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              <text>&lt;a href="http://doi.org/10.1038/oby.2004.187" target="_blank" rel="noreferrer noopener"&gt;http://doi.org/10.1038/oby.2004.187&lt;/a&gt;</text>
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                <text>Longitudinal Relationship Between Elapsed Time In The Action Stages Of Change And Weight Loss</text>
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                <text>balance; decisional; Endocrinology &amp; Metabolism; exercise; health behaviors; longitudinal study; Nutrition &amp; Dietetics; obesity; physical-activity; primary care; primary care; reducing dietary-fat; self-efficacy; transtheoretical model; weight loss; women</text>
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                <text>Logue E E; Jarjoura D G; Sutton K S; Smucker W D; Baughman K R; Capers C F</text>
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                <text>Objective: The objective of this study was to examine the longitudinal relationship between the elapsed time in the action and maintenance stages of change for multiple target behaviors and weight loss or gain. Research Methods and Procedures: The research design was a prospective cohort study of overweight and obese primary care patients randomized to an obesity management intervention based on the Transtheoretical Model and a chronic disease paradigm. The target behaviors included increased planned exercise and usual physical activity, decreased dietary fat, increased fruit and vegetable consumption, and increased dietary portion control. The participants were 329 middle-aged men and women with elevated body mass indices recruited from 15 primary care practices in Northeastern Ohio; 28% of the participants were African Americans. The main outcomes were weight loss (5% or more) or weight gain (5% or more) after 18 or 24 months of follow-up. Results: There were significant (p &lt; 0.05) longitudinal relationships between the number of periods (0 to 4) in action or maintenance for each of the five target behaviors, or a composite score taken across the five target behaviors, and weight loss. In all cases, there was a significant (p &lt; 0.05) stepped (graded) relationship between the time in action or maintenance and weight loss (or gain). Discussion: The data support the concept of applying the Transtheoretical Model to the problem of managing obesity in primary care settings. The remaining challenge is to identify those factors that reliably move patients into the action and maintenance stages for long periods.</text>
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              <text>&lt;a href="http://doi.org/10.1038/oby.2005.106" target="_blank" rel="noreferrer noopener"&gt;http://doi.org/10.1038/oby.2005.106&lt;/a&gt;</text>
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              <text>13</text>
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              <text>&lt;p&gt;Users with a NEOMED Library login can search for full-text journal articles at the following url: &lt;a href="https://libraryguides.neomed.edu/home"&gt;https://libraryguides.neomed.edu/home&lt;/a&gt;&lt;/p&gt;</text>
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                <text>Transtheoretical Model-chronic Disease Care For Obesity In Primary Care: A Randomized Trial</text>
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                <text>chronic disease; clinical-trials; cognitive-behavioral therapy; dietary-fat intake; Endocrinology &amp; Metabolism; exercise behavior; intervention; motivational readiness; Nutrition &amp; Dietetics; physical-activity; program; randomized controlled trial; self-efficacy; services task-force; treatment; weight management; weight loss</text>
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                <text>Objective: To compare health benefits achieved in a transtheoretical model-chronic disease (TM-CD) minimal intervention for obesity vs. augmented usual care (AUC). Research Method and Procedures: This was a 2-year, randomized clinical trial with overweight or obese men and women from 15 primary care sites. AUC (n = 336) included dietary and exercise advice, prescriptions, and three 24-hour dietary recalls every 6 months. TM-CD care (n = 329) included AUC elements plus "stage of change" (SOC) assessments for five target behaviors every other month, mailed SOC and target behavior-matched-workbooks, and monthly telephone calls from a weight-loss advisor. Weight change was the primary outcome. Results: Repeated measures models under the missing at random assumption yielded nonsignificant adjusted differences between. the AUC and TM-CD groups for weight change, waist circumference, energy intake or expenditure, blood pressure, and blood lipids. The pattern of change over time suggested that TM-CD participants were trying harder to impact target behaviors during the first 6 to 12 months of the trial but relapsed afterward. Sixty percent of trial participants maintained their baseline weights for 18 to 24 months. Discussion: A combination of mailed patient materials and monthly telephone calls based on, the transtheoretical model and some elements of chronic disease care is not powerful enough, relative to AUC, to alter target behaviors among overweight primary care patients in an obesogenic environment. AUC may be sufficient to maintain weights among at-risk primary care patients.</text>
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                <text>&lt;a href="http://doi.org/10.1038/oby.2005.106" target="_blank" rel="noreferrer noopener"&gt;10.1038/oby.2005.106&lt;/a&gt;</text>
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              <text>&lt;a href="http://doi.org/10.1016/j.ygcen.2012.07.011" target="_blank" rel="noreferrer noopener"&gt;http://doi.org/10.1016/j.ygcen.2012.07.011&lt;/a&gt;</text>
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              <text>3</text>
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              <text>178</text>
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                <text>Knockdown Of Leptin A Expression Dramatically Alters Zebrafish Development</text>
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                <text>General and Comparative Endocrinology</text>
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                <text>atlantic salmon; Auditory; bhlh genes; bone; carp cyprinus-carpio; cell fate specification; central-nervous-system; cloning; danio-rerio; differentiation; Endocrinology &amp; Metabolism; gene; metabolism; n-cadherin; receptor; sensory ganglia; Visual; visual-system</text>
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                <text>Liu Q; Dalman M; Chen Y; Akhter M; Brahmandam S; Patel Y; Lowe J; Thakkar M; Gregory A V; Phelps D; Riley C; Londraville R L</text>
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                <text>Using morpholino antisense oligonucleotide (MO) technology, we blocked leptin A or leptin receptor expression in embryonic zebrafish, and analyzed consequences of leptin A knock-down on fish development. Embryos injected with leptin A or leptin receptor MOs (leptin A or leptin receptor morphants) had smaller bodies and eyes, undeveloped inner ear, enlarged pericardial cavity, curved body and/or tail and larger yolk compared to control embryos of the same stages. The defects persisted in 6-9 days old larvae. We found that blocking leptin A function had little effect on the development of early brain (1 day old), but differentiation of both the morphant dorsal brain and retinal cells was severely disrupted in older (2 days old) embryos. Despite the enlarged pericardial cavity, differentiation of cardiac cells appeared to be similar to control embryos. Formation of the morphants' inner ear is also severely disrupted, which corroborates existing reports of leptin receptor expression in inner ear of both zebrafish and mammals. Co-injection of leptin A MO and recombinant leptin results in partial rescue of the wild-type phenotype. Our results suggest that leptin A plays distinct roles in zebrafish development. (c) 2012 Elsevier Inc. All rights reserved.</text>
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                <text>&lt;a href="http://doi.org/10.1016/j.ygcen.2012.07.011" target="_blank" rel="noreferrer noopener"&gt;10.1016/j.ygcen.2012.07.011&lt;/a&gt;</text>
