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[PMID]:28845935
[Au] Autor:Bozhedomov VA; Lipatova NA; Bozhedomova GE; Rokhlikov IM; Shcherbakova EV; Komarina RA
[Ad] Endereço:Polyclinic 3 of the ADP of the RF, 2N.A. Semashko Railroad Hospital, 3I.M. Sechenov First MSMU, 4City Polyclinic 68, Moscow Health Department, Moscow, Russia.
[Ti] Título:[Using L- and acetyl-L-carnintines in combination with clomiphene citrate and antioxidant complex for treating idiopathic male infertility: a prospective randomized trial].
[So] Source:Urologiia;(3):22-32, 2017 Jul.
[Is] ISSN:1728-2985
[Cp] País de publicação:Russia (Federation)
[La] Idioma:rus
[Ab] Resumo:The most common cause of male infertility is idiopathic oligo-, and or astheno-, and /or teratozoospermia. In such cases, anti-estrogens, antioxidants (vitamins and trace elements) or carnitines are used, but the evidence on their effectiveness is inconsistent; there are currently no published studies exploring their concurrent use. AIM: To investigate the efficacy and safety of the L- and acetyl-L-carnitine complex, vitamins A, E, C, selenium, zinc and other antioxidants ("SpermActin" + "More than vitamins") in combination with clomiphene citrate (CC) in managing male idiopathic infertility in the form of oligo, and/or astheno-, and/or teratozoospermia. MATERIALS AND METHODS: The study comprised 173 men from infertile couples aged 25-45 years who were divided into two groups - the study group (n=88) and control group (n=85). All the patients were examined according to the WHO recommendations. Patients of the study group received L-carnitine fumarate (1 g), acetyl-L-carnitine (0.5 g) twice daily, a complex of vitamins and microelements and CC 25 mg twice daily orally. Patients of the control group were administered the same dosages of CC and a complex of vitamins. Ejaculate was evaluated before and after 3-4 months of treatment. Six months after the start of treatment, information about the onset or absence of pregnancy over the last six months was collected via telephone or online survey. RESULTS: Co-administration of L- and acetyl-L-carnitines concurrently with CC and antioxidant complex (vitamins and minerals) in patients with idiopathic oligo- and/or asteno- and/or teratozoospermia provides some additional positive effect on the concentration of spermatozoa, more pronounced in patients with multiple impaired semen parameters - oligoasthenoteratozoospermia, but does not improve the morphology, progressive sperm motility and pregnancy rates compared to patients receiving basic treatment.
[Mh] Termos MeSH primário: Acetilcarnitina/uso terapêutico
Antioxidantes/uso terapêutico
Astenozoospermia/tratamento farmacológico
Clomifeno/uso terapêutico
Oligospermia/tratamento farmacológico
Teratozoospermia/tratamento farmacológico
[Mh] Termos MeSH secundário: Acetilcarnitina/administração & dosagem
Acetilcarnitina/farmacologia
Adulto
Antioxidantes/administração & dosagem
Antioxidantes/farmacologia
Clomifeno/administração & dosagem
Clomifeno/farmacologia
Quimioterapia Combinada
Seres Humanos
Masculino
Meia-Idade
Minerais/administração & dosagem
Minerais/farmacologia
Minerais/uso terapêutico
Selênio/administração & dosagem
Selênio/farmacologia
Selênio/uso terapêutico
Sêmen/efeitos dos fármacos
Motilidade Espermática/efeitos dos fármacos
Espermatozoides/efeitos dos fármacos
Vitaminas/administração & dosagem
Vitaminas/farmacologia
Vitaminas/uso terapêutico
Zinco/administração & dosagem
Zinco/farmacologia
Zinco/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Antioxidants); 0 (Minerals); 0 (Vitamins); 1HRS458QU2 (Clomiphene); 6DH1W9VH8Q (Acetylcarnitine); H6241UJ22B (Selenium); J41CSQ7QDS (Zinc)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171109
[Lr] Data última revisão:
171109
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170829
[St] Status:MEDLINE


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[PMID]:28445364
[Au] Autor:Catapano J; Zhang J; Scholl D; Chiang C; Gordon T; Borschel GH
[Ad] Endereço:Toronto, Ontario, Canada From the Division of Plastic and Reconstructive Surgery, The Hospital for Sick Children; and the Institute of Medical Science, University of Toronto.
