Latent profiles of bullying perpetration and victimization: Gender differences and family variables.

BACKGROUND: School bullying is a prevalent issue that threatens the psychological and social well-being of adolescents. However, little research has investigated how gender and family variables were related to bullying-involvement patterns among adolescents with siblings. OBJECTIVE: This study explored gender differences in the profiles of bullying involvement and the relationship between sibling, parental variables, and these profiles among Chinese adolescents. PARTICIPANTS AND SETTING: Participants (N = 1,060; 46.0 % boys; Mage = 15.53) were recruited from junior and senior high schools in Jiangxi and Guizhou Provinces, China. METHODS: Bullying involvement, sibling warmth and conflict, and parental psychological maltreatment and neglect were assessed by self-report questionnaire. Latent profile analysis was used to identify subgroups with distinct bullying involvement patterns, then multiple logistic regressions were performed to investigate the associations between family variables and bullying-involvement subgroups. RESULTS: We found gender differences in both the latent profiles of bullying involvement and the associations between profiles and family variables. Only boys were identified severe bully-victims (3.39 %), while only girls were categorized as relational bully-victims (20.18 %). Boys and girls were similarly represented among uninvolved students (70.76 % vs. 66.85 %), moderate bully-victims (15.25 % vs. 6.49 %), and victims (10.59 % vs. 6.49 %). Students with more sibling warmth manifested less likelihood of engaging in bullying-related profiles, with more parental psychological maltreatment, and more parental neglect manifested more likelihood of engaging in bullying-related profiles only among girls. While students with more sibling conflict were related to more bullying-related profiles among boys than girls. CONCLUSIONS: The findings emphasize the importance of developing gender-specific bullying intervention strategies that also consider relevant family factors.

Uniaxial Compressive Stress-Strain Model of Jujube Nucleus Concrete following Exposure to Elevated Temperatures.

Aiming to provide a solution for natural resource consumption and agricultural waste pollution, jujube nucleus is utilized as a substitute for coarse aggregate in the preparation of lightweight aggregate concrete. The effect of the jujube nucleus (JN) replacement ratio and the elevated temperature on the uniaxial compressive stress-strain curves of jujube nucleus concrete (JNC) are experimentally studied. The results show that the failure of the JNC prisms became more serious with the increase in the JN replacement ratio. The linear proportion in ascending branch and the descending slope of the stress-strain curves for JNC increased gradually with the increase in the JN replacement ratio and elevated temperature, which is probably owing to the higher porosity and lower stiffness of the jujube nucleus, compared to natural aggregate. Moreover, as the JN replacement ratio and the elevated temperature increase, the peak stress and elastic modulus in the stress-strain curves of JNC decrease gradually, whilst an increase in the peak strain shows up, which is possibly due to the growth of hydrate calcium silicate and calcium hydroxide hampered by sucrose molecules. Based on the test results, a series of theoretical formulas are proposed to predict the compressive performance of JNC. A material constitutive model is developed for describing the stress-strain relationship of JNC by considering the JN replacement ratio and elevated temperature.

Local Cooling as a Step of Treatment for Tissue Ischemia Caused by Hyaluronic Acid Injection-induced Embolism-A Report of 9 Cases.

Hyaluronic acid injection is 1 of the most popular procedures in facial rejuvenation and augmentation. It is widely popular in the cosmetic surgery due to several advantages, which include rapid effect, minimal injury, and a short postoperative recovery period. With continuous increase in hyaluronic acid injections, many cases of hyaluronic acid injection-induced embolism have been reported. At present, methods for early treatment of hyaluronic acid injection-induced embolism include local injection of hyaluronidase, topical application of nitroglycerin ointment, massage, hot compression, and intravenous injections of antibiotics and hormones. Although early warm massage may facilitate hyaluronic acid degradation by hyaluronidase, local application of heat will also increase metabolic rate in the tissue, thereby reducing the ischemic tolerance of the tissue. Therefore, in this study, warm massage was limited to the first 30 minutes after hyaluronidase injection and was followed by local cooling using a gauze pad soaked with antibiotic saline solution. Excellent therapeutic effects were achieved with this approach. The methods of treatment for tissue ischemia caused by hyaluronic acid injection-induced embolism and clinical cases are introduced in the article.

