Microarrays, antiobesity and the liver.
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2004 Oct-D3(4):137-45.Microarrays, antiobesity and the liver.1.1Departamento de Biología Molecular en Medicina, Hospital Civil de Belén, Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara, México. AbstractIn this review, the microarray technology and especially oligonucleotide arrays are exemplified with a practical example taken from the perilipin-/- mice and using the dChip software, available for non-lucrative purposes. It was found that the liver of perilipin-/- mice was healthy and normal, even under high-fat diet when compared with the results published for the scd1-/- mice, which under high-fat diets had a darker liver, suggestive of hepatic steatosis. Scd1 is required for the biosynthesis of monounsaturated fatty acids and plays a key role in the hepatic synthesis of triglycerides and of very-low-density lipoproteins. Both models of obesity resistance share many similar phenotypic antiobesity features, however, the perilipin-/- mice had a significant downregulation of stearoyl CoA desaturases scd1 and scd2 in its white adipose tissue, but a normal level of both genes inside the liver, even under high-fat diet. Here, different microarray methodologies are discussed, and also some of the most recent discoveries and perspectives regarding the use of microarrays, with an emphasis on obesity gene expression, and a personal remark on my findings of increased expression for hemoglobin transcripts and other hemo related genes (hemo-like), and for leukocyte like (leuko-like) genes inside the white adipose tissue of the perilipin-/- mice. In conclusion, microarrays have much to offer in comparative studies such as those in antiobesity, and also they are methodologies adequate for new astounding molecular discoveries [free full text of this article Online].PMID:
[PubMed - indexed for MEDLINE] Methodology used in the microarray fabrication and application in a practical experimental design.Ann Hepatol. ;3(4):137-145.Hierarchical clustering of the gene expression changes between tissues of plin-/- (ko) vs. wild-type (wt) mice. Metabolic genes are upregulated in plin-/- WAT, brown rectangle. Transcription related genes are downregulated in plin-/- WAT, black rectangle, translation related genes appear below, after a short gap (not highlighted). Location of scd1, green rectangle and scd2, purple rectangle. The columns represent the organism and its tissues as labeled, and the rows represent the individual genes. A red color inside a cell in this figure represents upregulation, whereas a blue color in a cell represents downregulation. The clusters are grouped according to the intensity of expression for each particular transcript (dChip V 1.2). Symbols: wt, wild type (replicas); ko, knock out (replicas); WAT, white adipose tissue.Ann Hepatol. ;3(4):137-145.Publication TypesMeSH TermsSubstancesGrant SupportFull Text SourcesMedical
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External link. Please review our .Altered ventricular torsion and transmural patterns of myocyte relaxation precede heart failure in aging F344 rats.
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2013 Sep 1;305(5):H676-86. doi: 10.1152/ajpheart.. Epub
2013 Jun 21.Altered ventricular torsion and transmural patterns of myocyte relaxation precede heart failure in aging F344 rats.1, , , , .1Department of Physiology and the Center for Muscle Biology, University of Kentucky, Lexington, Kentucky.AbstractThe purpose of this study was to identify and explain changes in ventricular and cellular function that contribute to aging-associated cardiovascular disease in aging F344 rats. Three groups of female F344 rats, aged 6, 18, and 22 mo, were studied. Echocardiographic measurements in isoflurane-anesthetized animals showed an increase in peak left ventricular torsion between the 6- and the 18-mo-old groups that was partially reversed in the 22-mo-old animals (P & 0.05). Epicardial, midmyocardial, and endocardial myocytes were subsequently isolated from the left ventricles of each group of rats. Unloaded sarcomere shortening and Ca(2+) transients were then measured in these cells (n = &75 cells for each of the nine age-region groups). The decay time of the Ca(2+) transient and the time required for 50% length relaxation both increased with age but not uniformly across the three regions (P & 0.02). Further analysis revealed a significant shift in the transmural distribution of these properties between 18 and 22 mo of age, with the largest changes occurring in epicardial myocytes. Computational modeling suggested that these changes were due in part to slower Ca(2+) dissociation from troponin in aging epicardial myocytes. Subsequent biochemical assays revealed a &50% reduction in troponin I phosphoprotein content in 22-mo-old epicardium relative to the other regions. These data suggest that between 18 and 22 mo of age (before the onset of heart failure), F344 rats display epicardial-specific myofilament-level modifications that 1) break from the progression observed between 6 and 18 mo and 2) coincide with aberrant patterns of cardiac torsion. KEYWORDS:
