The patient was a 70-year-old man who had complained of a terminal miction pain and gross hematuria. A left total nephroureterectomy and partial cystectomy were carried out under the diagnosis of ureteral tumor and bladder tumor. Histopathological examination revealed a spindle cell carcinoma consisting of transitional cell carcinoma grade 3 with sarcomatous proliferation. There were histologically direct transformation of the transitional cell carcinoma into squamous cells, and transformation of the squamous cells into sarcomatous spindle cells. Five months after operation, the patient died from recurrence.
Oral administration of forphenicinol stimulated the production of lipopolysaccharide (LPS)-induced interferon (IFN) in mice up to 21-fold over control when given more than 10 days before the elicitation. The IFN production in mice sensitized with bacillus Calmette-Guerin (BCG) 14 days before LPS injection was further augmented by forphenicinol given after BCG. In addition to the IFN production, forphenicinol increased production of LPS-induced tumor necrosis factor (TNF) in mice sensitized with BCG, and the dose of LPS required to induce TNF was reduced by the drug. Furthermore, forphenicinol augmented the antitumor effect of BCG and LPS on Meth A fibrosarcoma.
Muscle strips from the longitudinal or circular muscle of the chicken rectum were used to determine changes in membrane potential during field stimulation as recorded using the sucrose-gap method. Stimulation with single square pulses (0.1 msec duration) evoked junction potentials elicited by transmitter released from nerve endings. Facilitation in amplitude of excitatory junction potentials (EJPs) was seen during repetitive stimulation in the longitudinal muscle, but in the circular muscle, EJPs reduced. Neither atropine nor hyoscine (up to 10(-5) g/ml) reduced EJPs. These drugs abolished the depression of EJPs in the circular muscle produced by repetitive stimulation. Anticholinesterases (2 X 10(--8)-2 X 10(-6) g/ml) reduced the EJPs. The inhibitory effect was produced without affecting the membrane resistance of smooth muscle and was completely antagonized by atropine (1-(-6) g/ml). Drugs that abolish the adrenergic functions did not affect the EJPs. These results suggest that nerves involved in the EJPs are non-cholinergic and non-adrenergic in nature, and the motor transmission to the smooth muscle may be inhibited by cholinergic nerves, presumably presynaptically.
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