Transitional cell carcinoma (TCC), a urinary bladder tumor with high mortality, is encountered commonly in dogs. Whereas overexpression of epidermal growth factor receptor (EGFR) is associated with development of human urinary bladder cancer, information on EGFR expression in canine TCC is lacking. In this study, EGFR protein and mRNA expression in canine normal bladder (n=5), polypoid cystitis (n=5) and TCC (n=25) were examined by immunohistochemistry and real-time polymerase chain reaction. EGFR protein expression was significantly higher in TCC than that in normal healthy bladder (P<0.001) and polypoid cystitis (P<0.005). High EGFR protein expression was significantly (P<0.01) associated with TCC with a sensitivity of 72% and specificity of 100%. Comparative analysis of protein and mRNA expression levels in TCC showed significant positive correlation (r=0.88, P<0.05) between mRNA and protein expression. These findings suggest that intense expression of EGFR protein could be used as a marker to help canine TCC diagnosis.

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The effects of progesterone (P) on the release of LRH and LH were examined in a sequential double chamber superfusion system by superfusing the medial basal hypothalamus (MBH) and/or pituitaries excised randomly from cycling female rats. Addition of 10 \g=m\lof 10\m=-\6 m oestradiol (E2) to the first chamber resulted in a gradual and significant (60\p=n-\160%) increase in LH release above the pre-injection level from the pituitary in series with MBH. Administration of 10\m=-\8m P after 10\m=-\6m E2 caused a prompt and marked increase (300%) of LH (P < 0.05), whereas 10\m=-\8m P alone had no effect. Administration of 10\m=-\6m E2, 10\m=-\8m P or E2 plus P did not significantly change LH secretion from the pituitary superfused alone. The concentration of LRH in the efflux was significantly increased (150\p=n-\200%) 150 min after 10\m=-\6m E2 administration. P administration after E2 injection produced a prompt and significant increase of LRH and the increase of LRH (300\p=n-\600%) was 2\p=n-\3-fold that produced by E2. P alone had no effect. These data clearly indicate that P enhances E2-induced LH release by increasing LRH secretion from the MBH.

We investigated expression of hsp70 and c-jun mRNA with in situ hybridization for evaluating hypothermia effect on the brain exposed to subarachnoid hemorrhage (SAH). SAH was induced in Wistar rats with endovascular perforation. Animals were divided arbitrarily into normothermic and hypothermic groups, and they were sacrificed at 3 h or 12 h after SAH. The SAH induced hsp70 and c-jun mRNAs in the cerebral cortex, hippocampus, thalamus, hypothalamus, and caudoputamen. Mild hypothermia depressed hsp70 mRNA expression in the cortex, thalamus, and hippocampus. The c-jun mRNA expression was reduced by hypothermia in the cortex, thalamus, and CA1 of the hippocampus. Based on these findings, we speculate that hypothermia protects the brain exposed to SAH by reducing this stress response. Although it is yet difficult to employ hypothermia in the clinical settings, this study suggests its utility to those patients sustaining severe subarachnoid hemorrhage.