Fgf15 is necessary to maintain BA homeostasis and prevent liver injury during liver regeneration. Moreover, Fgf15 is an essential mediator of the liver growth-promoting effects of BA. Preoperative administration of this enterokine to patients undergoing liver resection might be useful to reduce damage and foster regeneration.

Data concerning the effects of GnRHa on weight gain are scarce. Objective: To assess the variation of the body mass index (BMI) in girls during GnRHa treatment for idiopathic central precocious puberty (CPP). Patients and Methods: Semestral anthropometric data from 176 girls treated with goserelin or leuprorelin were analyzed. Results: BMI z-score increased from 1.5 ± 0.1 SD before treatment (n = 176) to 1.7 ± 0.2 SD after 24 months (n = 61, ρ = 0.008). In girls with normal weight before treatment, this variation was greater (n = 112,0.2 ± 0.1 SD, ρ = 0.01) than in those who were overweight (n = 63, -0.9 ± 0.2 SD, ρ = 0.7). In the goserelin group the weight change adjusted for bone age was greater (n = 28, 0.4 ± 0.1 SD) than in the leuprorelin group (n = 5, 0.04 ± 0.1 SD, ρ = 0.05). Conclusions: A slight increase in BMI was noted, mainly in girls with normal weight before treatment. The influence of different GnRHa on weight must be further investigated.We studied the BMI follow-up of girls treated with GnRHa for CPP. PATIENTS AND METHODSThe aim of this longitudinal retrospective study was to evaluate semestral changes in BMI of 176 Brazilian girls treated with GnRHa for idiopatic central precocious puberty (ICPP), regularly seen at a public health reference center (CEDEBA) in the state of Bahia, Brazil, during a 6-year period (1998)(1999)(2000)(2001)(2002)(2003)(2004).

No abstract

Hepatocyte transplantation is the best approach to maintain and propagate differentiated hepatocytes from different species. Host liver has to be adapted for transplanted hepatocytes productive engraftment and proliferation being required a chronic liver injury to eliminate host hepatocytes and provide a proliferative advantage to the transplanted hepatocytes. Most valuable mouse models for xenograft hepatocyte transplantation are based on genetically modified animals to cause a chronic liver damage and to limit host hepatocyte regeneration potential. We present a methodology that generates a chronic liver damage and can be applied to any host mouse strain and animal species based on the inoculation of a recombinant adenovirus to express herpes simplex thymidine kinase in host hepatocytes sensitizing them to ganciclovir treatment. This causes a prolonged liver damage that allows hepatocyte transplantation and generation of regenerative nodules in recipient mouse liver integrated by transplanted cells and host sinusoidal. Obtained chimeric animals maintain functional chimeric nodules for several weeks, ready to be used in any study.

No abstract