Photosynthesis, yield, energy balance, and water-use of intercropped maize and soybean

By 2050, the U.S. Corn Belt will likely face a 23% increase in leaf-to-air vapor pressure deficit (VPDL), the driving force of evapotranspiration (ET), which may restrict maize yield improvements for rainfed agroecosystems. Alternative cropping systems, such as maize and legume intercrops, have previously demonstrated yield and resource-use advantages over monocultures. In this study, the residual energy balance approach was used to gain insights into how an additive simultaneous maize and soybean intercrop system regulates ET and water-use efficiency (WUE) compared to standard maize and soybean monoculture systems of the U.S. Corn Belt. Experimental field plots were rain-fed and arranged in a randomized complete block design in three blocks. Photosynthetic capacity and grain yield of maize were conserved in the intercrop. However, its competitive dominance shaded 80%–90% of incident light for intercropped soybean at canopy closure, leading to a 94% decrease in grain yield compared to soybean monoculture. The total grain yield per unit area of the additive intercrop (land-use efficiency) increased by 11% ± 6% (1 SE). Compared to maize monoculture, the intercrop had higher latent heat fluxes (λET) at night but lower daytime λET as the intercrop canopy surface temperature was approximately.25°C warmer, partitioning more energy to sensible heat flux. However, the diel differences in λET fluxes were not sufficient to establish a statistically significant or biologically relevant decrease in seasonal water-use (ΣET). Likewise, the increase in land-use efficiency by the intercrop was not sufficient to establish an increase in seasonal water-use efficiency. Intercropping high-performing maize and soybean cultivars in a dense configuration without negative impact suggests that efforts to increase yield and WUE may lead to improved benefits

An amphitropic cAMP-binding protein in yeast mitochondria

ABSTRACT: We describe the first example of a mitochondrial protein with a covalently attached phos-phatidylinositol moiety acting as a membrane anchor. The protein can be metabolically labeled with both stearic acid and inositol. The stearic acid label is removed by phospholipase D whereupon the protein with the retained inositol label is released from the membrane. This protein is a cAMP receptor of the yeast Saccharomyces cereuisiae and tightly associated with the inner mitochondrial membrane. However, it is converted into a soluble form during incubation of isolated mitochondria with Ca2+ and phospholipid (or lipid derivatives). This transition requires the action of a proteinaceous, N-ethylmaleimide-sensitive component of the intermembrane space and is accompanied by a decrease in the lipophilicity of the cAMP receptor. We propose that the component of the intermembrane space triggers the amphitropic behavior of the mitochondrial lipid-modified CAMP-binding protein through a phospholipase activity. Only in recent years specific fatty acids have been recog-nized to play important roles in the association of proteins with membranes. Both noncovalent and covalent interactions be-tween fatty acids and proteins have been reported. Among the latter are GTP-binding proteins (Molenaar et al., 1988)

Faculty writing groups: a support for women balancing family and career on the academic tightrope

Open access article. Creative Commons Attribution-NonCommercial-No Derivative Works 2.5 Canada license (CC BY-NC-ND 2.5 CA) appliesThis qualitative research project explored the experiences of women who juggle the demands of family or parenthood while engaging in academic careers at a faculty of education. The researcher-participants consisted of 11 women; 9 women provided a written narrative, and all women participated in the data analysis. The data consisted of the personal, reflective narratives of 9 women who participated in a faculty writing group. Analysis of narratives uncovered 5 themes common to the researchers and participants in this study: genderspecific experiences surrounding parenting, second-career academics, pressure surrounding academic work, human costs, and commitment to work and family. Implications of the findings are discussed with particular emphasis on how a faculty writing group framed by a relational model of interaction can be used to support untenured faculty who experience difficulty balancing the demands of family and academia.Ye

Overexpression of CD97 in Intestinal Epithelial Cells of Transgenic Mice Attenuates Colitis by Strengthening Adherens Junctions

