Zinc-finger protein 143 (ZNF143) is a human homolog of Xenopus transcriptional activator staf that is involved in selenocystyl tRNA transcription. We previously showed that ZNF143 expression is induced by treatment with DNA-damaging agents and that it preferentially binds to cisplatin-modified DNA. In this study, the potential function of ZNF143 was investigated. ZNF143 was overexpressed in cisplatin-resistant cells. ZNF143 knockdown in prostate cancer caused increased sensitivity for cisplatin, but not for oxaliplatin, etoposide and vincristine. We also showed that ZNF143 is associated with tumor suppressor gene product p73 but not with p53. p73 could stimulate the binding of ZNF143 to both ZNF143 binding site and cisplatin-modified DNA, and modulate the function of ZNF143. We provide a direct evidence that both Rad51 and flap endonuclease-1 are target genes of ZNF143 and overexpressed in cisplatin-resistant cells. Taken together, these experiments demonstrate that an interplay of ZNF143, p73 and ZNF143 target genes is involved in DNA repair gene expression and cisplatin resistance.

We have generated rats bearing an oxytocin (OXT)-monomeric red fluorescent protein 1 (mRFP1) fusion transgene. The mRFP1 fluorescence was highly visible in ventral part of the supraoptic nucleus (SON) and the posterior pituitary in a whole mount. mRFP1 fluorescence in hypothalamic sections was also observed in the SON, the paraventricular nucleus (PVN), and the internal layer of the median eminence. Salt loading for 5 d caused a marked increase in mRFP1 fluorescence in the SON, the PVN, the median eminence, and the posterior pituitary. In situ hybridization histochemistry revealed that the expression of the mRNA encoding the OXT-mRFP1 fusion gene was observed in the SON and the PVN of euhydrated rats and increased dramatically after chronic salt loading. The expression of the endogenous OXT and the arginine vasopressin (AVP) genes were significantly increased in the SON and the PVN after chronic salt loading in both nontransgenic and transgenic rats. These responses were not different between male and female rats. Compared with nontransgenic rats, euhydrated and salt-loaded male and female transgenic rats showed no significant differences in plasma osmolality, sodium concentration, OXT, and AVP levels. Finally, we succeeded in generating a double-transgenic rat that expresses both the OXT-mRFP1 fusion gene and the AVP-enhanced green fluorescent protein fusion gene. Our new transgenic rats are valuable new tools to study the physiology of the hypothalamo-neurohypophysial system.

The portal triad around the hepatic hilum, including the caudate lobe, was investigated using 106 adult cadavers. The portal vein showed regular branching at the hepatic hilum. The round ligament was attached mainly to the pars umbilicalis of the left branch of the portal vein (81.3%), especially to its lower portion (64.6%). Typical extrahepatic branching of the hepatic artery was noted in 67% of the cadavers. Intrahepatic branching of the middle and left hepatic arteries showed some variations in 9.4% and 12.5% of the cadavers, respectively. The cystic artery originated from the right hepatic artery in 84.4% of the cadavers, and a dual cystic artery was observed in 30.2%.An aberrant hepatic duct, previously reported as an accessory hepatic duct, was observed in 9.0% of the cadavers; each entered the common hepatic duct on the right side. With reference to the course of bile duct and hepatic artery, the middle hepatic artery traversed the left main hepatic duct anteriorly in 13.5% of the cadavers, and ran partly in front of the duct in 52.0%. Furthermore, the right hepatic artery or its branches traversed the right main hepatic duct anteriorly in 9.4% of the cadavers and ran partly in front of the duct in 38.5%. The caudate lobe is supplied by both the right and left branches of the portal triad, mainly by the left. The caudate process is mainly supplied by the posterior branches of the portal triad, being continuous with the posterior segment of the liver.

The patients showed a remarkable improvement of > or = 80%, with the exception of two patients who had an approximately 50% reduction of the total symptomatic scores. Four of eight patients with anosmia subjectively improved whereas the other four patients felt unchanged. All patients who underwent rhinomanometry (n=15) and nasal provocation testing (n = 15) both before and after surgery showed a significant improvement. There were no intraoperative complications. Postoperative epistaxis occurred in one patient. One patient complained of a transient hypesthesia of the soft palate and dry eye. Nasal mucosal tears were observed in approximately 30% of the patients who otherwise showed no severe synechia or persistent crusting.

In our controlled retrospective analysis of medical records in tertiary care academic medical center, we aimed to investigate the therapeutic effects of hyperbaric oxygen (HBO) therapy combined with steroid administration for idiopathic sudden sensorineural hearing loss (ISSNHL) in comparison with that of steroid administration alone. Our subjects were 130 consecutive inpatients with ISSNHL (hearing levels >/=40 dB; time from the onset of hearing loss to the start of treatment /=80 dB, the hearing improvement rate was significantly higher in the HBO group than in the steroid group (51.1 +/- 7.0% vs. 27.1 +/- 7.8%; P < 0.05), while in patients whose initial hearing levels were <80 dB, hearing outcomes were not statistically different between the two groups. In both the HBO and steroid groups, patients with initial hearing levels of <80 dB showed a better hearing improvement rate than those with initial hearing levels of >/=80 dB. In conclusion HBO therapy shows a significant additional effect in combination with steroid therapy for ISSNHL, particularly in patients with severe hearing loss.