Point-of-care test of heart-type fatty acid-binding protein for the diagnosis of early acute myocardial infarction.

AIM: To investigate the efficacies of point-of-care test of heart-type fatty-acid binding protein (H-FABP) and its combinations with the conventional biomarkers in the diagnosis of early acute myocardial infarction (AMI). METHODS: 227 patients suspected of AMI were consecutively recruited in two centers. Biomarkers including H-FABP, myoglobin (MYO), creatine kinase-myocardial band (CK-MB) and cardiac troponin T (cTnT) were determined simultaneously at admission. AMI was defined according to the universal definition of myocardial infarction. Chi-Square test was adopted for the analysis. RESULTS: In patients presenting within 12 h of symptom onset, the sensitivity of H-FABP[93.0% (95% CI: 86.6%-96.9%)] was significantly higher than that of initial CK-MB [67.5% (95% CI: 58.1%-76.0%), P<0.0001], cTnT [69.3% (95%CI: 60.0%-77.6%), P<0.0001] and MYO [68.6% (95% CI: 54.1%-80.9%), P<0.05]. The negative predictive value of H-FABP [92.8% (95%CI: 86.3%-96.8%)] was significantly higher than that of initial CK-MB [74.7% (95% CI: 66.8%-81.5%), P<0.001] and cTnT [75.9% (95% CI: 68.1%-82.6%), P<0.001]. The sensitivity of H-FABP+cTnT combination [94.7% (95% CI: 88.9%-98.0%)] was significantly higher than that of admission cTnT [69.3% (95% CI: 60.0%-77.6%), P<0.0001], CK-MB+cTnT [75.4% (95% CI: 66.5%-83.0%), P<0.0001] and MYO+CK-MB+cTnT [74.5% (95% CI: 60.4%-85.7%), P<0.05]. The negative predictive value of H-FABP+cTnT [94.5% (95% CI: 88.4%-98.0%] was significantly higher than that of initial cTnT [75.9% (95% CI: 68.1%-82.6%), P<0.001] and CK-MB+cTnT [79.1% (95% CI: 71.2%-85.6%), P<0.001]. Subgroup analysis showed that the superiorities of both the sensitivities and the negative predictive values of H-FABP and H-FABP+cTnT combination occurred only in patients who presented within 6 h of the symptom onset. CONCLUSION: Point-of-care test of H-FABP can be used as a valuable biomarker to detect or exclude an early-stage AMI. Combining H-FABP and cTnT provides the best performance for early AMI diagnosis.

Atorvastatin reduces tissue factor expression in adipose tissue of atherosclerotic rabbits.

BACKGROUND: We have recently demonstrated that tissue factor (TF) expression increases in adipose tissues/adipocytes of cholesterol-fed rabbit, which is associated with a hypercoagulable state that contributes to thrombosis. In this study, we evaluated the ability of atorvastatin to modulate TF expression in cholesterol-fed rabbit and the regulatory mechanism. METHODS: Male rabbits were randomly fed with normal diet and high-cholesterol diet for 8 weeks, following 4 weeks, those fed high-cholesterol diet were randomly assigned to atorvastatin or starch. At the end of 12 weeks, subcutaneous adipose was collected, and culture adipocyte. TF mRNA was detected by reverse transcription-polymerase chain reaction (RT-PCR). TF concentrations were determined with ELISA. The in vitro effect of atorvastatin and mevalonate (MVA) on TF production in adipocytes was observed. RESULTS: Atorvastatin reduced serum TC and LDL-C levels (P<0.05), and decreased plasma TF concentration and expression in adipose tissues/adipocytes from cholesterol-fed rabbits. In vitro, atorvastatin dose-dependently suppressed TF expression and protein secretion in adipocytes. MVA reversed the inhibitory effect of atorvastatin on TF expression in concentration-dependent manner. CONCLUSIONS: Results provide further support for the antithrombotic effect of atorvastatin. It also indicated that mevalonate pathway may play an important role in TF expression in adipocyte.

