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The rat STSL locus: characterization, chromosomal assignment, and genetic variations in sitosterolemic hypertensive rats
Hongwei Yu, Bhaswati Pandit, Eric Klett, Mi-Hye Lee, Kangmo Lu, Khalil Helou, Ikuo Ikeda, Nami Egashira, Masao Sato, Richard Klein, Ashok Batta, Gerald Salen, Shailendra B Patel
BMC Cardiovascular Disorders , 2003, DOI: 10.1186/1471-2261-3-4
Abstract: To investigate whether mutations in Abcg5 or Abcg8 exist in SHR, SHRSP, WKY and GH rats, we initiated a systematic search for the genetic variation in coding and non-coding region of Abcg5 and Abcg8 genes in these strains. We isolated the rat cDNAs for these genes and characterized the genomic structure and tissue expression patterns, using standard molecular biology techniques and FISH for chromosomal assignments.Both rat Abcg5 and Abcg8 genes map to chromosome band 6q12. These genes span ~40 kb and contain 13 exons and 12 introns each, in a pattern identical to that of the STSL loci in mouse and man. Both Abcg5 and Abcg8 were expressed only in liver and intestine. Analyses of DNA from SHR, SHRSP, GH, WKY, Wistar, Wistar King A (WKA) and Brown Norway (BN) rat strains revealed a homozygous G to T substitution at nucleotide 1754, resulting in the coding change Gly583Cys in sterolin-1 only in rats that are both sitosterolemic and hypertensive (SHR, SHRSP and WKY).The rat STSL locus maps to chromosome 6q12. A non-synonymous mutation in Abcg5, Gly583Cys, results in sitosterolemia in rat strains that are also hypertensive (WKY, SHR and SHRSP). Those rat strains that are hypertensive, but not sitosterolemic (e.g. GH rat) do not have mutations in Abcg5 or Abcg8. This mutation allows for expression and apparent apical targeting of Abcg5 protein in the intestine. These rat strains may therefore allow us to study the pathophysiological mechanisms involved in the human disease of sitosterolemia.The human disorder of sitosterolemia, also known as phytosterolemia (MIM 210250), is an autosomal recessive disorder characterized by the marked elevation of plasma phytosterols e.g. β-sitosterol, campesterol and stigmasterol [1,2]. Hypercholesterolemia primarily during childhood, accelerated atherosclerosis in some adult patients leading to premature death, as well a hemolytic anaemia, arthralgias and tendon and tuberous xanthoma formations are other clinical features. Studies have sho
Localization of ABCG5 and ABCG8 proteins in human liver, gall bladder and intestine
Eric L Klett, Mi-Hye Lee, David B Adams, Kenneth D Chavin, Shailendra B Patel
BMC Gastroenterology , 2004, DOI: 10.1186/1471-230x-4-21
Abstract: Here we report the biochemical and immuno-localization of ABCG5 and ABCG8 in human liver, gallbladder and intestine using cell fractionation and immunohistochemical analyses.We raised peptide antibodies against ABCG5 and ABCG8 proteins. Using human liver samples, cell fractionation studies showed both proteins are found in membrane fractions, but they did not co-localize with caveolin-rafts, ER, Golgi or mitochondrial markers. Although their distribution in the sub-fractions was similar, they were not completely contiguous. Immunohistochemical analyses showed that while both proteins were readily detectable in the liver, ABCG5 was found predominately lining canalicular membranes, whereas ABCG8 was found in association with bile duct epithelia. At the cellular level, ABCG5 appeared to be apically expressed, whereas ABCG8 had a more diffuse expression pattern. Both ABCG5 and ABCG8 appeared to localize apically as shown by co-localization with MRP2. The distribution patterns of ABCG5 and ABCG8 in the gallbladder were very similar to each other. In the small intestine both ABCG5 and ABCG8 appear to line the brush border. However, at the level of the enterocyte, the cellular distribution patterns of ABCG5 and ABCG8 differed, such that ABCG5 was more diffuse, but ABCG8 was principally apical. Using standard deglycosylation methods, ABCG5 and ABCG8 do not appear to be glycosylated, suggesting a difference between human and mouse proteins.We report the distribution patterns of ABCG5 and ABCG8 in human tissues. Cell fractionation studies showed that both proteins co-fractionated in general, but could also be found independent of each other. As predicted, they are expressed apically in both intestine and liver, although their intracellular expression patterns are not completely congruent. These studies support the concept of heterodimerization of ABCG5 and ABCG8, but also support the notion that these proteins may have an independent function.The gastrointestinal tract is the
