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[PMID]: 25630876
[Au] Autor:Vaillancourt M; Ruffenach G; Meloche J; Bonnet S
[Ad] Address:Pulmonary Hypertension Research Group of The Quebec Heart And Lung Institute Research Centre, Québec City, Québec, Canada....
[Ti] Title:Adaptation and remodelling of the pulmonary circulation in pulmonary hypertension.
[So] Source:Can J Cardiol;31(4):407-15, 2015 Apr.
[Is] ISSN:1916-7075
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Pulmonary arterial hypertension (PAH) is characterized by remodelling of pulmonary arteries caused by a proliferation/apoptosis imbalance within the vascular wall. This pathological phenotype seems to be triggered by different environmental stress and injury events such as increased inflammation, DNA damage, and epigenetic deregulation. It appears that one of the first hit to occur is endothelial cells (ECs) injury and apoptosis, which leads to paracrine signalling to other ECs, pulmonary artery smooth muscle cells (PASMCs), and fibroblasts. These signals promote a phenotypic change of surviving ECs by disturbing different signalling pathways leading to sustained vasoconstriction, proproliferative and antiapoptotic phenotype, deregulated angiogenesis, and formation of plexiform lesions. EC signalling also recruits proinflammatory cells, leading to pulmonary infiltration of lymphocytes, macrophages, and dendritic cells, sustaining the inflammatory environment and autoimmune response. Finally, EC signalling promotes proliferative and antiapoptotic PAH-PASMC phenotypes, which acquire migratory capacities, resulting in increased vascular wall thickness and muscularization of small pulmonary arterioles. Adaptation and remodelling of pulmonary circulation also involves epigenetic components, such as microRNA deregulation, DNA methylation, and histone modification. This review will focus on the different cellular and epigenetic aspects including EC stress response, molecular mechanisms contributing to PAH-PASMC and PAEC proliferation and resistance to apoptosis, as well as epigenetic control involved in adaptation and remodelling of the pulmonary circulation in PAH.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Em] Entry month:1504
[Js] Journal subset:IM
[St] Status:In-Data-Review

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[PMID]: 25534940
[Au] Autor:Cardoso TM; Machado Á; Costa DL; Carvalho LP; Queiroz A; Machado P; Scott P; Carvalho EM; Bacellar O
[Ad] Address:Serviço de Imunologia, Hospital Universitário Prof. Edgard Santos, Universidade Federal da Bahia, Salvador, BA, Brazil Instituto Nacional de Ciência e Tecnologia de Doenças Tropicais (INCT-DT) (CNPq/MCT), Salvador, BA, Brazil....
[Ti] Title:Protective and pathological functions of CD8+ T cells in Leishmania braziliensis infection.
[So] Source:Infect Immun;83(3):898-906, 2015 Mar.
[Is] ISSN:1098-5522
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Cutaneous leishmaniasis (CL) caused by Leishmania braziliensis is characterized by a strong Th1 response that leads to skin lesion development. In areas where L. braziliensis transmission is endemic, up to 15% of healthy subjects have tested positive for delayed-type hypersensitivity to soluble leishmania antigen (SLA) and are considered to have subclinical (SC) infection. SC subjects produce less gamma interferon (IFN-γ) and tumor necrosis factor alpha (TNF-α) than do CL patients, but they are able to control the infection. The aim of this study was to characterized the role of CD8(+) T cells in SC infection and in CL. Peripheral blood mononuclear cells (PBMC) were stimulated with SLA to determine the frequencies of CD4(+) IFN-γ(+) and CD8(+) IFN-γ(+) T cells. Monocytes from PBMC were infected with L. braziliensis and cocultured with CD8(+) T cells, and the frequencies of infected monocytes and levels of cytotoxicity markers, target cell apoptosis, and granzyme B were determined. The frequency of CD8(+) IFN-γ(+) cells after SLA stimulation was higher for SC individuals than for CL patients. The frequency of infected monocytes in SC cells was lower than that in CL cells. CL CD8(+) T cells induced more apoptosis of infected monocytes than did SC CD8(+) T cells. Granzyme B production in CD8(+) T cells was higher in CL than in SC cells. While the use of a granzyme B inhibitor decreased the number of apoptotic cells in the CL group, the use of z-VAD-FMK had no effect on the frequency of these cells. These results suggest that CL CD8(+) T cells are more cytotoxic and may be involved in pathology.
