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Patients with depression have a high prevalence of developing dyslipidemia. In this study, we aim to investigate the difference of serum lipids, including total cholesterol (TCH), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), and triglycerides (TG), between the depressed patients and healthy controls. Sex differences in lipids and their psychological correlations were also included. The study included 56 healthy controls (males/females = 26/30) and 110 first-diagnosed drug-naïve outpatients (males/females = 35/75). A total of 42 patients (males/females = 14/28) were followed for 3 months. A significant difference was found in TCH and LDL-C among healthy control and patients. Interestingly, female patients with first-diagnosed, drug-naïve depression had lower atherogenic indices than male patients. After 3 months of antidepressants therapy, female patients exhibited detrimental changes in serum lipids, namely increased TG and atherogenic index. Moreover, correlation analysis showed significant correlations between changes of depression inventory (HAMD and BDI) score and serum lipids (TCH, HDL-C) in depressed patients. We found that dyslipidemia was more common in female patients with depression during therapy with antidepressants. Moreover, the altered serum lipids and atherogenic index might be a hallmark of female patients. Further investigation of sex differences in lipid metabolism of depression is warranted. [ABSTRACT FROM AUTHOR]

The possible organic acid emission sources in PM10 in Xiamen urban atmosphere such as cooking, biomass burning, vehicle exhaust and soil/dust were obtained using a re-suspension test chamber. A total of 15 organic acids including dicarboxylic acids, fatty acids and aromatic acids were determined using GC/MS after derivatization with BF3/n-butanol. The results showed that the highest total concentration of 15 organic acids (53%) was found in cooking emission and the average concentration of the sum of linoleic acid and oleic acid was 24% +/- 14%. However, oxalic acid was the most abundant species followed by phthalic acid in gasoline vehicle exhaust. The ratios of adipic to azelaic acid in gasoline combustion emissions were significantly higher than those in other emission sources, which can be used to qualitatively differentiate anthropogenic and biological source of dicarboxylic acids in atmospheric samples. The ratios of malonic to succinic acid in source emissions (except gasoline generator emissions) were lower (0.07-0.44) than ambient PM10 samples (0.61-3.93), which can be used to qualitatively differentiate the primary source and the secondary source of dicarboxylic acids in urban PM10.

Objective: To explore the protective effects and potential mechanisms of 1α, 25(OH)(2) D(3) (VitD(3)) on pancreatic β-cells., Methods: The apoptosis of NIT-1 cells was induced by interleukin-1β (IL-1β) and interferon-γ (IFN-γ) in vitro. Then the apoptotic rate of NIT-1 cells was determined by Hoechest33342 staining and Annexin V-FITC/PI flow cytometry. The insulin secretion level of NIT-1 cells was measured by ELISA. The NIT-1 cells were treated with VitD(3) at the final concentrations of 10(-8) mol/L or underwent transient transfection with vitamin D receptor (VDR)-SiRNA., Results: After the treatment of VitD(3), the apoptotic rate of NIT-1 cells decreased to 39.7%. There were significant differences in apoptotic rate between the VitD(3) treatment and IL-1β/IFN-γ groups (68.4%) (P < 0.01). Similarly impaired glucose-stimulated insulin secretion (GSIS) of NIT-1 cells recovered ((7.34 ± 0.21) ng/ml) after the treatment of VitD(3) as compared with the IL-1β/IFN-γ group ((4.88 ± 0.32) ng/ml, P < 0.01). Moreover, most of the protective effects of VitD(3) on pancreatic β-cells could be blocked by the transfection of VDR-SiRNA., Conclusion: VitD(3) may protect pancreatic β-cells from cytokine-induced apoptosis and impaired insulin secretion through its conjugation with VDR.

The levels and congener patterns of 28 PCBs compounds were investigated in soil and dust fallout collected in a capacitor storage site and an industrial brownfield, respectively in Sichuan Ziyang Locomotive Factory. The highest concentration of the total PCBs(sigma PCBs =227 502 ng x g(-1)) was found in soil collected from the front gate (unsealed) of the capacitor storage tunnel. Very high levels of sigma PCBs, exceed 10 microg x g(-1), were also found in the dust collected from the window sill of an iron foundry. There were significant positive correlations (P < 0.01) among PCB congener concentration in the storage site and the iron foundry samples. The major contribution to the total content of PCBs in the high contaminated samples was tetrachlorinated biphenyls, followed by tri- and penta-chlorinated biphenyls. Hexa- and higher chlorinated biphenyls contributed more to sigma PCBs in the iron foundry than those in the storage site. The total toxicity equivalents (TEQ) of 12 dioxin-like congeners varied in the range of 75.43-24 027 pg x g(-1) and were much higher than those in soils of e-waste recycling sites. However, PCB126 contribute the most to the TEQ in most cases.

During the period from August 10, 2010 through August 14, 2010, particle and gas phase PAHs were collected and analyzed using double filters plus PUFs (Poly Urethane Foam) sampling system, and the uncertainties of gas/particle partitioning coefficients of PAHs were investigated using the propagation of errors formulas. The results showed that low-molecular weight PAHs such as naphthalene, acenaphthylene, acenaphthene and fluorene possessed the strong breakthrough capacity with the breakthrough rates close to 50% in double PUF cartridges. The corrected K(p) values based on the sorption of PAHs to the primary filter were more than an order of magnitude higher than those without sorption correction for naphthalene, acenaphthylene and acenaphthene. The uncertainties for all the 19 PAHs ranged from 28.14% to 50.37% based on the standard error propagation formulas, with higher values for volatile and involatile PAHs and lower values for semi-volatile PAHs. The results also showed that the uncertainties of K(p) were mainly contributed from the measurements of particle (average variance contribution was 77.9%) and gas (average variance contribution was 22.0%) phase PAHs while the contributions of total suspended particle were ignorable. Thus, getting more accurate data for gaseous PAHs using an appropriate sampling system is the key to increase the accuracy of gas/particle partitioning coefficients of PAHs.

