335 research outputs found
Data for: Leptin and HPA axis activity in diabetic rats: Effects of adrenergic agonists
No full textThis study explores the effect of diabetes on norepinephrine release in the paraventricular nucleus of the hypothalamus and its relationship to circulating corticosterone. Leptin treatment helps to partially reverse the increase in noradrenergic activity in diabetic rats. Adrenergic agonists were used to reverse the effect of leptin. It was found that while the alpha adrenergic agonist clonidine reversed the effect of leptin on norepinephrine release towards the end of the observation period, the beta adrenergic agonist, isoproterenol, did not have a similar effect. We conclude that the hypothalamus remains sensitive to alpha adernergic agonists in diabetes, but not to beta adrenergic agonists. Leptin treatment produces a dramatic drop in circulating corticosterone indicating that the adrenals remain sensitive to leptin during diabetes. Moreover, both adrenergic agonists were able to counter leptin's effects on corticosterone. These results indicate that the adrenals continue to be sensitive to both adrenergic receptors in diabetes
Microstructure and mechanical properties of nickel coated multi walled carbon nanotube reinforced stainless steel 316L matrix composites by laser sintering process
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Anthocyanin modified triphenylamine based organic sensitizer for dye sensitized solar cells (DSSC) - A theoretical approach
No full textHOXA1-stimulated oncogenicity is mediated by selective upregulation of components of the p44/42 MAP kinase pathway in human mammary carcinoma cells
No full textExpression of homeobox A1 (HOXA1) results in oncogenic transformation of immortalized human mammary epithelial cells with aggressive tumor formation in vivo. However, the mechanisms by which HOXA1 mediates oncogenic transformation is not well defined. To identify molecules that could potentially be involved in HOXA1-mediated oncogenic transformation, microarray analysis was utilized to characterize and compare the gene expression pattern in response to forced expression or depletion of HOXA1 in human mammary carcinoma cells. Gene expression profiling identified that genes involved in the p44/42 mitogen-activated protein (MAP) kinase activation pathway (GRB2, MAP kinase kinase (MEK1) and SDFR1) or p44/42 MAP kinase-regulated genes (IER3, EPAS1, PCNA and catalase) are downstream expression targets of HOXA1. Forced expression of HOXA1 increased GRB2 and MEK1 mRNA and protein expression and increased p44/42 MAP kinase phosphorylation, activity and Elk-1-mediated transcription. Use of a MEK1 inhibitor demonstrated that increased p44/42 MAP kinase activity is required for the HOXA1-mediated increase in cell proliferation, survival, oncogenicity and oncogenic transformation. Thus, modulation of the p44/42 MAP kinase pathway is one mechanism by which HOXA1 mediates oncogenic transformation of the human mammary epithelial cell
Search for the human homolog of S. cerevisiae PTR2 gene
No full textPeptide transport is an evolutionarily conserved phenomenon with functional significance in cell nutrition. An attempt to identify a human homolog of the S. cerevisiae peptide transport gene (PTR2) was made in order to study the molecular features of the putative human gene. S. cerevisiae ptr2 mutant PB1X-9B was transformed with a HeLa cell cDNA library and ptr2+ transformants were selected directly on dipeptide medium. A single clone with a 10kb insert was obtained. Subsequently, the complementing region was subcloned as a 6kb fragment of the insert. Southern and DNA sequence analyses showed that the isolated clone was identical to the S. cerevisiae PTR2 and not derived from HeLa cell DNA. The explanation for this result is not apparent
The effects of aging and dual task performance on language production
No full textThis is an electronic version of an article published in Kemper, S., Schmalzried, R., Herman, R., Leedahl, S., & Mohankumar, D. (2009). The effects of aging and dual task performance on language production. Aging, Neuropsychology, and Cognition, 16, 241-259. PM#2674132. Aging, Neuropsychology, and Cognition
is available online at www.taylorandfrancis.comA digital pursuit rotor task was used to measure dual task costs of language production by young and older adults. After training on the pursuit rotor, participants were asked to track the moving target while providing a language sample. When simultaneously engaged, young adults experienced greater dual task costs to tracking, fluency, and grammatical complexity than older adults. Older adults were able to preserve their tracking performance by speaking more slowly. Individual differences in working memory, processing speed, and Stroop interference affected vulnerability to dual task costs. These results demonstrate the utility of using a digital pursuit rotor to study the effects of aging and dual task demands on language production and confirm prior findings that young and older adults use different strategies to accommodate to dual task demands
