[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 10 of about 17779329
1. Nesbitt TS, Gilbert WM, Herrchen B: Shoulder dystocia and associated risk factors with macrosomic infants born in California. Am J Obstet Gynecol; 1998 Aug;179(2):476-80
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Shoulder dystocia and associated risk factors with macrosomic infants born in California.
  • OBJECTIVE: The purpose of this study was to examine the 1-year incidence statewide in California of shoulder dystocia and its associated risk factors.
  • STUDY DESIGN: With a data set that contains computer-linked records from the birth certificate and hospital discharge records of both mother and baby, all births of infants >3500 g in >300 civilian acute care hospitals in California in 1992 were analyzed.
  • All cases of shoulder dystocia were identified from discharge records, birth certificates, or both and were analyzed with both bivariate and multivariate techniques to identify specific risk factors.
  • RESULTS: A total of 175,886 vaginal births of infants >3500 g were included in our database, of which 6238 infants (3%) had shoulder dystocia.
  • The percentages of births complicated by shoulder dystocia for unassisted births not complicated by diabetes were 5.2% for infants 4000 to 4250 g, 9.1% for those 4250 to 4500 g, 14.3% for 4500 to 4750, and 21.1% for those 4750 to 5000 g.
  • Shoulder dystocia increased by approximately 35% to 45% in vacuum- or forceps-assisted births to nondiabetic mothers.
  • Similar increases were seen in unassisted births to diabetic mothers.
  • The risk of shoulder dystocia for assisted births to diabetic mothers was even more dramatic: 12.2% for infants 4000 to 4250 g, 16.7% for those 4250 to 4500 g, 27.3% for those 4500 to 4750 g, and 34.8% for those 4750 to 5000 g.
  • After controlling for other parameters, there was an increased risk of shoulder dystocia associated with diabetes (odds ratio 1.7), assisted delivery (odds ratio 1.9), and induction of labor (odds ratio 1.3).
  • Rates of birth trauma, asphyxia, and length of stay were all increased among births complicated by shoulder dystocia.
  • CONCLUSION: This information on the incidence of shoulder dystocia and associated risk factors for a large statewide population may assist providers of obstetric care in counseling patients when macrosomia is suspected.
  • The inaccuracy of estimating fetal weight is a severe limitation in attempting to establish guidelines designed to prevent shoulder dystocia.
  • [MeSH-major] Dystocia / etiology. Fetal Macrosomia / complications
  • [MeSH-minor] Birth Weight. Female. Humans. Infant, Newborn. Logistic Models. Pregnancy. Risk Factors

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Am J Obstet Gynecol. 1999 Apr;180(4):1047 [10203684.001]
  • (PMID = 9731856.001).
  • [ISSN] 0002-9378
  • [Journal-full-title] American journal of obstetrics and gynecology
  • [ISO-abbreviation] Am. J. Obstet. Gynecol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] UNITED STATES
  •  go-up   go-down


2. Vekshina NL, Khristoliubova NA: [Changes in the properties of the brain opiate, DA2, GABA, and 5-HT1 receptors in the progeny of female rats consuming ethanol for a long time during pregnancy and lactation]. Eksp Klin Farmakol; 1993 Mar-Apr;56(2):58-60
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Changes in the properties of the brain opiate, DA2, GABA, and 5-HT1 receptors in the progeny of female rats consuming ethanol for a long time during pregnancy and lactation].
  • [Transliterated title] Izmenenie svoĭstv opiatnykh, DA2-, GAMK- i 5HT1-retseptorov mozga u potomkov krys-samok, dlitel'no potrebliavshikh étanol vo vremia beremennosti i laktatsii.
  • The study was undertaken to examine two-week and two-month rats whose mothers had been given alcohol for a long period of time during pregnancy and lactation.
  • Profound changes were found in the properties of all types of the receptors under study.
  • The changes were found in the receptors of both group animals.
  • Substantial changes were encountered in the properties of GABA and DA2 receptors in the brain of two-month rats after acute alcoholization.
  • The changes were differentiated from those seen in GABA and DA2 receptors in the brain of the rats whose mothers had not been given ethanol.
  • [MeSH-major] Alcohol Drinking / adverse effects. Brain / drug effects. Lactation / drug effects. Prenatal Exposure Delayed Effects. Receptors, Cell Surface / drug effects
  • [MeSH-minor] Aging / drug effects. Animals. Brain Chemistry / drug effects. Female. Pregnancy. Rats. Receptors, Dopamine D2 / analysis. Receptors, Dopamine D2 / drug effects. Receptors, GABA-A / analysis. Receptors, GABA-A / drug effects. Receptors, Opioid / analysis. Receptors, Opioid / drug effects. Receptors, Serotonin / analysis. Receptors, Serotonin / drug effects

