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11.
A viable option for increasing nitrogen (N) use efficiency and mitigation of negative impacts of N on the environment is to capitalize on multi-element interactions through implementation of nutrient management programs that provide balanced nutrition. Numerous studies have demonstrated the immediate efficacy of this approach in the developing regions like China and India as well as developed countries in North America. Based on 241 site-years of experiments in these countries, the first-year N recovery efficiency (RE) for the conventional or check treatments averaged 21% while the balanced treatments averaged 54% RE, for an average increase of 33% in RE due to balanced nutrition. Effective policies to promote adoption are most likely those that enable site-specific approaches to nutrient management decisions rather than sweeping, nation-wide incentives supporting one nutrient over another. Local farmers, advisers and officials need to be empowered with tools and information to help them define necessary changes in practices to create more balanced nutrient management. 相似文献
12.
A Puri R Sethi B Singh SK Dwivedi VS Narain RK Saran VK Puri 《Indian pacing and electrophysiology journal》2009,9(3):186-189
A 25-year-old previously asymptomatic pregnant woman at 36 weeks'' gestation was noticed to have repetitive monomorphic ventricular tachycardia. A dilated left ventricle with moderately reduced systolic function was found on echocardiographic examination. This is a very rare presentation of peripartum cardiomyopathy (PPCMP) presenting with repetitive monomorphic ventricular tachycardia. 相似文献
13.
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14.
Allophanate lyase can be induced by urea or acetamide 20-40-fold within 4 h in NH4 + -deprived cultures of Chlamydomonas reinhardi. In light-synchronized cultures, allophanate lyase induction appeared to be limited to the light phase of the cell cycle, provided that culture samples were induced under ongoing illumination conditions (i.e. light induction of light phase cells and dark induction of dark phase cells). However, when culture samples were induced under constant light conditions this cell cycle pattern was abolished. Light was found to be required for allophanate lyase induction and this was shown to be due, in part, to the light requirement for inducer uptake. The relationship between allophanate lyase induction and gametogenesis is discussed. 相似文献
15.
The murid rodent subfamily Sigmodontinae contains 79 genera which are
distributed throughout the New World. The time of arrival of the first
sigmodontines in South America and the estimated divergence time(s) of the
different lineages of South American sigmodontines have been controversial
due to the lack of a good fossil record and the immense number of extant
species. The "early-arrival hypothesis" states that the sigmodontines must
have arrived in South America no later than the early Miocene, at least 20
MYA, in order to account for their vast present-day diversity, whereas the
"late-arrival hypothesis" includes the sigmodontines as part of the
Plio-Pleistocene Great American Interchange, which occurred approximately
3.5 MYA. The phylogenetic relationships among 33 of these genera were
reconstructed using mitochondrial DNA (mtDNA) sequence data from the ND3,
ND4L, arginine tRNA, and ND4 genes, which we show to be evolving at the
same rate. A molecular clock was calibrated for these genes using published
fossil dates, and the genetic distances were estimated from the DNA
sequences in this study. The molecular clock was used to estimate the dates
of the South American sigmodontine origin and the main sigmodontine
radiation in order to evaluate the "early-" and "late-arrival" scenarios.
We estimate the time of the sigmodontine invasion of South America as
between approximately 5 and 9 MYA, supporting neither of the scenarios but
suggesting two possible models in which the invading lineage was either (1)
ancestral to the oryzomyines, akodonts, and phyllotines or (2) ancestral to
the akodonts and phyllotines and accompanied by the oryzomyines. The
sigmodontine invasion of South America provides an example of the advantage
afforded to a lineage by the fortuitous invasion of a previously
unexploited habitat, in this case an entire continent.
相似文献
16.
Plasmin-mediated Proteolysis Is Required for Hepatocyte Growth Factor
Activation during Liver
Repair
Kumar Shanmukhappa Ursula Matte Jay L. Degen Jorge A. Bezerra 《The Journal of biological chemistry》2009,284(19):12917-12923
The physiological relevance of the activation of hepatocyte growth factor
(Hgf) by the plasminogen (Plg) system of proteases and its contribution to
tissue repair are largely undefined. Here, we investigated whether the
defective liver repair in mice lacking Plg is due to impaired activation of
Hgf. Loss of Plg in vivo suppressed Hgf activation and signaling
through its Met tyrosine kinase receptor. Without Plg, hepatocytes were
unresponsive to Hgf-induced proliferation and migration, with a more
pronounced impairment in hepatocyte movement within the hepatic environment.
Most notably, circumventing the defect in proteolytic activation of Hgf by the
downstream expression of an activated Met receptor corrected the functional
deficits and improved liver repair in Plg-deficient mice. These findings
support a fibrinolysis-unrelated role for Plg in modulating cell proliferation
and migration by activation of Hgf.Tissue repair requires a prompt proliferative response in concert with the
timely reorganization of the extracellular matrix. Each one of these processes
can be disrupted by the loss of individual growth factors or proteases, but
the precise regulatory relationship between these molecules in supporting
tissue repair is not fully understood. Multiple in vitro studies have
inferred that proteases in the plasminogen
(Plg)2 activation
system may be important in the proteolytic activation of the hepatocyte growth
factor (Hgf)
(1–4),
the ligand for the Met tyrosine kinase receptor that exerts potent mitogenic
and motogenic properties to mesenchymal and epithelial cells. This concept is
made even more attractive by the fact that Hgf is structurally related to Plg,
with multiple kringle domains and a catalytically inactive serine
protease-like domain. However, the physiological relevance of Plg to Hgf
activation and Hgf-related reparative processes are controversial and
effectively unexplored in vivo.We previously reported that a genetically imposed loss of circulating Plg
severely impairs clearance of necrotic cells and the repopulation of injured
zones by newly formed cells but without compromising the general hepatic
proliferative response (5).
