problem with importing files

Thanks for the reply, that was a quick one!

Yes it has to do something with the format of the exported files. Me and another student have exactly the same issue, but have different seach string topics.

Attached is the Scopus (csv file format) and the WOS (Mac UTF-8 format).

All the best,

Alex

Best regards,

Alexander Aloy Unit 8, 42 Meeks St Kingsford NSW 2032 AUSTRALIA Mobile +61424507588

On Mon, Apr 9, 2018 at 2:06 PM, Maxime Rivest notifications@github.com wrote:

Hi,

Thank you for reaching out.

Because the problem is at the import step, I would need to see the content of the Wos/ and Scopus/ folder. Or, at least, a very representative sample of it.

Would you be willing to share those file by email? If so, maxime(dot)rivest2(at)mail(dot)mcgill(dot)ca

The first thing I would check is whether each folder contains only wos or scopus files and not both, and whether they have the approriate format.

Based on the cause of the problem I will try to improve the error message.

— You are receiving this because you authored the thread. Reply to this email directly, view it on GitHub https://github.com/MaximeRivest/scimeetr/issues/4#issuecomment-379624456, or mute the thread https://github.com/notifications/unsubscribe-auth/AitmZUFzKZEYbFJwqdPP3Vft2O2EF2EJks5tmt4qgaJpZM4TL5KA .

