Ad4BP (or SF-1) has been identified as a transcription factor which regulates all the steroidogenic P450 genes in the peripheral organs, and is encoded by the mammalian homologue of Drosophila FTZ-F1 gene. mRNA coding for Ad4BP was detected in the hypothalamus and pituitary of rats by RT-PCR. Immunohistochemical analyses using an antiserum to Ad4BP in the brain and pituitary revealed that the transcription factor is expressed in nuclei of the dorsomedial part of the ventromedial hypothalamus (dmVMH) and in some subpopulation of the adenohypophysial cells. Double immunostaining of the pituitary for Ad4BP and trophic peptide hormones, FSH, TSH, and ACTH, indicated a restricted localization of Ad4BP to the gonadotroph. Disruption of the mouse Ftz-FI gene was clarified to induce severe defects in the organization of the dmVMH and the function of the pituitary gonadotroph. However, some of the dm VMH neurons and pituitary gonadotrophs persisted, which provided a sharp contrast to complete agenesis of the peripheral steroidogenic tissues (adrenal and gonads) in the mutant mouse. Additional abnormalities were seen in the ventrolateral part of VMH and dorsomedial hypothalamic nucleus, both of which do not express Ad4BP but have strong reciprocal fiber-connections with the dmVMH. Aromatase P450-containing cells in the medial preoptico-amygdaloid region, which were devoid of Ad4BP, persisted even in the brain of the gene disrupted mice. The present results clearly showed that the hypothalamic and pituitary Ad4BPs are essential to normal development of the functional VMH and gonadotroph through some mechanism distinct from that in the peripheral steroidogenic tissues. 8 1995 Wiley-Liss, Inc.

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Single dose QIV showed sufficient immunogenicity in patients with inflammatory bowel disease, and a boost in immunization by additional vaccination was not obtained. Additionally, immunogenicity was low in patients receiving infliximab therapy.

Varicella-zoster virus (VZV) is a member of the human alphaherpesvirus family and the causative agent of varicella (chickenpox) and zoster (shingles) (46,47). Varicella is a manifestation of lytic infection that presents as fever and a generalized vesicular rash, usually in childhood; herpes zoster is a localized, painful, vesicular rash caused by VZV reactivation from latency, a characteristic of Herpesviridae infections.One conundrum in VZV research is that VZV is highly infectious as airborne virions during outbreaks of chickenpox, but once it is grown in vitro, it becomes highly cell associated and is propagated only by cell-cell spread. In vitro, VZV particles are degraded in the late endosome (11,12). The degradation depends on the mannose 6-phosphate receptor (5) and occurs after nucleocapsids are released from nuclei and become coated with the tegument and envelope at the transGolgi network (TGN) (45). Recently, insulin-degrading enzyme was identified as a cellular receptor for infection, which VZV binds via its glycoprotein E (gE). This binding occurs under both cell-free and cell-associated conditions (22), but the mechanism of the cell-cell spread of VZV infection has not been elucidated.