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  1 / 18612 MEDLINE  
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[PMID]:29268133
[Au] Autor:Zhu G; Xu Y; Cen X; Nandakumar KS; Liu S; Cheng K
[Ad] Endereço:Guangdong Provincial Key Laboratory of New Drug Screening and Guangzhou Key Laboratory of Drug Research for Emerging Virus Prevention and Treatment, School of Pharmaceutical Sciences, Southern Medical University, Guangzhou, 510515, China.
[Ti] Título:Targeting pattern-recognition receptors to discover new small molecule immune modulators.
[So] Source:Eur J Med Chem;144:82-92, 2018 Jan 20.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:Pattern recognition receptors (PRRs) are key immune receptors of the innate immune system, which recognize the conserved pathogen-associated molecular patterns (PAMPs) of the invading pathogens. Compared to the adaptive immune receptors, PRRs have three distinguishing features, viz., universal expression, fast response and recognizing many kinds of microbes. Toll-like receptors (TLRs), RIG-I-like receptors (RLRs), C-type lectin receptors (CLRs) and NOD-like receptors (NLRs) recognize viral nucleic acid/bacterial fragments and trigger anti-microbial innate immune responses. Upon recognition of their ligand species, PRRs recruit specific intracellular adaptor proteins to initiate signaling pathways culminating in the activation of nuclear factor-κB (NF-κB), mitogen-activated protein (MAP) kinases and interferon regulatory factors (IRFs) that control the transcription of genes encoding pro-inflammatory factors including type I interferon and other inflammatory cytokines, which are critical for eliminating the potential threat to the host. Here, we summarize the effects of small molecule regulators acting on signaling pathways initiated by TLR, RLR and NLR as well as their influence on innate and adaptive immune responses leading to therapy.
[Mh] Termos MeSH primário: Imunidade Adaptativa/efeitos dos fármacos
Imunidade Inata/efeitos dos fármacos
Fatores Imunológicos/química
Fatores Imunológicos/farmacologia
Receptores de Reconhecimento de Padrão/imunologia
[Mh] Termos MeSH secundário: Animais
Descoberta de Drogas
Seres Humanos
Inflamação/tratamento farmacológico
Inflamação/imunologia
Terapia de Alvo Molecular
Bibliotecas de Moléculas Pequenas/química
Bibliotecas de Moléculas Pequenas/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Immunologic Factors); 0 (Receptors, Pattern Recognition); 0 (Small Molecule Libraries)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171222
[St] Status:MEDLINE


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[PMID]:29157614
[Au] Autor:Dispenzieri A; Kourelis T; Buadi F
[Ad] Endereço:Division of Hematology, Department of Medicine, Medicine, Mayo Clinic, 200 First Street Southwest, Rochester, MN 55905, USA. Electronic address: Dispenzieri.angela@mayo.edu.
[Ti] Título:POEMS Syndrome: Diagnosis and Investigative Work-up.
[So] Source:Hematol Oncol Clin North Am;32(1):119-139, 2018 02.
[Is] ISSN:1558-1977
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:POEMS syndrome is a rare paraneoplastic syndrome secondary to a plasma cell dyscrasia. Recognition of a combination of peripheral neuropathy, organomegaly, endocrinopathy, monoclonal plasmaproliferative disorder, skin changes, papilledema, extravascular volume overload, sclerotic bone lesions, thrombocytosis, and Castleman disease is the first step in managing the disease. Increased blood levels of vascular endothelial growth factor are usually confirmatory. This rare disorder should not be missed, especially if the patient has a putative diagnosis of chronic inflammatory polyradiculoneuropathy, a lambda restricted monoclonal gammopathy, and thrombocytosis, and is not responding as expected to immunomodulatory therapy commonly used for chronic inflammatory polyradiculoneuropathy.