Prenatal stress-mediated fetal programming of obesity in diet-induced obese and dietary resistant rats
No full textGenotype, diet and environment or life style factors are known to be associated with the development of obesity and metabolic syndrome in adults. However, recent evidence suggests that prenatal factors could contribute to obesity as well. One of the prenatal factors implicated in the development of metabolic syndrome in the offspring is stress, which is known to increase circulating glucocorticoids during pregnancy. Prolonged exposure of the developing fetus to excess glucocorticoid levels results in long lasting neuroendocrine changes which predispose the offspring to obesity and other cardiovascular disorders. Considering the fact that 30% of today's maternal population is obese, it is also important to address the impact of prenatal stress in the background of maternal obesity. Hence, we used diet-induced obese (DIO) and dietary resistant (DR) rat model to explore the mechanisms underlying prenatal stress mediated fetal programming of obesity in DIO and DR rats. Prenatal stress was associated with catch up growth and hyperinsulinemia in the DIO offspring. Although, prenatal stress reduced birth weight in the DR offspring, it did not result in any other adverse metabolic outcomes. Next, we investigated the role of stress axis hyperactivation in prenatal stress-induced metabolic programming in the DIO offspring. In the DIO rats, prenatal stress resulted in hyperactivation of stress axis marked by increased norepinephrine (NE) levels in the paraventricular nucleus in the  hypothalamus and increased corticotrophin releasing hormone levels in the median eminence. However, the serum corticosterone (CORT) levels were not altered in the prenatally stressed DIO and DR offspring. Despite, no change in circulating CORT levels, glucocorticoids might play a role in metabolic syndrome through increasing 11β-hydroxysteroid dehydrogenase enzyme (11βHSD1) in the target tissues. 11βHSD1 is highly expressed in metabolically active tissues like liver and adipose tissue and is involved in the intracellular generation of CORT by converting inactive 11-dehydroCORT to active CORT. Hence, we investigated the role of 11βHSD1 in the liver and adipose tissue in prenatal stress mediated metabolic programming. Prenatal stress significantly increased 11βHSD1 mRNA and protein expression in the visceral adipose tissue accompanied with hypertrophied adipocytes in the DIO offspring. There were no differences in 11βHSD1 expression in the liver suggesting prenatal stress results in tissue-specific programming of 11βHSD1 expression. Taken together, the results suggest that prenatal stress produces differential metabolic effects in DIO and DR rats. Further, 11βHSD1 could mediate the metabolic effects observed in the prenatally stressed offspring and thus may be a potential mechanism for fetal origins of obesity.Thesis (Ph. D.)--Michigan State University. Pharmacology and Toxicology-Environmental Toxicology, 2012Includes bibliographical references (pages 159-178
Application of comparative genomics in developing molecular markers tightly linked to the virus resistance gene Rsv4 in soybean
No full textThe Rsv4 gene confers resistance to all the known strain groups of soybean mosaic virus in soybean (Glycine max (L.) Merr.). To construct a fine genetic map near Rsv4 in soybean, we employed a comparative genomics approach that used genome sequence information of the model legume Lotus japonicus. Sequences of the soybean expressed sequence tags (ESTs) AI856415 and BF070293 mapping to one side of the Rsv4 gene showed high similarity with gene sequences of the transformation-competent artificial chromosome (TAC) clone LjT32P24 of Lotus. LjT32P24 is tightly linked to another sequenced TAC clone, LjT26I01, in Lotus. A new marker, AW307114A, developed from soybean EST AW307114, which is homologous to a Lotus gene within LjT26I01, was mapped to the other side of the Rsv4 gene. The identification of the microsyntenic relationship facilitated the development of additional 2 EST markers between BF070293-S and AW307114A bracketing the Rsv4 gene. Several other markers developed in this study were mapped to putative homoeologous or duplicated chromosomal regions in soybean. Alignment between the soybean maps indicated that Rsv4 is located near a local chromosomal rearrangement. This targeted comparative mapping serves to provide a foundation for marker-assisted selection and cloning of the Rsv4 gene.open