  • MedlinePlus Health Information. consumer health - Alcohol.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 8394167.001).
  • [ISSN] 0869-2092
  • [Journal-full-title] Eksperimental'naia i klinicheskaia farmakologiia
  • [ISO-abbreviation] Eksp Klin Farmakol
  • [Language] rus
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] RUSSIA
  • [Chemical-registry-number] 0 / Receptors, Cell Surface; 0 / Receptors, Dopamine D2; 0 / Receptors, GABA-A; 0 / Receptors, Opioid; 0 / Receptors, Serotonin
  •  go-up   go-down


3. Airò R, Carusillo MG, Rivetti I: [Specific immune response in asymptomatic bacteriuria in pregnancy]. Boll Ist Sieroter Milan; 1980;59(6):625-31
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Specific immune response in asymptomatic bacteriuria in pregnancy].
  • [Transliterated title] Risposta immunitaria specifica nella batteriuria asintomatica della gravidanza.
  • Specific antibodies against bacteria isolated from urine have been searched in the serum of pregnant women with asymptomatic bacteriuria, utilizing passive hemagglutination, direct agglutination and indirect immunofluorescence methods.
  • Of the 475 examined women 35 (7.3%) showed positive urine culture; 88.5% of these women had an elevated specific antibody titer in their serum.
  • Our studies support the hypothesis that asymptomatic bacteriuria in pregnant women might represent a signal of latent urinary tract infection.
  • [MeSH-major] Bacteriuria / immunology. Pregnancy Complications, Infectious / immunology. Urinary Tract Infections / immunology
  • [MeSH-minor] Adult. Agglutination Tests. Antibodies, Bacterial / analysis. Escherichia coli / immunology. Female. Fluorescent Antibody Technique. Hemagglutination Tests. Humans. Pregnancy. Proteus / immunology

  • Genetic Alliance. consumer health - Pregnancy.
  • MedlinePlus Health Information. consumer health - Infections and Pregnancy.
  • MedlinePlus Health Information. consumer health - Urinary Tract Infections.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 7016137.001).
  • [ISSN] 0021-2547
  • [Journal-full-title] Bollettino dell'Istituto sieroterapico milanese
  • [ISO-abbreviation] Boll Ist Sieroter Milan
  • [Language] ita
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] ITALY
  • [Chemical-registry-number] 0 / Antibodies, Bacterial
  •  go-up   go-down


Advertisement
4. Blum J, Fridovich I: Superoxide, hydrogen peroxide, and oxygen toxicity in two free-living nematode species. Arch Biochem Biophys; 1983 Apr 1;222(1):35-43
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Superoxide, hydrogen peroxide, and oxygen toxicity in two free-living nematode species.
  • Two species of free-living nematodes, Turbatrix aceti and Caenorhabditis elegans, exhibited a marked sensitivity to 3 atm of 100% O2.
  • Environmental changes in pH and temperature, which altered nematode respiration, resulted in alterations in the survival of these organisms under high pO2.
  • Levels of defensive enzymes such as superoxide dismutase, catalase, glutathione peroxidase, and dianisidine peroxidase were measured in the two species.
  • No changes in the level of superoxide dismutase or catalase activity were induced by exposure of the nematodes to high pO2.
  • Manipulation of these two enzymes was however achieved using the inhibitors 3-amino-1,2,4-triazole and diethyldithiocarbamate.
  • 3-Amino-1,2,4-triazole (20 mM) eliminated greater than or equal to 80% of the catalase activity in vivo and diethyldithiocarbamate (5 mM) decreased the level of CuZn superoxide dismutase by greater than or equal to 70%.
  • Both of these compounds increased the sensitivity of C. elegans to high pO2 toxicity.
  • Compounds capable of intracellular redox-cycling with O2- -production, such as plumbagin, increased CN- -resistant respiration in the nematodes and imposed an O2-dependent toxicity.
  • These experiments demonstrate the toxicity of intracellular O2- and H2O2 in nematodes and the importance of superoxide dismutase and catalase in providing a defense against these toxic molecules in vivo.
  • [MeSH-major] Hydrogen Peroxide / toxicity. Nematoda / drug effects. Oxygen / toxicity. Superoxide Dismutase / metabolism
  • [MeSH-minor] Animals. Caenorhabditis / drug effects. Dihydrolipoamide Dehydrogenase. Free Radicals. Oxidation-Reduction. Oxygen Consumption

