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  1 / 1227 MEDLINE  
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[PMID]:25468774
[Au] Autor:Horvathova L; Tillinger A; Sivakova I; Mikova L; Mravec B; Bucova M
[Ad] Endereço:Institute of Experimental Endocrinology, Slovak Academy of Sciences, Vlarska 3, 833 06 Bratislava, Slovakia. Electronic address: ueenlack@savba.sk.
[Ti] Título:Chemical sympathectomy increases neutrophil-to-lymphocyte ratio in tumor-bearing rats but does not influence cancer progression.
[So] Source:J Neuroimmunol;278:255-61, 2015 Jan 15.
[Is] ISSN:1872-8421
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The sympathetic nervous system regulates many immune functions and modulates the anti-tumor immune defense response, too. Therefore, we studied the effect of 6-hydroxydopamine induced sympathectomy on selected hematological parameters and inflammatory markers in rats with Yoshida AH130 ascites hepatoma. We found that chemically sympathectomized tumor-bearing rats had significantly increased neutrophil-to-lymphocyte ratio, leukocyte-to-lymphocyte ratio, and plasma levels of tumor necrosis factor alpha. Although our findings showed that sympathetic denervation in tumor-bearing rats led to increased neutrophil-to-lymphocyte ratio, that is an indicator of the disease progression, we found no significant changes in tumor growth and survival of sympathectomized tumor-bearing rats.
[Mh] Termos MeSH primário: Linfócitos/fisiologia
Neutrófilos/fisiologia
Sarcoma de Yoshida/imunologia
Sarcoma de Yoshida/patologia
Simpatectomia Química
[Mh] Termos MeSH secundário: Animais
Peso Corporal/efeitos dos fármacos
Modelos Animais de Doenças
Progressão da Doença
Eritrócitos
Estimativa de Kaplan-Meier
Leucócitos/efeitos dos fármacos
Leucócitos/fisiologia
Linfócitos/efeitos dos fármacos
Masculino
Neutrófilos/efeitos dos fármacos
Norepinefrina/metabolismo
Oxidopamina/farmacologia
Ratos
Ratos Wistar
Sarcoma de Yoshida/mortalidade
Baço/metabolismo
Simpatolíticos/farmacologia
Fatores de Tempo
Fator de Necrose Tumoral alfa/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Sympatholytics); 0 (Tumor Necrosis Factor-alpha); 8HW4YBZ748 (Oxidopamine); X4W3ENH1CV (Norepinephrine)
[Em] Mês de entrada:1503
[Cu] Atualização por classe:150117
[Lr] Data última revisão:
150117
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:141204
[St] Status:MEDLINE


  2 / 1227 MEDLINE  
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[PMID]:24981848
[Au] Autor:Hori K; Akita H; Nonaka H; Sumiyoshi A; Taki Y
[Ad] Endereço:Division of Cancer Science, Department of Vascular Biology, Institute of Development, Aging and Cancer, Tohoku University, Sendai, Japan.
[Ti] Título:Prevention of cancer recurrence in tumor margins by stopping microcirculation in the tumor and tumor-host interface.
[So] Source:Cancer Sci;105(9):1196-204, 2014 Sep.
[Is] ISSN:1349-7006
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Combretastatins interrupt blood flow of solid tumor vascular networks and lead to necrosis by blocking nutrients. However, tumors recover from tumor blood flow interruption-induced damage and develop viable rims. To investigate why cancer recurs and its prevention, we used a combretastatin derivative, Cderiv (=AC7700), and analyzed changes in tumor-host interface (T-HI) vessels, which were closest to cancer cells in the tumor margin after tumor vessel disruption, and the microenvironment surrounding them. Treatment with Cderiv (10 mg/kg) interrupted tumor blood flow in all regions of LY80 (a variant of Yoshida sarcoma) tumor, but not T-HI vessel blood flow. The same Cderiv dose given 72 h after 5 Gy irradiation stopped T-HI vessel blood flow and prevented cancer recurrence. Treatment in the reverse order, however, did not affect T-HI vessel blood flow. The greatest difference between the two treatments was the occurrence of gradual T-HI edema with the former. Severe T-HI edema compressed T-HI blood vessels, so that circulation stopped. Thus, the distance between a tumor margin and its nearest functioning host vessel became much larger, and the tumor marginal region became a microenvironment that lacked a nutritional supply. Cancer cells in tumor margins received nutrients through two circulation routes: tumor vessels and T-HI vessels. Our starvation methods, which involved treatment with Cderiv 72 h after 5 Gy irradiation, blocked both circulation routes and may have great potential as a clinical strategy to prevent cancer recurrence.
