Inverse gradients in leaf wax δD and δ13C values along grass blades of Miscanthus sinensis: Implications for leaf wax reproduction and plant physiology

Compound specific hydrogen and carbon isotopic ratios of higher plant leaf waxes have been extensively used in paleoclimate and paleoenvironmental reconstructions. However, studies so far have focused on the comparison of leaf wax isotopic differences in bulk leaf samples between different plant species. We sampled three different varieties of tall grasses (Miscanthus sinensis) in six segments from base to tip and determined hydrogen and carbon isotopic ratios of leaf waxes, as well as hydrogen and oxygen isotopic ratios of leaf water samples. We found an increasing, base-to-tip hydrogen isotopic gradient along the grass blades that can probably be attributed to active leaf wax regeneration over the growth season. Carbon isotopic ratios, on the other hand, show opposite trends to hydrogen isotopic ratios along the grass blades, which may reflect different photosynthetic efficiencies at different blade locales.     

The first Praesiricidae (Hymenoptera) from Northeast China

A new subfamily Rudisiricinae Gao, Rasnitsyn, Ren & Shih, n. subfam. and a new genus Rudisiricius Gao, Rasnitsyn, Ren & Shih, n. gen. with three new species R. belli Gao, Rasnitsyn, Ren & Shih n. sp., R. crassinodus Gao, Rasnitsyn, Ren & Shih, n. sp., and R. celsus Gao, Rasnitsyn, Ren & Shih, n. sp. are described and illustrated from the family Praesiricidae. The type specimens were collected from the Late Jurassic to Early Cretaceous Yixian Formation, northeastern China. The new subfamily also includes Aulidontes Rasnitsyn from the Upper Jurassic of Karatau in Kazakhstan. This is the first record of Praesiricidae in China. These well-preserved nearly-complete new fossils reported here provide additional material and structure characters about this family, which helps filling some gap in the evolution of Lower Hymenoptera.     

Influence of sucrose concentration and phosphate source on biomass and metabolite accumulation in adventitious roots of Pseudostellaria heterophylla

In this study, we investigated the induction of Pseudostellaria heterophylla adventitious root and the effects of sucrose concentration and phosphate source on biomass increase and metabolites accumulation. These roots were initially cultured in Murashige and Skoog medium for 4 weeks. IBA 3.0 mg L^?1 proved to be the best auxin for inducing adventitious roots and the frequency of adventitious roots induced from roots (100 %) was higher than that from leaves (78 %) and stems (27 %). The medium with 4 % sucrose resulted in the optimum biomass i.e. 1.04 g/flask DW, and the content of saponin and polysaccharides reached the peak i.e. 0.676 and 24.4 %, respectively. With regards to phosphate source, 1.25 mM phosphate concentration was more favorable for biomass of roots (0.87 g/flask of DW), whereas the optimum saponin (0.74 %) and polysaccharides (22.09 %) were achieved with 2.5 mM phosphate. However, the saponin content at 2.5 mM phosphate did not show significant difference from the saponin content at 0.625 mM (0.69 %) or 3.75 mM phosphate (0.69 %).     

9-Phenanthrol and flufenamic acid inhibit calcium oscillations in HL-1 mouse cardiomyocytes