[Mh] Termos MeSH primário: Fatores Imunológicos/uso terapêutico
Síndrome POEMS
[Mh] Termos MeSH secundário: Seres Humanos
Síndrome POEMS/sangue
Síndrome POEMS/diagnóstico
Síndrome POEMS/tratamento farmacológico
Síndrome POEMS/patologia
Plasmócitos/metabolismo
Plasmócitos/patologia
Fator A de Crescimento do Endotélio Vascular/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Immunologic Factors); 0 (Vascular Endothelial Growth Factor A)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171122
[St] Status:MEDLINE


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[PMID]:29231623
[Au] Autor:Alstadhaug KB; Myhr KM; Rinaldo CH
[Ti] Título:Progressive multifocal leukoencephalopathy.
[Ti] Título:Progredierende multifokal leukoencefalopati..
[So] Source:Tidsskr Nor Laegeforen;137(23-24), 2017 12 12.
[Is] ISSN:0807-7096
[Cp] País de publicação:Norway
[La] Idioma:eng; nor
[Ab] Resumo:Progressive multifocal leukoencephalopathy is a rare, opportunistic infection of the central nervous system caused by the John Cunningham virus (JCV). There is no effective antiviral treatment available, and restoring immunocompetence is essential for survival. If this occurs too quickly, however, the inflammatory response may prove fatal. This is an up-to-date review of the disorder, intended for clinicians responsible for immunomodulatory therapy.
[Mh] Termos MeSH primário: Leucoencefalopatia Multifocal Progressiva
[Mh] Termos MeSH secundário: Idoso
Feminino
Seres Humanos
Fatores Imunológicos/efeitos adversos
Vírus JC/isolamento & purificação
Leucoencefalopatia Multifocal Progressiva/induzido quimicamente
Leucoencefalopatia Multifocal Progressiva/diagnóstico
Leucoencefalopatia Multifocal Progressiva/diagnóstico por imagem
Leucoencefalopatia Multifocal Progressiva/terapia
Imagem por Ressonância Magnética
Masculino
Meia-Idade
Tomografia Computadorizada por Raios X
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Immunologic Factors)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171213
[St] Status:MEDLINE
[do] DOI:10.4045/tidsskr.16.1092


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[PMID]:29374471
[Au] Autor:Abu N; Zamberi NR; Yeap SK; Nordin N; Mohamad NE; Romli MF; Rasol NE; Subramani T; Ismail NH; Alitheen NB
[Ad] Endereço:UKM Molecular Biology Institute (UMBI), UKM Medical Center, Jalan Yaacob Latif, Bandar Tun Razak 56000 Cheras, Kuala Lumpur, Malaysia.
[Ti] Título:Subchronic toxicity, immunoregulation and anti-breast tumor effect of Nordamnacantal, an anthraquinone extracted from the stems of Morinda citrifolia L.
[So] Source:BMC Complement Altern Med;18(1):31, 2018 Jan 27.
[Is] ISSN:1472-6882
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Morinda citrifolia L. that was reported with immunomodulating and cytotoxic effects has been traditionally used to treat multiple illnesses including cancer. An anthraquinone derived from fruits of Morinda citrifolia L., nordamnacanthal, is a promising agent possessing several in vitro biological activities. However, the in vivo anti-tumor effects and the safety profile of nordamnacanthal are yet to be evaluated. METHODS: In vitro cytotoxicity of nordamnacanthal was tested using MTT, cell cycle and Annexin V/PI assays on human MCF-7 and MDA-MB231 breast cancer cells. Mice were orally fed with nordamnacanthal daily for 28 days for oral subchronic toxicity study. Then, the in vivo anti-tumor effect was evaluated on 4T1 murine cancer cells-challenged mice. Changes of tumor size and immune parameters were evaluated on the untreated and nordamnacanthal treated mice. RESULTS: Nordamnacanthal was found to possess cytotoxic effects on MDA-MB231, MCF-7 and 4T1 cells in vitro. Moreover, based on the cell cycle and Annexin V results, nordamnacanthal managed to induce cell death in both MDA-MB231 and MCF-7 cells. Additionally, no mortality, signs of toxicity and changes of serum liver profile were observed in nordamnacanthal treated mice in the subchronic toxicity study. Furthermore, 50 mg/kg body weight of nordamncanthal successfully delayed the progression of 4T1 tumors in Balb/C mice after 28 days of treatment. Treatment with nordamnacanthal was also able to increase tumor immunity as evidenced by the immunophenotyping of the spleen and YAC-1 cytotoxicity assays. CONCLUSION: Nordamnacanthal managed to inhibit the growth and induce cell death in MDA-MB231 and MCF-7 cell lines in vitro and cease the tumor progression of 4T1 cells in vivo. Overall, nordamnacanthal holds interesting anti-cancer properties that can be further explored.