ABCG5-positivity in tumor buds is an indicator of poor prognosis in node-negative colorectal cancer patients  [cached]
lsabel Hostettler, Inti Zlobec, Luigi Terracciano, Alessandro Lugli
World Journal of Gastroenterology , 2010,
Abstract: AIM: To analyze the expression of 8 putative cancer stem cell (CSC) markers within colorectal cancer tumor buds and to determine their prognostic impact in patients with this disease.METHODS: Immunohistochemistry was performed on 101 colorectal cancer resections for CK22 (to identify tumor buds) as well as CD133, CD166, CD24, CD44s, CD90, EpCAM, ALDH1, and ABCG5, and their expression within tumor buds was evaluated.RESULTS: CD90, CD44s, and CD133 expression in tumor buds was found in less than 5% of all cases. ALDH1, CD24, CD166 were expressed in 16.5%, 16.2%, and 34% cases, respectively, while ABCG5 and EpCAM expression was more frequent and found in 35% and 69% of cases, respectively. Of the 8 markers studied, EpCAM and ABCG5 positivity in tumor buds were significantly associated with poor prognosis (P = 0.023, P = 0.038, respectively) in multivariable analysis with pT and pN classification [P = 0.048; hazard ratio (HR): 2.64; 95% CI: 1.0-6.9, for EpCAM and P = 0.029; HR: 2.22; 95% CI: 1.0-4.5, for ABCG5]. Poor survival time was particularly striking for lymph node-negative patients with ABCG5-positive buds (P < 0.001).CONCLUSION: Expression of putative stem cell markers EpCAM and ABCG5 within the tumor buds of colorectal cancer are frequently noted and are associated with poor prognosis.
Acetylcholine and bradykinin enhance hypotension and affect the function of remodeled conduit arteries in SHR and SHR treated with nitric oxide donors
Gerová, M.;Kristek, F.;Cacányiová, S.;Cebová, M.;
Brazilian Journal of Medical and Biological Research , 2005, DOI: 10.1590/S0100-879X2005000600019
Abstract: discrepancy was found between enhanced hypotension and attenuated relaxation of conduit arteries in response to acetylcholine (ach) and bradykinin (bk) in nitric oxide (no)-deficient hypertension. the question is whether a similar phenomenon occurs in spontaneously hypertensive rats (shr) with a different pathogenesis. wistar rats, shr, and shr treated with no donors [molsidomine (50 mg/kg) or pentaerythritol tetranitrate (100 mg/kg), twice a day, by gavage] were studied. after 6 weeks of treatment systolic blood pressure (bp) was increased significantly in experimental groups. under anesthesia, the carotid artery was cannulated for bp recording and the jugular vein for drug administration. the iliac artery was used for in vitro studies and determination of geometry. compared to control, shr showed a significantly enhanced (p < 0.01) hypotensive response to ach (1 and 10 μg, 87.9 ± 6.9 and 108.1 ± 5.1 vs 35.9 ± 4.7 and 64.0 ± 3.3 mmhg), and bk (100 μg, 106.7 ± 8.3 vs 53.3 ± 5.2 mmhg). shr receiving no donors yielded similar results. in contrast, maximum relaxation of the iliac artery in response to ach was attenuated in shr (12.1 ± 3.6 vs 74.2 ± 8.6% in controls, p < 0.01). iliac artery inner diameter also increased (680 ± 46 vs 828 ± 28 μm in controls, p < 0.01). wall thickness, wall cross-section area, wall thickness/inner diameter ratio increased significantly (p < 0.01). no differences were found in this respect among shr and shr treated with no donors. these findings demonstrated enhanced hypotension and attenuated relaxation of the conduit artery in response to no activators in shr and in shr treated with no donors, a response similar to that found in no-deficient hypertension.
