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The objective of this study was to assess whether vitamin D (VD) treatment alters the overall all-cause and cardiovascular mortalities in a chronic kidney disease (CKD) population. We systematically searched PubMed, EMBASE, Web of Science, and Cochrane Central Register of Controlled Trials without language restriction, until the publication date of 22 February 2016. All related literatures that compared VD treatment with non-VD treatment and reported the mortality of patients with CKD (including those undergoing dialysis) were identified. Pooled risk ratios (RR) and 95% confidence intervals (CI) were calculated by using the random- and fixed-effects models. Randomised controlled trials (RCTs) that used the intention-to-treat principle and observational studies (OSs) were analysed separately. For this study, 38 studies involving 223 429 patients (17 RCTs, n=1819 and 21 OSs, n=221610) were included. In the OSs, VD treatment was significantly associated with reductions in both all-cause and cardiovascular mortalities; however, such significant association was not found in the RCTs. The existing RCTs do not provide sufficient or precise evidence that VD supplementation affects the mortality of patients with CKD, although subsets of patients that could potentially benefit from VD treatment can be identified by using the existing data from the RCTs. Nevertheless, large-size RCTs are needed in the future to assess any potential differences in survival prospectively., Author(s): R J Lu [sup.1] , S M Zhu [sup.1] , F L Tang [sup.1] , X S Zhu [sup.2] , Z D Fan [sup.1] , G L Wang [sup.2] [...]

The PbPd1 − xNixO2 nanograin films with different Ni-doping levels (x = 0.037–0.150) were synthesized by the sol–gel spin-coating method and an oxidation treatment. The films with a thickness of about 210 nm were found to be single phase with a body-centered orthorhombic structure and to possess a large number of Pb vacancies. High-temperature ferromagnetism discovered in these films can be maintained above 380 K. Paramagnetism was also found in the films with high Ni-doping levels. The analysis on the XANES spectra and their first derivatives offered the evidences for the facts that the film’s ferromagnetism is intrinsic and the increase in the Pb valence from 2+ towards 4+, caused by the appearance of large amount of Pb vacancies and low electronegativity of Pb2+ ion, provides magnetic moments to the film’s magnetism. A carrier-mediated mechanism bridged to the bound magnetic polaron model based on the Pb vacancies, the doped Ni ions and the Pb ions with a valence higher than 2+ was adopted to interpret the origin of the magnetism within these PbPd1 − xNixO2 nanograin films. The variation of the specific area of the grain boundary was believed to have a great influence on the proportions of the film’s ferromagnetism and paramagnetism. [ABSTRACT FROM AUTHOR]

