Is the surgical stress associated with worse survival in patients with esophageal cancer?--Analysis of colon substitution for 37 patients with remnant stomach

BACKGROUND/AIMS: Colon substitution is a standard method of reconstruction, although an aggressive surgery, for patients with esophageal carcinoma who have remnant stomach. Presence of postoperative complication was reported to be a risk factor for worse survival in the patients with esophageal cancer. We evaluated the affect of this surgical stress on the postoperative course and long-term survival of patients with esophageal carcinoma. METHODOLOGY: Between 1980 and 2002, a total of 37 patients with primary thoracic esophageal squamous cell carcinoma, who had history of gastrectomy due to gastric ulcer, underwent R0 esophagectomy followed by colon substitution (colon group). The clinical affect of colon substitution was retrospectively evaluated in comparison with gastric substitution as the control group (stomach group). RESULTS: The postoperative hospital morbidity rate was significantly higher in the patients with remnant stomach than in the control group. Although the clinicopathological features in both groups were similar, except operative time and bleeding volume, the overall and cause-specific survival of the remnant stomach group were significantly worse than those of the control group. Multivariate analysis suggested that remnant stomach was an independent risk factor for a worse survival. CONCLUSIONS: Surgical stress and postoperative complications, resulted by colon substitution for the patients with remnant stomach, might be associated with worse survival of patients with esophageal cancer.     

A new Late Miocene great ape from Kenya and its implications for the origins of African great apes and humans

Extant African great apes and humans are thought to have diverged from each other in the Late Miocene. However, few hominoid fossils are known from Africa during this period. Here we describe a new genus of great ape (Nakalipithecus nakayamai gen. et sp. nov.) recently discovered from the early Late Miocene of Nakali, Kenya. The new genus resembles Ouranopithecus macedoniensis (9.6-8.7 Ma, Greece) in size and some features but retains less specialized characters, such as less inflated cusps and better-developed cingula on cheek teeth, and it was recovered from a slightly older age (9.9-9.8 Ma). Although the affinity of Ouranopithecus to the extant African apes and humans has often been inferred, the former is known only from southeastern Europe. The discovery of N. nakayamai in East Africa, therefore, provides new evidence on the origins of African great apes and humans. N. nakayamai could be close to the last common ancestor of the extant African apes and humans. In addition, the associated primate fauna from Nakali shows that hominoids and other non-cercopithecoid catarrhines retained higher diversity into the early Late Miocene in East Africa than previously recognized.     

Familial adenomatous polyposis complicated by chronic myelogenous leukemia: response to imatinib mesylate

Familial adenomatous polyposis (FAP) is an autosomal dominant disorder characterized by colonic polyposis and a predisposition for developing colorectal cancer. FAP is frequently complicated by extracolonic disease, but complications of leukemia are rare. We present the first case of FAP complicated by chronic myelogenous leukemia (CML) in a 38-year-old man. The patient had numerous adenomas in the colorectum and a family history compatible with FAP. He was diagnosed as having FAP in February 2000. Two years after the diagnosis, he developed leukocytosis with the Philadelphia chromosome abnormality, indicating complication with CML. Imatinib mesylate was administered for the treatment of CML, and hematologic and cytogenetic remission of CML was achieved in 6 months. Numerous polyps, 2 to 3 mm in diameter, observed in the rectum prior to the administration of imatinib, regressed in size, but not in number, after 1 year of treatment with imatinib. Eighteen months later, however, the polyps were enlarged. In this patient, imatinib administration led to the remission of CML and might also have been responsible for the temporary regression of adenomatous polyps of FAP.     

The mechanism of Axl-mediated Ebola virus infection

We previously reported that expression of the receptor-type tyrosine kinase Axl, which regulates cell survival and activation, enhances both pseudotype and live Ebola virus (EBOV) infection. To clarify the mechanistic basis of this enhancement, we created a series of Axl mutants and identified amino acids/domains necessary for this function, by using a pseudotype virus carrying the EBOV glycoprotein (GP). Analyses of the Axl mutants showed the importance of extracellular and intracellular regions for Axl functions, including ligand binding and signal transduction, in EBOV GP-mediated infection. These data suggest that EBOV uses the physiological functions of Axl to enter cells.     

Ghrelin differentially modulates glucose-induced insulin secretion according to feeding status in sheep

The present study was conducted to investigate roles of ghrelin in glucose-induced insulin secretion in fasting- and meal-fed state in sheep. Castrated Suffolk rams were fed a maintenance diet of alfalfa hay cubes once a day. Hyperglycemic clamp (HGC) was carried out to examine glucose-induced insulin response from 48 to 53 h (fasting state) and from 3 to 8 h (meal-fed state) after feeding in Experiment 1 and 2 respectively. Total dose of 70 nmol/kg body weight of D-Lys3-GHRP6, a GH secretagogue receptor 1a (GHS-R1a) antagonist, was intravenously administered at 0, 60, and 120 min after the commencement of HGC. In the fasting state, the ghrelin antagonist significantly (P < 0.01) enhanced glucose-induced insulin secretion. In the meal-fed state, i.v. administration of synthetic ovine ghrelin (0.04 microg/kg body weight per min during HGC) significantly (P < 0.05) enhanced glucose-induced insulin secretion. d-Lys3-GHRP6 treatment suppressed ghrelin-induced enhancement of the insulin secretion. In conclusion, ghrelin has an inhibitory and stimulatory role in glucose-induced insulin secretion via GHS-R1a in fasting- and meal-fed state respectively.