[Mh] Termos MeSH primário: Aldeídos/farmacologia
Antraquinonas/farmacologia
Antineoplásicos/farmacologia
Neoplasias da Mama/metabolismo
Fatores Imunológicos/farmacologia
Morinda/química
Extratos Vegetais/farmacologia
[Mh] Termos MeSH secundário: Aldeídos/química
Aldeídos/toxicidade
Animais
Antraquinonas/química
Antraquinonas/toxicidade
Antineoplásicos/química
Antineoplásicos/toxicidade
Apoptose/efeitos dos fármacos
Linhagem Celular Tumoral
Feminino
Seres Humanos
Fatores Imunológicos/química
Fatores Imunológicos/toxicidade
Células MCF-7
Masculino
Camundongos
Camundongos Endogâmicos BALB C
Extratos Vegetais/química
Extratos Vegetais/toxicidade
Testes de Toxicidade Subcrônica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aldehydes); 0 (Anthraquinones); 0 (Antineoplastic Agents); 0 (Immunologic Factors); 0 (Plant Extracts); 0 (nordamnacanthal)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180129
[St] Status:MEDLINE
[do] DOI:10.1186/s12906-018-2102-3


  5 / 18612 MEDLINE  
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[PMID]:29301743
[Au] Autor:Dowlatshahi EA; Diercks G; van Doorn M
[Ad] Endereço:Erasmus Medical Centre, Rotterdam, Netherlands emmilia.dowlat@gmail.com.
[Ti] Título:Blisters in disguise.
[So] Source:BMJ;360:j5364, 2018 01 04.
[Is] ISSN:1756-1833
[Cp] País de publicação:England
[La] Idioma:eng
[Mh] Termos MeSH primário: Vesícula/imunologia
Vesícula/patologia
Pênfigo/imunologia
Pênfigo/patologia
Pele/patologia
[Mh] Termos MeSH secundário: Corticosteroides/administração & dosagem
Corticosteroides/uso terapêutico
Idoso
Vesícula/tratamento farmacológico
Vesícula/epidemiologia
Desmogleínas/imunologia
Diagnóstico Diferencial
Ensaio de Imunoadsorção Enzimática/métodos
Técnica Direta de Fluorescência para Anticorpo/métodos
Seres Humanos
Fatores Imunológicos/administração & dosagem
Fatores Imunológicos/uso terapêutico
Imunossupressores/administração & dosagem
Imunossupressores/uso terapêutico
Incidência
Masculino
Pênfigo/tratamento farmacológico
Pênfigo/epidemiologia
Rituximab/administração & dosagem
Rituximab/uso terapêutico
Pele/imunologia
Resultado do Tratamento
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adrenal Cortex Hormones); 0 (Desmogleins); 0 (Immunologic Factors); 0 (Immunosuppressive Agents); 4F4X42SYQ6 (Rituximab)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180106
[St] Status:MEDLINE
[do] DOI:10.1136/bmj.j5364


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Registro de Ensaios Clínicos
Registro de Ensaios Clínicos
Registro de Ensaios Clínicos
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[PMID]:29224502
[Au] Autor:Connors JM; Jurczak W; Straus DJ; Ansell SM; Kim WS; Gallamini A; Younes A; Alekseev S; Illés Á; Picardi M; Lech-Maranda E; Oki Y; Feldman T; Smolewski P; Savage KJ; Bartlett NL; Walewski J; Chen R; Ramchandren R; Zinzani PL; Cunningham D; Rosta A; Josephson NC; Song E; Sachs J; Liu R; Jolin HA; Huebner D; Radford J; ECHELON-1 Study Group
[Ad] Endereço:From the University of British Columbia and the Department of Medical Oncology, British Columbia Cancer Agency Centre for Lymphoid Cancer, Vancouver, Canada (J.M.C., K.J.S.); the Department of Hematology, Jagiellonian University, Krakow (W.J.), the Department of Hematology, Institute of Hematology a
[Ti] Título:Brentuximab Vedotin with Chemotherapy for Stage III or IV Hodgkin's Lymphoma.