[Mh] MeSH terms primary: CD4-Positive T-Lymphocytes/pathology
Leishmania braziliensis/pathogenicity
Leishmaniasis, Cutaneous/pathology
T-Lymphocytes, Cytotoxic/pathology
[Mh] MeSH terms secundary: Amino Acid Chloromethyl Ketones/pharmacology
Antigens, Protozoan/immunology
Antigens, Protozoan/pharmacology
Apoptosis/drug effects
Asymptomatic Diseases
CD4-Positive T-Lymphocytes/drug effects
CD4-Positive T-Lymphocytes/immunology
Chronic Disease
Coculture Techniques
Cytotoxicity, Immunologic
Enzyme Inhibitors/pharmacology
Granzymes/antagonists & inhibitors
Granzymes/metabolism
Humans
Interferon-gamma/biosynthesis
Interferon-gamma/secretion
Leishmania braziliensis/immunology
Leishmaniasis, Cutaneous/immunology
Leishmaniasis, Cutaneous/parasitology
Lymphocyte Count
Monocytes/immunology
Monocytes/parasitology
Primary Cell Culture
T-Lymphocytes, Cytotoxic/drug effects
T-Lymphocytes, Cytotoxic/immunology
Tumor Necrosis Factor-alpha/biosynthesis
Tumor Necrosis Factor-alpha/secretion
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Name of substance:0 (Amino Acid Chloromethyl Ketones); 0 (Antigens, Protozoan); 0 (Enzyme Inhibitors); 0 (Tumor Necrosis Factor-alpha); 0 (benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone); 82115-62-6 (Interferon-gamma); EC 3.4.21.- (Granzymes)
[Em] Entry month:1504
[Cu] Class update date: 150516
[Lr] Last revision date:150516
[Js] Journal subset:IM
[Da] Date of entry for processing:150214
[St] Status:MEDLINE
[do] DOI:10.1128/IAI.02404-14

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[PMID]: 25623449
[Au] Autor:Yang D; Zhao H; Gao G; Wei K; Zhang L; Han N; Xiao J; Li X; Wang F; Liang H; Zhang W; Wu L
[Ad] Address:The Infectious Diseases Center, Beijing Ditan Hospital, Capital Medical University, Beijing 100015, China....
[Ti] Title:[Relationship between CD4(+) T lymphocyte cell count and the prognosis (including the healing of the incision wound) of HIV/AIDS patients who had undergone surgical operation].
[So] Source:Zhonghua Liu Xing Bing Xue Za Zhi;35(12):1333-6, 2014 Dec.
[Is] ISSN:0254-6450
[Cp] Country of publication:China
[La] Language:chi
[Ab] Abstract:OBJECTIVE: To explore the relationship between CD4(+) T lymphocyte cell count and prognosis as well as healing of the surgical incision in HIV/AIDS patients who had received operation. METHODS: Data were collected and analysed retrospectively from 234 HIV/AIDS patients hospitalized at the Beijing Ditan hospital who underwent operation between January 2008 and December 2012. Following factors were taken into consideration that including:age, gender, time and where that anti-HIV(+) was diagnosed, CD4(+)T lymphocyte cell count at the time of operation, part of the body that being operated, typology of incision, different levels of healing on the surgical incision, infection at the incision site, post-operative complications and the prognosis, etc. Wilcoxon rank sum test, χ(2) test, Kruskal-Wallis H test and Spearman rank correlation were used for statistical analysis to compare the different levels on healing of the incision in relation to the different CD4(+)T lymphocyte cell counts. Rates of level A healing under different CD4(+)T cell counts were also compared. RESULTS: 1) Among the 234 patients including 125 males and 109 females, the average age was 36.17±11.56 years old. Time after discovery of anti-HIV(+)was between 0 and 204 months. The medium CD4(+)T cell count was 388.5 cell/µl; 23.93% of the patients having CD4(+)T lymphocyte cell counts as <200 cell/µl. 2) 7.26% of the operations were emergent. There were 23 different organs affected at the time of operation, due to 48 different kinds of illness. 21.37% of the operations belonged to class I incision, 49.57% was class II incision and 29.06% was class III incision. 86.32% of the incisions resulted in level A healing, 12.51% resulted in level B and 1.71% in level C. 4.27% of the patients developed post-operative complications. Differences between level A healing and level B or C healing in terms of CD4(+)T lymphocyte cell count were not significant (P > 0.05). There was no statistically significant difference on the CD4(+) T lymphocyte count in patients with or without postoperative complications. Difference of the HIV infection time was also not statistically significant between the two groups of patients. Rate of level A healing for the different CD4(+)T lymphocyte cell count was not significant (P > 0.05). Healing of the incision did not show significant correlation with CD4(+) T lymphocyte cell count, duration of antiretroviral therapy or the time that HIV infection was discovered (P > 0.05). CONCLUSION: As long as both the in/exclusion criteria were strictly followed, prognosis for operation on HIV/AIDS seemed to be generally good. Low CD4(+)T lymphocyte cell count should not be taken as a exclusion criteria for operation on HIV/AIDS patients.
