Modification of pea dietary fibre by superfine grinding assisted enzymatic modification: Structural, physicochemical, and functional properties.

Using the optimal extraction conditions determined by response surface optimisation, the yield of soluble dietary fibre (SDF) modified by superfine grinding combined with enzymatic modification (SE-SDF) was significantly increased from 4.45 % ± 0.21 % (natural pea dietary fibre) to 16.

A simple "turn-on" fluorescent sensor for reversible recognition of aluminum ion in living cell.

A simple and reliable "turn-on" fluorescent sensor (E)-1-[((2-hydroxyethyl)imino) methyl] naphthalen-2-ol (HNP) has been designed, synthesized, and characterized by H-NMR, C-NMR, FT-IR, and EI-MS analysis. The binding property of HNP was examined employing UV-Vis and fluorescence spectroscopy. HNP exhibited high selectivity towards Al among other cations and anions.

The Composition of Fungal Communities in the Rumen of Gayals (), Yaks (), and Yunnan and Tibetan Yellow Cattle ().

The rumen is a microbial-rich ecosystem in which rumen fungi play an important role in the feed digestion of ruminants. The composition of rumen fungi in free-range ruminants such as gayals, yaks, Tibetan yellow cattle, and the domesticated Yunnan yellow cattle was investigated by sequencing an internal transcribed spacer region 1 (ITS1) using Illumina MiSeq. A total of 285 092 optimized sequences and 904 operational taxonomic units (OTUs) were obtained from the four cattle breeds.

Cooperation of the agonistic DR5 antibody apomab with chemotherapy to inhibit orthotopic lung tumor growth and improve survival.

Purpose: Apomab is a fully human monoclonal antibody that induces programmed cell death through the proapoptotic receptor DR5 in various cancer cells but not in normal cells. Several lung cancer cell lines express DR5 and exhibit apoptosis in response to apomab in vitro.

Experimental Design: We investigated the efficacy of apomab and its interaction with chemotherapy in xenograft models based on human NCI-H460 non-small-cell lung carcinoma cells.

MetMAb, the one-armed 5D5 anti-c-Met antibody, inhibits orthotopic pancreatic tumor growth and improves survival.

The hepatocyte growth factor (HGF) and its receptor, c-Met, have been implicated in driving proliferation, invasion, and poor prognosis in pancreatic cancer. Here, we investigated the expression of HGF and c-Met in primary pancreatic cancers and described in vitro and in vivo models in which MetMAb, a monovalent antibody against c-Met, was evaluated. First, expression of HGF and MET mRNA was analyzed in 59 primary pancreatic cancers and 51 normal samples, showing that both factors are highly expressed in pancreatic cancer.

Imaging tumors with an albumin-binding Fab, a novel tumor-targeting agent.

Association with albumin as a means to improve biodistribution and tumor deposition of a Fab was investigated using AB.Fab4D5, a bifunctional molecule derived from trastuzumab (HERCEPTIN) capable of binding albumin and tumor antigen HER2 (erbB2) simultaneously. AB.

Inhibitory effects of interferon-gamma on myocardial hypertrophy.

Prostaglandin F(2alpha) (PGF(2alpha)) plays an important role in pathologic cardiac growth. After testing several immune cytokines, we found that interferon-gamma (IFN-gamma) inhibited responsiveness of adult myocytes to PGF(2alpha). The present study was designed to test the hypothesis that IFN-gamma inhibits cardiac hypertrophy induced by PGF(2alpha).

The therapeutic potential of hepatocyte growth factor for myocardial infarction and heart failure.

Hepatocyte growth factor (HGF) is a cytokine whose multipotent actions are mediated by c-Met receptor. This review focuses on effects of HGF on myocardial infarction (MI) and heart failure. Circulating concentrations of HGF and myocardial concentrations of HGF and c-Met mRNA and protein are substantially increased following acute MI.

Apo2 ligand/tumor necrosis factor-related apoptosis-inducing ligand cooperates with chemotherapy to inhibit orthotopic lung tumor growth and improve survival.

Apo2 ligand/tumor necrosis factor-related apoptosis-inducing ligand (Apo2L/TRAIL) is a tumor necrosis factor superfamily member that induces apoptosis through the death receptors DR4 and/or DR5 in various cancer cell types but not in most normal cells. Several lung cancer cell lines express DR4 and DR5 and undergo apoptosis in vitro in response to Apo2L/TRAIL. We investigated the efficacy of recombinant soluble human Apo2L/TRAIL and its interaction with chemotherapy in xenograft models based on human NCI-H460 non-small cell lung carcinoma cells.

Thyrotropin-releasing hormone is induced in the left ventricle of rats with heart failure and can provide inotropic support to the failing heart.

Background: We reported previously that left ventricular gene expression for thyrotropin-releasing hormone (TRH) precursor was increased in rats with heart failure 8 weeks after myocardial infarction (MI) and that early ACE inhibition tended to cause further myocardial induction of this gene.

Methods And Results: Here, we show that after MI, the expression of pro-TRH is induced in the heart coordinately with the protease PC1, an important enzyme in TRH biosynthesis. Pro-TRH gene expression was induced in cardiac interstitial cells after MI, and this effect was restricted to the heart, because no increase in TRH mRNA abundance was observed in the hypothalamus, kidney, or lung.

Early treatment with hepatocyte growth factor improves cardiac function in experimental heart failure induced by myocardial infarction.

Plasma levels of hepatocyte growth factor (HGF) are increased within hours of cardiac ischemia/reperfusion in rats, and HGF has been shown to be cardioprotective toward acute ischemic injury. Myocardial levels of HGF mRNA and protein are increased for several days after myocardial infarction (MI), however, indicating a possible additional protective effect of HGF toward the progression of MI to heart failure. The purpose of this study was to determine whether HGF administration during the time course of endogenous cardiac HGF induction would lead to long-term improvement in cardiac function in rats with MI.

Effects of early treatment with growth hormone on infarct size, survival, and cardiac gene expression after acute myocardial infarction.

Objective: This study examined the effects of growth hormone (GH) on infarct size, survival, and cardiac gene expression in rats with acute myocardial infarction.

Design: Animals randomly received sc injection of either saline vehicle (n = 98) or GH (2mg/kg/day, n = 105) for 14 days commencing the day of left coronary artery ligation. Infarct size was determined by morphometric analysis at the time of death or at 52 weeks post-surgery.

KDR (VEGF receptor 2) is the major mediator for the hypotensive effect of VEGF.

Vascular endothelial growth factor (VEGF) exerts vasodilation-induced hypotension as a major side effect for treatment of ischemic diseases. VEGF has 2 receptor tyrosine kinases, KDR and Flt-1. Little is known about which receptor mediates VEGF-induced hypotension.

Exaggerated hypotensive effect of vascular endothelial growth factor in spontaneously hypertensive rats.

Vascular endothelial growth factor (VEGF) induces hypotension in normotensive subjects, which is considered to be a major side effect for treatment of ischemic diseases. However, the hypotensive effect of VEGF has not been investigated in the setting of hypertension. This study determined effects of VEGF on hemodynamics, pharmacokinetics, and release of NO and prostaglandin I2 (PGI2) in vivo and on vasorelaxation of mesentery artery rings in vitro in spontaneously hypertensive rats (SHR) compared with Wistar-Kyoto rats (WKY).