Sweet taste sensitivities vary among different inbred mouse strains, partially due to sequence variations in Tas1r3 gene. Whether polymorphisms in Tas1r3 are responsible for the low nerve responses to sweet and umami compounds in these MRL mouse strains is currently under investigation. Nevertheless, our data from gene expression, histology, nerve recording, and behavioral tests all support the conclusion that type II taste receptor cells are selectively affected in MRL/lpr mice. While the etiology may be complex, taste abnormalities are well recognized in patients with Sjo��gren��s syndrome. In human psychophysical studies, Sjo��gren��s syndrome patients show Carfilzomib decreased sensitivities for sweet, bitter, salty, and sour taste compounds. Taste abnormalities in systemic lupus patients, although previously recognized, are not well characterized. The autoimmune disease developed in MRL/lpr mice shares some characteristics with systemic lupus and Sjo��gren��s syndrome. Yet, MRL/lpr mice did not differ significantly in their responses to salty and sour taste compounds in both behavioral and nerve recording experiments compared with controls. However, when SB431542 comparing taste alterations between MRL/lpr model and Sjo��gren��s syndrome patients, one has to consider that many Sjo��gren��s syndrome patients also develop other illnesses and take various medications for treatment, which may complicate their taste abnormalities. One of the advantages of using animal models to study the mechanisms of taste dysfunction is to minimize the effects of other factors. Although not without limitations, these models can provide valuable information for understanding the molecular and cellular bases of taste disorders associated with various diseases. Over the last 100 years there has been a substantial increase in diseases of the male reproductive system including developmental abnormalities, poor semen quality and testicular cancer, especially in developed countries. The rising incidence of type II testicular cancer is highly correlated with infertility as well as more overt problems of reproductive health suggesting that it is an indicator of a broader problem with the general reproductive health of the population. There is concern that exposure to environmental toxicants in utero, especially endocrine disruptors, augments a genetic predisposition for testicular germ cell tumours such as defects in kit signalling, apoptosis, sex determination and telomere regulation. This is particularly pertinent given that the gonocyte-to-spermatogonia transition occurs in late gestation in humans and that Carcinoma in Situ cells have previously been identified as arising from arrested/dysfunctional gonocytes. Taken together these findings suggest that the risk for testicular cancer must therefore be established in utero.