Obesity is a public health problem that has reached epidemic proportions with an increasing worldwide prevalence. The global emergence of obesity increases the risk of developing chronic metabolic disorders. Thus, it is an economic issue that increased the costs of the comorbidities associated. Moreover, in recent years, it has been demonstrated that obesity is associated with chronic systemic inflammation, this status is conditioned by the innate immune system activation in adipose tissue that promotes an increase in the production and release of pro-inflammatory cytokines that contribute to the triggering of the systemic acute-phase response which is characterized by elevation of acute-phase protein levels. On this regard, low-grade chronic inflammation is a characteristic of various chronic diseases such as metabolic syndrome, cardiovascular disease, diabetes, hypertension, non-alcoholic fatty liver disease, and some cancers, among others, which are also characterized by obesity condition. Thus, a growing body of evidence supports the important role that is played by the inflammatory response in obesity condition and the pathogenesis of chronic diseases related.

Collagen degradation by matrix metalloproteinases is the limiting step in reversing liver fibrosis. Although collagen production in cirrhotic livers is increased, the expression and/or activity of matrix metalloproteinases could be normal, increased in early fibrosis, or decreased during advanced liver cirrhosis. Hepatic stellate cells are the main producers of collagens and matrix metalloproteinases in the liver. Therefore, we sought to investigate whether they simultaneously produce alpha1(I) collagen and matrix metalloproteinase-13 mRNAs. In this communication we show that expression of matrix metalloproteinase-13 mRNA is reciprocally modulated by tumor necrosis factor-alpha and transforming growth factor-beta1. When hepatic stellate cells are co-cultured with hepatocytes, matrix metalloproteinase-13 mRNA is up-regulated and alpha1(I) collagen is down-regulated. Injuring hepatocytes with galactosamine further increased matrix metalloproteinase-13 mRNA production. Confocal microscopy and differential centrifugation of co-cultured cells revealed that matrix metalloproteinase-13 is localized mainly within hepatic stellate cells. Studies performed with various hepatic stellate cell lines revealed that they are heterogeneous regarding expression of matrix metalloproteinase-13. Those with myofibroblastic phenotypes produce more type I collagen whereas those resembling freshly isolated hepatic stellate cells express matrix metalloproteinase-13. Overall, these findings strongly support the notion that alpha1(I) collagen and matrix metalloproteinase-13 mRNAs are reciprocally modulated.

Background: HPV infection in women from developing countries is an important public health problem. Therefore, we sought to determine the prevalences of HPV infection and HPV genotypes in a female population of Durango City, Mexico. Also to determine whether any socio-demographic characteristic from the women associated with HPV infection exists.

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-α (TNF-α) 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-α and CRP were determined. Two cohorts were established (leptin ≤10 ng/ml and >10 ng/ml). Death or survival was followed through 30 days. The relationship between leptin (≤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-α 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 ≧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.

Functional and morphological alterations were generated by p.o. (per os) administration of a single oral dose of carbon tetrachloride (CCl4; 0.125 mL/kg b.w., equivalent to 293 mg/kg) to adult male Wistar rats. CCl4 significantly increased (p < 0.05) the serum activities of alanine aminotransferase (ALT; 7478 ± 1044%) and aspartate aminotransferase (AST; 6964 ± 833%), compared to control rats; CCl4 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). CCl4 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 CCl4: significantly decreased the serum activities of ALT and AST (54 and 65%, respectively), compared to CCl4-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 CCl4-treated rats.