Objective To examine the relationship between plasma homocysteine level and status of congestive heart failure. Methods Plasma homocysteine level was determined in 106 patients with congestive heart failure(CHF).Among them,40 patients were diagnosed as having recent onset of CHF(group 1) and the remaining 66 were receiving conventional treatment(group 2).Thirty healthy subjects were served as a control group. Results(The plasma) homocysteine levels in group 1,group 2 and the control group were(14.87?5.22),(13.25?5.45) and((7.52)?1.73) ?mol/L,respectively.The plasma homocysteine level was significantly higher in group 1 and group 2 than in the control group(P

Objective To evaluate the influence of right ventricular outflow tract septal ( RVS) pacing with right ventricular apical ( RVA) pacing on left ventricular remodeling and brain natriuretic peptide ( BNP). Methods Sixty patients with indication of pacemaker implantation were randomized into two groups, RVA group and RVS group. BNP was measured with ELISA, and echocardiography was performed to measure the left ventricular end diastolic volume ( LVEDD), left ventricular end systolic volume ( LVEDV) and left ventricular ejection fraction (LVEF) at pre-operation,and after 6,12,24 months pacing. The difference of cardiac remodeling and BNP in the two groups was observed. Results Compared to BNP at pre-operation (( 60. 2 ± 15. 7 ) ng/L) , BNP increased significantly in the RVA group at the 6th,12th and 24th month after operation( ( 108. 2 ±29. 8) , ( 190. 3 ±46. 7) ,(308. 2 ±56. 5)ng/L,respectively) (P <0. 05). In the RVS group,BNP increased only at 24 months after pacing ( (75. 2 ± 15. 8) ng/L vs. (63. 9 ± 15. 1 ) ng/L) (P < 0. 05). There was significant difference on BNP between the two groups. LVEDD,LVEDV increased,LVEF declined at 12 months after pacing in the RVA group,which were not observed in the RVS group. There was significant difference on LVEDD,LVEDV and LVEF in the RVA group (P< 0. 05) between the 12th month and pre-operation,and there were no significant difference in the RVS group (P > 0. 05). Conclusions Compared to RVA pacing,RVS pacing was more beneficial to improve heart function,prevent cardiac remodeling and decline the activation of nerve-endocrine.

We predicted the anti-hepatitis B virus (HBV) active components and mechanism of Salvia miltiorrhiza based on network pharmacology. The active components of S. miltiorrhiza were obtained through TCMSP, PubChem database and literature research. The potential targets of the active components and HBV infection were predicted by SwissTargetPrediction and GeneCards databases, respectively. The protein-protein interaction (PPI) network was constructed by String database. Cytoscape software was adopted to construct a visual network of active component-disease target and perform topological analysis. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed using DAVID platform. The molecular docking of key components and core targets was carried out by AutoDock Vina software. We screened out a total of 38 active components and 178 disease-component overlapping targets. Enrichment analyses obtained 405 related GO items and 68 signaling pathways, such as T/B cell receptor signaling pathways, PI3K/AKT signaling pathway, and mTOR signaling pathway. According to the results of molecular docking, most characteristic components of S. miltiorrhiza (miltionone Ⅱ, miltirone, protocatechuic acid, lithospermic acid, protocatechualdehyde) showed good affinity with the key targets (PIK3CA, APP, STAT3,AKT1 and mTOR). Furthermore, the anti-HBV activity of lithospermic acid, the representative active component of S. miltiorrhiza, and its regulation on PI3K/AKT and mTOR signaling pathways were investigated in an HBV replicating mouse model. Animal welfare and experimental procedures follow the regulations of the Animal Ethics and Welfare Committee of Hubei University. The results showed that lithospermic acid significantly inhibited HBV DNA replication, reduced serum HBsAg and HBeAg levels, and decreased the phosphorylation protein expression levels of AKT and mTOR in liver, indicating that lithospermic acid might exert the anti-HBV activity by regulating PI3K/AKT and mTOR signaling pathways.

Objective　To explore the risk factors and causes affecting the operative mortality in esophagectomy patients with esophageal can cer. Methods　1400 cases with a curative esophagectomy for neopl asm of esophagus hospitalized from Mar,1973 to June, 2000 were reviewed. There w ere 31 died within 30 d or during hospitalization after esophagectomy as a group , and 1 369 survival cases, after operation, as another group. Sixteen factors t hat may influence the operational mortality were selected. A multi-variate anal ysis of these individual variables was performed by the computer′s logistic reg ression model. Results　The operative mortality was 2.2%(31/1400 ). The causes of death included respiratory complication 17 cases (including res piratory failure caused by pneumonia or atelectasis), 15 cases, and adult respir atory distress syndrome (ARDS) 2 cases, the mortality was 54.8% in the death gro up), anastomotic leak 11 cases (34.5%), Chylothorax 2 cases (6.5%) and postopera tive digestive tract hemorrhage 1 case (3.2%). The results showed that the major risk factors that affected operative mortality in cases with esophageal cancer were history of long-herm heavy smoking, duration of operation and the year of operational (P<0.05). Conclusion　To minimize operative mort ality of esophagectomy, some means must be noticed, including the reinforcemen t of the perioperative care, the improvement of anastomotic methods and surgical skill, reduing operative time as p ossible, disposing pulmonary complications in time and using respirator if neces sary.

