118 research outputs found
Captopril prevents intestinal fibrosis by TGF-1 downregulation in TNBS-induced colitis in rats.
No full textNerve growth factor displays stimulatory effects on human skin and lung fibroblasts, demonstrating a direct role for this factor in tissue repair
No full textPrevention of fibrosis in experimental colitis by captopril: the role of TGFβ1. Inflamm Bowel Dis 2004;10:536-545
No full textBACKGROUND & AIMS: There is a body of evidence to suggest that the local
activation of angiotensin II (ANG II) plays a pivotal role in fibrogenic response
involving the kidney, heart, lung, pancreas and liver. In such conditions,
fibrosis is mediated, at least partially, through ANG II induction of the
cytokine transforming growth factor-beta1 (TGF-beta1). Both ANG II and TGF-beta1
also seem to be involved in intestinal fibrosis and stenosis, particularly in
Crohn's disease. The aim of the present study was, firstly, to determine the
effects of the angiotensin-converting enzyme inhibitor, captopril, on colonic
fibrosis in experimental colitis in rats and, secondly, to check the role of
TGF-beta1 on these effects.
METHODS: Colitis was induced in rats by intracolonic administration of TNBS.
Colonic fibrosis was assessed 21 days later by macroscopic and microscopic
evaluation. Levels of collagen alpha1 gene expression, hydroxyproline,
angiotensin II and TGF-beta1 proteins, and TGF-beta1 mRNA were measured on the
colonic tissue.
RESULTS: In chronic colitis, captopril significantly reduced the score of
macroscopic and histologic lesions, as well as the colonic tissue levels of
collagen alpha1, hydroxyproline, ANG II and TGF-beta1 proteins, and TGF-beta1
mRNA.
CONCLUSIONS: These data demonstrate for the first time that the prophylactic
administration of captopril is effective in preventing colonic fibrosis in
TNBS-induced colitis. The antifibrotic action of captopril could be due to the
blockade of TGFbeta-1 overexpression, and/or to a direct down-regulation of
TGFbeta-1 transcript
Desloratadine: a new approach in the treatment of allergy as a systematic disease--pharmacology and clinical overview. Introduction
No full textVerbreitungsmittel der Früchte und Samen
No full textBotanische Wandrafeln. Blatt 10. La tavola raffigura il frutto di un olmo, quello di un carpino, il seme di un pino, un altro alato, il frutto di una clematide, il frutto di un dente di leone, quello di un tipo di epilobio, un seme con pappo, il frutto di un papavero, quello di una carota, di un\u27agrimonia, il frutto di una bidens, quello di una bardana, quello di un geranio, ..., il seme di una celidonia, il frutto di un sorbo, quello del vischio, il frutto del ginepro e quello dell\u27euonimo.Restauro nel 200
Lack of galectin-1 exacerbates chronic hepatitis, liver fibrosis, and carcinogenesis in murine hepatocellular carcinoma model
No full textChronic liver inflammation (CLI) is a risk factor for development of hepatocellular carcinoma (HCC). Galectin-1 (Gal1) is involved in the regulation of inflammation, angiogenesis, and tumorigenesis, exhibiting multiple anti-inflammatory and protumorigenic activities. We aimed to explore its regulatory role in CLI and HCC progression using an established model of CLI-mediated HCC development, Abcb4 [multidrug-resistance 2 (Mdr2)]-knockout (KO) mice, which express high levels of Gal1 in the liver. We generated double-KO (dKO) Gal1- KO/Mdr2-KO mice on C57BL/6 and FVB/N genetic backgrounds and compared HCC development in the generated strains with their parentalMdr2-KO strains. Loss of Gal1 increased liver injury, inflammation, fibrosis, and ductular reaction in dKO mice of both strains starting from an early age. Aged dKO mutants displayed earlier hepatocarcinogenesis and increased tumor size compared with control Mdr2-KO mice. We found that osteopontin, a well-knownmodulator of HCC development, and oncogenic proteins Ntrk2 (TrkB) and S100A4 were overexpressed in dKO compared with Mdr2-KO livers. Our results demonstrate that in Mdr2-KO mice, a model of CLI-mediated HCC, Gal1-mediated protection from hepatitis, liver fibrosis, and HCC initiation dominates over its known procarcinogenic activities at later stages of HCC development. These findings suggest that anti-Gal1 treatmentsmay not be applicable at all stages of CLI-mediated HCC.