[Ti] Título:N-Acetylcysteine Prevents Retrograde Motor Neuron Death after Neonatal Peripheral Nerve Injury.
[So] Source:Plast Reconstr Surg;139(5):1105e-1115e, 2017 May.
[Is] ISSN:1529-4242
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Neuronal death may be an overlooked and unaddressed component of disability following neonatal nerve injuries, such as obstetric brachial plexus injury. N-acetylcysteine and acetyl-L-carnitine improve survival of neurons after adult nerve injury, but it is unknown whether they improve survival after neonatal injury, when neurons are most susceptible to retrograde neuronal death. The authors' objective was to examine whether N-acetylcysteine or acetyl-L-carnitine treatment improves survival of neonatal motor or sensory neurons in a rat model of neonatal nerve injury. METHODS: Rat pups received either a sciatic nerve crush or transection injury at postnatal day 3 and were then randomized to receive either intraperitoneal vehicle (5% dextrose), N-acetylcysteine (750 mg/kg), or acetyl-L-carnitine (300 mg/kg) once or twice daily. Four weeks after injury, surviving neurons were retrograde-labeled with 4% Fluoro-Gold. The lumbar spinal cord and L4/L5 dorsal root ganglia were then harvested and sectioned to count surviving motor and sensory neurons. RESULTS: Transection and crush injuries resulted in significant motor and sensory neuron loss, with transection injury resulting in significantly less neuron survival. High-dose N-acetylcysteine (750 mg/kg twice daily) significantly increased motor neuron survival after neonatal sciatic nerve crush and transection injury. Neither N-acetylcysteine nor acetyl-L-carnitine treatment improved sensory neuron survival. CONCLUSIONS: Proximal neonatal nerve injuries, such as obstetric brachial plexus injury, produce significant retrograde neuronal death after injury. High-dose N-acetylcysteine significantly increases motor neuron survival, which may improve functional outcomes after obstetrical brachial plexus injury.
[Mh] Termos MeSH primário: Acetilcarnitina/uso terapêutico
Acetilcisteína/uso terapêutico
Morte Celular/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Neurônios Motores/efeitos dos fármacos
Neurônios Motores/patologia
Traumatismos dos Nervos Periféricos/complicações
[Mh] Termos MeSH secundário: Animais
Feminino
Distribuição Aleatória
Ratos
Ratos Endogâmicos Lew
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
6DH1W9VH8Q (Acetylcarnitine); WYQ7N0BPYC (Acetylcysteine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170427
[St] Status:MEDLINE
[do] DOI:10.1097/PRS.0000000000003257


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[PMID]:28369834
[Au] Autor:Schoeler NE; Bell G; Yuen A; Kapelner AD; Heales SJR; Cross JH; Sisodiya S
[Ad] Endereço:UCL Great Ormond Street Institute of Child Health, London, United Kingdom.
[Ti] Título:An examination of biochemical parameters and their association with response to ketogenic dietary therapies.
[So] Source:Epilepsia;58(5):893-900, 2017 May.
[Is] ISSN:1528-1167
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: In the absence of specific metabolic disorders, accurate predictors of response to ketogenic dietary therapies (KDTs) for treating epilepsy are largely unknown. We hypothesized that specific biochemical parameters would be associated with the effectiveness of KDT in humans with epilepsy. The parameters tested were ß-hydroxybutyrate, acetoacetate, nonesterified fatty acids, free and acylcarnitine profile, glucose, and glucose-ketone index (GKI). METHODS: Biochemical results from routine blood tests conducted at baseline prior to initiation of KDT and at 3-month follow-up were obtained from 13 adults and 215 children with KDT response data from participating centers. One hundred thirty-two (57%) of 228 participants had some data at both baseline and 3 months; 52 (23%) of 228 had data only at baseline; 22 (10%) of 228 had data only at 3 months; and 22 (10%) of 228 had no data. KDT response was defined as ≥50% seizure reduction at 3-month follow-up. RESULTS: Acetyl carnitine at baseline was significantly higher in responders (p < 0.007). It was not associated with response at 3-month follow-up. There was a trend for higher levels of free carnitine and other acylcarnitine esters at baseline and at 3-month follow-up in KDT responders. There was also a trend for greater differences in levels of propionyl carnitine and in ß-hydroxybutyrate measured at baseline and 3-month follow-up in KDT responders. No other biochemical parameters were associated with response at any time point. SIGNIFICANCE: Our finding that certain carnitine fractions, in particular baseline acetyl carnitine, are positively associated with greater efficacy of KDT is consistent with the theory that alterations in energy metabolism may play a role in the mechanisms of action of KDT.