[Mh] Termos MeSH primário: Inibidores da Angiogênese/farmacologia
Bibenzilas/farmacologia
Recidiva Local de Neoplasia/prevenção & controle
Sarcoma de Yoshida/terapia
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Quimiorradioterapia
Ensaios de Seleção de Medicamentos Antitumorais
Edema/induzido quimicamente
Edema/metabolismo
Masculino
Transplante de Neoplasias
Ratos
Fluxo Sanguíneo Regional/efeitos dos fármacos
Sarcoma de Yoshida/irrigação sanguínea
Sarcoma de Yoshida/patologia
Microambiente Tumoral/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Angiogenesis Inhibitors); 0 (Bibenzyls); 0 (Cderiv)
[Em] Mês de entrada:1411
[Cu] Atualização por classe:160221
[Lr] Data última revisão:
160221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140702
[St] Status:MEDLINE
[do] DOI:10.1111/cas.12477


  3 / 1227 MEDLINE  
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[PMID]:24897498
[Au] Autor:Honors MA; Kinzig KP
[Ad] Endereço:a Department of Psychological Sciences and Ingestive Behavior Research Center , Purdue University , West Lafayette , Indiana , USA.
[Ti] Título:Diet-induced obesity and insulin resistance spur tumor growth and cancer cachexia in rats bearing the Yoshida sarcoma.
[So] Source:Nutr Cancer;66(5):872-8, 2014.
[Is] ISSN:1532-7914
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Obesity and insulin resistance are associated with increased risk of cancer and cancer mortality. However, it is currently unknown whether they contribute to the development of cancer cachexia, a syndrome that contributes significantly to morbidity and mortality in individuals with cancer. The present experiment addresses the question of whether preexisting obesity and insulin resistance alter tumor growth and cancer cachexia symptoms in Yoshida sarcoma bearing male rats. Obesity and insulin resistance were induced through 5 weeks of high-fat (HF) diet feeding and insulin resistance was confirmed by intraperitoneal glucose tolerance testing. Chow-fed animals were used as a control group. Following the establishment of insulin resistance, HF- and chow-fed animals were implanted with fragments of the Yoshida sarcoma or received a sham surgery. Tumor growth rate was greater in HF-fed animals, resulting in larger tumors. In addition, cancer cachexia symptoms developed in HF-fed animals but not chow-fed animals during the 18-day experiment. These results support a stimulatory effect of obesity and insulin resistance on tumor growth and cancer cachexia development in Yoshida sarcoma-bearing rats. Future research should investigate the relationship between obesity, insulin resistance, and cancer cachexia in human subjects.
[Mh] Termos MeSH primário: Caquexia/patologia
Dieta Hiperlipídica/efeitos adversos
Resistência à Insulina
Obesidade/patologia
Sarcoma de Yoshida/patologia
[Mh] Termos MeSH secundário: Animais
Glicemia/metabolismo
Composição Corporal
Peso Corporal
Caquexia/etiologia
Ingestão de Energia
Insulina/sangue
Masculino
Obesidade/complicações
Ratos
Ratos Sprague-Dawley
Sarcoma de Yoshida/etiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Insulin)
[Em] Mês de entrada:1502
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140605
[St] Status:MEDLINE
[do] DOI:10.1080/01635581.2014.916325


  4 / 1227 MEDLINE  
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[PMID]:24101584
[Au] Autor:Honors MA; Kinzig KP
[Ad] Endereço:Department of Psychological Sciences and Ingestive Behavior Research Center, Purdue University, 703 Third Street, West Lafayette, IN, 47907, USA, mhonors@purdue.edu.
