Photosystem II photochemistry and photosynthetic pigment composition in salt-adapted halophyte Artimisia anethifolia grown under outdoor conditions

The effects of high salinity (0-400 mmol/L NaCl) on photosystem II (PSII) photochemistry and photosynthetic pigment composition were investigated in the halophyte Artimisia anethifolia grown under outdoor conditions and exposed to full sunlight. High salinity resulted in an inhibition in plant growth and a significant accumulation of sodium and chloride in leaves. However, high salinity induced no effects on the actual PSII efficiency, the efficiency of excitation energy capture by open PSII reaction centres, photochemical quenching, and non-photochemical quenching at midday. High salinity also induced neither changes in the maximum efficiency of PSII photochemistry, the efficiency with which a trapped exciton can move an electron into the electron transport chain further than QA and the quantum yield of electron transport beyond QA, nor changes in absorption, trapping and electron transport fluxes per PSII reaction centre. No significant changes were observed in the levels of neoxanthin, lutein, beta-carotene, violaxanthin, antheraxanthin, and zeaxanthin expressed on a total chlorophyll basis in salt-adapted plants. Our results suggest that Artimisia anethifolia showed high resistance not only to high salinity, but also to photoinhibition even if it was treated with high salinity as high as 400 mmol/L NaCl and exposed to full sunlight. The results indicate that tolerance of PSII to high salinity and photoinhibition can be viewed as an important strategy for Artimisia anethifolia, a halophyte plant, to grow in very high saline soil.     

p38-MAPK signaling pathway is not involved in osteogenic differentiation during early response of mesenchymal stem cells to continuous mechanical strain

Quercetin has been reported to protect testicular cells from oxidative damage induced by environmental chemicals. In this study, we isolated interstitial Leydig cells (ILCs) from immature rats, set-up ILCs culture, co-treated cells with atrazine (ATZ) and quercetin (QT), evaluated toxicity, and measured the expression levels of antioxidant enzymes and nuclear factor-kappaB (NF-κB) and levels of steroidogenic enzymes. ATZ decreased ILCs viability at concentrations higher than 10 μg/mL and increased reactive oxygen species, malondialdehyde (MDA), and glutathione levels. ATZ also increased glutathione peroxidase, glutathione reductase, and glutathione-S-transferase and decreased superoxide dismutase-1 (sod1) and superoxide dismutase-2 (sod2) messenger RNA (mRNA) levels which were prevented by QT. The changes in the MDA levels and lactate dehydrogenase leakage induced by ATZ (50 μg/mL) were also prevented on co-treatment with QT (50 μM). Furthermore, ATZ-induced 3β- and 17β-hydroxysteroid dehydrogenase activities and NF-κB-expressions at the mRNA and protein levels were also recovered to control value on co-treatment with QT. These data showed that QT protected against ATZ-induced ILCs toxicity by restoring the expression of NF-κB and steroidogenic activity and by preventing the oxidative stress.     

Functional Nucleic Acid Nanoparticle-Based Resonance Scattering Spectral Probe

Highly sensitive and selective resonance Rayleigh scattering (RRS) and surface enhanced resonance Raman scattering (SERRS) spectral detection technique are developed by combining the functional nucleic acid including aptamer and DNAzyme, and nanoparticle such as gold/silver (NG/NS) aggregation and catalysis reaction. The recent progress of resonance scattering spectral technologies including RRS and SERRS are reviewed in this paper.     

The association between CD14 gene C-260T polymorphism and coronary heart disease risk: a meta-analysis

Monocyte differentiation antigen CD14 is considered an important cell-activating mediator of inflammatory responses that may result in atherosclerosis, coronary heart disease (CHD), thrombus formation, and myocardial infarction (MI). A common C-260T polymorphism in the promoter of the CD14 gene, the trans-membrane receptor of lipopolysaccharides, has been inconsistently associated with CHD. To investigate this inconsistency, we performed a meta-analysis of 28 studies involving a total of 13,335 CHD cases and 7,979 controls for C-260T of the CD14 gene to evaluate the effect of CD14 on genetic susceptibility for CHD. An overall random effects odds ratio of 1.24 (95 % CI: 1.12–1.36, P < 10^?5) was found for T allele. Significant results were also observed using dominant (OR = 1.34, 95 % CI: 1.17–1.54, P < 10^?4) or recessive genetic model (OR = 1.25, 95 % CI: 1.10–1.41, P = 0.0004). There was strong evidence of heterogeneity (P < 10^?5), which largely disappeared after stratification by ethnicity. After stratified by ethnicity, significant results were found in East Asians; whereas no significant associations were found among Caucasians and other ethnic populations in all genetic models. In the stratified analysis according to sample size, CHD endpoints, and HWE status, significantly increased risks for the polymorphism were found in all genetic models. In conclusion, our results indicate that the CD14 C-260T polymorphism is a risk factor of CHD, especially in East Asians. However, additional very large-scale studies are warranted to confirm our results.     