Objective: To evaluate the relationship between different indexes of weight variability and the risk of diabetic kidney disease (DKD) in patients with type 2 diabetes mellitus (T2DM). Methods: A retrospective cohort study. The clinical data of 2 180 T2DM patients without DKD who underwent case management at Lee's United Clinic in Taiwan, China from 2002 to 2018 were retrospectively analyzed, including 1 103 females and 1 077 males, with an average age of (64.8±12.4) years. Regular follow-up was conducted for patients for at least 2 years, and their metabolic indexes were monitored annually. BMI variability independent of the mean (BMI-VIM), average yearly mean square successive difference (BMI-ASV), coefficient of variation (BMI-CV) and standard deviation (BMI-SD) were calculated,based on the body mass index (BMI) recorded annually by the patients. Patients were divided into four groups ( Q 1 - Q 4 ) based on the quartiles of the four weight variability indexes. DKD group and non-DKN group(NDKD group) were defined based on the occurrence of DKD at the end of the follow-up. Cox proportional hazards regression models were used to analyze the relationship between the four weight variability indicators and the incidence of DKD. Subgroup analysis was performed by categorizing patients into non-obesity (BMI<28 kg/m 2 ) and obesity groups (BMI≥28 kg/m 2 ) to investigate the impact of the four weight variability indicators on the risk of DKD. Results: After a follow-up of (4.55±2.13) years, 904 patients developed DKD. Compared with the NDKD group, patients in the DKD group had a higher proportion of females, older age, longer duration of diabetes, more insulin users, higher waist-to-hip ratio, higher levels of BMI-VIM, BMI-ASV, BMI-CV, BMI-SD, systolic blood pressure, diastolic blood pressure, and urine albumin - creatinine ratio, a lower proportion of hypoglycemic drugs, estimated glomerular filtration rate, and high-density lipoprotein cholesterol level, with statistically significant differences between the two groups(all P <0.05). Cox proportional hazards regression analysis results revealed that the risk of DKD in T2DM patients increased with the increase in BMI-SD, BMI-CV, BMI-VIM, and BMI-ASV after correcting a series of influencing factors. In the BMI-VIM subgroup, compared with the Q 1 group, the risk of DKD in the Q 4 group increased by 22.4% [ HR =1.224 (95% CI :1.008-1.487), P =0.041]. In the BMI-ASV group, compared with the Q 1 group, the risk of DKD in the Q 4 group increased by 51.1% [ HR =1.511 (95% CI :1.240-1.841), P <0.01]. In the BMI-CV group, compared with the Q 1 group, the risk of DKD in the Q 4 group increased by 22.2% [ HR =1.222 (95% CI :1.006-1.485), P =0.044]. In the BMI-SD subgroup, compared with the Q 1 group, the risk of DKD in the Q 4 group increased by 22.2% [ HR =1.222 (95% CI :1.002-1.490), P =0.048]. Sub-group analysis showed that when the non-obesity group was grouped by BMI-ASV, after correcting a series of influencing factors, compared with the Q 1 group, the highest risk of DKD occurred in the Q 4 group [ HR =1.551 (95% CI :1.228-1.958), P <0.001];when the obesity group was grouped by BMI-ASV, after correcting a series of influencing factors, compared with the Q 1 group, the highest risk of DKD occurred in the Q 4 group [ HR =1.703 (95% CI :1.168-2.485), P =0.006]. Conclusion: Increases in BMI-VIM, BMI-ASV, BMI-CV, and BMI-SD are associated with an increased risk of DKD in T2DM patients.

Acrylonitrile in ambient air was collected by Tenax GC and then thermo-desorbed. It was separated on GDX-502 chromatographic column from other pollutants and determined by flame-ion ization detector. The minimum detectable concentration was 0.01 mg/m3 when 2 L ambient air was collected. The recoveries were 85.6%-105.4% and RSDs were 4.5%-6.2%.

Objective: To assess the ability of T cells from patients with systemic lupus erythematosus (SLE) to respond to a mitogenic combination of anti-CD2 monoclonal antibodies (MAb), and to learn the molecular basis of the documented defect., Methods: Peripheral blood mononuclear cell (PBMC) populations from individuals with SLE and paired controls were stimulated in vitro with anti-CD2, and the proliferative response was compared with that evoked by stimulation with phytohemagglutinin (PHA) and anti-CD3. Surface markers on lymphocyte populations were assessed by flow cytometry after staining with specific MAb., Results: The proliferative response to anti-CD2 was decreased to a greater extent than was the response to anti-CD3 or PHA in SLE patients. This defect was found in approximately one-half of the patients examined, was not associated with disease activity, and was maintained upon repeated testing. Since either monocytes or resting B cells can serve as accessory cells for T cells following activation by anti-CD2, we examined the T cell response after depletion of adherent cells. In approximately two-thirds of the individuals with a decreased response, depletion of monocytes or substitution of monocytes with allogeneic, resting B cells from normal donors corrected the defect. The addition to PBMC of anti-CD28, but not of a neutralizing antibody to interleukin-10, largely reversed the anti-CD2 proliferative defect. Significantly fewer CD8+ T cells expressed CD28 in SLE, and this defect was also documented, to a lesser extent, in CD4+ cells., Conclusion: This study provides evidence that some functional T cell defects in SLE may be due, at least in part, to decreased CD28-mediated costimulatory activity following the interaction of T cells with conventional accessory cells.

