p53 protein expression in extrahepatic bile duct cancer

p53 mutations, a tumor suppressor gene located on chromosome 17p, are the most common genetic alterations found in human cancers. Although the p53 expression or mutation has been investigated in a variety of cancers there have been very few studies in extrahepatic bile duct cancers. In this study, we investigated the immunohistochemical expression of p53 in formalin fixed paraffin embedded archival specimens of 36 extrahepatic bile duct cancers in which p53 expression was found in eighteen (50%) cases. There was no significant difference in age, gender, size of tumor, histologic grade, extent of tumor involvement, lymph node metastasis and tumor resectability according to p53 immunoreactivity. Comparison of survival duration according to p53 expression showed no significant difference. In conclusion, we reported 50 percent of p53 expression in extrahepatic bile duct cancers by immunohistochemical staining and we found no prognostic significance of p53 expression in dinicopathologic parameters.     

Symptomatic recurrent carotid stenosis and aneurysmal degeneration after endarterectomy

BACKGROUND: Aneurysmal degeneration of a carotid reconstruction was not recognized until the patient, who was known to have recurrent carotid artery stenosis, had a thromboembolic stroke. This sequelae of carotid endarterectomy is a serious complication, associated with a high morbidity and mortality rate. This review was conducted to establish the risk of transient ischemic attack and stroke for patients found to have recurrent carotid stenosis associated with aneurysmal degeneration of the carotid artery after endarterectomy. METHODS: A case is reported, and 100 literature references of aneurysmal degeneration of the carotid artery after endarterectomy were reviewed. RESULTS: False aneurysm from anastomotic disruption was the most common presentation identified in the cases reviewed. Nineteen of the patients had a significant neurologic event; however, three (50%) of six patients with aneurysm and recurrent carotid artery stenosis had a transient ischemic attack or stroke. CONCLUSIONS: The incidence of neurologic symptoms is markedly increased when recurrent carotid artery stenosis is associated with carotid aneurysm. During postoperative surveillance after endarterectomy, the identification of recurrent carotid artery stenosis requires evaluation for aneurysmal degeneration of the carotid artery with duplex scanning. These patients are at significant risk for transient ischemic attack and stroke. This rare complication merits operative repair.     

Treatment of chronic autoimmune thrombocytopenic purpura with monoclonal anti-D

BACKGROUND: The platelet count increases transiently after treatment with polyclonal anti-D in about 50 percent of D+ patients with autoimmune thrombocytopenic purpura (AITP). The effect is usually attributed to macrophage Fc-receptor blockade by antibody-coated red cells. As polyclonal anti-D is in limited supply, prospective testing was performed on a monoclonal anti-D (MoAb D) in such patients. STUDY DESIGN AND METHODS: Seven D+ patients with chronic AITP received MoAb D intravenously at doses of 47 to 95 microg per kg of body weight. Response was assessed by studying platelet count increment. Hemolysis and red cell-bound MoAb D were measured before and after MoAb D administration. RESULTS: MoAb D red cell binding was demonstrated in all patients at a ratio higher than that observed in AITP patients successfully treated with polyclonal anti-D. However, little or no platelet count increment was observed in six patients, while a transient response was observed in only one (platelet count 97 x 10(9)/L before MoAb D infusion and 163 x 10(9)/L 4 days later). Furthermore, because five patients showed signs of hemolysis and two became anemic, higher doses of MoAb D should be used only with caution in patients with AITP. CONCLUSION: The MoAb D used in this study cannot be proposed as an alternative treatment for patients with AITP.     

Postembryonic neurogenesis in the central nervous system of the tobacco hornworm, Manduca sexta. III. Spatial and temporal patterns of proliferation

Postembryonic neurogenesis leads to a dramatic increase in the number of functional neurons within the segmental ganglia of the moth, Manduca sexta. These adult-specific neurons are generated during larval life by segment-specific arrays of individually identifiable stem cells, or neuroblasts (Nbs). By the end of the feeding larval stage, each Nb has generated a discrete nest of progeny, which ranges in size from less than 10 to more than 70 progeny. The sizes of these identifiable nests of progeny vary in a segment-specific manner, with the thoracic nests containing a greater number of progeny compared with their homologues in the simpler abdominal ganglia. In order to describe those factors that influence the size of the post-embryonic neuronal lineages, we examined the spatial and temporal pattern of postembryonic neurogenesis in the segmental ganglia of Manduca. The rates at which the identifiable nests accumulated progeny were estimated by counting the number of progeny within the nests, using sectioned material isolated from animals at stages ranging from embryonic hatching until the end of the feeding larval stage. All of the postembryonic Nbs began to generate progeny at around the time of the molt to the third larval instar. Each nest added progeny at a rate that was a characteristic of its identity and segment of origin. Although all of the nests within the thorax continued to accumulate progeny throughout the feeding larval stage, several of the abdominal nests showed little or no growth following the molt to the fifth larval instar. The thymidine analog 5-bromo 2-deoxyuridine (5-BrdU) was used to estimate the mitotic rates of the identifiable Nbs. The number of labeled progeny within a nest 24 h after application of 5-BrdU ranged from a low of 1 to 2 to a high of 11 to 13 labeled cells. In some instances there was a good correlation between the estimated mitotic rate of an identified Nb and the rate of growth of its associated nest of progeny. However, several of the identifiable nests accumulated progeny at a slower rate than predicted based on the estimated mitotic rate of the Nb. Cell death appears to be responsible for slowing the growth of the nests during the feeding larval stage. We estimate that 10% to 70% of the neurons generated during the feeding larval stage degenerate within 24 h of their birth. The level of cell death observed within a nest was dependent on both its identity and its segment of origin.