Network analysis of internet addiction and sleep disturbance symptoms.

BACKGROUND: Internet addiction (IA) is a behavioral addiction to problematic internet use. IA is associated with poorer sleep quality. Few studies to date, however, have explored the interactions between symptoms of IA and symptoms of sleep disturbance. This study uses network analysis to identify bridge symptoms by analyzing these interactions in a large sample of students. METHOD: We recruited 1977 university students to participate in our study. Each student completed the Internet Addiction Test (IAT) and the Pittsburgh Sleep Quality Index (PSQI). We used these collected data for network analysis to identify the bridge symptoms in the IAT-PSQI network by calculating the bridge centrality. Furthermore, the closest symptom connected with the bridge symptom was found to identify the comorbidity mechanisms. RESULTS: The core symptom of IA and the sleep disturbance network was "I08" (Study efficiency suffers due to internet use). The bridge symptoms between IA and sleep disturbance were "I14" (Surfing the internet late instead of sleeping), "P_DD" (Daytime dysfunction), and "I02" (Spending much time online instead of socializing in real life). Among the symptoms, "I14" had the highest bridge centrality. The edge connecting nodes "I14" and "P_SDu" (Sleep duration) had the strongest weight (0.102) around all the symptoms of sleep disturbance. Nodes "I14" and "I15" (Thinking about online shopping, games, social networking, and other network activities when unable to access the internet) had the strongest weight (0.181), connecting all the symptoms of IA. CONCLUSIONS: IA leads to poorer sleep quality, most likely by shortening sleep duration. Preoccupation with and craving the internet while being offline may lead to this situation. Healthy sleep habits should be learned, and craving may be a good point at which to treat the symptoms of IA and sleep disturbance.

Glucocorticoids offer protection against myocardial injury in a murine model of sepsis.

Sepsis is a serious infection-related complication that, in causing significant inflammation, often leads to myocardial injury. Severe inflammation, including in sepsis, is sometimes treated with exogenous glucocorticoids (GCs). Here, to explore the potential effect of GCs to protect against myocardial injury, we created a model of sepsis in rats by performing cecal ligation and puncture (CLP) in 96 rats randomly divided into sham-operated control (N=32), untreated sepsis (CLP, N=32), and GC-treated sepsis (N=32) groups. At 3, 6, 12, and 24 h after surgery, the changes in cardiac hemodynamic indexes, serum inflammatory response factor levels, and myocardial enzymes were measured, along with mitochondrial membrane potential in myocardial cells, apoptosis of myocardial cells, and the expression of nuclear factor kappa B (NF-κB p65) in myocardial tissues. Pathological changes in myocardial cells were also observed. Compared to the sham-operated group, CLP rats experienced deterioration of left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVEDP), maximum rate of left ventricular pressure rise (+dP/dtmax), and the maximum rate of left ventricular pressure drop (-dP/dtmax). CLP rats also had a rise in serum tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), C-reactive protein (CRP), cardiac troponin I (cTnI), creatine kinase (CK), lactate dehydrogenase (LDH), aspartate aminotransferase (AST), and NF-κB p65 in myocardial tissues. The GCs-treated group had lower levels of these inflammatory response molecules than the CLP group, with the exception of anti-inflammatory cytokine interleukin-10 (IL-10), which was higher in the GC-treated rats than the CLP group at each time point post-surgery. Compared to the sham group, CLP rats had a rise in myocardial cell apoptosis and a drop in mitochondrial membrane potential in myocardial cells. In addition, GCs-treated rats had a marked drop in the myocardial cell apoptosis rate and a rise in the mitochondrial membrane potential compared to CLP rats. After intervention with GCs, the pathological changes in heart tissues were also reduced compared to those in the sepsis group. Based on these results, we conclude that exogenous GCs can inhibit a drop in myocardial mitochondrial membrane potential and inhibit myocardial cell apoptosis by blocking the activation of NF-κB, decreasing the generation of proinflammatory cytokines, and relieving inflammatory injury in heart tissues.

Polymorphism in Integrin ITGA2 is Associated with Ischemic Stroke and Altered Serum Cholesterol in Chinese Individuals.