[Ti] Título:Chronic exendin-4 treatment prevents the development of cancer cachexia symptoms in male rats bearing the Yoshida sarcoma.
[So] Source:Horm Cancer;5(1):33-41, 2014 Feb.
[Is] ISSN:1868-8500
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cancer cachexia is the syndrome of weight loss, loss of appetite, and wasting of skeletal muscle and adipose tissue experienced by many individuals with cancer. Currently, few effective treatment and prevention strategies are available for these patients, due in part to a poor understanding of the mechanisms contributing to cachexia. Insulin resistance has been associated with cancer cachexia in epidemiological, human, and animal research. The present experiment was designed to examine the ability of Exendin-4, a GLP-1 agonist and insulin sensitizing agent, to prevent the development of cachexia symptoms in male Sprague Dawley rats bearing the Yoshida sarcoma. Following tumor implantation or sham surgery, rats were treated daily with saline or Exendin-4 (3 µg/kg body weight/day) and were monitored for tumor growth and cachexia symptoms for 21-23 days. As a result of large variability in treatment effects, data were analyzed separately for animals with large and small tumors. Exendin-4 treatment reduced tumor growth and prevented the development of cancer cachexia symptoms in animals with small, but not large, tumors. In addition, insulin levels were preserved in Exendin-4-treated tumor-bearing animals. The results of this experiment demonstrate a novel preventative therapy for cancer cachexia and a novel use of Exendin-4. Further research is necessary to determine the mechanisms through which Exendin-4 exerts these potent effects.
[Mh] Termos MeSH primário: Caquexia/prevenção & controle
Incretinas/administração & dosagem
Insulina/metabolismo
Peptídeos/administração & dosagem
Sarcoma de Yoshida/tratamento farmacológico
Peçonhas/administração & dosagem
[Mh] Termos MeSH secundário: Animais
Caquexia/etiologia
Carcinogênese
Peptídeo 1 Semelhante ao Glucagon/agonistas
Seres Humanos
Incretinas/farmacologia
Resistência à Insulina
Masculino
Transplante de Neoplasias
Peptídeos/farmacologia
Ratos
Ratos Sprague-Dawley
Sarcoma de Yoshida/complicações
Carga Tumoral/efeitos dos fármacos
Peçonhas/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Incretins); 0 (Insulin); 0 (Peptides); 0 (Venoms); 89750-14-1 (Glucagon-Like Peptide 1); 9P1872D4OL (exenatide)
[Em] Mês de entrada:1409
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:131009
[St] Status:MEDLINE
[do] DOI:10.1007/s12672-013-0163-9


  5 / 1227 MEDLINE  
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[PMID]:23689977
[Au] Autor:Honors MA; Kinzig KP
[Ad] Endereço:Department of Psychological Sciences and Ingestive Behavior Research Center, Purdue University, 703 Third Street, West Lafayette, IN, 47907, USA, mhonors@purdue.edu.
[Ti] Título:Characterization of the Yoshida sarcoma: a model of cancer cachexia.
[So] Source:Support Care Cancer;21(10):2687-94, 2013 Oct.
[Is] ISSN:1433-7339
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:PURPOSE: Cancer cachexia contributes significantly to morbidity and mortality in individuals with cancer. Currently, the mechanisms contributing to the development of cachexia are largely unknown, leading to a paucity of treatment and prevention options. Animal models are necessary in determining causal mechanisms and in testing potential treatments. While the Yoshida sarcoma has been utilized for more than 50 years, the cachexia syndrome produced by this model has not been well characterized in the literature. METHODS: Tumor allografts were subcutaneously implanted in male Sprague Dawley rats (n = 16) and allowed to grow for 23 days. Control animals (n = 16) received a sham surgery. All rats were monitored daily for the presence of hallmark cachexia symptoms. RESULTS: The results demonstrate the presence of decreased body weight gain, as well as lower levels of body adiposity and skeletal muscle mass, in tumor-bearing animals, as compared to controls. CONCLUSIONS: While a large tumor burden was reached, the extent of cachexia was similar to that which is observed in many individuals with cancer cachexia. Future experiments utilizing this model are encouraged to identify mechanisms and effective treatment and prevention strategies.
