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Principal Regulator (principal + regulator)
Selected AbstractsPristine New Zealand forest soil is a strong methane sinkGLOBAL CHANGE BIOLOGY, Issue 1 2004Sally J. Price Abstract Methanotrophic bacteria oxidize methane (CH4) in forest soils that cover ,30% of Earth's land surface. The first measurements for a pristine Southern Hemisphere forest are reported here. Soil CH4 oxidation rate averaged 10.5±0.6 kg CH4 ha,1 yr,1, with the greatest rates in dry warm soil (up to 17 kg CH4 ha,1 yr,1). Methanotrophic activity was concentrated beneath the organic horizon at 50,100 mm depth. Water content was the principal regulator of (r2=0.88) from the most common value of field capacity to less than half of this when the soil was driest. Multiple linear regression analysis showed that soil temperature was not very influential. However, inverse co-variability confounded the separation of soil water and temperature effects in situ. Fick's law explained the role of water content in regulating gas diffusion and substrate supply to the methanotrophs and the importance of pore size distribution and tortuosity. This analysis also showed that the chambers used in the study did not affect the oxidation rate measurements. The soil was always a net sink for atmospheric CH4 and no net CH4 (or nitrous oxide, N2O) emissions were measured over the 17-month long study. For New Zealand, national-scale extrapolation of our data suggested the potential to offset 13% of CH4 emissions from ca. 90 M ruminant animals. Our average was about 6.5 times higher than rates reported for most Northern Hemisphere forest soils. This very high was attributed to the lack of anthropogenic disturbance for at least 3000,5000 years and the low rate of atmospheric nitrogen deposition. Our truly baseline data could represent a valid preagricultural, preindustrial estimate of the soil sink for temperate latitudes. [source] Vitamin D and multiple sclerosisJOURNAL OF CELLULAR BIOCHEMISTRY, Issue 2 2008Anita Raghuwanshi Abstract Vitamin D is a principal regulator of calcium homeostasis. However, recent evidence has indicated that vitamin D can have numerous other physiological functions including inhibition of proliferation of a number of malignant cells including breast and prostate cancer cells and protection against certain immune mediated disorders including multiple sclerosis (MS). The geographic incidence of MS indicates an increase in MS with a decrease in sunlight exposure. Since vitamin D is produced in the skin by solar or UV irradiation and high serum levels of 25-hydroxyvitamin D (25(OH)D) have been reported to correlate with a reduced risk of MS, a protective role of vitamin D is suggested. Mechanisms whereby the active form of vitamin D, 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) may act to mediate this protective effect are reviewed. Due to its immunosuppressive actions, it has been suggested that 1,25(OH)2D3 may prevent the induction of MS. J. Cell. Biochem. 105: 338,343, 2008. © 2008 Wiley-Liss, Inc. [source] Methods in Nutrition ScienceNUTRITION REVIEWS, Issue 10 2001The Bone Remodeling Transient: Interpreting Interventions Involving Bone-related Nutrients The bone remodeling transient is a temporary alteration in the balance between bone formation and bone resorption, brought about by any agency that affects bone remodeling. Ascertaining the steady state effect of an intervention requires factoring the component of the change due to the transient out of the total bony response. Since parathyroid hormone (PTH) is the principal regulator of the quantity of remodeling activity, and since calcium intake influences PTH secretion, it follows that altering calcium intake will always induce a remodeling transient. Worked examples from three published calcium intervention studies are presented, and the errors that can be made by ignoring the transient and simply measuring change in bone mass across treatment are described. [source] Reproductive Functions of Corticotropin-Releasing Hormone.AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 4 2004Potential Clinical Utility of Antalarmins (CRH Receptor Type 1 Antagonists), Research Background:, The hypothalamic-pituitary-adrenal (HPA) axis exerts a complex, mostly inhibitory, effect on the female reproductive system. In addition, the principal regulator of this axis, the