METHODS: One hundred thirty-one FH patients, 68 RUC and 214 matched NC were recruited. Fasting lipid profile, biomarkers of inflammation (hsCRP), endothelial activation (sICAM-1 and E-selectin) and oxidative stress [oxidized LDL (oxLDL), malondialdehyde (MDA) and F2-isoprostanes (ISP)] were analyzed and independent predictor was determined using binary logistic regression analysis.
RESULTS: hsCRP was higher in FH and RUC compared to NC (mean ± SD = 1.53 ± 1.24 mg/L and mean ± SD = 2.54 ± 2.30 vs 1.10 ± 0.89 mg/L, p LDL, MDA and ISP) were elevated in FH compared to NC [mean ± SD = (48.2 ± 26.8 vs 27.3 ± 13.2 mU/L, p 0.05). FH was an independent predictor for sICAM-1 (p = 0.007), ox-LDL (p
Methods: A cross-sectional study was conducted at the Sulaimani Blood Bank, during the period of April 1, 2016 to March 28, 2017, on convenient samples of 100 regular and 100 first-time blood donors. Donor particulars were obtained from blood bank records. The cholesterol, triglyceride, low-density lipoprotein, ferritin, vitamin D3, and uric acid concentrations of blood samples were determined.
Results: The main reason for blood donation by regular blood donors was headache (45%), while for the first-timers it was to help relatives (31%). The low-density lipoprotein and ferritin concentrations were significantly (p=0.001) lower in the blood of regular donors than first-timers.
Conclusion: The study shows that regular blood donation is beneficial for the maintenance of health of donors.
METHODS: The Cochrane Central Register of Controlled Trials (CENTRAL), EMBASE, MEDLINE, China National Knowledge Infrastructure (CNKI) and Wanfang Database were searched for relevant randomized controlled trials up to March 2016. Two review authors independently selected trials for inclusion, extracted data, assessed the methodological quality and rated the quality of evidence with the Grading of Recommendations, Assessment, Development and Evaluation approach.
RESULTS: Twelve studies involving 655 participants were included. Evidence of low to moderate-quality showed that cordyceps plus conventional treatment compared to conventional treatment alone significantly improved C-reactive protein [standardized mean difference (SMD) －0.61; 95% confidence intervals (CI) －1.00 to －0.22], high-sensitivity C-reactive protein [weighted mean difference (WMD) －3.44 mg/L; 95% CI －3.89 to －2.99], serum albumin (WMD 3.07 g/L; 95% CI 1.59 to 4.55), malondialdehyde (WMD －1.95 nmol/L; 95% CI －2.24 to －1.66), and hemoglobin (WMD 9.56 g/L; 95% CI 3.65 to 15.47) levels. However, there was no significant improvement for serum creatinine and low-density lipoprotein cholesterol. Overall, most trials either did not monitor adverse events or poorly documented them.
CONCLUSION: Given the small number of trials included, the unclear methodological quality of the included trials, and the high heterogeneity in pooled analyses, the evidence obtained in this review is insufficient to recommend the use of cordyceps as adjunctive treatment in hemodialysis patients.
Methods: An in vitro cell model for tamoxifen-resistant HER2 overexpressed UACC732 cells was created using the pulse method. Cells were exposed to oxidized LDL (oxLDL) and very low density lipoprotein (VLDL) separately. Effects on cell morphology was studied using phase contrast microscopic changes. Percentage of cell viability was measured using proliferation assay kit. Development of tamoxifen resistance was determined based on P-gp expression with flow cytometry. Further analysis includedcell death measurement with flow cytometry method.
Results: UACC732 cells exposed to VLDL exhibited fibroblast-like morphology. This was further supported by proliferation assay, where the percentage of cell viability achieved more than 100% with 100 μg/ml of VLDL exposure, indicating cell proliferation. Findings also showed that VLDL caused reduction in expression of Pgp in resistant cells compared to resistant cells alone (p = 0.02).
Conclusion: Results of this study suggest that VLDL may play a role in growth of drug-resistant HER2-overexpressing cells. Lower expression of P-gp in presence of VLDL need to be investigated further.
MATERIALS AND METHODS: This was a retrospective cohort study undertaken at a public tertiary care centre in the state of Perak, Malaysia. Information of obese patients who underwent bariatric surgery was obtained from their medical records. The changes in the BMI, HbA1C, systolic and diastolic blood pressure (SBP and DBP), and lipid levels between three months before and after the surgery were assessed.