Despite the indisputable role of Plg in fibrin clearance
(6), complementary studies in
mice with no capacity for fibrin deposition have shown that the loss of
fibrinolytic function alone in Plg-deficient mice cannot account for the
impediment in tissue repair
(5). Multiple nonfibrin targets
of plasmin-mediated proteolysis are known (e.g. serine and
metalloprotease zymogens, and extracellular matrix glycoproteins, latent
growth factors), and it is feasible that they may contribute to the focal
clearance of necrotic tissue. However, based on recent findings pointing to a
strikingly similar defect in hepatic repair in mice lacking Plg or a
conditional loss of Met (7), an
attractive hypothesis emerged that the Plg activation system supports
physiological liver repair by activation of the Met ligand, Hgf. Testing this
hypothesis, we found that the loss of Plg impairs Hgf activation, suppresses
Met phosphorylation and signaling, and prevents Hgf-induced migration of
hepatocytes. Most notably, consistent with a physiologically relevant
contribution of Plg to Hgf-Met signaling, the expression of an
autophosphorylated Met largely corrected the defective repair in Plg-deficient
livers. 相似文献
17.
KK Chan B Dassanayake R Deen RE Wickramarachchi SK Kumarage S Samita KI Deen 《World journal of surgical oncology》2010,8(1):1-11
Introduction
Male breast cancer (MBC) is a rare, yet potentially aggressive disease. Although literature regarding female breast cancer (FBC) is extensive, little is known about the etiopathogenesis of male breast cancer. Studies from our laboratory show that MBCs have a distinct immunophenotypic profile, suggesting that the etiopathogenesis of MBC is different from FBCs. The aim of this study was to evaluate and correlate the immunohistochemical expression of cell cycle proteins in male breast carcinoma to significant clinico-biological endpoints.Methods
75 cases of MBC were identified using the records of the Saskatchewan Cancer Agency over 26 years (1970-1996). Cases were reviewed and analyzed for the immunohistochemical expression of PCNA, Ki67, p27, p16, p57, p21, cyclin-D1 and c-myc and correlated to clinico-biological endpoints of tumor size, node status, stage of the disease, and disease free survival (DFS).Results
Decreased DFS was observed in the majority of tumors that overexpressed PCNA (98%, p = 0.004). The overexpression of PCNA was inversely correlated to the expression of Ki67 which was predominantly negative (78.3%). Cyclin D1 was overexpressed in 83.7% of cases. Cyclin D1 positive tumors were smaller than 2 cm (55.6%, p = 0.005), had a low incidence of lymph node metastasis (38.2%, p = 0.04) and were associated with increased DFS of >150 months (p = 0.04). Overexpression of c-myc (90%) was linked with a higher incidence of node negativity (58.3%, p = 0.006) and increased DFS (p = 0.04). p27 over expression was associated with decreased lymph node metastasis (p = 0.04). P21 and p57 positive tumors were related to decreased DFS (p = 0.04). Though p16 was overexpressed in 76.6%, this did not reach statistical significance with DFS (p = 0.06) or nodal status (p = 0.07).Conclusion
Aberrant cell cycle protein expression supports our view that these are important pathways involved in the etiopathogenesis of MBC. Tumors with overexpression of Cyclin D1 and c-myc had better outcomes, in contrast to tumors with overexpression of p21, p57, and PCNA with significantly worse outcomes. P27 appears to be a predictive marker for lymph nodal status. Such observation strongly suggests that dysregulation of cell cycle proteins may play a unique role in the initiation and progression of disease in male breast cancer. Such findings open up new avenues for the treatment of MBC as a suitable candidate for novel CDK-based anticancer therapies in the future. 相似文献18.
19.
Proliferating cell nuclear antigen (PCNA) as a proliferative marker during embryonic and adult zebrafish hematopoiesis 总被引:4,自引:1,他引:3
Leung AY Leung JC Chan LY Ma ES Kwan TT Lai KN Meng A Liang R 《Histochemistry and cell biology》2005,124(2):105-111
We investigated the expression of proliferative cell nuclear antigen (PCNA) in zebrafish to delineate the proliferative hematopoietic
component during adult and embryonic hematopoiesis. Immunostaining for PCNA and enhanced green fluorescence protein (eGFP)
was performed in wild-type and fli1-eGFP (endothelial marker) and gata1-eGFP (erythroid cell marker) transgenic fish. Expression
of PCNA mRNA was examined in wild-type and chordin morphant embryos. In adult zebrafish kidney, the renal tubules are surrounded
by endothelial cells and it is separated into hematopoietic and excretory compartments. PCNA was expressed in hematopoietic
progenitor cells but not in mature neutrophils, eosinophils or erythroid cells. Some PCNA+ cells are scattered in the hematopoietic
compartment of the kidney while others are closely associated with renal tubular cells. PCNA was also expressed in spermatogonial
stem cells and intestine crypts, consistent with its role in cell proliferation and DNA synthesis. In embryos, PCNA is expressed
in the brain, spinal cord and intermediate cell mass (ICM) at 24 h-post fertilization. In chordin morphants, PCNA is significantly
upregulated in the expanded ICM. Therefore, PCNA can be used to mark cell proliferation in zebrafish hematopoietic tissues
and to identify a population of progenitor cells whose significance would have to be further investigated. 相似文献
20.
Escargot maintains stemness and suppresses differentiation in Drosophila intestinal stem cells 下载免费PDF全文