Fibrolytic enzyme treatment of barley grain and source of forage in high-grain diets fed to growing cattle

We conducted a study to determine the effects of treating barley grain with a fibrolytic enzyme mixture on chewing activities, ruminal fermentation, and total tract digestibility in cattle. We also investigated the potential benefits of using barley straw rather than barley silage as a roughage source in high-grain diets for feedlot cattle. Steers were given ad libitum access to one of four diets that consisted of 95% barley-based concentrate and 5% forage (DM basis). The concentrate was either control or enzyme-treated, and the forage was either barley silage or barley straw. Applying the enzyme mixture onto the barley lowered the concentrations of dietary ADF and NDF. However, it is not certain when this fiber hydrolysis occurred relative to feed consumption because the fiber analyses were conducted after the study was completed. Enzyme treatment of barley increased total tract dietary ADF digestibility by 28% (P<.05). Acetate-to-propionate ratio tended to decrease, which suggests that enzymes may have increased ruminal starch digestion as a result of enhanced digestion of barley hulls. Replacing silage with straw increased ADF intake (P<.05) and resulted in 1-h/d increase in rumination time (P<.05). Even though there was no effect of diet on ruminal pH, replacing silage with straw increased ruminal acetate, as a percentage of total VFA, and total tract ADF digestion (P<.01). This study demonstrates that using a fibrolytic enzyme mixture in high-grain diets that contain mainly barley grain can improve fiber digestion and grain utilization, but the mode of action is unclear. Straw can be used rather than silage to increase the effective fiber content of a high-grain feedlot diet.     

Enhanced radioresponse of paclitaxel-sensitive and -resistant tumours in vivo

Functional assembly of the plasminogen-dependent proteolytic system on the cell surface requires multiple interactions involving urokinase (uPA), urokinase receptor (uPAR), plasminogen activator inhibitors, and other molecules that mediate cell migration and adhesion. We analyzed the in vitro interaction of uPAR-containing particulate cell fractions with the amino-terminal fragment (ATF) of human urokinase and the matrix-like form of vitronectin. Binding and cross-linking of 125I-labeled ATF to crude membrane extracts from LB6-19 mouse cells overexpressing human uPARs in the presence of 25 nM urea-denatured vitronectin led to the formation of Mr 137,000, 92, 000, and 82,000 covalent complexes. Immunoprecipitation of the preformed cross-linked 125I-labeled complexes with anti-vitronectin, anti-uPA, or anti-uPAR antibodies revealed that the Mr 82,000 and 92, 000 species do contain ATF and vitronectin and identified the Mr 137, 000 species as a ternary complex formed by ATF, uPAR, and vitronectin. A similar electrophoretic pattern was displayed by acid-pretreated membranes extracted from MCF-7 breast carcinoma or HT1080 fibrosarcoma cell lines, as well as a ductal breast carcinoma specimen; the latter exhibited complex formation at concentrations of vitronectin lower than 10 nM. Finally, uPAR-vitronectin interaction was further documented by the decreased reactivity of an anti-uPAR polyclonal antibody to acid-pretreated sections of 10 breast carcinomas that had been preincubated with vitronectin. Our findings highlight the ability of uPAR to interact simultaneously with vitronectin and uPA in breast cancer, supporting a dynamic coupling of the molecular mechanisms underlying plasminogen-dependent matrix degradation and cell adhesion.     

Chronic pain in the lives of older women

We investigated the effect of chlorpromazine (CPZ) in a murine model of T-cell-dependent liver injury caused by concanavalin A (ConA). CPZ (3 and 10 mg/kg) treatment 1 h before ConA injection prevented liver injury. CPZ (3, 10 mg/kg) administered 1 h after a ConA injection was also hepatoprotective, whereas cyclosporin (CsA, 100 mg/kg) was active only when given before ConA. Under either condition, CsA but not CPZ prevented concurrent increases in splenic ornithine decarboxylase (ODC) activity, a putative index of T-cell proliferation/differentiation. CPZ down-regulated tumor necrosis factor-alpha (TNF-alpha) and up-regulated IL-10 in mice that then received ConA, whereas delayed administration of CPZ had no effect. These results suggest that CPZ prevented liver injury without affecting the proliferation/differentiation of T-cells. The dissociation of hepatoprotection by CPZ from cytokine modulation indicates that this drug intervenes in the adherence of T-cells or the death of hepatocytes in the ConA-model.     

Misinterpretation of body sensations in panic disorder

Cognitive accounts of panic predict that panic disorder patients will be particularly prone to misinterpret autonomic sensations. Several studies have produced results consistent with this prediction, but each is open to alternative interpretation. To clarify matters, 2 studies administered the Body Sensations Interpretation Questionnaire (BSIQ) to panic patients and controls. Panic patients were more likely to interpret ambiguous autonomic sensations as signs of immediately impending physical or mental disaster and were more likely than other anxiety disorder patients and nonpatients to believe these interpretations. In a 3rd study, a brief version of the BSIQ was shown to have satisfactory test-retest reliability, to change with treatment, and to discriminate treatments that varied in their effects on panic.     