[Mh] Termos MeSH primário: Biomarcadores/sangue
Dieta Cetogênica
Epilepsia/sangue
Epilepsia/dietoterapia
[Mh] Termos MeSH secundário: Acetilcarnitina/sangue
Adolescente
Adulto
Fatores Etários
Criança
Pré-Escolar
Epilepsia/genética
Feminino
Seguimentos
Seres Humanos
Masculino
Resultado do Tratamento
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 6DH1W9VH8Q (Acetylcarnitine)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170404
[St] Status:MEDLINE
[do] DOI:10.1111/epi.13729


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[PMID]:28326943
[Au] Autor:Notartomaso S; Mascio G; Bernabucci M; Zappulla C; Scarselli P; Cannella M; Imbriglio T; Gradini R; Battaglia G; Bruno V; Nicoletti F
[Ad] Endereço:1 I.R.C.C.S. Neuromed, Pozzilli, Italy.
[Ti] Título:Analgesia induced by the epigenetic drug, L-acetylcarnitine, outlasts the end of treatment in mouse models of chronic inflammatory and neuropathic pain.
[So] Source:Mol Pain;13:1744806917697009, 2017 Jan.
[Is] ISSN:1744-8069
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Background L-acetylcarnitine, a drug marketed for the treatment of chronic pain, causes analgesia by epigenetically up-regulating type-2 metabotropic glutamate (mGlu2) receptors in the spinal cord. Because the epigenetic mechanisms are typically long-lasting, we hypothesized that analgesia could outlast the duration of L-acetylcarnitine treatment in models of inflammatory and neuropathic pain. Results A seven-day treatment with L-acetylcarnitine (100 mg/kg, once a day, i.p.) produced an antiallodynic effect in the complete Freund adjuvant mouse model of chronic inflammatory pain. L-Acetylcarnitine-induced analgesia persisted for at least 14 days after drug withdrawal. In contrast, the analgesic effect of pregabalin, amitryptiline, ceftriaxone, and N-acetylcysteine disappeared seven days after drug withdrawal. L-acetylcarnitine treatment enhanced mGlu2/3 receptor protein levels in the dorsal region of the spinal cord. This effect also persisted for two weeks after drug withdrawal and was associated with increased levels of acetylated histone H3 bound to the Grm2 gene promoter in the dorsal root ganglia. A long-lasting analgesic effect of L-acetylcarnitine was also observed in mice subjected to chronic constriction injury of the sciatic nerve. In these animals, a 14-day treatment with pregabalin, amitryptiline, tramadol, or L-acetylcarnitine produced a significant antiallodynic effect, with pregabalin displaying the greatest efficacy. In mice treated with pregabalin, tramadol or L-acetylcarnitine the analgesic effect was still visible 15 days after the end of drug treatment. However, only in mice treated with L-acetylcarnitine analgesia persisted 37 days after drug withdrawal. This effect was associated with an increase in mGlu2/3 receptor protein levels in the dorsal horns of the spinal cord. Conclusions Our findings suggest that L-acetylcarnitine has the unique property to cause a long-lasting analgesic effect that might reduce relapses in patients suffering from chronic pain.
