Dual band tunable EBG

An electromagnetic bandgap (EBG) surface that can be independently tuned over two separate frequency bands is demonstrated. The EBG consists of a dual layer of square element based designs with varactor diodes. The EBG tuning ranges for each band were from 600 to 1200 and 1700 to 2600 MHz.     

The role of physical health functioning, mental health, and sociodemographic factors in determining the intensity of mental health care use among primary care medical patients.

The present study examined sociodemographic and attitudinal predisposing factors (gender, age, marital status, health insurance, household income, attitudes about mental health care), and need/illness variables (depression severity, physical and mental health functional status) as predictors of past-year mental health care use intensity (i.e., visit counts) and use/nonuse. The sample included 283 adult primary care patients from the Midwestern United States in a cross-sectional study. Nonlinear regression models demonstrated that past-year treatment use intensity was significantly associated with both married status and poorer physical health functioning, while the use (vs. nonuse) of treatment was associated with depression severity. A sociodemographic and attitudinal multivariate predictor model only explained 5% of the variance in treatment use intensity, but a need/illness model significantly contributed an additional 23% variance. Poorer physical health functioning was significant in predicting treatment use intensity, while depression severity was significant in predicting the use (vs. nonuse) of treatment. Results demonstrate the particular importance of physical health problems in determining the intensity of mental health care use, and depression severity in determining the use/nonuse of treatment, notwithstanding the restricted sociodemographic contour of the sample. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Role of decay-accelerating factor in regulating complement activation on the erythrocyte surface as revealed by gene targeting

Decay-accelerating factor (DAF) is a glycosylphosphatidylinositol (GPI)-anchored membrane protein that inhibits both the classical and the alternative pathways of complement activation. DAF has been studied extensively in humans under two clinical settings: when absent from the erythrocytes of paroxysmal nocturnal hemoglobinuria (PNH) patients, who suffer from complement-mediated hemolytic anemia, and in transgenic pigs expressing human DAF, which have been developed to help overcome complement-mediated hyperacute rejection in xenotransplantation. Nevertheless, the exact role of DAF in regulating complement activation in vivo on the cell surface and the species specificity of this molecule remain to be fully characterized. To address these issues, we have used gene targeting to produce mice lacking GPI-anchored DAF. We found that erythrocytes from mice deficient in GPI-anchored DAF showed no increase in spontaneous complement activation in vivo but exhibited impaired regulation of zymosan-initiated bystander and antibody-triggered classical pathway complement activation in vitro, resulting in enhanced complement deposition. Despite a high level of C3 fixation, no homologous hemolysis occurred. It is noteworthy that GPI-linked DAF knockout erythrocytes, when tested with human and guinea pig sera, were more susceptible to heterologous complement lysis than were normal erythrocytes. These results suggest that DAF is capable of regulating homologous as well as heterologous complement activation via the alternative or the classical pathway. They also indicate that DAF deficiency alone is not sufficient to cause homologous hemolysis. In contrast, when the assembly of the membrane-attack complex is not properly regulated, as in the case of heterologous complement activation or in PNH patients, impaired erythrocyte DAF activity and enhanced C3 deposition could lead to increased hemolytic reaction.     

Diabetes mellitus and serum carotenoids: findings from the Third National Health and Nutrition Examination Survey

Little is known about carotenoids, a diverse group of plant compounds with antioxidant activity, and their association with diabetes, a condition characterized by oxidative stress. Data from phase I of the Third National Health and Nutrition Examination Survey (1988-1991) were used to examine concentrations of alpha-carotene, beta-carotene, cryptoxanthin, lutein/zeaxanthin, and lycopene in 40- to 74-year-old persons with a normal glucose tolerance (n = 1,010), impaired glucose tolerance (n = 277), newly diagnosed diabetes (n = 148), and previously diagnosed diabetes (n = 230) based on World Health Organization criteria. After adjustment for age, sex, race, education, serum cotinine, serum cholesterol, body mass index, physical activity, alcohol consumption, vitamin use, and carotene and energy intake, geometric means of beta-carotene were 0.363, 0.316, and 0.290 micromol/liter for persons with a normal glucose tolerance, impaired glucose tolerance, and newly diagnosed diabetes, respectively (p = 0.004 for linear trend), and geometric means for serum lycopene were 0.277, 0.259, and 0.231 micromol/liter, respectively (p = 0.044 for linear trend). All serum carotenoids were inversely related to fasting serum insulin after adjustment for confounders (p < 0.05 for each carotenoid). If confirmed, these data suggest new opportunities for research that include exploring a possible role for carotenoids in the pathogenesis of insulin resistance and diabetes.     