PT AU BA BE GP AF BF CA TI SO SE BS LA DT CT CY CL SP HO DE ID AB C1 RP EM RI OI FU FX CR NR TC Z9 U1 U2 PU PI PA SN EI BN J9 JI PD PY VL IS PN SU SI MA BP EP AR DI D2 EA EY PG WC SC GA UT PM OA HC HP DA J Lima, TD; Avila, ETP; Fraga, GA; Sena, MD; Dias, ABD; de Almeida, PC; Trombeta, JCD; Vieira, RC; Damazo, A; Navalta, J; Prestes, J; Voltarelli, F Lima, Thiago da Rosa; Pereira Avila, Eudes Thiago; Fraga, Gessica Alves; Sena, Mariana de Souza; de Souza Dias, Arlyson Batista; de Almeida, Paula Caroline; dos Santos Trombeta, Joice Cristina; Vieira Junior, Roberto Carlos; Damazo, Amilcar Sabino; Navalta, James Wilfred; Prestes, Jonato; Voltarelli, Fabrcio Azevedo Effect of administration of high-protein diet in rats submitted to resistance training EUROPEAN JOURNAL OF NUTRITION English Article Dietary management; High-protein diet; Resistance training; Aquatic jump training; Tissue morphology BODY-WEIGHT GAIN; SKELETAL-MUSCLE; ENERGY-BALANCE; EXERCISE; REQUIREMENTS; STRENGTH; APPETITE; SUPPLEMENTATION; ADAPTATION; METABOLISM Although there is limited evidence regarding the pathophysiological effects of a high-protein diet (HD), it is believed that this type of diet could overload the body and cause damage to the organs directly involved with protein metabolism and excretion. The aim of this study was to verify the effects of HD on biochemical and morphological parameters of rats that completed a resistance training protocol (RT; aquatic jump) for 8 weeks. Thirty-two adult male Wistar rats were divided into four groups (n = 8 for each group): sedentary normal protein diet (SN-14%), sedentary high-protein diet (SH-35%), trained normal protein diet (TN-14%), and trained high-protein diet (TH-35%). Biochemical, tissue, and morphological measurements were made. Kidney (1.91 +/- 0.34) and liver weights (12.88 +/- 1.42) were higher in the SH. Soleus muscle weight was higher in the SH (0.22 +/- 0.03) when compared to all groups. Blood glucose (123.2 +/- 1.8), triglycerides (128.5 +/- 44.0), and HDL cholesterol levels (65.7 +/- 20.9) were also higher in the SH compared with the other experimental groups. Exercise reduced urea levels in the trained groups TN and TH (31.0 +/- 4.1 and 36.8 +/- 6.6), respectively. Creatinine levels were lower in TH and SH groups (0.68 +/- 0.12; 0.54 +/- 0.19), respectively. HD negatively altered renal morphology in SH, but when associated with RT, the apparent damage was partially reversed. In addition, the aquatic jump protocol reversed the damage to the gastrocnemius muscle caused by the HD. A high-protein diet promoted negative metabolic and morphological changes, while RT was effective in reversing these deleterious effects. [Lima, Thiago da Rosa; Pereira Avila, Eudes Thiago; Fraga, Gessica Alves; Sena, Mariana de Souza; de Souza Dias, Arlyson Batista; de Almeida, Paula Caroline; Damazo, Amilcar Sabino; Voltarelli, Fabrcio Azevedo] Univ Fed Mato Grosso, Fernando Correa da Costa Ave 2367, BR-78060600 Cuiaba, MT, Brazil; [dos Santos Trombeta, Joice Cristina] Mato Grosso State Univ, Diamantino, MT, Brazil; [Vieira Junior, Roberto Carlos] Mato Grosso State Univ, Caceres, MT, Brazil; [Navalta, James Wilfred] Univ Nevada, Las Vegas, NV 89154 USA; [Prestes, Jonato] Univ Catolica Brasilia, Graduat Program Phys Educ, Brasilia, DF, Brazil Voltarelli, F (reprint author), Univ Fed Mato Grosso, Fernando Correa da Costa Ave 2367, BR-78060600 Cuiaba, MT, Brazil. faunesp8@yahoo.com.br 62 0 0 0 0 SPRINGER HEIDELBERG HEIDELBERG TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY 1436-6207 1436-6215 EUR J NUTR Eur. J. Nutr. APR 2018 57 3 1083 1096 10.1007/s00394-017-1391-5 14 Nutrition & Dietetics Nutrition & Dietetics FZ9YC WOS:000427967500019 28236109 2018-04-09
J Gaynullina, DK; Borzykh, AA; Sofronova, SI; Selivanova, EK; Shvetsova, AA; Martyanov, AA; Kuzmin, IV; Tarasova, OS Gaynullina, D. K.; Borzykh, A. A.; Sofronova, S. I.; Selivanova, E. K.; Shvetsova, A. A.; Martyanov, A. A.; Kuzmin, I. V.; Tarasova, O. S. Voluntary exercise training restores anticontractile effect of NO in coronary arteries of adult rats with antenatal/early postnatal hypothyroidism NITRIC OXIDE-BIOLOGY AND CHEMISTRY English Article Coronary arteries; Endothelium; Hypothyroidism; Nitric oxide; 6-Propyl-2-thiouracil; Voluntary exercise ISCHEMIA-REPERFUSION INJURY; CARDIAC-FUNCTION; MATERNAL HYPOTHYROIDISM; ENDOTHELIAL DYSFUNCTION; FETAL HYPOTHYROIDISM; NITRIC-OXIDE; BLOOD-FLOW; DISEASE; ADAPTATIONS; PREGNANCY Introduction: Our recent study showed that NO-mediated anticontractile effect of endothelium is absent in coronary arteries of adult rats, which suffered from antenatal/early postnatal hypothyroidism. This study tested the hypothesis that exercise training would improve such detrimental consequences of early thyroid deficiency. Design and methods: Wistar dams received propylthiouracil (PTU, 7 ppm) in drinking water during gestation and two weeks postpartum; control dams received tap water. Six-week-old male offspring of control (CON) and PTU dams was divided into sedentary (CON-Sed, n = 12; PTU-Sed, n = 10) and trained (CON-Tr, n = 12; PTU-Tr, n = 10) groups; the latter had 24-h access to running wheels. Eight weeks later coronary arteries were studied by wire myography. Anticontractile effect of NO was assessed by the effects of NOS inhibitor L-NNA on the basal tone and contractile response to U46619. Oxidative phosphorylation complexes and eNOS were estimated by Western blotting. Results: T-3/T-4 and TSH levels (ELISA) were normalized in the progeny of PTU-treated dams at the age of 6 weeks and were not affected by training. Total running distance did not differ between CON-Tr and PTU-Tr. The contents of oxidative phosphorylation complexes were increased post-training in triceps brachii muscle from CON-Tr and PTU-Tr and in heart from PTU-Tr. Coronary arteries of PTU-Sed compared to CON-Sed demonstrated higher basal tone and contractile response to U46619, which were not further increased by L-NNA. The effects of L-NNA on the basal tone and contractile response to U46619 did not differ in CON-Tr and PTU-Tr groups, but were elevated in PTU-Tr compared to PTU-Sed group. PTU-Tr rats in comparison to PTU-Sed group had higher eNOS content in heart. Responses of coronary arteries to DEA/NO did not differ among all experimental groups. Conclusions: Long-lasting coronary endothelial dysfunction resulted from transient thyroid deficiency during the antenatal/early postnatal period can be corrected by voluntary exercise training. [Gaynullina, D. K.; Sofronova, S. I.; Selivanova, E. K.; Shvetsova, A. A.; Martyanov, A. A.; Kuzmin, I. V.; Tarasova, O. S.] Moscow MV Lomonosov State Univ, Fac Biol, Leninskie Gory 1-12, Moscow 119234, Russia; [Gaynullina, D. K.; Borzykh, A. A.; Sofronova, S. I.; Selivanova, E. K.; Shvetsova, A. A.; Martyanov, A. A.; Kuzmin, I. V.; Tarasova, O. S.] Russian Acad Sci, Inst Biomed Problems, Khoroshevskoe Shosse 76A, Moscow 123007, Russia; [Gaynullina, D. K.] Russian Natl Res Med Univ, Dept Physiol, Ostrovitianova Str 1, Moscow 117997, Russia Gaynullina, DK (reprint author), Moscow MV Lomonosov State Univ, Fac Biol, Leninskie Gory 1-12, Moscow 119234, Russia. gaynullina@mail.bio.msu.ru Russian Science Foundation [N14-15-00704] This study was supported by the Russian Science Foundation (grant N14-15-00704). 49 0 0 5 5 ACADEMIC PRESS INC ELSEVIER SCIENCE SAN DIEGO 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA 1089-8603 1089-8611 NITRIC OXIDE-BIOL CH Nitric Oxide-Biol. Chem. APR 1 2018 74 10 18 10.1016/j.niox.2018.01.001 9 Biochemistry & Molecular Biology; Cell Biology Biochemistry & Molecular Biology; Cell Biology FY0YJ WOS:000426538300002 29307633 2018-04-09
J Guo, Y; Luo, F; Zhang, X; Chen, JY; Shen, L; Zhu, Y; Xu, DY Guo, Yuan; Luo, Fei; Zhang, Xv; Chen, Jingyuan; Shen, Li; Zhu, Yi; Xu, Danyan TPPU enhanced exercise-induced epoxyeicosatrienoic acid concentrations to exert cardioprotection in mice after myocardial infarction JOURNAL OF CELLULAR AND MOLECULAR MEDICINE English Article myocardial infarction; exercise; soluble epoxide hydrolase inhibitor; endothelial progenitor cells; angiogenesis; microRNA-126 SOLUBLE EPOXIDE HYDROLASE; ENDOTHELIAL PROGENITOR CELLS; SENSITIVE POTASSIUM CHANNELS; CARDIAC REHABILITATION; ISCHEMIC ANGIOGENESIS; PATHWAY; INHIBITORS; INCREASES; MEDIATOR; RATS Exercise training (ET) is a safe and efficacious therapeutic approach for myocardial infarction (MI). Given the numerous benefits of exercise, exercise-induced mediators may be promising treatment targets for MI. C57BL/6 mice were fed 1-trifluoromethoxyphenyl-3-(1-propionylpiperidine-4-yl) urea (TPPU), a novel soluble epoxide hydrolase inhibitor (sEHI), to increase epoxyeicosatrienoic acid (EET) levels, for 1week before undergoing MI surgery. After 1-week recovery, the mice followed a prescribed exercise programme. Bone marrow-derived endothelial progenitor cells (EPCs) were isolated from the mice after 4weeks of exercise and cultured for 7days. Angiogenesis around the ischaemic area, EPC functions, and the expression of microRNA-126 (miR-126) and its target gene Spred1 were measured. The results were confirmed invitro by adding TPPU to EPC culture medium. ET significantly increased serum EET levels and promoted angiogenesis after MI. TPPU enhanced the effects of ET to reduce the infarct area and improve cardiac function after MI. ET increased EPC function and miR-126 expression, which were further enhanced by TPPU, while Spred1 expression was significantly down-regulated. Additionally, the protein kinase B/glycogen synthase kinase 3 beta (AKT/GSK3 beta) signalling pathway was activated after the administration of TPPU. EETs are a potential mediator of exercise-induced cardioprotection in mice after MI. TPPU enhances exercise-induced cardiac recovery in mice after MI by increasing EET levels and promoting angiogenesis around the ischaemic area. [Guo, Yuan; Luo, Fei; Chen, Jingyuan; Shen, Li; Xu, Danyan] Cent S Univ, Dept Cardiovasc Med, Xiangya Hosp 2, Changsha, Hunan, Peoples R China; [Zhang, Xv; Zhu, Yi] Tianjin Med Univ, Dept Physiol & Pathophysiol, Collaborat Innovat Ctr Tianjin Med Epigenet, Tianjin, Peoples R China Xu, DY (reprint author), Cent S Univ, Dept Cardiovasc Med, Xiangya Hosp 2, Changsha, Hunan, Peoples R China. xudanyan02@sina.com National Natural Science Foundation of China [81372117, 81672264]; Fundamental Research Funds for the Central Universities of Central South University [2016zzts132] This work was supported by the grant from the National Natural Science Foundation of China (Nos. 81372117 and 81672264). This work was supported by the Fundamental Research Funds for the Central Universities of Central South University (No. 2016zzts132). 36 0 0 0 0 WILEY HOBOKEN 111 RIVER ST, HOBOKEN 07030-5774, NJ USA 1582-4934 J CELL MOL MED J. Cell. Mol. Med. MAR 2018 22 3 1489 1500 10.1111/jcmm.13412 12 Cell Biology; Medicine, Research & Experimental Cell Biology; Research & Experimental Medicine FX4SU WOS:000426069300010 29265525 gold 2018-04-09
J Martins, EL; Ricardo, JC; De-Souza-Ferreira, E; Camacho-Pereira, J; Ramos, D; Galina, A Martins, Eduarda Lopes; Ricardo, Juliana Carvalho; de-Souza-Ferreira, Eduardo; Camacho-Pereira, Juliana; Ramos-Filho, Dionizio; Galina, Antonio Rapid regulation of substrate use for oxidative phosphorylation during a single session of high intensity interval or aerobic exercises in different rat skeletal muscles COMPARATIVE BIOCHEMISTRY AND PHYSIOLOGY B-BIOCHEMISTRY & MOLECULAR BIOLOGY English Article Exercise; Skeletal muscle adaptations; Mitochondria; Substrate oxidation; High intensity interval exercise; Reactive oxygen species production and mitochondrial biogenesis FATTY-ACID OXIDATION; HYDROGEN-PEROXIDE; MITOCHONDRIAL BIOGENESIS; SUPEROXIDE; ADAPTATION; FIBERS; PERFORMANCE; GENERATION; TISSUE; PRESCRIPTION Different exercise protocols lead to long-term adaptations that are related to increased mitochondrial content through the activation of mitochondrial biogenesis. However, immediate mitochondrial response to exercise and energetic substrate utilization is still unknown. We evaluate the mitochondrial physiology of two types rat skeletal muscle fibres immediately after a single session of high intensity interval exercise (HIIE) or aerobic exercise (AER). We found AER was able to reduce the ATP synthesis dependent oxygen flux in the tibialis (TA) when stimulated by complex I and II substrates. On the other hand, there was an increase of the maximum velocity (V-max) for glycerol-phosphate oxidation and V-max and affinity (K-M) of palmitoyl-carnitine oxidation (PC). The exercise did not affect oxygen flux coupled to ATP synthesis in red gastrocnemius (RG) but, surprisingly, reduced its affinity for PC, decreasing the apparent catalytic efficiency (V-max/K-M) of oxidation for PC. Neither exercise protocol was able to change the electron transfer system capacity of the mitochondria or markers of mitochondrial content. The AER group had increased H2O2 production compared to the SED and HIIE groups, with the mechanism being predominantly the escape of electrons through reverse flux in complex I and other sites in TA, and only through other sites in RG. There were no changes in the activities of antioxidant enzymes. Our results show that mitochondria from different muscles submitted to distinct exercise protocols show alterations in the specific fluxes of substrate utilization and oxygen metabolism, indicating that the dynamics of mitochondria are linked to the metabolic flexibility. [Martins, Eduarda Lopes; Ricardo, Juliana Carvalho; de-Souza-Ferreira, Eduardo; Camacho-Pereira, Juliana; Ramos-Filho, Dionizio; Galina, Antonio] Univ Fed Rio de Janeiro, Fed Univ Rio de Janeiro, Inst Med Biochem Leopoldo Meis, Lab Bioenerget & Mitochondrial Physiol, Rio de Janeiro, RJ, Brazil Martins, EL; Galina, A (reprint author), Univ Fed Rio de Janeiro, Fed Univ Rio de Janeiro, Inst Med Biochem Leopoldo Meis, Lab Bioenerget & Mitochondrial Physiol, Rio de Janeiro, RJ, Brazil.; Galina, A (reprint author), Av Carlos Chagas Filho 373,BL D,SL Dss13, BR-21941902 Rio De Janeiro, Brazil. eglopes@bioqmed.ufrj.br; galina@bioqmed.ufrj.br FAPERJ (Fundacao de Amparo a Pesquisa do Estado do Rio de Janeiro) [E_26/2014]; CNPq (Conselho Nacional de Desenvolvimento Cientifico e Tecnologico) [483093/2012-2]; CAPES (Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior) [PROEX - 0487] This work was supported by FAPERJ (Fundacao de Amparo a Pesquisa do Estado do Rio de Janeiro) - E_26/2014, CNPq (Conselho Nacional de Desenvolvimento Cientifico e Tecnologico) 483093/2012-2 and CAPES (Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior) PROEX - 0487. 59 0 0 5 5 ELSEVIER SCIENCE INC NEW YORK 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA 1096-4959 1879-1107 COMP BIOCHEM PHYS B Comp. Biochem. Physiol. B-Biochem. Mol. Biol. MAR 2018 217 40 50 10.1016/j.cbpb.2017.11.013 11 Biochemistry & Molecular Biology; Zoology Biochemistry & Molecular Biology; Zoology FV6VO WOS:000424720400005 29222029 2018-04-09
J Ganguly, BB; Mandal, S; Kadam, NN Ganguly, Bani Bandana; Mandal, Shouvik; Kadam, Nitin N. Spectrum of health condition in methyl isocyanate (MIC)-exposed survivors measured after 30 years of disaster ENVIRONMENTAL SCIENCE AND POLLUTION RESEARCH English Article Methyl isocyanate (MIC); Health of the MIC victims; Systemic complications; 30 years post MIC-disaster GAS LEAK; MYELODYSPLASTIC SYNDROMES; EXPOSURE SURROGATE; BHOPAL DISASTER; B6C3F1 MICE; F344/N RATS; MORBIDITY; RESIDENCE; RECOVERY; TOXICITY Health effects of methyl isocyanate (MIC) exposure were mostly reported on the one-time acute exposure in Bhopal population. Epidemiological survey conducted by the Indian apex body of health research has been reported as Technical Reports, which were lacking in peer review by the expert epidemiologic scientists. The present pilot survey was aimed to measure the health effects 30 years post disaster in MIC-exposed survivors. Questionnaire-based survey has captured every health complaint in 168 individuals and grouped as systemic functions for interpreting the long-term effects of MIC. Key health parameters, including reproductive outcome and respiratory/orthopedic/general morbidity, were prevalent among the severely exposed population compared to control and moderately exposed groups. The collective incidence of diabetes, hypertension, and cancer also was prevalent in the severely exposed group. Ophthalmic morbidity was almost similar in the three groups, rather with higher incidence in the control group, though not statistically significant. Among all health parameters, reproductive, ophthalmic, and respiratory effects were prevalent over others. Although the incidence of health problems has been declined among the survivors, long-term effect is apparent as scars of one-time acute exposure might trigger sequel of long-term effects. Additionally, acquisition of genetic rearrangements, survival of T cell sub-populations, variable latency of chemical effect on DNA nucleosides, nutritional status, occupational exposure, living environment, lifestyle, and overall gene-environment interaction might perturb individual immunity and favor onset of long-term illness in a scenario of background exposure to MIC. However, the exercise should be continued on a larger sample size for drawing a conclusive result on long-term MIC effect on survivors' health. [Ganguly, Bani Bandana; Mandal, Shouvik] MGM New Bombay Hosp, MGM Ctr Genet Res & Diag, Vashi Sect 3, Navi Mumbai 400703, India; [Kadam, Nitin N.] MGM Med Coll, Navi Mumbai, India Ganguly, BB (reprint author), MGM New Bombay Hosp, MGM Ctr Genet Res & Diag, Vashi Sect 3, Navi Mumbai 400703, India. mgmgeneticlab@yahoo.com Indian Council of Medical Research, New Delhi, India The authors acknowledge the financial support of Indian Council of Medical Research, New Delhi, India, and administrative support of National Institute for Research in Environmental Health, Bhopal, India. 49 0 0 0 0 SPRINGER HEIDELBERG HEIDELBERG TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY 0944-1344 1614-7499 ENVIRON SCI POLLUT R Environ. Sci. Pollut. Res. FEB 2018 25 5 SI 4963 4973 10.1007/s11356-017-0865-6 11 Environmental Sciences Environmental Sciences & Ecology FX0XG WOS:000425770300086 29204942 2018-04-09
