Database : MEDLINE Search on : brain [Words] References found : 1149468 [refine] Displaying: 1 .. 10   in format [Detailed]

page 1 of 114947

go to page

1 / 1149468

MEDLINE

select to print Photocopy

[PMID]: 23648293 [Au] Autor: Hu YZ; Wang DH; Luan Y; Gong HD [Ad] Address: Department of Neurosurgery, the First Affiliated Hospital of Harbin Medical University, Harbin 150001, China. [Ti] Title: [Antitumor effect of baicalin on rat brain glioma]. [So] Source: Zhonghua Zhong Liu Za Zhi;35(1):11-6, 2013 Jan. [Is] ISSN: 0253-3766 [Cp] Country of publication: China [La] Language: chi [Ab] Abstract: OBJECTIVE: To investigate the therapeutic mechanism of baicalin on rat brain glioma. METHODS: Deep brain glioma models were established by injection of glioma cell line C6 cells into the brain of Wistar rats. The rats at 7 days after modeling were randomly divided into tumor control group (0.9% NaCl solution 30 mg×kg(-1)×d(-1) gavage)and experimental groups. The experimental rats was divided into 3 groups: low dose group (50 mg×kg(-1)×d(-1)), middle dose group (100 mg×kg(-1)×d(-1)) and high dose group (200 mg×kg(-1)×d(-1)), given the baicalin by gavage. Pathological and electron microscopic changes were observed. The expressions of p53 and Bcl-2 were determined by immunohistochemistry, and the changes of MRI, the average survival time and body weight of the rats in each group after treatments were analyzed. RESULTS: Compared with the control group, the tumor diameter and volume of high dose group rats before sacrifice were significantly reduced (P < 0.01), and the survival time was significantly prolonged (P < 0.01). Immunohistochemistry revealed strong positive expression rate of mutant p53 (84.47 ± 3.74)% and moderately positive rate (47.28 ± 2.38)% in the control group, significantly higher than that in the negative group (12.91 ± 1.07)% (P < 0.01). The positive rate of mutant p53 of the high dose group was (46.42 ± 2.19)%, significantly lower than that of the control group (84.47 ± 3.74)% (P < 0.01). The expression rate of Bcl-2 in the control group was strongly positive (86.51 ± 4.17)% and moderate positive (48.19 ± 2.11)%, significantly higher than that of the negative group (10.36 ± 1.43)% (P < 0.01). Electron microscopy revealed that baicalin caused damages of the cell nuclei and organelles in the gliomas. CONCLUSIONS: Baicalin has significant inhibitory effect on glioma in vivo, and its mechanism may be related to cell apoptosis induced by down-regulated expression of mutant p53, but not related with Bcl-2 expression. [Pt] Publication type: ENGLISH ABSTRACT; JOURNAL ARTICLE [Em] Entry month: 1305 [Js] Journal subset: IM [St] Status: In-Data-Review

2 / 1149468

MEDLINE

select to print Photocopy

[PMID]: 23648292 [Au] Autor: Chen YM; Fei XF; Wang AD; Dai XL; Zhang JS; Cui BQ; Zhang QB; Zhao YD; Chen H; Wang ZM; Lan Q; Dong J; Huang Q [Ad] Address: Department of Neurosurgery, 2nd Affiliated Hospital, Soochow University, Suzhou 215004, China. [Ti] Title: [Host glial cell canceration induced by glioma stem cells in GFP/RFP dual fluorescence orthotopic glioma models in nude mice]. [So] Source: Zhonghua Zhong Liu Za Zhi;35(1):5-10, 2013 Jan. [Is] ISSN: 0253-3766 [Cp] Country of publication: China [La] Language: chi [Ab] Abstract: OBJECTIVE: During the process of tissue remodeling in human tumor transplantation models, the roles of the inoculated tumor cells and host tissue in tumor progression is still largely unknown. The aim of this study was to investigate the relationships and interactions between these two sides using GFP-RFP double fluorescence tracing technique. METHODS: Red fluorescence protein (RFP) gene was stably transfected into glioma stem cell line SU3, then SU3-RFP cells were transplanted into the brain of athymic nude mice with green fluorescence protein (GFP) expression. After the intracerebral tumors were formed, the relationship and interaction between GFP cells and RFP cells were analyzed. Highly proliferative GFP cells were screened out, and monocloned with micro-pipetting. DNA content assay, chromosome banding and carcinogenicity test of the GFP cells were performed to observe the GFP cells' cancerous phenotype in nude mice. RESULTS: In the transplantable tumor tissue, besides a great quantity of RFP cells, there were still a proportion of GFP cells and GFP/RFP fusion cells. The proportion of RFP cells, GFP cells and GFP/RFP cells were (88.99 ± 1.46)%, (5.59 ± 1.00)%, and (4.11 ± 1.020)%, respectively. Two monoclonal host GFP cells (H1 and H9) were cloned, which demonstrated the properties of immortality, loss of contact inhibition, and ultra-tetraploid when cultured in vitro. Both H1 and H9 cells expressed CNP, a specific marker of oligodendrocytes. The GFP cells also demonstrated 100% tumorigenic rate and high invasive properties in vivo. CONCLUSIONS: In this glioma transplantation model, the transplanted tumor tissues contained not only transplanted glioma stem cells but also cancerous host GFP cells. Our findings offer important clues to further research on the relationships among different members in the tumor microenvironment. [Pt] Publication type: ENGLISH ABSTRACT; JOURNAL ARTICLE [Em] Entry month: 1305 [Js] Journal subset: IM [St] Status: In-Data-Review

