Histology and histopathology Vol.21, nº 6 (2006)
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- PublicationOpen AccessConjugated linoleic acids CLAs and white adipose tissue: how both in vitro and in vivo studies tell the story of a relationship(Murcia : F. Hernández, 2006) Domeneghini, C.; Di Giancamillo, A.; Corino, C.The distribution of adipose tissue in mammals is dependent on genetic and environmental factors, and in health the fundamental role of adipocytes is to store triacylglycerol during energetic excess and to mobilize this reserve during energy expenditure or reduced food intake. This requires an accurate balance, which is maintained through the interactions of several regulatory factors, as well as dietary manipulations. Dietary supplementation with CLAs (conjugated linoleic acids) is regarded as promising in many mammalian species for obtaining good body mass repartition and diminution of fat depots. CLAs are a group of positional and geometric isomers of conjugated dienoic derivatives of linoleic acid, naturally present in foods originating from ruminant species, and normally present in human adipose tissue. CLAs can, however, also be obtained as commercial supplements, usually containing synthetically prepared isomeric mixtures, and as dietary supplements CLAs are widely used by obese people, above all in the USA and Europe. CLAs are claimed to have protective effects against human degenerative pathologies, such as cancer, atherosclerosis, and diabetes, as well as showing beneficial effects on immune functions and food and energy intakes. The mechanisms of action of CLAs are not fully clarified at present, because in vitro and in vivo studies are not always in agreement, and possibly because CLAs act in different ways and with different consequences when administered in the diet to different species. The present review summarizes the ascertained mechanisms of action of CLAs, the mammalian species of major interest in which important studies have been conducted, and the future prospects for the use of CLAs in both humans and food animal species.
- PublicationOpen AccessPrognostic value of bronchioloalveolar carcinoma component in lung adenocarcinoma(Murcia : F. Hernández, 2006) Lin, D.M.; Ma, Y.; Zheng, S.; Liu, X.Y.; Zou, S.M.; Wei, W.Q.BAC is a common pattern in conventional lung adenocarcinoma. In the past, however, there were no well-defined criteria for BAC. As a result, it was difficult to evaluate the prognosis on this type of lung adenocarcinoma. Though the 1999 WHO classification of BAC provides a useful framework, it does not provide detailed enough information to predict prognosis in lung adenocarcinomas with BAC feature. The aim of this study was to address the prognostic value of bronchioloalveolar carcinoma (BAC) component in lung adenocarcinoma. Ninety-one consecutive surgically treated patients with adenocarcinoma exhibiting various degrees of BAC features and complete follow-up records were retrospectively studied. According to the percentage of BAC component designed as less than 50%, 50%-79%, 80%-99%, and 100% , tumors were classified as type I, type II, type III, and type IV respectively. The overall 5- year survival rate was 64.84%. Multivariate analysis revealed that the four classified types are independent prognostic factors (P=0.0008), as is tumor stage (P=0.0000). The 5-year survival rates were 39.29%, 58.82%, 81.25%, 85.71% for the four classified types respectively, and were 88.89% for stage I, 46.15% for stage II, and 23.81% for stage III. However, the size of tumor (>2 cm) was significant only in the univariate analysis (P=0.0275). In the patients with tumor size exceeding 2 cm in diameter, the BAC component was also significant to predict prognosis (p=0.0008). In lung adenocarcinoma, the BAC component may prove to be useful to predict the outcome of the patients, and the percentage of BAC pattern and pathological stage appear to be two independent prognostic factors.
- PublicationOpen AccessSmad3 phosphoisoform-mediated signaling during sporadic human colorectal carcinogenesis(Murcia : F. Hernández, 2006) Matsuzaki, K.Transforming growth factor-ß (TGF-ß) signaling occurring during human colorectal carcinogenesis involves a shift in TGF-ß function, reducing the cytokine’s antiproliferative effect, while increasing actions that promote invasion and metastasis. TGF-ß signaling involves phosphorylation of Smad3 at serine residues 208 and 213 in the linker region and serine residues 423 and 425 in the C-terminal region. Exogenous TGF-ß activates not only TGF-ß type I receptor (TßRI) but also c-Jun N-terminal kinase (JNK), changing unphosphorylated Smad3 to its phosphoisoforms: C-terminally phosphorylated Smad3 (pSmad3C) and linker phosphorylated Smad3 (pSmad3L). Either pSmad3C or pSmad3L oligomerizes with Smad4, and translocates into nuclei. While the TßRI/pSmad3C pathway inhibits growth of normal epithelial cells in vivo, JNK/pSmad3L-mediated signaling promotes tumor cell invasion and extracellular matrix synthesis by activated mesenchymal cells. Furthermore, hepatocyte growth factor signaling interacts with TGF-ß to activate the JNK/pSmad3L pathway, accelerating nuclear transport of cytoplasmic pSmad3L. This reduces accessibility of unphosphorylated Smad3 to membrane-anchored TßRI, preventing Smad3C phosphorylation, pSmad3Cmediated transcription, and antiproliferative effects of TGF-ß on epithelial cells. As neoplasia progresses from normal colorectal epithelium through adenoma to invasive adenocarcinoma with distant metastasis, nuclear pSmad3L gradually increases while pSmad3C decreases. The shift from TßRI/pSmad3C-mediated to JNK/pSmad3L-mediated signaling is a major mechanism orchestrating a complex transition of TGF-ß signaling during sporadic human colorectal carcinogenesis. This review summarizes the recent understanding of Smad3 phosphoisoform-mediated signaling, particularly “cross-talk” between Smad3 and JNK pathways that cooperatively promote oncogenic activities. Understanding of these actions should help to develop more effective therapy against human colorectal cancer, involving inhibition of JNK/pSmad3L pathway.