[Mh] Termos MeSH primário: Caquexia/metabolismo
Caquexia/patologia
Modelos Animais de Doenças
Sarcoma de Yoshida/metabolismo
Sarcoma de Yoshida/patologia
[Mh] Termos MeSH secundário: Animais
Glicemia/metabolismo
Caquexia/sangue
Caquexia/etiologia
Ingestão de Alimentos
Xenoenxertos
Insulina/sangue
Masculino
Ratos
Ratos Sprague-Dawley
Sarcoma de Yoshida/sangue
Perda de Peso
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Insulin)
[Em] Mês de entrada:1404
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130522
[St] Status:MEDLINE
[do] DOI:10.1007/s00520-013-1839-y


  6 / 1227 MEDLINE  
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[PMID]:23200745
[Au] Autor:Fontes-Oliveira CC; Busquets S; Toledo M; Penna F; Paz Aylwin M; Sirisi S; Silva AP; Orpí M; García A; Sette A; Inês Genovese M; Olivan M; López-Soriano FJ; Argilés JM
[Ad] Endereço:Cancer Research Group, Departament de Bioquímica i Biologia Molecular, Facultat de Biologia, Universitat de Barcelona, Diagonal 645 08028-Barcelona, Spain.
[Ti] Título:Mitochondrial and sarcoplasmic reticulum abnormalities in cancer cachexia: altered energetic efficiency?
[So] Source:Biochim Biophys Acta;1830(3):2770-8, 2013 Mar.
[Is] ISSN:0006-3002
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Cachexia is a wasting condition that manifests in several types of cancer, and the main characteristic is the profound loss of muscle mass. METHODS: The Yoshida AH-130 tumor model has been used and the samples have been analyzed using transmission electronic microscopy, real-time PCR and Western blot techniques. RESULTS: Using in vivo cancer cachectic model in rats, here we show that skeletal muscle loss is accompanied by fiber morphologic alterations such as mitochondrial disruption, dilatation of sarcoplasmic reticulum and apoptotic nuclei. Analyzing the expression of some factors related to proteolytic and thermogenic processes, we observed in tumor-bearing animals an increased expression of genes involved in proteolysis such as ubiquitin ligases Muscle Ring Finger 1 (MuRF-1) and Muscle Atrophy F-box protein (MAFBx). Moreover, an overexpression of both sarco/endoplasmic Ca(2+)-ATPase (SERCA1) and adenine nucleotide translocator (ANT1), both factors related to cellular energetic efficiency, was observed. Tumor burden also leads to a marked decreased in muscle ATP content. CONCLUSIONS: In addition to muscle proteolysis, other ATP-related pathways may have a key role in muscle wasting, both directly by increasing energetic inefficiency, and indirectly, by affecting the sarcoplasmic reticulum-mitochondrial assembly that is essential for muscle function and homeostasis. GENERAL SIGNIFICANCE: The present study reports profound morphological changes in cancer cachectic muscle, which are visualized mainly in alterations in sarcoplasmic reticulum and mitochondria. These alterations are linked to pathways that can account for energy inefficiency associated with cancer cachexia.