Acetylcholine and bradykinin enhance hypotension and affect the function of remodeled conduit arteries in SHR and SHR treated with nitric oxide donors  [cached]
Gerová M.,Kristek F.,Cacányiová S.,Cebová M.
Brazilian Journal of Medical and Biological Research , 2005,
Abstract: Discrepancy was found between enhanced hypotension and attenuated relaxation of conduit arteries in response to acetylcholine (ACh) and bradykinin (BK) in nitric oxide (NO)-deficient hypertension. The question is whether a similar phenomenon occurs in spontaneously hypertensive rats (SHR) with a different pathogenesis. Wistar rats, SHR, and SHR treated with NO donors [molsidomine (50 mg/kg) or pentaerythritol tetranitrate (100 mg/kg), twice a day, by gavage] were studied. After 6 weeks of treatment systolic blood pressure (BP) was increased significantly in experimental groups. Under anesthesia, the carotid artery was cannulated for BP recording and the jugular vein for drug administration. The iliac artery was used for in vitro studies and determination of geometry. Compared to control, SHR showed a significantly enhanced (P < 0.01) hypotensive response to ACh (1 and 10 μg, 87.9 ± 6.9 and 108.1 ± 5.1 vs 35.9 ± 4.7 and 64.0 ± 3.3 mmHg), and BK (100 μg, 106.7 ± 8.3 vs 53.3 ± 5.2 mmHg). SHR receiving NO donors yielded similar results. In contrast, maximum relaxation of the iliac artery in response to ACh was attenuated in SHR (12.1 ± 3.6 vs 74.2 ± 8.6% in controls, P < 0.01). Iliac artery inner diameter also increased (680 ± 46 vs 828 ± 28 μm in controls, P < 0.01). Wall thickness, wall cross-section area, wall thickness/inner diameter ratio increased significantly (P < 0.01). No differences were found in this respect among SHR and SHR treated with NO donors. These findings demonstrated enhanced hypotension and attenuated relaxation of the conduit artery in response to NO activators in SHR and in SHR treated with NO donors, a response similar to that found in NO-deficient hypertension.
RESEARCH OF SDH UNIDIRECTIONAL SHR
SDH单向复用段自愈环的研究

Wu Xiang,Wang Yichao,Feng Zhongxi,
伍翔
,王一超,冯重熙

电子与信息学报 , 2001,
Abstract: This paper reviews the SDH SHR, summarily depicts the architecture of U-SHR. Two APS methods of U-SHR are compared. Finally, this paper addresses the problems of lowering the cost of ADM device, timing manners in the U-SHR and working mode of the network element.
An Evolutionary approach for solving Shr?dinger Equation  [PDF]
Khalid jebari,Mohammed Madiafi,Abdelaziz Elmoujahid
Computer Science , 2014,
Abstract: The purpose of this paper is to present a method of solving the Shr\"odinger Equation (SE) by Genetic Algorithms and Grammatical Evolution. The method forms generations of trial solutions expressed in an analytical form. We illustrate the effectiveness of this method providing, for example, the results of its application to a quantum system minimal energy, and we compare these results with those produced by traditional analytical methods
Testosterone influences renal electrolyte excretion in SHR/y and WKY males
Jonathan Toot, Cathy Jenkins, Gail Dunphy, Shannon Boehme, Mike Hart, Amy Milsted, Monte Turner, Daniel Ely
BMC Physiology , 2008, DOI: 10.1186/1472-6793-8-5
Abstract: To investigate the role of the Yc and T, consomic borderline hypertensive (SHR/y) and normotensive Wistar-Kyoto (WKY) rat strains were used (15 weeks) in three T treatment groups: castrate, castrate with T implant and gonadally intact males. Urine was collected (24 hrs at 15 weeks of age) for Na and K measurements by flame photometry. RT-PCR was used to demonstrate the presence of renal androgen receptor (AR) transcripts. Plasma T and aldosterone were measured by RIA. In another experiment the androgen receptor was blocked using flutamide in the diet.Na and K excretion were decreased by T in SHR/y and WKY. AR transcripts were identified in SHR/y and WKY kidneys. Plasma aldosterone was decreased in the presence of T. Blockade of the AR resulted in a significant increase in Na excretion but not in K excretion in both SHR/y and WKY males.T influences electrolyte excretion through an androgen receptor dependent mechanism. There was not a