J Townsend, LK; Peppler, WT; Bush, ND; Wright, DC Townsend, Logan K.; Peppler, Willem T.; Bush, Natasha D.; Wright, David C. Obesity exacerbates the acute metabolic side effects of olanzapine PSYCHONEUROENDOCRINOLOGY English Article Obesity; Olanzapine; Glucose; Insulin resistance; Schizophrenia HEPATIC INSULIN-RESISTANCE; BODY-MASS INDEX; 2ND-GENERATION ANTIPSYCHOTICS; WEIGHT-GAIN; IN-VIVO; ATYPICAL ANTIPSYCHOTICS; INDUCED HYPERGLYCEMIA; GLUCOSE-INTOLERANCE; FAT OXIDATION; ANIMAL-MODEL Olanzapine is a second-generation antipsychotic used in the management of schizophrenia and various off-label conditions. The acute metabolic responses of olanzapine recapitulate many of the side effects associated with obesity. Obesity rates are high in the schizophrenic population, but it is unknown whether pre-existing obesity associated metabolic dysfunction augments the acute side effects of olanzapine. To address this question, we compared the responses to olanzapine in lean and high-fat diet-induced (HFD) obese mice. Four weeks of HFD (60% kcal from fat) led to obese, hyperglycemic, and insulin resistant mice. Olanzapine-induced hyperglycemia and systemic insulin resistance were exacerbated in HFD-induced obese mice. Olanzapine also profoundly inhibited insulin signalling in skeletal muscle and liver, which appears to be exacerbated by obesity. The greater olanzapine-induced hyperglycemia may also result from increased hepatic glucose output in obese mice as pyruvate challenge led to significantly higher blood glucose concentrations, with associated increases in hepatic content of gluconeogenic enzymes. Olanzapine also suppressed RER while acutely increasing oxygen consumption in obese mice. A single olanzapine treatment reduced physical activity for up to 24 h, regardless of obesity. Considering obesity is very common in the schizophrenic population, these data suggest that previous research may be under-estimating the severity of olanzapine's acute side effects. [Townsend, Logan K.; Peppler, Willem T.; Bush, Natasha D.; Wright, David C.] Univ Guelph, Dept Human Hlth & Nutr Sci, 50 Stone Rd E, Guelph, ON N1G 2W1, Canada Wright, DC (reprint author), Univ Guelph, Dept Human Hlth & Nutr Sci, 50 Stone Rd E, Guelph, ON N1G 2W1, Canada. dcwright@uoguelph.ca Natural Sciences and Engineering Research Council of Canada (NSERC) Discovery grant; Tier II Canada Research Chair in Lipids, Metabolism, and Health; Queen Elizabeth II Scholarship in Science and Technology; Canadian Institute of Health Research Scholarship - Masters; Ontario Graduate Scholarship; NSERC Post-Graduate Scholarship DCW is funded by a Natural Sciences and Engineering Research Council of Canada (NSERC) Discovery grant and is a Tier II Canada Research Chair in Lipids, Metabolism, and Health. WTP is supported by a Queen Elizabeth II Scholarship in Science and Technology. NDB is supported by a Canadian Institute of Health Research Scholarship - Masters. LKT is supported by an Ontario Graduate Scholarship and NSERC Post-Graduate Scholarship. The funders were not involved in the study design, collection, analysis and interpretation of data and in writing of the manuscript. 52 0 0 1 1 PERGAMON-ELSEVIER SCIENCE LTD OXFORD THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND 0306-4530 PSYCHONEUROENDOCRINO Psychoneuroendocrinology FEB 2018 88 121 128 10.1016/j.psyneuen.2017.12.004 8 Endocrinology & Metabolism; Neurosciences; Psychiatry Endocrinology & Metabolism; Neurosciences & Neurology; Psychiatry FX6ZO WOS:000426236000015 29241148 2018-04-09
J Auguste, S; Sharma, S; Fisette, A; Fernandes, MF; Daneault, C; Des Rosiers, C; Fulton, S Auguste, Stephanie; Sharma, Sandeep; Fisette, Alexandre; Fernandes, Maria F.; Daneault, Caroline; Des Rosiers, Christine; Fulton, Stephanie Perinatal deficiency in dietary omega-3 fatty acids potentiates sucrose reward and diet-induced obesity in mice INTERNATIONAL JOURNAL OF DEVELOPMENTAL NEUROSCIENCE English Article Obesity; Energy balance; Lipids; Perinatal; Anxiety; Food-motivated behaviour FATTY-ACIDS; DOCOSAHEXAENOIC ACID; BRAIN; ADAPTATIONS; DISEASE; BETA Insufficient dietary intake of essential omega-3 polyunsaturated fatty acids (N-3), especially during critical stages of development, is well-associated with negative neurological and metabolic consequences. The increased availability and intake of foods rich in saturated fat coincides with reduced N-3 consumption, yet how N-3 dietary deficiency during perinatal development modulates motivation for palatable food and interacts with a high-fat diet to affect body weight and emotional states is not clear. Pregnant C57BI6 mice and pups were subjected to diets either deficient or adequate (control) in N-3 until postnatal day 21. Adult male N-3 deficient or control offspring were tested in a progressive ratio operant task for sucrose motivated behavior or given pro-longed access to a saturated high-fat diet or chow followed by measures of energy balance and anxiety-like behavior in the elevated-plus maze and open field test. Brain fatty acid profiles were measured via gas chromatography mass spectrometry. Perinatal dietary N-3 deficiency lowered brain N-3 levels, augmented the rewarding effects of sucrose, heightened diet-induced weight gain and fat mass accumulation and diminished spontaneous physical activity. Finally, perinatal N-3 deficiency increased anxiety-like behaviour independent of diet in the open field but not in the elevated-plus maze test. Insufficient dietary N-3 during critical periods of developmental can amplify the obesogenic effects of saturated fat intake, enhance motivated behaviour for palatable foods and may elicit negative emotional states that can perpetuate overeating and obesity. [Auguste, Stephanie; Sharma, Sandeep; Fisette, Alexandre; Fernandes, Maria F.; Fulton, Stephanie] CRCHUM, Montreal, PQ H3T 1J4, Canada; [Auguste, Stephanie; Sharma, Sandeep; Fisette, Alexandre; Fernandes, Maria F.; Fulton, Stephanie] Montreal Diabet Res Ctr, Montreal, PQ H3T 1J4, Canada; [Auguste, Stephanie; Fisette, Alexandre; Des Rosiers, Christine; Fulton, Stephanie] Univ Montreal, Dept Nutr, Fac Med, Montreal, PQ H3T 1J4, Canada; [Daneault, Caroline; Des Rosiers, Christine] Montreal Heart Inst, Montreal, PQ H3T 1J4, Canada Fulton, S (reprint author), Univ Montreal, CRCHUM, 900 St Denis St,R08-428, Montreal, PQ H2X 0A9, Canada.; Fulton, S (reprint author), Montreal Diabet Res Ctr, 900 St Denis St,R08-428, Montreal, PQ H2X 0A9, Canada. stephanie.fulton@umontreal.ca Natural Sciences and Engineering Research Council of Canada [355881-2013]; CIHR [MOP9575]; Department of Nutrition, Universite de Montreal; Canadian Diabetes Association This project was supported by a grant to SF from the Natural Sciences and Engineering Research Council of Canada (355881-2013), a CIHR grant (MOP9575) to CD, graduate awards to SA from the Department of Nutrition, Universite de Montreal and a postdoctoral fellowship to AF from the Canadian Diabetes Association. 30 0 0 2 2 PERGAMON-ELSEVIER SCIENCE LTD OXFORD THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND 0736-5748 1873-474X INT J DEV NEUROSCI Int. J. Dev. Neurosci. FEB 2018 64 SI 8 13 10.1016/j.ijdevneu.2017.09.003 6 Developmental Biology; Neurosciences Developmental Biology; Neurosciences & Neurology FU9NC WOS:000424181600003 28919371 2018-04-09
J Pak, ME; Jung, DH; Lee, HJ; Shin, MJ; Kim, SY; Shin, YB; Yun, YJ; Shin, HK; Choi, BT Pak, Malk Eun; Jung, Da Hee; Lee, Hong Ju; Shin, Myung Jun; Kim, Soo-Yeon; Shin, Yong Beom; Yun, Young Ju; Shin, Hwa Kyoung; Choi, Byung Tae Combined therapy involving electroacupuncture and treadmill exercise attenuates demyelination in the corpus callosum by stimulating oligodendrogenesis in a rat model of neonatal hypoxia-ischemia EXPERIMENTAL NEUROLOGY English Article Neonatal hypoxia-ischemia; Electroacupuncture; Exercise; Oligodendrogenesis; Brain-derived neurotrophic factor SPINAL-CORD-INJURY; WHITE-MATTER INJURY; PROLONGED CEREBRAL HYPOPERFUSION; NEUROTROPHIC FACTOR; BRAIN-INJURY; CREB FAMILY; TRANSCRIPTION FACTORS; SUBVENTRICULAR ZONE; NERVOUS-SYSTEM; MOUSE MODEL We investigated whether electroacupuncture (EA) and treadmill (TM) exercise improve behaviors related to motor and memory dysfunction in a cerebral palsy-like rat model via activation of oligodendrogenesis. A neonatal hypoxia-ischemia model was created using Sprague-Dawley rats (P7), and these underwent EA stimulation and treadmill training from 3 to 5 weeks after hypoxia-ischemia induction. FA treatment was delivered via electrical stimulation (2 Hz, 1 mA) at two acupoints, Baihui (GV20) and Zusanli (ST36). Behavioral tests showed that EA alleviated motor dysfunction caused by hypoxia-ischemia on a rotarod test, and TM exercise alleviated motor and memory dysfunction seen on cylinder and passive avoidance tests. Combined therapy with EA and TM exercise showed synergistic effects on the