Expression,purification and functional characterization of a recombinant scorpion venom peptide BmTXKbeta

BmTXKbeta, a scorpion toxin isolated from the Chinese scorpion Buthus martensii Karsch (BmK), was expressed as a GST fusion protein in BL21 (DE3) strain. The recombinant GST-BmTXKbeta protein was purified by affinity chromatography. When treated with enterokinase, the GST-BmTXKbeta fusion protein released an approximate 6.5kDa protein which was the expected size for correctly processed. About 2mg purified recombinant BmTXKbeta protein (rBmTXKbeta) was produced from 1l bacterial culture, using this expression and purification system. The function of rBmTXKbeta was studied on the rabbit atrial myocyte by whole-cell patch clamp technique. The results showed that rBmTXKbeta inhibited the transient outward current (I(to)) of rabbit atrial myocyte with recovery after washout and the inhibition was concentration-dependent. The rBmTXKbeta prolonged the action potential duration of rabbit atrial myocyte in a concentration-dependent manner, whereas it did not affect the action potential amplitude.     

Powering DNA repair through substrate electrostatic interactions

The reaction catalyzed by the DNA repair enzyme uracil DNA glycosylase (UDG) proceeds through an unprecedented stepwise mechanism involving a positively charged oxacarbenium ion sugar and uracil anion leaving group. Here we use a novel approach to evaluate the catalytic contribution of electrostatic interactions between four essential phosphodiester groups of the DNA substrate and the cationic transition state. Our strategy was to substitute each of these phosphate groups with an uncharged (R)- or (S)-methylphosphonate linkage (MeP). We then compared the damaging effects of these methylphosphonate substitutions on catalysis with their damaging effects on binding of a cationic 1-azadeoxyribose (1-aza-dR(+)) oxacarbenium ion analogue to the UDG-uracil anion binary complex. A plot of log k(cat)/K(m) for the series of MeP-substituted substrates against log K(D) for binding of the 1-aza-dR(+) inhibitors gives a linear correlation of unit slope, confirming that the electronic features of the transition state resemble that of the 1-aza-dR(+), and that the anionic backbone of DNA is used in transition state stabilization. We estimate that all of the combined phosphodiester interactions with the substrate contribute 6-8 kcal/mol toward lowering the activation barrier, a stabilization that is significant compared to the 16 kcal/mol catalytic power of UDG. However, unlike groups of the enzyme that selectively stabilize the charged transition state by an estimated 7 kcal/mol, these phosphodiester groups also interact strongly in the ground state. To our knowledge, these results provide the first experimental evidence for electrostatic stabilization of a charged enzymatic transition state and intermediate using the anionic backbone of DNA.     

Cutting edge: bacterial lipoprotein induces endotoxin-independent tolerance to septic shock

Tolerance to bacterial cell wall components is an adaptive host response. Endotoxin/LPS tolerance is characterized by a survival advantage against subsequent lethal LPS challenge. However, it is uncertain whether LPS tolerance can afford protection against other septic challenges. In this study, we show that tolerance induced by bacterial lipoprotein (BLP) protects mice against not only BLP-induced lethality, but also LPS-, live bacteria-, and polymicrobial sepsis-induced lethality. In contrast, LPS tolerance offers no survival benefit against the latter two challenges. Furthermore, induction of BLP tolerance results in overexpression of complement receptor type 3 and FcgammaIII/IIR on neutrophils (polymorphonuclear neutrophils) and peritoneal macrophages, with increased bacterial recognition and bactericidal activity, whereas LPS-tolerized mice exhibit an impaired ability to ingest and to kill bacteria. These results indicate that BLP tolerance is a novel adaptive host response associated with a unique protective effect during septic shock.     

