Enzyme-linked immunosorbent assay of ochratoxin A in barley

A noncompetitive, double antibody enzyme-linked immunosorbent assay for ochratoxin A using microtitration plates has been developed and applied to samples of barley. The anti-ochratoxin A antiserum, which is used at high dilution, does not cross-react significantly with ochratoxin B or ochratoxin a. Assay sensitivity for determination of the toxin in barley samples is 60 ng/kg. Minimal sample preparation is required before assay.     

空心菜对入星云湖河水的净化及其生物产出分析

为充分开发利用入星云湖河水的N、P等营养资源,降低其富营养化水平,改善和保护星云湖生态系统,于2010—2013年采用微区试验与大区试验相结合、静态试验与动态试验相结合的方法,研究了漂浮空心菜(Ipomoea aquatica)对入星云湖河水净化及其生物产出的规律。结果表明:漂浮空心菜对入湖河水具有较好的水质净化效应,静态条件下空心菜对入湖河水全N、水溶性P的去除率高达90%以上,动态条件下则达50%左右,空心菜吸收入湖河水N、P、K的量分别平均为348.4、50.9、530.4 kg·hm-2·a-1,且其绝大部分被空心菜的茎叶吸收(占93.0%,为864.5 kg·hm-2·a-1)。空心菜对入湖河水的净化量,以水溶性N计平均为27 321 m3·hm-2·a-1,以水溶性P计平均为67 569 m3·hm-2·a-1;空心菜的生长主要依赖入湖河水中N、P等营养物质(两者呈正相关),通过茎叶大量吸收并同化入湖河水中的N、P等养分后,空心菜获得了较高的茎叶生物产出量(占90.9%,鲜重量平均为112 032.0 kg·hm-2·a-1)。利用入星云湖河水漂浮种植空心菜,产生了明显的生态效益和经济效益。     

Mutations in a human ROBO gene disrupt hindbrain axon pathway crossing and morphogenesis

The mechanisms controlling axon guidance are of fundamental importance in understanding brain development. Growing corticospinal and somatosensory axons cross the midline in the medulla to reach their targets and thus form the basis of contralateral motor control and sensory input. The motor and sensory projections appeared uncrossed in patients with horizontal gaze palsy with progressive scoliosis (HGPPS). In patients affected with HGPPS, we identified mutations in the ROBO3 gene, which shares homology with roundabout genes important in axon guidance in developing Drosophila, zebrafish, and mouse. Like its murine homolog Rig1/Robo3, but unlike other Robo proteins, ROBO3 is required for hindbrain axon midline crossing.     

Rapid changes in throughput from single motor cortex neurons to muscle activity

Motor cortex output is capable of considerable reorganization, which involves modulation of excitability within the cortex. Does such reorganization also involve changes beyond the cortex, at the level of throughput from single motor cortex neurons to muscle activity? We examined such throughput during a paradigm that provided incentive for enhancing functional connectivity from motor cortex neurons to muscles. Short-latency throughput from a recorded neuron to muscle activity not present during some behavioral epochs often appeared during others. Such changes in throughput could not always be attributed to a higher neuron firing rate, to more ongoing muscle activity, or to neuronal synchronization, indicating that reorganization of motor cortex output may involve rapid changes in functional connectivity from single motor cortex neurons to alpha-motoneuron pools.     

Structural basis of type II topoisomerase inhibition by the anticancer drug etoposide

Type II topoisomerases (TOP2s) resolve the topological problems of DNA by transiently cleaving both strands of a DNA duplex to form a cleavage complex through which another DNA segment can be transported. Several widely prescribed anticancer drugs increase the population of TOP2 cleavage complex, which leads to TOP2-mediated chromosome DNA breakage and death of cancer cells. We present the crystal structure of a large fragment of human TOP2β complexed to DNA and to the anticancer drug etoposide to reveal structural details of drug-induced stabilization of a cleavage complex. The interplay between the protein, the DNA, and the drug explains the structure-activity relations of etoposide derivatives and the molecular basis of drug-resistant mutations. The analysis of protein-drug interactions provides information applicable for developing an isoform-specific TOP2-targeting strategy.     

Increased insulin sensitivity and obesity resistance in mice lacking the protein tyrosine phosphatase-1B gene

Protein tyrosine phosphatase-1B (PTP-1B) has been implicated in the negative regulation of insulin signaling. Disruption of the mouse homolog of the gene encoding PTP-1B yielded healthy mice that, in the fed state, had blood glucose concentrations that were slightly lower and concentrations of circulating insulin that were one-half those of their PTP-1B+/+ littermates. The enhanced insulin sensitivity of the PTP-1B-/- mice was also evident in glucose and insulin tolerance tests. The PTP-1B-/- mice showed increased phosphorylation of the insulin receptor in liver and muscle tissue after insulin injection in comparison to PTP-1B+/+ mice. On a high-fat diet, the PTP-1B-/- and PTP-1B+/- mice were resistant to weight gain and remained insulin sensitive, whereas the PTP-1B+/+ mice rapidly gained weight and became insulin resistant. These results demonstrate that PTP-1B has a major role in modulating both insulin sensitivity and fuel metabolism, thereby establishing it as a potential therapeutic target in the treatment of type 2 diabetes and obesity.     

Erythropoiesis in the rat: differential rates of DNA synthesis and cell proliferation

Direct in vivo estimates of DNA synthesis time in early and late erythroblasts were obtained by using the H(3)- and C(14)-thymidine double-la-beling technique. A double-emulsion autoradiographic procedure was used to resolve the two isotopes. Early erythroblasts were found to proliferate at a rate about five times that of late cells. This results primarily from a shorter mean DNA synthesis time in early cells (2.5 hours) than in late cells (6.5 hours).     

Hypertensive action of 18-hydroxydeoxycorticosterone

18-Hydroxydeoxycorticosterone is an adrenal steroid hormone causing salt and water retention and is secreted in greatly increased amounts in response to the pituitary hormone adrenocorticotropic hormone. Its production is abnormally high in some forms of hypertension in man and rat. Direct proof that 18-hydroxydeoxycorticosterone is capable of causing hypertension is present. Daily subcutaneous injections of 200 micrograms, a low physiological dose, significantly increase the blood pressure of unilaterally nephrectomized saline-treated rats after 2 weeks. This strengthens the hypothesis that 18-hydroxydeoxycorticosterone contributes to the etiology of hypertension, possibly by a mechanism involving stressinduced release of adrenocorticotropic hormone.