RESULTS: The patients (n=106) were mostly Malay (66.0%), had at least one comorbidity (61.3%), and had a mean age of 40.38±11.75 years. Following surgery, the BMI of the patients was found to reduce by 9.78±5.82kg/m2. For the patients who had diabetes (n=24) and hypertension (n=47), their mean HbA1C, SBP and DBP were also shown to reduce significantly by 2.02±2.13%, 17.19±16.97mmHg, and 11.45±12.63mmHg, respectively. Meanwhile, the mean total cholesterol, triglyceride and low-density lipoprotein levels of those who had dyslipidaemia (n=21) were, respectively, lowered by 0.91±1.18mmol/L, 0.69±1.11mmol/L and 0.47±0.52mmol/L.
CONCLUSION: The findings suggest that in addition to weight reduction, bariatric surgery is helpful in improving the diabetes, hypertension and dyslipidaemia control among obese patients. However, a large-scale trial with a control group is required to verify our findings.
Methods: In the experimental study, the rats were randomly divided into four groups of five rats in each and fed with high-fat diet for 12 weeks as follows: One group (normal diet group) was fed with a standard diet, one group was fed with HFD, and two groups were fed with HFD and orally fed with 150 and 450 mg/kg/day HAEM. The serum samples and liver tissues were used for measuring the biochemical and oxidative parameters and histopathological studies. HFD induced hepatosteatosis in rats as evidenced by the altered liver enzymes activity, serum lipid profile and oxidative status.
Results: Serum lipid profile (triglyceride, cholesterol and low-density lipoprotein) in rats fed with HFD + HAEM (150 and 450 mg/kg/day) was significantly decreased. Furthermore, the evaluation of oxidative stress showed a reduction of the malondialdehyde (MDA) level and an increase in ferric-reducing anti-oxidant power. Meanwhile, liver enzyme activities declined in response to HAEM.
Conclusion: Using the HAEM could be a future therapeutic agent in treating hepatosteatosis and reducing oxidative damages of HFD in the liver.
AIM OF THE STUDY: The present study was performed to determine underlying mechanism of G. procumbens ethanol extract and its fractions such as aqueous, chloroform, ethyl acetate and hexane affect macrophage derived foam cell formation.
MATERIALS AND METHODS: Lipid droplets accumulation in treated macrophages were visualized by Oil Red O staining while the total cholesterol present in the treated macrophages were measured using Cholestryl Ester quantification assay kit. Enzyme-Linked Immunosorbent Assay (ELISA) were used to detect TNF-α and IL-1β secretion in the supernatant of treated macrophages. Gene expression of Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) and ATP-binding cassette transporter A-1 (ABCA-1) in treated macrophages were analyzed using Real-Time Quantitative Polymerase Chain Reaction (RT-qPCR).
RESULTS: G. procumbens ethanol extract and its fractions reduced lipid droplet accumulation and total cholesterol in oxLDL-treated macrophages together with significantly reduction of TNF-α and IL-1β secretions in supernatant oxLDL-treated macrophages. LOX-1 gene expression was significantly reduced when G. procumbens ethanol extract and its fractions were added in oxDL-treated macrophages. In contrast, G. procumbens ethanol extract and its fractions significantly increased the expression of ABCA-1 gene in oxLDL-treated macrophages.
CONCLUSION: In conclusion, G. procumbens ethanol extract and its fractions inhibit the formation of macrophage derived foam cell by reducing TNF-α and IL-1β expression, which usually highly expressed in atherosclerotic plaques, suppressing scavenger receptor LOX-1 gene that binds oxLDL but induced ABCA-1 gene that mediate lipid efflux from macrophages.
MATERIALS AND METHODS: Cell viability was determined using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Reactive oxygen species (ROS) and membrane potential was detected using 2',7'-dichlorofluorescein diacetate and 5,5',6,6'-tetrachloro-1,1',3,3'-tetraethylbenzimidazolcarbocyanine iodide (JC-1) dye staining, respectively. While, cell apoptosis was determined by Annexin-V staining and protein expression was measured using Western blot.
RESULTS: Our results suggested that melatonin inhibited glucose-induced ROS elevation, mitochondria dysfunction and apoptosis on HUVEC. Melatonin inhibited glucose-induced HUVEC apoptosis via PI3K/Akt signaling pathway. Activation of Akt further activated BcL-2 pathway through upregulation of Mcl-1 expression and downregulation Bax expression in order to inhibit glucose-induced HUVEC apoptosis. Besides that, melatonin promoted downregulation of oxLDL/LOX-1 in order to inhibit glucose-induced HUVEC apoptosis.
CONCLUSIONS: In conclusion, our results suggested that melatonin exerted vasculoprotective effects against glucose-induced apoptosis in HUVEC through PI3K/Akt, Bcl-2 and oxLDL/LOX-1 signaling pathways.