[Mh] MeSH terms primary: Acquired Immunodeficiency Syndrome/immunology
CD4 Lymphocyte Count
Surgical Procedures, Operative
[Mh] MeSH terms secundary: Adult
Communicable Diseases
Female
Hospitals
Humans
Male
Middle Aged
Prognosis
Retrospective Studies
T-Lymphocytes
Wound Healing
Young Adult
[Pt] Publication type:ENGLISH ABSTRACT; JOURNAL ARTICLE
[Em] Entry month:1505
[Js] Journal subset:IM
[Da] Date of entry for processing:150127
[St] Status:MEDLINE

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[PMID]: 25482020
[Au] Autor:Hulse KE; Stevens WW; Tan BK; Schleimer RP
[Ad] Address:Division of Allergy-Immunology, Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
[Ti] Title:Pathogenesis of nasal polyposis.
[So] Source:Clin Exp Allergy;45(2):328-46, 2015 Feb.
[Is] ISSN:1365-2222
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Chronic rhinosinusitis with nasal polyps (CRSwNP) is a complex inflammatory condition that affects a large proportion of the population world-wide and is associated with high cost of management and significant morbidity. Yet, there is a lack of population-based epidemiologic studies using current definitions of CRSwNP, and the mechanisms that drive pathogenesis in this disease remain unclear. In this review, we summarize the current evidence for the plethora of factors that likely contribute to CRSwNP pathogenesis. Defects in the innate function of the airway epithelial barrier, including diminished expression of antimicrobial products and loss of barrier integrity, combined with colonization by fungi and bacteria likely play a critical role in the development of chronic inflammation in CRSwNP. This chronic inflammation is characterized by elevated expression of many key inflammatory cytokines and chemokines, including IL-5, thymic stromal lymphopoietin and CCL11, that help to initiate and perpetuate this chronic inflammatory response. Together, these factors likely combine to drive the influx of a variety of immune cells, including eosinophils, mast cells, group 2 innate lymphoid cells and lymphocytes, which participate in the chronic inflammatory response within the nasal polyps. Importantly, however, future studies are needed to demonstrate the necessity and sufficiency of these potential drivers of disease in CRSwNP. In addition to the development of new tools and models to aid mechanistic studies, the field of CRSwNP research also needs the type of robust epidemiologic data that has served the asthma community so well. Given the high prevalence, costs and morbidity, there is a great need for continued research into CRS that could facilitate the development of novel therapeutic strategies to improve treatment for patients who suffer from this disease.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Entry month:1501
[Cu] Class update date: 150516
[Lr] Last revision date:150516
[Js] Journal subset:IM
[St] Status:In-Process
[do] DOI:10.1111/cea.12472

  5 / 451857 MEDLINE  
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[PMID]: 25608891
[Au] Autor:Xu X; Li X; Liu Y
[Ad] Address:Shenzhen Center for Disease Control and Prevention, Shenzhen 518055, China.
[Ti] Title:[Involvement of cellular immunity and humoral immunity in mixed allergy induced by trichloroethylene].
