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Residual tumor at the esophageal stump was found in 103, or 14.3%, of a series of 719 resected esophageal specimens for carcinoma. The residual tumor pathologically presented as basal epithelial-cell carcinomatous change in 16 (15.5%), carcinoma in situ in 26 (25.5%), invasive carcinoma in 51 (49.5%), and cancerous emboli in 6 (5.8%) cases. A follow-up study of the 719 patients showed that the long-term survival rate of those with residual tumor was significantly lower than that of those without. Factors of occurrence besides inadequate resection were analyzed, and indications of surgical treatment were recommended. The presence of residual tumor is not an important factor in the development of anastomotic leakage.

Twenty-four patients, 12 children and 12 adults, with the Henoch-Schoenlein syndrome had their renal biopsy specimens studied by light and electron microscopic and immunofluorescent antibody techniques. The principal glomerular lesion was a focal and segmental proliferative glomerulonephritis in 15, a diffuse proliferative glomerulonephritis in 6 and a animal or minor change lesion with mesangial hypertrophy in 3 cases. The proliferation of the cells was mainly mesangial. Renal biopsies taken earlier in the course of the disease showed a greater number with a focal lesion. Electron dense deposits with cellular proliferation and increased matrix were seen in the mesangium. Less frequent subendothelial and occasional subepithelial deposits were found. Capillary loop changes were seen more frequently in the later stages of the disease. Heavy deposits of IgA were found in the mesangium in all cases, and less intense deposits of IgG in 60%. beta 1 C globulin and fibrinogen were found in 80% and IgD and IgM less frequently. Complement activation was via the alternate pathway as early complement components C1q and C4 were absent. Overt allergies, streptococal infections and the HBsAg could not explain the pathogenesis of the disease. Henoch-Schoenlein syndrome is a chronic disease of the mesangium; only 5 patients showed complete recovery, 15 had persistent microscopic hematuria and 3 died or developed renal insufficiency within 8 years. The prognosis was worst with diffuse proliferative glomerulonephritis, widespread focal glomerulonephritis or epithelial cresents formation.

Two simple cerebral ischemic models of mice were used for studying brain energy metabolism and the effects of drugs. Model one is partial occlusion of the left carotid artery and total occlusion of the right one including the vagus. The behavior of the animals appeared splaying of the contralateral extremities, circling around counterclockwise and in a comatose motionless state. Following the designated ischemic time, the animals were put into liquid N2. Model two is decapitation induced ischemia of mouse brain. The whole animal (control) and the severed head were rapidly frozen in liquid nitrogen 0, 10, 30, 60 s after decapitation. Brain samples were powdered at liquid N2 temperature, extracted and determined for ATP, phosphocreatine (Pcr) and lactic acid (LA). The data from model one indicate that after an ischemic period of 10 min, brain LA level increased significantly compared with values from the sham operated group, while no significant alteration was observed in brain ATP, and Pcr level. At 180 min of ischemia, levels of ATP and Pcr were considerably reduced while LA level increased significantly. The degree of symptoms induced by brain ischemia showed good correlation with brain energy metabolism. In model 2 brain LA level was found to be increased, while ATP and Pcr levels decreased after whole brain ischemia. However, brain ATP and Pcr levels were increased and LA level was decreased significantly in the normal and ischemic animal after administration of phenobarbital (225 mg/kg ip). LA level decreased significantly in the unischemic mice treated with Rb1 (100 mg/kg ip). It is indicated that both models of cerebral ischemia were simple and sensitive methods for studying brain ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

The effect of dose on the absorption and excretion of [14C]benzene was studied using 13-week old male F344/N rats, Sprague-Dawley rats, and B6C3F1 mice. Gastrointestinal absorption of benzene administered by gavage was greater than 97% in these species for doses between 0.5 and 150 mg benzene/kg body wt. At oral doses below 15 mg/kg, greater than 90% of the 14C excreted was in the urine as nonethylacetate extractable material. Above 15 mg/kg, in both rats and mice, an increasing percentage of the administered benzene was exhaled unmetabolized, suggesting saturation of metabolic pathways. Above 50 mg/kg, total metabolites (as determined by 14C in the urine, feces, and carcass after 2 days) were not linearly related to administered dose. Total metabolites per unit body weight was equal in F344/N rats and B6C3F1 mice at gavage doses up to 50 mg/kg; however, total metabolites in mice did not increase at higher doses. For inhalation exposures, the percentage of inhaled benzene that was absorbed and retained during a 6-hr exposure decreased from 33 +/- 6% (mean +/- standard deviation) to 15 +/- 9% in rats, and from 50 +/- 15 to 10 +/- 2% in mice as the exposure concentration was increased from approximately 26 to 2600 micrograms/liter (10 to 1000 ppm at 615 Torr, 23 degrees C). Total metabolite formation was exponentially related to the benzene exposure concentration with one-half the maximal amount of metabolite formation occurring at 220 micrograms/liter (84 ppm) for B6C3F1 mice and 650 micrograms/liter (250 ppm) for F344/N rats. Total metabolites were higher in mice than in rats at any of the vapor concentrations used due mainly to the higher amount inhaled by mice. Saturation of overall metabolism in mice but not in rats at high doses by both routes of administration indicates species differences in metabolism of benzene.

To determine accurately the potential genetic damage induced by toxic inhaled agents, the cells that receive a high concentration of such agents should be analyzed. Pulmonary alveolar macrophages (PAMs) represent such cells. We compared the cytogenetic effects of cigarette smoke on PAMs of rats exposed repeatedly by different methods. This study was part of a larger investigation of the health effects resulting from different methods of exposing rats to cigarette smoke. Fischer 344/N male rats (4/group) were randomly selected from five different exposure groups: 1) nose-only sham-exposed (air) control, 2) whole-body sham-exposed control, 3) nose-only intermittent, 4) nose-only continuous, and 5) whole-body continuous. The rats were exposed 6 hr/day, 5 days/week for 22-24 days. All smoke-exposed rats received the same daily concentration x time product (600 mg.hr.m-3 for the first week, 1200 mg.hr.m-3 thereafter) of cigarette smoke. Rats were injected intraperitoneally with colchicine at the end of exposure. PAMs were obtained by lung lavage and chromosomal damage was measured. Highly significant smoke-induced differences in both structural and numerical aberrations were observed in continuously exposed rats vs. sham controls, regardless route of exposure. The structural aberrations observed were chromatid-type deletions. Both hypoploid and hyperploid cells were detected. Our data suggest that cigarette smoke is clastogenic and may disrupt spindle-fiber formation. These activities may play a role in the induction of human carcinogenesis caused by cigarette smoke exposure.