[So] Source:N Engl J Med;378(4):331-344, 2018 01 25.
[Is] ISSN:1533-4406
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Brentuximab vedotin is an anti-CD30 antibody-drug conjugate that has been approved for relapsed and refractory Hodgkin's lymphoma. METHODS: We conducted an open-label, multicenter, randomized phase 3 trial involving patients with previously untreated stage III or IV classic Hodgkin's lymphoma, in which 664 were assigned to receive brentuximab vedotin, doxorubicin, vinblastine, and dacarbazine (A+AVD) and 670 were assigned to receive doxorubicin, bleomycin, vinblastine, and dacarbazine (ABVD). The primary end point was modified progression-free survival (the time to progression, death, or noncomplete response and use of subsequent anticancer therapy) as adjudicated by an independent review committee. The key secondary end point was overall survival. RESULTS: At a median follow-up of 24.6 months, 2-year modified progression-free survival rates in the A+AVD and ABVD groups were 82.1% (95% confidence interval [CI], 78.8 to 85.0) and 77.2% (95% CI, 73.7 to 80.4), respectively, a difference of 4.9 percentage points (hazard ratio for an event of progression, death, or modified progression, 0.77; 95% CI, 0.60 to 0.98; P=0.04). There were 28 deaths with A+AVD and 39 with ABVD (hazard ratio for interim overall survival, 0.73 [95% CI, 0.45 to 1.18]; P=0.20) [corrected]. All secondary efficacy end points trended in favor of A+AVD. Neutropenia occurred in 58% of the patients receiving A+AVD and in 45% of those receiving ABVD; in the A+AVD group, the rate of febrile neutropenia was lower among the 83 patients who received primary prophylaxis with granulocyte colony-stimulating factor than among those who did not (11% vs. 21%). Peripheral neuropathy occurred in 67% of patients in the A+AVD group and in 43% of patients in the ABVD group; 67% of patients in the A+AVD group who had peripheral neuropathy had resolution or improvement at the last follow-up visit. Pulmonary toxicity of grade 3 or higher was reported in less than 1% of patients receiving A+AVD and in 3% of those receiving ABVD. Among the deaths that occurred during treatment, 7 of 9 in the A+AVD group were associated with neutropenia and 11 of 13 in the ABVD group were associated with pulmonary-related toxicity. CONCLUSIONS: A+AVD had superior efficacy to ABVD in the treatment of patients with advanced-stage Hodgkin's lymphoma, with a 4.9 percentage-point lower combined risk of progression, death, or noncomplete response and use of subsequent anticancer therapy at 2 years. (Funded by Millennium Pharmaceuticals and Seattle Genetics; ECHELON-1 ClinicalTrials.gov number, NCT01712490 ; EudraCT number, 2011-005450-60 .).
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Doença de Hodgkin/tratamento farmacológico
Imunoconjugados/administração & dosagem
Fatores Imunológicos/administração & dosagem
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Idoso de 80 Anos ou mais
Protocolos de Quimioterapia Combinada Antineoplásica/efeitos adversos
Bleomicina/administração & dosagem
Dacarbazina/administração & dosagem
Intervalo Livre de Doença
Doxorrubicina/administração & dosagem
Feminino
Seguimentos
Doença de Hodgkin/mortalidade
Seres Humanos
Imunoconjugados/efeitos adversos
Fatores Imunológicos/efeitos adversos
Masculino
Meia-Idade
Estadiamento de Neoplasias
Neutropenia/induzido quimicamente
Taxa de Sobrevida
Vimblastina/administração & dosagem
Adulto Jovem
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE III; COMPARATIVE STUDY; JOURNAL ARTICLE; MULTICENTER STUDY; RANDOMIZED CONTROLLED TRIAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Immunoconjugates); 0 (Immunologic Factors); 11056-06-7 (Bleomycin); 5V9KLZ54CY (Vinblastine); 7GR28W0FJI (Dacarbazine); 7XL5ISS668 (brentuximab vedotin); 80168379AG (Doxorubicin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171212
[Cl] Clinical Trial:ClinicalTrial
[St] Status:MEDLINE
[do] DOI:10.1056/NEJMoa1708984


  7 / 18612 MEDLINE  
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[PMID]:29465579
[Au] Autor:Wang L; Qi CH; Zhong R; Yuan C; Zhong QY
[Ad] Endereço:Department of Pharmacy, Jining No.1 People's Hospital, Jining.