[Mh] Termos MeSH primário: Acetilcarnitina/farmacologia
Acetilcarnitina/uso terapêutico
Epigênese Genética/efeitos dos fármacos
Inflamação/tratamento farmacológico
Neuralgia/tratamento farmacológico
[Mh] Termos MeSH secundário: Amitriptilina/uso terapêutico
Analgésicos/farmacologia
Analgésicos/uso terapêutico
Animais
Doença Crônica
Modelos Animais de Doenças
Adjuvante de Freund/efeitos adversos
Hiperalgesia/tratamento farmacológico
Hiperalgesia/etiologia
Inflamação/induzido quimicamente
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Manejo da Dor
Pregabalina/uso terapêutico
Receptores de Glutamato Metabotrópico/metabolismo
Fatores de Tempo
Tramadol/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Analgesics); 0 (Receptors, Metabotropic Glutamate); 0 (metabotropic glutamate receptor 2); 1806D8D52K (Amitriptyline); 39J1LGJ30J (Tramadol); 55JG375S6M (Pregabalin); 6DH1W9VH8Q (Acetylcarnitine); 9007-81-2 (Freund's Adjuvant)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170323
[St] Status:MEDLINE
[do] DOI:10.1177/1744806917697009


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[PMID]:28289166
[Au] Autor:Zeidman LA
[Ad] Endereço:From the Department of Neurology and Rehabilitation, University of Illinois at Chicago. lzeidm1@uic.edu.
[Ti] Título:Hans Jacob and brain research on Hamburg "euthanasia" victims: "Awaiting further brains!"
[So] Source:Neurology;88(11):1089-1094, 2017 Mar 14.
[Is] ISSN:1526-632X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Several neuropathologists conducted brain research on victims of so-called euthanasia programs carried out by the National Socialist (Nazi) regime in Germany from 1940 to 1945. Some published their results in German journals or books during and after the war. One of these neuropathologists was Hans Jacob of Hamburg, a former Nazi party member and the leader of the same laboratory previously run by Alfons Jakob (Creutzfeldt-Jakob disease). Though much has been published on the unethical actions of Jacob's fellow neuropathologist from Berlin, Julius Hallervorden, Jacob's actions were remarkably similar and have not been previously analyzed in the neuroscience literature. Jacob dissected at least 42 patient brains from euthanasia centers near Hamburg, and saved the specimens from at least 17 of them. He published a 1956 book chapter featuring 2 such specimens. Jacob was denazified, had a notable career, and never publicly addressed his actions during the war. His ethical violations may not have been on the same scale as Hallervorden's, but the effect of his work echoes to the modern era. As responsible researchers, we must always be conscious of the provenance of material provided and not succumb to opportunistic temptation despite the ethical consequences.
[Mh] Termos MeSH primário: Eutanásia/história
Nacional-Socialismo/história
Neurologia/história
[Mh] Termos MeSH secundário: Acetilcarnitina
Alemanha
História do Século XIX
História do Século XX
Seres Humanos
Masculino
[Pt] Tipo de publicação:HISTORICAL ARTICLE; JOURNAL ARTICLE; PORTRAITS
[Nm] Nome de substância:
6DH1W9VH8Q (Acetylcarnitine)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170522
[Lr] Data última revisão:
170522
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170315
[St] Status:MEDLINE
[do] DOI:10.1212/WNL.0000000000003712


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[PMID]:28287417
[Au] Autor:Yu M; Jia HM; Cui FX; Yang Y; Zhao Y; Yang MH; Zou ZM
[Ad] Endereço:Institute of Medicinal Plant Development, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100193, China. yumeng.5555@163.com.
[Ti] Título:The Effect of Chinese Herbal Medicine Formula mKG on Allergic Asthma by Regulating Lung and Plasma Metabolic Alternations.
[So] Source:Int J Mol Sci;18(3), 2017 Mar 10.
[Is] ISSN:1422-0067
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Asthma is a chronic inflammatory disorder of the airway and is characterized by airway remodeling, hyperresponsiveness, and shortness of breath. Modified Kushen Gancao Formula (mKG), derived from traditional Chinese herbal medicines (TCM), has been demonstrated to have good therapeutic effects on experimental allergic asthma. However, its anti-asthma mechanism remains currently unknown. In the present work, metabolomics studies of biochemical changes in the lung tissue and plasma of ovalbumin (OVA)-induced allergic asthma mice with mKG treatment were performed using ultra high-performance liquid chromatography coupled with quadrupole time-of-flight mass spectrometry (UPLC-Q-TOF/MS). Partial least squares-discriminate analysis (PLS-DA) indicated that the metabolic perturbation induced by OVA was reduced after mKG treatment. A total of twenty-four metabolites involved in seven metabolic pathways were identified as potential biomarkers in the development of allergic asthma. Among them, myristic acid ( or ), sphinganine ( or ), and lysoPC(15:0) ( or ) were detected both in lung tissue and plasma. Additionally, l-acetylcarnitine ( ), thromboxane B2 ( ), 10-HDoHE ( ), and 5-HETE ( ) were first reported to be potential biomarkers associated with allergic asthma. The treatment of mKG mediated all of those potential biomarkers except lysoPC(15:0) ( ). The anti-asthma mechanism of mKG can be achieved through the comprehensive regulation of multiple perturbed biomarkers and metabolic pathways.
