The PBDE-209 Exposure during Pregnancy and Lactation Impairs Immune Function in Rats

In the present study, we assessed the treatment effects of PBDE-209 administration on the immune function in rats during pregnancy and lactation. We harvested the blood and organs for flow cytometry, viability assay, enzyme-linked immunosorbent assay, and histological evaluation. The results of this study were the PBDE-209 exposure during pregnancy and lactation impairs immune function in rats. The results may contribute to understanding the mechanism of PBDE-209 in immune function

Mitigating heat-related mortality risk in Shanghai, China: system dynamics modeling simulations

Numerous studies in epidemiology, meteorology, and climate change research have demonstrated a significant association between abnormal ambient temperature and mortality. However, there is a shortage of research attention to a systematic assessment of potential mitigation measures which could effectively reduce the heat-related morbidity and mortality risks. This study first illustrates a conceptualization of a systems analysis version of urban framework for climate service (UFCS). It then constructs a system dynamics (SD) model for the UFCS and employs this model to quantify the impacts of heat waves on public health system in Shanghai and to evaluate the performances of two mitigation measures in the context of a real heat wave event in July 2013 in the city. Simulation results show that in comparison with the baseline without mitigation measures, if the hospital system could prepare 20% of beds available for emergency response to heat waves once receiving the warning in advance, the number of daily deaths could be reduced by 40–60 (15.8–19.5%) on the 2 days of day 7 and day 8; if increasing the minimum living allowance of 790 RMB/month in 2013 by 20%, the number of daily deaths could be reduced by 50–70 (17.7–21.9%) on the 2 days of day 8 and day 12. This tool can help policy makers systematically evaluate adaptation and mitigation options based on performance assessment, thus strengthening urban resilience to changing climate

Role of dexmedetomidine in IL-4 and IFN-γ expression in rats with multiple organ dysfunction syndrome induced by postpartum bleeding

Bleeding-induced multiple organ dysfunction syndrome (MODS) is one of the major causes of death in pregnant women. MODS is thought to result from an inappropriate generalized host inflammatory response to a variety of acute insults. In this study we established a MODS model in postpartum rats, in which MODS was induced by the combination of induced hypotension for 60 min and clamping of the superior mesenteric artery for a period of 40 min. We sacrificed all the rats 24 h after dexmedetomidine (DEX) treatment. Thymus, spleen, and mesenteric lymph node tissue were collected to detect interferon-γ (IFN-γ) and interleukin-4 (IL-4) protein expression; lung and intestine tissue were collected to measure IFN-γ and IL-4 gene expression. In the present study, IFN-γ and IL-4 mRNA were increased in the lungs and intestines of the MODS rats. DEX administration decreased IFN-γ and IL-4 mRNA expression. IFN-γ and IL-4 expression for the thymus, spleen, and mesenteric lymph nodes were higher in the MODS postpartum rats relative to control rats, and these expression levels decreased upon DEX administration, But there were no significant differences between DEX doses. In conclusion DEX administration appeared to reduce IFN-γ and IL-4 protein expression in thymus, spleen, and mesenteric lymph node tissue and reduce IFN-γ and IL-4 gene expression in the lungs and intestines in the MODS postpartum rats but was not dose-dependent

Dexmedetomidine Reduced Cytokine Release during Postpartum Bleeding-Induced Multiple Organ Dysfunction Syndrome in Rats

Dexmedetomidine (DEX) is an α2-adrenergic agonist. It decreases the levels of norepinephrine release, resulting in a reduction of postsynaptic adrenergic activity. In the present study, the effects of DEX on postpartum bleeding-induced multiple organ dysfunction syndrome (BMODS) were studied in rats in which BMODS was induced by the combination of hypotension and clamping of the superior mesenteric artery. We evaluated the role of dexmedetomidine (DEX) in cytokine release during postpartum BMODS in rats. In summary, the present study demonstrated that DEX administration reduced IFN-r and IL-4 release and decreased lung injury during postpartum BMODS. It is possible that DEX administration decreased inflammatory cytokine production in BMODS by inhibiting inflammation and free radical release by leukocytes independent of the DEX dose

Application of Quadratic Rotation-Orthogonal Composite Experimental Design to Assess the Relationship between Growth Environment and Ultraweak Luminescence of Mint

International audienceQuadratic rotation-orthogonal composite experimental design was applied in this experiment to obtain the ultraweak luminescence property of mint affected by multilateral growth environmental factors including illumination, temperature, humidity, and moisture. The influence models of four factors on luminescence were established. Analysis showed that different factors and their interactions had different effect on luminous value, among which the interaction of illumination and humidity had the most significant influence on luminescence of mint (p ≤ 0.01). And the maximum luminous value was obtained when ten stick of lamp tube (intensity of illumination value 4229 Lx) was used, mean temperature, humidity and water were 35 ℃, 85% and 90 mL/d respectively. On the base of that, linear effects and their interactions that affected ultraweak luminescence were also studied