Objective: To investigate the protective effects of glitazones on islet beta cells and PPAR gamma dependence of such effects., Methods: IL-1beta and IFN-gamma were used to treat NIT-1 cells, a beta cell line, to induce beta cell damage. The cells were pretreated with rosiglitazone and pioglitazone at different concentrations to study the protective effects of these drugs. The cell apoptosis rate was determined with Annexin V-FITC by flow cytometry, and the insulin secretion capacity of the cells was assessed with ELISA. GW9662 and PPARgamma-SiRNA were used to specifically inhibit PPAR to investigate the PPAR gamma-dependent mechanisms., Results: Rosiglitazone and pioglitazone at 10 micromol/L could significantly decrease the apoptosis of beta cells induced by the cytokines (apoptotic rates of 13.99% and 16.67% vs 51.33%, P<0.01). Rosiglitazone at 10 micromol/L and pioglitazone at 20 micromol/L were less effective than 10 micromol/L rosiglitazone and pioglitazone. The insulin secretion of the cytokine-treated cells decreased from 8.5-/+0.6 ng/ml of the control group to 3.6-/+0.5 ng/ml, while rosiglitazone and pioglitazone could increase the insulin secretion to 6.8-/+0.7 ng/ml and 5.9-/+0.9 ng/ml, respectively. When PPAR gamma was specifically inhibited by GW9662 and PPARgamma-SiRNA, the protective effects of rosiglitazone and pioglitazone were almost undetectable, and the apoptotic rate increased and insulin secretion decreased to the level of the cytokine-treated cells., Conclusion: Glitazones can protect beta cells from apoptosis and impairment of insulin secretion function resulting from the cytotoxic cytokines via a PPAR gamma-dependent mechanism.

Objectives: To explore the effect of transient continuous subcutaneous insulin infusion (CSII) on ß cell function, insulin resistance and vascular endothelial injury in newly diagnosed type 2 diabetic patients and its potential mechanism., Methods: Ten patients with newly diagnosed type 2 diabetes mellitus (T2DM) accepted CSII for two weeks. Intravenous glucose tolerance test (IVGTT) and hyperinsulinemia euglycemia clamp test were performed before and after CSII. Serum soluble E-selectin (sE-selectin) was used to evaluate the injury of vascular endothelial cell, while serum high sensitivity C reactive protein (hsCRP) and soluble CD₁₄ (sCD₁₄) were both used to assess inflammatory condition., Results: (1) Compared with those before treatment, the blood glucose levels of IVGTT, the area under the curve of the blood glucose, glycosylated hemoglobin, TC and LDL-C in the patients were decreased after CSII (P < 0.05 or 0.01). (2) Compared with those before treatment, the insulin levels of IVGTT (except the fasting insulin), the area under the curve of insulin and acute insulin response were all increased after CSII (P < 0.05 or 0.01). (3) Compared with that before treatment, the glucose infusion ratio in the clamp test [(3.46 ± 1.66) mg x kg⁻¹ x min⁻¹ increased to (7.14 ± 2.37) mg x kg⁻¹ x min⁻¹] and HOMA-beta elevated, while HOMA-IR declined (P < 0.05 or 0.01 in all). (4) Compared with those before treatment, the levels of serum sE-selectin, sCD₁₄ and hsCRP were decreased (P < 0.01, except for hsCRP)., Conclusion: Transient intensive insulin therapy in patients with newly diagnosed T2DM is useful to restore beta cell function, attenuate insulin resistance, repair vascular endothelial injury and improve the disorder of blood sugar and lipid. The mechanism may be related with the inhibition of inflammation in patients.

Objective: To investigate the protective effects and potential mechanisms of TZD upon pancreatic beta-cells., Methods: Apoptosis was induced in vitro by interleukin-1beta (IL-1beta) and interferon-gamma (IFN-gamma). After treatment with rosiglitazone (RSG)/pioglitazone (PIG) at the final concentrations of 1 micromol/L, 10 micromol/L, 20 micromol/L respectively, the apoptotic rate of NIT-1 cells was determined by Hoechest33342 staining and Annexin V-FITC/PI flow cytometry respectively. Caspase-3 specific activity of NIT-1 cells was determined by Caspase-3 assay and insulin secretion measured by ELISA., Results: After treatment of different concentrations of RSG/PIG, the apoptotic rate of NIT-1 cells decreased to 29.3%, 14.0%, 28.1% and 27.4%, 16.7%, 23.5% respectively. There were significant differences in apoptotic rate between the RSG/PIG treatment group and IL-1beta/IFN-gamma group (P < 0.01). After treatment with RSG/PIG, glucose-stimulated insulin secretion (GSIS) of NIT-1 cells recovered in different degrees [(6.8 +/- 0.7) ng/ml, (5.9 +/- 0.9) ng/ml, P < 0.01]. There were significant differences in GSIS between the RSG/PIG treatment group and IL-1beta/IFN-gamma group (P < 0.01). Moreover, most of the protective effects of TZD upon pancreatic beta-cells could be blocked by a PPAR-gamma inhibitor, GW9662., Conclusion: TZD might protect pancreatic beta-cells directly via inhibiting cytokine-induced apoptosis and recovering insulin secretion. And the mechanism may be correlated with the down-regulation of caspase-3 activity.