Atorvastatin reduces plasminogen activator inhibitor-1 expression in adipose tissue of atherosclerotic rabbits.

BACKGROUND: Plasminogen activator inhibitor-1 (PAI-1) expression are increased in adipose tissues/adipocytes of obese mice, which is associated with a hypofibrinolytic state that contributes to thrombosis. We recently demonstrated that PAI-1 expression increases in adipose tissues/adipocytes of cholesterol-fed rabbits. In this study, we evaluated the ability of atorvastatin to modulate PAI-1 expression in cholesterol-fed rabbits and the regulatory mechanism. METHODS: Male rabbits were randomly fed with normal diet and high-cholesterol diet for 8 weeks, following 4 weeks, those fed high-cholesterol diet were randomly assigned to 2.5 mg/kg/day atorvastatin or starch. At the end of 12 weeks, subcutaneous adipose was collected, and culture adipocyte. PAI-1 mRNA was detected by RT-PCR. PAI-1 concentrations were determined with ELISA. The effect of atorvastatin and mevalonate (MVA) on PAI-1 production in adipocytes in vitro was observed. RESULTS: Atorvastatin significantly reduced serum TC and LDL-C concentrations (p<0.05), and decreased plasma PAI-1 concentration and PAI-1 expression in adipose tissues/adipocytes from cholesterol-fed rabbits. In vitro, atorvastatin dose-dependently suppressed PAI-1 expression and protein secretion in adipocytes. MVA reversed the inhibitory effect of atorvastatin on PAI-1 expression in concentration-dependent manner. CONCLUSIONS: Atorvastatin reduces plasma PAI-1 concentration and PAI-1 expression in adipose tissue and adipocyte of atherosclerotic rabbit, and inhibits PAI-1 expression and protein secretion in adipocytes in vitro, suggesting that it may have an antithrombtic effect. We also suggest that the mevalonate pathway may play an important role in PAI-1 expression in adipocyte.

Valsartan reduces interleukin-1beta secretion by peripheral blood mononuclear cells in patients with essential hypertension.

BACKGROUND: Chronic low-grade inflammation response may contribute to the pathology of essential hypertension. Angiotensin II (Ang II) may be partly responsible for this process. Our early studies showed that individuals with essential hypertension had increased interleukin-1beta (IL-1beta) secretion by peripheral blood mononuclear cells (PBMCs). In this study, we investigated whether treatment with valsartan, an angiotensin receptor blocker, lowered IL-1beta secretion by PBMCs in patients with essential hypertension. METHODS: Twenty-four patients with essential hypertension were randomized to treatment with valsartan (80 mg/day, group B) or matching routine therapy group (group A) for 2 weeks. PBMCs were isolated by gradient centrifugation. IL-1beta concentrations in supernatant from PBMCs were measured by enzyme-linked immunosorbent assay (ELISA). RESULTS: Compared with routine therapy group, patients treated with valsartan had decreased secretion of IL-1beta in PBMCs after stimulated by lipopolysaccharide (2857+/-643 vs. 2146+/-508 pg/ml, P<0.05). CONCLUSIONS: We suggest a direct anti-inflammatory effect of valsartan and a pro-inflammatory effect of Ang II in patients with essential hypertension.

Fenofibrate enhances CD36 mediated endocytic uptake and degradation of oxidized low density lipoprotein in adipocytes from hypercholesterolemia rabbit.

