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61.
Joseph E. Knoll William F. Anderson Ravindra Malik Robert K. Hubbard Timothy C. Strickland 《Bioenergy Research》2013,6(3):974-983
Napiergrass (Pennisetum purpureum Schum.) is a high-yielding perennial biomass crop that is well adapted to the Southeast USA where poultry litter is readily available. This research was conducted to compare biomass production and nutrient utilization of napiergrass fertilized with either poultry litter or inorganic fertilizer. Each spring, approximately 100 kg ha?1 of N, 40 kg ha?1 P, and 90 kg ha?1 K were applied as poultry litter or equivalent inorganic fertilizer. Biomass was harvested each winter after senescence. For the first 2 years, dry matter yield did not differ among treatments, but in the third and fourth years, yields declined in all treatments and were lowest in the unfertilized treatment. Biomass N concentration and N removal were greatest in the inorganic treatment. In general, N removal exceeded the amount applied, suggesting that higher application rates may be necessary to maintain yields. Biomass P concentration and total P uptake were greatest in the litter fertilized treatment, demonstrating that napiergrass can remove some of the excess P from applied litter. Soil cores were taken periodically to assess changes in soil properties. After 2 years of production, soil pH in the surface layer (0–15 cm) was lower in the inorganic treatment than in the other treatments. After 4 years, total soil C had increased by an average of 3,180 kg ha?1 though fertilizer treatments did not differ. Yield declined in all treatments after 4 years and N supplementation is recommended for production in upland fields. 相似文献
62.
Unlike prototypical receptor tyrosine kinases (RTKs), which are single-chain polypeptides, the insulin receptor (InsR) is a preformed, covalently linked tetramer with two extracellular α subunits and two membrane-spanning, tyrosine kinase-containing β subunits. A single molecule of insulin binds asymmetrically to the ectodomain, triggering a conformational change that is transmitted to the cytoplasmic kinase domains, which facilitates their trans-phosphorylation. As in prototypical RTKs, tyrosine phosphorylation in the juxtamembrane region of InsR creates recruitment sites for downstream signaling proteins (IRS [InsR substrate] proteins, Shc) containing a phosphotyrosine-binding (PTB) domain, and tyrosine phosphorylation in the kinase activation loop stimulates InsR’s catalytic activity. For InsR, phosphorylation of the activation loop, which contains three tyrosine residues, also creates docking sites for adaptor proteins (Grb10/14, SH2B2) that possess specialized Src homology-2 (SH2) domains, which are dimeric and engage two phosphotyrosines in the activation loop.Insulin is a highly potent anabolic hormone that is critical for tissue development and for glucose homeostasis (Taniguchi et al. 2006). Released from the β cells of the pancreas, insulin regulates glucose output from the liver and glucose uptake into (primarily) skeletal muscle and adipose tissue. In addition, insulin promotes the synthesis and storage of carbohydrates, lipids, and protein. Insulin’s actions are mediated by the insulin receptor (InsR), a plasma membrane-resident glycoprotein and member of the receptor tyrosine kinase (RTK) family. Other members of the InsR subfamily of RTKs include the insulinlike growth factor-1 receptor (IGF1R) and insulin receptor-related receptor, the latter of which has no known ligand. As an RTK, InsR is ligand-activated through mechanisms that are both prototypical and atypical of RTKs. These mechanisms will be the focus of this article. 相似文献
63.
Julie In Valeriy Lukyanenko Jennifer Foulke-Abel Ann L. Hubbard Michael Delannoy Anne-Marie Hansen James B. Kaper Nadia Boisen James P. Nataro Chengru Zhu Edgar C. Boedeker Jorge A. Girón Olga Kovbasnjuk 《PloS one》2013,8(7)
Life-threatening intestinal and systemic effects of the Shiga toxins produced by enterohemorrhagic Escherichia coli (EHEC) require toxin uptake and transcytosis across intestinal epithelial cells. We have recently demonstrated that EHEC infection of intestinal epithelial cells stimulates toxin macropinocytosis, an actin-dependent endocytic pathway. Host actin rearrangement necessary for EHEC attachment to enterocytes is mediated by the type 3 secretion system which functions as a molecular syringe to translocate bacterial effector proteins directly into host cells. Actin-dependent EHEC attachment also requires the outer membrane protein intimin, a major EHEC adhesin. Here, we investigate the role of type 3 secretion in actin turnover occurring during toxin macropinocytosis. Toxin macropinocytosis is independent of EHEC type 3 secretion and intimin attachment. EHEC soluble factors are sufficient to stimulate macropinocytosis and deliver toxin into enterocytes in vitro and in vivo; intact bacteria are not required. Intimin-negative enteroaggregative Escherichia coli (EAEC) O104:H4 robustly stimulate Shiga toxin macropinocytosis into intestinal epithelial cells. The apical macropinosomes formed in intestinal epithelial cells move through the cells and release their cargo at these cells’ basolateral sides. Further analysis of EHEC secreted proteins shows that a serine protease EspP alone is able to stimulate host actin remodeling and toxin macropinocytosis. The observation that soluble factors, possibly serine proteases including EspP, from each of two genetically distinct toxin-producing strains, can stimulate Shiga toxin macropinocytosis and transcellular transcytosis alters current ideas concerning mechanisms whereby Shiga toxin interacts with human enterocytes. Mechanisms important for this macropinocytic pathway could suggest new potential therapeutic targets for Shiga toxin-induced disease. 相似文献
64.