  • Hazardous Substances Data Bank. HYDROGEN PEROXIDE .
  • Hazardous Substances Data Bank. OXYGEN .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 6687666.001).
  • [ISSN] 0003-9861
  • [Journal-full-title] Archives of biochemistry and biophysics
  • [ISO-abbreviation] Arch. Biochem. Biophys.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Free Radicals; BBX060AN9V / Hydrogen Peroxide; EC 1.15.1.1 / Superoxide Dismutase; EC 1.8.1.4 / Dihydrolipoamide Dehydrogenase; S88TT14065 / Oxygen
  • [Other-IDs] NASA/ 83177107
  •  go-up   go-down


5. Stass SA, Holloway ML, Peterson V, Creegan WJ, Gallivan M, Schumacher HR: Cytoplasmic fragments causing spurious platelet counts in the leukemic phase of poorly differentiated lymphocytic lymphoma. Am J Clin Pathol; 1979 Jan;71(1):128-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytoplasmic fragments causing spurious platelet counts in the leukemic phase of poorly differentiated lymphocytic lymphoma.
  • A patient with a leukemic phase of poorly differentiated lymphocytic lymphoma had a spuriously high automated platelet count because of cytoplasmic fragments.
  • The number and relative percentage of cytoplasmic fragments increased during chemotherapy.
  • The cytoplasmic fragments did not interfere with platelet aggregation using adenosine diphosphate, collagen, and epinephrine even though they were found in platelet-rich plasma.
  • The ultrastructure of the cytoplasmic fragments is discussed.
  • Cytoplasmic fragments as a cause of spuriously high automated platelet counts should be considered in cases of leukemic patients.
  • [MeSH-major] Blood Platelets. Cytoplasm. Lymphoma, Non-Hodgkin / pathology
  • [MeSH-minor] Adult. Blood Cell Count / methods. Humans. Male

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 581717.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] UNITED STATES
  •  go-up   go-down


6. Dithmer S, Staat C, Müller C, Ku MC, Pohlmann A, Niendorf T, Gehne N, Fallier-Becker P, Kittel Á, Walter FR, Veszelka S, Deli MA, Blasig R, Haseloff RF, Blasig IE, Winkler L: Claudin peptidomimetics modulate tissue barriers for enhanced drug delivery. Ann N Y Acad Sci; 2017 Jun;1397(1):169-184
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Claudin peptidomimetics modulate tissue barriers for enhanced drug delivery.
  • The blood-brain barrier (BBB) formed by the microvascular endothelium limits cerebral drug delivery.
  • The paraendothelial cleft is sealed by tight junctions (TJs) with a major contribution from claudin-5, which we selected as a target to modulate BBB permeability.
  • For this purpose, drug-enhancer peptides were designed based on the first extracellular loop (ECL) of claudin-5 to allow transient BBB permeabilization.
  • Peptidomimetics (C5C2 and derivatives, nanomolar affinity to claudin-5) size-selectively (≤40 kDa) and reversibly (12-48 h) increased the permeability of brain endothelial and claudin-5-transfected epithelial cell monolayers.
  • Upon peptide uptake, the number of TJ strand particles diminished, claudin-5 was downregulated and redistributed from cell-cell contacts to the cytosol, and the cell shape was altered.
  • Cellular permeability of doxorubicin (cytostatic drug, 580 Da) was enhanced after peptide administration.
  • Mouse studies (3.5 μmol/kg i.v.) confirmed that, for both C5C2 and a d-amino acid derivative, brain uptake of Gd-diethylene-triamine penta-acetic acid (547 Da) was enhanced within 4 h of treatment.
  • On the basis of our functional data, circular dichroism measurements, molecular modeling, and docking experiments, we suggest an association model between β-sheets flanked by α-helices, formed by claudin-5 ECLs, and the peptides.
  • In conclusion, we identified claudin-5 peptidomimetics that improve drug delivery through endothelial and epithelial barriers expressing claudin-5.
  • [MeSH-major] Blood-Brain Barrier / drug effects. Claudin-5 / pharmacology. Endothelial Cells / drug effects. Peptidomimetics / pharmacology
  • [MeSH-minor] Animals. Antibiotics, Antineoplastic / administration & dosage. Antibiotics, Antineoplastic / pharmacokinetics. Brain / drug effects. Brain / metabolism. Cell Line. Cells, Cultured. Circular Dichroism. Doxorubicin / administration & dosage. Doxorubicin / pharmacokinetics. Drug Delivery Systems / methods. Gadolinium DTPA / administration & dosage. Gadolinium DTPA / pharmacokinetics. HEK293 Cells. Humans. Mice, Inbred C57BL. Microscopy, Confocal. Microscopy, Electron / methods. Models, Molecular. Permeability / drug effects. Protein Conformation. Rats. Rhodamines / administration & dosage. Rhodamines / pharmacokinetics. Tight Junctions / drug effects. Tight Junctions / metabolism. Tight Junctions / ultrastructure. Time-Lapse Imaging / methods

