Next-to-leading order QCD predictions for Z0H0+jetZ^0 H^0 + {\rm jet} production at LHC

We calculate the complete next-to-leading order (NLO) QCD corrections to the $Z^0H^0$ production in association with a jet at the LHC. We study the impacts of the NLO QCD radiative corrections to the integrated and differential cross sections and the dependence of the cross section on the factorization/renormalization scale. We present the transverse momentum distributions of the final $Z^0$-, Higgs-boson and leading-jet. We find that the NLO QCD corrections significantly modify the physical observables, and obviously reduce the scale uncertainty of the LO cross section. The QCD K-factors can be 1.183 and 1.180 at the $\sqrt{s}=14 TeV$ and $\sqrt{s}=7 TeV$ LHC respectively, when we adopt the inclusive event selection scheme with $p_{T,j}^{cut}=50 GeV$, $m_H=120 GeV$ and $\mu=\mu_r=\mu_f=\mu_0 \equiv 1/2(m_Z+m_H)$. Furthermore, we make the comparison between the two scale choices, $\mu=\mu_0$ and $\mu=\mu_1=1/2(E_{T}^{Z}+E_{T}^{H}+ \sum_{j}E_{T}^{jet})$, and find the scale choice $\mu=\mu_1$ seems to be more appropriate than the fixed scale $\mu=\mu_0$.Comment: 18 pages, 7 figure

Nuclear receptors in vascular biology

Nuclear receptors sense a wide range of steroids and hormones (estrogens, progesterone, androgens, glucocorticoid, and mineralocorticoid), vitamins (A and D), lipid metabolites, carbohydrates, and xenobiotics. In response to these diverse but critically important mediators, nuclear receptors regulate the homeostatic control of lipids, carbohydrate, cholesterol, and xenobiotic drug metabolism, inflammation, cell differentiation and development, including vascular development. The nuclear receptor family is one of the most important groups of signaling molecules in the body and as such represent some of the most important established and emerging clinical and therapeutic targets. This review will highlight some of the recent trends in nuclear receptor biology related to vascular biology

Cover to Volume 3

The fibroblast mitogen platelet-derived growth factor -BB (PDGF-BB) induces a transient expression of the orphan nuclear receptor NR4A1 (also named Nur77, TR3 or NGFIB). The aim of the present study was to investigate the pathways through which NR4A1 is induced by PDGF-BB and its functional role. We demonstrate that in PDGF-BB stimulated NIH3T3 cells, the MEK1/2 inhibitor CI-1040 strongly represses NR4A1 expression, whereas Erk5 downregulation delays the expression, but does not block it. Moreover, we report that treatment with the NF-κB inhibitor BAY11-7082 suppresses NR4A1 mRNA and protein expression. The majority of NR4A1 in NIH3T3 was found to be localized in the cytoplasm and only a fraction was translocated to the nucleus after continued PDGF-BB treatment. Silencing NR4A1 slightly increased the proliferation rate of NIH3T3 cells; however, it did not affect the chemotactic or survival abilities conferred by PDGF-BB. Moreover, overexpression of NR4A1 promoted anchorage-independent growth of NIH3T3 cells and the glioblastoma cell lines U-105MG and U-251MG. Thus, whereas NR4A1, induced by PDGF-BB, suppresses cell growth on a solid surface, it increases anchorage-independent growth

Thyrotropin-releasing hormone (TRH) promotes wound re-epithelialisation in frog and human skin

There remains a critical need for new therapeutics that promote wound healing in patients suffering from chronic skin wounds. This is, in part, due to a shortage of simple, physiologically and clinically relevant test systems for investigating candidate agents. The skin of amphibians possesses a remarkable regenerative capacity, which remains insufficiently explored for clinical purposes. Combining comparative biology with a translational medicine approach, we report the development and application of a simple ex vivo frog (Xenopus tropicalis) skin organ culture system that permits exploration of the effects of amphibian skin-derived agents on re-epithelialisation in both frog and human skin. Using this amphibian model, we identify thyrotropin-releasing hormone (TRH) as a novel stimulant of epidermal regeneration. Moving to a complementary human ex vivo wounded skin assay, we demonstrate that the effects of TRH are conserved across the amphibian-mammalian divide: TRH stimulates wound closure and formation of neo-epidermis in organ-cultured human skin, accompanied by increased keratinocyte proliferation and wound healing-associated differentiation (cytokeratin 6 expression). Thus, TRH represents a novel, clinically relevant neuroendocrine wound repair promoter that deserves further exploration. These complementary frog and human skin ex vivo assays encourage a comparative biology approach in future wound healing research so as to facilitate the rapid identification and preclinical testing of novel, evolutionarily conserved, and clinically relevant wound healing promoters