[Mh] Termos MeSH primário: Caquexia/metabolismo
Núcleo Celular/metabolismo
Mitocôndrias/metabolismo
Músculo Esquelético/metabolismo
Atrofia Muscular/metabolismo
Sarcoma de Yoshida/metabolismo
Retículo Sarcoplasmático/metabolismo
[Mh] Termos MeSH secundário: Translocador 1 do Nucleotídeo Adenina/genética
Translocador 1 do Nucleotídeo Adenina/metabolismo
Trifosfato de Adenosina/deficiência
Animais
Apoptose/genética
Caquexia/complicações
Caquexia/patologia
Núcleo Celular/ultraestrutura
Metabolismo Energético/genética
Expressão Gênica
Masculino
Mitocôndrias/ultraestrutura
Proteínas Musculares/genética
Proteínas Musculares/metabolismo
Músculo Esquelético/patologia
Atrofia Muscular/complicações
Atrofia Muscular/patologia
Proteólise
Ratos
Ratos Wistar
Proteínas Ligases SKP Culina F-Box/genética
Proteínas Ligases SKP Culina F-Box/metabolismo
Sarcoma de Yoshida/complicações
Sarcoma de Yoshida/patologia
Retículo Sarcoplasmático/ultraestrutura
ATPases Transportadoras de Cálcio do Retículo Sarcoplasmático/genética
ATPases Transportadoras de Cálcio do Retículo Sarcoplasmático/metabolismo
Proteínas com Motivo Tripartido
Ubiquitina-Proteína Ligases/genética
Ubiquitina-Proteína Ligases/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Adenine Nucleotide Translocator 1); 0 (Atp2a1 protein, rat); 0 (Muscle Proteins); 0 (Tripartite Motif Proteins); 8L70Q75FXE (Adenosine Triphosphate); EC 2.3.2.27 (Fbxo32 protein, rat); EC 2.3.2.27 (SKP Cullin F-Box Protein Ligases); EC 2.3.2.27 (Trim63 protein, rat); EC 2.3.2.27 (Ubiquitin-Protein Ligases); EC 3.6.3.8 (Sarcoplasmic Reticulum Calcium-Transporting ATPases)
[Em] Mês de entrada:1306
[Cu] Atualização por classe:161126
[Lr] Data última revisão:
161126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:121204
[St] Status:MEDLINE


  7 / 1227 MEDLINE  
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[PMID]:19544373
[Au] Autor:Hori K; Nishihara M; Yokoyama M
[Ad] Endereço:Division of Cancer Control, Department of Vascular Biology, Institute of Development, Aging and Cancer, Tohoku University, Sendai, Miyagi, Japan. k-hori@idac.tohoku.ac.jp
[Ti] Título:Vital microscopic analysis of polymeric micelle extravasation from tumor vessels: macromolecular delivery according to tumor vascular growth stage.
[So] Source:J Pharm Sci;99(1):549-62, 2010 Jan.
[Is] ISSN:1520-6017
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Particles larger than a specific size have been thought to extravasate from tumor vessels but not from normal vessels. Therefore, various nanoparticles incorporating anticancer drugs have been developed to realize selective drug delivery to solid tumors. However, it is not yet clear whether nanoparticles extravasate readily from all tumor vessels including vessels of microtumors. To answer this question, we synthesized new polymeric micelles labeled with fluorescein isothiocyanate (FITC) and injected them into the tail vein of rats with implanted skinfold transparent chambers. We also analyzed, by means of time-lapse vital microscopy with image analysis, extravasation of FITC micelles from tumor vessels at different stages of growth of Yoshida ascites sarcoma LY80. Polymeric micelles readily leaked from vessels at the interface between normal and tumor tissues and those at the interface between tumor tissues and necrotic areas. The micelles showed negligible extravasation, however, from the vascular network of microtumors less than 1 mm in diameter and did not accumulate in the microtumor. Our results suggest that we must develop a novel therapeutic strategy that can deliver sufficient nanomedicine to microtumors.