- PublicationOpen AccessZinc ions in the endocrine andexocrine pancreas of zinc deficient rats(Murcia : F. Hernández, 2006) Søndergaard, L.G.; Stoltenberg, M.; Doering, P.; Flyvbjerg, A.; Rungby, J.Objective: Zinc deficiency is a problem world-wide. Zinc and insulin are intimately related, and a reduced zinc intake may affect glucose metabolism. The present study investigates how subclinical zinc deficiency in rats affects glucose metabolism and zinc distribution in the pancreas. Methods: Glucose metabolism was evaluated by blood-glucose, serum insulin, homeostasis model assessment (HOMA), and intraperitoneal glucose tolerance tests. Immersion zincsulphide autometallography (iZnSAMG) was used to describe zinc ion distribution. Results: After 4 weeks on a zinc deficient diet (<10 ppm), the zinc deficient rats had a slightly impaired glucose metabolism characterized by significantly increased blood-glucose levels. No differences in serum insulin, insulin resistance, beta-cell function were observed. The zinc deficient rats had significantly decreased serum zinc without any clinical signs of zinc deficiency. Zinc ion staining intensity of the islets of Langerhans was unaffected by the zinc deficiency. In contrast, the acinar cells in the exocrine pancreas appeared depleted of iZnSAMG grains in the zinc deficient rats when compared with their controls. Though statistically non-significant, a reduction in total zinc of the pancreas was found. Conclusions: The present findings suggest that the endocrine pancreas is able to compensate for the subclinical zinc deficiency as it maintains an adequate zinc ion level in the secretory vesicles for insulin storage. The exocrine pancreas lacks this ability; it exhibits decreased levels of zinc ion staining as a consequence of 4 weeks of reduced zinc intake.
- PublicationOpen AccessExpression of matrix metalloproteinase-9 (gelatinase B) in benign, premalignant and malignant laryngeal lesions(Murcia : F. Hernández, 2006) Peschos, D.; Damala, C.; Stefanou, D.; Tsanou, E.; Assimakopoulos, D.; Vougiouklakis, T.; Charalabopoulos, K.; Agnantis, N.J.The matrix metalloproteinases (MMPs) are a family of proteolytic zinc-containing enzymes, which are responsible for the breakdown of the extracellular matrix components in pathological and physiological conditions. They are involved in basement membrane disruption, stroma and blood vessel penetration, metastasis and more recently there is evidence that they participate in tumor growth and angiogenic events. Matrix metalloproteinase 2 and 9 (MMP 2 and 9) belong to the gelatinases, a subgroup of MMPs, and have the capacity to degrade the triple helix type IV collagen of basal lamina of the basement membrane. With the present study, we tried to demonstrate the expression of MMP-9 immunohistochemically, comparatively in benign, premalignant and malignant lesions of the larynx. We studied 154 laryngeal lesions including 55 squamous cell carcinomas, 8 in situ carcinomas, 54 cases of dysplasia (of low and intermediate grade), 13 papillomas and 24 cases of keratosis. Overexpression of MMP 9 was observed in 74.4% and 50% in invasive and in situ squamous cell carcinomas respectively. In dysplastic cases, in papillomas and in keratoses the percentage of overexpression was 62.9%, 61.53% and 54.16% respectively and the expression of MMP-9 was significantly higher in invasive squamous cell carcinomas compared to dysplasias (p=0.000004). Also significantly higher was the expression of MMP-9 in dysplastic cases compared to papillomas (p=0.023). The MMP-9 expression was related neither to survival nor to the other available clinicopathological parameters (tumor size, grade, clinical stage, lymph node status and patient age). In conclusion, our study indicates that the expression of MMP-9 is up-regulated in a stepwise fashion, with two main steps, the first one, when a dysplastic lesion evolves and the next one, when the dysplasia progresses to invasive carcinoma.
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