[Ti] Título:Efficacy of alemtuzumab and natalizumab in the treatment of different stages of multiple sclerosis patients.
[So] Source:Medicine (Baltimore);97(8):e9908, 2018 Feb.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Multiple sclerosis (MS) is an autoimmune disease, in which the insulating covers of nerve cells in the brain and spinal cord are demyelinated. This study was conducted to compare the efficacy of alemtuzumab and natalizumab in the treatment of different stages of MS patients. METHODS: A total of 585 patients diagnosed with MS and hospitalized were included and analyzed after which they were divided into the primary progressive MS A and B groups, the relapsing-remitting MS (RRMS) C and D groups, and the secondary progressive MS E and F groups. Patients in A, C, and E groups were administered alemtuzumab while those in B, D, and F groups were administered natalizumab for the treatment. The expanded disability status scale (EDSS) scores and the EDSS difference were calculated before and after treatment. The number of head magnetic resonance imaging enhanced lesions in the patients, recurrence time and recurrence rate were measured before and after treatment. RESULTS: The EDSS score of the RRMS group was significantly lower than that of the primary progressive MS group and the secondary progressive MS group. After 12 months of treatment, the EDSS score of RRMS patients treated with natalizumab was significantly lower compared with the patients with alemtuzumab, and the difference before and after treatment was significantly higher than alemtuzumab. The recurrence rate of the RRMS-D group was significantly lower than the RRMS-C group. After 12 months of treatment, compared with the RRMS-C group, a significant reduction was observed in the number of head magnetic resonance imaging enhanced lesions and longer recurrence time in the RRMS-D group. CONCLUSION: The efficacy of natalizumab was better than alemtuzumab in the treatment of patients in the RRMS group, while there was no significant difference among other stages of MS patients, which provided the theoretical basis and clinical guidance for the treatment of different stages of MS.
[Mh] Termos MeSH primário: Alemtuzumab/uso terapêutico
Fatores Imunológicos/uso terapêutico
Esclerose Múltipla Crônica Progressiva/tratamento farmacológico
Esclerose Múltipla Recidivante-Remitente/tratamento farmacológico
Natalizumab/uso terapêutico
[Mh] Termos MeSH secundário: Adulto
Feminino
Seres Humanos
Imagem por Ressonância Magnética
Masculino
Esclerose Múltipla Crônica Progressiva/diagnóstico por imagem
Esclerose Múltipla Recidivante-Remitente/diagnóstico por imagem
Resultado do Tratamento
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Immunologic Factors); 0 (Natalizumab); 3A189DH42V (Alemtuzumab)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180222
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009908


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[PMID]:28471112
[Au] Autor:Yao F; Lu YQ; Jiang JK; Gu LH; Mou HZ
[Ad] Endereço:Department of Emergency Medicine, the First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310003, China.
[Ti] Título:Immune recovery after fluid resuscitation in rats with severe hemorrhagic shock.
[So] Source:J Zhejiang Univ Sci B;18(5):402-409, 2017 May.
