Interaction of sleep duration and depression on cardiovascular disease: a retrospective cohort study.

BACKGROUND: To assess the interaction of sleep duration and depression on the risk of cardiovascular disease (CVD). METHODS: A total of 13,488 eligible participants were enrolled in this retrospective cohort study eventually. Baseline characteristics were extracted from the China Health and Retirement Longitudinal Study (CHARLS) database, including age, sex, diabetes, high-density lipoprotein (HDL), blood glucose (GLU), glycosylated hemoglobin (GHB) etc. Univariate and multivariate negative binomial regression models were carried out to assess the statistical correlation of sleep duration and depression on CVD separately. Additionally, multivariate negative binomial regression model was used to estimate the interaction of sleep duration and depression on CVD risk. RESULTS: After adjusting for age, sex, educational background, hypertension, diabetes, dyslipidemia, the use of hypnotics, disability, nap, drinking, deposit, sleep disturbance, HDL, triglyceride, total cholesterol, GLU and GHB, the risk of CVD in participants with the short sleep duration was increased in comparison with the normal sleep duration [relative risk (RR)=1.02, 95% confidence interval (CI):1.01-1.03]; compared to the participants with non-depression, participants suffered from depression had an increased risk of CVD (RR=1.05, 95%CI:1.04-1.06). Additionally, the result also suggested that the interaction between short sleep duration and depression on the risk of CVD was statistically significant in these patients with diabetes and was a multiplicative interaction. CONCLUSION: An interaction between short sleep duration and depression in relation to an increased risk of CVD among Chinese middle-aged and elderly individuals was noticed, which may provide a reference that people with diabetes should focus on their sleep duration and the occurrence of depression, and coexisting short sleep duration and depression may expose them to a higher risk of CVD.

Thrombocytopenia as a predictor of severe acute kidney injury in patients with heat stroke.

BACKGROUND: Abnormalities of blood system often occur several days before acute kidney injury (AKI) in patients with heat stroke (HS). We aimed to investigate the prevalence and prognostic value of the early hematological markers in patients with AKI induced by HS. METHODS: In a retrospective cohort study, we analyzed the case records of 176 patients with HS and evaluated the hematological markers for early prediction and risk classification in the patients with AKI. RESULTS: Of 176, 103 (58%) HS cases developed AKI, and men comprised more than half (75%) of the sample population. The nadir platelet count significantly correlated with the levels of peak serum creatinine (r = -0.608, p < 0.01) and blood urea nitrogen (r = -0.546, p < 0.01), and the length of hospital stay (r = -0.393, p < 0.01). The areas under the receiver operating characteristic curves (AU-ROC) indicated the prognostic accuracy of hematological markers, AU-ROC was significantly higher with the nadir platelet count than that with the admission platelet count (AU-ROC of the nadir platelet: 0.73; 95% CI: 0.67-0.82; vs. AU-ROC of the admission platelet: 0.67; 95% CI: 0.59-0.75; p < 0.01). Multiple logistic regression results indicated that the nadir platelet count (adjusted ORs: 37.92; 95% CI: 2.18-87.21; p < 0.01) was independent predictor of AKI in HS. CONCLUSION: The high mortality observed in HS complicated with AKI, and among the various hematological parameters assessed, thrombocytopenia is associated with AKI induced by HS independently.

Urine neutrophil gelatinase-associated lipocalin in septic patients with and without acute kidney injury.

INTRODUCTION: Urine neutrophil gelatinase-associated lipocalin (uNGAL) is a rapidly emerging biomarker for early detection of acute kidney injury (AKI). We aimed to investigate the prevalence and prognostic value of the early uNGAL in patients with AKI induced by sepsis. METHODS: In this prospective cohort study, we analyzed the case records of 126 septic patients with and without AKI and evaluated the uNGAL for early prediction and risk stratification of septic patients with AKI. RESULTS: Of 126 patients analyzed, 58 (46%) developed septic AKI. Men comprised more than half (68%) of the sample population, the mean age (SD) was 57 years. The prognostic accuracy of uNGAL, as quantified by the area under the receiver-operating-characteristic curve (AU-ROC), was highest with peak uNGAL (AU-ROC: 0.86; 95% CI: 0.81-0.93), as compared with the admission uNGAL (AU-ROC: 0.81; 95% CI: 0.73-0.89). The peak uNGAL correlated with the levels of peak blood urea nitrogen (r = 0.674) and serum creatinine (r = 0.608), the length of hospital stay (r = 0.602) and weakly correlated with the number of hemodialysis sessions that each patient received during hospital stay (r = 0.405). By multivariate analysis, increased peak uNGAL remained independently associated with the development of septic AKI (odds ratio: 32.12; 95% CI: 6.21-90.37; p < 0.0001). CONCLUSIONS: uNGAL is independently associated with subsequent AKI among patients with sepsis.