cylinder, rotarod, and catwalk tests. TM exercise significantly restored corpus callosum thickness, and combined therapy with EA and TM restored myelin basic protein (MBP) levels in this region. While EA stimulation only increased activation of cAMP-response element hinging protein (CREB) in oligodendrocytes of the corpus callosum, TM exercise increased newly generated oligodendrocyte progenitor cells or oligodendrocytes via activation of CREB. Synergistic effects on oligodendrogenesis were also observed by the combined therapy. Furthermore, the combined therapy induced mature brain-derived neurotrophic factor (BDNF) expression in the cerebral cortex. These results demonstrate that combined therapy with EA and TM exercise may restore myelin components following neonatal hypoxia-ischemia via upregulation of oligodendrogenesis involving CREB/BDNF signaling, which subsequently improves motor and memory function. Therefore, combined therapy with EA and TM exercise offers another treatment option for functional recovery from injuries caused by neonatal hypoxia-ischemia, such as cerebral palsy. [Pak, Malk Eun; Jung, Da Hee; Lee, Hong Ju; Shin, Hwa Kyoung; Choi, Byung Tae] Pusan Natl Univ, Sch Korean Med, Dept Korean Med Sci, Yangsan 50612, South Korea; [Pak, Malk Eun; Jung, Da Hee; Lee, Hong Ju; Shin, Hwa Kyoung; Choi, Byung Tae] Pusan Natl Univ, Grad Training Program Korean Med Hlth Aging, Sch Korean Med, Yangsan 50612, South Korea; [Shin, Myung Jun] Pusan Natl Univ, Sch Med, Dept Rehabil Med, Busan 49241, South Korea; [Shin, Myung Jun; Shin, Yong Beom] Pusan Natl Univ Hosp, Biomed Res Inst, Busan 49241, South Korea; [Kim, Soo-Yeon] Pusan Natl Univ, Yangsan Hosp, Dept Rehabil Med, Yangsan 50612, South Korea; [Kim, Soo-Yeon] Pusan Natl Univ, Yangsan Hosp, Res Inst Convergence Biomed Sci & Technol, Yangsan 50612, South Korea; [Yun, Young Ju] Pusan Natl Univ, Sch Korean Med, Dept Integrat Med, Yangsan 50612, South Korea; [Shin, Hwa Kyoung; Choi, Byung Tae] Pusan Natl Univ, Korean Med Sci Res Ctr Hlth Aging, Yangsan 50612, South Korea Choi, BT (reprint author), Pusan Natl Univ, Sch Korean Med, Yangsan 50612, South Korea. choibt@pusan.ac.kr Convergence of Conventional Medicine and Traditional Korean Medicine R&D project - Ministry of Health & Welfare through the Korea Health Industry Development Institute (KHIDI) [HI14C0704] This research was supported by the Convergence of Conventional Medicine and Traditional Korean Medicine R&D project funded by the Ministry of Health & Welfare through the Korea Health Industry Development Institute (KHIDI) (Grant No. HI14C0704). 61 0 0 3 3 ACADEMIC PRESS INC ELSEVIER SCIENCE SAN DIEGO 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA 0014-4886 1090-2430 EXP NEUROL Exp. Neurol. FEB 2018 300 222 231 10.1016/j.expneurol.2017.11.014 10 Neurosciences Neurosciences & Neurology FT1JZ WOS:000422893300021 29199131 2018-04-09
J Ahmadalipour, A; Ghodrati-Jaldbakhan, S; Samaei, SA; Rashidy-Pour, A Ahmadalipour, Ali; Ghodrati-Jaldbakhan, Shahrbanoo; Samaei, Seyed Afshin; Rashidy-Pour, Ali Deleterious effects of prenatal exposure to morphine on the spatial learning and hippocampal BDNF and long-term potentiation in juvenile rats: Beneficial influences of postnatal treadmill exercise and enriched environment NEUROBIOLOGY OF LEARNING AND MEMORY English Article Morphine; Prenatal; Exercise; Enriched environment; Learning; BDNF; LIP ADULT MALE RATS; SYNAPTIC PLASTICITY; NEUROTROPHIC FACTOR; FEMALE RATS; VOLUNTARY EXERCISE; MESSENGER-RNA; DENTATE GYRUS; IN-VIVO; SEIZURE SUSCEPTIBILITY; COGNITIVE PERFORMANCE Prenatal morphine exposure causes a variety of neurobehavioral alterations observed in later life. The present study investigated the effects of postnatal exercise and enriched environment (EE) on alterations in water maze learning and hippocampal long-term potentiation (LIP) and brain derived neurotrophic factor (BDNF) levels induced by exposure to morphine during prenatal period in rats. On gestation days 11-18, pregnant rats were injected twice daily with saline or morphine. Offspring were subjected to postnatal exercise and EE for 30 days and afterward, spatial learning and hippocampal LIP and BDNF levels were investigated. Prenatal morphine exposure impaired the spatial learning and hippocampal LIP in both male and female offspring. Interestingly, postnatal exercise and EE increased performance in the water maze and improved LIP in both prenatally saline and morphine-exposed male and female rats. Prenatal morphine exposure also caused a reduction in the hippocampal BDNF levels in the female, but not male rats, and postnatal exercise and EE alleviated this deficit. Our results demonstrate that postnatal exercise and EE can improve deficits in water maze learning and hippocampal LTP and BDNF levels caused by prenatal morphine exposure. [Ahmadalipour, Ali] Tabriz Univ Med Sci, Res Ctr Psychiat & Behav Sci, Tabriz, Iran; [Ahmadalipour, Ali; Ghodrati-Jaldbakhan, Shahrbanoo; Rashidy-Pour, Ali] Semnan Univ Med Sci, Sch Med, Res Ctr, Lab Learning & Memory, Semnan 1513138111, Iran; [Ahmadalipour, Ali; Ghodrati-Jaldbakhan, Shahrbanoo; Rashidy-Pour, Ali] Semnan Univ Med Sci, Sch Med, Dept Physiol, Semnan 1513138111, Iran; [Ghodrati-Jaldbakhan, Shahrbanoo] Seaman Univ Med Sci, Sch Med, Student Res Comm, Semnan, Iran; [Samaei, Seyed Afshin] Semnan Univ Med Sci, Sch Med, Neuromuscular Rehabil Res Ctr, Semnan, Iran; [Samaei, Seyed Afshin] Semnan Univ Med Sci, Sch Med, Dept Neurol, Semnan, Iran Rashidy-Pour, A (reprint author), Semnan Univ Med Sci, Sch Med, Res Ctr, Lab Learning & Memory, Semnan 1513138111, Iran.; Rashidy-Pour, A (reprint author), Semnan Univ Med Sci, Sch Med, Dept Physiol, Semnan 1513138111, Iran. Rashidy-pour@semums.ac.ir Ghodrati-Jaldbakhan, shahrbanoo/0000-0002-1822-9618 Semnan University of Medical Sciences (Semnan, Iran); Cognitive Sciences and Technologies Council of Iran This work was supported by grants from the Semnan University of Medical Sciences (Semnan, Iran) and Cognitive Sciences and Technologies Council of Iran. In addition, Mr. Ali Ahmadalipour carried out this work in partial project fulfillment of the requirements to obtain a PhD degree in Medical Physiology. 92 0 0 2 2 ACADEMIC PRESS INC ELSEVIER SCIENCE SAN DIEGO 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA 1074-7427 1095-9564 NEUROBIOL LEARN MEM Neurobiol. Learn. Mem. JAN 2018 147 54 64 10.1016/j.nlm.2017.11.013 11 Behavioral Sciences; Neurosciences; Psychology; Psychology, Multidisciplinary Behavioral Sciences; Neurosciences & Neurology; Psychology FT8QY WOS:000423419500007 29175674 2018-04-09
J Perez-Dominguez, M; Tovar-y-Romo, LB; Zepeda, A Perez-Dominguez, Martha; Tovar-y-Romo, Luis B.; Zepeda, Angelica Neuroinflammation and physical exercise as modulators of adult hippocampal neural precursor cell behavior REVIEWS IN THE NEUROSCIENCES English Article adult neurogenesis; dentate gyrus; differentiation; hippocampus; microglia; proliferation ENDOTHELIAL GROWTH-FACTOR; MOUSE DENTATE GYRUS; IN-VIVO ANALYSIS; STEM-CELLS; PROGENITOR CELLS; NEUROTROPHIC FACTOR; SONIC HEDGEHOG; AGED MICE; ASTROCYTIC DIFFERENTIATION; NEURONAL DIFFERENTIATION The dentate gyrus of the hippocampus is a plastic structure where adult neurogenesis constitutively occurs. Cell components of the neurogenic niche are source of paracrine as well as membrane-bound factors such as Notch, Bone Morphogenetic Proteins, Wnts, Sonic Hedgehog, cytokines, and growth factors that regulate adult hippocampal neurogenesis and cell fate decision. The integration and coordinated action of multiple extrinsic and intrinsic cues drive a continuous decision process: if adult neural stem cells remain quiescent or proliferate, if they take a neuronal or a glial lineage, and if new cells proliferate, undergo apoptotic death, or survive. The proper balance in the molecular milieu of this neurogenic niche leads to the production of neurons in a higher rate as that of astrocytes. But this rate changes in face of microenvironment modifications as those driven by physical exercise or with neuroinflammation. In this work, we first review the cellular and molecular components of the subgranular zone, focusing on the molecules, active signaling pathways and genetic programs that maintain quiescence, induce proliferation, or promote differentiation. We then summarize the evidence regarding the role of neuroinflammation and physical exercise in the modulation of adult hippocampal neurogenesis with emphasis on the activation of progression from adult neural stem cells to lineage-committed progenitors to their progeny mainly in murine models. [Perez-Dominguez, Martha; Zepeda, Angelica] Univ Nacl Autonoma Mexico, Inst Invest Biomed, Dept Med Genom & Toxicol Ambiental, Circuito Exterior S-N, Mexico City 04510, DF, Mexico; [Tovar-y-Romo, Luis B.] Univ Nacl Autonoma Mexico, Inst Fisiol Celular, Div Neurociencias, Mexico City 04510, DF, Mexico Zepeda, A (reprint author), Univ Nacl Autonoma Mexico, Inst Invest Biomed, Dept Med Genom & Toxicol Ambiental, Circuito Exterior S-N, Mexico City 04510, DF, Mexico. azepeda@biomedicas.unam.mx Zepeda, Angelica/0000-0003-0857-1652 Consejo Nacional de Ciencia y Tecnologia CONACyT; Direccion General del Personal Academico-Programa de Apoyo a Proyectos de Investigacion e Innovacion Tecnologica, DGAPA PAPIIT [IN203015]; DGAPA PAPIIT [IA201315] M.P.D. is supported by a Consejo Nacional de Ciencia y Tecnologia CONACyT scholarship; A.Z. is supported by Direccion General del Personal Academico-Programa de Apoyo a Proyectos de Investigacion e Innovacion Tecnologica, DGAPA PAPIIT IN203015; L.B.T. is supported by DGAPA PAPIIT IA201315. 161 0 0 5 5 WALTER DE GRUYTER GMBH BERLIN GENTHINER STRASSE 13, D-10785 BERLIN, GERMANY 0334-1763 1607-8470 REV NEUROSCIENCE Rev. Neurosci. JAN 2018 29 1 1 20 10.1515/revneuro-2017-0024 20 Neurosciences Neurosciences & Neurology FR1DR WOS:000418806700001 28873068 gold 2018-04-09
