Objective To investigate the effects and related risk factors of different vascular access types on new atrial fibrillation in maintenance hemodialysis (MHD) patients.Methods This was a single-center prospective cohort study.Patients who established long-term dialysis access and were voluntarily followed up in the Second Hospital of Tianjin Medical University from January 1,2013 to June 30,2013 were enrolled to follow-up for 5 years.Patients were divided into fistula group (patients with autogenous arteriovenous fistula) and catheter group (patients with tunneled cuffed internal jugular vein catheter).The incidences of new atrial fibrillation in the two groups were compared by Kaplan-Meier survival analysis.Cox regression analysis and receiver operator characteristic curve (ROC) were used to assess the risk factors of new atrial fibrillation.Results A total of 315 eligible patients were enrolled,including 150 males (47.62％).There were 189 patients (60.00％) in the fistula group,and 126 patients (40.00％) in the catheter group.Multivariate Cox regression analysis showed that older age (HR=1.021,95％CI 1.003-1.040),arteriovenous fistula (HR=1.899,95％CI 1.019-3.539),increased dialysis blood flow (HR=1.030,95％CI 1.010-1.051) and left atrial diameter (HR=1.097,95％CI 1.022-1.177) were independent risk factors for new atrial fibrillation in MHD patients (all P ＜ 0.05).Kaplan-Meier survival analysis showed that the incidence of new atrial fibrillation in fistula group was higher than that in catheter group (Log-rank A2=9.53,P=0.002).ROC curve analysis showed that age [the area under the curve (AUC)=0.608,P=0.008],arteriovenous fistula (AUC=0.594,P=0.021),dialysis blood flow (AUC=0.659,P＜0.001) and left atrial diameter (AUC=0.604,P=0.011) could predict the occurrence of new atrial fibrillation.Condusions Older age,arteriovenous fistula,increased blood flow during dialysis and left atrial diameter are independent risk factors for new atrial fibrillation in MHD patients,which can predict the occurrence of atrial fibrillation.The incidence of new atrial fibrillation in patients with arteriovenous fistula is higher than that in patients with catheter.

One hundred and twenty maintenance hemodialysis patients with secondary hyperparathyroidism were randomly assigned to receive cinacalce,calcitriol or combination of cinacalce and cacitriol for treatment,with 40 cases in each group.Patients were followed up for 12 months;and the blood tests,echocardiography,examinations for osteoporosis and soft tissue calcification were performed every month.After 3 months of treatment,the serum levels of parathyroid hormone were decreased in all three groups (P ＜ 0.01);while the parathyroid hormone decreased more markedly with less influence on serum calcium and phosphorus levels in combination group.There were no significant changes in alkaline phosphatase,osteoporosis and cardiac valve calcification after treatment,compared with before treatment.There were no cases of hypercalcemia and hypocalcemia appearing in combination group after treatment.The study indicates that the combination of cinacalcet with calcitriol has better therapeutic effect for treatment of secondary hyperparathyroidism in maintenance dialysis patients.

Objective To investigate the possible risk factors for the progression of abdominal aortic calcification (AAC) in MHD patients.Methods Total of 170 patients on MHD between June 2014 and October 2014 in the dialysis center of the Second Hospital of Tianjin Medical University were included prospectively.Lateral lumbar radiography were applied to evaluate patients' AAC score (AACs) at baseline and after two-years of follow-up respectively.According to the change of AACs,the patients were divided into rapid AAC progression group and non-rapid AAC progression group.Multivariable Logistic regression models were used to determine the risk factors for the progression of AAC in MHD patients.Results At baseline,the presence of AAC (AACs≥1) was 43.5％(74/170).The mean follow-up duration was 27.6(24.7,28.0) months.AACs were available in 111 patients,and the presence of AAC was 78.4％(87/111).During the follow up,36 patients developed new AAC;rapid AAC progression was seen in 54 patients,and non-rapid AAC progression was seen in 57 patients.Multivariate Logistic regression analysis demonstrated that hyperphosphatemia (OR=4.373,95％ CI 1.562-7.246,P=0.005) and high density lipoprotein (HDL) (OR=0.031,95％CI 0.003-0.338,P=0.004) were independent risk factors for AAC progression in MHD patients.Conclusions Hyperphosphatemia and low HDL may promote the progression of AAC.Well-controlled serum phosphate and lipid metabolism may slow the progression of vascular calcification,reducing cardiovascular morbidity and mortality.