  • Hazardous Substances Data Bank. DOXORUBICIN .
  • Hazardous Substances Data Bank. GADOPENTETATE DIMEGLUMINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] © 2017 New York Academy of Sciences.
  • (PMID = 28505395.001).
  • [ISSN] 1749-6632
  • [Journal-full-title] Annals of the New York Academy of Sciences
  • [ISO-abbreviation] Ann. N. Y. Acad. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 5-carboxytetramethylrhodamine succinimidyl ester; 0 / Antibiotics, Antineoplastic; 0 / Claudin-5; 0 / Peptidomimetics; 0 / Rhodamines; 80168379AG / Doxorubicin; K2I13DR72L / Gadolinium DTPA
  • [Keywords] NOTNLM ; blood-brain barrier / cell-cell contact / claudin protein family / peptide / tight junction / tissue barrier
  •  go-up   go-down


7. Freeman SM, Itthipuripat S, Aron AR: High Working Memory Load Increases Intracortical Inhibition in Primary Motor Cortex and Diminishes the Motor Affordance Effect. J Neurosci; 2016 May 18;36(20):5544-55
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High Working Memory Load Increases Intracortical Inhibition in Primary Motor Cortex and Diminishes the Motor Affordance Effect.
  • Motor affordances occur when the visual properties of an object elicit behaviorally relevant motor representations.
  • Typically, motor affordances only produce subtle effects on response time or on motor activity indexed by neuroimaging/neuroelectrophysiology, but sometimes they can trigger action itself.
  • This is apparent in "utilization behavior," where individuals with frontal cortex damage inappropriately grasp affording objects.
  • This raises the possibility that, in healthy-functioning individuals, frontal cortex helps ensure that irrelevant affordance provocations remain below the threshold for actual movement.
  • In Experiment 1, we tested this "frontal control" hypothesis by "loading" the frontal cortex with an effortful working memory (WM) task (which ostensibly consumes frontal resources) and examined whether this increased EEG measures of motor affordances to irrelevant affording objects.
  • Under low WM load, there were typical motor affordance signatures: an event-related desynchronization in the mu frequency and an increased P300 amplitude for affording (vs nonaffording) objects over centroparietal electrodes.
  • Contrary to our prediction, however, these affordance measures were diminished under high WM load.
  • In Experiment 2, we tested competing mechanisms responsible for the diminished affordance in Experiment 1.
  • We used paired-pulse transcranial magnetic stimulation over primary motor cortex to measure long-interval cortical inhibition.
  • We found greater long-interval cortical inhibition for high versus low load both before and after the affording object, suggesting that a tonic inhibition state in primary motor cortex could prevent the affordance from provoking the motor system.
  • Overall, our results suggest that a high WM load "sets" the motor system into a suppressed state that mitigates motor affordances.
  • SIGNIFICANCE STATEMENT: Is an irrelevant motor affordance more likely to be triggered when you are under low or high cognitive load?
  • We examined this using physiological measures of the motor affordance while working memory load was varied.
  • We observed a typical motor affordance signature when working memory load was low; however, it was abolished when load was high.
  • Further, there was increased intracortical inhibition in primary motor cortex under high working memory load.
  • This suggests that being in a state of high cognitive load "sets" the motor system to be imperturbable to distracting motor influences.
  • This makes a novel link between working memory load and the balance of excitatory/inhibitory activity in the motor cortex and potentially has implications for disorders of impulsivity.
  • [MeSH-major] Memory, Short-Term. Motor Cortex / physiology. Neural Inhibition
  • [MeSH-minor] Adult. Evoked Potentials. Female. Humans. Male

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright © 2016 the authors 0270-6474/16/365544-12$15.00/0.
  • (PMID = 27194334.001).
  • [ISSN] 1529-2401
  • [Journal-full-title] The Journal of neuroscience : the official journal of the Society for Neuroscience
  • [ISO-abbreviation] J. Neurosci.
  • [Language] eng
  • [Grant] United States / NIDA NIH HHS / DA / R01 DA026452
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Keywords] NOTNLM ; EEG / GABA / inhibition / motor affordance / working memory
  •  go-up   go-down