hypothalamic neuropeptide corticotropin-releasing hormone (CRH) and its receptors have been identified in most female reproductive tissues, including the ovary, uterus, and placenta. Furthermore, CRH is secreted in peripheral inflammatory sites where it exerts strong inflammatory actions. Antalarmins (CRH receptor type 1 antagonists) have been used to elucidate the roles of CRH in stress, inflammation and reproduction. Method of study:, We review existing data on the effects of CRH in the female reproductive system. Results:, Ovarian CRH participates in female sex steroid production, follicular maturation, ovulation and luteolysis. Uterine CRH participates in decidualization, implantation, and early maternal tolerance. Placental CRH participates in the physiology of pregnancy and the onset of parturition. Circulating placental CRH is secreted mostly during the latter half of pregnancy and is responsible for the concurrently increasing physiologic hypercortisolism of this period. After labor and delivery, this hypercortisolism is ensued by a transient suppression of hypothalamic CRH secretion, which may explain the postpartum blues and depression and the increased autoimmune manifestations depression of period, the postpartum period. Conclusions:, These data show that CRH is present in female reproductive tissues, and is regulating key reproductive functions with an inflammatory component, such as ovulation, luteolysis, implantation, and parturition. [source] Erythropoietin stimulates growth and STAT5 phosphorylation in human prostate epithelial and prostate cancer cellsTHE PROSTATE, Issue 2 2006Laurie Feldman Abstract BACKGROUND Erythropoietin (Epo), the principal regulator of erythroid progenitor survival, growth, and differentiation, initiates its action by binding to its cognate cell surface receptor (EpoR). EpoR have been identified on a variety of non-hematopoietic cells, both normal and malignant, however, little is known about the function of EpoR on malignant cells. METHODS RT-PCR, Western blotting, and immunohistochemistry were used to demonstrate that prostate cancer cells express EpoR at both the gene and protein level. Cell proliferation assays and STAT5 phosphorylation were used to demonstrate Epo's mitogenic action and intracellular signaling, respectively. RESULTS We have demonstrated that transformed prostate epithelial and prostate cancer cell lines, as well as primary prostate tissue, express the EpoR. Importantly, the EpoR on prostate cells are functional, as demonstrated by the observation that each of the cell lines exhibited a dose-dependent proliferative response to Epo, and that Epo triggered STAT5b phosphorylation in the cells. CONCLUSION Human prostatic epithelial cells and prostate cancer cells express functional EpoR, and Epo serves as a growth factor for these cells. These results have implications for our understanding of normal prostatic growth and development and of the pathobiology of human prostate cancer. © 2005 Wiley-Liss, Inc. [source] Pharmacological targeting of CDK9 in cardiac hypertrophyMEDICINAL RESEARCH REVIEWS, Issue 4 2010Vladimír Kry Abstract Cardiac hypertrophy allows the heart to adapt to workload, but persistent or unphysiological stimulus can result in pump failure. Cardiac hypertrophy is characterized by an increase in the size of differentiated cardiac myocytes. At the molecular level, growth of cells is linked to intensive transcription and translation. Several cyclin-dependent kinases (CDKs) have been identified as principal regulators of transcription, and among these CDK9 is directly associated with cardiac hypertrophy. CDK9 phosphorylates the C -terminal domain of RNA polymerase II and thus stimulates the elongation phase of transcription. Chronic activation of CDK9 causes not only cardiac myocyte enlargement but also confers predisposition to heart failure. Due to the long interest of molecular oncologists and medicinal chemists in CDKs as potential targets of anticancer drugs, a portfolio of small-molecule inhibitors of CDK9 is available. Recent determination of CDK9's crystal structure now allows the development of selective inhibitors and their further optimization in terms of biochemical potency and selectivity. CDK9 may therefore constitute a novel target for drugs against cardiac hypertrophy. © 2009 Wiley Periodicals, Inc. Med Res Rev 30, No. 4, 646,666, 2010 [source] | |||||||||||||