differential Yc involvement in electrolyte excretion between WKY and SHR/y males.Human [1,2] and animal studies [3] have implicated Y-chromosome (Yc) loci as influencing the onset of male hypertension. In the Spontaneously Hypertensive Rat strain (SHR), the SHR Yc contains a locus which increases blood pressure (BP) approximately 20 mmHg compared to the normotensive Wistar Kyoto (WKY) Y chromosome. The Yc is only one genetic component of the total SHR hypertension. In SHR males, the presences of testosterone and androgen receptors through puberty are required for development of the hypertension and associated sympathetic nervous system potentiation, including the Yc component [4,5]. In examining phenotypes that mapped to the Yc and differed between SHR and WKY, our laboratory demonstrated an earlier rise of testosterone (T) levels in SHR males leading into puberty [4] and this phenotype mapped to the SHR Yc. Because of the unique biology of the mammalian Yc the blood pressure phenotype and the T timing phenotype cannot be separated usin
How Channel Segregates Originates: The Flow of Accumulated Impurity Clusters in Solidifying Steels  [PDF]
Dianzhong Li,Xing-Qiu Chen,Paixian Fu,Xiaoping Ma,Hongwei Liu,Yun Chen,Yikun Luan,Yiyi Li
Physics , 2013,
Abstract: The phenomenon, channel segregates (CS) as a result of gravity-driven flow due to density contrast occurred in the solid-liquid mushy zones1during solidification, often causes the severe destruction of homogeneity and even some fatal damages. Investigation on its mechanism sheds light on the understanding and controlling of the formation of solidifying metals,earth's core, igneous rock and sea ice. Until now, it still remains controversial what composes the density contrasts and, to what extent, how it affects channel segregates. Here, we show that in experimental 500kg and 100 ton commercial cast steel ingots CS originates from oxide Al2O3/MnS impurity clusters (OICs) initially nucleated from the oxide (Al2O3) particles, which induce an extra flow due to sharp density contrast between clusters and melt. The results uncover that, as OICs enrich and grow, their driven flow becomes stronger than the traditionally recognized inter-dendritic thermo-solutal convection, dominating the subsequent opening of the channels. This study extends the classical macrosegregation theory, highlights a significant technological breakthrough to control CS, and could quickly yield practical benefits to the worldwide manufacture of over 50 million tons of ingots, super-thick slab and heavy castings annually, as well as has general implications for the elaboration of other related natural phenomena.
Spatial Memory in Spontaneously Hypertensive Rats (SHR)  [PDF]
Thomas-A. Sontag, Anselm B. M. Fuermaier, Joachim Hauser, Ivo Kaunzinger, Oliver Tucha, Klaus W. Lange
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0074660
Abstract: The spontaneously hypertensive rat (SHR) is an established animal model of ADHD. It has been suggested that ADHD symptoms arise from deficits in executive functions such as working memory, attentional control and decision making. Both ADHD patients and SHRs show deficits in spatial working memory. However, the data on spatial working memory deficits in SHRs are not consistent. It has been suggested that the reported cognitive deficits of SHRs may be related to the SHRs’ locomotor activity. We have used a holeboard (COGITAT) to study both cognition and activity in order to evaluate the influence of the activity on the cognitive performance of SHRs. In comparison to Wistar-Kyoto (WKY) rats, SHRs did not have any impairment in spatial working memory and reference memory. When the rats’ locomotor activity was taken into account, the SHRs’ working memory and reference memory were significantly better than in WKY rats. The locomotor activity appears to be a confounding factor in spatial memory tasks and should therefore be controlled for in future studies. In the SHR model of ADHD, we were unable to demonstrate an impairment of working memory which has been reported in patients with ADHD.
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