8. Lorenz TK, Demas GE, Heiman JR: Interaction of menstrual cycle phase and sexual activity predicts mucosal and systemic humoral immunity in healthy women. Physiol Behav; 2015 Dec 1;152(Pt A):92-8
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Interaction of menstrual cycle phase and sexual activity predicts mucosal and systemic humoral immunity in healthy women.
  • Several studies have documented shifts in humoral immune parameters (e.g., immunoglobulins) across the menstrual cycle in healthy women.
  • It is thought that these shifts may reflect dynamic balancing between reproduction and pathogen defense, as certain aspects of humoral immunity may disrupt conception and may be temporarily downregulated at ovulation.
  • If so, one could expect maximal cycle-related shifts of humoral immunity in individuals invested in reproduction - that is, women who are currently sexually active - and less pronounced shifts in women who are not reproductively active (i.e., abstinent).
  • We investigated the interaction of sexual activity, menstrual cycle phase, and humoral immunity in a sample of 32 healthy premenopausal women (15 sexually active, 17 abstinent).
  • Participants provided saliva samples during their menses, follicular phase, ovulation (as indicated by urine test for LH surge), and luteal phase, from which IgA was assayed.
  • Participants also provided blood samples at menses and ovulation, from which IgG was assayed.
  • Sexually active participants provided records of their frequency of sexual activity as well as condom use.
  • At ovulation, sexually active women had higher IgG than abstinent women (d=0.77), with women reporting regular condom use showing larger effects (d=0.63) than women reporting no condom use (d=0.11).
  • Frequency of sexual activity predicted changes in IgA (Cohen's f(2)=0.25), with women reporting high frequency of sexual activity showing a decrease in IgA at ovulation, while women reporting low frequency or no sexual activity showing an increase in IgA at ovulation.
  • Taken together, these findings support the hypothesis that shifts in humoral immunity across the menstrual cycle are associated with reproductive effort, and could contribute to the mechanisms by which women's physiology navigates tradeoffs between reproduction and immunity.