增强蛋白与多角体蛋白共包埋的研究

颗粒体病毒的增强蛋白（enhancin)是一种能显著提高核型多角体病毒（NPV）对昆虫感染力的病毒蛋白。构建了一种不形成多角体但表达粉纹夜蛾颗粒体病毒增强蛋白的重组病毒AcBBH-TnEn,将它与野生型AcMNPV共同感染SF21细胞,经SDS－PAGE、免疫印迹分析、荧光免疫等方法检测证实,增强蛋白与多角体可在同一细胞中同时表达,而且发现所形成的病毒多角体带有增强蛋白。这表明,可以通过混合感染的方式生产带有增强蛋白的病毒多角体。     

Dose-dependent metabolic response of mammary carcinoma to photodynamic therapy

The metabolic response of mammary carcinoma in the C3H mouse to photodynamic therapy (PDT) was measured using in vivo 31P nuclear magnetic resonance (31P-NMR) spectroscopy and pH microelectrodes. Twenty-four hours after administration of Photofrin II (12.5 mg/kg), the tumor was subjected to photoactivation using an argon dye laser. Optical treatment doses were 200, 400, and 600 J/cm2 and corresponded to the following tumor control doses: TCD10/30, TCD50/30, and TCD90/30, respectively. In vivo 31P-NMR spectra and pH micro-electrode measurements were obtained prior to treatment and at 4, 24, 48, and 72 h and 1 week post-treatment. The data revealed a significant (P less than 0.0002) alkalosis as indicated by the pH measured by NMR compared to pH measured by microelectrodes at all treatment levels and time points. Spectral differences between treatment groups were apparent as early as 4 h after treatment. The ratio of beta-nucleoside triphosphate to inorganic phosphate at 4 h after treatment was significantly (P less than 0.01) smaller for 600 J/cm2 treatment than for 200 J/cm2 treatment. At curative (600 J/cm2) levels, from 48 h on, no phosphate resonances were detected in the spectra. The pH measured by NMR transiently decreased from pretreatment levels after 200 and 400 J/cm2 treatment (P less than 0.002, P less than 0.009, respectively), while no change in pH from pretreatment values was found after 600 J/cm2 treatment. The data suggest that the early metabolic response of mammary carcinoma to PDT, as indicated by 31P-NMR spectroscopy, is dose dependent, and may be a sensitive indicator of biological outcome to treatment.     

MiR‐616‐3p modulates cell proliferation and migration through targeting tissue factor pathway inhibitor 2 in preeclampsia

Objectives

Despite improvements in diagnosis and treatment, preeclampsia (PE) continues to pose a significant risk of maternal and foetal morbidity and mortality if not addressed promptly. An increasing number of studies have suggested that tissue factor pathway inhibitor 2 (TFPI2) acts as a suppressor gene, possibly inhibiting multiple serine proteases affecting cell proliferation and migration. It plays an essential role in the occurrence and development of PE, but the pathogenesis remains unclear.

Materials and methods

In our research, we performed western blotting, immunohistochemistry and qPCR assays to investigate TFPI2 and miR‐616‐3p expression in preeclamptic placental tissues. Cell assays were performed in HTR‐8/SVneo and JEG3 cell lines. Cell proliferation and migration events were investigated by MTT, EdU and transwell assays. In conjunction with bioinformatics analysis, luciferase reporter assays were performed to elucidate the mechanism by which miR‐616‐3p binds to TFPI2 mRNA.

Results

We established that TFPI2 protein levels were significantly upregulated in PE placental tissues. In addition, we found that miR‐616‐3p binds specifically to the 3′‐UTR region of TFPI2 mRNA. Furthermore, miR‐616‐3p knockdown or TFPI2 overexpression substantially impaired cell growth and migration, whereas miR‐616‐3p upregulation or TFPI2 knockdown stimulated cell proliferation and migration. This miR‐616‐3p / TFPI2 axis was also found to affect the epithelial‐mesenchymal transition process in PE.

Conclusions

Our results demonstrated that TFPI2 plays a vital role in the progression of PE and might provide a prospective therapeutic strategy to mitigate the severity of the disorder.