[So] Source:Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi;32(12):881-6, 2014 Dec.
[Is] ISSN:1001-9391
[Cp] Country of publication:China
[La] Language:chi
[Ab] Abstract:OBJECTIVE: To investigate whether cellular immunity and humoral immunity are involved in trichlorethylene (TCE)-induced mixed allergy, then provide the scientific basis for the mechanism of this disease. METHODS: Guinea pigs and rats were tested for this study by application of guinea pig maximization test (GPMT), the animals were randomly divided into negative control, positive control and TCE treatment groups. Animals of these groups were administrated with olive oil, 2, 4-dinitrochlorobenzene (DNCB), and TCE, respectively, by intradermal injection. After TCE administration, rat peripheral blood samples were collected by flow cytometry to detect lymphocytes CD3⁺, CD4⁺, CD8⁺. Guinea pig peripheral blood samples were collected to detect the levels of IgG, IgA, IgM, C3, C4, and the spleens were taken out from guinea pigs after various treatment, mRNA expression of GATA3, T-bet, CTLA4 and Foxp3 in lymphocytes of guinea pig spleen was detected by real-time fluorescent PCR assay. Additionally, TCE allergic dermatitis patients were selected for the study, the peripheral blood samples were collected from the TCE patients group and control group, quantitative PCR was applied to detect mRNA expression of immune-related genes Foxp3, GATA3, CTLA4, T-bet. RESULTS: TCE induced obvious skin allergic reaction in guinea pigs, the sensitization rate was 83.3%, IgG levels in TCE group and positive control increased significantly. Additionally, mRNA expression levels of GATA3, T-bet, CTLA4 significantly elevated in TCE group and positive control, but Foxp3 mRNA levels decreased. The lymphocytes CD3⁺ ratio in TCE group and positive control of rats was higher than that in negative control, we found that there was no statistical difference of CD4⁺, CD8⁺, CD4⁺/CD8⁺ between TCE group and negative control of rats. The mRNA expression levels of Foxp3, GATA3, CTLA4 in TCE patients increased by 115%, 97%, 241%, respectively as compared with the control, T-bet levels decreased by 47%when compared with the control. CONCLUSIONS: TCE could induce obvious changes of cellular immunity and humoral immunity in guinea pigs, rats, and TCE patients, these findings indicated that TCE-induced immunological disorder belongs to the mixed allergy with involvment of cellular immunity and humoral immunity, the mixed allergy might be type IV and type II allergy.
[Mh] MeSH terms primary: Hypersensitivity
Immunity, Cellular/drug effects
Immunity, Humoral/drug effects
Trichloroethylene/toxicity
[Mh] MeSH terms secundary: Allergens
Animals
CTLA-4 Antigen
Guinea Pigs
Humans
Lymphocytes
RNA, Messenger
Rats
Spleen
[Pt] Publication type:ENGLISH ABSTRACT; JOURNAL ARTICLE
[Nm] Name of substance:0 (Allergens); 0 (CTLA-4 Antigen); 0 (RNA, Messenger); 290YE8AR51 (Trichloroethylene)
[Em] Entry month:1505
[Js] Journal subset:IM
[Da] Date of entry for processing:150122
[St] Status:MEDLINE

  6 / 451857 MEDLINE  
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[PMID]: 25106478
[Au] Autor:Yang Y; Boss IW; McIntyre LM; Renne R
[Ti] Title:A systems biology approach identified different regulatory networks targeted by KSHV miR-K12-11 in B cells and endothelial cells.
[So] Source:BMC Genomics;15:668, 2014.