J Jiang, T; Zhang, LY; Pan, XN; Zheng, HQ; Chen, X; Li, LL; Luo, J; Hu, XQ Jiang, Ting; Zhang, Liying; Pan, Xiaona; Zheng, Haiqing; Chen, Xi; Li, Lili; Luo, Jing; Hu, Xiquan Physical Exercise Improves Cognitive Function Together with Microglia Phenotype Modulation and Remyelination in Chronic Cerebral Hypoperfusion FRONTIERS IN CELLULAR NEUROSCIENCE English Article physical exercise; vascular cognitive impairment; remyelination; M2 microglia; CX3CL1/CX3CR1 axis WHITE-MATTER INJURY; MULTIPLE-SCLEROSIS; PRONEUROGENIC PHENOTYPE; ISCHEMIC MICE; ADULT CNS; MYELINATION; CELLS; BRAIN; RAT; DIFFERENTIATION Myelin is closely associated with cognitive function and is extremely vulnerable to damage in ischemic cerebrovascular diseases. The failure of remyelination is mainly due to limitations in oligodendrocyte progenitor cells (OPCs) differentiation in the damaged area. Previous studies have shown that physical exercise can improve vascular cognitive impairment, but whether it can reverse the defect in remyelination during ischemic injury and the underlying mechanism remains unclear. In this study, we observed the effects of physical exercise on chronic cerebral hypoperfusion (CCH) established by bilateral carotid artery occlusion. The cognitive function, myelin integrity, OPCs proliferation and differentiation, as well as microglia polarization were analyzed at 28 days after CCH. Besides, the expression of CX3CL1/CX3CR1 axis and activation of mitogen-activated protein kinase (MAPK) signal cascades were also evaluated. We found that physical exercise improved the cognitive function of rats with CCH, alleviated myelin injury, triggered OPCs proliferation and differentiation, facilitated microglia polarization toward M2, augmented the expression of CX3CL1/CX3CR1 axis, and reduced ERK and JNK phosphorylation. The results indicated that physical exercise improved the cognitive function of rats with CCH, possibly through microglial phenotype modulation and enhancement of oligodendrocytegenesis and remyelination. Moreover, the CX3CL1/CX3CR1 axis played an important role in this process by mediating ERK- and JNK-dependent pathways. [Jiang, Ting; Zhang, Liying; Pan, Xiaona; Zheng, Haiqing; Chen, Xi; Li, Lili; Luo, Jing; Hu, Xiquan] Sun Yat Sen Univ, Affiliated Hosp 3, Dept Rehabil Med, Guangzhou, Guangdong, Peoples R China Hu, XQ (reprint author), Sun Yat Sen Univ, Affiliated Hosp 3, Dept Rehabil Med, Guangzhou, Guangdong, Peoples R China. xiquhu@hotmail.com National Natural Science Foundation of China [81372107, 81672261, 81301674]; Natural Science Foundation of Guangdong Province, China [S2013020012648, 2017A030313493]; Guangdong Provincial Key Laboratory for Diagnosis and Treatment of Major Neurological Diseases [2014B030301035]; Southern China International Cooperation Base for Early Intervention and Functional Rehabilitation of Neurological Diseases [2015B050501003]; Guangdong Provincial Engineering Center for Major Neruolgoical Disease Treatment, Science and Technology Planning Project of Guangzhou [201604020010] The authors would like to thank Prof. Zhong Pei in Department of Neurology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China for kind guidance and help with the design and performance of the experiments. This work was supported by the National Natural Science Foundation of China [No: 81372107, No: 81672261 and No: 81301674], Natural Science Foundation of Guangdong Province, China [No: S2013020012648 and No: 2017A030313493], the Guangdong Provincial Key Laboratory for Diagnosis and Treatment of Major Neurological Diseases (No. 2014B030301035), the Southern China International Cooperation Base for Early Intervention and Functional Rehabilitation of Neurological Diseases (No. 2015B050501003), Guangdong Provincial Engineering Center for Major Neruolgoical Disease Treatment, Science and Technology Planning Project of Guangzhou (No. 201604020010). 47 0 0 3 3 FRONTIERS MEDIA SA LAUSANNE PO BOX 110, EPFL INNOVATION PARK, BUILDING I, LAUSANNE, 1015, SWITZERLAND 1662-5102 FRONT CELL NEUROSCI Front. Cell. Neurosci. DEC 22 2017 11 404 10.3389/fncel.2017.00404 14 Neurosciences Neurosciences & Neurology FQ9WW WOS:000418713400001 29311834 gold 2018-04-09
J Quiclet, C; Dubouchaud, H; Berthon, P; Sanchez, H; Vial, G; Siti, F; Fontaine, E; Batandier, C; Couturier, K Quiclet, Charline; Dubouchaud, Herve; Berthon, Phanelie; Sanchez, Herve; Vial, Guillaume; Siti, Farida; Fontaine, Eric; Batandier, Cecile; Couturier, Karine Maternal exercise modifies body composition and energy substrates handling in male offspring fed a high-fat/high-sucrose diet JOURNAL OF PHYSIOLOGY-LONDON English Article gestation; exercise; offspring; insulin sensitivity; pancreas; metabolism HIGH-FAT DIET; SKELETAL-MUSCLE; INSULIN SENSITIVITY; DIABETES-MELLITUS; IN-UTERO; CARDIOVASCULAR-DISEASE; MITOCHONDRIAL-FUNCTION; GLUCOSE-HOMEOSTASIS; HEPATIC STEATOSIS; BLOOD-PRESSURE Maternal exercise during gestation has been reported to modify offspring metabolism and health. Whether these effects are exacerbated when offspring are receiving a high-fat diet remains unclear. Our purpose was to evaluate the effect of maternal exercise before and during gestation on the offspring fed a high-fat/high-sucrose diet (HF) by assessing its body composition, pancreatic function and energy substrates handling by two major glucose-utilizing tissues: liver and muscle. Fifteen-week-old nulliparous female Wistar rats exercised 4weeks before as well as during gestation at a constant submaximal intensity (TR) or remained sedentary (CT). At weaning, pups from each group were fed either a standard diet (TRCD or CTCD) or a high-fat/high-sucrose diet (TRHF or CTHF) for 10weeks. Offspring from TR dams gained less weight compared to those from CT dams. Selected fat depots were larger with the HF diet compared to control diet (CD) but significantly smaller in TRHF compared to CTHF. Surprisingly, the insulin secretion index was higher in islets from HF offspring compared to CD. TR offspring showed a higher muscle insulin sensitivity estimated by the ratio of phosphorylated protein kinase B to total protein kinase B compared with CT offspring (+48%, P<0.05). With CD, permeabilized isolated muscle fibres from TR rats displayed a lower apparent affinity constant (K-m) for pyruvate and palmitoyl coenzyme A as substrates compared to the CT group (-46% and -58%, respectively, P<0.05). These results suggest that maternal exercise has positive effects on young adult offspring body composition and on muscle carbohydrate and lipid metabolism depending on the nutritional status. Key points Maternal training during gestation enhances offspring body composition and energy substrates handling in early adulthood. Offspring nutrition also plays a role as some beneficial effects of maternal training during gestation disappear after consumption of a high-fat diet. [Quiclet, Charline; Dubouchaud, Herve; Siti, Farida; Fontaine, Eric; Batandier, Cecile; Couturier, Karine] Univ Grenoble Alpes, Lab Fundamental & Appl Bioenerget LBFA, Grenoble, France; [Quiclet, Charline; Dubouchaud, Herve; Siti, Farida; Fontaine, Eric; Batandier, Cecile; Couturier, Karine] INSERM, U1055, Grenoble, France; [Quiclet, Charline; Dubouchaud, Herve; Vial, Guillaume; Couturier, Karine] Univ Grenoble Alpes, UFR STAPS, SFR SEM, Grenoble, France; [Berthon, Phanelie] Univ Savoie Mt Blanc, Lab Interdisciplinaire Biol Motricite, Le Bourget Du Lac, France; [Sanchez, Herve] French Armed Biomed Res Inst, Bretigny Sur Orge, France; [Vial, Guillaume] INSERM, U1042, Grenoble, France; [Siti, Farida] Fac Univ Indonesia, Jakarta, Indonesia; [Fontaine, Eric] Grenoble Univ Hosp, Grenoble, France Quiclet, C (reprint author), Univ Grenoble Alpes, INSERM U1055, Lab Bioenerget Fondamentale & Appl, CS 40700, F-38058 Grenoble 9, France. charline.quiclet@gmail.com Vial, Guillaume/0000-0002-7333-8526; Batandier, Cecile/0000-0003-1173-458X; Quiclet, Charline/0000-0001-8641-0374 INSERM; SFR Sport Exercice Motricite (SEM); French Ministry of Research This work was supported by INSERM and SFR Sport Exercice Motricite (SEM). C.Q. was funded by a 3 year fellowship from the French Ministry of Research. 60 1 1 2 2 WILEY HOBOKEN 111 RIVER ST, HOBOKEN 07030-5774, NJ USA 0022-3751 1469-7793 J PHYSIOL-LONDON J. Physiol.-London DEC 1 2017 595 23 7049 7062 10.1113/JP274739 14 Neurosciences; Physiology Neurosciences & Neurology; Physiology FO6FL WOS:000416958000009 2018-04-09