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                <text>Spaceflight Effects On Cultured Embryonic Chick Bone Cells</text>
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                <text>biomechanics; bone adaptation; collagen; differentiation; Endocrinology &amp; Metabolism; in-vitro; mechanical strain; messenger-rna expression; microgravity; osteoblast; osteoblasts; osteopontin; restriction; signal-transduction; space-flight</text>
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                <text>A model calcifying system of primary osteoblast cell cultures derived from normal embryonic chicken calvaria has been flown aboard the shuttle, Endeavour, during the National Aeronautics and Space Administration (NASA) mission STS-59 (April 9-20, 1994) to characterize unloading and other spaceflight effects on the bone cells. Aliquots of cells (similar to 7 x 10(6)) grown in Dulbecco's modified Eagle's medium (DMEM) + 10% fetal bovine serum (FBS) were mixed with microcarrier beads, inoculated into cartridge culture units of artificial hollow fiber capillaries, and carried on the shuttle. To promote cell differentiation, cartridge media were supplemented with 12.5 mu g/ml ascorbate and 10 mM P-glycerophosphate for varying time periods before and during Right. Four cartridges contained cells from 17-day-old embryos grown for 5 days in the presence of ascorbate prior to launch (defined as flight cells committed to the osteoblastic lineage) and four cartridges supported cells from 14-day-old embryos grown for 10 days with ascorbate before launch (uncommitted flight cells). Eight cartridges prepared in the same manner were maintained under normal gravity throughout the Right (control cells) and four additional identical cartridges under normal gravity were terminated on the day of launch (basal cells). From shuttle launch to landing, all cartridges were contained in closed hardware units maintaining 5% CO2, 37 degrees C, and media delivery at a rate of similar to 1.5 ml/6 h. During day 3 and day 5 of flight, duplicate aliquots of conditioned media and accumulated cell products were collected in both the Right and the control hardware units. At the mission end, comparisons among Right, basal, and control samples were made in cell metabolism gene expression for type I collagen and osteocalcin, and ultrastructure. Both committed and uncommitted flight cells were metabolically active, as measured by glucose uptake and lactate production, at approximately the same statistical levels as control counterparts. Flight cells elaborated a less extensive extracellular matrix, evidenced by a reduced collagen gene expression and collagen protein appearance compared with controls. Osteocalcin was expressed by all cells, a result indicating progressive differentiation of both flight and control osteoblasts, but its message levels also were reduced in flight cells compared with ground samples. This finding suggested that osteoblasts subjected to flight followed a slower progression toward a differentiated function. The summary of data indicates that spaceflight, including microgravity exposure, demonstrably affects bone cells by down-regulating type I collagen and osteocalcin gene expression and thereby inhibiting expression of the osteogenic phenotype notably by committed osteoblasts. The information is important for insight into the response of bone cells to changes of gravity and of force in general.</text>
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              <text>12</text>
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                <text>Gene Therapy Strategy To Improve Bone Quality In Osteogenesis Imperfecta</text>
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                <text>1997</text>
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                <text>1997-08</text>
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                <text>King D; Beamer W; Chase J; Havey R; Patwardhan A; Saban J; Schneider G; Sparks S E; Steinke B; Zussman M</text>
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                <text>a-i; cardiovascular-disease; cholesterol; Endocrinology &amp; Metabolism; expression; glycation end-products; Gycation; high-density-lipoprotein; increases; Lipoproteins; metformin; methylglyoxal; oxidative stress; Type II diabetes; type-2</text>
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                <text>Kheniser K G; Kashyap S R; Kasumov T</text>
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                <text>Aims Metformin is a commonly prescribed anti-hyperglycaemic pharmacological agent, and it remains a staple in the management of type II diabetes. In addition to metformin's glucose lowering effects, research has indicated that metformin inhibits glycation-mediated and oxidative modification of lipoprotein residues. The purpose was to discuss the effects of metformin as it relates to high-density lipoprotein (HDL) and low-density lipoprotein (LDL) modification. Materials and methods The purpose was to conduct a narrative and pragmatic review on the effects of metformin as it pertains to HDL and LDL modification. Results High-density lipoprotein (HDL) concentration is a quantitative measure and therefore does not provide insight into its function, which is a qualitative property. Dysfunctional HDLs are unable to carry out functions normally associated with HDL because they can be modified by glycating agents. Metformin may counteract HDL dysfunction by abating HDL modification. Reductions in HDL modification may improve reverse cholesterol transport ability and thus possibly diminish cardiovascular risk. Similarly, metformin-mediated attenuations in LDL modification may reduce their atherogenic potency. Conclusion Metformin may partially ameliorate HDL dysfunction and reduce LDL modification by inhibiting alpha-dicarbonyl-mediated modification of apolipoprotein residues; consequently, the results are salient because cardiovascular disease incidence may be reduced given that reverse cholesterol transport activity predicts risk, and modified LDL are proatherogenic.</text>
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                <text>&lt;a href="http://doi.org/10.1002/osp4.309" target="_blank" rel="noreferrer noopener"&gt;10.1002/osp4.309&lt;/a&gt;</text>
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        <name>Kheniser K G</name>
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              <text>&lt;a href="http://doi.org/10.1016/j.freeradbiomed.2017.10.300" target="_blank" rel="noreferrer noopener"&gt;http://doi.org/10.1016/j.freeradbiomed.2017.10.300&lt;/a&gt;</text>
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            <elementText elementTextId="135654">
              <text>191-191</text>
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            <elementText elementTextId="135655">
              <text>112</text>
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              <text>&lt;p&gt;Users with a NEOMED Library login can search for full-text journal articles at the following url: &lt;a href="https://libraryguides.neomed.edu/home"&gt;https://libraryguides.neomed.edu/home&lt;/a&gt;&lt;/p&gt;</text>
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                <text>Pleiotropic Roles Of Nrf2 As Regulators Of Chondrocyte Apoptosis, Oxidative Stress, Inflammatory Response And Catabolic And Anabolic Pathways In Osteoarthritis</text>
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                <text>Free Radical Biology and Medicine</text>
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                <text>Biochemistry &amp; Molecular Biology; Endocrinology &amp; Metabolism</text>
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              <elementText elementTextId="135650">
                <text>Khan N M; Haqqi T M</text>
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        <name>Khan N M</name>
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      <name>Text</name>
      <description>A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.</description>
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            <elementText elementTextId="134823">
              <text>&lt;a href="http://doi.org/10.1016/j.freeradbiomed.2017.10.170" target="_blank" rel="noreferrer noopener"&gt;http://doi.org/10.1016/j.freeradbiomed.2017.10.170&lt;/a&gt;</text>
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          <elementTextContainer>