[Is] ISSN:1471-2164
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Kaposi's sarcoma associated herpes virus (KSHV) is associated with tumors of endothelial and lymphoid origin. During latent infection, KSHV expresses miR-K12-11, an ortholog of the human tumor gene hsa-miR-155. Both gene products are microRNAs (miRNAs), which are important post-transcriptional regulators that contribute to tissue specific gene expression. Advances in target identification technologies and molecular interaction databases have allowed a systems biology approach to unravel the gene regulatory networks (GRNs) triggered by miR-K12-11 in endothelial and lymphoid cells. Understanding the tissue specific function of miR-K12-11 will help to elucidate underlying mechanisms of KSHV pathogenesis. RESULTS: Ectopic expression of miR-K12-11 differentially affected gene expression in BJAB cells of lymphoid origin and TIVE cells of endothelial origin. Direct miRNA targeting accounted for a small fraction of the observed transcriptome changes: only 29 genes were identified as putative direct targets of miR-K12-11 in both cell types. However, a number of commonly affected biological pathways, such as carbohydrate metabolism and interferon response related signaling, were revealed by gene ontology analysis. Integration of transcriptome profiling, bioinformatic algorithms, and databases of protein-protein interactome from the ENCODE project identified different nodes of GRNs utilized by miR-K12-11 in a tissue-specific fashion. These effector genes, including cancer associated transcription factors and signaling proteins, amplified the regulatory potential of a single miRNA, from a small set of putative direct targets to a larger set of genes. CONCLUSIONS: This is the first comparative analysis of miRNA-K12-11's effects in endothelial and B cells, from tissues infected with KSHV in vivo. MiR-K12-11 was able to broadly modulate gene expression in both cell types. Using a systems biology approach, we inferred that miR-K12-11 establishes its GRN by both repressing master TFs and influencing signaling pathways, to counter the host anti-viral response and to promote proliferation and survival of infected cells. The targeted GRNs are more reproducible and informative than target gene identification, and our approach can be applied to other regulatory factors of interest.
[Mh] MeSH terms primary: B-Lymphocytes/virology
Endothelial Cells/virology
Herpesvirus 8, Human/genetics
MicroRNAs/genetics
RNA, Viral/genetics
[Mh] MeSH terms secundary: B-Lymphocytes/metabolism
Cell Line, Tumor
Endothelial Cells/metabolism
Gene Regulatory Networks
Herpesviridae Infections/genetics
Herpesviridae Infections/metabolism
Host-Pathogen Interactions
Humans
Immunity, Innate/genetics
Interferons/genetics
Interferons/metabolism
MicroRNAs/metabolism
RNA Interference
RNA, Viral/metabolism
Signal Transduction
Systems Biology
Transcriptome
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Name of substance:0 (MIRN155 microRNA, human); 0 (MicroRNAs); 0 (RNA, Viral); 9008-11-1 (Interferons)
[Em] Entry month:1505
[Cu] Class update date: 150516
[Lr] Last revision date:150516
[Js] Journal subset:IM
[Da] Date of entry for processing:140825
[St] Status:MEDLINE
[do] DOI:10.1186/1471-2164-15-668

  7 / 451857 MEDLINE  
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[PMID]: 25014774
[Au] Autor:Efanov A; Zanesi N; Coppola V; Nuovo G; Bolon B; Wernicle-Jameson D; Lagana A; Hansjuerg A; Pichiorri F; Croce CM
[Ad] Address:Division of Hematology, College of Medicine, Comprehensive Cancer Center, The Ohio State University, Columbus, OH, USA....
[Ti] Title:Human HMGA2 protein overexpressed in mice induces precursor T-cell lymphoblastic leukemia.
[So] Source:Blood Cancer J;4:e227, 2014.
[Is] ISSN:2044-5385
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:T-cell acute lymphoblastic leukemia (T-ALL) is a neoplasia of thymocytes characterized by the rapid accumulation of the precursors of T lymphocytes. HMGA2 (high-mobility group AT-hook 2) gene expression is extremely low in normal adult tissues, but it is overexpressed in many tumors. To identify the biological function of HMGA2, we generated transgenic mice carrying the human HMGA2 gene under control of the VH promoter/Eµ enhancer. Approximately 90% of Eµ-HMGA2 transgenic mice became visibly sick between 4 and 8 months due to the onset and progression of a T-ALL-like disease. Characteristic features included severe alopecia (30% of mice); enlarged lymph nodes and spleen; and profound immunological abnormalities (altered cytokine levels, hypoimmunoglobulinemia) leading to reduced immune responsiveness. Immunophenotyping showed accumulation of CD5+CD4+, CD5+CD8+ or CD5+CD8+CD4+ T-cell populations in the spleens and bone marrow of sick animals. These findings show that HMGA2-driven leukemia in mice closely resembles spontaneous human T-ALL, indicating that HMGA2 transgenic mice should serve as an important model for investigating basic mechanisms and potential new therapies of relevance to human T-ALL.