left transmural heterogeneityPMID:
[PubMed - indexed for MEDLINE] Left ventricular (LV) torsion assessed using echocardiography. A: representative short axis B-mode echocardiographic image taken at the basal plane of an 18-mo-old F344 rat showing the right ventricle (RV), posterior wall (PW), and centroid (+) of manually traced sub-endocardial points (white markers). B: depiction of base and apex image planes with normal distance (dBA). Angular displacements of basal (θB) and apical (θA) PW points (four in each plane) were used to calculate an average torsion time course. C: representative paths of tracked PW points during systole (solid lines) and diastole (shaded dashed lines). Circles indicate PW points at end-diastole. D: mean LV torsion values during a complete cardiac cycle for 6- (n = 3), 18- (n = 6), and 22-mo-old (n = 6) animals. Error bars show ± SE for clarity, positive and negative SE have been omitted from 6- and 18-mo traces, respectively. *Signficant difference vs. 6-mo-old animals (P & 0.05). +Significant difference vs. 22-mo-old animals (P & 0.05).Am J Physiol Heart Circ Physiol. 2013 September 1;305(5):H676-H686.Intracellular Ca2+ transients and contractile dynamics vary by myocardial region and animal age. A and B: representative normalized Ca2+ transients (A) and sarcomere length records (B) for endocardial (ENDO), midmyocardial (MID), and epicardial (EPI) cells from rats of 6, 18, and 22 mo of age. C: histograms showing the distributions of the Ca2+ transient amplitude (ΔF340/380) and decay constant (τCa) for each age-region group (n = 75 to 176 cells/group). Arrows indicate the population mean. D: same as C but showing distributions of contractile parameters maximum shortening (ΔSL), time to peak shortening (TP), and time from peak to 50% re-lengthening (RT50).Am J Physiol Heart Circ Physiol. 2013 September 1;305(5):H676-H686.Transmural patterns of Ca2+ handling and contraction dynamics are altered with age. A: means ± SE of the time constant of F340/380 decay after peak (τCa) for each age-region group. B and C: same as A but showing unloaded sarcomere TP (B) and RT50 (C). *Significant difference vs. cells from the same region at 6 mo of age (P & 0.05). +Significant difference vs. endocardial cells at the same age (P & 0.05). ?Significant difference vs. midmyocardial cells at the same age (P & 0.05).Am J Physiol Heart Circ Physiol. 2013 September 1;305(5):H676-H686.Aging alters Ca2+-relaxation coupling in epicardial myocytes. Plotted points show RT50 vs. τCa for each cell in the study, grouped according to region and animal age. Analysis of covariance on τCa-RT50 relations indicates that the slope depends significantly on the age-region group (P & 0.001). RT50 in epicardial myocytes from 6-mo-old rats was significantly less sensitive to τCa than in 18- and 22-mo-old cells from the same region.Am J Physiol Heart Circ Physiol. 2013 September 1;305(5):H676-H686.Computer simulations of unloaded sarcomere shortening. Ca2+ transients with various rates of decay (τCa) were used as inputs to predict relationships between τCa and RT50 under different conditions. A: example input Ca2+ transients of increasing τCa and corresponding SL outputs for the baseline model (40% β-MHC, 0.3 μM TnC Ca2+ affinity). B: sensitivity of the τCa-RT50 relation to doubling and halving relative β-MHC content. C: sensitivity of the τCa-RT50 relation to a 20% increase in TnC Ca2+ affinity.Am J Physiol Heart Circ Physiol. 2013 September 1;305(5):H676-H686.Biochemical analyses of tissue homogenates obtained from each age-region group (n = 3 animals per age group). Representative Western blot images (A) and summary data from densitometry (B) showing expression of SERCA2a (arbitrary units). Representative bands from midmyocardial samples of various ages showing separated α- and β-MHC isoforms (C) and the mean α-MHC isoform percentages across groups (D). E: representative TnI bands from gels stained for phosphoprotein (Pro-Q Diamond) and total protein content (Sypro Ruby). F: mean values of phosphoprotein-to-total protein ratios from densitometric analysis. +Significant difference vs. endocardial cells at the same age (P & 0.05). ?Significant difference vs. midmyocardial cells at the same age (P & 0.05).Am J Physiol Heart Circ Physiol. 2013 September 1;305(5):H676-H686.Publication TypesMeSH TermsSubstancesGrant SupportFull Text SourcesMedicalMiscellaneous
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External link. Please review our .Antioxidants as potential therapeutics for lung fibrosis.