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright © 2015 Elsevier Inc. All rights reserved.
  • [Cites] Endocrinology. 2012 Jun;153(6):2544-50 [22434079.001]
  • [Cites] Psychophysiology. 1996 Mar;33(2):175-83 [8851245.001]
  • [Cites] Ann N Y Acad Sci. 1993 Sep 20;694:184-94 [8215054.001]
  • [Cites] Epidemiol Rev. 2014;36:71-82 [24042431.001]
  • [Cites] Clin Exp Immunol. 1996 Jun;104(3):538-42 [9099941.001]
  • [Cites] Brain Behav Immun. 1997 Dec;11(4):286-306 [9512816.001]
  • [Cites] J Clin Endocrinol Metab. 1998 Jul;83(7):2454-60 [9661628.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Apr 19;102(16):5808-13 [15817686.001]
  • [Cites] Evolution. 2005 Jul;59(7):1510-7 [16153036.001]
  • [Cites] Curr Biol. 2005 Sep 20;15(18):1690-4 [16169493.001]
  • [Cites] Arch Sex Behav. 2014 Feb;43(2):231-50 [23807216.001]
  • [Cites] J Sex Med. 2014 Apr;11(4):966-79 [23448297.001]
  • [Cites] Natl Health Stat Report. 2012 Oct 18;(60):1-25 [24988814.001]
  • [Cites] Horm Behav. 2014 Jul;66(2):330-8 [24954690.001]
  • [Cites] PLoS One. 2014;9(12):e114824 [25479383.001]
  • [Cites] J Clin Immunol. 2015 Feb;35(2):125-34 [25572592.001]
  • [Cites] Nat Rev Immunol. 2015 Apr;15(4):217-30 [25743222.001]
  • [Cites] Clin Chim Acta. 2015 Apr 15;444:29-36 [25659295.001]
  • [Cites] Fertil Steril. 2015 Dec;104(6):1513-21.e1-4 [26385401.001]
  • [Cites] Infect Immun. 1999 Dec;67(12):6321-8 [10569744.001]
  • [Cites] Psychoneuroendocrinology. 2000 Feb;25(2):187-99 [10674282.001]
  • [Cites] Fertil Steril. 2000 Nov;74(5):1008-13 [11056250.001]
  • [Cites] J Clin Invest. 2001 Jul;108(1):15-23 [11435451.001]
  • [Cites] Early Pregnancy. 2000 Apr;4(2):154-64 [11723544.001]
  • [Cites] Neurosci Biobehav Rev. 2002 Jan;26(1):31-44 [11835982.001]
  • [Cites] Clin Endocrinol (Oxf). 2001 Dec;55(6):701-10 [11895208.001]
  • [Cites] Clin Exp Immunol. 2002 Apr;128(1):10-20 [11982585.001]
  • [Cites] J Clin Endocrinol Metab. 2002 May;87(5):2013-7 [11994334.001]
  • [Cites] J Immunol. 2002 Jul 1;169(1):566-74 [12077289.001]
  • [Cites] Brain Behav Immun. 2002 Dec;16(6):785-98 [12480507.001]
  • [Cites] Psychol Rep. 2004 Jun;94(3 Pt 1):839-44 [15217036.001]
  • [Cites] Hum Reprod. 2004 Jul;19(7):1539-43 [15190016.001]
  • [Cites] J Clin Invest. 1970 Apr;49(4):673-80 [5443170.001]
  • [Cites] J Reprod Fertil. 1981 Sep;63(1):237-40 [7277324.001]
  • [Cites] Obstet Gynecol. 1983 Sep;62(3):388-92 [6410312.001]
  • [Cites] Scand J Dent Res. 1984 Feb;92(1):33-7 [6372061.001]
  • [Cites] J Reprod Fertil. 1985 Jul;74(2):361-70 [3900380.001]
  • [Cites] Am J Reprod Immunol Microbiol. 1985 Sep;9(1):1-5 [4051082.001]
  • [Cites] J Reprod Med. 1989 Apr;34(4):292-4 [2715991.001]
  • [Cites] J Acquir Immune Defic Syndr. 1992;5(4):325-32 [1347787.001]
  • [Cites] Gut. 1992 Jul;33(7):882-6 [1644326.001]
  • [Cites] Am J Reprod Immunol. 1993 May;29(4):219-23 [8397811.001]
  • [Cites] J Am Coll Health. 2005 Nov-Dec;54(3):143-7 [16335313.001]
  • [Cites] Biol Psychol. 2006 Mar;71(3):312-5 [16095799.001]
  • [Cites] Scand J Clin Lab Invest. 2006;66(2):121-7 [16537245.001]
  • [Cites] Trends Ecol Evol. 2007 Feb;22(2):80-6 [17056152.001]
  • [Cites] AIDS. 2007 Feb 19;21(4):467-76 [17301565.001]
  • [Cites] Perspect Sex Reprod Health. 2008 Jun;40(2):94-104 [18577142.001]
  • [Cites] J Infect Dis. 2009 Feb 1;199(3):455-63 [19133811.001]
  • [Cites] AIDS Res Hum Retroviruses. 2009 Jan;25(1):83-92 [19108692.001]
  • [Cites] Front Biosci (Landmark Ed). 2009;14:4444-56 [19273362.001]
  • [Cites] Women Health. 2008;48(4):429-44 [19301532.001]
  • [Cites] Biol Reprod. 2009 May;80(5):1036-45 [19164169.001]
  • [Cites] Am J Phys Anthropol. 2011;146 Suppl 53:134-54 [22101690.001]
  • [Cites] Psychophysiology. 2012 Jan;49(1):111-7 [22092348.001]
  • [Cites] Immunol Cell Biol. 2012 Feb;90(2):137-48 [21537340.001]
  • [Cites] PLoS One. 2013;8(10):e76176 [24098437.001]
  • [Cites] Curr Opin Allergy Clin Immunol. 2012 Dec;12(6):602-8 [23026772.001]
  • (PMID = 26394125.001).
  • [ISSN] 1873-507X
  • [Journal-full-title] Physiology & behavior
  • [ISO-abbreviation] Physiol. Behav.
  • [Language] ENG
  • [Grant] United States / NICHD NIH HHS / HD / T32 HD049336; United States / NICHD NIH HHS / HD / T32HD049336-09
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Immunoglobulin A; 0 / Immunoglobulin G
  • [Other-IDs] NLM/ NIHMS726165 [Available on 12/01/16]; NLM/ PMC4633338 [Available on 12/01/16]
  • [Keywords] NOTNLM ; Immunity / Immunoglobulins / Menstrual cycle / Reproduction / Sexual behavior
  •  go-up   go-down