11192U90 was submitted to receptor binding and monoamine uptake assays. It bound potently at serotonin 5-HT2, dopaminergic D2, serotonin 5-HT1A, and adrenergic alpha 1 and alpha 2 receptors. It also bound to dopaminergic D1, serotonin 5-HT3, serotonin 5-HT4, and sigma sites, albeit with lower affinity. It was essentially inactive at 22 other sites, including those for cholinergic M1 and M2. It weakly inhibited uptake of 3H-norepinephrine, 3H-serotonin and 3H-dopamine. Acute doses of 1192U90 (5 and 20 mg/kg P.O.) increased whole-brain levels of dopamine metabolites but did not affect levels of norepinephrine, dopamine, and serotonin. Subcutaneous injection of 1192U90 (0.8 mg/kg/day) and clozapine (20 mg/kg/day) for 28 days preferentially decreased the number of spontaneously active dopamine cells in the ventral tegmental area (VTA) but not the substantia nigra (SN) of rats, as measured by population sampling. This outcome is characteristics of atypical antipsychotics like clozapine. Acute injections of 1192U90 reversed the rate-inhibiting effects of microiontophoretically applied dopamine and intravenously injected apomorphine and d-amphetamine on dopamine cell firing. Intravenous injection or iontophoretic application of 1192U90 or the 5-HT1A agonist (+/-)8-OH-DPAT inhibited the firing rates of dorsal raphe nucleus (DRN) neurons in rats, and the effects of both compounds were blocked by iontophoretically applied S(-) propranolol, a 5-HT1A antagonist. The results suggest that 1192U90 is a preferential dopamine D2 antagonist as well as a 5-HT1A agonist that may prove to be an atypical antipsychotic.

PBMC proliferation in patients with SLE was assessed by incorporation of 3H-Tdr in an accessory cell-dependent response to anti-CD2 specific monoclonal antibody. The response was compared to monoclonal anti-CD3 and PHA response. There was a marked decrease in the response to anti-CD2 in SLE patients (9257 +/- 8543) than in normal controls (20619 +/- 15279) (P < 0.005). It was more obvious in 8 patients with less active and untreated disease, but not in 10 patients with less active or inactive disease. In contrast, no statistical difference was noted in the response to anti-CD3 and PHA between SLE patients and normal controls. We also examined the response of purified T cells to anti-CD2 and the response was depressed in SLE, but no marked decrease in the response to anti-CD3 was found in SLE patients. Our results demonstrate that SLE patients with active disease have T cells that respond poorly to CD2 activation, but that response via the CD3/TCR complex is essentially intact. It might be reflect intrinsic T cell defects in some SLE patients.

The American Rheumatism Association (ARA) 1958 and 1987 criteria for the classification of rheumatoid arthritis (RA) were applied to 111 consecutive RA patients and 54 patients with non-RA connective tissue diseases from three hospitals of tertiary level in Beijing. Comparison of the two criteria showed that the specificity was the same, being 88% for both, whereas the sensitivity varied from 94% of the 1958 criteria to 91% of the 1987 criteria. Factors affecting the sensitivity were morning stiffness for more than one hour and increase of number of swollen joints from one to three in the 1987 revised criteria.

Biochemical studies have shown that the ability of erythrosine to inhibit dopamine uptake into brain synaptosomal preparations is dependent on the concentration of tissue present in the assay mixture. Thus, the finding that erythrosine inhibits dopamine uptake (which, if true, would provide a plausible explanation of the Feingold hypothesis of childhood hyperactivity) may simply be an artifact that results from nonspecific interactions with brain membranes. In addition, although erythrosine given parenterally (50 milligrams per kilogram) did not alter locomotor activity of control of 6-hydroxydopamine-treated rats, erythrosine (50 to 300 milligrams per kilogram) attenuated the effect of punishment in a "conflict" paradigm.