Characterisation of rhizobia from African acacias and other tropical woody legumes using Biolog and partial 16S rRNA sequencing

Blood was collected from two Sahelian goats, experimentally infected with either a drug-sensitive cloned population of Trypanosoma congolense (IL 1180) or a multiple drug-resistant T. congolense stock (Samorogouan/89/CRTA/267) and incubated at 37 degrees C for 30 min and 12 h, respectively, in the presence of different drug concentrations (0.5, 1.0, 10.0 and 100.0 microg/ml blood) of diminazene aceturate or isometamidium chloride. After that, the trypanosome/blood/drug suspensions were offered to tsetse flies (2100 teneral Glossina morsitans submorsitans) through an in vitro feeding system, using a silicone membrane. All tsetse flies were dissected and examined for the presence of trypanosomes in labrum, hypopharynx and midgut 20 days after their infective blood-meals. Infectivity of the drug-sensitive cloned population was already completely abolished after incubation with 0.5 microg/ml of both drugs; however, 13.6-42.2% of tsetse having been fed on untreated blood had developed an infection. In contrast, no significant differences were observed in the infection rates between the experimental groups and their control groups when fed on blood infected with the multiple drug-resistant stock after incubation for 30 min with up to 10 microg/ml of diminazene or isometamidium. In consequence, tsetse appear to be a useful tool in the assessment of drug susceptibility of typanosome populations.     

Role of Ca2+-ATPase inhibitors in activation of cytosolic phospholipase A2 in human polymorphonuclear neutrophils

In the present study, we investigated the involvement of Ca2+-signaling and protein kinases in the effect of Ca2+-ATPase inhibitors on the activation of cytosolic phospholipase A2 (cPLA2) in human polymorphonuclear neutrophils. We found that activity and mobility on electrophoresis gels of the cPLA2 protein were significantly increased by f-Met-Leu-Phe (fMLP), 12-myristate 13-acetate (PMA) and the Ca2+-ATPase inhibitors, thapsigargin and cyclopiazonic acid. This effect was completely suppressed by staurosporine. Calphostin C partially inhibited the fMLP- and PMA-induced cPLA 2 activation, but had no influence on thapsigargin- and cyclopiazonic acid-treated cells. Thapsigargin and cyclopiazonic acid also showed no effect on protein kinase C activity. However, the thapsigargin- and cyclopiazonic acid-induced cPLA2 activation was completely inhibited by the tyrosine kinase inhibitor, erbstatin, and Ca2+ chelator, EGTA. In addition, the cPLA2 activity was reduced after pretreatment with the mitogen-activated protein kinase kinase inhibitor PD98059. The arachidonic acid release was significantly reduced in cells pretreated with the cPLA2 inhibitor, AACOCF3. Furthermore, we found that the human neutrophil cPLA2 cDNA contain a Ca2+-dependent-lipid binding domain which shares homology to several other enzymes such as protein kinase C and phospholipase C. Our results suggest that tyrosine kinases and the MAP kinase cascade are involved in Ca2+-ATPase inhibitor-induced activation and phosphorylation of cPLA2. Protein kinase C is not required in this event.     

