盐碱胁迫下羊草种子的萌发特性

时羊草Leymus chinensis种子在NaCl,Na2CO3和混合盐胁迫下的发芽率进行测定.在NaCl 12.5～600mmol/L,Na2CO312.5～150 mmol/L和混合盐37.5～250 mmol/L条件下羊草的发芽率均高于对照,在NaCl,Na2CO3浓度为1 2.5 mmol/L,混合盐75 mmol/L时发芽率最高,并且NaCl胁迫下的发芽率高于Na2CO3和混合盐,表明适宜的盐碱能促进种子发芽,中性盐更有助于促进种子发芽.方差分析表明羊草种子在3种胁迫下的发芽响应已产生分化,发芽率的变异系数为64.190 5%～66.625 5%.在不同环境条件下,羊草种子具有生态可塑性.     

PASS的制备及其在污水处理中的应用

以Na2SiO4和Al2(SO4)3为原料,采用复合法制备聚合硅酸硫酸铝(PASS):先在碱性条件下制备聚硅酸,然后在酸性条件下制备PASS。将自制的PASS应用于实际废水的处理并与聚合氯化铝(PAC)进行了比较,研究结果表明,所制备的PASS具有优良的絮凝性能,其在除浊、脱色及去除COD等方面较PAC具有更好的絮凝效果,是一种有广阔发展前景的新型高效净水剂。     

Mechanism of AKT1 negatively regulating breast cancer cell migration

AIM: To investigate the molecular mechanism and downstream signaling pathway by which AKT1 inhibition regulates breast cancer cell migration. METHODS: RNA interference was used to knockdown the expression of AKT1. Western blot assay was performed to examine the expression of AKT1 total protein, β-catenin total protein and β-catenin nuclear protein. Immunofluorescence was used to examine the cellular localization of β-catenin. Transwell assay was used to investigate whether β-catenin nuclear accumulation as an alternative pathway was responsible for breast cancer metastasis induced by AKT1 inhibition. RESULTS: The total protein expression of AKT1 was decreased in MCF-7 and MDA-MB-231 cells treated with AKT1 siRNA. A significant increase in the protein expression of β-catenin was observed in MCF-7 cells and MDA-MB-231 cells treated with AKT1 siRNA. Immunofluorescence staining showed that MCF-7 cells and MDA-MB-231 cells displayed strong β-catenin staining in the cytoplasm and nucleus after knockdown of AKT1 expression. The ability of tumor cell migration increased dramatically after treated with AKT1 specific siRNA in the breast cancer MCF-7 cells and MDA-MB-231 cells in Transwell assay. XAV-939 reversed breast cancer cell migration induced by knockdown of AKT1 expression. CONCLUSION: β-catenin nuclear accumulation contributes to AKT1 inhibition-mediated breast cancer cell migration.     

Suspected mitochondrial myopathy in a Jack Russell terrier

A Jack Russell terrier with a history of progressive exercise intolerance was examined at the age of four months and again 10 months later. Clinical examination revealed a stunted, thin dog with a stilted gait. The dog had raised lactate levels before and after feeding and a raised lactate/pyruvate ratio after feeding, indicating a metabolic abnormality. Histochemical evaluation of muscle biopsies revealed subsarcolemmal accumulation of oxidative activity when stained with nicotinamide adenine dinucleotide tetrazolium reductase and ragged red fibres when stained with modified Gomori trichrome; all fibre types were involved. Ultrastructural examination of the muscle confirmed the presence of subsarcolemmal accumulations of mitochondria. Histochemical staining for the activity of enzymes of the Krebs cycle, oxidative phosphorylation and other metabolic cytosolic enzymes failed to demonstrate an abnormality. In view of the clinical picture and the biochemical and histological findings, a tentative diagnosis of mitochondrial myopathy was made. The difficulties associated with diagnosing mitochondrial disorders are discussed.     

Case of angiosarcoma of the nasal passage of the horse--ultrastructure and differential diagnosis from progressive haematoma

An angiosarcoma involving the right frontal and maxillary sinuses in a nine-year-old Thoroughbred mare was studied post mortem by light and electron microscopy. Important diagnostic features included malignant endothelial cells lining ill-defined vascular spaces, supported by other vasoformative elements. Rhabdomyoblasts were also found. The tumour is apparently rarely seen in the nasal passages of the horse.     

Effect of ginsenosides on glucose uptake in human Caco-2 cells is mediated through altered Na+/glucose cotransporter 1 expression

In this study, we measured the effect of ginsenosides on glucose uptake using the Caco-2 cell system. At submicromolar concentrations, these compounds exhibited marked effects on the rate of glucose transport across the differentiated Caco-2 cell monolayer. Compound K (CK), the main intestinal bacterial metabolite of the protopanaxadiol ginsenosides, significantly enhanced the steady-state glucose transport rate to about 50% of the control sample rate (from 1.54 +/- 0.09 to 2.25 +/- 0.15 nmol/min). Conversely, the protopanaxatriol ginsenoside Rg1 inhibited glucose transport to about 70% of the original rate (from 1.54 +/- 0.09 to 1.02 +/- 0.05 nmol/min). Consistent with the effect on glucose uptake rate, CK and Rg1 conferred a significant and paralleled alteration on both the protein and mRNA expression levels of the Na+/glucose cotransporter 1 (SGLT1) gene. Unlike SGLT1, there is no significant alteration on the protein or mRNA levels of GLUTs in CK- or Rg1-treated cells. Taken together, our results demonstrate that ginsenosides CK and Rg1 elicited potent enhancing and suppressing effects, respectively, on glucose uptake across human intestinal Caco-2 monolayer through modulation of SGLT1 expression.