Low dose chronic estradiol-17beta exposure induces ovarian pathology and inhibits tuberoinfundibular dopaminergic neuronal function by inducing a proinflammatory state within the arcuate nucleus
No full textEstrogen exposure is known to cause hyperprolactinemia which can lead to the development of mammary and pituitary tumors. This hyperprolactinemia is associated with a decrease in the activity of tuberoinfundibular dopaminergic (TIDA) neurons of the hypothalamus. Perikarya of TIDA neurons are located in the arcuate nucleus (AN) of the hypothalamus and their axon terminals extend to the median eminence (ME). Here, dopamine is secreted into the hypophyseoportal circulation and acts on lactotrophs in the anterior pituitary gland to provide tonic inhibition of prolactin release. Therefore, if the activity of TIDA neuronal function is inhibited by estrogen, there is a decrease in dopamine (DA) levels, prolactin is no longer inhibited and a state of hyperprolactinemia ensues. Though it has been established that estrogens inhibit TIDA function, the mechanism by which estrogen exerts this effect has not been clearly elucidated. We hypothesized that a low dose of estradiol17-\ue2 (E2) would cause an increase in IL-1\ue2 and nitrate levels within the arcuate nucleus (AN), and that this local proinflammatory environment would damage TIDA neurons through nitration of tyrosine hydroxylase, which is the rate-limiting enzyme in DA synthesis. To test this hypothesis, we exposed reproductivelyintact and ovariectomized female Sprague-Dawley rats to E2 by subcutaneously implanting them with slow-release E2 pellets which release E2 at 20ng per day for 90 days. After 90 days of exposure, the animals were sacrificed and serum was collected for hormonal analysis, brain sections were microdissected to analyze IL-1\ue2 and nitrate levels in the AN via ELISA and modified Griess assay, respectively, the ME was microdissected and analyzed for the neurotransmitter DA using high performance liquid chromatography (HPLC), and western blot was performed to measure tyrosine hydroxylase (TH) and nitration of TH (nT) in the ME. Our results demonstrate that indeed, chronic exposure to a low dose of E2 increased serum prolactin, decreased DA levels in the ME, increased IL-1\ue2 and nitrate concentrations in the AN and increased the ratio of nT to TH in the ME. These findings provide strong evidence that chronic exposure to a low level of E2 induces a proinflammatory state within the AN and this may be a possible mechanism by which E2 exposure causes inhibition of TIDA activity and hyperprolactinemia.Additionally, estrogen exposure is known to affect the reproductive axis and to induce ovarian follicular cysts. Exposure to estrogen has been implicated as a model for polycystic ovary syndrome (PCOS) in women. However, most studies claiming this association, have primarily focused on the ovarian morphologic phenotype and have not thoroughly assessed the other clinical parameters that would correlate with those seen in women with PCOS. We explored whether our paradigm of chronic exposure to low levels E2 could cause changes in ovarian morphology and hormonal profiles similar to that of PCOS. Adult female rats were sham-implanted (control) or implanted with slow-release E2 (20 ng/day) pellets for 30 (E-30), 60 (E-60), or 90 (E-90) days. Old constant estrous (OCE) rats were used for comparison. At the end oftreatment, ovaries were collected and subjected to histological examination and Mullerian inhibiting substance (MIS) immunohistochemistry. We found that follicular size increased with E2 exposure and the number of corpora lutea (CL) decreased in a exposure-dependent manner indicating failure of ovulation. Estradiol treatment was associated with a decrease of MIS immunolabeling in follicles. Serum testosterone (T) levels decreased in a duration dependent manner with E2 treatment. Also, the ratio of serum LH to FSH remained unaffected in different groups. While ovarian changes observed in this model are similar to that seen in PCOS, the hormonal profiles are very different from that observed in PCOS and we therefore determined that this may not be a true model for this condition.Thesis (Ph. D.)--Michigan State University. Pathology, 2011Includes bibliographical references (pages 142-158
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