BACKGROUND: Recent studies have reported contrasting results regarding the association of polymorphisms in two integrin genes, ITGA2 and ITGB3, with ischemic stroke. AIMS: The present study aimed to investigate the correlation between the ITGA2 C807T and ITGB3 T176C polymorphic loci with ischemic stroke, as well as plasma lipid and lipoprotein levels. STUDY DESIGN: Case control study. METHODS: Human venous blood samples were collected from patients admitted for ischemic stroke (n=350, 'patients') and healthy individuals (n=300, 'controls'). Blood was genotyped at these loci by polymerase chain reaction-restriction fragment length polymorphism. Plasma lipid and lipoprotein levels were measured by routine enzymatic, masking, and turbidimetry methods. RESULTS: As expected, total cholesterol, triglycerides, and low-density lipoprotein were all significantly higher in patients than in controls (p<0.05). Genotype and allele frequencies of ITGA2 C807T were significantly different between patients and controls (p<0.05), but no difference was detected in genotype or allele frequencies for ITGA3 T176C. For ITGA-2, the T allele conferred a 1.226 times higher relative risk of ischemic stroke than the C allele (odds ratio=1.226, 95% confidence interval=1.053-1.428). Similarly, total cholesterol was higher in T allele carriers than in non-carriers (p<0.05). CONCLUSION: ITGA2 C807T polymorphism is associated with ischemic stroke, with the T allele acting as a susceptibility allele that appears to confer increased cholesterol levels.

Correlation between interleukin-18 promoter -607C/A polymorphism and susceptibility to ischemic stroke

Single nucleotide polymorphisms in the promoter region of interleukin-18 (IL-18), an inflammatory cytokine, have been linked to susceptibility to many diseases, including cancer and immune dysfunction. Here, we explored the potential association between the IL-18 -607C/A (rs1946518) promoter region polymorphism and susceptibility to ischemic stroke (IS). This locus was amplified from peripheral blood samples of 386 IS patients (cases) and 364 healthy individuals (controls) by the polymerase chain reaction with sequence-specific primers. Significant differences were observed by the χ2 test in the -607C/A (rs1946518) genotype and allele frequencies between cases and controls (P < 0.05). Furthermore, after excluding for age, gender, smoking status, and hypertension, logistic regression indicated that IS susceptibility of -607C carriers increased 1.6 times (OR = 1.601, 95%CI = 1.148-2.233, P = 0.006) compared to -607A carriers. Additionally, similar increases in IS risk were noted for male patients or patients less than 65 years old. In conclusion, IL-18 -607C/A (rs1946518) promoter polymorphism is associated with IS susceptibility, and the C allele may confer increased IS risk.

Correlation between interleukin-18 promoter -607C/A polymorphism and susceptibility to ischemic stroke.

Single nucleotide polymorphisms in the promoter region of interleukin-18 (IL-18), an inflammatory cytokine, have been linked to susceptibility to many diseases, including cancer and immune dysfunction. Here, we explored the potential association between the IL-18 -607C/A (rs1946518) promoter region polymorphism and susceptibility to ischemic stroke (IS). This locus was amplified from peripheral blood samples of 386 IS patients (cases) and 364 healthy individuals (controls) by the polymerase chain reaction with sequence-specific primers. Significant differences were observed by the χ2 test in the -607C/A (rs1946518) genotype and allele frequencies between cases and controls (P < 0.05). Furthermore, after excluding for age, gender, smoking status, and hypertension, logistic regression indicated that IS susceptibility of -607C carriers increased 1.6 times (OR = 1.601, 95%CI = 1.148-2.233, P = 0.006) compared to -607A carriers. Additionally, similar increases in IS risk were noted for male patients or patients less than 65 years old. In conclusion, IL-18 -607C/A (rs1946518) promoter polymorphism is associated with IS susceptibility, and the C allele may confer increased IS risk.

Effect of aloe polysaccharide on caspase-3 expression following cerebral ischemia and reperfusion injury in rats.