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              <text>Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).</text>
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          <elementTextContainer>
            <elementText elementTextId="134825">
              <text>113-114</text>
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          <elementTextContainer>
            <elementText elementTextId="134826">
              <text>112</text>
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          <description>Locate full-text within NEOMED Library's e-journal collections</description>
          <elementTextContainer>
            <elementText elementTextId="134827">
              <text>&lt;p&gt;Users with a NEOMED Library login can search for full-text journal articles at the following url: &lt;a href="https://libraryguides.neomed.edu/home"&gt;https://libraryguides.neomed.edu/home&lt;/a&gt;&lt;/p&gt;</text>
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          <element elementId="50">
            <name>Title</name>
            <description>A name given to the resource</description>
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              <elementText elementTextId="134816">
                <text>Increased Cysteine Sulfonation Of The Hydrophilic Domain Of Complex I Mediates Mitochondrial Dysfunction In The Post-ischemic Heart</text>
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              <elementText elementTextId="134817">
                <text>Free Radical Biology and Medicine</text>
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            <description>A point or period of time associated with an event in the lifecycle of the resource</description>
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            <description>The topic of the resource</description>
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              <elementText elementTextId="134820">
                <text>Biochemistry &amp; Molecular Biology; Endocrinology &amp; Metabolism</text>
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              <elementText elementTextId="134821">
                <text>Kang P T; Chen C L; Lin P; Zhang L W; Chen Y R</text>
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            <description>An unambiguous reference to the resource within a given context</description>
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        <name>Chen C L</name>
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              <text>1517-1528</text>
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              <text>11</text>
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            <elementText elementTextId="134541">
              <text>6</text>
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          <elementTextContainer>
            <elementText elementTextId="134542">
              <text>&lt;p&gt;Users with a NEOMED Library login can search for full-text journal articles at the following url: &lt;a href="https://libraryguides.neomed.edu/home"&gt;https://libraryguides.neomed.edu/home&lt;/a&gt;&lt;/p&gt;</text>
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                <text>Decreasing Cb1 Receptor Signaling In Kupffer Cells Improves Insulin Sensitivity In Obese Mice</text>
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              <elementText elementTextId="134530">
                <text>Molecular Metabolism</text>
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                <text>2017-11</text>
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              <elementText elementTextId="134533">
                <text>adiponectin receptors; adipose-tissue; CB1 receptors; disruption; endocannabinoid system; Endocrinology &amp; Metabolism; fatty liver-disease; Inflammation; Insulin resistance; Kupffer cells; macrophage polarization; nf-kappa-b; nonalcoholic steatohepatitis; protein-2; reactive oxygen; siRNA; targeted; uncoupling</text>
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              <elementText elementTextId="134534">
                <text>Jourdan T; Nicoloro S M; Zhou Z; Shen Y F; Liu J; Coffey N J; Cinar R; Godlewski G; Gao B; Aouadi M; Czech M P; Kunos G</text>
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                <text>Objective: Obesity-induced accumulation of ectopic fat in the liver is thought to contribute to the development of insulin resistance, and increased activity of hepatic CB1R has been shown to promote both processes. However, lipid accumulation in liver can be experimentally dissociated from insulin resistance under certain conditions, suggesting the involvement of additional mechanisms. Obesity is also associated with pro-inflammatory changes which, in turn, can promote insulin resistance. Kupffer cells (KCs), the liver's resident macrophages, are the major source of pro-inflammatory cytokines in the liver, such as TNF-alpha, which has been shown to inhibit insulin signaling in multiple cell types, including hepatocytes. Here, we sought to identify the role of CB1R in KCs in obesity-induced hepatic insulin resistance. Methods: We used intravenously administered beta-D-glucan-encapsulated siRNA to knock-down CB1R gene expression selectively in KCs. Results: We demonstrate that a robust knock-down of the expression of Cnr1, the gene encoding CB1R, results in improved glucose tolerance and insulin sensitivity in diet-induced obese mice, without affecting hepatic lipid content or body weight. Moreover, Cnr1 knock-down in KCs was associated with a shift from pro-inflammatory M1 to anti-inflammatory M2 cytokine profile and improved insulin signaling as reflected by increased insulin-induced Akt phosphorylation. Conclusion: These findings suggest that CB1R expressed in KCs plays a critical role in obesity-related hepatic insulin resistance via a pro inflammatory mechanism. Published by Elsevier GmbH.</text>
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        <name>Nicoloro S M</name>
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        <name>Reactive oxygen</name>
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        <name>Shen Y F</name>
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        <name>siRNA</name>
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        <name>targeted</name>
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        <name>uncoupling</name>
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      <tag tagId="33925">
        <name>Zhou Z</name>
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              <text>&lt;a href="http://doi.org/10.1210/en.2004-0487" target="_blank" rel="noreferrer noopener"&gt;http://doi.org/10.1210/en.2004-0487&lt;/a&gt;</text>
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          <name>Pages</name>
          <description/>
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            <elementText elementTextId="134164">
              <text>4330-4343</text>
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              <text>9</text>
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        <element elementId="57">
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          <elementTextContainer>
            <elementText elementTextId="134166">
              <text>145</text>
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          <name>Search for Full-text</name>
          <description>Locate full-text within NEOMED Library's e-journal collections</description>
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              <text>&lt;p&gt;Users with a NEOMED Library login can search for full-text journal articles at the following url: &lt;a href="https://libraryguides.neomed.edu/home"&gt;https://libraryguides.neomed.edu/home&lt;/a&gt;&lt;/p&gt;</text>
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            <name>Title</name>
            <description>A name given to the resource</description>
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                <text>Gonadal Hormones And Frontocortical Expression Of Vascular Endothelial Growth Factor In Male Stroke-prone, Spontaneously Hypertensive Rats, A Model For Attention-deficit/hyperactivity Disorder</text>
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            <description>An entity responsible for making the resource available</description>
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              <elementText elementTextId="134155">