It is well established that intracellular calcium ([Ca²⁺]_i) controls the inotropic state of the myocardium, and evidence mounts that a “Ca²⁺ clock” controls the chronotropic state of the heart. Recent findings describe a calcium-activated nonselective cation channel (NSC_Ca) in various cardiac preparations sharing hallmark characteristics of the transient receptor potential melastatin 4 (TRPM4). TRPM4 is functionally expressed throughout the heart and has been implicated as a NSC_Ca that mediates membrane depolarization. However, the functional significance of TRPM4 in regards to Ca²⁺ signaling and its effects on cellular excitability and pacemaker function remains inconclusive. Here, we show by Fura2 Ca-imaging that pharmacological inhibition of TRPM4 in HL-1 mouse cardiac myocytes by 9-phenanthrol (10 μM) and flufenamic acid (10 and 100 μM) decreases Ca²⁺ oscillations followed by an overall increase in [Ca²⁺]_i. The latter occurs also in HL-1 cells in Ca²⁺-free solution and after depletion of sarcoplasmic reticulum Ca²⁺ with thapsigargin (10 μM). These pharmacologic agents also depolarize HL-1 cell mitochondrial membrane potential. Furthermore, by on-cell voltage clamp we show that 9-phenanthrol reversibly inhibits membrane current; by fluorescence immunohistochemistry we demonstrate that HL-1 cells display punctate surface labeling with TRPM4 antibody; and by immunoblotting using this antibody we show these cells express a 130–150 kDa protein, as expected for TRPM4. We conclude that 9-phenanthrol inhibits TRPM4 ion channels in HL-1 cells, which in turn decreases Ca²⁺ oscillations followed by a compensatory increase in [Ca²⁺]_i from an intracellular store other than the sarcoplasmic reticulum. We speculate that the most likely source is the mitochondrion.     

Selenium Attenuates Adriamycin-Induced Cardiac Dysfunction via Restoring Expression of ATP-Sensitive Potassium Channels in Rats

The possible mechanism of adriamycin (ADR) and/or selenium (Se) deficiency-induced cardiac dysfunction, and cardioprotective effects of Se against ADR-induced cardiac toxicity were investigated in this study. Cardiac function was evaluated by plasma brain natriuretic peptide level and echocardiographic and hemodynamic parameters. Cardiac glutathione peroxidase (GPx) activity was assessed spectrophotometrically. Expression of ATP-sensitive potassium channels (K_ATP) subunits—SUR2A and Kir6.2—were examined by real-time PCR and Western blotting. The results showed that cardiac function and cardiac GPx activity decreased remarkably after administration of ADR or Se deficiency; more dramatic impairment of cardiac function and cardiac GPx activity were observed after co-administration of ADR and Se deficiency. Mechanically, it is novel for us to find down-regulation of K_ATP subunits gene expression in cardiac tissue after administration of ADR or Se deficiency, and more significant inhibition of cardiac K_ATP gene expression was identified after co-administration of ADR and Se deficiency. Furthermore, cardiac toxicity of ADR was found alleviated by Se supplementation, accompanied by restoring of cardiac GPx activity and cardiac K_ATP gene expression. These results indicate that decreased expression of cardiac K_ATP is involved in adriamycin and/or Se deficiency-induced cardiac dysfunction; Se deficiency exacerbates adriamycin-induced cardiac dysfunction by future inhibition of K_ATP expression; Se supplementation seems to protect against adriamycin-induced cardiac dysfunction via restoring K_ATP expression, showing potential clinical application in cancer chemotherapy.     

Selenoprotein P and Yunnan Endemic Sudden Cardiac Death—an Ecological Study

The aim of the present study was to explore the role of selenoprotein P (SePP) in the etiology of the endemic sudden cardiac death in Yunnan, China. The levels of SePP of 124 subjects and glutathione peroxidase (GPx) of 119 subjects were measured. The subjects were from the old and new endemic areas and non-endemic areas. The levels of SePP and GPx of the subjects of the old endemic area were significantly higher than those of the subjects of the new endemic area and the non-endemic areas, respectively. The Pearson’s correlation among SePP, GPx, and the number of the incident cases of the disease were statistically significant. These correlations show that there is an inverse relationship among the number of patients and the levels of SePP (r? = ?? 0.9800, P ?= ?0.0200) and GPx (r? = ?? 0.961, P ?= ?0.009). The results show that selenium deficiency might play an important role in the incidence of the disease.     