3 / 1149468

MEDLINE

select to print Photocopy Full text

[PMID]: 23648159 [Au] Autor: Su ZY; Li CS [Ad] Address: Department of Emergency, Beijing Chaoyang Hospital Affiliated to Capital Medical University, Beijing 100020, China. Corresponding author: Li Chun-sheng, Email: lcscyyy@163.com. [Ti] Title: [The evaluation of cerebral function by diffusion weighted imaging after norepinephrine-induced hypertensive perfusion therapy in pig model of cardiac arrest]. [So] Source: Zhonghua Wei Zhong Bing Ji Jiu Yi Xue;25(2):92-5, 2013 Feb. [Is] ISSN: 2095-4352 [Cp] Country of publication: China [La] Language: chi [Ab] Abstract: OBJECTIVE: To evaluate the changes in cerebral function of pigs with cardiac arrest (CA) after recovery of spontaneous circulation (ROSC) after hypertension perfusion therapy induced by norepinephrine (NE). METHODS: Ventricular fibrillation (VF) was induced by electrical stimulation, and standard cardiopulmonary resuscitation (CPR) was performed after VF for 4 minutes. The pigs with successful ROSC were randomly divided into two group, each n=5. The pigs in the hypertensive reperfusion group were given with NE immediately to maintain the mean arterial pressure (MAP) at 130% before VF for 4 hours; MAP of the pigs in normal reperfusion group was maintained for 4 hours as baseline. The changes in hemodynamics were observed for 4 hours in both groups. Cerebral cortex was scanned with diffusion weighted imaging (DWI) before VF and 1 hour and 3 hours after ROSC, and the dynamic changes in brain functional imaging were observed. Twenty-four hours after ROSC, brain biopsy were collected and examined after hematoxylin and eosin staining (HE). RESULTS: Compared with the normal reperfusion group, heart rate (HR), MAP, cardiac output (CO) and coronary perfusion pressure (CPP) in the hypertensive reperfusion group showed a tendency to increase (ROSC 30 minutes HR: 167±8 bpm vs. 140±15 bpm, ROSC 1 hour MAP: 131±9 mm Hg vs. 108±10 mm Hg, ROSC 1 hour CO: 4.9±0.1 L/min vs. 3.4±0.5 L/min, ROSC 2 hours CPP: 118±12 mm Hg vs. 88±1 mm Hg, P<0.05 or P<0.01). There was no obvious abnormality as shown by DWI before and after resuscitation, and the apparent diffusion coefficient (ADC) showed a tendency to decrease after resuscitation in both groups. The ADC in the normal reperfusion group was decreased more than that in the hypertensive reperfusion. Pathological study showed that the protective effect of the hypertensive reperfusion on brain tissue was better than that of the normal reperfusion group. CONCLUSION: Hypertensive reperfusion can produce hemodynamic changes, and an increase in cerebral blood flow, thus it produces a protective effect on brain to promote the recovery of neurological function in pigs with CA after resuscitation. [Pt] Publication type: ENGLISH ABSTRACT; JOURNAL ARTICLE [Em] Entry month: 1305 [Js] Journal subset: IM [St] Status: In-Data-Review [do] DOI: 10.3760/cma.j.issn.2095-4352.2013.02.010

