50 research outputs found

    Nickel-Catalyzed Reductive Alkene Cross-Dialkylation with Unactivated Alkyl Electrophiles

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    A Ni-catalyzed reductive dialkylation of 8-aminoquinoline-tethered aliphatic alkenes with two unactivated alkyl electrophiles is disclosed here. Key to the development of this transformation is the combination of primary alkyl (pseudo)halides and secondary alkyl iodides that produce products in a single regioselective manner. The reaction exhibits good functional group compatibility, and its synthetic utility was demonstrated by the concise synthesis of the precursors of biologically relevant molecules

    Association between intrauterine mild hyperglycemia and post-natal high-fat diet with adiponectin and AMPK pathway genes

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    <p>To investigate the mechanisms of maternal–fetal interactions in the setting of gestational diabetes mellitus. We investigated the long-term effects of intrauterine mild hyperglycemia and a postnatal high-fat diet on the glucose metabolism of adult offspring, and explored the role of adiponectin on hepatic gluconeogenesis. Twenty-one pregnant Wistar rats were randomly divided into an intrauterine hyperglycemia group (group D, <i>n</i> = 14) and a control group (group C, <i>n</i> = 7). Offspring were divided into four groups according to intrauterine blood glucose level and post-weaning dietary patterns (high-fat diet groups: DF and CF or normal diet groups: DN and CN, <i>n</i> = 8 per group). The average birth weights of group D offspring were higher than for group C. In the DF rats, low adiponectin mRNA expression in perirenal and epididymal fat was significantly positively correlated with low hepatic AdipoR1 mRNA expression and significantly correlated with high hepatic PEPCK, G-6-Pase, and PGC-1α mRNA levels. In DF rats, hepatic P-AMPK was cytoplasmically located and its level was decreased; in these rats, hepatic CRTC2 was expressed in the nucleus and its level was significantly increased. Our study shows that the dietary structure of offspring has a large influence on the incidence of abnormal glucose tolerance.</p

    GDM rat model induced high blood pressure in male offspring.

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    <p>(<b>A–B</b>) Blood pressure and heart rate were determined in conscious rats from all offspring groups by an indirect tail-cuff method. Three stable consecutive measurements of blood pressure and heart rate were averaged. Data are means ± sem. N = 9. * p<0.05 vs. CN, # p<0.05 vs. CS, $ p<0.05 vs. DN.</p

    GDM rat model induced glucose intolerance in male offspring.

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    <p>(<b>A</b>) No significant difference of blood glucose level at birth in offspring born from control and diabetic mothers. (<b>B–E</b>) Glucose tolerance test (GTT) was performed at 16, 20, 24, 28 weeks using glucose (2 g/kg body weight) given by gavage. N = 9. Results are mean ± sem. * indicates p<0.05.</p

    GDM rat model with moderate hyperglycemia was induced by streptozotocin.

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    <p>(<b>A</b>) Study design: The male offspring were studied and fed with either normal diet or high salt diet (8% NaCl) after weaning: control group fed with normal diet (CN, n = 9) or high salt diet (CS, n = 9), diabetic group fed with normal diet (DN, n = 9) or high salt diet (DS, n = 9). (<b>B</b>) GDM rat model with moderate hyperglycemia after pregnancy was established by a single intraperitoneal injection of streptozotocin (STZ). The average glucose level of diabetic mothers during pregnancy was 11.2–15.0 mmol/L. (<b>C</b>) HE staining images (400X) of pancreatic islets obtained from control and diabetic rat mothers. (<b>D</b>) Pancreatic islets area and diameters were measured using an image analysis program, Image-Pro Plus 6.0, Media Cybernetics. Ten different fields were analyzed for each group. Results are mean ± sem. * indicates p<0.05.</p

    Kidney weight of male offspring.

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    <p>Data are means ± sem.</p>a<p>p<0.05 vs. CN;</p>c<p>p<0.05 vs. DN.</p

    Water intake, urine volume and urinary ion excretion in male offspring.

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    <p><i>In vivo</i> studies were carried out in metabolic cages with rats to compare water intake (<b>A</b>), urine volume (<b>B</b>) and Na<sup>+</sup>, K<sup>+</sup>, Cl<sup>−</sup> excretion (<b>C</b>) between offspring groups. Data are means ± sem. N = 9. * p<0.05 vs. CN, # p<0.05 vs. CS, $ p<0.05 vs. DN.</p

    Intrarenal expression of RAS components.

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    <p>Components of RAS in kidney in offspring groups were measured by real-time quantitative PCR. The gene expression of angiotensinogen, renin, angiotensin converting enzyme 1, angiotensin II type 1A receptor and angiotensin II type 1B receptor (<b>A–E</b>) was detected.</p

    Immunostaining for TLR4 in normal term placentae.

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    <p>(A) The expression of CK7 in the maternal surfaces of placentae; (B) The expression of vimentin in the maternal surfaces of placentae; (C) The expression of TLR4 in the maternal surfaces of placentae. In the serial sections of maternal surfaces of normal placentae, TLR4 expressions were observed in trophoblast, decidual cells and in the vascular endothelial cells (n = 36). (D) In the fetal sections of placentae, the straining of CK7 were observed; (E) The expression of vimentin in fetal section of normal placentae (n = 36); (F) The expression of TLR4 in the fetal surface of placentae. Except in trophoblasts and vascular endothelial cells, TLR4 staining were also observed in amniotic epithelium (n = 36). STB, syncytiotrophoblast; BV: blood vascul; DC, decidual cells; AE, amniotic epithelium. CK7: cytokeratin 7; TLR4: toll like receptor 4. Positive staining is brown. Magnification ×100.</p
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