Objective To study the effects of cisapride on symptoms of digestive and gastrointestinal hormones in chronic renal failure patients.Methods There were 46 cases of chronic renal failure patients in this paper,all patients were given routine treatment of the underlying disease and were randomly divided into two groups.23 patients were additionally treated with cisapride as research group,and the others as control group.The gastrointestinal symptoms,serum somatostatin (SS),motilin (MOT) and vasoactive intestinal peptide (VIP) and other gastrointestinal hormones and renal function in two groups of patients were compared before and after treatment.Results The score of acid reflux,nausea,vomiting,abdominal distension,belching and other symptoms of hard feces and other gastrointestinal after treatment were significantly lower than that before treatment in research group and after treatment in control group (all P ＜ 0.05).There was no significant change between before and after treatment in SS and VIP of two group (all P ＞ 0.05),and MOT in control group (P ＞0.05),but the MOT in research group was decreased significantly(P ＜ 0.05).There was no significant difference in Scr,Ccr and BUN between the control and research group after treatment (all P ＞ 0.05).Conclusion Conventional treatment combined with cisapride can improve the effect of gastrointestinal symptoms in patients with chronic renal failure,while reducing serum motilin level.

Objective To evaluate the role of autophagy in hydrogen-induced reduction of lung injury in septic mice.Methods Sixty pathogen-free healthy male ICR mice,aged 6 weeks,weighing 20-25 g,were divided into 5 groups (n =12 each) using a random number table:sham operation group (group Sh),sepsis group (group Sep),sepsis plus hydrogen group (group Sep+H2),sepsis plus autophagy inhibitor 3-methyladenine (3-MA) group (group Sep+3-MA) and sepsis plus 3-MA plus hydrogen group (group Sep+3-MA+H2).Sepsis was produced by cecal ligation and puncture.At 1 h before operation,3-MA 10 mg/kg was intraperitoneally injected.The mice inhaled 2％ H2 for 1 h starting from 1 and 6 h after operation.Blood samples were collected from the common carotid artery at 24 h after operation for measurement of arterial oxygen partial pressure,and the oxygenation index (OI) was calculated.Pulmonary specimens were obtained for examination of the pathological changes which were scored.Pulnonary mitochondria were isolated for determination of mitochondrial membrane potential (MMP) and ATP content using fluorescence spectrophotometry and a bioluminescence assay,respectively,and the respiratory control rate (RCR) was calculated.The expression of autophagy-related protein microtubule-associated protein 1 light chain 3 (LC3) was determined by Western blot,and the ratio of LC3-Ⅱ to LC3-Ⅰ expression (LC3-Ⅱ/LC3-Ⅰ ratio) was calculated.Results Compared with group Sh,the pathological scores were significantly increased,the OI and contents of mitochondrial RCR,MMP and ATP were decreased,and the LC3-Ⅱ/LC3-Ⅰ ratio was increased in Sep and Sep+H2 groups (P＜0.05).Compared with group Sep,the pathological scores were significantly decreased,the OI and contents of mitochondrial RCR,MMP and ATP were increased,and the LC3-Ⅱ/LC3-Ⅰ ratio was increased in group Sep+H2,and the pathological scores were significantly increased,the OI and contents of mitochondrial RCR,MMP and ATP were decreased,and the LC3-Ⅱ/LC3-Ⅰ ratio was decreased in group Sep+3-MA (P＜0.05),and no significant change was found in each parameter mentioned above in group Sep+3-MA+H2 (P＞0.05).Compared with group Sep+H2,the pathological scores were significantly increased,the OI and contents of mitochondrial RCR,MMP and ATP were decreased,and the LC3-Ⅱ/LC3-Ⅰ ratio was decreased in group Sep+3-MA+H2 (P＜0.05).Conclusion The mechanism by which hydrogen ameliorates lung injury is related to enhanced level of autophagy in septic mice.

