Effects of physostigmine on ketamine-induced anesthesia and analgesia were studied in male Sprague-Dawley rats using behavioral tests. Rats were divided into six groups. Immediately after loss of the righting reflex following an intraperitoneal injection of ketamine 75 mg/kg, each group of rats was given an intraperitoneal injection of either physostigmine 0.05, 0.1, 0.2, 0.4, 0.6 mg/kg or saline as the control, respectively. Physostigmine 0.1 mg/kg caused the greatest antagonistic effect on ketamine anesthesia as indicated by sleeping time, duration of ataxia and motor coordination. The antagonistic effects of physostigmine were reduced by a dose of physostigmine of greater than 0.1 mg/kg. However, at no dose did physostigmine antagonize ketamine analgesia as indicated by the tail-flick latency. Physostigmine (0.4 and 0.6 mg/kg) itself had analgesic and motor-suppressive actions. It can therefore be presumed that there is a limited threshold of the dose of physostigmine which develops an antagonistic effect on ketamine anesthesia due to the motor-suppressive action. It is also confirmed that physostigmine itself produces analgesia, and does not antagonize ketamine-induced analgesia.
To compare the histological features of non-drug-induced and drug-induced coma blister, we performed histopathological and immunopathological studies of four biopsy specimens from three patients with non-drug-induced coma. These results were compared with the previously well-documented histology of drug-induced coma. The findings of the present study of non-drug-induced coma included (a) a variable degree of epidermal cell degeneration, including vacuolation of basal cells, intraepidermal blister formation with pale cytoplasm, and extensive coagulation necrosis with pale nuclei; (b) alteration of the outer root sheath of telogen follicles, ranging from focal necrosis to total coagulation necrosis, and degeneration of sebaceous gland with disappearance of the germinative cell layer; (c) secretory eccrine cells with pyknotic nuclei, vacuolation of the cytoplasm, and intercellular edema, resulting in poorly defined cytoplasm, although the nuclei of the outer basal layer were partially preserved; (d) from slight edema of the vessel wall of the venules to fibrinoid, thrombosis and/or fibrinoid necrotic degeneration of arterioles and venules; and (e) deposits of immunoglobulins or complement as detected by direct immunofluorescent technique in all the three cases. One significant difference between non-drug-induced and drug-induced coma blister was the presence of fibrinoid thrombi in the lumina of non-drug-induced coma blisters. Since one of the three cases of non-drug-induced coma studied in the present report did not show thrombi in the lumina, this feature may not always be available for the differential diagnosis of these two conditions. However, fibrinoid thrombi may be a good marker for the differentiation of these two conditions, when the depth and duration of non-drug-induced coma are severe enough to induce these lesions.
A spinal block was performed in a post-laminectomy patient, using both ultrasound imaging and X-ray imaging. Ultrasound imaging clearly identified the L3/4 intervertebral level, the spinal canal, the corpus vertebrae, and the dura mater. Using ultrasound imaging, we measured the distance from the skin surface to the dura mater (39 mm). A 25-G needle for the spinal block was accurately advanced into the spinal canal with the use of X-ray imaging (43 mm from the skin to the subarachnoid space). We report here that ultrasound imaging was useful for performing a spinal block in a post-laminectomy patient in whom there was anatomical change around the spine.
Recent evidence has suggested that carcinoma is accompanied by the loss of cell polarity. An epithelial cell-specific form of the AP-1 clathrin adaptor complex, AP1B, is involved in the polarized transport of membrane proteins to the basolateral surface of epithelial cells. In our study, we investigated whether AP1B is involved in intestinal tumorigenesis. The cellular polarity of intestinal tumor cells was examined using APC Min/1 mice as an in vivo model and SW480 cells with a truncating mutation in the adenomatous polyposis coli (APC) gene as an in vitro model by confocal microscopy. Next, the expression of AP1B in intestinal tumor cells was examined by real-time polymerase chain reaction (PCR) and Western blotting. The localization of b-catenin and the expression of AP1B in the tumor tissue of patients with colorectal cancer were evaluated by confocal microscopy and real-time PCR, respectively, and the relationships among cell polarity, AP1B expression and intestinal tumorigenesis were examined. Cellular polarity was lost in intestinal tumor cells, and the expression of AP1B was downregulated. In addition, the reduction in the expression level of AP1B correlated with the nuclear localization of b-catenin in human colorectal cancer. Our study indicates the close associations between AP1B, intestinal tumorigenesis and mutations in the APC gene. This is the first report to reveal the relationships among AP1B, cellular polarity and intestinal tumorigenesis, and achieving a detailed understanding of AP1B will hopefully lead to discovery of therapeutic targets and novel biomarkers for intestinal cancer.Some of the components involved in basolateral transport have recently been identified, including an epithelial cell-specific form of the AP-1 clathrin adaptor complex, AP1B.
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