The adhesion G-protein-coupled receptor CD97 is present in normal colonic enterocytes but overexpressed in colorectal carcinoma. To investigate the function of CD97 in colorectal carcinogenesis, transgenic Tg(villin-CD97) mice overexpressing CD97 in enterocytes were generated and subjected to azoxymethane (AOM)/dextran sodium sulfate (DSS)-induced colitis-associated tumorigenesis. Unexpectedly, we found a CD97 cDNA copy number-dependent reduction of DSS-induced colitis in Tg compared to wild-type (WT) mice that was confirmed by applying a simple DSS protocol. Ultrastructural analysis revealed that overexpression of CD97 strengthened lateral cell-cell contacts between enterocytes, which, in contrast, were weakened in CD97 knockout (Ko) mice. Transepithelial resistance was not altered in Tg and Ko mice, indicating that tight junctions were not affected. In Tg murine and normal human colonic enterocytes as well as in colorectal cell lines CD97 was localized preferentially in E-cadherin-based adherens junctions. CD97 overexpression upregulated membrane-bound but not cytoplasmic or nuclear β-catenin and reduced phospho-β-catenin, labeled for degradation. This was associated with inactivation of glycogen synthase kinase-3β (GSK-3β) and activation of Akt. In summary, CD97 increases the structural integrity of enterocytic adherens junctions by increasing and stabilizing junctional β-catenin, thereby regulating intestinal epithelial strength and attenuating experimental colitis

Phono-spectrographic analysis of heart murmur in children

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Institutional shared resources and translational cancer research

The development and maintenance of adequate shared infrastructures is considered a major goal for academic centers promoting translational research programs. Among infrastructures favoring translational research, centralized facilities characterized by shared, multidisciplinary use of expensive laboratory instrumentation, or by complex computer hardware and software and/or by high professional skills are necessary to maintain or improve institutional scientific competitiveness. The success or failure of a shared resource program also depends on the choice of appropriate institutional policies and requires an effective institutional governance regarding decisions on staffing, existence and composition of advisory committees, policies and of defined mechanisms of reporting, budgeting and financial support of each resource. Shared Resources represent a widely diffused model to sustain cancer research; in fact, web sites from an impressive number of research Institutes and Universities in the U.S. contain pages dedicated to the SR that have been established in each Center, making a complete view of the situation impossible. However, a nation-wide overview of how Cancer Centers develop SR programs is available on the web site for NCI-designated Cancer Centers in the U.S., while in Europe, information is available for individual Cancer centers. This article will briefly summarize the institutional policies, the organizational needs, the characteristics, scientific aims, and future developments of SRs necessary to develop effective translational research programs in oncology

Downstream signalling and specific inhibition of c-MET/HGF pathway in small cell lung cancer: implications for tumour invasion

The c-MET receptor can be overexpressed, amplified, or mutated in solid tumours including small cell lung cancer (SCLC). In c-MET-overexpressing SCLC cell line NCI-H69, hepatocyte growth factor (HGF) dramatically induced c-MET phosphorylation at phosphoepitopes pY1230/1234/1235 (catalytic tyrosine kinase), pY1003 (juxtamembrane), and also of paxillin at pY31 (CRKL-binding site). We utilised a global proteomics phosphoantibody array approach to identify further c-MET/HGF signal transduction intermediates in SCLC. Strong HGF induction of specific phosphorylation sites in phosphoproteins involved in c-MET/HGF signal transduction was detected, namely adducin-α [S724], adducin-γ [S662], CREB [S133], ERK1 [T185/Y187], ERK1/2 [T202/Y204], ERK2 [T185/Y187], MAPKK (MEK) 1/2 [S221/S225], MAPKK (MEK) 3/6 [S189/S207], RB [S612], RB1 [S780], JNK [T183/Y185], STAT3 [S727], focal adhesion kinase (FAK) [Y576/S722/S910], p38α-MAPK [T180/Y182], and AKT1[S473] and [T308]. Conversely, inhibition of phosphorylation by HGF in protein kinase C (PKC), protein kinase R (PKR), and also CDK1 was identified. Phosphoantibody-based immunohistochemical analysis of SCLC tumour tissue and microarray established the role of c-MET in SCLC biology. This supports a role of c-MET activation in tumour invasive front in the tumour progression and invasion involving FAK and AKT downstream. The c-MET serves as an attractive therapeutic target in SCLC, as shown through small interfering RNA (siRNA) and selective prototype c-MET inhibitor SU11274, inhibiting the phosphorylation of c-MET itself and its downstream molecules such as AKT, S6 kinase, and ERK1/2. Investigation of mechanisms of invasion and, ultimately, metastasis in SCLC would be very useful with these signal transduction molecules