[Is] ISSN:1862-1783
[Cp] País de publicação:China
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To investigate the effects of resuscitation with normal saline (NS), hypertonic saline (HTS), and hydroxyethyl starch (HES) on regulatory T cells (Tregs), helper T 1 (Th1)/Th2 and cytotoxic T 1 (Tc1)/Tc2 profiles in the treatment of hemorrhagic shock. METHODS: Rats subjected to severe hemorrhagic shock were resuscitated for 30 min with NS (n=8), HTS (n=8), or HES (n=8); sham (n=8) and naive control (n=8) groups were used for comparison. Following fluid resuscitation, the whole shed blood was reinfused for 30 min, and the rats were observed with continuous hemodynamic monitoring for 120 min. CD4 CD25 Foxp3 Treg proportions, Th1/Th2 and Tc1/Tc2 profiles in spleen were analyzed by three-color flow cytometry. RESULTS: The proportion of CD4 CD25 Foxp3 Tregs and ratios of Th1/Th2 and Tc1/Tc2 did not differ among control, sham, and HTS groups, but were significantly lower in NS and HES groups (both P<0.05 vs. sham); NS and HES levels were similar. The level of Tc1 was significantly increased in HTS (P<0.05 vs. sham), and levels of Tc2 were increased in NS, HES, and HTS groups compared to sham (all P<0.05), but did not differ from each other. CONCLUSIONS: HTS resuscitation has a greater impact on immune system recovery than NS or HES by preserving the proportion of Tregs and maintaining the balance between Th1/Th2 and Tc1/Tc2 cells in the spleen. Thus, HTS resuscitation provides potential immunomodulatory activity in the early stage after hemorrhagic shock.
[Mh] Termos MeSH primário: Hidratação/métodos
Derivados de Hidroxietil Amido/administração & dosagem
Ressuscitação/métodos
Solução Salina Hipertônica/administração & dosagem
Choque Hemorrágico/imunologia
Choque Hemorrágico/terapia
Cloreto de Sódio/administração & dosagem
[Mh] Termos MeSH secundário: Animais
Imunidade Inata/imunologia
Fatores Imunológicos/administração & dosagem
Masculino
Ratos
Ratos Sprague-Dawley
Recuperação de Função Fisiológica/efeitos dos fármacos
Recuperação de Função Fisiológica/imunologia
Resultado do Tratamento
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Hydroxyethyl Starch Derivatives); 0 (Immunologic Factors); 0 (Saline Solution, Hypertonic); 451W47IQ8X (Sodium Chloride)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1631/jzus.B1600370


  9 / 18612 MEDLINE  
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[PMID]:29353038
[Au] Autor:Yao C; Guo X; Yao WX; Zhang C
[Ad] Endereço:Department of Plastic Surgery, The Second Affiliated Hospital of Xi'an Jiao Tong University, Xi'an, 710004, China.
[Ti] Título:Cereblon (CRBN) deletion reverses streptozotocin induced diabetic osteoporosis in mice.
[So] Source:Biochem Biophys Res Commun;496(3):967-974, 2018 02 12.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Diabetes mellitus is a major cause to induce osteoporosis. Though the pathogenesis of osteoporosis progression has been well investigated, its still not fully understood. Recently, cereblon (CRBN) was considered as a negative modulator of adenosine monophosphate-activated protein kinase (AMPK) in vitro and in vivo. Here, we presented results indicating that CRBN could effectively regulate osteoporosis development. In STZ-induced wild type (WT) mice with diabetes, the osteoclasts were highly increased along with the deterioration of bone structure. However, CRBN knockout (KO) reduced blood glucose the levels and attenuated insulin resistance. What's more, CRBN ablation suppressed osteoclast differentiation and rescued diabetic bone loss in vivo, accompanied with decreased receptor activator of NF-kB ligand (RANKL), RANKL/osteoprotegerin (OPG), and tartrate-resistant acid phosphatase (TRAP) levels, as well as improved AMP-activated kinase (AMPK) α/acetyl-CoA carboxylase (ACC)αactivation. In vitro, suppressing CRBN expression could reduce RANKL-induced osteoclastogenesis, supported by the reduction of TRAP-positive cells. CRBN knockdown (KD) obviously reduced RANKL-induced activity of IκBα/nuclear factor-κB (NF-κB) pathway. In addition, osteoclast-specific genes expression levels stimulated by RANKL were also decreased by CRBN silence. More importantly, CRBN blockage increased phosphorylated AMPK-α and ACC-α expressions in RANKL-incubated cells. However, these processes could be abolished by suppressing AMPK-α with its inhibitor, Compound C. Collectively, our data suggested that CRBN is a potential treatment option against diabetes-induced osteolytic bone disease.