[Mh] Termos MeSH primário: Permeabilidade Capilar
Sistemas de Liberação de Medicamentos/métodos
Substâncias Macromoleculares/administração & dosagem
Micelas
Neovascularização Patológica/prevenção & controle
Sarcoma de Yoshida/irrigação sanguínea
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/administração & dosagem
Antineoplásicos/uso terapêutico
Ácido Aspártico/química
Biopolímeros/química
Permeabilidade Capilar/fisiologia
Fluoresceína-5-Isotiocianato/administração & dosagem
Fluoresceína-5-Isotiocianato/farmacocinética
Substâncias Macromoleculares/uso terapêutico
Masculino
Microscopia de Fluorescência/métodos
Transplante de Neoplasias
Neovascularização Patológica/patologia
Polietilenoglicóis/química
Ratos
Ratos Endogâmicos
Sarcoma de Yoshida/tratamento farmacológico
Sarcoma de Yoshida/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Biopolymers); 0 (Macromolecular Substances); 0 (Micelles); 0 (poly(ethylene oxide)-block-poly(beta-benzyl aspartate)); 30IQX730WE (Polyethylene Glycols); 30KYC7MIAI (Aspartic Acid); I223NX31W9 (Fluorescein-5-isothiocyanate)
[Em] Mês de entrada:1011
[Cu] Atualização por classe:151119
[Lr] Data última revisão:
151119
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:090623
[St] Status:MEDLINE
[do] DOI:10.1002/jps.21848


  8 / 1227 MEDLINE  
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[PMID]:19604139
[Au] Autor:Luboldt W; Pinkert J; Matzky C; Wunderlich G; Kotzerke J
[Ad] Endereço:Clinic and Policlinic of Nuclear Medicine, University Hospital Dresden, Fetscherstr. 74, 01307 Dresden, Germany. wolfgang.luboldt@uniklinikum-dresden.de
[Ti] Título:Radiopharmaceutical tracking of particles injected into tumors: a model to study clearance kinetics.
[So] Source:Curr Drug Deliv;6(3):255-60, 2009 Jul.
[Is] ISSN:1567-2018
[Cp] País de publicação:United Arab Emirates
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: Success of selective drug therapies depends on the drug's depot time in the target to treat. Depot time is currently being prolonged, using drug-eluting beads or microspheres for selective internal radiation therapy. The purpose of this study was to establish a model for investigating the depot time of particles injected into tumors in relation to tumor vascularization and particle size. MATERIALS AND METHODS: An animal model with two different vascularized tumors (Walker Carcinoma 256 (hypervascularized) and Yoshida Sarcoma (hypovascularized)) was used. The tumors were implanted into the hind leg of Wistar rats. When the tumors reached 10-15mm, rhenium radiolabeled particles of 25microm and 0.3microm were percutaneously injected into the tumors: large particles (Re-188 microspheres) in 10 hypo- and 10 hypervascularized tumors and small particles (Re-186 sulfid colloid) in 4 hypo- and 16 hypervascularized tumors with the co-injection of the vasoconstrictor, adrenalin (0.01 mg), into 8 hypervascularized tumors. Tumor activity was measured with a gamma camera at 10 min, 1h, 3h, 6h, 14h and 48h p.i. In addition, activity in the lung, liver, spleen, kidneys, and lymph nodes was measured at 48 h p.i. Measurements were adjusted for decay times and then compared. RESULTS: Drainage of the injected particles is bi-phasic, characterized by a fast wash-out. At 10 min p.i., intratumoral activity decreases to 70% of the initially injected activity. This is followed by a slow decline at 48 h p.i in which intratumoral activity decreases to at least 60% of the initially injected activity. Slow decline is independent of particle size and vascularization, whereas fast leakage depends on both. Co-injecting adrenalin significantly reduced the wash-out of the small particles. Radiolabeled microspheres accumulated mainly in the lungs, smaller colloids in the liver. CONCLUSIONS: Particle stay time, biodistribution, and stability can be easily monitored as shown in this animal model. The hematogeneous wash-out can be reduced, using larger particles and vasoconstrictors. Prolonged retention is independent of vascularization and particle size and appears to be sufficient for therapy.
[Mh] Termos MeSH primário: Microesferas
Modelos Animais
Neoplasias/metabolismo
Compostos Radiofarmacêuticos/química
Compostos Radiofarmacêuticos/farmacocinética
[Mh] Termos MeSH secundário: Animais
Carcinoma 256 de Walker/irrigação sanguínea
Carcinoma 256 de Walker/metabolismo
Epinefrina/farmacologia
Feminino
Seres Humanos
Injeções Intralesionais
Rim/metabolismo
Fígado/metabolismo
Pulmão/metabolismo
Neoplasias/irrigação sanguínea
Radioisótopos/química
Compostos Radiofarmacêuticos/análise
Ratos
Ratos Wistar
Rênio/química
Sarcoma de Yoshida/irrigação sanguínea
Sarcoma de Yoshida/metabolismo
Albumina Sérica/química
Baço/metabolismo
Enxofre/química
Distribuição Tecidual/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Radioisotopes); 0 (Radiopharmaceuticals); 0 (Serum Albumin); 0 (rhenium sulfur colloid); 70FD1KFU70 (Sulfur); 7440-15-5 (Rhenium); YKH834O4BH (Epinephrine)
[Em] Mês de entrada:0908
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:090717
[St] Status:MEDLINE


  9 / 1227 MEDLINE  
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[PMID]:18366320
[Au] Autor:Rassweiler J; Prager P; Haferkamp A; Alken P; Kauffmann GW; Richter G
[Ad] Endereço:Department of Urology, SLK Kliniken Heilbronn, University of Heidelberg, Germany. jens.rassweiler@slk-kliniken.de
[Ti] Título:Transarterial nephrectomy: the current status of experimental and clinical studies.