N-cadherin-catenin interaction: necessary component of cardiac cell compartmentalization during early vertebrate heart development

During early heart development the expression pattern of N-cadherin, a calcium-dependent cell adhesion molecule, suggests its involvement in morphoregulation and the stabilization of cardiomyocyte differentiation. N-cadherin's adhesive activity is dependent upon its interaction with the intracellular catenins. An association with alpha-catenin and beta-catenin also is believed to be involved in cell signaling. This study details the expression patterns of alpha-catenin, beta-catenin, and gamma-catenin, during definition of the cardiac cell population as distinct compartments in the anterior regions of the chick embryo between stages 5 and 9. The restriction of N-cadherin/catenin localization at stage 5+ from a uniform pattern in vivo, to specific cell clusters that demarcate areas where mesoderm separation is initiated, suggests that the N-cadherin/catenin complex is involved in boundary formation and in the subsequent cell sorting. The latter two processes lead to the specification and formation of the somatic and cardiac splanchnic mesoderm. N-cadherin colocalized with alpha- and beta-catenin at the cell membrane before and during the time that its expression becomes restricted to the lateral mesoderm and continues cephalocaudad into stage 8. These proteins continue to colocalize in the myocardium of the tubular heart. Plakoglobin is not expressed in this region during stages 6-8, but is detected in the myocardium later at stage 13. The observed in vivo expression patterns of alpha-catenin, beta-catenin, and plakoglobin suggest that these proteins are directly linked with the developmental regulation of cell junctions, as cardiac cells become stably committed and phenotypically differentiated to eventually form a mature myocardium. The localization of N-CAM also was analyzed during these stages to determine whether the N-cadherin-catenin localization was unique or whether other cell adhesion molecules were expressed similarly. The results indicate that the unique pattern of N-cadherin expression is not shared with N-CAM. We also show that perturbation of N-cadherin using a function perturbing N-cadherin antibody (NCD-2) inhibits normal early heart development and myogenesis in a cephalocaudad, stage-dependent manner. We propose a model whereby myocardial cell compartmentalization also defines the endocardial population. The presence of beta-catenin suggests that a similar signaling pathway involving Wnt (wingless)-mediated events may function in myocardial cell compartmentalization during early vertebrate heart development, as in Drosophila contractile vessel development.     

Nanostructured polymer blends: Synthesis and structure

Nanostructured polymer blends prepared via anionic ring opening polymerizations of cyclic monomers in the presence of a pre-made polymer melt exhibit a number of special properties over traditional polymer blends and homopolymers. Here, we report on a simple and versatile method of in situ polymerization of macrocyclic carbonates in the presence of a maleic anhydride polypropylene (mPP) matrix and a surface-active compatibilizer (i.e. PC grafted onto a mPP backbone generated in situ) to yield a micro- and nanostructured polymer blends consisting of a polycarbonate (PC) minor phase, and a polypropylene (PP) major phase. By varying the processing conditions and concentration of the macrocyclic carbonate it was possible to reduce the size of the PC dispersions to an average minor diameter of 150 nm. NMR and TEM characterizations indicate that the PC dispersions do not influence crystal content in the PP phase. Overall, the results point to a simple strategy and versatile route to new polymeric materials with enhanced benefits.     

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显示器用的液晶面板价格近期呈全线上扬的态势，从17英寸、19英寸到19英寸宽屏，都有2～6美元的价格上涨，这很可能预示着主流液晶显示器的价格即将全面反弹。不过，20英寸以上的液晶面板将改用第七代生产线，因此成本又会大幅度下调。因此，业界的普遍预期是液晶显示器价格短期内会有所波动，而大屏幕产品价格将长期走低。     

Hypotension following acute hypovolaemia depends on the caudal midline medulla

Acute hypovolaemia evokes abrupt, life-threatening hypotension and bradycardia. Hypotension can be evoked also by excitation of the caudal midline medulla (CMM). This study investigated the possible contribution of the CMM depressor area to hypotension evoked by acute hypovolaemia. Inactivation of the CMM, with either lignocaine or cobalt chloride did not alter resting arterial pressure. However lignocaine injections blocked the fall in arterial pressure, and cobalt chloride injections delayed the onset and significantly attenuated the size of hypovolaemic-evoked hypotension. These findings suggest that the CMM is a key region triggering hypotension after blood loss, and that the brain areas mediating cardiovascular response to challenges such as acute hypovolaemia are not the same areas that regulate resting arterial pressure.