4 / 1149468

MEDLINE

select to print Photocopy Full text

[PMID]: 23648154 [Au] Autor: Zhang D; Li N; Chen Y; Wang YS [Ad] Address: Department of Intensive Care Unit, the First Hospital, Jilin University, Changchun 130021, Jilin, China. Corresponding author: Wang Yu-shan, Email: wang-yushan@tom.com. [Ti] Title: [Reproducing and evaluating a rabbit model of multiple organ dysfunction syndrome after cardiopulmonary resuscitation resulted from asphyxia]. [So] Source: Zhonghua Wei Zhong Bing Ji Jiu Yi Xue;25(2):72-5, 2013 Feb. [Is] ISSN: 2095-4352 [Cp] Country of publication: China [La] Language: chi [Ab] Abstract: OBJECTIVE: To evaluate the reproduction of a model of post resuscitation multiple organ dysfunction syndrome (PR-MODS) after cardiac arrest (CA) in rabbit, in order to provide new methods for post-CA treatment. METHODS: Thirty-five rabbits were randomly divided into three groups, the sham group (n=5), the 7-minute asphyxia group (n=15), and the 8-minute asphyxia group (n=15). The asphyxia CA model was reproduced with tracheal occlusion. After cardiopulmonary resuscitation (CPR), the ratio of recovery of spontaneous circulation (ROSC), the mortality at different time points and the incidence of systemic inflammatory response syndrome (SIRS) were observed in two asphyxia groups. Creatine kinase isoenzyme (CK-MB), alanine aminotransferase (ALT), creatinine (Cr), glucose (Glu) and arterial partial pressure of oxygen (PaO2) levels in blood were measured in the two asphyxia groups before CPR and 12, 24 and 48 hours after ROSC. The survived rabbits were euthanized at 48 hours after ROSC, and heart, brain, lung, kidney, liver, and intestine were harvested for pathological examination using light microscope. PR-MODS after CA was defined based on the function of main organs and their pathological changes. RESULTS: (1) The incidence of ROSC was 100.0% in 7-minute asphyxia group and 86.7% in 8-minute asphyxia group respectively (P>0.05). The 6-hour mortality in 8-minute asphyxia group was significantly higher than that in 7-minute asphyxia group (46.7% vs. 6.7%, P<0.05), and the mortality of 8-minute asphyxia group at 12 - 48 hours was slightly higher compared with that of 7-minute asphyxia group (all P>0.05). (2) There was a variety of organ dysfunctions in survived rabbits after ROSC, including chemosis, respiratory distress, hypotension, abdominal distension, weakened or disappearance of bowel peristalsis and oliguria. (3) There was no SIRS or associated changes in major organ function in the sham group. SIRS was observed at 12 - 24 hours after ROSC in the two asphyxia groups. CK-MB was increased significantly at 12 hours after ROSC compared with that before asphyxia (7-minute asphyxia group: 786.88±211.84 U/L vs. 468.20±149.45 U/L, 8-minute asphyxia group: 894.88±248.80 U/L vs. 462.11±115.15 U/L, both P<0.05), ALT, Cr and Glu were elevated obviously at 24 hours after ROSC (7-minute asphyxia group ALT: 174.25±36.28 U/L vs. 50.27±9.37 U/L, Cr: 144.25±41.64 µmol/L vs. 67.71±16.47 µmol/L, Glu: 11.21±1.14 mmol/L vs. 5.59±1.10 mmol/L; 8-minute asphyxia group ALT: 205.50±10.61 U/L vs. 51.13±10.37 U/L, Cr: 230.50±88.39 µmol/L vs. 65.93±13.81 µmol/L, Glu: 11.55±0.35 mmol/L vs. 6.41±1.23 mmol/L, all P<0.05), and PaO2 was lowered significantly at 48 hours after ROSC (7-minute asphyxia group: 5.03±0.73 kPa vs. 9.07±1.03 kPa, P<0.05). (4) There were pathological changes in major organ in the survived rabbits at 48 hours after ROSC (only 4 rabbits survived in 7-minute asphyxia group), including infiltration of inflammatory cells, partial cellular degeneration, edema, necrosis and tissue bleeding in major organs. CONCLUSION: If the SIRS and dysfunction of two or more organ were defined in animals after ROSC, the signs, biochemical markers and nonspecific pathological changes could be accepted to evaluate the PR-MODS. [Pt] Publication type: ENGLISH ABSTRACT; JOURNAL ARTICLE [Em] Entry month: 1305 [Js] Journal subset: IM [St] Status: In-Data-Review [do] DOI: 10.3760/cma.j.issn.2095-4352.2013.02.005