                <text>Endocrinology</text>
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            <name>Date</name>
            <description>A point or period of time associated with an event in the lifecycle of the resource</description>
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                <text>2004-09</text>
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            <name>Subject</name>
            <description>The topic of the resource</description>
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                <text>aged female rats; animal-model; central-nervous-system; cerebral-blood-flow; computed tomography; deficit-hyperactivity-disorder; emission; Endocrinology &amp; Metabolism; estrogen-receptor-alpha; in-situ hybridization; insulin-resistant; messenger-ribonucleic-acid; stage</text>
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            <name>Creator</name>
            <description>An entity primarily responsible for making the resource</description>
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              <elementText elementTextId="134159">
                <text>Jesmin S; Togashi H; Sakuma I; Mowa C N; Ueno K I; Yamaguchi T; Yoshioka M; Kitabatake A</text>
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            <name>Description</name>
            <description>An account of the resource</description>
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                <text>Attention-deficit/hyperactivity disorder (AD/HD) is a common pediatric behavioral disorder associated, in part, with male preponderance and reduced regional cerebral blood flow (rCBF). However, mechanism(s) underlying male preponderance and reduced rCBF in AD/HD are unclear. The present study profiles the expression of angiogenic and hormonal factors likely to underlie these symptoms using a recently characterized AD/HD animal model, juvenile male stroke-prone spontaneously hypertensive rats (SHRSP). Because vascular endothelial growth factor (VEGF) signaling cascade and gonadal steroids are key regulators of angiogenesis and gender-based behavior, respectively, we profiled their patterns of expression in the frontal cortex of SHRSP to elucidate their roles in the genesis of AD/HD male preponderance and rCBF. Interestingly, levels of VEGF, VEGF receptors (KDR, Flt-1), endothelial nitric oxide synthase, phosphorylated. Akt (pAkt), estrogen receptor-alpha, aromatase, and capillary density in sham-operated SHRSP were remarkably down-regulated, whereas androgen receptor levels were up-regulated, compared with age-matched genetic control, Wistar-Kyoto rats. Castration, estrogen, and androgen receptor antagonist (flutamide) counteracted these effects. Dihydrotestosterone, but not testosterone, reversed the beneficiary effects of castration. Estrogen receptor-beta levels remained unchanged in all groups examined. We postulate that changes in androgen metabolism that tend to up-regulate local dihydrotestosterone concentration and diminish estrogen synthesis, in the frontal cortex of juvenile male SHRSP, may lower levels and/or activity of VEGF and its signaling cascade and, subsequently, reduce rCBF. These findings could, in part, help explain the pathogenesis of reduced rCBF and male preponderance in AD/HD.</text>
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                <text>&lt;a href="http://doi.org/10.1210/en.2004-0487" target="_blank" rel="noreferrer noopener"&gt;10.1210/en.2004-0487&lt;/a&gt;</text>
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        <name>central-nervous-system</name>
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        <name>Jesmin S</name>
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        <name>Journal Article or Conference Abstract Publication</name>
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        <name>Kitabatake A</name>
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      <tag tagId="8422">
        <name>Mowa C N</name>
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      <tag tagId="17137">
        <name>Sakuma I</name>
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        <name>stage</name>
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      <tag tagId="17138">
        <name>Togashi H</name>
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      <tag tagId="48596">
        <name>Ueno K I</name>
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      <tag tagId="48588">
        <name>Yamaguchi T</name>
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        <name>Yoshioka M</name>
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              <text>&lt;a href="http://doi.org/10.1677/jme.101548" target="_blank" rel="noreferrer noopener"&gt;http://doi.org/10.1677/jme.101548&lt;/a&gt;</text>
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            <elementText elementTextId="134134">
              <text>343-359</text>
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        <element elementId="56">
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            <elementText elementTextId="134135">
              <text>2</text>
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        <element elementId="57">
          <name>Volume</name>
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          <elementTextContainer>
            <elementText elementTextId="134136">
              <text>33</text>
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          <name>Search for Full-text</name>
          <description>Locate full-text within NEOMED Library's e-journal collections</description>
          <elementTextContainer>
            <elementText elementTextId="134137">
              <text>&lt;p&gt;Users with a NEOMED Library login can search for full-text journal articles at the following url: &lt;a href="https://libraryguides.neomed.edu/home"&gt;https://libraryguides.neomed.edu/home&lt;/a&gt;&lt;/p&gt;</text>
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        <description>The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.</description>
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          <element elementId="50">
            <name>Title</name>
            <description>A name given to the resource</description>
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              <elementText elementTextId="134124">
                <text>Aromatase Is Abundantly Expressed By Neonatal Rat Penis But Downregulated In Adulthood</text>
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            <name>Publisher</name>
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              <elementText elementTextId="134125">
                <text>Journal of Molecular Endocrinology</text>
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            <name>Date</name>
            <description>A point or period of time associated with an event in the lifecycle of the resource</description>
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                <text>2004-10</text>
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            <name>Subject</name>
            <description>The topic of the resource</description>
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              <elementText elementTextId="134128">
                <text>androgen receptor; beta messenger-rnas; brain; cytochrome-p450 aromatase; Endocrinology &amp; Metabolism; estrogen-receptor-alpha; female reproductive organ; in-situ hybridization; leydig-cells; ribonucleic-acid; tract</text>
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            <name>Creator</name>
            <description>An entity primarily responsible for making the resource</description>
            <elementTextContainer>
              <elementText elementTextId="134129">
                <text>Jesmin S; Mowa C N; Sakuma I; Matsuda N; Togashi H; Yoshioka M; Hattori Y; Kitabatake A</text>
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            </elementTextContainer>
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            <description>An account of the resource</description>
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              <elementText elementTextId="134130">
