BORIS and CTCF are overexpressed in squamous intraepithelial lesions and cervical cancer.

We investigated the expression of Brother of Regulator of Imprinted Sites (BORIS) and CCCTC-binding factor (CTCF) in squamous intraepithelial lesions and cervical cancer. To analyze BORIS and CTCF expression, an endocervical cytobrush sample was taken for total RNA isolation. CTCF and BORIS mRNA was quantified from total RNA using quantitative reverse transcription-polymerase chain reaction. A total of 71 samples were collected and classified according to the Bethesda Classification of squamous intraepithelial lesions. BORIS expression was observed in 9 (12.7%) samples; of these, 5.3, 5.9, 14.8, and 37.5% in the groups that were cytology negative for intraepithelial lesion or malignancy, low-grade squamous intraepithelial lesions (LSIL), high-grade squamous intraepithelial lesions (HSIL), and invasive cervical carcinoma, respectively. The expression level of BORIS was significantly higher in the group with invasive cervical carcinoma as compared with the groups negative for intraepithelial lesion or malignancy, LSIL, and HSIL (P < 0.0005). CTCF mRNA was expressed in all samples. CTCF expression was significantly higher in carcinoma groups compared with LSIL, HSIL, and negative for intraepithelial lesion or malignancy groups. We found that BORIS and CTCF expressions in the LSIL and invasive cervical carcinoma groups were higher than expression in cytological normal samples. Additional studies should be conducted to examine the function of transcription factors during different stages of the transformation of cervical cancer cells.

Protective effect of Ginkgo biloba extract on liver damage by a single dose of CCl(4) in male rats.

Functional and morphological alterations were generated by p.o. (per os) administration of a single oral dose of carbon tetrachloride (CCl(4); 0.125 mL/kg b.w., equivalent to 293 mg/kg) to adult male Wistar rats. CCl(4) significantly increased (p < 0.05) the serum activities of alanine aminotransferase (ALT; 7478 ± 1044%) and aspartate aminotransferase (AST; 6964 ± 833%), compared to control rats; CCl(4) also significantly decreased serum concentration of albumin (23 ± 5.5%) and increased the concentration of malondialhdeyde (MDA) in liver (300 ± 33%). Furthermore, CCl(4) down-regulated the mRNA steady-state level of tumor necrosis factor a(TNF-a). CCl(4) produced necrosis in the central lobe area, extended to the periphery, nuclear alterations (pycnosis, karyolysis and karyorrhexis), and cytoplasmic acidophilia. The pretreatment with 4 mg/kg (p.o.) of Ginkgo biloba extract (GbE), for 5 days, prevented most of the damage caused by CCl(4): significantly decreased the serum activities of ALT and AST (54 and 65%, respectively), compared to CCl(4)-treated rats; GbE partially prevented the increase of liver MDA (55 ± 14%) and the decrease of albumin concentration to 12 ± 0.2%. This pretreatment prevented the down-regulation of TNF-a and up-regulated the interleukine 6 (IL-6) mRNA steady-state level. Moreover, the GbE reduced the amount of necrotic areas in the central lobe area, compared to CCl(4)-treated rats.

Establishment and characterization of porcine aortic endothelial cell cultures with prolonged replicative lifespan by a non-enzymatic method.

The aim of this work was the establishment and characterization of porcine aortic endothelial cell cultures with prolonged lifespan. Endothelial cells where isolated from porcine thoracic aorta and established in primary culture; after sub cultivation, the cells showed typical morphology of endothelial phenotype with cobblestone appearance and growth in monolayer; they were positive against anti-CD31 and anti-CD54 immunostaining and Ac-LDL-Dil uptake. The cells were able to migrate in culture and showed a normal growth curve. The phenotype of our in vitro model of endothelial cells was stable through subcultivation; so, it should be a valuable tool for diverse studies of the endothelial response against physiological and pathological stimulus, particularly it could be useful to study interactions of endothelium with pathogenic bacteria causing diseases in pigs, as they are difficult to study in vivo.

A leptin serum concentration less than 10 ng/ml is a predictive marker of outcome in patients with moderate to severe secondary peritonitis.