BACKGROUND: CD36 as a fatty acid transporter is predominantly expressed in adipocytes. We studied whether adipocytes could uptake and degrade OxLDL through CD36 and explored the effect of fenofibrate on OxLDL uptake in adipocytes from hypercholesterolemia rabbits. METHODS: Subcutaneous adipose tissues were collected from normal, high-cholesterol and high-cholesterol plus fenofibrate treatment rabbits for adipocytes culture. CD36 and peroxisome proliferator-activated receptor gamma (PPARgamma) mRNA expression were evaluated by RT-PCR. RESULTS: Cellular expression of CD36 was confirmed during differentiation of adipose cell by RT-PCR. Upon incubation at 37 degrees C, (125)I-OxLDL was endocytosed in a dose-dependent fashion and underwent lysosomal degradation by adipocytes. In binding experiments at 4 degrees C, (125)I-OxLDL exhibited specific and saturable binding to adipocytes (K(D) = 4.2 microg/mL). The endocytic uptake and degradation of (125)I-OxLDL by adipocytes were inhibited by 56 and 54% with anti-CD36 antibody. Fenofibrate treatment enhanced the (125)I-OxLDL uptake and degradation and up-regulated CD36 mRNA expression in adipocytes and suppressed PPARgamma mRNA expression in adipose tissue from hypercholesterolemia rabbits. CONCLUSION: CD36 plays a novel role in adipose tissues and adipocytes possibly involve in clearance of OxLDL in blood. Fenofibrate treatment improved the OxLDL uptake and degradation in adipocytes from hypercholesterolemia rabbits.

Fenofibrate inhibits thrombogenic and fibrinolytic factors expression in adipose tissue of atherosclerotic rabbits.

BACKGROUND: Tissue factor (TF) and plasminogen activator inhibitor-1 (PAI-1) activity and/or expression are upregulated in obesity. We investigated TF and PAI-1 mRNA expression in adipose tissues of cholesterol-fed rabbits, and the effects of fenofibrate. METHODS: Male rabbits were fed either a normal or high-cholesterol diet for 8 weeks. After 4 weeks, those fed high-cholesterol diets were randomly assigned to 30 mg/kg/day fenofibrate and starch. At the end of 12 weeks, subcutaneous adipose was collected. The concentration of TF and PAI-1 mRNA was detected by reverse transcription-polymerase chain reaction (RT-PCR). The plasma activities of TF and PAI-1 were determined with ELISA and chromogenic substrate method, respectively. RESULTS: The atherogenic diet caused a consistent increase in serum concentrations of total cholesterol (TC) (p<0.05) and did not significantly affect serum triglyceride (TG) concentrations, and increased TF and PAI-1 mRNA expression in adipose tissues (1.149+/-0.014 and 1.200+/-0.012, respectively) as compared to the normal diet (1.034+/-0.011 and 1.098+/-0.013, respectively) (p<0.01). The plasma activities of TF [(74.4+/-28.8) ng/l] and PAI-1 [(15.6+/-1.9) x 10(3) AU/l] in high-cholesterol diet group were higher than those of normal diet group [(33.1+/-10.7) ng/l and (6.9+/-0.9) x 10(3) AU/l, respectively, p<0.05]. Four-week fenofibrate treatment resulted in significant decrease of TF (1.017+/-0.010) and PAI-1 mRNA (1.061+/-0.011, p<0.01), the plasma activity of TF [(40.3+/-12.2) ng/l, p<0.05] and PAI-1 [(7.5+/-1.5) x 10(3) AU/l, p<0.01] also decreased significantly, and the concentrations of lipids were not changed. CONCLUSION: TF and PAI-1 mRNA expression and plasma activities increased in adipose tissue of cholesterol-fed rabbits. Fenofibrate reduced TF and PAI-1 expression and plasma activity in adipose, suggesting that fenofibrate treatment reduces thrombosis risk, and may have an antithrombotic effect independent of its lipid-lowering.