Acute pancreatitis associated with hemorrhagic fever with renal syndrome: clinical analysis of 12 cases.

BACKGROUND: Acute pancreatitis is one of the rare complications of hemorrhagic fever with renal syndrome (HFRS), which easy to be misdiagnosed as acute abdomen, usually critically ill, poor treatment effect, highly mortality. In this study, we retrospectively analyzed to explore the clinical characteristics, 12 cases of hemorrhagic fever with renal syndrome complicated with acute pancreatitis treatment methods and prognosis. METHODS: We conducted a retrospective study of HFRS in patients complicated with acute pancreatitis. 12 cases were collected from Ningbo first hospital between January 2001 and December 2012. Clinical information and laboratory parameters were obtained by reviewing literature and records. RESULTS: Twelve from 156 cases (7.69%) HFRS complicated with acute pancreatitis. Men comprised more than half (75%) of the sample population, the mean age was (38 ± 19) years. Abdominal pain was the main clinical manifestations in all the patients, all of their serum amylase and serum lipase were increased, 10 patients were given the total abdomen CT examination, eight cases showed enlargement of the pancreas and surrounding leakage, two cases showed pancreatic necrosis and hemorrhage. Three cases complicated with pulmonary edema. In 12 cases, four of them received hemodialysis treatment, one gives surgical intervention. Eight cases were complete remission, three cases were partial remission and one case was death. CONCLUSIONS: Acute pancreatitis is one of rare of the serious complications of HFRS, whereas the correct diagnosis and clear the cause of disease is critical for improve the quality of life of patients and reduce the mortality, timely hemodialysis treatment is effective, early intervention can improve the prognosis.

Palmitoylation modification of Galpha(o) depresses its susceptibility to GAP-43 activation.

Interaction between GAP-43 (growth associated protein-43) and Galpha(o) (alpha subunit of Go protein) influences the signal transduction pathways leading to differentiation of neural cells. GAP-43 is known to increase guanine nucleotide exchange by Galpha(o), which is a major component of neuronal growth cone membranes. However, it is not clear whether GAP-43 stimulation is related to the Galpha(o) palmitoylation or the conversion of Galpha(o) from oligmers to monomers, which was shown to be a necessary regulatory factor in GDP/GTP exchange of Galpha(o). Here we expressed and purified GAP-43, GST-GAP-43 and Galpha(o) proteins, detected their stimulatory effect on [(35)S]-GTPgammaS binding of Galpha(o). It was found that the EC(50) of both GAP-43 and GST-GAP-43 activation were tenfold lower in case of depalmitoylated Galpha(o) than palmitoylated Galpha(o). Non-denaturing gel electrophoresis and p-PDM cross-linking analysis revealed that addition of GST-GAP-43 induced disassociation of depalmitoylated Galpha(o) from oligomers to monomers, but did not influence the oligomeric state of palmitoylated Galpha(o), which suggests that palmitoylation is a key regulatory factor in GAP-43 stimulation on Galpha(o). These results indicated the interaction of GAP-43 and Galpha(o) could accelerate conversion of depalmitoylated Galpha(o) but not palmitoylated Galpha(o) from oligomers to monomers, so as to increase the GTPgammaS binding activity of Galpha(o). Results here provide new evidence about how signaling protein palmitoylation is involved in the G-protein-coupled signal transduction cascade, and give a useful clue on the participation of GAP-43 in G-protein cycle by its preferential activation of depalmitoylated Galpha(o).

[Association of platelet endothelial cell adhesion molecule-1 gene polymorphism with coronary heart disease].

OBJECTIVE: To investigate the association of Leu125Val and Ser563Asn polymorphism of the gene encoding platelet endothelial cell adhesion molecule-1(PECAM-1) with coronary heart disease. METHODS: This study included 156 patients with the diagnoses of coronary heart disease (CHD) and coronary lesions derived from electrocardiography, myocardial enzyme analysis and coronary angiography as the CHD group, and another 75 in-patients admitted within the same period who showed no signs of CHD in the above examinations constituted the control group. Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) was employed to examine the missense polymorphism of PECAM-1gene in the position of Leu125Val and Ser563Asn. RESULTS: There were significant differences between CHD and control group in terms of the allele frequencies and genotype distributions of PECAM-1 gene, and the differences were especially conspicuous in the allele frequencies of 125Val and 563Asn (P<0.05) and genotype distributions of 125Val/Val and 563Asn/Asn. CONCLUSION: PECAM-1 gene polymorphism 1 may be a genetic risk factor for coronary heart disease.