                <text>Although synthesis of estrogen by male gonads has been well documented for over half a century, it is only recently that the role of estrogen in male reproductive events has gained appreciation. We recently reported abundant expression of estrogen receptor (ER)-alpha and -beta in different cell types of the rat penis, whose levels diminished with advancing age. The present study, which builds on data from the ER study, was designed to determine whether the penis is capable of generating its own local estrogen by examining evidence of the expression of aromatase, a microsomal enzymatic complex which irreversibly converts androgens to estrogens, using immunohistochemistry, Western blotting, in situ hybridization and real-time PCR analyses. Secondly, the effects of sex steroid hormones on penile aromatase were examined. Discrete aromatase immunoreactive cells were localized in primordial corpus cavernosum, corpus spongiosus and os penis, blood vessels and sensory corpuscle of glans penis. In situ hybridization signals corresponded with immunohistochemical findings. Western blot, enzyme immunoassay and real-time PCR analyses of rat penile samples revealed an age-dependent expression of aromatase and estrogen, with levels at week 1 almost resembling those of the ovary, but they decreased sharply by week 8, and decreased further by week 35. This expression pattern was strikingly similar to that of ER-alpha reported previously. Testosterone and diethylstilbesterol administered prenatally upregulate levels of aromatase mRNA and protein, and estrogen postnatally. Dihydrotestosterone upregulated aromatase mRNA and protein, but not estrogen. We conclude that estrogen acts via ER in a paracrine and/or autocrine manner to regulate penile events, particularly during development, and that estrogen synthesis is regulated by estrogen and androgens.</text>
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            <description>An unambiguous reference to the resource within a given context</description>
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              <elementText elementTextId="134131">
                <text>&lt;a href="http://doi.org/10.1677/jme.101548" target="_blank" rel="noreferrer noopener"&gt;10.1677/jme.101548&lt;/a&gt;</text>
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        <name>Endocrinology &amp; Metabolism</name>
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        <name>female reproductive organ</name>
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        <name>Hattori Y</name>
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        <name>in-situ hybridization</name>
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        <name>Jesmin S</name>
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        <name>Matsuda N</name>
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        <name>Mowa C N</name>
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        <name>ribonucleic-acid</name>
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        <name>Sakuma I</name>
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        <name>Togashi H</name>
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        <name>Yoshioka M</name>
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              <text>&lt;a href="http://doi.org/10.1210/en.2002-220628" target="_blank" rel="noreferrer noopener"&gt;http://doi.org/10.1210/en.2002-220628&lt;/a&gt;</text>
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          <description/>
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            <elementText elementTextId="134118">
              <text>Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).</text>
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          </elementTextContainer>
        </element>
        <element elementId="55">
          <name>Pages</name>
          <description/>
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            <elementText elementTextId="134119">
              <text>4764-4774</text>
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            <elementText elementTextId="134120">
              <text>12</text>
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        <element elementId="57">
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          <description/>
          <elementTextContainer>
            <elementText elementTextId="134121">
              <text>143</text>
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        <element elementId="58">
          <name>Search for Full-text</name>
          <description>Locate full-text within NEOMED Library's e-journal collections</description>
          <elementTextContainer>
            <elementText elementTextId="134122">
              <text>&lt;p&gt;Users with a NEOMED Library login can search for full-text journal articles at the following url: &lt;a href="https://libraryguides.neomed.edu/home"&gt;https://libraryguides.neomed.edu/home&lt;/a&gt;&lt;/p&gt;</text>
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          <element elementId="50">
            <name>Title</name>
            <description>A name given to the resource</description>
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              <elementText elementTextId="134109">
                <text>Evidence For A Potential Role Of Estrogen In The Penis: Detection Of Estrogen Receptor-alpha And -beta Messenger Ribonucleic Acid And Protein</text>
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            <name>Publisher</name>
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              <elementText elementTextId="134110">
                <text>Endocrinology</text>
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          <element elementId="40">
            <name>Date</name>
            <description>A point or period of time associated with an event in the lifecycle of the resource</description>
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              <elementText elementTextId="134111">
                <text>2002</text>
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                <text>2002-12</text>
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          <element elementId="49">
            <name>Subject</name>
            <description>The topic of the resource</description>
            <elementTextContainer>
              <elementText elementTextId="134113">
                <text>androgen receptor; differential expression; dorsal-root ganglion; Endocrinology &amp; Metabolism; hyena crocuta-crocuta; in-situ hybridization; male reproductive-system; molecular-cloning; rat pituitary; sexual-behavior; spinal-cord</text>
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            <name>Creator</name>
            <description>An entity primarily responsible for making the resource</description>
            <elementTextContainer>
              <elementText elementTextId="134114">
                <text>Jesmin S; Mowa C N; Matsuda N; Salah-Eldin A E; Togashi H; Sakuma I; Hattori Y; Kitabatake A</text>
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            <name>Description</name>
            <description>An account of the resource</description>
            <elementTextContainer>
              <elementText elementTextId="134115">
                <text>Body tissues are traditionally classified as estrogen targets based on both the response to the hormone and the presence of estrogen receptors (ERs). We undertook the study on expression of ERalpha and ERbeta in the penis to identify compartments/cells responsive to estrogen, using immunohistochemistry, Western blotting, in situ hybridization, and RT-PCR analyses. Expressions of ERalpha and ERbeta in the rat penis were age dependent at both mRNA and protein levels, with the most intense signals being observed during the perinatal period and declining thereafter with age. Initial signals (fetal d 17) of ERalpha were localized to the mesenchyme and subepithelial stroma and later (postnatal d 2) to the corpus spongiosus, corpus cavernosus; and urethral epithelia. ERbeta was initially detected by postnatal d 2 and was localized diffusely in corpus spongiosus and cavernosus in immature rats. In the. adult, both ERs were concentrated largely to the urethral eithelia and vascular and neuronal structures. The present study provides the first evidence for ER expression in the penis. Thus, our data add the penis to the list of estrogen-responsive tissues in males and provide a base and insight for future studies aimed at investigating a functional role of estrogen in the penis, especially in development.</text>