Stroke is a leading cause of cardiovascular morbidity, economic and social burden and mortality. Novel approaches are needed to address stroke prevention and treatment. The purpose of this study was to explore the effects of aloe polysaccharide on caspase-3 expression following cerebral ischemia reperfusion injury in rats. Male Wistar rats were randomly divided into 5 groups (16 rats in each group): aloe polysaccharide, ginkgo leaf tablet, nimodipine, model and sham surgery groups. The rats were administered the appropriate drug or normal saline for 7 days by gavage. A rat model of cerebral ischemia and reperfusion injury was established using the middle cerebral artery occlusion (MCAO) model. Caspase-3 protein and mRNA expression levels in the cerebral cortex were detected by immunohistochemistry and reverse transcription-polymerase chain reaction (RT-PCR), respectively. Results showed that caspase-3 protein and mRNA expression levels in the cerebral cortex in the aloe polysaccharide, ginkgo leaf tablet and nimodipine groups were significantly lower compared with the model group and were higher than the sham surgery group (P<0.05). No significant difference was observed in caspase-3 protein and mRNA expression among the aloe polysaccharide, the ginkgo leaf tablet and the nimodipine groups (P>0.05). In conclusion, aloe polysaccharide has a protective effect on cerebral ischemia that may be due to the inhibition of neuronal cell apoptosis.

[The expression and significance of ANXA2 in human glioma].

AIM: to investigate the relation between the expression of ANXA2 in human glioma and its pathological grades, and research the possibility that if ANXA2 could be as a useful diagnostic marker for glioma. METHOD: Semi-quantity RT-PCR and immunohistochemistry were proceeded fro corresponding specimens to detect the level of ANXA2 and ANXA2mRNA. RESULTS: In RT-PCR, the expression level of ANXA2mRNA in glioma was higher than that in surrounding brain tissue. (P < 0.05), as the same, in immunohistochemistry, the expression level of ANXA2 in glioma is higher than that is surrounding brain tissues (P< 0.05). CONCLUSION: ANXA2 expression was much higher in glioma samples than in the surrounding brain tissues, and positive correlation between its expression and pathological grades was found. It could be used as an assistant diagnostic index for glioma.

In situ fabrication of nanostructured titania coating on the surface of titanium wire: A new approach for preparation of solid-phase microextraction fiber.

Nanostructured titania-based solid-phase microextraction (SPME) fibers were fabricated through the in situ oxidation of titanium wires with H(2)O(2) (30%, w/w) at 80 degrees C for 24h. The obtained SPME fibers possess a approximately 1.2microm thick nanostructured coating consisting of approximately 100nm titania walls and 100-200nm pores. The use of these fibers for headspace SPME coupled with gas chromatography with electron capture detection (GC-ECD) resulted in improved analysis of dichlorodiphenyltrichloroethane (DDT) and its degradation products. The presented method to detect DDT and its degradation products has high sensitivity (0.20-0.98ngL(-1)), high precision (relative standard deviation R.S.D.=9.4-16%, n=5), a wide linear range (5-5000ngL(-1)), and good linearity (coefficient of estimation R(2)=0.991-0.998). As the nanostructured titania was in situ formed on the surface of a titanium wire, the coating was uniformly and strongly adhered on the titanium wire. Because of the inherent chemical stability of the titania coating and the mechanical durability of the titanium wire substrate, this new SPME fiber exhibited long life span (over 150 times).

QSAR analysis of cyclooxygenase inhibitor using particle swarm optimization and multiple linear regression.

Quantitative structure-activity relationship (QSAR) models of inhibiting action of some diarylimidazole derivatives on cylcooxygenase (COX) enzyme were constructed using modified particle swarm optimization (PSO) method. As a comparison to this method, the genetic algorithm (GA) was also tested. It has been demonstrated that the modified PSO is a useful tool for variable selection comparable to GA and even superior to GA. QSAR models are constructed separately for COX-2 inhibitory activity and selectivity of COX-2 inhibition over COX-1. The spatial descriptors play a key role in the compounds' activity and selectivity to COX-2, especially Jurs descriptors. Polar interactions are the principal binding strength between compounds and COX-2 enzyme. In addition, the aqueous desolvation free energy (FH2O) value of substituent will affect the COX-2 inhibitory activity, while the charge distribution can affect the selectivity to COX-2.