9. Morino-Koga S, Yano S, Kondo T, Shimauchi Y, Matsuyama S, Okamoto Y, Suico MA, Koga T, Sato T, Shuto T, Arima H, Wada I, Araki E, Kai H: Insulin receptor activation through its accumulation in lipid rafts by mild electrical stress. J Cell Physiol; 2013 Feb;228(2):439-46
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Insulin receptor activation through its accumulation in lipid rafts by mild electrical stress.
  • Insulin resistance is due to the reduced cellular response to insulin in peripheral tissues.
  • The interaction of insulin with its receptor is the first step in insulin action and thus the identified target of insulin resistance.
  • It has been well established that defects or mutations in the insulin receptor (IR) cause insulin resistance.
  • Therefore, an IR activator might be a novel therapeutic approach for insulin resistance.
  • Our previous report showed that mild electrical stress (MES) enhanced the insulin-induced signaling pathway.
  • However, the molecular mechanism of the effect of MES remains unclear.
  • We assessed the effect of MES, which is characterized by low-intensity direct current, on insulin signaling in vitro and in vivo.
  • Here, we showed that MES activated the insulin signaling in an insulin-independent manner and improved insulin resistance in peripheral tissues of high fat-fed mice.
  • Moreover, we found that MES increased the localization of IR in lipid rafts and enhanced the level of phosphorylated Akt in insulin-resistant hepatic cells.
  • Ablation of lipid rafts disrupted the effect of MES on Akt activation.
  • Our findings indicate that MES has potential as an activator of IR in an insulin-independent manner, and might be beneficial for insulin resistance in type 2 diabetes.
  • [MeSH-major] Electric Stimulation. Membrane Microdomains / metabolism. Receptor, Insulin / metabolism. Stress, Physiological
  • [MeSH-minor] Animals. Diet, High-Fat. Hep G2 Cells. Humans. Hyperglycemia / complications. Insulin / pharmacology. Insulin Resistance / physiology. Liver / drug effects. Liver / metabolism. Male. Mice. Mice, Inbred C57BL. Phosphorylation. Proto-Oncogene Proteins c-akt / metabolism. Signal Transduction / drug effects. Signal Transduction / physiology

  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright © 2012 Wiley Periodicals, Inc.
  • (PMID = 22740366.001).
  • [ISSN] 1097-4652
  • [Journal-full-title] Journal of cellular physiology
  • [ISO-abbreviation] J. Cell. Physiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Insulin; EC 2.7.10.1 / Receptor, Insulin; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
  •  go-up   go-down


10. Dronamraju R, Mason JM: MU2 and HP1a regulate the recognition of double strand breaks in Drosophila melanogaster. PLoS One; 2011;6(9):e25439
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] MU2 and HP1a regulate the recognition of double strand breaks in Drosophila melanogaster.
  • Chromatin structure regulates the dynamics of the recognition and repair of DNA double strand breaks; open chromatin enhances the recruitment of DNA damage response factors, while compact chromatin is refractory to the assembly of radiation-induced repair foci.
  • MU2, an orthologue of human MDC1, a scaffold for ionizing radiation-induced repair foci, is a widely distributed chromosomal protein in Drosophila melanogaster that moves to DNA repair foci after irradiation.
  • Here we show using yeast 2 hybrid screens and co-immunoprecipitation that MU2 binds the chromoshadow domain of the heterochromatin protein HP1 in untreated cells.
  • We asked what role HP1 plays in the formation of repair foci and cell cycle control in response to DNA damage.
  • After irradiation repair foci form in heterochromatin but are shunted to the edge of heterochromatic regions an HP1-dependent manner, suggesting compartmentalized repair.
  • Hydroxyurea-induced repair foci that form at collapsed replication forks, however, remain in the heterochromatic compartment.
  • HP1a depletion in irradiated imaginal disc cells increases apoptosis and disrupts G2/M arrest.
  • Further, cells irradiated in mitosis produced more and brighter repair foci than to cells irradiated during interphase.
  • Thus, the interplay between MU2 and HP1a is dynamic and may be different in euchromatin and heterochromatin during DNA break recognition and repair.