Synthesis and Cytotoxic Evaluation of Steroidal Copper (Cu (II)) Complexes

Using estrone and pregnenolone as starting materials, some steroidal copper complexes were synthesized by the condensation of steroidal ketones with thiosemicarbazide or diazanyl pyridine and then complexation of steroidal thiosemicarbazones or steroidal diazanyl pyridines with Cu (II). The complexes were characterized by IR, NMR, and HRMS. The synthesized compounds were screened for their cytotoxicity against HeLa, Bel-7404, and 293T cell lines in vitro. The results show that all steroidal copper (II) complexes display obvious antiproliferative activity against the tested cancer cells. The IC50 values of complexes 5 and 12 against Bel-7404 (human liver carcinoma) are 5.0 and 7.0 μM

Characterization of the complete chloroplast genome sequence of Vicia costata (Fabaceae) and its phylogenetic implications

Vicia costata Ledeb. is a fine leguminous pasture which has advantages of drought resistance and barren tolerance. In this study, the complete chloroplast (cp) genome of V. costata was assembled and annotated. The total genome size of V. costata was 134,184 bp in length with IR loss. The cp genome encoded a set of 112 genes, containing 74 protein-coding genes, 34 tRNA genes, and 4 rRNA genes. The overall GC content was 34.82%. Phylogenetic analysis showed that V. costata got together with the same genus species V. ramuliflora, V. bungei, V. faba, V. sativa and V. sepium with high support value, and V. costata had a close relationship with V. ramuliflora. The whole cp genome of V. costata will be a useful resource for future studies on phylogeny and conservation in Vicia

Triptolide Prevents Bone Destruction in the Collagen-Induced Arthritis Model of Rheumatoid Arthritis by Targeting RANKL/RANK/OPG Signal Pathway

Focal bone destruction within inflamed joints is the most specific hallmark of rheumatoid arthritis (RA). Our previous study indicated that the therapeutic efficiency of triptolide in RA may be due partially to its chondroprotective and anti-inflammatory effects. However, its roles in bone destruction are still unclear. In this study, our data firstly showed the therapeutic effects of triptolide on severity of arthritis and arthritis progression in collagen-induced arthritis (CIA) mice. Then, by micro-CT quantification, triptolide treatment significantly increased bone mineral density, bone volume fraction, and trabecular thickness and decreased trabecular separation of inflamed joints. Interestingly, triptolide treatment could prevent the bone destruction by reducing the number of osteoclasts in inflamed joints, reducing the expression of receptor activator of NF-κB (RANK) ligand (RANKL) and RANK, increasing the expression of osteoprotegerin (OPG), at both mRNA and protein levels, and decreasing the ratio of RANKL to OPG in sera and inflamed joints of CIA mice, which were further confirmed in the coculture system of human fibroblast-like synovial and peripheral blood mononuclear cells. These findings offer the convincing evidence for the first time that triptolide may attenuate RA partially by preventing the bone destruction and inhibit osteoclast formation by regulating RANKL/RANK/OPG signal pathway

A long noncoding RNA distributed in both nucleus and cytoplasm operates in the PYCARD-regulated apoptosis by coordinating the epigenetic and translational regulation.

Long noncoding RNAs (lncRNAs) participate in various biological processes such as apoptosis. The function of lncRNAs is closely correlated with their localization within the cell. While regulatory potential of many lncRNAs has been revealed at specific subcellular location, the biological significance of discrete distribution of an lncRNA in different cellular compartments remains largely unexplored. Here, we identified an lncRNA antisense to the pro-apoptotic gene PYCARD, named PYCARD-AS1, which exhibits a dual nuclear and cytoplasmic distribution and is required for the PYCARD silencing in breast cancer cells. The PYCARD-regulated apoptosis is controlled by PYCARD-AS1; moreover, PYCARD-AS1 regulates apoptosis in a PYCARD-dependent manner, indicating that PYCARD is a critical downstream target of PYCARD-AS1. Mechanistically, PYCARD-AS1 can localize to the PYCARD promoter, where it facilitates DNA methylation and H3K9me2 modification by recruiting the chromatin-suppressor proteins DNMT1 and G9a. Moreover, PYCARD-AS1 and PYCARD mRNA can interact with each other via their 5' overlapping region, leading to inhibition of ribosome assembly in the cytoplasm for PYCARD translation. This study reveals a mechanism whereby an lncRNA works at different cellular compartments to regulate the pro-apoptotic gene PYCARD at both the epigenetic and translational levels, contributing to the PYCARD-regulated apoptosis, and also sheds new light on the role of discretely distributed lncRNAs in diverse biological processes