[Mh] MeSH terms primary: HMGA2 Protein/biosynthesis
Precursor T-Cell Lymphoblastic Leukemia-Lymphoma/metabolism
[Mh] MeSH terms secundary: Animals
Cell Proliferation/physiology
Female
HMGA2 Protein/genetics
HMGA2 Protein/metabolism
Humans
Male
Mice
Mice, Transgenic
Phenotype
Precursor T-Cell Lymphoblastic Leukemia-Lymphoma/genetics
Precursor T-Cell Lymphoblastic Leukemia-Lymphoma/pathology
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (HMGA2 Protein)
[Em] Entry month:1504
[Cu] Class update date: 150516
[Lr] Last revision date:150516
[Js] Journal subset:IM
[Da] Date of entry for processing:140712
[St] Status:MEDLINE
[do] DOI:10.1038/bcj.2014.46

  8 / 451857 MEDLINE  
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[PMID]: 23916838
[Au] Autor:Evans CF; Davtyan H; Petrushina I; Hovakimyan A; Davtyan A; Hannaman D; Cribbs DH; Agadjanyan MG; Ghochikyan A
[Ad] Address:Ichor Medical Systems, San Diego, CA, USA....
[Ti] Title:Epitope-based DNA vaccine for Alzheimer's disease: translational study in macaques.
[So] Source:Alzheimers Dement;10(3):284-95, 2014 May.
[Is] ISSN:1552-5279
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: Clinical trials with passive and active Alzheimer's disease (AD) vaccines suggest that early interventions are needed for improvement of cognitive and/or functional performance in patients, providing impetus for the development of safe and immunologically potent active vaccines targeting amyloid ß (Aß). The AN-1792 trial has indicated that Aß-specific T cells may be unsafe for humans; therefore, other vaccines based on small Aß epitopes are undergoing preclinical and clinical testing. METHODS: Humoral and cellular immune responses elicited in response to a novel DNA epitope-based vaccine (AV-1955) delivered to rhesus macaques using the TriGrid electroporation device were evaluated. Functional activities of anti-Aß antibodies generated in response to vaccination were assessed in vitro. RESULTS: AV-1955 generates long-term, potent anti-Aß antibodies and cellular immune responses specific to foreign T-helper epitopes but not to self-Aß. CONCLUSIONS: This translational study demonstrates that a DNA-based epitope vaccine for AD could be appropriate for human clinical testing.
[Mh] MeSH terms primary: Alzheimer Disease/immunology
Alzheimer Disease/therapy
Alzheimer Vaccines/therapeutic use
Lymphocyte Activation
T-Lymphocytes, Helper-Inducer/physiology
[Mh] MeSH terms secundary: Amyloid beta-Peptides/immunology
Animals
Antibodies/blood
Antibodies/immunology
Cell Line, Tumor
Dose-Response Relationship, Immunologic
Epitopes, T-Lymphocyte
Humans
Immunoglobulin G/blood
Immunoglobulin G/immunology
Longitudinal Studies
Macaca mulatta
Male
Plaque, Amyloid/immunology
Random Allocation
Time Factors
Translational Medical Research
Vaccines, DNA/immunology
Vaccines, DNA/therapeutic use
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Name of substance:0 (Alzheimer Vaccines); 0 (Amyloid beta-Peptides); 0 (Antibodies); 0 (Epitopes, T-Lymphocyte); 0 (Immunoglobulin G); 0 (Vaccines, DNA)
[Em] Entry month:1412
[Cu] Class update date: 150516
[Lr] Last revision date:150516
[Js] Journal subset:IM
[Da] Date of entry for processing:140430
[St] Status:MEDLINE

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[PMID]: 25575489
[Au] Autor:Ago Y; Condro MC; Tan YV; Ghiani CA; Colwell CS; Cushman JD; Fanselow MS; Hashimoto H; Waschek JA
[Ad] Address:Semel Institute for Neuroscience and Human Behavior, Department of Psychiatry and Biobehavioral Sciences, David Geffen School of Medicine, University of California Los Angeles, 635 Charles E. Young Drive South, Los Angeles, CA, 90095, USA.