[Mh] Termos MeSH primário: Asma/metabolismo
Medicamentos de Ervas Chinesas/farmacologia
Hipersensibilidade/metabolismo
Pulmão/efeitos dos fármacos
Metaboloma/efeitos dos fármacos
[Mh] Termos MeSH secundário: Acetilcarnitina/sangue
Acetilcarnitina/metabolismo
Animais
Asma/etiologia
Biomarcadores/sangue
Biomarcadores/metabolismo
Feminino
Hipersensibilidade/complicações
Pulmão/metabolismo
Camundongos
Camundongos Endogâmicos BALB C
Ácido Mirístico/sangue
Ácido Mirístico/metabolismo
Esfingosina/análogos & derivados
Esfingosina/sangue
Esfingosina/metabolismo
Tromboxano B2/sangue
Tromboxano B2/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Drugs, Chinese Herbal); 0I3V7S25AW (Myristic Acid); 54397-85-2 (Thromboxane B2); 6DH1W9VH8Q (Acetylcarnitine); NGZ37HRE42 (Sphingosine); OWA98U788S (safingol)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170420
[Lr] Data última revisão:
170420
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170314
[St] Status:MEDLINE


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[PMID]:28233701
[Au] Autor:Sun R; Zhang J; Wei H; Meng X; Ding Q; Sun F; Cao M; Yin L; Pu Y
[Ad] Endereço:Key Laboratory of Environmental Medicine Engineering, Ministry of Education, School of Public Health, Southeast University, Nanjing, 210009, Jiangsu, China.
[Ti] Título:Acetyl-l-carnitine partially prevents benzene-induced hematotoxicity and oxidative stress in C3H/He mice.
[So] Source:Environ Toxicol Pharmacol;51:108-113, 2017 Apr.
[Is] ISSN:1872-7077
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Benzene is an environmental pollutant and occupational toxicant which induces hematotoxicity. Our previous metabonomics study suggested that acetyl-l-carnitine (ALCAR) decreased in the mouse plasma and bone marrow (BM) cells due to benzene exposure. In the present study, the topic on whether ALCAR influences hematotoxicity caused by benzene exposure was explored. Thirty-two male C3H/He mice were divided into four groups: control group (C: vehicle, oil), benzene group (150mg/kg body weight (b.w.) benzene), benzene+A1 group (150mg/kg b.w. benzene+100mg/kg b.w. ALCAR), and benzene+A2 group (150mg/kg b.w. benzene+200mg/kg b.w. ALCAR). Benzene was injected subcutaneously, and ALCAR was orally administrated via gavage once daily for 4 weeks consecutively. After the experimental period, the blood routine, BM cell number and frequency of hematopoietic stem/progenitor cell (HS/PC) were assessed. The mitochondrial membrane potential and ATP level were determined to evaluate the mitochondrial function. Reactive oxygen species (ROS), hydrogen peroxide (H O ) and malondialdehyde (MDA) levels were also examined, and the comet assay was performed to measure oxidative stress. Results showed that ALCAR intervention can partially reduce the benzene-induced damage on BM and HS/PCs and can simultaneously alleviate the DNA damage by reducing benzene-induced H O ROS, and MDA.