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          <element elementId="43">
            <name>Identifier</name>
            <description>An unambiguous reference to the resource within a given context</description>
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              <elementText elementTextId="134116">
                <text>&lt;a href="http://doi.org/10.1210/en.2002-220628" target="_blank" rel="noreferrer noopener"&gt;10.1210/en.2002-220628&lt;/a&gt;</text>
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            <name>Format</name>
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                <text>COL27A1 is a member of the collagen fibrillar gene family and is expressed in cartilaginous tissues including the anlage of endochondral bone. To begin to understand its role in skeletogenesis, the temporospatial distributions of its RNA message and protein product, type XXVII collagen, were determined in developing human skeletal tissues. Laser capture microdissection and quantitative reverse-transcription polymerase chain reaction demonstrated that gene expression occurred throughout the growth plate and that it was higher in the resting and proliferative zones than in hypertrophic cartilage. Immunohistochemical analyses showed that type XXVII collagen was most evident in hypertrophic cartilage at the primary ossification center and at the growth plate and that it accumulated in the pericellular matrix. Synthesis of type XXVII collagen overlapped partly with that of type X collagen, a marker of chondrocyte hypertrophy, preceded the transition of cartilage to bone, and was associated with cartilage calcification. Immunogold electron microscopy of extracted ECM components from mouse growth plate showed that type XXVII collagen was a component of long non-banded fibrous structures, filamentous networks, and thin banded fibrils. The timing and location of synthesis suggest that type XXVII collagen plays a role during the calcification of cartilage and the transition of cartilage to bone. (C) 2007 Elsevier Inc. All rights reserved.</text>
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          <description>Locate full-text within NEOMED Library's e-journal collections</description>
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              <text>&lt;p&gt;Users with a NEOMED Library login can search for full-text journal articles at the following url: &lt;a href="https://libraryguides.neomed.edu/home"&gt;https://libraryguides.neomed.edu/home&lt;/a&gt;&lt;/p&gt;</text>
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                <text>Testosterone Decreases 3 Beta-hydroxysteroid Dehydrogenase-isomerase Messenger Ribonucleic Acid In Cultured Mouse Leydig Cells By A Strain-specific Mechanism</text>
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                <text>17-alpha-hydroxylase/c17-20 lyase; adult-rats; androgen; denovo synthesis; Endocrinology &amp; Metabolism; expression; human chorionic-gonadotropin; inbred mice; luteinizing-hormone; receptor; rna; side-chain cleavage; steroidogenesis; testicular cells; testis</text>
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                <text>We previously reported a strain-related difference in basal 3 beta-hydroxysteroid dehydrogenase-isomerase (3 beta HSD) activity in response to testosterone in cultured Leydig cells. The data suggested that the response to testosterone was androgen receptor mediated and that testosterone was acting via a irans-acting factor distal to the androgen receptor to regulate Leydig cell basal 3 beta HSD activity. This study was designed to determine whether the previous reported strain-related difference in basal 3 beta HSD activity in response to testosterone was due to a difference at the 3 beta HSD protein and/or at the mRNA level, In C57BL/6J Leydig cells, 2.0 mu M testosterone significantly decreased basal 3 beta HSD immunoreactive mass by day 6 in culture. Treatment with 2.0 mu M testosterone and 2.0 mu M hydroxyflutamide, an androgen receptor antagonist, negated the inhibitory effect of testosterone on C57BL/6J 3 beta HSD immunoreactive mass, Treatment with 2.0 mu M testosterone also significantly decreased 3 beta HSD mRNA content in C57BL/6J Leydig cells, which was detectable on day 3 in culture, In contrast to Leydig cells from C57BL/6J mice, Leydig cells from C3H/HeJ mice were not susceptible to the inhibitory effect of testosterone on 3 beta HSD. Treatment with 2.0 mu M testosterone had no detectable effect on C3H/HeJ 3 beta HSD immunoreactive mass or mRNA content at any time point in culture. These data indicate that the testosterone-induced loss of basal 3 beta HSD activity in C57BL/6J Leydig cells can he accounted for by the lass of 3 beta HSD immunoreactive mass, which is preceded by the loss of 3 beta HSD mRNA, and that the strain-related difference in the regulation of 3 beta HSD is present at all three levels. Thus, the putative trans-acting factor involved in the mechanism whereby testosterone decreases basal 3 beta HSD is likely to regulate the amount of 3 beta HSD mRNA.</text>
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              <text>Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).</text>
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              <text>S402-S402</text>
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              <text>25</text>
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          <description>Locate full-text within NEOMED Library's e-journal collections</description>
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            <description>A name given to the resource</description>
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                <text>Mcpip1 Is A Regulator Of Interleukin-6 Expression In Human Osteoarthritis Chondrocytes</text>
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                <text>Osteoporosis International</text>
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                <text>Endocrinology &amp; Metabolism</text>
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                <text>Haqqi T; Haseeb A; Makki M S</text>
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        <name>Osteoporosis International</name>
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        <element elementId="53">
          <name>URL Address</name>
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              <text>n/a</text>
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              <text>25</text>
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          <description>Locate full-text within NEOMED Library's e-journal collections</description>
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            <name>Title</name>
            <description>A name given to the resource</description>
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                <text>Regulation Of Interleukin-6 Expression By A Ribonucleotidyl Transferase Zcchc6 In Human Chondrocytes</text>
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              <elementText elementTextId="130216">
                <text>Osteoporosis International</text>
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            <description>A point or period of time associated with an event in the lifecycle of the resource</description>
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            <description>An entity primarily responsible for making the resource</description>
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                <text>Haqqi T; Arida A; Akhtar N</text>
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            <description>An unambiguous reference to the resource within a given context</description>
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            <elementText elementTextId="129702">
              <text>88</text>
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          <description>Locate full-text within NEOMED Library's e-journal collections</description>
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            <elementText elementTextId="129703">
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            <description>A name given to the resource</description>
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                <text>Low Level Suppression Of Hpa Axis From Ciclesonide</text>
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                <text>Haidet J; Garibaldi L</text>
