Objective To explore the expression profile of adenosine A1 receptor in the paraventricular thalamic nucleus(PVT)in wakefulness/sleep state and its role in regulating sleep.Methods Male C57BL/6J mice(6～12 weeks old,weighing 22～28 g)were randomly divided into ZT0,ZT6,ZT10,ZT12,and sleep deprivation and recover0y sleep groups(n=16 or n=4).RT-qPCR and fluorescence in situ hybridization were used to observe the changes of adenosine A1 receptor in PVT.Whole-cell patch-clamp recording was conducted to determine the effects of adenosine on the membrane potential and discharge frequency of PVT neurons.The experimental animals were divided into adenosine A1 receptor interference group(n=8)and interference control group(n=7).After RNA interference,electroencephalography(EEG)and electromyography(EMG)were applied simultaneously to observe the changes in wake and sleep time between the 2 groups during sleep deprivation for 6 h and sleep recovery for 4 h.Results RT-qPCR and fluorescence in situ hybridization confirmed that the expression of adenosine A1 receptor in PVT was affected by wakefulness/sleep state,with the level in the ZT0 group(active stage)significantly higher than that in the ZT12 group(non-active stage,P<0.05).Whole-cell patch clamp recording indicated that adenosine exerted inhibitory effects on PVT neurons through 2 distinct response types(P<0.05),and the inhibition was in a diminishing trend with a decrease in the expression level of adenosine A1 receptor.After sleep deprivation,the expression level of adenosine A1 receptor showed significant intergroup differences:the level was significantly higher in the sleep deprivation group than the recovery sleep group(P<0.05),while that of the recovery sleep group was higher than that of the ZT6 group and that of the ZT10 group(P<0.05).After knocking down adenosine A1 receptor(shRNA-A1R)in the PVT,the wakefulness timing of the shRNA-A1R group was significantly increased,while the sleep timing was significantly decreased within 1 h after sleep recovery when compared with the interference control group(P<0.05).Conclusion The expression of adenosine A1 receptor in the PVT is dynamically regulated by sleep pressure,which was increasing as sleep pressure rises.

Objective : To investigate the factors affecting concurrent sarcopenia among patients with cardiovascular diseases, so as to provide insights into early identification and prevention of cardiovascular diseases complicated with sarcopenia. Methods: A total of 250 inpatients with cardiovascular diseases in the Sixth Division Hospital of Xinjiang Production and Construction Corps were recruited and divided into the sarcopenia and non-sarcopenia groups according to the diagnostic criteria of sarcopenia. Subjects' basic characteristics, body mass index, blood biochemical indicators and human body composition parameters were collected using questionnaire surveys, and factors affecting concurrent sarcopenia among patients with cardiovascular diseases using a multivariable logistic regression model. Results: Among the 250 patients with cardiovascular diseases, there were 149 males (59.60%) and 101 females (40.40%). The overall prevalence of sarcopenia was 8.40% among the study subjects. The mean age and body mass index were (75.19±9.74) and (20.77±2.19) kg/m2 in the sarcopenia group and (65.24±11.50) years and (25.85±2.87) kg/m2 in the non-sarcopenia group. Multivariable logistic regression analysis identified age (OR=1.115, 95%CI: 1.030-1.207) and body mass index (OR=0.582, 95%CI: 0.445-0.761) were as factors affecting concurrent sarcopenia among patients with cardiovascular diseases. Conclusion Advanced age and low body mass index may increase the risk of concurrent sarcopenia among patients with cardiovascular diseases.

Objective:To investigate the clinical application and efficacy of microsurgical peripheral nerve decompression in the treatment of painful diabetic peripheral neuropathy (PDPN) .Methods:From Sep. 2017 to Jun. 2018, 33 PDPN patients of our department were treated with DELLON microsurgical peripheral nerve decompression. All surgeries were assisted with neuroelectrophysiological monitoring during the operation and were followed up for 0.5 to 1 years. Electromyography and VAS pain scores were performed 0.5 years before and after surgery, and the preoperative and postoperative results were compared.Results:Postoperative electromyography showed that sensory nerve conduction velocity (SNCV) was significantly improved compared with preoperative ( P<0.05) , while the postoperative VAS score (4.6±1.8) was significantly lower than that (8.3±2.6) of before ( P<0.05) . Conclusions:Microsurgical peripheral nerve decompression is an effective therapeutic method for PDPN. Intraoperative electrophysiological monitoring can effectively avoid iatrogenic nerve injury. Neurophysiological examination can be used as an objective evidence for definitive diagnosis and evaluation of surgical outcomes.

OBJECTIVE: To investigate the mechanism by which epigallocatechin gallate (EGCG) induces gene demethylation and promotes the apoptosis of acute myeloid leukemia KG-1 and THP-1 cell lines. METHODS: KG-1 and THP-1 cells treated with 25, 50, 75, 100 or 150 μg/mL EGCG for 48 h were examined for gene methylation using MSP and for cell proliferation using MTT assay. The changes in cell cycle and apoptosis of the two cell lines after treatment with EGCG for 48 h were detected using flow cytometry. The mRNA and protein expressions of DNMT1, CHD5, p19, p53 and p21 in the cells were detected using RT-quantitative PCR and Western blot. RESULTS: EGCG dose-dependently reversed hypermethylation of gene and reduced the cell viability in both KG-1 and THP-1 cells ( < 0.05). EGCG treatment caused obvious cell cycle arrest in G1 phase, significantly increased cell apoptosis, downregulated the expression of DNMT1 and upregulated the expressions of CHD5, p19, p53 and p21 in KG-1 and THP-1 cells ( < 0.05). CONCLUSIONS EGCG reduces hypermethylation of gene in KG-1 and THP-1 cells by downregulating DNMT1 to restore its expression, which results in upregulated expressions of p19, p53 and p21 and induces cell apoptosis.

Objective To investigate the clinical characteristics of DCD donor-derived CRKP infection and bleeding in kidney transplantation,and to summarize the experience of diagnosis,treatment and prevention.Methods A retrospective analysis was carried out from July 2016 to December 2017 in hospital,containing clinical data of 4 cases of CRKP-infected DCD donors and 7 cases of kidney transplantation recipients.Results In the CRKP culture of 4 cases of DCD donors,1 case was positive for blood culture,1 case was positive for urine culture,1 case was positive for sputum culture,and 1 case was negative for blood,urine and sputum culture.The corresponding 7 recipients were all positive for blood culture after renal transplantation,4 cases were positive for urine culture,3 cases were positive for sputum culture,and 5 cases were positive for perirenal drainage.Of the 7 patients,4 cases had renal artery hemorrhage,1 of them was died.The average bleeding time was 17.75 days after operation (14-19 days).In 7 patients with renal transplantation,CRP increasd.And in 3 cases of deaths,CRP was stably higher than normal.Meanwhile,CRP in 4 surviving patients gradually decreased to the normal range after effective anti-infection treatment.All 7 patients were treated with carbapenems;2 patients were dead without avibactam therapy;and 5 cases were treated with avibactam and carbapenems and survived,1 case died and 1 case had good renal function recovery.Conclusion Positive CRKP in blood,urine and sputum of DCD donors can lead to CRKP infection in kidney transplant recipients.Even if the body fluids of donors are all negative,the false negative results could not be excluded.Persistent or increased high-level CRP after operation is an early warning on CRKP infection.And CRP can be used as an indicator for evaluating the effectiveness of anti CRKP therapy.The combination of avibactam and carbapenem antibiotics is an effective regimen in the treatment of DCD donor-derived CRKP.