[Ti] Title:Reductions in synaptic proteins and selective alteration of prepulse inhibition in male C57BL/6 mice after postnatal administration of a VIP receptor (VIPR2) agonist.
[So] Source:Psychopharmacology (Berl);232(12):2181-9, 2015 Jun.
[Is] ISSN:1432-2072
[Cp] Country of publication:Germany
[La] Language:eng
[Ab] Abstract:RATIONALE: An abundance of genetic and epidemiologic evidence as well as longitudinal neuroimaging data point to developmental origins for schizophrenia and other mental health disorders. Recent clinical studies indicate that microduplications of VIPR2, encoding the vasoactive intestinal peptide (VIP) receptor VPAC2, confer significant risk for schizophrenia and autism spectrum disorder. Lymphocytes from patients with these mutations exhibited higher VIPR2 gene expression and VIP responsiveness (cAMP induction), but mechanisms by which overactive VPAC2 signaling may lead to these psychiatric disorders are unknown. OBJECTIVES: We subcutaneously administered the highly selective VPAC2 receptor agonist Ro 25-1553 to C57BL/6 mice from postnatal day 1 (P1) to P14 to determine if overactivation of VPAC2 receptor signaling during postnatal brain maturation affects synaptogenesis and selected behaviors. RESULTS: Western blot analyses on P21 revealed significant reductions of synaptophysin and postsynaptic density protein 95 (PSD-95) in the prefrontal cortex, but not in the hippocampus in Ro 25-1553-treated mice. The same postnatally restricted treatment resulted in a disruption in prepulse inhibition of the acoustic startle measured in adult mice. No effects were observed in open-field locomotor activity, sociability in the three-chamber social interaction test, or fear conditioning or extinction. CONCLUSION: Overactivation of the VPAC2 receptor in the postnatal mouse results in a reduction in synaptic proteins in the prefrontal cortex and selective alterations in prepulse inhibition. These findings suggest that the VIPR2-linkage to mental health disorders may be due in part to overactive VPAC2 receptor signaling during a critical time of synaptic maturation.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1505
[Cu] Class update date: 150515
[Lr] Last revision date:150515
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1007/s00213-014-3848-z

  10 / 451857 MEDLINE  
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[PMID]: 25866806
[Au] Autor:Dobrovinskaya O; Delgado-Enciso I; Quintero-Castro LJ; Best-Aguilera C; Rojas-Sotelo RM; Pottosin I
[Ad] Address:Center for Biomedical Research, University of Colima, 28045 Colima, COL, Mexico....
[Ti] Title:Placing ion channels into a signaling network of T cells: from maturing thymocytes to healthy T lymphocytes or leukemic T lymphoblasts.
[So] Source:Biomed Res Int;2015:750203, 2015.
[Is] ISSN:2314-6141
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:T leukemogenesis is a multistep process, where the genetic errors during T cell maturation cause the healthy progenitor to convert into the leukemic precursor that lost its ability to differentiate but possesses high potential for proliferation, self-renewal, and migration. A new misdirecting "leukemogenic" signaling network appears, composed by three types of participants which are encoded by (1) genes implicated in determined stages of T cell development but deregulated by translocations or mutations, (2) genes which normally do not participate in T cell development but are upregulated, and (3) nondifferentially expressed genes which become highly interconnected with genes expressed differentially. It appears that each of three groups may contain genes coding ion channels. In T cells, ion channels are implicated in regulation of cell cycle progression, differentiation, activation, migration, and cell death. In the present review we are going to reveal a relationship between different genetic defects, which drive the T cell neoplasias, with calcium signaling and ion channels. We suggest that changes in regulation of various ion channels in different types of the T leukemias may provide the intracellular ion microenvironment favorable to maintain self-renewal capacity, arrest differentiation, induce proliferation, and enhance motility.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Em] Entry month:1504
[Cu] Class update date: 150515
[Lr] Last revision date:150515
[Js] Journal subset:IM
[St] Status:In-Process
[do] DOI:10.1155/2015/750203


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