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                <text>Detecting Dna Synthesis Of Neointimal Formation After Catheter Balloon Injury In Gk And In Wistar Rats: Using 5-ethynyl-2 '-deoxyuridine</text>
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                <text>Cardiovascular Diabetology</text>
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                <text>2012-12</text>
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            <description>The topic of the resource</description>
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                <text>alkynes; arterial injury; balloon injury; Cardiovascular System &amp; Cardiology; carotid-artery; Catheter; cell-cycle progression; click chemistry; diabetes-mellitus; diabetes-mellitus; DNA synthesis; EdU; eluting stents; Endocrinology &amp; Metabolism; in-vitro; mammalian target; Neointimal formation; PCNA; proliferation; terminal</text>
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                <text>Guo J S; Li D Y; Bai S R; Xu T D; Zhou Z M; Zhang Y B</text>
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                <text>Background: Neointimal formation plays an important role in the pathogenesis of coronary restenosis after percutaneous coronary intervention (PCI), especially in patients with diabetes mellitus. Recently, some studies have shown that 5-ethynyl-2'-deoxyuridine (EdU) incorporation can serve as a novel alternative to the 5-bromo-2'-deoxyuridine (BrdU) antibody detection method for detection of DNA synthesis in regenerating avian cochlea, chick embryo and the adult nervous system. However, few studies have been performed to assess the suitability of EdU for detecting DNA synthesis in vascular neointima. Methods: The carotid artery balloon injury model was established in Goto-Kakizaki (GK) and Wistar rats. A Cell-Light (TM) EdU Kit was used to detect EdU-labeled cell nuclei of common carotid arteries at day 7 after catheter balloon injury. Different methods of injecting EdU were tested. The protein levels of proliferating cell nuclear antigen (PCNA) and p-Akt (Ser473), as well as the mRNA levels of PCNA were evaluated by Western blotting and quantitative real-time PCR (qRT-PCR), respectively. Immunohistochemical staining was also employed to visualize PCNA-positive cells. Results: At day 7 after catheter balloon injury, far more EdU-positive and PCNA-positive cells were observed in GK rats. When comparing groups that received different EdU doses, it was found that the percentage of EdU-positive cells at a dose of 100 mg/kg body weight was than at doses of 25 mg/kg and 50 mg/kg. The number of positive cells was significantly higher in the repeated injection group compared to the single injection group. Further, after balloon injury DNA synthesis in GK rats was more notable than in Wistar rats. Neointimal formation in GK rats was more obvious than in Wistar rats. The protein levels of PCNA and p-Akt (Ser473) and the mRNA levels of PCNA were increased in injured rats as compared to uninjured rats, and were significantly higher in GK rats than in Wistar rats. Conclusion: By intraperitoneal injections of EdU at a dose of 100 mg/kg three times, EdU incorporation can detect carotid arterial DNA synthesis caused by neointimal formation in GK rats and Wistar rats at day 7 after balloon injury by the EdU click reaction quickly and effectively. Moreover, more obvious DNA synthesis in the vascular neointima could be observed in GK rats than in Wistar rats.</text>
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            <description>An unambiguous reference to the resource within a given context</description>
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                <text>&lt;a href="http://doi.org/10.1186/1475-2840-11-150" target="_blank" rel="noreferrer noopener"&gt;10.1186/1475-2840-11-150&lt;/a&gt;</text>
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        <name>Bai S R</name>
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        <name>Zhou Z M</name>
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              <text>&lt;a href="http://doi.org/10.1016/s8756-3282(01)00594-4" target="_blank" rel="noreferrer noopener"&gt;http://doi.org/10.1016/s8756-3282(01)00594-4&lt;/a&gt;</text>
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              <text>Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).</text>
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          <name>Pages</name>
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            <elementText elementTextId="129101">
              <text>453-457</text>
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              <text>5</text>
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            <elementText elementTextId="129103">
              <text>29</text>
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          <name>Search for Full-text</name>
          <description>Locate full-text within NEOMED Library's e-journal collections</description>
          <elementTextContainer>
            <elementText elementTextId="129104">
              <text>&lt;p&gt;Users with a NEOMED Library login can search for full-text journal articles at the following url: &lt;a href="https://libraryguides.neomed.edu/home"&gt;https://libraryguides.neomed.edu/home&lt;/a&gt;&lt;/p&gt;</text>
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          <element elementId="50">
            <name>Title</name>
            <description>A name given to the resource</description>
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                <text>Age- And Genotype-dependence Of Bone Material Properties In The Osteogenesis Imperfecta Murine Model (oim)</text>
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            <description>An entity responsible for making the resource available</description>
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                <text>Bone</text>
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            <description>A point or period of time associated with an event in the lifecycle of the resource</description>
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                <text>2001</text>
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                <text>2001-11</text>
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          <element elementId="49">
            <name>Subject</name>
            <description>The topic of the resource</description>
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                <text>(SAXS); calcified tissues; children; collagen; density; density distribution; electron-microscopy; Endocrinology &amp; Metabolism; mechanical-properties; mice exhibit; microhardness; mineral; mineral crystals; murine model; osteogenesis imperfecta (OI); quantitative backscattered electron imaging (qBEI); small-angle X-ray scattering; tendon; x-ray-scattering</text>
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            <description>An entity primarily responsible for making the resource</description>
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                <text>Grabner B; Landis W J; Roschger P; Rinnerthaler S; Peterlik H; Klaushofer K; Fratzl P</text>
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            <description>An account of the resource</description>
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                <text>Cortical mineralization of long bones was studied in collagen alpha2(I)-deficient mice (oim) used as a model for human osteogenesis imperfecta. Aspects of the age development of the mice were characterized by combining nanometer- to micrometer-scale structural analysis with microhardness measurements. Bone structure was determined from homozygous (oini/oim) and heterozygous (oim/+) mice and their normal (+/+) littermates as a function of animal age by small-angle X-ray scattering (SAXS) and quantitative backscattered electron imaging (qBEI) measurements. SAXS studies found anomalies in the size and arrangement of bone mineral crystals in both homozygous and heterozygous mice aged 1-14 months. Generally, the crystals were smaller in thickness and less well aligned in these mice compared with control animals. An increase in the mean crystal thickness of the bone was found within all three genotypes up to an age of 3 months. Vicker's hardness measurements were significantly enhanced for oim bone (homozygotes and heterozygotes) compared with controls. The microhardness values were correlated directly with increased mineral content of homozygous and heterozygous compared with control bone, as determined by qBEI analysis. There was also a significant increase of mineral content with age. Two possibilities for collagen-mineral association are discussed for explaining the increased hardness and mineral content of oim/oim bone, together with its decreased toughness and thinner mineral crystals. As a consequence of the present measurements, one model for oim bone could incorporate small and densely packed mineral crystals. A second model for possible collagen-mineral association in oim material would consist of two families of mineral crystals, one being smaller and the other being much larger than the crystals found in normal mouse long bones. (C) 2001 by Elsevier</text>