[Mh] Termos MeSH primário: Acetilcarnitina/farmacologia
Antioxidantes/farmacologia
Benzeno/toxicidade
Poluentes Ambientais/toxicidade
Células-Tronco Hematopoéticas/efeitos dos fármacos
Estresse Oxidativo/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Contagem de Células Sanguíneas
Células da Medula Óssea/citologia
Células da Medula Óssea/efeitos dos fármacos
Ensaio Cometa
Dano ao DNA/efeitos dos fármacos
Eritrócitos/citologia
Eritrócitos/efeitos dos fármacos
Células-Tronco Hematopoéticas/citologia
Células-Tronco Hematopoéticas/metabolismo
Leucócitos/citologia
Leucócitos/efeitos dos fármacos
Masculino
Potencial da Membrana Mitocondrial/efeitos dos fármacos
Camundongos Endogâmicos
Espécies Reativas de Oxigênio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antioxidants); 0 (Environmental Pollutants); 0 (Reactive Oxygen Species); 6DH1W9VH8Q (Acetylcarnitine); J64922108F (Benzene)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170808
[Lr] Data última revisão:
170808
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170225
[St] Status:MEDLINE


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[PMID]:27240534
[Au] Autor:Lau T; Bigio B; Zelli D; McEwen BS; Nasca C
[Ad] Endereço:Laboratory of Neuroendocrinology, The Rockefeller University, New York, NY, USA.
[Ti] Título:Stress-induced structural plasticity of medial amygdala stellate neurons and rapid prevention by a candidate antidepressant.
[So] Source:Mol Psychiatry;22(2):227-234, 2017 Feb.
[Is] ISSN:1476-5578
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The adult brain is capable of adapting to internal and external stressors by undergoing structural plasticity, and failure to be resilient and preserve normal structure and function is likely to contribute to depression and anxiety disorders. Although the hippocampus has provided the gateway for understanding stress effects on the brain, less is known about the amygdala, a key brain area involved in the neural circuitry of fear and anxiety. Here, in mice more vulnerable to stressors, we demonstrate structural plasticity within the medial and basolateral regions of the amygdala in response to prolonged 21-day chronic restraint stress (CRS). Three days before the end of CRS, treatment with the putative, rapidly acting antidepressant, acetyl-l-carnitine (LAC) in the drinking water opposed the direction of these changes. Behaviorally, the LAC treatment during the last part of CRS enhanced resilience, opposing the effects of CRS, as shown by an increased social interaction and reduced passive behavior in a forced swim test. Furthermore, CRS mice treated with LAC show resilience of the CRS-induced structural remodeling of medial amygdala (MeA) stellate neurons. Within the basolateral amygdala (BLA), LAC did not reduce, but slightly enhanced, the CRS-increased length and number of intersections of pyramidal neurons. No structural changes were observed in MeA bipolar neurons, BLA stellate neurons or in lateral amygdala stellate neurons. Our findings identify MeA stellate neurons as an important component in the responses to stress and LAC action and show that LAC can promote structural plasticity of the MeA. This may be useful as a model for increasing resilience to stressors in at-risk populations.
[Mh] Termos MeSH primário: Antidepressivos/farmacologia
Ansiedade/fisiopatologia
[Mh] Termos MeSH secundário: Acetilcarnitina/metabolismo
Acetilcarnitina/uso terapêutico
Tonsila do Cerebelo/fisiologia
Animais
Antidepressivos/metabolismo
Complexo Nuclear Basolateral da Amígdala/fisiologia
Encéfalo/fisiopatologia
Complexo Nuclear Corticomedial
Dendritos
Depressão
Medo/fisiologia
Hipocampo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Plasticidade Neuronal/fisiologia
Neurônios/fisiologia
Células Piramidais/fisiologia
Estresse Psicológico/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antidepressive Agents); 6DH1W9VH8Q (Acetylcarnitine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171003
[Lr] Data última revisão:
171003
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160601
[St] Status:MEDLINE
[do] DOI:10.1038/mp.2016.68


  9 / 1133 MEDLINE  
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[PMID]:28262191
[Au] Autor:Dundar HA; Kiray M; Kir M; Kolatan E; Bagriyanik A; Altun Z; Aktas S; Ellidokuz H; Yilmaz O; Mutafoglu K; Olgun N
[Ad] Endereço:Department of Pediatrics, Faculty of Medicine, Dokuz Eylul University, Izmir, Turkey. Electronic address: haticeadiguzel@hotmail.com.
[Ti] Título:Protective Effect of Acetyl-L-Carnitine Against Doxorubicin-induced Cardiotoxicity in Wistar Albino Rats.