J Ju, LP; Tong, WX; Qiu, MY; Shen, WL; Sun, JC; Zheng, S; Chen, Y; Liu, WT; Tian, JY Ju, Liping; Tong, Wenxin; Qiu, Miaoyan; Shen, Weili; Sun, Jichao; Zheng, Sheng; Chen, Ying; Liu, Wentao; Tian, Jingyan Antioxidant MMCC ameliorates catch-up growth related metabolic dysfunction ONCOTARGET English Article catch-up growth; MMCC (MitoQuinone mesylate beta cyclodextrin complex); mitochondria; metabolic dysfunction; skeletal functions LOW-BIRTH-WEIGHT; SKELETAL-MUSCLE; ADULT HEALTH; MITOCHONDRIA; EXERCISE; WATER; FAT; UNDERNUTRITION; ORIGINS; DISEASE Postnatal catch-up growth may be related to reduce mitochondrial content and oxidation capacity in skeletal muscle. The aim of this study is to explore the effect and mechanism of antioxidant MitoQuinone mesylate beta cyclodextrin complex (MMCC) ameliorates catch-up growth related metabolic disorders. Catch-up growth mice were created by restricting maternal food intake during the last week of gestation and providing high fat diet after weaning. Low birthweight mice and normal birthweight controls were randomly subjected to normal fat diet, high fat diet and high fat diet with MMCC drinking from the 4th week. MMCC treatment for 21 weeks slowed down the catch up growth and ameliorated catch-up growth related obesity, glucose intolerance and insulin resistance. MMCC administration significantly inhibited the peroxidation of the membrane lipid and up-regulated the antioxidant enzymes Catalase and MnSOD. In addition, MMCC treatment effectively enhanced mitochondrial functions in skeletal muscle through the up-regulation of the ATP generation, and the promotion of mitochondrial replication and remodeling. To conclude, this study demonstrates that antioxidant MMCC effectively ameliorates catch-up growth related metabolic dysfunctions by increasing mitochondrial functions in skeletal muscle. [Ju, Liping; Tong, Wenxin; Qiu, Miaoyan; Zheng, Sheng; Chen, Ying; Tian, Jingyan] Shanghai Jiao Tong Univ, Shanghai Inst Endocrine & Metab Dis, Ruijin Hosp,Sch Med, Shanghai Clin Ctr Endocrine & Metab Dis,Dept Endo, Shanghai, Peoples R China; [Tong, Wenxin; Tian, Jingyan] City Hope Natl Med Ctr, Dept Diabet Complicat & Metab, Beckman Res Inst, Duarte, CA 91010 USA; [Shen, Weili] Shanghai Jiao Tong Univ, Sch Med, Ruijin Hosp, Shanghai Inst Hypertens, Shanghai, Peoples R China; [Sun, Jichao] Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Hlth Sci, Lab Endocrine & Metab Dis, Shanghai, Peoples R China; [Sun, Jichao] Shanghai Jiao Tong Univ, Sch Med, Shanghai, Peoples R China; [Liu, Wentao] Shanghai Jiao Tong Univ, Shanghai Inst Digest Surg, Dept Surg, Key Lab Shanghai Gastr Neoplasms,Ruijin Hosp, Shanghai, Peoples R China Tian, JY (reprint author), Shanghai Jiao Tong Univ, Shanghai Inst Endocrine & Metab Dis, Ruijin Hosp,Sch Med, Shanghai Clin Ctr Endocrine & Metab Dis,Dept Endo, Shanghai, Peoples R China.; Tian, JY (reprint author), City Hope Natl Med Ctr, Dept Diabet Complicat & Metab, Beckman Res Inst, Duarte, CA 91010 USA.; Liu, WT (reprint author), Shanghai Jiao Tong Univ, Shanghai Inst Digest Surg, Dept Surg, Key Lab Shanghai Gastr Neoplasms,Ruijin Hosp, Shanghai, Peoples R China. wt_mygod@163.com; tianjypaper@163.com National Natural Science Foundation of China [81270935]; Transform Medicine Innovation Foundation of Shanghai Jiao Tong University School of Medicine [15ZH2001]; Shanghai Municipal Health Bureau Foundation [20114301]; Fund of the Key Laboratory of Stem Cell Biology of Chinese Academy of Sciences [201601] We gratefully acknowledge grants supported by the National Natural Science Foundation of China (81270935), Transform Medicine Innovation Foundation of Shanghai Jiao Tong University School of Medicine (15ZH2001), Shanghai Municipal Health Bureau Foundation (20114301), and the Fund of the Key Laboratory of Stem Cell Biology of Chinese Academy of Sciences (201601). 27 0 0 0 0 IMPACT JOURNALS LLC ORCHARD PARK 6666 E QUAKER ST, STE 1, ORCHARD PARK, NY 14127 USA 1949-2553 ONCOTARGET Oncotarget NOV 21 2017 8 59 99931 99939 10.18632/oncotarget.21965 9 Oncology; Cell Biology Oncology; Cell Biology FS1TR WOS:000419561600065 29245950 gold 2018-04-09
J Cunningham, LA; Newville, J; Li, L; Tapia, P; Allan, AM; Valenzuela, CF Cunningham, Lee Anna; Newville, Jessie; Li, Lu; Tapia, Phillip; Allan, Andrea M.; Valenzuela, C. Fernando Prenatal Alcohol Exposure Leads to Enhanced Serine 9 Phosphorylation of Glycogen Synthase Kinase-3 beta (GSK-3 beta) in the Hippocampal Dentate Gyrus of Adult Mouse ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH English Article Fetal Alcohol Spectrum Disorders; Glycogen Synthase Kinase; Hippocampal Neurogenesis; Hippocampal Plasticity; Hilar Mossy Cells GRANULE CELLS; SYNAPTIC PLASTICITY; SPECTRUM DISORDERS; VOLUNTARY EXERCISE; ENRICHED ENVIRONMENT; SUBVENTRICULAR ZONE; STEM-CELLS; NEUROGENESIS; MEMORY; INHIBITION Background: The goal of this study was to evaluate the expression and serine 9 phosphorylation of glycogen synthase kinase (GSK-3 beta) within the adult hippocampal dentate gyrus (DG) in a preclinical mouse model of fetal alcohol spectrum disorders. GSK-3 beta is a multifunctional kinase that modulates many hippocampal processes affected by gestational alcohol, including synaptic plasticity and adult neurogenesis. GSK-3 beta is a constitutively active kinase that is negatively regulated by phosphorylation at the serine 9 residue. Methods: We utilized a well-characterized limited access "drinking-in-the-dark" paradigm of prenatal alcohol exposure (PAE) and measured p(Ser9) GSK-3 beta and total GSK-3 beta within adult DG by Western blot analysis. In addition, we evaluated the expression pattern of both p(Ser9) GSK-3 beta and total GSK-3 beta within the adult hippocampal dentate of PAE and control mice using high-resolution confocal microscopy. Results: Our findings demonstrate a marked 2.0-fold elevation of p(Ser9) GSK-3 beta in PAE mice, concomitant with a more moderate 36% increase in total GSK-3 beta. This resulted in an approximate 63% increase in the p(Ser9) GSK-3 beta/GSK-3 beta ratio. Immunostaining revealed robust GSK-3 beta expression within Cornu Ammonis (CA) pyramidal neurons, hilar mossy cells, and a subset of GABAergic interneurons, with low levels of expression within hippocampal progenitors and dentate granule cells. Conclusions: These findings suggest that PAE may lead to a long-term disruption of GSK-3 beta signaling within the DG, and implicate mossy cells, GABAergic interneurons, and CA primary neurons as major targets of this dysregulation. [Cunningham, Lee Anna; Newville, Jessie; Li, Lu; Tapia, Phillip; Allan, Andrea M.; Valenzuela, C. Fernando] Univ New Mexico, Hlth Sci Ctr, Dept Neurosci, Albuquerque, NM 87131 USA Cunningham, LA (reprint author), 1 Univ New Mexico, Hlth Sci Ctr, Dept Neurosci, Univ New Mexico, MSC08 4740, Albuquerque, NM 87131 USA. leeanna@salud.unm.edu cunningham, lee anna/0000-0003-0294-5262 NIH-NIAAA [P50-AA022534] This work was supported by the NIH-NIAAA (P50-AA022534). 61 0 0 2 2 WILEY HOBOKEN 111 RIVER ST, HOBOKEN 07030-5774, NJ USA 0145-6008 1530-0277 ALCOHOL CLIN EXP RES Alcoholism (NY) NOV 2017 41 11 1907 1916 10.1111/acer.13489 10 Substance Abuse Substance Abuse FP2GU WOS:000417435800010 28865114 2018-04-09
J De Gasperi, R; Hamidi, S; Harlow, LM; Ksiezak-Reding, H; Bauman, WA; Cardozo, CP De Gasperi, Rita; Hamidi, Sayyed; Harlow, Lauren M.; Ksiezak-Reding, Hanna; Bauman, William A.; Cardozo, Christopher P. Denervation-related alterations and biological activity of miRNAs contained in exosomes released by skeletal muscle fibers SCIENTIFIC REPORTS English Article EXTRACELLULAR VESICLES; GENE-EXPRESSION; SATELLITE CELLS; CIRCULATING MICRORNAS; LINEAGE PROGRESSION; MUSCULAR-DYSTROPHY; MIR-206; EXERCISE; MICE; DIFFERENTIATION Exosomes are vesicles released by many eukaryotic cells; their cargo includes proteins, mRNA and microRNA (miR) that can be transferred to recipient cells and regulate cellular processes in an autocrine or paracrine manner. While cells of the myoblast lineage secrete exosomes, it is not known whether skeletal muscle fibers (myofibers) release exosomes. In this study, we found that cultured myofibers release nanovesicles that have bilamellar membranes and an average size of 60-130 nm, contain typical exosomal proteins and miRNAs and are taken up by C2C12 cells. miR-133a was found to be the most abundant myomiR in these vesicles while miR-720 was most enriched in exosomes compared to parent myofibers. Treatment of NIH 3T3 cells with myofiber-derived exosomes downregulated the miR-133a targets proteins Smarcd1 and Runx2, confirming that these exosomes have biologically relevant effects on recipient cells. Denervation resulted in a marked increase in miR-206 and reduced expression of miRs 1, 133a, and 133b in myofiber-derived exosomes. These findings demonstrate that skeletal