5 / 1149468

MEDLINE

select to print Photocopy

[PMID]: 23649390 [Au] Autor: Yabuki Y; Nakagawasai O; Tadano T; Fukunaga K [Ad] Address: Department of Pharmacology, Graduate School of Pharmaceutical Sciences, Tohoku University. [Ti] Title: Imaging Monitoring Method of CaMKII Activity by Immunohistochemical Analysis in Schizophrenic Model Rats. [So] Source: Yakugaku Zasshi;133(5):501-6, 2013. [Is] ISSN: 1347-5231 [Cp] Country of publication: Japan [La] Language: eng [Ab] Abstract:   Schizophrenia is characterized by various behavioral abnormalities including cognitive dysfunction. Neonatal ventral hippocampus (NVH)-lesioned rats had been known as neurodevelopmental animal model similar to schizophrenia. Previous observations indicate that postpubertal NVH-lesioned rats exhibit impairments in prepulse inhibition (PPI), spontaneous locomotion, social interaction behavior and working memory. Here, we document the neurochemical basis of those defects in NVH-lesioned rats. Since Ca(2+)/calmodulin-dependent protein kinase II (CaMKII), which is NMDA receptor downstream kinase, is essential for memory and learning acquisition, we developed a protocol to monitor the spatial changes in CaMKII autophosphorylation using immunohistochemical imaging of whole brain slices with anti-autophosphorylated CaMKII antibody in order to address mechanisms underlying impaired cognitive function in NVH-lesioned rats. Immunohistochemical analyses using anti-autophosphorylated CaMKII antibody revealed that CaMKII autophosphorylation was significantly reduced in the medial prefrontal cortex (mPFC) of NVH-lesioned rats compared with control animals. This immunohistochemical technique is useful to investigate temporal and special changes in CaMKII activity in rodent brain and to evaluate drugs to improve the cognitive impairment. [Pt] Publication type: JOURNAL ARTICLE [Em] Entry month: 1305 [Js] Journal subset: IM [St] Status: In-Data-Review

6 / 1149468

MEDLINE

select to print Photocopy

[PMID]: 23649389 [Au] Autor: Nishinaka T; Matsumoto K; Nakamoto K; Anbo A; Mankura M; Koyama Y; Tokuyama S [Ad] Address: Department of Clinical Pharmacy, School of Pharmaceutical Sciences, Kobe Gakuin University. [Ti] Title: Elucidation of Mechanisms Underlying Docosahexaenoic Acid-induced Antinociception. [So] Source: Yakugaku Zasshi;133(5):493-9, 2013. [Is] ISSN: 1347-5231 [Cp] Country of publication: Japan [La] Language: eng [Ab] Abstract:   Docosahexaenoic acid (DHA), a predominant of n-3 polyunsaturated fatty acids (n-3 PUFA), has numerous beneficial physiological effects, including neuroprotection and cardiovascular protection. Recently, a possible involvement of n-3 PUFA in pain control has gathered considerable attention because numerous studies have reported a regulatory role of n-3 PUFAs. However, the mechanisms underlying how DHA exerts antinociceptive effect remain unknown. Here, we performed elucidation of mechanisms underlying DHA-induced antinociception. DHA administration dose-dependently exerted an antinociceptive effect. This effect was abolished by pretreated with the ß-funaltrexamine (ß-FNA), a µ-opioid receptor antagonist, and the nartrindole (NTI), a δ-opioid receptor antagonist, but not by the nor-binaltorphimine (nor-BNI), a κ-opioid receptor antagonist. In the radioligand binding assay, DHA itself did not have the affinity for µ-, δ- and κ- opioid receptor. Furthermore, the pretreatment of anti ß-endorphin antiserum inhibited DHA-induced antinociception. The plasma levels of ß-endorphin increased 30 min after DHA administration. The ß-endorphin immunoreactivity in the brain increased at 30 min after DHA treatment. Expression of GPR40 protein was widely observed in the brain as well as the spinal cord. The intracerebroventricular but not intrathecal injection of DHA and GW9508, a GPR40/GPR120 agonist, significantly reduced formalin-induced pain behavior. The ß-endorphin immunoreactivity in the brain increased at 10 and 20 min after intracerebroventricular injection of DHA and GW9508. These findings suggest that DHA-induced antinociception via ß-endorphin release may be mediated through GPR40 signaling in the supraspinal area. [Pt] Publication type: JOURNAL ARTICLE [Em] Entry month: 1305 [Js] Journal subset: IM [St] Status: In-Data-Review