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):355-70.Antioxidants as potential therapeutics for lung fibrosis.1.1Division of Environmental and Occupational Health Sciences, Department of Medicine, National Jewish Medical and Research Center, Denver, Colorado 80206, USA. dayb@njc.orgAbstractInterstitial lung disease encompasses a large group of chronic lung disorders associated with excessive tissue remodeling, scarring, and fibrosis. The evidence of a redox imbalance in lung fibrosis is substantial, and the rationale for testing antioxidants as potential new therapeutics for lung fibrosis is appealing. Current animal models of lung fibrosis have clear involvement of ROS in their pathogenesis. New classes of antioxidant agents divided into catalytic antioxidant mimetics and antioxidant scavengers are being developed. The catalytic antioxidant class is based on endogenous antioxidant enzymes and includes the manganese-containing macrocyclics, porphyrins, salens, and the non-metal-containing nitroxides. The antioxidant scavenging class is based on endogenous antioxidant molecules and includes the vitamin E analogues, thiols, lazaroids, and polyphenolic agents. Numerous studies have shown oxidative stress to be associated with many interstitial lung diseases and that these agents are effective in attenuating fibroproliferative responses in the lung of animals and humans.PMID:
[PubMed - indexed for MEDLINE] Several phosphatases contain sensitive thiol residues that are inhibited on oxidation. As steady-state levels of oxidants increase, an increase in the inactivation of phosphatases and a corresponding increase in the levels and duration of phosphorylated proteins occur. An increase in steady-state ROS results in altering the cellular glutathione (GSH)/glutathione disulfide (GSSG) redox couple, which can in turn alter the relative oxidation status of protein thiols. In addition, ROS can alter cell signaling directly by reacting with specific thiols on transcription factors. Many of these types of mechanisms are thought to contribute to the often observed unregulated tissue-repair responses associated lung fibrosis.Antioxid Redox Signal. ;10(2):355-370.Chemical structures of macrocyclic catalytic antioxidant mimetics with SOD activity.Antioxid Redox Signal. ;10(2):355-370.Chemical structures of metalloporphyrin catalytic antioxidant mimetics with SOD and catalase activities.Antioxid Redox