  • FlyBase. FlyBase .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Cell Biochem. 2006 Dec 15;99(6):1463-75 [16927314.001]
  • [Cites] Genetics. 2006 Jul;173(3):1447-54 [16648644.001]
  • [Cites] Nat Cell Biol. 2007 Jun;9(6):683-90 [17486112.001]
  • [Cites] PLoS One. 2007;2(10):e1057 [17957241.001]
  • [Cites] EMBO Rep. 2008 Jan;9(1):91-6 [18064046.001]
  • [Cites] Mutat Res. 2008 Mar 1;639(1-2):108-12 [18179804.001]
  • [Cites] Cell. 2008 Mar 7;132(5):731-2 [18329359.001]
  • [Cites] Biotechniques. 2008 Feb;44(2):265-73 [18330356.001]
  • [Cites] Nat Protoc. 2008;3(4):606-11 [18388942.001]
  • [Cites] Nature. 2008 May 29;453(7195):682-6 [18438399.001]
  • [Cites] Curr Opin Genet Dev. 2008 Apr;18(2):169-74 [18329871.001]
  • [Cites] Curr Opin Genet Dev. 2008 Apr;18(2):204-11 [18372168.001]
  • [Cites] Methods Mol Biol. 2008;420:207-18 [18641949.001]
  • [Cites] Mol Cell. 2008 Jul 25;31(2):167-77 [18657500.001]
  • [Cites] Mol Cell. 2008 Aug 8;31(3):303-4 [18691960.001]
  • [Cites] Chromosome Res. 2008;16(6):851-62 [18704724.001]
  • [Cites] Biochim Biophys Acta. 2008 Dec;1783(12):2398-414 [18706456.001]
  • [Cites] Int Rev Cell Mol Biol. 2009;273:1-47 [19215901.001]
  • [Cites] PLoS Genet. 2009 Mar;5(3):e1000435 [19325889.001]
  • [Cites] Methods Mol Biol. 2009;523:125-40 [19381917.001]
  • [Cites] PLoS Genet. 2009 May;5(5):e1000473 [19424425.001]
  • [Cites] Cell Cycle. 2009 May 15;8(10):1494-500 [19377276.001]
  • [Cites] Biochem Soc Trans. 2009 Jun;37(Pt 3):569-76 [19442252.001]
  • [Cites] J Cell Biol. 2009 May 18;185(4):577-86 [19451271.001]
  • [Cites] Proc Natl Acad Sci U S A. 2009 Jun 2;106(22):8998-9003 [19443688.001]
  • [Cites] Cell Cycle. 2009 Sep 15;8(18):2945-50 [19657222.001]
  • [Cites] Annu Rev Genet. 2009;43:467-92 [19919324.001]
  • [Cites] Mol Cell Biol. 2009 Dec;29(24):6335-40 [19805510.001]
  • [Cites] J Cell Biol. 2010 Jul 26;190(2):197-207 [20660628.001]
  • [Cites] Cell. 2011 Mar 4;144(5):732-44 [21353298.001]
  • [Cites] Oncogene. 1999 Nov 1;18(45):6135-44 [10557105.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Jun 6;97(12):6499-503 [10823906.001]
  • [Cites] Mol Biol Cell. 2001 Jun;12(6):1671-85 [11408576.001]
  • [Cites] Carcinogenesis. 2002 May;23(5):687-96 [12016139.001]
  • [Cites] Curr Biol. 2002 Oct 29;12(21):1797-806 [12419179.001]
  • [Cites] Biochem Soc Trans. 2003 Feb;31(Pt 1):40-4 [12546650.001]
  • [Cites] Biochem Cell Biol. 2003 Jun;81(3):123-9 [12897845.001]
  • [Cites] Development. 2004 Aug;131(15):3571-80 [15215206.001]
  • [Cites] Genes Dev. 2004 Aug 1;18(15):1850-61 [15256487.001]
  • [Cites] Nucleic Acids Res. 1983 Mar 11;11(5):1475-89 [6828386.001]
  • [Cites] Proc Natl Acad Sci U S A. 1984 Oct;81(19):6090-4 [6435123.001]
  • [Cites] Cancer Res. 1988 Mar 15;48(6):1618-22 [3345532.001]
  • [Cites] EMBO J. 1988 Apr;7(4):1081-6 [2841109.001]
  • [Cites] Eur J Cell Biol. 1989 Oct;50(1):170-80 [2515059.001]
  • [Cites] Prog Clin Biol Res. 1989;318:73-80 [2516630.001]
  • [Cites] Development. 1993 Jan;117(1):29-43 [8223253.001]
  • [Cites] Development. 1993 Jun;118(2):401-15 [8223268.001]
  • [Cites] Curr Opin Genet Dev. 1994 Apr;4(2):281-91 [8032206.001]
  • [Cites] J Cell Sci. 1995 Apr;108 ( Pt 4):1407-18 [7615662.001]
  • [Cites] Genetics. 1997 Aug;146(4):1381-97 [9258681.001]
  • [Cites] J Cell Biol. 1998 Aug 24;142(4):1013-22 [9722613.001]
  • [Cites] Mol Cell. 1998 Nov;2(5):527-38 [9844626.001]
  • [Cites] Genetics. 1999 Jul;152(3):1025-35 [10388821.001]
  • [Cites] Science. 2005 Apr 22;308(5721):510-1 [15845843.001]
  • [Cites] Nucleic Acids Res. 2005;33(9):2852-8 [15905474.001]
  • [Cites] Nat Genet. 2005 Dec;37(12):1361-6 [16258543.001]
  • [Cites] PLoS Genet. 2006 May;2(5):e71 [16710445.001]
  • [Cites] Chromosome Res. 2006;14(4):377-92 [16821134.001]
  • [Cites] J Cell Biol. 2007 Apr 23;177(2):219-29 [17438073.001]
  • (PMID = 21966530.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chromosomal Proteins, Non-Histone; 0 / DNA-Binding Proteins; 0 / Drosophila Proteins; 0 / MU2 protein, Drosophila; 107283-02-3 / heterochromatin-specific nonhistone chromosomal protein HP-1
  • [Other-IDs] NLM/ PMC3179522
  •  go-up   go-down






Advertisement