Role of Pigment Epithelium-Derived Factor (PEDF) in Arsenic-Induced Cell Apoptosis of Liver and Brain in a Rat Model

Although studies have shown that arsenic exposure can induce apoptosis in a variety of cells, the exact molecular mechanism of chronic arsenicosis remains unclear. Based on our previous study on human serum, the present study was to determine whether pigment epithelium-derived factor (PEDF) plays a role in the damage induced by chronic arsenic exposure in a rat model and to explore the possible signaling pathway involved. Thirty male Wistar rats were randomly divided into three groups and the arsenite doses administered were 0, 10, and 50 mg/L, respectively. The experiment lasted for 6 months. Our results showed that level of arsenic increased significantly in serum, liver, brain, and kidney in arsenic-exposed groups. It was indicated that PEDF protein was widely distributed in the cytoplasm of various types of cells in liver, brain, and kidney. PEDF protein level was only changed when the arsenite dose reached 50 mg/L in liver and brain, whereas it was not changed in the kidney. In order to investigate the possible mechanism of PEDF-exerted damages upon arsenite exposure, apoptosis in liver and brain was assessed. The proportion of apoptotic cells gradually increased with increasing arsenic administration. The ratio of Bax/Bcl-2 in the high arsenic group (50 mg/L) was significantly higher than that in the control group. Therefore, we thought PEDF played a role in cell apoptosis of liver and brain which induced by sodium arsenite exposure, and the results also demonstrated that Bax and Bcl-2 might be two key targets in the action of PEDF.     

The Alteration of MiR-222 and Its Target Genes in Nickel-Induced Tumor

Nickel is an important kind of metal and a necessary trace element in people’s production and livelihood; it is also a well-confirmed human carcinogen. In the past few years, researchers did a large number of studies about the molecular mechanisms of nickel carcinogenesis, and they focused on activation of proto-oncogenes and inactivation of anti-oncogenes caused by gene point mutation, gene deletion, gene amplification, DNA methylation, chromosome condensation, and so on that were induced by nickel. However, the researches on tumorigenic molecular mechanisms regulated by microRNAs (miRNAs) are rare. In this study, we established nickel-induced tumor by injecting Ni₃S₂ compounds to Wistar Rattus. By establishing a cDNA library of miRNA from rat muscle tumor tissue induced by Ni₃S₂, we found that the expression of miR-222 was significantly upregulated in tumor tissue compared with the normal tissue. As we expected, the expression levels of target genes of miR-222, CDKN1B and CDKN1C, were downregulated in the nickel-induced tumor. The same alteration of miR-222 and its target genes was also found in malignant 16HBE cells induced with Ni₃S₂ compounds. We conclude that miR-222 may promote cell proliferation infinitely during nickel-induced tumorigenesis in part by regulating the expression of its target genes CDKN1B and CDKN1C. Our study elucidated a novel molecular mechanism of nickel-induced tumorigenesis.     

PRIP (Phospholipase C-related but Catalytically Inactive Protein) Inhibits Exocytosis by Direct Interactions with Syntaxin 1 and SNAP-25 through Its C2 Domain

Membrane fusion for exocytosis is mediated by SNAREs, forming trans-ternary complexes to bridge vesicle and target membranes. There is an array of accessory proteins that directly interact with and regulate SNARE proteins. PRIP (phospholipase C-related but catalytically inactive protein) is likely one of these proteins; PRIP, consisting of multiple functional modules including pleckstrin homology and C2 domains, inhibited exocytosis, probably via the binding to membrane phosphoinositides through the pleckstrin homology domain. However, the roles of the C2 domain have not yet been investigated. In this study, we found that the C2 domain of PRIP directly interacts with syntaxin 1 and SNAP-25 but not with VAMP2. The C2 domain promoted PRIP to co-localize with syntaxin 1 and SNAP-25 in PC12 cells. The binding profile of the C2 domain to SNAP-25 was comparable with that of synaptotagmin I, and PRIP inhibited synaptotagmin I in binding to SNAP-25 and syntaxin 1. It was also shown that the C2 domain was required for PRIP to suppress SDS-resistant ternary SNARE complex formation and inhibit high K⁺-induced noradrenalin release from PC12 cells. These results suggest that PRIP inhibits regulated exocytosis through the interaction of its C2 domain with syntaxin 1 and SNAP-25, potentially competing with other SNARE-binding, C2 domain-containing accessory proteins such as synaptotagmin I and by directly inhibiting trans-SNARE complex formation.