Our previous results have demonstrated that insulin reduces myocardial ischemia/reperfusion (MI/R) injury and increases the postischemic myocardial functions via activating the cellular survival signaling, i.e., phosphatidylinositol 3-kinase (PI3-K)-Akt-endothelial nitric oxide synthase (eNOS)-nitric oxide (NO) cascade. However, it remains largely controversial whether c-Jun NH2-terminal kinase (JNK) is involved in the effects of insulin on MI/R injury. Therefore, the aims of the present study were to investigate the role of JNK, especially the cross-talk between JNK and previously expatiated Akt signaling, in the protective effect of insulin on I/R myocardium. Isolated hearts from adult Sprague-Dawley rats were subjected to 30 min of regional ischemia and followed by 2 or 4 h of reperfusion (n=6). The hearts were pretreated with PI3-K inhibitor LY294002, or phosphorylated-JNK inhibitor SP600125, respectively, then perfused retrogradely with insulin, and the mechanical functions of hearts, including the heart rate (HR), left ventricular developed pressure (LVDP) and instantaneous first derivation of left ventricular pressure (+/-LVdp/dt(max)) were measured. At the end of reperfusion, the infarct size (IS) and apoptotic index (AI) were examined. MI/R caused significant cardiac dysfunction and myocardial apoptosis (strong TUNEL-positive staining). Compared with the control group, insulin treatment in MI/R rats exerted protective effects as evidenced by reduced myocardial IS [(28.9 +/- 2.0)% vs (45.0 +/- 4.0) %, n=6, P<0.01], inhibited cardiomyocyte apoptosis [decreased AI: (16.0 +/- 0.7) % vs (27.6 +/- 1.3) %, n=6, P<0.01] and improved recovery of cardiac systolic/diastolic function (including LVDP and +/-LVdp/dt(max)) at the end of reperfusion. Moreover, insulin resulted in 1.7-fold and 1.5-fold increases in Akt and JNK phosphorylation in I/R myocardium, respectively (n=6, P<0.05). Inhibition of Akt activation with LY294002 abolished, and inhibition of JNK activation with SP600125 enhanced the cardioprotection by insulin, respectively. And the abolishment by LY294002 could be partly converted by SP600125 pretreatment. In addition, SP600125 also decreased the Akt phosphorylation (n=6, P<0.05). These results demonstrate that insulin simultaneously activates both Akt and JNK, and the latter further increases the phosphorylation of Akt which attenuates MI/R injury and improves heart function; this cross-talk between Akt and JNK in the insulin signaling is involved in insulin-induced cardioprotective effect.
Animals ; Apoptosis ; Heart ; Insulin ; metabolism ; JNK Mitogen-Activated Protein Kinases ; MAP Kinase Signaling System ; Myocardial Infarction ; Myocardial Ischemia ; Myocardial Reperfusion Injury ; Myocardium ; Myocytes, Cardiac ; Nitric Oxide Synthase Type III ; Phosphatidylinositol 3-Kinase ; metabolism ; Phosphatidylinositol 3-Kinases ; metabolism ; Phosphorylation ; Proto-Oncogene Proteins c-akt ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; Signal Transduction

INTRODUCTIONThis study aimed to determine the early growth patterns of preterm infants who required prolonged hospitalisation in terms of body weight Z-score, and to explore the influencing factors and predictors of their growth.

METHODSThe criteria of enrolment included preterm birth, singleton pregnancy, hospitalisation within the first 24 hours of life, hospital stay ≥ 28 days and clinical follow-up beyond 91 days of corrected age. Body weight Z-scores and the incidence of underweight infants were reviewed periodically, and the influencing factors and possible predictors of growth analysed.

RESULTSBody weight Z-scores of all infants of gestational age (GA) groups kept decreasing, with a trough seen at 36 weeks corrected gestational age (CGA). At corrected full-term, body weight Z-scores for all birth weight groups achieved birth level and were higher than that at 36 weeks CGA. Body weight Z-scores at 61 days corrected age was (-0.300 × GA [weeks] + 0.210 × birth weight [g] + 0.682 × body weight Z-score) at 40 weeks CGA. The cut-off values for body weight Z-score at birth (cut-off, -1.79; sensitivity, 100%; specificity, 91.3%) and 61 days corrected age (cut-off, -1.95; sensitivity, 100%; specificity, 97.1%) were selected to predict the risk of being underweight at 183 days corrected age.