muscle fibers release exosomes which can exert biologically significant effects on recipient cells, and that pathological muscle conditions such as denervation induce alterations in exosomal miR profile which could influence responses to disease states through autocrine or paracrine mechanisms. [De Gasperi, Rita; Harlow, Lauren M.; Bauman, William A.; Cardozo, Christopher P.] James J Peters VA Med Ctr, Nat Ctr Med Consequences Spinal Cord Injury, Bronx, NY 10468 USA; [Hamidi, Sayyed; Bauman, William A.; Cardozo, Christopher P.] James J Peters VA Med Ctr, Med Serv, Bronx, NY 10468 USA; [Bauman, William A.; Cardozo, Christopher P.] Icahn Sch Med Mt Sinai, Dept Med, New York, NY 10029 USA; [Bauman, William A.; Cardozo, Christopher P.] Icahn Sch Med Mt Sinai, Dept Rehabil Med, New York, NY 10029 USA; [Cardozo, Christopher P.] Icahn Sch Med Mt Sinai, Dept Pharmacol Sci, New York, NY 10029 USA; [Ksiezak-Reding, Hanna] Icahn Sch Med Mt Sinai, Dept Neurol, New York, NY 10029 USA; [De Gasperi, Rita] Icahn Sch Med Mt Sinai, Dept Psychiat, New York, NY 10029 USA; [De Gasperi, Rita] Icahn Sch Med Mt Sinai, Friedman Brain Inst, New York, NY 10029 USA Cardozo, CP (reprint author), James J Peters VA Med Ctr, Nat Ctr Med Consequences Spinal Cord Injury, Bronx, NY 10468 USA.; Cardozo, CP (reprint author), James J Peters VA Med Ctr, Med Serv, Bronx, NY 10468 USA.; Cardozo, CP (reprint author), Icahn Sch Med Mt Sinai, Dept Med, New York, NY 10029 USA.; Cardozo, CP (reprint author), Icahn Sch Med Mt Sinai, Dept Rehabil Med, New York, NY 10029 USA.; Cardozo, CP (reprint author), Icahn Sch Med Mt Sinai, Dept Pharmacol Sci, New York, NY 10029 USA. christopher.cardozo@mssm.edu Department of Veterans Affair, Veterans Health Administration; Rehabilitation Research and Development Service [B-9212-C, B-2020-C]; James J. Peters VA Medical Center The research reported here was supported by the Department of Veterans Affair, Veterans Health Administration, Rehabilitation Research and Development Service (B-9212-C and B-2020-C) and the James J. Peters VA Medical Center. 56 0 0 3 3 NATURE PUBLISHING GROUP LONDON MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND 2045-2322 SCI REP-UK Sci Rep OCT 16 2017 7 12888 10.1038/s41598-017-13105-9 11 Multidisciplinary Sciences Science & Technology - Other Topics FJ8XU WOS:000413052700001 29038428 gold 2018-04-09
J Tashiro, S; Nishimura, S; Iwai, H; Sugai, K; Shinozaki, M; Iwanami, A; Toyama, Y; Liu, M; Okano, H; Nakamura, M Tashiro, S.; Nishimura, S.; Iwai, H.; Sugai, K.; Shinozaki, M.; Iwanami, A.; Toyama, Y.; Liu, M.; Okano, H.; Nakamura, M. Functional recovery secondary to neural stem/progenitor cells transplantation combined with treadmill training in mice with chronic spinal cord injury JOURNAL OF THE NEUROLOGICAL SCIENCES English Meeting Abstract 23rd World Congress of Neurology (WCN) SEP 16-21, 2017 Kyoto, JAPAN [Tashiro, S.; Liu, M.] Keio Univ, Sch Med, Dept Rehabil Med, Tokyo, Japan; [Nishimura, S.; Iwai, H.; Sugai, K.; Iwanami, A.; Toyama, Y.; Nakamura, M.] Keio Univ, Sch Med, Dept Orthopaed Surg, Tokyo, Japan; [Shinozaki, M.; Okano, H.] Keio Univ, Sch Med, Dept Physiol, Tokyo, Japan 0 0 0 0 0 ELSEVIER SCIENCE BV AMSTERDAM PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS 0022-510X 1878-5883 J NEUROL SCI J. Neurol. Sci. OCT 15 2017 381 S 11 4 4 10.1016/j.jns.2017.08.036 1 Clinical Neurology; Neurosciences Neurosciences & Neurology FZ2YT WOS:000427450300012 2018-04-09
J Locatelli, J; Paiva, NCN; Carvalho, SHR; Lavorato, VN; Gomes, LHLS; Castro, QJT; Grabe-Guimaraes, A; Carneiro, CM; Natali, AJ; Isoldi, MC Locatelli, Jamille; Paiva, Nivia C. N.; Carvalho, Sara H. R.; Lavorato, Victor N.; Gomes, Luis Henrique L. S.; Castro, Quenia J. T.; Grabe-Guimaraes, Andrea; Carneiro, Claudia M.; Natali, Antonio J.; Isoldi, Mauro C. Swim training attenuates the adverse remodeling of LV structural and mechanical properties in the early compensated phase of hypertension LIFE SCIENCES English Article Cardiac remodeling; Hypertension; Spontaneously hypertensive rats; Swim training; Cardiomyocytes RENIN-ANGIOTENSIN SYSTEM; HEART-FAILURE; GENETIC-HYPERTENSION; CARDIAC-HYPERTROPHY; MATRIX PROTEIN; RATS; EXERCISE; INHIBITION; EXPRESSION; FIBROSIS Aim: Investigate to what extent low-intensity swim training for six weeks counterbalances the adverse remodeling due to the advance of pathological hypertrophy in the left ventricle (LV) structural and mechanical properties in the early compensated phase of hypertension in male SHR. Main methods: Four-month-old male SHR and Wistar rats were randomly divided into Sed (sedentary) and Ex (exercised) groups. The exercised rats were submitted to a swimming protocol (1 h/day, 5 times/week, no additional load) for six weeks. LV tissue and isolated myocytes were used to assess structural and mechanical properties. Myocytes were stimulted at frequencies (F) of 1 and 3 Hz at 37 degrees C. Key findings: Exercised SHR showed improvement in cardiovascular parameters compared to sedentary SHR (mean arterial pressure: 13.22%; resting HR: 14.28.%). About structural and mechanical properties, swim training induced a decrease in LV myocyte thickness (10.85%), number of inflammatory cells (21.24%); collagen type III (74.23%) and type I (85.6%) fiber areas; amplitude of single myocyte shortening (47% to F1 and 28.46% to F3), timecourses of shortening (16.5% to F1 and 7.55% to F3) and relaxation (15.31% to F3) compared to sedentary SHR. Significance: Six weeks of swim training attenuates the adverse remodeling of LV structural and mechanical properties in the early compensated phase of hypertension in male SHR. [Locatelli, Jamille] Univ Fed Ouro Preto, Sports Ctr, BR-35400000 Ouro Preto, MG, Brazil; [Paiva, Nivia C. N.; Carvalho, Sara H. R.; Carneiro, Claudia M.; Isoldi, Mauro C.] Univ Fed Ouro Preto, Ctr Res Biol Sci, Ouro Preto, MG, Brazil; [Lavorato, Victor N.; Gomes, Luis Henrique L. S.; Natali, Antonio J.] Univ Fed Vicosa, Dept Phys Educ, Lab Exercise Biol, Vicosa, MG, Brazil; [Castro, Quenia J. T.; Grabe-Guimaraes, Andrea] Univ Fed Ouro Preto, Sch Pharm, Lab Expt Pharmacol, Ouro Preto, MG, Brazil Locatelli, J (reprint author), Univ Fed Ouro Preto, Sports Ctr, BR-35400000 Ouro Preto, MG, Brazil. jahefi@cedufop.ufop.br Fundacao de Amparo a Pesquisa do Estado de Minas Gerais (FAPEMIG) [APQ-00793-13]; Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPQ) [307033/2013-9]; Pro-Reitoria de Pesquisa e Pos-Graduacao da Universidade Federal de Ouro Preto (PROPP-UFOP) [02/2015, 09/2016 (23109.003209/2016-98)] The research was supported by Fundacao de Amparo a Pesquisa do Estado de Minas Gerais (FAPEMIG), grant APQ-00793-13, Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPQ), grant 307033/2013-9, Pro-Reitoria de Pesquisa e Pos-Graduacao da Universidade Federal de Ouro Preto (PROPP-UFOP), grant numbers 02/2015 and 09/2016 (23109.003209/2016-98) and we thank Nucleo de Pesquisas em Ciencias Biologicas (NUPEB) and Laboratory of Exercise Biology (UFV) for technical support. 42 0 0 5 5 PERGAMON-ELSEVIER SCIENCE LTD OXFORD THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND 0024-3205 1879-0631 LIFE SCI Life Sci. OCT 15 2017 187 42 49 10.1016/j.lfs.2017.08.014 8 Medicine, Research & Experimental; Pharmacology & Pharmacy Research & Experimental Medicine; Pharmacology & Pharmacy FG7TD WOS:000410626500006 28823565 2018-04-09
J Bull, C; Cooper, C; Lindahl, V; Fitting, S; Persson, AI; Grander, R; Alborn, AM; Bjork-Eriksson, T; Kuhn, HG; Blomgren, K Bull, Cecilia; Cooper, Christiana; Lindahl, Veronica; Fitting, Sylvia; Persson, Anders I.; Grander, Rita; Alborn, Ann-Marie; Bjork-Eriksson, Thomas; Kuhn, H. Georg; Blomgren, Klas Exercise in Adulthood after Irradiation of the Juvenile Brain Ameliorates Long-Term Depletion of Oligodendroglial Cells RADIATION RESEARCH English Article WHITE-MATTER VOLUME; YOUNG-MOUSE BRAIN; SPONTANEOUSLY HYPERTENSIVE-RAT; NEURAL STEM-CELLS; VOLUNTARY EXERCISE; DENTATE GYRUS; IN-VIVO; HIPPOCAMPAL NEUROGENESIS; NEUROCOGNITIVE DEFICITS; DEVELOPMENTAL MODEL Cranial radiation severely affects brain health and function, including glial cell production and myelination. Recent studies indicate that voluntary exercise has beneficial effects on oligodendrogenesis and myelination. Here, we hypothesized that voluntary running would increase oligodendrocyte numbers in the corpus callosum after irradiation of the juvenile mouse brain. The brains of C57Bl/6J male mice were 6 Gy irradiated on postnatal day 9 during the main gliogenic developmental phase, resulting in a loss of oligodendrocyte precursor cells. Upon adulthood, the mice were injected with bromodeoxyuridine and allowed to exercise on a running wheel for four weeks. Cell proliferation and survival, Ascl1(+) oligodendrocyte precursor and Olig2(+) oligodendrocyte cell numbers as well as CC1(+) mature oligodendrocytes were quantified using immunohistology. Radiation induced a reduction in the number of Olig2(+) oligodendrocytes by nearly 50% without affecting production or survival of new

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