; CAD→T2DM: OR = 1.12, 95% CI: 1.07-1.18), which was confirmed in multiancestry individuals (T2DM→CAD: OR = 1.13, 95% CI: 1.10-1.16; CAD→T2DM: OR = 1.08, 95% CI: 1.04-1.13). This bidirectional relationship was significantly mediated by systolic blood pressure and intake of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors, with mediation proportions of 54.1% (95% CI: 24.9-83.4%) and 90.4% (95% CI: 29.3-151.5%), respectively. Conclusion::Our observational and genetic analyses demonstrated an intrinsic bidirectional relationship between T2DM and CAD and clarified the biological mechanisms underlying this relationship.