Biomedical subjects
Publications and source records attributed to E Butruk.
A series of 20 patients with 24 squamous cell papillomas of the esophagus are presented. Nonspecific symptoms not directly connected with esophageal disorders were the reason for esophagoscopy. Clinical findings, treatment, and follow-up of the patients in the context of the world literature review of 141 cases reported to date, are discussed.
The present studies were designed to evaluate the parietal cell acid production in response to short-time stimulation by epidermal growth factor (EGF). Studies were performed in vitro using isolated cells from rat stomachs, and acid production was indirectly determined by [14C]aminopyrine accumulation. EGF inhibited histamine-stimulated aminopyrine accumulation from standard incubation medium (K+ = 5 mM) but not from that with increased K+ concentration (K+ = 70 mM). EGF significantly stimulated ornithine decarboxylase (ODC) activity, an effect that was blocked by the specific ODC inhibitor, difluoromethylornithine (DFMO). In the presence of DFMO, EGF failed to inhibit histamine-stimulated aminopyrine uptake. Like EGF, the polyamine spermine, which is a direct product of enhanced ODC activity, also inhibited histamine-stimulated aminopyrine uptake. Unlike EGF, the spermine-induced inhibition of aminopyrine accumulation was not altered by DFMO. Thus the DFMO effect was specific to EGF. Taken together, these results are consistent with the postulate that EGF inhibits parietal cell secretory response through the induction of ODC activity and increased synthesis of polyamines.
Mucosal gastric injury was induced in vivo by oral administration of 75% ethanol to rats that were intraperitoneally pretreated with saline (controls), 4 mg/kg of verapamil, 0.4 mg/kg of nifedipine or 160 mg/kg of MgCl2. The glandular stomachs were used for macroscopic and histologic evaluation of mucosal lesions. The gastroprotective effects of substances tested against ethanol-induced mucosal damage in vitro were examined: 1). in rats intraperitoneally pretreated with calcium antagonists and 2). after adding of 10(-4) M verapamil, 10(-6) M nifedipine or 10(-2) M MgCl2 directly to minced gastric mucosa of untreated rats. This effect was measured by DNA synthesis. Gross and histologic evaluation showed that rats pretreated with nifedipine or MgCl2 had significantly decreased ethanol-induced gastric injury compared to controls, whereas those pretreated with verapamil had significantly increased injury. On the contrary, all verapamil, nifedipine and MgCl2 treatments, administrated intraperitoneally or by exposure to an incubation mixture were equally effective in reducing gastric mucosal damage following to ethanol treatment in vitro. We conclude that the differential effects of verapamil and nifedipine on ethanol-damaged gastric mucosa in vivo, but not in vitro, suggests the existence of different actions of these calcium antagonists more on systemic rather than local protective mechanisms, such as gastric mucosal blood flow, mucosal barrier, or cell renewal.
We present here four patients with six granular cell tumors of the esophagus: all are women, 22, 38, 47, and 49 yr old. In three of them, single polyps were encountered. In the fourth, age 38, two lesions were found in 1982, and a new one, a satellite polyp, has appeared after 5 yr of follow-up. All of the patients' conditions were followed up [mean time 65 months (16 months to 10 yr)]. In connection with these case reports, we include an up-to-date review of the world literature on this subject.
To examine the role of protein kinase C (PKC) in induction of human colon adenocarcinoma cell line, DETA/W, by polypeptide growth-promoting factors, ornithine decarboxylase activity (ODC) and DNA synthesis were determined in cells depleted of PKC. PKC depletion was achieved by prolonged cultivation (more than 30 passages) with 10(-6) M phorbol 12-myristate 13-acelate. Lack of PKC in studied cells was proved by measurements of PKC activity and immunoreactivity. Although ODC activities and DNA syntheses in PKC-depleted cells were decreased by about 40-50% compared to normal DETA/W cells, the percentage increase of these mitogen-responsive reactions was quantitatively similar in both cell sublines. These results raise the possibility that not all of the biological responses to growth factors are connected with the activation of calcium-dependent PKC.
The formation of carcinoma in the hyperplastic gastric polyp is extremely rare. This paper presents two cases of carcinomas which developed in hyperplastic polyps of the stomach in a 39-year-old man and an 82-year-old man. The problem of malignant transformation of gastric hyperplastic polyps is stressed and discussed in the light of data in the literature.
The aim of this study was to determine serum retinol levels in patients with inflammatory bowel disease and to attempt to elucidate the mechanism of changes in vitamin A metabolism in these disorders. It was found that in 15 patients with active ulcerative colitis, 14 patients with active Crohn's disease and in 3 operated patients with recurrent Crohn's disease serum retinol levels and retinol-binding protein were significantly lower than in controls. Concentrations of vitamin A did not depend on the localization of inflammatory bowel disease, previous ileal resections, duration of the disease or age and sex of the patients. During successful treatment of active ulcerative colitis normalization of serum retinol levels without substitution of vitamin A was observed. Repeated determinations in patients with Crohn's disease who had low serum retinol levels in an active phase of disease revealed normal vitamin A levels in an inactive phase. The absorption of vitamins A and E in patients with inflammatory bowel disease was normal. The normal serum retinol concentrations in patients with diarrhea due to irritable bowel syndrome, and in those with anorexia nervosa exclude the influence of diarrhea and body weight itself on vitamin A levels. The results of this study indicate that serum retinol levels in patients with active inflammatory bowel disease are secondary to the decreased serum retinol-binding protein concentrations, and probably depend on the increased protein catabolism in these disorders.