Signal. ;10(2):355-370.Chemical structures of salen catalytic antioxidant mimetics with SOD and catalase activities.Antioxid Redox Signal. ;10(2):355-370.Chemical structures of nitroxide catalytic antioxidant mimetics with SOD activity.Antioxid Redox Signal. ;10(2):355-370.Chemical structures of selenium-containing catalytic antioxidant mimetics with glutathione peroxidase activity.Antioxid Redox Signal. ;10(2):355-370.Chemical structures of antioxidant scavengers.Antioxid Redox Signal. ;10(2):355-370.Publication TypesMeSH TermsSubstancesGrant SupportFull Text SourcesOther Literature SourcesMedical
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External link. Please review our .请问路由器的原始户名和密码是什么？_百度知道
请问路由器的原始户名和密码是什么？
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用户名：adsl 密码：adsl831
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出门在外也不愁现在看到很多人都在QQ上说什么TP、TP啊，还什么TP名，TP姐妹，到底是什么意思啊？求大神帮忙解答~ ~_百度知道
现在看到很多人都在QQ上说什么TP、TP啊，还什么TP名，TP姐妹，到底是什么意思啊？求大神帮忙解答~ ~
提问者采纳
双方在TP界就是姐妹了。
希望您能满意。
TP姐妹就是双方各自取一个网络名。
TP名就是真实名字或是网络上的名字。
网络上的两个冒充明星的人互相摊牌。这个一般都是在QQ上的，比如＂陌馨＂＂安汐＂TP的意思就是摊牌，以后就用TP名称呼对方，说名字，然后记住对方的TP名。
摊牌后就只能相信对方
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T这个词最初是一种男性化的存在;　　台湾一直奉行儒教。另有H向偏T，P就是有着传统的女性言行举止和思维的女人、偏P的说法……【T和P的由来】　　T的说法，最早来自台湾的女同志运动，男尊女卑的思想深入人心、P和H】　　　　P是指比较女性化的女性同性恋者。比如，就是那些爱上T的女人，本来并不只是用于形容女同志。最初浮出水面的女同志。&　　P的说法，一般喜欢穿女装，很多人都歪曲了Tomboy的真实词义，T模仿的是传统社会中的男性形象：梓菜团的梓，外形特征一般中性。T是英文Tomboy的缩写，可P也可T简称H即TP不分，TP关系也是模拟的两性关系。&nbsp，梓菜团的团和梓菜团的团……诸如此类。（由此可见为什么许多T恐惧P的“回归主流”，就是婆的意思，Tomboy原意是“男子气的女人”。但是这都不重要，也不乏双性倾向和异性倾向的，显然是一个附属的名词，角色也可因对象角色而定，这些人，只要她们（表面上）爱上了一个显性的女同志。再超一步就是网络虚拟夫妇了……然后是真人同性夫妇……等等等等……【T，成为的网络用户名，一般喜欢留短发。）&　　所以说，穿着上也一般以休闲装为主H不分是界于P和T之间，TP姐妹则是以此做引申，或者扮演男性角色的女同志（也就是“显性的”女同志）以后，是一些举止打扮甚至思维都非常男性化的女性。相对于T的男性化，自称为T，但是T被台湾同志用来指代那些男性化的，也就是所谓的“正常的女人”、留长发等T是比较男性化的女性同性恋者。最初定义的P，她们中固然有同性倾向的女性，那就是P了女同（拉拉）特定用语，原意是“T的老婆”，是个传统文化力量非常强大的地方
百度知道有：TP的意思就是摊牌（摊牌的缩写就是TP）。TP姐妹就是双方各自取一个网络名，比如＂陌馨＂＂安汐＂，然后记住对方的TP名，以后就用TP名称呼对方，双方在TP界就是姐妹了。这个一般都是在QQ上的。
TP笼统的可以翻译为摊牌（摊牌的缩写就是TP），TP界也就是摊牌界。TP界的人们都有TP名字的，掩盖自己的身份，玩自己喜欢的人。TP并不是冒充明星什么的，而是网络深交，在网络上付出真心，找到姐妹。但是普遍都是冒充明星的居多，就代表玩明星，找合作，因为TP的缩写是摊牌。每个玩明星的都有一个TP名，然后ta会有大量和ta合作的明星，在空间经常进行互动，网络上的两个冒充明星的人互相摊牌，然后合作一起骗粉丝，TP名就是网络上的名字。 摊牌后就只能相信对方。 TP姐妹就是双方各自取一个网络名，然后记住对方的TP名，以后就用TP名称呼对方，双方在TP界就是姐妹了。
TP的意思就是摊牌（摊牌的缩写就是TP）。TP姐妹就是双方各自取一个网络名，比如＂陌馨＂＂安汐＂，然后记住对方的TP名，以后就用TP名称呼对方，双方在TP界就是姐妹了。这个一般都是在QQ上的。
深交做姐妹,就是姐妹,tp界有许多人,tp界很强大的!!!
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