Seongah Han Taro E. Akiyama Stephen F. Previs Kithsiri Herath Thomas P. Roddy Kristian K. Jensen Hong-Ping Guan Beth A. Murphy Lesley A. McNamara Xun Shen Walter Strapps Brian K. Hubbard Shirly Pinto Cai Li Jing Li 《Journal of lipid research》2013,54(10):2615-2622
Hepatic glucose overproduction is a major characteristic of type 2 diabetes. Because glucagon is a key regulator for glucose homeostasis, antagonizing the glucagon receptor (GCGR) is a possible therapeutic strategy for the treatment of diabetes mellitus. To study the effect of hepatic GCGR inhibition on the regulation of lipid metabolism, we generated siRNA-mediated GCGR knockdown (si-GCGR) in the db/db mouse. The hepatic knockdown of GCGR markedly reduced plasma glucose levels; however, total plasma cholesterol was increased. The detailed lipid analysis showed an increase in the LDL fraction, and no change in VLDL HDL fractions. Further studies showed that the increase in LDL was the result of over-expression of hepatic lipogenic genes and elevated de novo lipid synthesis. Inhibition of hepatic glucagon signaling via siRNA-mediated GCGR knockdown had an effect on both glucose and lipid metabolism in db/db mice. 相似文献
65.
Alison M. Strack Ester Carballo-Jane Sheng-ping Wang Jiyan Xue Xiaoli Ping Lesley Ann McNamara Anil Thankappan Olga Price Michael Wolff T. J. Wu Douglas Kawka Michele Mariano Charlotte Burton Ching H. Chang Jing Chen John Menke Silvi Luell Emanuel I. Zycband Xinchun Tong Richard Raubertas Carl P. Sparrow Brian Hubbard John Woods Gary O'Neill M. Gerard Waters Ayesha Sitlani 《Journal of lipid research》2013,54(1):177-188
The use of nicotinic acid to treat dyslipidemia is limited by induction of a “flushing” response, mediated in part by the interaction of prostaglandin D2 (PGD2) with its G-protein coupled receptor, DP1 (Ptgdr). The impact of DP1 blockade (genetic or pharmacologic) was assessed in experimental murine models of atherosclerosis. In Ptgdr−/−ApoE−/− mice versus ApoE−/− mice, both fed a high-fat diet, aortic cholesterol content was modestly higher (1.3- to 1.5-fold, P < 0.05) in Ptgdr−/−ApoE−/− mice at 16 and 24 weeks of age, but not at 32 weeks. In multiple ApoE−/− mouse studies, a DP1-specific antagonist, L-655, generally had a neutral to beneficial effect on aortic lipids in the presence or absence of nicotinic acid treatment. In a separate study, a modest increase in some atherosclerotic measures was observed with L-655 treatment in Ldlr−/− mice fed a high-fat diet for 8 weeks; however, this effect was not sustained for 16 or 24 weeks. In the same study, treatment with nicotinic acid alone generally decreased plasma and/or aortic lipids, and addition of L-655 did not negate those beneficial effects. These studies demonstrate that inhibition of DP1, with or without nicotinic acid treatment, does not lead to consistent or sustained effects on plaque burden in mouse atherosclerotic models. 相似文献
66.
67.
68.
KB Cullberg T Christiansen SK Paulsen JM Bruun SB Pedersen B Richelsen 《Obesity (Silver Spring, Md.)》2013,21(3):454-460
Background:
Vascular growth is a prerequisite for adipose tissue (AT) development and expansion. Some AT cytokines and hormones have effects on vascular development, like vascular endothelial growth factor (VEGF‐A), angiopoietin (ANG‐1), ANG‐2 and angiopoietin‐like protein‐4 (ANGPTL‐4).Methods:
In this study, the independent and combined effects of diet‐induced weight loss and exercise on AT gene expression and proteins levels of those angiogenic factors were investigated. Seventy‐nine obese males and females were randomized to: 1. Exercise‐only (EXO; 12‐weeks exercise without diet‐restriction), 2. Hypocaloric diet (DIO; 8‐weeks very low energy diet (VLED) + 4‐weeks weight maintenance diet) and 3. Hypocaloric diet and exercise (DEX; 8‐weeks VLED + 4‐weeks weight maintenance diet combined with exercise throughout the 12 weeks). Blood samples and fat biopsies were taken before and after the intervention.Results:
Weight loss was 3.5 kg in the EXO group and 12.3 kg in the DIO and DEX groups. VEGF‐A protein was non‐significantly reduced in the weight loss groups. ANG‐1 protein levels were significantly reduced 22‐25% after all three interventions (P < 0.01). The ANG‐1/ANG‐2 ratio was also decreased in all three groups (P < 0.05) by 27‐38%. ANGPTL‐4 was increased in the EXO group (15%, P < 0.05) and 9% (P < 0.05) in the DIO group. VEGF‐A, ANG‐1, and ANGPTL‐4 were all expressed in human AT, but only ANGPTL‐4 was influenced by the interventions.Conclusions:
Our data show that serum VEGF‐A, ANG‐1, ANG‐2, and ANGPTL‐4 levels are influenced by weight changes, indicating the involvement of these factors in the obese state. Moreover, it was found that weight loss generally was associated with a reduced angiogenic activity in the circulation. 相似文献69.
Correction: Targeting Homologous Recombination in Notch-Driven C. elegans Stem Cell and Human Tumors
70.
Renato Sathler-Avelar Danielle Marquete Vitelli-Avelar Armanda Moreira Mattoso-Barbosa Marcelo Perdig?o-de-Oliveira Ronaldo Peres Costa Silvana Maria Elói-Santos Matheus de Souza Gomes Laurence Rodrigues do Amaral Andréa Teixeira-Carvalho Olindo Assis Martins-Filho Edward J. Dick Jr Gene B. Hubbard Jane F. VandeBerg John L. VandeBerg 《PLoS neglected tropical diseases》2016,10(1)