The effects of extracellular K+ in relation to extracellular Ca2+ on acid production were studied. Studies were performed in vitro using isolated cells from rat stomachs, and acid production was indirectly determined by 14C-aminopyrine (AP) accumulation. In the absence of K+ in the incubation medium histamine-stimulated AP accumulation ratios were significantly decreased independently in the presence or absence of extracellular Ca2+. Under basal conditions, in the absence of extracellular Ca2+, increasing concentrations of extracellular K+ enhanced AP accumulation ratios to significantly higher than those found in the presence of Ca2+. In histamine-, cAMP-, and carbachol-stimulated parietal cells, high K+ concentrations increased AP accumulation significantly less in Ca(2+)-free than in Ca(2+)-containing media. High K+ also induced significantly both an increase in cytosolic free Ca2+ concentration and 45Ca2+ uptake. The present results confirmed the importance of K+ in gastric acid production and suggested a role for Ca2+ as a modulator of mechanisms of parietal cell stimulation.
The present studies were designed to examine the effect of changes in membrane potential by means of protonophore carbonyl cyanide m-chlorophenylhydrazone (CCCP) and variations in the pH of the medium on the secretory response of parietal cells. Studies were performed in vitro using isolated cells from rat stomachs and acid production was indirectly determined by 14C-aminopyrine (AP) accumulation. CCCP affected both basal and histamine-stimulated AP accumulation in a concentration-dependent manner. The AP accumulation ratios depended on pH of the incubation medium; the ratio was lowest at pH 6.6, and increased progressively as the pH of the medium increased to 7.8. Moreover, the decreases in AP accumulation ratios caused by simultaneous addition of CCCP and AP to cell suspensions compared to those in which CCCP was added to incubated cells after achieving the steady-state of AP accumulation were quantitatively similar. These findings suggest that the decrease in AP accumulation due to CCCP treatment is a consequence of an activation of acid secretion rather than an inhibitor of acid production. From the present and previously published data, we propose a working hypothesis: membrane recycling is dependent on changes in apical membrane potential.
Insertion of biliary endoprosthesis was attempted in 151 patients with obstructive jaundice and was successful in 124 patients (82%). The indications for the procedure were: 1) biliary and pancreatic neoplasms (79 patients) and 2) non-neoplastic diseases such as common bile duct stones or postoperative biliary strictures (45 patients). Successful drainage of bile was obtained in 95% of patients from the first group and in 93% of those from the second group. The mean survival time of patients with neoplasms was 4.5 months and the majority of them were free of jaundice and itching. In 32 patients with non-neoplastic diseases there was no recurrence of jaundice after a mean time of 20 months. Serious complications occurred in 5 patients (4%), 4 of them died (3.2%). The most frequent late complication was clogging of the endoprosthesis (19% of patients from the first group after a mean time of 5 months and in 28% of those from the second group after a mean time of 16 months). Replacement of the endoprosthesis was carried out mainly on the ambulatory basis. Endoscopic biliary stenting is an effective method of palliative biliary drainage in patients with non-operable biliary and pancreatic tumours. In high risk patients with non-neoplastic obstructive jaundice the technique may be an alternative for surgical treatment.
The present studies were designed to examine the effect of local anesthetics (benzyl alcohol, lidocaine, and procainamide) on the secretory response of parietal cells to histamine, dbcAMP, and carbachol. Studies were performed in vitro using isolated cells from rat stomachs, and acid production was determined by 14C-aminopyrine accumulation. In addition, the (H(+)-K+)-ATPase activity of microsomal vesicles isolated from parietal cells was determined. Lower concentrations of the drugs studied increased the basal aminopyrine accumulation and potentiated the secretory response of parietal cells to histamine and dbcAMP. At higher concentrations local anesthetics progressively inhibited both the basal 14C-aminopyrine accumulation and that stimulated by histamine, dbcAMP or carbachol. While a low concentration of local anesthetics increased gastric microsomal (H(+)-K+)-ATPase activity, higher concentrations inhibited enzyme activity to about 80% of those activities found in resting parietal cells. We conclude that increased aminopyrine accumulation may reflect the activation of membrane-bound enzyme(s) involved in the cAMP-dependent signal transduction pathway mediating acid secretion by parietal cells. In turn, it is possible that the inhibition of aminopyrine accumulation by local anesthetics at higher concentrations can relate to two different mechanisms: (1) the nonspecific effect of local anesthetics that causes simple proton neutralization (as weak bases), and (2) to a minor extent their inhibitory effect on proton pump activity.
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The concentrations of vitamin A in liver samples obtained at autopsy of patients who died of cancer was investigated. It was found that liver vitamin A levels in cancer patients were significantly lower than in controls. Although our recent results have suggested that the decreased serum retinol level in cancer patients reflects rather a functional impairment of vitamin A release from the liver, the results of this study suggest that this phenomenon can also indicate a true vitamin A deficiency in patients with neoplastic process.
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Serum retinol levels were determined by a fluorometric method in patients with colorectal cancer or polyps and those with inflammatory bowel disease. Serum retinol levels in patients with benign or malignant colorectal polyps and stage B cancer (modified Dukes' classification) were similar to those found in controls. By contrast, serum retinol levels were significantly lower in patients with Dukes' stage C or D. Among cancer patients that were followed after surgical treatment serum retinol levels did not differ significantly from those found in controls. Patients who died of metastases during follow-up possessed very low serum retinol levels. These findings suggest that a decreased serum retinol level in cancer patients is a consequence rather than a precursor of the neoplastic process. Furthermore, this study suggests that the marked decrease in serum retinol level might be an indicator of poor prognosis in colorectal cancer patients after surgery.
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