7 / 1149468

MEDLINE

select to print Photocopy Full text

[PMID]: 23561718 [Au] Autor: Deco G; Jirsa VK; McIntosh AR [Ad] Address: Center for Brain and Cognition, Computational Neuroscience Group, Department of Information and Communication Technologies, Universitat Pompeu Fabra, Roc Boronat 138, Barcelona, 08018, Spain; Institució Catalana de la Recerca i Estudis Avançats (ICREA), Universitat Pompeu Fabra, Passeig Lluís Companys 23, Barcelona, 08010, Spain. Electronic address: gustavo.deco@upf.edu. [Ti] Title: Resting brains never rest: computational insights into potential cognitive architectures. [So] Source: Trends Neurosci;36(5):268-74, 2013 May. [Is] ISSN: 1878-108X [Cp] Country of publication: England [La] Language: eng [Ab] Abstract: Resting-state networks (RSNs), which have become a main focus in neuroimaging research, can be best simulated by large-scale cortical models in which networks teeter on the edge of instability. In this state, the functional networks are in a low firing stable state while they are continuously pulled towards multiple other configurations. Small extrinsic perturbations can shape task-related network dynamics, whereas perturbations from intrinsic noise generate excursions reflecting the range of available functional networks. This is particularly advantageous for the efficiency and speed of network mobilization. Thus, the resting state reflects the dynamical capabilities of the brain, which emphasizes the vital interplay of time and space. In this article, we propose a new theoretical framework for RSNs that can serve as a fertile ground for empirical testing. [Pt] Publication type: JOURNAL ARTICLE [Em] Entry month: 1305 [Js] Journal subset: IM [St] Status: In-Data-Review

8 / 1149468

MEDLINE

select to print Photocopy Full text

[PMID]: 23415112 [Au] Autor: Zilles K; Palomero-Gallagher N; Amunts K [Ad] Address: Research Centre Juelich, Institute for Neuroscience and Medicine (INM-1), Juelich, Germany; Juelich-Aachen Research Alliance (JARA), Translational Brain Medicine, Juelich, Germany; C. & O. Vogt Institute for Brain Research, University of Düsseldorf, Düsseldorf, Germany; Rheinisch-Westfaelische Technische Hochschule (RWTH) Aachen University, Department of Psychiatry, Psychotherapy, and Psychosomatics, Aachen, Germany. Electronic address: k.zilles@fz-juelich.de. [Ti] Title: Development of cortical folding during evolution and ontogeny. [So] Source: Trends Neurosci;36(5):275-84, 2013 May. [Is] ISSN: 1878-108X [Cp] Country of publication: England [La] Language: eng [Ab] Abstract: Cortical folding is a hallmark of many, but not all, mammalian brains. The degree of folding increases with brain size across mammals, but at different scales between orders and families. In this review we summarize recent studies that have shed light on cortical folding and discuss new models that arise from these data. Genetic analyses argue for an independent development of brain volume and gyrification, but more recent data on the cellular development of the cortex and its connectivity highlight the role of these processes in cortical folding (grey matter hypothesis). This, and the widely discussed tension hypothesis, further tested by analyzing the mechanical properties of maturing nerve fibers, synapses, and dendrites, can provide the basis for a future integrative view on cortical folding. [Pt] Publication type: JOURNAL ARTICLE [Em] Entry month: 1305 [Js] Journal subset: IM [St] Status: In-Data-Review