[So] Source:Arch Med Res;47(7):506-514, 2016 Oct.
[Is] ISSN:1873-5487
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND AND AIMS: Anthracyclines are one of the most preferred agents in practical pediatric oncology despite their dose-dependent cardiotoxic effects. The aim of this study was to investigate whether or not acetyl-L-carnitine (ALCAR) has protective effects on doxorubicin (DOX)-induced cardiotoxicity. METHODS: Wistar rats were divided into four groups; control, DOX, ALCAR and ALCAR+DOX. Rats in the first group were given saline on study days, whereas those in the second group were given a single dose of DOX on the 5 day and saline on the other days. Rats in the third group were given ALCAR and those in the fourth group were given ALCAR on study days but also given only a single dose of DOX on the fifth day of the study. Ejection fractions (EF) were measured by echocardiography before and after drug administration. Heart tissues were evaluated by light and electron microscopy. Apoptotic cells were determined with TUNEL and caspase-3 staining. RESULTS: DOX significantly decreased the EF values, whereas ALCAR did not. Cardiac functions were higher in the ALCAR+DOX group when compared to the DOX group. DOX administration caused a cardiac injury not only functionally, but also structurally, whereas ALCAR prevented it. CONCLUSIONS: ALCAR has a capacity of preventing DOX-induced cardiac injury at both functional and structural levels.
[Mh] Termos MeSH primário: Acetilcarnitina/farmacologia
Antibióticos Antineoplásicos/efeitos adversos
Antioxidantes/farmacologia
Doxorrubicina/efeitos adversos
Coração/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Cardiotoxicidade/patologia
Cardiotoxicidade/fisiopatologia
Cardiotoxicidade/prevenção & controle
Caspase 3/metabolismo
Feminino
Coração/fisiopatologia
Miocárdio/patologia
Ratos Wistar
Função Ventricular Esquerda/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibiotics, Antineoplastic); 0 (Antioxidants); 6DH1W9VH8Q (Acetylcarnitine); 80168379AG (Doxorubicin); EC 3.4.22.- (Caspase 3)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170706
[Lr] Data última revisão:
170706
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170307
[St] Status:MEDLINE


  10 / 1133 MEDLINE  
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[PMID]:27786574
[Au] Autor:Saribas GS; Erdogan D; Goktas G; Akyol SN; Hirfanoglu IM; Gurgen SG; Coskun N; Ozogul C
[Ad] Endereço:a Faculty of Medicine, Department of Histology and Embryology , Gazi University , Ankara , Turkey.
[Ti] Título:Examining the protective effects of acetyl l-carnitine on cisplatin-induced uterine tube toxicity.
[So] Source:J Obstet Gynaecol;36(8):1086-1092, 2016 Nov.
[Is] ISSN:1364-6893
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The aim of this study was to investigate the effects of cisplatin and the protective role of acetyl l-carnitine against uterine tube toxicity. Twenty-four female Wistar albino rats were divided into four groups: control group was injected with saline (control); group 2 was injected with acetyl l-carnitine; group 3 was injected with cisplatin; and group 4 was pre-treated with acetyl l-carnitine before cisplatin intraperitoneal injection. According to our results, a significant weight loss was observed in rats from group 3. The thickness of the wall and epithelium of uterine tube were decreased in group 3 rats. We elaborate the protein expression of caspase in epithelium and stroma by IHC. We found that the expression of caspase and the number of TUNEL-positive cells were increased in group 3 rats compared to the other groups. In our study, we showed the protective role of acetyl l-carnitine against uterine tube toxicity caused by cisplatin.
[Mh] Termos MeSH primário: Acetilcarnitina/farmacologia
Antineoplásicos/toxicidade
Cisplatino/toxicidade
Tubas Uterinas/efeitos dos fármacos
Complexo Vitamínico B/farmacologia
[Mh] Termos MeSH secundário: Animais
Tubas Uterinas/patologia
Feminino
Substâncias Protetoras/farmacologia
Ratos
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Protective Agents); 12001-76-2 (Vitamin B Complex); 6DH1W9VH8Q (Acetylcarnitine); Q20Q21Q62J (Cisplatin)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170626
[Lr] Data última revisão:
170626
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161028
[St] Status:MEDLINE



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