Influence of blood supply of the esophageal and gastric stumps on anastomotic healing after esophagogastrostomy in rabbits]

OBJECTIVE: To study how blood supply of the esophageal and gastric stumps influences the anastomotic healing after esophagogastrostomy in rabbits. METHODS: Twenty-seven New Zealand rabbits were randomly divided into 3 groups to receive esophagogastrostomy, followed by different procedures. Except for those in group I, all the rabbits were subjected to procedures of reducing the blood supply either of the esophageal or the gastric stump (group II and group III, respectively), followed by single-layer esophagogastric anastomoses using interrupted 5-0 polypropylene sutures. Ten days after operation, all the rats were killed and the anastomotic sites excised for measurement of the inner diameter, tensile strength, and hydroxyproline concentration. RESULTS: Healing of the esophagograstric anastomosis was obtained in all the rabbits but one with anastomotic leakage in group I and one with perforation of the gastric fundus in group III. The anastomotic inner diameters were similar in all the three groups, whereas the tensile strength and hydroxyproline concentration at the anastomoses decreased in group III in comparison with the other two groups (P<0.05) that had similar measurements (P>0.05). CONCLUSIONS: Extended length of the free esophageal stump does not significantly affect anastomotic healing as decrease of blood supply in the gastric stump.     

Pro-opiomelanocortin messenger ribonucleic acid and posttranslational processing of beta endorphin in spleen macrophages.

We have previously demonstrated low levels of immunoreactive (ir)-beta-endorphin (beta-EP) and ir-ACTH in a subpopulation of mouse spleen macrophages, which is consistent with an involvement of opioid peptides in modulation of immune responses. Gel chromatography studies suggested the presence of an approximately 3.5,000-molecular weight (mol wt) species, putatively beta-EP, an approximately 11.5,000-mol-wt species, putatively beta-lipotropin, and a higher molecular weight species (putative beta-EP precursor, pro-opiomelanocortin (POMC). In this study we have extended our original findings by demonstrating the presence of messenger RNA for POMC by the use of a complementary DNA probe and Northern blot analysis of extracts of mouse and rat spleen. In addition, using high performance liquid chromatography (HPLC), we have shown that the major endorphin species in mouse spleen macrophages is beta-EP1-31, and that there are smaller amounts of each of the acetylated forms, N-acetyl-beta-EP1-16 (alpha-endorphin), N-acetyl-beta-EP1-17 (gamma-endorphin), N-acetyl-beta-EP1-27, and N-acetyl-beta-EP1-31. We interpret these studies as showing that (a) the spleen is an organ of POMC synthesis and that (b) the predominant COOH-terminal product of macrophage POMC is the opiate-receptor active species beta-EP1-31.     

Spinal cord injury: prognosis for ambulation based on quadriceps recovery.

The purpose of this study was to determine if early recovery of quadricep muscle strength post spinal cord injury (SCI) is a useful predictor of future ambulation. Seventeen C4-T10 motor incomplete (Frankel C) spinal cord injured patients admitted to our center between March 1988 and April 1990 were examined within 72 hours to one week post injury. All patients had initial quadricep strengths < or = 2/5 in both legs. Strength in the strongest quadricep was followed prospectively at intervals from admission to one year post injury. Recovery time to a > 3/5 quadricep was established for each patient. Patients were categorized into 2 groups: FA (n = 11) were those patients who achieved functional ambulation and NA (n = 6) were those subjects who were nonambulators. Functional ambulators were defined as those patients who were able to walk in the household and/or the community while non ambulators were those who either did not ambulate or did so only for exercise. All patients (n = 9) who achieved a > 3/5 quadricep by 2 months post SCI became functional ambulators whereas in the group of 8 patients who did not achieve a > 3/5 by 2 months, only 2 became functional ambulators. This result was found to be significant using a point-by-serial correlation with p < 0.05. In conclusion, motor incomplete spinal cord injured patients who recovered to a > 3/5 quadricep strength by 2 months post injury had an excellent prognosis for subsequent ambulation by 6 months post injury.     

Gains of chromosomes 7, 17, 12, 16, and 20 and loss of Y occur early in the evolution of papillary renal cell neoplasia: a fluorescent in situ hybridization study.

It has been suggested that gains of chromosomes 7 and 17 and loss of Y occur in renal papillary adenoma and that progression to papillary renal cell carcinoma is marked by gains of additional chromosomes, most frequently 12, 16, and 20. Previous studies have included very few lesions of <5 mm in diameter, a requirement of the present definition of papillary adenoma. Ten papillary adenomas (ranging from 1 to 5 mm in diameter) from autopsy material and 10 surgically resected papillary renal cell carcinomas were studied with fluorescence in situ hybridization in paraffin sections using centromeric probes for chromosomes 7, 12, 16, 17, 20, and Y diluted 1:100 with tDenHyb1 buffer. The signals in 50 to 150 nuclei were counted in each tumor. Controls for all the probes were normal renal tissues from the same patients. Three or more signals per nucleus were frequently observed in papillary adenomas: chromosome 7 (range, 10 to 50%; > or = 30% in 9 of 10), 17 (range, 10 to 47%; > or = 30% in 7), 16 (range, 1 to 63%; > or = 10% in 5), 12 (range, 0 to 32%; > or =10% in 4), and 20 (range, 5 to 49%; > or = 10% in 5). Loss of the Y chromosome was observed in 80 to 90% of nuclei in 9 adenomas from males. Three or more signals were frequent in papillary renal cell carcinomas: chromosome 7 (range, 32 to 63%; > or =30% in 10 of 10), 17 (range, 28 to 61%; > or = 30% in 7), 16 (range, 0 to 45%; > or = 10% in 6), 12 (range, 1 to 37, > or = 10% in 5), 20 (range, 2 to 44%; > or = 10% in 4). No signal for Y was observed in 12 to 88% (> or = 81% in 6) of nuclei in 7 carcinomas from males. Statistical analysis showed no difference between adenomas and carcinomas. Gains of chromosomes 7, 17, 16, 12, and 20 and loss of the Y chromosome occur early in the evolution of papillary renal cell neoplasia in tumors that are only a few millimeters in diameter. Progressive gains of these chromosomes do not appear to correlate with the transition from adenoma to carcinoma.