9 / 1149468

MEDLINE

select to print Photocopy Full text

[PMID]: 23384445 [Au] Autor: Foster JA; McVey Neufeld KA [Ad] Address: Department of Psychiatry and Behavioural Neurosciences, McMaster University, at St. Joseph's Healthcare, 50 Charlton Ave. E, T3308, Hamilton, ON, L8N 4A6, Canada. Electronic address: jfoster@mcmaster.ca. [Ti] Title: Gut-brain axis: how the microbiome influences anxiety and depression. [So] Source: Trends Neurosci;36(5):305-12, 2013 May. [Is] ISSN: 1878-108X [Cp] Country of publication: England [La] Language: eng [Ab] Abstract: Within the first few days of life, humans are colonized by commensal intestinal microbiota. Here, we review recent findings showing that microbiota are important in normal healthy brain function. We also discuss the relation between stress and microbiota, and how alterations in microbiota influence stress-related behaviors. New studies show that bacteria, including commensal, probiotic, and pathogenic bacteria, in the gastrointestinal (GI) tract can activate neural pathways and central nervous system (CNS) signaling systems. Ongoing and future animal and clinical studies aimed at understanding the microbiota-gut-brain axis may provide novel approaches for prevention and treatment of mental illness, including anxiety and depression. [Pt] Publication type: JOURNAL ARTICLE [Em] Entry month: 1305 [Js] Journal subset: IM [St] Status: In-Data-Review

10 / 1149468

MEDLINE

select to print Photocopy Full text

[PMID]: 23380665 [Au] Autor: Castrén E; Hen R [Ad] Address: Neuroscience Center, University of Helsinki, P.O. Box 56, 00014 Helsinki, Finland. Electronic address: eero.castren@helsinki.fi. [Ti] Title: Neuronal plasticity and antidepressant actions. [So] Source: Trends Neurosci;36(5):259-67, 2013 May. [Is] ISSN: 1878-108X [Cp] Country of publication: England [La] Language: eng [Ab] Abstract: Antidepressant treatments enhance plasticity and increase neurogenesis in the adult brain, but it has been unclear how these effects influence mood. We propose that, like environmental enrichment and exercise, antidepressant treatments enhance adaptability by increasing structural variability within the nervous system at many levels, from proliferating precursors to immature synaptic contacts. Conversely, sensory deprivation and chronic stress reduce this structural variability. Activity-dependent competition within the mood-related circuits, guided by rehabilitation, then selects for the survival and stabilization of those structures that best represent the internal or external milieu. Increased variability together with competition-mediated selection facilitates normal function, such as pattern separation within the dentate gyrus and other mood-related circuits, thereby enhancing adaptability toward novel experiences. [Pt] Publication type: JOURNAL ARTICLE [Em] Entry month: 1305 [Js] Journal subset: IM [St] Status: In-Data-Review

---

page 1 of 114947

go to page

Refine the search

Database : MEDLINE

Advanced form

		Search	in field
1			WordsSubject descriptorMajor Subject descriptorLimitsAuthorTitle wordsAbstract wordsLanguageCountry of publicationName of substancePersonal name as subjectJournalJournal DescriptorISSNPublication typeUnique identifierEntry monthYear of PublicationFulltextClass update dateDeCS CategoryDeCS Category explodedICD-10 CategorySubSetsAffiliation CountryAffiliation
2	and or and not		WordsSubject descriptorMajor Subject descriptorLimitsAuthorTitle wordsAbstract wordsLanguageCountry of publicationName of substancePersonal name as subjectJournalJournal DescriptorISSNPublication typeUnique identifierEntry monthYear of PublicationFulltextClass update dateDeCS CategoryDeCS Category explodedICD-10 CategorySubSetsAffiliation CountryAffiliation
3	and or and not		WordsSubject descriptorMajor Subject descriptorLimitsAuthorTitle wordsAbstract wordsLanguageCountry of publicationName of substancePersonal name as subjectJournalJournal DescriptorISSNPublication typeUnique identifierEntry monthYear of PublicationFulltextClass update dateDeCS CategoryDeCS Category explodedICD-10 CategorySubSetsAffiliation CountryAffiliation

Search engine: iAH v2.6 powered by WWWISIS

BIREME/PAHO/WHO - Latin American and Caribbean Center on Health Sciences Information