—Potikha, T., Pappo, O., Mizrahi, L., Olam, D., Maller, S. M., Rabinovich, G. A., Galun, E., Goldenberg, D. S. Lack of galectin-1 exacerbates chronic hepatitis, liver fibrosis, and carcinogenesis in murine hepatocellular carcinoma model.Fil: Potikha, Tamara. Universidad Academica de Hadassa Jerusalem; IsraelFil: Pappo, Orit. Universidad Academica de Hadassa Jerusalem; IsraelFil: Mizrahi, Lina. Universidad Academica de Hadassa Jerusalem; IsraelFil: Olam, Devorah. Universidad Academica de Hadassa Jerusalem; IsraelFil: Maller, Sebastián M.. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; ArgentinaFil: Rabinovich, Gabriel Adrián. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; ArgentinaFil: Galun, Eithan. Universidad Academica de Hadassa Jerusalem; IsraelFil: Goldenberg, Daniel S.. Universidad Academica de Hadassa Jerusalem; Israe
NON-METASTATIC UNRESECTED PAEDIATRIC NON-RHABDOMYOSARCOMA SOFT TISSUE SARCOMAS: RESULTS OF A POOLED ANALYSIS FROM UNITED STATES AND EUROPEAN GROUPS
No full textBACKGROUND: Non-rhabdomyosarcoma soft tissue sarcomas (NRSTS) with initially unresected tumours represent a particular subset of patients with a poor outcome. Various international research groups pooled their data in a joint study in order to investigate prognostic variables and treatment modalities.
METHODS: The study population consisted of 304 patients <21 years old treated between 1980 and 2005 using a multimodality therapeutic strategy.
RESULTS: Synovial sarcoma and malignant peripheral nerve sheath tumour (MPNST) were the most frequent histotypes. Most patients received initial chemotherapy: major responses were recorded in 41% and minor in 16% of cases. Overall survival (OS) was 60.0% and 51.5% at 5 and 10 years, respectively, and it was significantly associated with patient's age, histological subtype, tumour site and size, quality of delayed surgical resection, radiotherapy administration and response to induction chemotherapy. MPNST associated to neurofibromatosis type 1 was the tumour type with the worst rate of response to chemotherapy and the worst outcome.
CONCLUSIONS: In unresected NRSTS patients, radiotherapy and delayed surgery are of crucial importance. Patients who respond to chemotherapy have better chance of survival. However, given the relatively poor prognosis, research on intensive multimodal treatment approaches and novel strategies is warranted
INITIALLY UNRESECTED PEDIATRIC NON RHABDOMYOSARCOMA SOFT TISSUE SARCOMAS: RESULTS OF A POOLED ANALYSIS FROM UNITED STATES AND EUROPEAN COOPERATIVE GROUPS
No full textNon-metastatic unresected paediatric non-rhabdomyosarcoma soft tissue sarcomas: results of a pooled analysis from United States and European groups.
No full textBACKGROUND: Non-rhabdomyosarcoma soft tissue sarcomas (NRSTS) with initially unresected tumours represent a particular subset of patients with a poor outcome. Various international research groups pooled their data in a joint study in order to investigate prognostic variables and treatment modalities.
METHODS: The study population consisted of 304 patients <21 years old treated between 1980 and 2005 using a multimodality therapeutic strategy.
RESULTS: Synovial sarcoma and malignant peripheral nerve sheath tumour (MPNST) were the most frequent histotypes. Most patients received initial chemotherapy: major responses were recorded in 41% and minor in 16% of cases. Overall survival (OS) was 60.0% and 51.5% at 5 and 10 years, respectively, and it was significantly associated with patient's age, histological subtype, tumour site and size, quality of delayed surgical resection, radiotherapy administration and response to induction chemotherapy. MPNST associated to neurofibromatosis type 1 was the tumour type with the worst rate of response to chemotherapy and the worst outcome.
CONCLUSIONS: In unresected NRSTS patients, radiotherapy and delayed surgery are of crucial importance. Patients who respond to chemotherapy have better chance of survival. However, given the relatively poor prognosis, research on intensive multimodal treatment approaches and novel strategies is warranted
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