Besides this, a recent work showed that spleen cells from infected female mice produced more TNF-a than those from males in response to paracoccin stimulus, which contributes to the greater resistance to PCM presented by female in relation to male mice. Summarizing, the rPb27 immunization combined to fluconazole chemotherapy was efficient to avoid fungal dissemination to spleen and liver of mice and to control yeast cells growth in the lungs after 40 days of treatment, but this control in lungs was lost after the suspension of chemotherapy, 90 days post treatment, this can be due to the short time of treatment, only thirty days. In the literature it was mentioned that resistance to P. brasiliensis infection is determined mainly by the ability of the host to restrict fungal dissemination rather than control fungal growth at the primary site of infection. This containment of the fungus in the lungs can be the first step to PCM control, and, possibly, with a larger time of chemotherapy this disease could be controlled. The specific antibody levels was also evaluated. We demonstrated that immunization of BALB/c mice with rPb27 induced significant levels of all isotypes evaluated after 40 and 90 days of treatment. When this immunization was combined with fluconazole chemotherapy mice developed a pulmonary-restricted PCM associated with low mortality rates and production of significant levels of IgG1, IgG2a and IgG2b isotypes after 40 and 90 days of treatment, with a small production of IgG3 only 40 days after treatment. The presented data showed that the immunization with rPb27 promoted enhanced antifungal protection by fluconazole chemotherapy, decreasing fungal load in lungs after 40 days of treatment and avoiding fungal dissemination to other sites of infection. Thus, rPb27 can be explored as an adjuvant for PCM therapy. FGF19 and its murine ortholog Fgf15 are the founding members of the endocrine FGF subfamily that also includes FGF21 and FGF23. FGF19 and Fgf15 influence a Tubacin variety of metabolic processes including glucose, lipid and bile acid metabolism as well as gall bladder filling. Transgenic overexpression of FGF19 in mouse skeletal muscle results in the accumulation of FGF19 in serum, and reverses high fat diet -induced weight gain and various metabolic defects associated with obesity, including hepatic lipid accumulation, insulin resistance, and increased serum lipid levels. Treatment of leptin deficient ob/ob mice or HFD-induced obese mice with recombinant FGF19 causes an increase in metabolic rate, resulting in weight loss, decreased hepatic triglyceride content and a dramatic improvement in glucose utilization and insulin sensitivity. Very similar metabolic effects have more recently been described for FGF21, the most closely related member of the FGF superfamily to FGF19, suggesting that FGF19 and FGF21 may act through a common receptor pathway.