Mesoscale flux-closure domain formation in single-crystal BaTiO3

Over 60 years ago, Charles Kittel predicted that quadrant domains should spontaneously form in small ferromagnetic platelets. He expected that the direction of magnetization within each quadrant should lie parallel to the platelet surface, minimizing demagnetizing fields,and that magnetic moments should be configured into an overall closed loop, or flux-closure arrangement. Although now a ubiquitous observation in ferromagnets, obvious flux-closure patterns have been somewhat elusive in ferroelectric materials. This is despite the analogous behaviour between these two ferroic subgroups and the recent prediction of dipole closure states by atomistic simulations research. Here we show Piezoresponse Force Microscopy images of mesoscopic dipole closure patterns in free-standing, single-crystal lamellae of BaTiO3. Formation of these patterns is a dynamical process resulting from system relaxation after the BaTiO3 has been poled with a uniform electric field. The flux-closure states are composed of shape conserving 90° stripe domains which minimize disclination stresses

Effect of Investment in Malaria Control on Child Mortality in Sub-Saharan Africa in 2002–2008

BACKGROUND: Around 8.8 million children under-five die each year, mostly due to infectious diseases, including malaria that accounts for 16% of deaths in Africa, but the impact of international financing of malaria control on under-five mortality in sub-Saharan Africa has not been examined. METHODS AND FINDINGS: We combined multiple data sources and used panel data regression analysis to study the relationship among investment, service delivery/intervention coverage, and impact on child health by observing changes in 34 sub-Saharan African countries over 2002-2008. We used Lives Saved Tool to estimate the number of lives saved from coverage increase of insecticide-treated nets (ITNs)/indoor residual spraying (IRS). As an indicator of outcome, we also used under-five mortality rate. Global Fund investments comprised more than 70% of the Official Development Assistance (ODA) for malaria control in 34 countries. Each $1 million ODA for malaria enabled distribution of 50,478 ITNs [95$3.90 vs. $7.05). Increased ITN/IRS coverage in high-burden countries led to 3,575 lives saved per 1 million children, as compared with 914 lives in lower-burden countries. Impact of ITN/IRS coverage on under-five mortality was significant among major child health interventions such as immunisation showing that 10% increase in households with ITN/IRS would reduce 1.5 [95%CI: 0.3-2.8] child deaths per 1000 live births. CONCLUSIONS: Along with other key child survival interventions, increased ITNs/IRS coverage has significantly contributed to child mortality reduction since 2002. ITN/IRS scale-up can be more efficiently prioritized to countries where malaria is a major cause of child deaths to save greater number of lives with available resources

Air–liquid interface cultures enhance the oxygen supply and trigger the structural and functional differentiation of intestinal porcine epithelial cells (IPEC)

The specific function of the epithelium as critical barrier between the intestinal lumen and the organism’s internal microenvironment is reflected by permanent maintenance of intercellular junctions and cellular polarity. The intestinal epithelial cells are responsible for absorption of nutritional components, facing mechanical stress and a changing oxygen supplementation via blood stream. Oxygen itself can regulate the barrier and the absorptive function of the epithelium. Therefore, we compared the dish cell culture, the transwell-like membrane culture and the oxygen enriched air–liquid interface (ALI) culture. We demonstrated strong influence of the different culture conditions on morphology and function of intestinal porcine epithelial cell lines in vitro. ALI culture resulted in a significant increase in cell number, epithelial cell layer thickness and expression as well as apical localisation of the microvilli-associated protein villin. Remarkable similarities regarding the morphological parameters were observed between ALI cultures and intestinal epithelial cells in vivo. Furthermore, the functional analysis of protein uptake and degradation by the epithelial cells demonstrated the necessity of sufficient oxygen supply as achieved in ALI cultures. Our study is the first report providing marked evidence that optimised oxygen supply using ALI cultures directly affects the morphological differentiation and functional properties of intestinal epithelial cells in vitro

Role of survivin and its splice variants in tumorigenesis

Survivin, a unique member of the inhibitor of apoptosis (IAP) protein family, is highly expressed in cancer but is undetectable in nonproliferating normal adult tissues, suggesting a potential role in tumorigenesis. Differential splicing of survivin pre-mRNA results in three new survivin variants, survivin-ΔEx3, survivin-2B, and survivin-3B. Loss of survivin-2B expression was found in the later stage of cancer development, while survivin and survivin-ΔEx3 are not, suggesting a differential role of them in tumour development. In this minireview, the author intends to summarise and discuss the current data relevant to the role of survivin and its splicing variants in tumorigenesis, which may facilitate further investigation in this interesting area