CONCLUSIONEarly growth restriction is a practical problem in preterm infants with prolonged hospitalisation. Body weight Z-scores at 40 weeks CGA and 61 days corrected age can be used to predict body weight gain prior to 183 days corrected age in these infants.

Female ; Follow-Up Studies ; Gestational Age ; Growth Disorders ; epidemiology ; etiology ; Humans ; Incidence ; Infant, Newborn ; Infant, Premature ; growth & development ; Infant, Premature, Diseases ; epidemiology ; etiology ; Length of Stay ; trends ; Male ; Pregnancy ; Retrospective Studies ; Singapore ; epidemiology

OBJECTIVETo study the relationship of protein intake and energy supply with the physical growth in very/extremely low birth weight infant at their early life.

METHODRetrospective survey was performed in Neonatal Intensive Care Unit (NICU) in Peking University First Hospital. Inclusion criteria were preterm infant, birth weight < 1500 g, hospitalization for longer than 2 weeks, discharge with body weight greater than 1800 g. The infants were divided into two groups according to gestational age (GA). GA < 32 weeks and ≥ 32 weeks. Physical growth and its relation with the protein intake and energy supply were analyzed. The predictive value of serum blood urea nitrogen (BUN) on protein intake was studied.

RESULTNinety-three very/extremely low birth weight infants were involved, 69 in GA < 32 weeks group and 24 in GA ≥ 32 weeks group.Compared with GA ≥ 32 group, GA < 32 weeks preterm infants had more weight loss, (9.2 ± 4.4)% vs. (5.0 ± 3.1)%, P = 0.000; slower birth weight recovery (10.6 ± 3.8) d vs. (7.1 ± 2.6) d, P = 0.000; poorer weight gain at 1, 4, 5 weeks of life, (-4.5 ± 9.3) g/ (kg·d) vs. (3.4 ± 6.9) g/ (kg·d), P = 0.000 , (13.5 ± 7.3) g/ (kg·d) vs. (19.2 ± 4.9) g/ (kg·d), P = 0.001, (14.6 ± 5.6) g/ (kg·d) vs. (18.2 ± 4.5) g/ (kg·d), P = 0.031; less energy supply at 1 to 5 weeks (P value was 0.000,0.000,0.025,0.001,0.008 respectively) and less protein intake at 1, 4, 5 weeks of life (P value was 0.009,0.006,0.032). Extrauterine growth retardation (EUGR) was still predominant in our subjects, 47.8% in GA < 32 weeks group, and 95.8% in GA ≥ 32 weeks group, P = 0.000. The incidence increased greater in GA < 32 weeks infants, 43.5% vs. 20.8%, P = 0.000.The duration of weight loss and mechanical ventilation correlated negatively with weight gain rate, respectively β = -0.591, P = 0.000 and β = -0.281, P = 0.005; the average energy supply and time taken to reach full enteral feeding were factors improving weight gain, respectively β = 0.202, P = 0.021 and β = 0.354, P = 0.000. After birth, serum BUN declined gradually. Positive relation showed between average protein intake at 3(rd) week and BUN level at the end of 3 weeks, r = 0.420, P = 0.000. Serum BUN 1.44, 1.49 mmol/L at the end of 3(rd) and 4(th) week were cut-off predictors for protein intake less than 3 g/(kg·d) at related period, sensitivity and specificity were 65.3%, 83.3% and 60%, 80% respectively.

CONCLUSIONNo enough protein intake and energy supply, poor weight gain are critical problems in the management of very/extremely low birth weight infants. Prevention from NEC, appropriate parenteral/enteral nutrition transforming will benefit their physical growth. Low serum BUN after 3 weeks of life is a valuable predictor of low protein intake.

Blood Urea Nitrogen ; Dietary Proteins ; administration & dosage ; Energy Intake ; Enteral Nutrition ; Humans ; Infant ; Infant Nutritional Physiological Phenomena ; Infant, Low Birth Weight ; growth & development ; Infant, Newborn ; Infant, Premature ; Infant, Premature, Diseases ; epidemiology ; etiology ; Infant, Very Low Birth Weight ; growth & development ; Intensive Care Units, Neonatal ; Nutritional Status ; Parenteral Nutrition ; Retrospective Studies ; Weight Gain