Objective To evaluate the effect of inhaling hydrogen (H2) on proteomics during acute lung injury in septic mice.Methods Sixty male ICR mice,aged 6 weeks,weighing 20-25 g,were divided into 4 groups (n=15 each) using a random number table:sham operation group (Sh group),sham operation plus H2 group (Sh+H2 group),sepsis group (S group) and sepsis plus H2 group (S+H2 group).Sepsis was produced by cecal ligation and puncture.The mice in Sh+H2 and S+H2 groups inhaled 2％ H2 for 1 h starting from 1 and 6 h after operation.At 24 h after operation,lungs were removed for identification of proteins by isobaric tags for relative and absolute quantification and liquid chromatography-tandem mass spectrometry analysis,and the differentially expressed proteins were screened.The differentially expressed proteins were used for KEGG pathway enrichment analysis and STRING protein-protein interaction networks analysis.Western blot was used to confirm the 4 differentially expressed proteins semaphorin 7A,transferrin,OTULIN and mitogen-activated protein kinase kinase kinase 1.Results A total of 4 472 quantifiable proteins were identified.A total of 192 proteins which were related to acute lung injury during H2 inhalationinduced reduction of sepsis were identified.The 192 proteins involved phosphatidylinositol 3-kinase/serine0threonine kinase signaling pathway,chemokine signaling pathway,hypoxia-inducible factor 1 signaling pathway,complement and coagulation cascades,peroxisome proliferator-activated receptor signaling pathway and proteins including ribosome proteins,myosin and troponin,collagen and adhesion-related proteins,coagulation-related proteins found in STRING protein-protein interaction networks.Conclusion Inhaling H2 can induce changes in the expression of 192 proteins,which may be the mechanism of lung protection in septic mice.

Objective To evaluate the effect of hydrogen on mitochondrial dynamics during endotoxin-induced damage to human umbilical vein endothelial cells (HUVECs).Methods HUVECs cultured in vitro were seeded in the culture plate and divided into 4 groups using a random number table:control group (group C),hydrogen-saturated culture medium group (H group),endotoxin group (group E) and endotoxin + hydrogen-saturated culture medium group (group E+H).The cells were cultured in the plain culture medium in C and E groups.The cells were cultured in the hydrogen-saturated culture medium containing lipopolysaccharide (LPS) with the final concentration of 10 μg/ml in H and E+H groups.At 2,8 and 24 h of culture or incubation with LPS,the cell viability was detected by methyl thiazolyl tetrazolium assay,the intracellular ATP content was measured using the phosphomolybdic acid colorimetric method,and the expression of dynamin-related protein 1 (DRP1) was detected by using Western blot.The expression of DRP1 was detected by immunofluorescence at 8 h of incubation with LPS.Results Compared with group C,the cell viability and ATP content were significantly decreased,and the expression of DRP1 was up-regulated at each incubation time point in E and E +H groups (P＜0.05),and no significant change was found in the parameters mentioned above in group H (P＞0.05).Compared with group E,the cell viability and ATP content were significantly increased,and the expression of DRP1 was down-regulated at each incubation time point in group E+H (P＜0.05).Conclusion The mechanism by which hydrogen reduces endotoxin-induced damage to HUVECs is related to down-regulation of DRP1 expression and inhibition of excessive mitochondrial fission.

Objective To investigate the efficacy and safety of neurotropin in the treatment of restless legs syndrome and sleep disorder in patients with maintenance hemodialysis. Methods Sixty eight patients who met the inclusion criteria were randomly assigned to control group (n=34) and treatment group (n=34). The trial lasted for 16 weeks, and all patients undergone thorough dialysis. 7.2 units (2 branches) neurotropin were slowly injected to the patients in the treatment group at the end of each hemodialysis and they were stopped after 8 weeks. The patients in the control group had no treatment for restless leg syndrome on the basis of adequate dialysis. All patients were assessed regularly as regards their biochemical indexes, restless legs syndrome rating scale and Pittsburgh sleep quality index. Results All the patients completed the experiment, and restless legs syndrome scores were decreased in two groups. Compared with the baseline, the restless legs syndrome scores decreased significantly in patients treated with neurotropin, and the differences between two groups were significant (P<0.01). In the Pittsburgh sleep quality index scores, the patients in the treatment group decreased in all scores and the difference was statistically significant (P<0.01). Conclusions Neurotropin can relieve the symptoms of restless legs syndrome and sleep disturbance in patients on maintenance hemodialysis and is safe, but symptoms may occur again after withdrawal.