[Mh] Termos MeSH primário: Citocinas/imunologia
Diabetes Mellitus Experimental/imunologia
Diabetes Mellitus Experimental/patologia
Proteínas do Tecido Nervoso/imunologia
Osteoporose/imunologia
Osteoporose/patologia
[Mh] Termos MeSH secundário: Animais
Diabetes Mellitus Experimental/complicações
Fatores Imunológicos/imunologia
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Proteínas do Tecido Nervoso/genética
Osteoporose/etiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Crbn protein, mouse); 0 (Cytokines); 0 (Immunologic Factors); 0 (Nerve Tissue Proteins)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180122
[St] Status:MEDLINE


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[PMID]:29278701
[Au] Autor:Chen C; Wang YY; Wang YX; Cheng MQ; Yin JB; Zhang X; Hong ZP
[Ad] Endereço:School of Pharmaceutical Sciences & Yunnan Key Laboratory of Pharmacology for Natural Products, Kunming Medical University, Kunming, Yunnan, China; Department of Urological Surgery, The 1st Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, China.
[Ti] Título:Gentiopicroside ameliorates bleomycin-induced pulmonary fibrosis in mice via inhibiting inflammatory and fibrotic process.
[So] Source:Biochem Biophys Res Commun;495(4):2396-2403, 2018 01 22.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Pulmonary fibrosis (PF) is a chronic and ultimately fatal interstitial lung disease of various causes. The advent of nintedanib and pirfenidone provides treatment options for PF patients for the first time. However, the adverse effects of the two drugs such as gastrointestinal disorders and hepatic dysfunction often lead to treatment discontinuation. Gentiopicroside (GPS) is a natural secoiridoid glycoside from gentian species of medicinal plants, and has a variety of pharmacological activities, including hepatoprotective and cholagogic, anti-inflammatory, antinociceptive, and smooth muscle relaxing activities. The present study aimed to investigate the therapeutical effects of GPS on bleomycin (BLM)-induced PF in mice. Severe lung inflammation and fibrosis were observed in BLM-treated mice. GPS significantly ameliorated inflammatory and fibrotic responses in lungs of PF mice which were confirmed by histopathological examinations including light microscopy and transmission electron microscopy. Additionally, GPS significantly decreased the levels of inflammatory cytokines including TNF-α and IL-1ß in bronchoalveolar lavage fluid and reduced the content of hydroxyproline in lungs of PF mice. Furthermore, GPS significantly downregulated the expression of TGF-ß1 and CTGF in lungs of PF mice. In vitro, GPS inhibited epithelial-mesenchymal transition of A549 cells stimulated by TGF-ß1, in a dose-dependent manner. Our findings suggest that GPS has the potential as an ideal drug candidate for PF, as it has both anti-inflammatory and anti-fibrotic effects. Alveolar epithelial cells and TGF-ß1 may be the main target cells and molecule of GPS on BLM-induced PF, respectively.
[Mh] Termos MeSH primário: Glucosídeos Iridoides/administração & dosagem
Pulmão/imunologia
Pneumonia/imunologia
Pneumonia/prevenção & controle
Fibrose Pulmonar/imunologia
Fibrose Pulmonar/prevenção & controle
[Mh] Termos MeSH secundário: Animais
Anti-Inflamatórios/administração & dosagem
Bleomicina
Citocinas/imunologia
Relação Dose-Resposta a Droga
Fatores Imunológicos/imunologia
Pulmão/efeitos dos fármacos
Masculino
Camundongos
Pneumonia/induzido quimicamente
Fibrose Pulmonar/induzido quimicamente
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Cytokines); 0 (Immunologic Factors); 0 (Iridoid Glucosides); 0WE09Z21RC (gentiopicroside); 11056-06-7 (Bleomycin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171227
[St] Status:MEDLINE



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