The angiotensinogen gene is expressed in both astrocytes and neurons in murine central nervous system

Two transgenic mouse models were used to examine the cellular localization of angiotensinogen (AGT) in the brain. The first model was previously described in detail and consists of a human AGT genomic transgene containing all exons and introns of the gene and 1. 2 kb of the 5' flanking DNA. The second model contains a fusion between 1.2 kb of HAGT 5' flanking DNA and the beta-gal reporter gene which exhibits a similar pattern of tissue-specific expression to the HAGT transgene. Expression of both transgenes qualitatively mirrors the expression of endogenous AGT. Double staining of transgenic mouse brain sections with X-gal and GFAP revealed that a majority of beta-gal activity was localized to astrocytes in almost all brain areas. However, both beta-gal activity as identified by X-gal, and HAGT mRNA as detected by in situ hybridization, were also found in neurons in restricted areas of the brain, including the mesencephalic trigeminal nucleus (meV), subfornical organ (SFO) and the external lateral parabrachial nucleus (elPB). The expression of these transgenes provides the first convincing evidence for AGT gene expression in neurons in the brain. We further report by angiotensin II (Ang-II) immunostaining in rat brains after selective lesioning, that Ang-II is likely involved in a neuronal pathway from the PB to the amygdala (Ce). Finally, we performed double-labeling, first by retrograde labeling of HRP injected into the Ce, and then by X-gal on PB neurons in beta-gal transgenic mice, and identified doubly labeled neurons. Based on these results, we propose that AGT is generated in neurons in the elPB, transported to the Ce and converted into Ang-II locally to exert is biological functions.     

The sec6/8 complex is located at neurite outgrowth and axonal synapse-assembly domains

The molecules that specify domains on the neuronal plasma membrane for the delivery and accumulation of vesicles during neurite outgrowth and synapse formation are unknown. We investigated the role of the sec6/8 complex, a set of proteins that specifies vesicle targeting sites in yeast and epithelial cells, in neuronal membrane trafficking. This complex was found in layers of developing rat brain undergoing synaptogenesis. In cultured hippocampal neurons, the sec6/8 complex was present in regions of ongoing membrane addition: the tips of growing neurites, filopodia, and growth cones. In young axons, the sec6/8 complex was also confined to periodic domains of the plasma membrane. The distribution of synaptotagmin, synapsin1, sec6, and FM1-43 labeling in cultured neurons suggested that the plasma membrane localization of the sec6/8 complex preceded the arrival of synaptic markers and was downregulated in mature synapses. We propose that the sec6/8 complex specifies sites for targeting vesicles at domains of neurite outgrowth and potential active zones during synaptogenesis.     

直面客户互联体验的新现实

<正>为了提供多重体验,企业需要创建适用于所有模式的应用,为每个客户提供个性化体验,且在不受任何互动的影响下,将后端一致性融入核心生态系统。因此,企业必须考虑如何使AR和VR技术在其数字化进程中发挥作用。随着互联网的发展,客户与品牌的互动渠道越来越多。世界每时每刻都在由物理化向数字化方向发展,而虚拟现实（VR）和增强现实（A R）等新兴技术的发展强化了这一转变。如今,良好的客户体验并非仅靠移动应用、稳定的网站或强大的服务产品就可以实现。     

Milk fat globule glycoproteins in human milk and in gastric aspirates of mother''s milk-fed preterm infants

The change of brain lesion load, measured on T2-weighted magnetic resonance imaging (MRI) using computer-assisted techniques, is a widely used secondary endpoint for phase III clinical trials in multiple sclerosis (MS). Collection, transfer, and analysis of the electronic data across multiple centers have all proved challenging and give rise to potential errors. However, many new acquisition schemes and postprocessing techniques have been developed; these may reduce scan times and result in better lesion conspicuity or lessen the human interaction needed for data analysis. This review considers many aspects of the use of MRI in clinical trials for MS and provides international consensus guidelines, derived from a task force of the European Magnetic Resonance Networks in Multiple Sclerosis (MAGNIMS) together with a group of North American experts. The main points considered are the organization of correctly powered trials and selection of participating sites; the appropriate choice of pulse sequences and image acquisition protocol given the current state of technology; quality assurance for data acquisition and analysis; accuracy and reproducibility of lesion load assessments; and the potential for the application of quantitative methods to other MRI-derived measures of disease burden.