Objective To evaluate the effect of hydrogen on the expression of Drp1 in the myocardial mitochondria of septic mice.Methods Fifty-four pathogen-free healthy male ICR mice,aged 6 weeks,weighing 20-25 g,were divided into 3 groups (n=18 each) using a random number table:sham operation group (S group),sepsis group (Sep group) and hydrogen group (H2 group).Sepsis was produced by cecal ligation and puncture in anesthetized mice.The mice inhaled 2％ hydrogen for 1 h starting from 1 and 6 h after operation in group H2.The mice were sacrificed at 1 day after operation,and hearts were removed for microscopic examination of the pathological changes which were scored and for determination of apoptosis in cardiomyocytes.Apoptosis rate was calculated.The myocardial mitochondria were isolated for measurement of respiratory control ratio (RCR) (using a Clark-type electrode),ATP content (by using a bioluminescence technique) and Drp1 expression (by Western blot).Results Compared with group S,the pathological score and apoptosis rate were significantly increased,the RCR and ATP content in mitochondria were decreased,and the expression of Drp1 was up-regulated in Sep and H2 groups (P＜0.05).Compared with group Sep,the pathological score and apoptosis rate were significantly decreased,the RCR and ATP content in mitochondria were increased,and the expression of Drp1 was down-regulated in group H2 (P＜0.05).Conclusion The mechanism by which hydrogen mitigates myocardial injury is related to down-regulating expression of Drp1 in the myocardial mitochondria and improving mitochondrial function in septic mice.

Objective To evaluate the effect of hydrogen ( H2 ) inhalation on mitochondrial bio?synthesis in lung tissues during acute lung injury in mice with sepsis. Methods One hundred and four male ICR mice, aged 6 weeks, weighing 20-25 g, were divided into 4 groups ( n=26 each) using a ran?dom number table: sham operation group ( group S) , sham operation + H2 group ( group S+H2 ) , sepsis group ( group Sep) and sepsis + H2 group ( group Sep+H2 ) . Sepsis was produced by cecal ligation and puncture. In S+H2 and Sep+H2 groups, the mice inhaled 2% H2 for 1 h starting from 1 and 6 h after opera?tion. Twenty mice in each group were selected, and the survival rates on postoperative days 1, 2, 3, 5 and 7 were recorded. On the postoperative day 1, 6 mice in each group were selected, and blood samples were collected from the common carotid artery for measurement of arterial oxygen partial pressure, and the oxygenation index was calculated. The pulmonary specimens were obtained for examination of the pathologi?cal changes which were scored and for determination of the expression of peroxisome proliferator?activated re?ceptor gamma coactivator?1α ( PGC?1α) in lung tissues by Western blot. The pulmonary mitochondria were isolated for determination of mitochndrial membrane potential ( MMP ) and ATP contents using spectropho?tometry and a bioluminescence technique, respectively. Results Compared with group S, the survival rate, oxygenation index and MMP and ATP content in lung tissues were significantly decreased, and the pathological scores and PGC?1α expression in lung tissues were significantly increased in Sep and Sep+H2 groups (P<0.05). Compared with group Sep, the survival rate, oxygenation index, and MMP, ATP content and PGC?1α expression in lung tissues were significantly increased, and the pathological scores were significantly decreased in group Sep+H2 ( P<0.05) . Conclusion H2 inhalation can ameliorate acute lung injury in mice with sepsis, and the mechanism is associated with the enhanced function of PGC?1αand promoted mitochondrial biosynthesis in lung tissues.