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            <name>Identifier</name>
            <description>An unambiguous reference to the resource within a given context</description>
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                <text>&lt;a href="http://doi.org/10.1016/s8756-3282(01)00594-4" target="_blank" rel="noreferrer noopener"&gt;10.1016/s8756-3282(01)00594-4&lt;/a&gt;</text>
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              <elementText elementTextId="129105">
                <text>Journal Article or Conference Abstract Publication</text>
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        <name>calcified tissues</name>
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        <name>tendon</name>
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        <name>x-ray-scattering</name>
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              <text>&lt;a href="http://doi.org/10.1210/en.2004-0728" target="_blank" rel="noreferrer noopener"&gt;http://doi.org/10.1210/en.2004-0728&lt;/a&gt;</text>
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              <text>Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).</text>
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              <text>5157-5167</text>
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              <text>11</text>
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          <description>Locate full-text within NEOMED Library's e-journal collections</description>
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            <elementText elementTextId="126630">
              <text>&lt;p&gt;Users with a NEOMED Library login can search for full-text journal articles at the following url: &lt;a href="https://libraryguides.neomed.edu/home"&gt;https://libraryguides.neomed.edu/home&lt;/a&gt;&lt;/p&gt;</text>
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            <description>A name given to the resource</description>
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                <text>Differential Regulation Of The Cell Cycle By Alpha(1)-adrenergic Receptor Subtypes</text>
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            <description>The topic of the resource</description>
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                <text>adventitial fibroblasts; alpha(1b)-adrenergic receptor; arterial blood-pressure; dna-synthesis; Endocrinology &amp; Metabolism; fibroblasts; gene-expression; kinase pathways; mitogen-activated protein; proliferation; rat-1; smooth-muscle-cells</text>
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            <description>An entity primarily responsible for making the resource</description>
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                <text>Gonzalez-Cabrera P J; Shi T; Yun J; McCune D F; Rorabaugh B R; Perez D M</text>
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            <name>Identifier</name>
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                <text>&lt;a href="http://doi.org/10.1210/en.2004-0728" target="_blank" rel="noreferrer noopener"&gt;10.1210/en.2004-0728&lt;/a&gt;</text>
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                <text>In Experiment I, castrated male and female CD-1 mice +/- estradiol benzoate (EB) treatment were tested for their performance on a skilled sensorimotor task consisting of walking across beams of varying widths (6, 9, 12, and 21 mm). To evaluate whether behavioral performance was related to nigrostriatal dopaminergic function, tissue dopamine concentrations were determined from the corpus striatum as well as the hypothalamus and olfactory tubercle. In general, sensorimotor performance improved for all treatment conditions as the beam width increased. Castrated male mice treated with oil vehicle showed the worst performance as indicated by significantly greater amounts of time to cross the beam. Treatment of castrated males with EB significantly improved their performance. Performance of the castrated females was not changed by EB treatment and was similar to that observed with the castrated + EB males. Significant gender differences in dopamine concentrations (female &gt; male) were obtained in the corpus striatum, as well as the olfactory tubercle and hypothalamus. Dopamine levels were unaltered by EB treatment. In Experiment II, behavioral and neurochemical determinations were directly compared between castrated and intact male mice. Behavioral performance of castrates was significantly reduced compared to intact males. No differences in dopamine concentrations were obtained between these two groups; however, the hypothalamic dopamine/DOPAC ratio of castrates was significantly greater than that of intact male mice. These results demonstrate significant modulatory effects of EB in castrated male, but not female, mice upon sensorimotor performance and indicate that this task may provide an effective means to partial out modulatory effects of gonadal steroid hormones upon skilled sensorimotor performance. When the data of Experiments I and II are combined, it appears that the basis of this sensorimotor deficit in the males is the absence of gonadal steroid hormones. In addition, these results reveal significant gender differences in various dopaminergic systems in these mice. (C) 1994 Academic Press, Inc.</text>
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                <text>Interactive effects of tamoxifen and oestrogen upon the nigrostriatal dopaminergic system: Long-term treatments</text>
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                <text>Journal of Neuroendocrinology</text>
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                <text>receptors; Neurosciences &amp; Neurology; Endocrinology &amp; Metabolism; estrogen; binding; catecholamines; brain; striatum; time; amphetamine; estradiol; antiestrogens; ovarian steroids; sexual-behavior; anti-oestrogens</text>
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                <text>McDermott J L; Anderson L I; Dluzen D E</text>
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                <text>In the present report adult female rats were ovariectomized (OVX) and assigned to one of four treatment conditions. Treatments consisted of administering pellets containing 17 beta-oestradiol (E), tamoxifen (TMX), a combination of TMX and E or no further treatment (OVX), Animals received these treatments immediately following OVX and were maintained in these conditions for a 40-day period. Subsequently, the corpus striatum (CS) was dissected from each animal and prepared for determinations of basal and amphetamine stimulated DA output using in-vitro superfusion. No statistically significant differences among the four treatment groups were obtained for basal dopamine output. The highest levels of amphetamine-stimulated dopamine responses were obtained from E treated rats. These values were significantly greater than that obtained from OVX rats and rats treated with a combination of TMX + E. The significance of these findings is that they indicate both a non-traditional central nervous system site and mechanism of action through which tamoxifen-oestrogen interactions can function. Such data may have important implications for administration of tamoxifen to premenopausal women as this anti-oestrogen may compromise nigrostriatal dopaminergic function under conditions where oestrogenic modulation is present.</text>
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