INTRODUCTION: Leptin is involved in the sepsis syndrome. A possible relationship exists between low leptin levels and peritonitis severity and a poorer prognosis. OBJECTIVES: We aimed to corroborate the relationship between low leptin serum levels and death in patients with peritonitis and to explore the associations between leptin and interleukin-6 (IL-6), interleukin-10 (IL-10), interleukin-13 (IL-13), tumor necrosis factor-alpha (TNF-alpha) and C-reactive protein (CRP). METHODS: In 230 adult patients with surgically confirmed secondary peritonitis, the Mannheim Peritonitis Index and the serum concentrations of leptin, IL-6, IL-10, IL-13, TNF-alpha and CRP were determined. Two cohorts were established (leptin < or = 10 ng/ml and > 10 ng/ml). Death or survival was followed through 30 days. The relationship between leptin (< or = 10 ng/ml) and death was evaluated using the accumulated incidence ratio (AIR). The association of leptin (dependent variable) with IL-6, IL-10, IL-13, TNF-alpha and CRP (independent variables) was studied by regression analysis. RESULTS: The general mortality rate was 7.8% and the death AIR was 3.15 (p nonsignificant). A subsample of patients with a Mannheim Peritonitis Index > or = 21 was studied, showing a significant AIR of 4.26 (p = 0.017). Regression analysis determined an association only between leptin and IL-6 (p < 0.001), IL-10 (p < 0.047) and CRP (p < 0.001). DISCUSSION: A serum leptin below the threshold of 10 ng/ml is an adverse prognostic marker in patients with moderate to severe secondary peritonitis. The results of the regression analysis suggest that the mechanisms involved are opposing, in that leptin associated with IL-6 has a proinflammatory effect and, through IL-10 and CRP production, restrains the inflammatory response.

The physiological role of estriol during human fetal development is to act as antioxidant at lipophilic milieus of the central nervous system.

Estriol is the most abundant estrogen during human pregnancy, it has a low estrogenic effect and its physiological role is not known. Recently it has been shown that estrogens have antioxidant and free-radical scavenging activity; in free form estrogens are lipophilic, here it is proposed that the role of estriol is to act as antioxidant at level of the developing fetal central nervous system, whose tissues are substantially lipid in nature.

[Bibliometric repercussions of adopting English as the sole language for publication]. / Repercusión bibliométrica de adoptar el inglés como idioma único de publicación.

OBJECTIVE: To determine the effect that the change from French to English had on the impact of the Annales de l' Institut Pasteur. THEORETICAL REFERENCE: The Pasteur Institute journals have a prestige of over 100 years of existence and eight Nobel Prize winners in Physiology and Medicine. Changes through time on the impact of these journals can be monitored as they are included in databases of the ISI (Institute for Scientific Information). METHODS: A year by year analysis from 1974 to 1992 was done using simple regression between percentage of articles published in English and: a) their impact factor; b) their ranking among journals of the same field. RESULTS: The determination coefficient (r2) between the percentage in English and the impact factor was 0.108, and that between percentage in English and the journal's rank in similar publications was 0.178 for the Ann Microbiol, 0.045 for the Ann Immunol and 0.122 for the Ann Virol. CONCLUSIONS: The change of language did not increase the impact factor of the French journals.

[Steroid hormones and the etiopathogenesis of liver lesions of a fibrotic nature]. / Las hormonas esteroides y la etiopatogénesis de padecimientos hepáticos de naturaleza fibrótica.

It has been hypothesized that the hormonal status is involved in the distinct susceptibility between men and women towards the development of hepatobiliary disease because the liver is target organ for steroid hormones. In the development of the fibrogenic phenomenon present in the hepatic cirrhosis of diverse etiology, Ito cells, myofibroblasts as well as some cytokines like transforming growth factor-beta, interleukin-6 and tumor necrosis factor-alpha are involved. It is known that in the organism exist regulatory loops among cytokines, glucocorticoids and sex steroids; in the liver this interaction could affect the fibrogenic phenomenon through Ito cells differentiation. The knowledge of the precise role of glucocorticoids and sex steroids on the fibrogenic mechanisms should allow to support rationally the viability of hormone manipulation for the treatment of hepatic diseases of fibrotic nature.

Are changes in expression of actin genes involved in estrogen-induced cholestasis?

It is postulated that cholestasis associated with high estrogen levels found in women in various conditions, is due to alterations in structure and/or function of the system of actin microfilaments by estrogen-induced changes on expression of actin genes and/or some regulatory actin-binding protein genes. Because bile secretion by hepatocytes is apparently mediated by the microfilamentous system of actin, the proposed hormonally induced dysfunction of this system could be translated to cholestasis.