This study was aimed to investigate the effect of 5-azacytidine (5-AZA) on XAF1 expression in myeloma cells and efficacy of 5-AZA treatment for myeloma in vitro. XAF1 expression was analyzed by semi-quantitative PCR. Methylation-specific PCR (MSP) was used to detect the methylation status of XAF1 promoter CpG islands. RPMI 8226 and XG-7 cells were treated with 0-5 micromol/L of 5-AZA. Expression of XAF1 mRNA variants was confirmed by gel electrophoresis. The results indicated that the untreated RPMI 8226 cell expressed XAF1 mRNA transcript 1 and transcript 2, untreated XG-7 cells did not express XAF1 mRNA. Hypermethylation of XAF1 promoter CpG islands could be detected in both cell lines. Both cell lines expressed full-length XAF1 transcript after being treated with 2.5 micromol/L of 5-AZA for 72 hours. 5-AZA treatment led XAF1 promoter CpG island to hypomethylation in both cell lines. 5-AZA exerted anti-myeloma activity in a time- and concentration-dependent manner. The IC(50) value of XG-7 cells treated with 5-AZA for 48 hours was 2.6 micromol/L. 1.0, 2.0, 2.5 and 5.0 micromol/L of 5-AZA treatment for 48 hours induced (34.3 +/- 8.0)%, (54.8 +/- 3.1)%, (64.1 +/- 3.4)%, (81.0 +/- 4.1)% apoptosis in XG-7 cell line respectively. The combination of 1.0 - 4.0 micromol/L of 5-AZA with 1.0 - 4.0 micromol/L of arsenic trioxide (ATO) exhibited synergistic toxicity in myeloma cells with all CI values less than 1.0. It is concluded that lack of XAF1 expression and abnormal expression of XAF1 in myeloma cell lines are associated with the hypermethylation of XAF1 gene promoter CpG island. 5-AZA treatment can induce the expression of XAF1 mRNA and protein in myeloma. 5-AZA exerts anti-myeloma activity via apoptosis at clinically achievable concentrations. The findings suggested that 5-AZA and ATO may be an effective combination in the therapy of patients with multiple myeloma.
Antimetabolites, Antineoplastic ; pharmacology ; Apoptosis ; drug effects ; Azacitidine ; pharmacology ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Humans ; Intracellular Signaling Peptides and Proteins ; metabolism ; Multiple Myeloma ; Neoplasm Proteins ; metabolism ; Promoter Regions, Genetic

OBJECTIVESTo investigate the incidence of intra- and extrauterine growth retardation (EUGR) and growth restriction in premature infants, and to illustrate the growth pattern of them in postnatal and infantile period.

METHODSAll premature infants were admitted to our neonatal intensive care unit (NICU) during the recent 7 years. The criteria for enrollment were (1) gestational age < 37 weeks; (2) single fetus; (3) admitted within the first 24 hours of life; (4) hospitalization period ≥ 14 days; (5) clinical follow-up persisted till ≥ 3 months of corrected gestational age. Intrauterine growth restriction (IUGR), EUGR and growth restriction were defined as having a measured growth value (weight) that was ≤ 10(th) percentile of Chinese infants' growth curve in corrected age on admission, discharge and follow-up period. Results were analyzed by using SPSS 12.0 statistical software package by chi-square test, rank-sum test, and t test.

RESULTSTwo hundred and thirty nine infants were involved, 134 were boys and 105 girls. The incidence of IUGR and EUGR assessed by weight was 25.5% and 40.6%, respectively. The lower the birth weight was, the higher the incidence of IUGR and EUGR was. The percentile of body weight in the growth curve at discharge was lower than that at birth (Z = -7.784, P = 0.000). The incidence of growth restriction assessed by weight was 20.5%, 15.0%, 8.8%, 17.0%, 10.4%, 10.1%, 11.9%, 7.0% at corrected gestational age of 38 - 40 weeks, corrected age of 28 d, 61 d, 91 d, 122 d, 152 d, 183 d, and 274 d, respectively. The incidences of growth restriction were stable when the corrected age was older than 91 days. The incidence of growth restriction in female premature infants at 183 days' corrected age was higher than that in male children (χ(2) = 6.181, P = 0.017), the incidence was 19.3% and 3.8% respectively. During the follow-up period, most of the average body weight of premature infants whose gestational age was < 32 weeks or birth weight ≤ 1500 g were lower than the 50(th) percentile of the growth curve except the average body weight of boys whose gestational age < 32 weeks at corrected age of 2 and 4 months.

CONCLUSIONSPremature and/or low birth weight infants are at high risk of growth restriction, especially very low birth weight infants. The incidence of growth restriction decreased with growth. Long-term prognosis requires further investigation.

Body Weight ; Female ; Fetal Growth Retardation ; Follow-Up Studies ; Humans ; Infant, Newborn ; Infant, Premature ; growth & development ; Male ; Weight Gain

Asian Continental Ancestry Group ; Bartter Syndrome ; genetics ; Child ; Chloride Channels ; genetics ; Humans ; Male ; Mutation