[So] Source:J Endourol;22(4):767-82, 2008 Apr.
[Is] ISSN:0892-7790
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Open nephrectomy is associated with significant morbidity. For several years, minimally invasive alternatives have been developed such as laparoscopic nephrectomy or transarterial renal ablation. This paper focuses on the different principles of vaso-occlusion and further improvements of the technique such as capillary chemoembolization in experimental as well as clinical studies. MATERIALS AND METHODS: Based on own in vitro studies, the principle of capillary embolization with occlusion of the entire arterial system up to the capillaries by a precipitating corn protein (Ethibloc) has been developed in animal studies (i.e., rat and canine kidney model). The precipitation speed of Ethibloc can be prolonged by 40% glucose per injection. The organ-ablative efficacy was evaluated in models of unilateral hypertension and chemically induced renal tumors (i.e., dimethyl-nitrosamine). Further studies using the model of unilateral transarterial implantation of Yoshida-sarcoma cells compared capillary chemoembolization using Ethibloc/mitomycin C (MMC) versus chemoperfusion and capillary embolization. Before starting clinical trials, the optimal mixture of Ethibloc and MMC was determined in vitro and in vivo. Prior to the vaso-occlusion, the volume of the arterial system of the kidney is determined by perfusion of the kidney with contrast-dye via a blocked balloon-catheter. Then 25% of the determined volume of 40% glucose is pre-injected followed by Ethibloc/MMC being injected with 1-cm(3) syringes. Once the capillary bed and tumor sinusoids are reached, the balloon catheter is emptied by postinjection of 40% glucose. RESULTS: Capillary embolization proved to be significantly superior to a central (i.e., ligation of renal artery) or peripheral type of occlusion resulting in complete coagulation necrosis of the normal rat and canine kidney with reduction of the elevated blood pressure, similar to nephrectomy in the model of renal hypertension. In the model of chemically induced renal tumors, complete necrosis of T2 stages could be achieved in 83% using Ethibloc compared to only 63% with Gelfoam particles, and 17% after ligation. In T3/T4 stages, the response rate was only 60% versus 0% after central and peripheral occlusion. In the highly aggressive Yoshida-sarcoma model, capillary chemoembolization yielded an 80% complete response rate compared to only 75% after capillary embolization and 70% after chemoperfusion. The optimal mixture of Ethibloc and MMC ranged between 1 and 2 mg of MMC to 1 cm(3) of Ethibloc, therefore for clinical trials 10 mg MMC was added to the 7.5 cm(3) syringe of Ethibloc. Clinical studies included 68 preoperatively as well as 62 palliatively embolized patients with renal cell carcinoma. The procedure was relatively well tolerated and usually associated with a mild postembolization syndrome. After an interval of up to 28 days, complete necrosis of the renal tumor could be achieved in tumors up to 9 cm in diameter. Hematuria ceased in all cases, and in selected cases long-lasting responses of very large tumors (i.e., vena cava involvement) could be achieved. DISCUSSION: Capillary chemoembolization represents an effective concept for ablation of malignant renal tumors. It offers control of tumor growth in case of temporary inoperability as well as cessation of hematuria in a palliative situation. Because of the local ablative efficiency, it may still represent a minimally invasive option in advanced stages of renal carcinoma (i.e., in combination with immunochemotherapy or targeted therapy).
[Mh] Termos MeSH primário: Quimioembolização Terapêutica/métodos
Nefrectomia/métodos
[Mh] Termos MeSH secundário: Animais
Carcinoma de Células Renais/terapia
Diatrizoato/uso terapêutico
Dimetilnitrosamina
Combinação de Medicamentos
Ácidos Graxos/uso terapêutico
Seres Humanos
Hipertensão Renal/terapia
Neoplasias Renais/induzido quimicamente
Neoplasias Renais/terapia
Propilenoglicóis/uso terapêutico
Ratos
Sarcoma de Yoshida/terapia
Soluções Esclerosantes/uso terapêutico
Zeína/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Drug Combinations); 0 (Fatty Acids); 0 (Propylene Glycols); 0 (Sclerosing Solutions); 117-96-4 (Diatrizoate); 9010-66-6 (Zein); 91196-33-7 (alcoholic prolamine solution); M43H21IO8R (Dimethylnitrosamine)
[Em] Mês de entrada:0807
[Cu] Atualização por classe:161018
[Lr] Data última revisão:
161018
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:080328
[St] Status:MEDLINE
[do] DOI:10.1089/end.2007.9826


  10 / 1227 MEDLINE  
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[PMID]:17261345
[Au] Autor:Busquets S; Fuster G; Ametller E; Olivan M; Figueras M; Costelli P; Carbó N; Argilés JM; López-Soriano FJ
[Ad] Endereço:Departament de Bioquímica i Biologia Molecular, Universitat de Barcelona, Diagonal 645, 08028 Barcelona, Spain.
[Ti] Título:Resveratrol does not ameliorate muscle wasting in different types of cancer cachexia models.
[So] Source:Clin Nutr;26(2):239-44, 2007 Apr.
[Is] ISSN:0261-5614
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND & AIMS: Resveratrol has been reported to have antitumoural effects and recently it has been demonstrated that resveratrol partially blocks skeletal muscle wasting by interfering with NF-kappaB activation. We decided to investigate the potential anti-wasting properties of resveratrol on different models of cancer cachexia in experimental animals. METHODS AND RESULTS: Incubations of isolated extensor digitorum longus muscles in the presence of 30 microM of resveratrol caused a significant decrease in the rate of protein degradation. However, administration of resveratrol in vivo to both rats bearing the Yoshida AH-130 ascites hepatoma (at the dose of 1 mg/kg body weight) and mice bearing the Lewis lung carcinoma (at two different doses, 5 and 25 mg/kg body weight) had no effect on skeletal muscle mass or body weight in tumour-bearing rodents. In addition, a combination of resveratrol (3 mg/kg body weight) and fish oil was also unable to induce any changes in skeletal muscle weights. CONCLUSIONS: It is therefore concluded from this study that resveratrol is unable to influence muscle mass in vivo and has no potential role as anticachectic agent for the treatment of muscle wasting associated with tumour growth.
[Mh] Termos MeSH primário: Caquexia/tratamento farmacológico
Proteínas Musculares/metabolismo
Músculo Esquelético/efeitos dos fármacos
Neoplasias Experimentais/metabolismo
Estilbenos/farmacologia
[Mh] Termos MeSH secundário: Animais
Peso Corporal/efeitos dos fármacos
Peso Corporal/fisiologia
Caquexia/metabolismo
Carcinoma Pulmonar de Lewis
Modelos Animais de Doenças
Ingestão de Energia/efeitos dos fármacos
Ingestão de Energia/fisiologia
Óleos de Peixe
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Músculo Esquelético/metabolismo
NF-kappa B/antagonistas & inibidores
Tamanho do Órgão/efeitos dos fármacos
Distribuição Aleatória
Ratos
Ratos Wistar
Sarcoma de Yoshida
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Fish Oils); 0 (Muscle Proteins); 0 (NF-kappa B); 0 (Stilbenes); Q369O8926L (resveratrol)
[Em] Mês de entrada:0706
[Cu] Atualização por classe:130603
[Lr] Data última revisão:
130603
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:070131
[St] Status:MEDLINE



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