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Biomedical subjects

A Pap

Publications and source records attributed to A Pap.

At least 73 records · Page 4Linked to original sources
PubMed1989

Studies into gastrinomas and combined carcinomatous carcinoid tumors. Optical light- and electron microscopy and immunohistochemistry.

The clinical, microscopic, immunohistochemical and ultrastructural features of 7 gastrinomas and 1 combined carcinoma-carcinoid tumor were evaluated. The tumors were located in the pancreas or duodenal wall in 6 cases, and on extragastro-enteropancreatic sites in 2 (liver or peripancreatic lymph node). All patients had the Zollinger-Ellison syndrome, 3 of them with additional bleeding and 1 with diarrhea. One patient with gastrinoma had additional tumors characteristic of the MEN-I syndrome. Immunohistochemistry showed gastrin and neuron-specific enolase-positivity in all of the tumors. Somatostatin was found in 4 cases, and single cell glucagon, pancreatic polypeptide. S-100 protein, keratin as well as carcino-embryonic antigen positivity in another few. Additional hormone production did not appear to be connected with biological behaviour of the tumors or with the clinical symptoms.

Adolescent↗
PubMed1989

Endocrine pancreas in chronic pancreatitis. A qualitative and quantitative study.

This study includes nine patients with diabetes mellitus (DM) and chronic pancreatitis (CP) (group I); 11 patients without DM and with CP (group II); and a control group (group III) consisting of five autopsy cases with neither DM nor CP. These groups were evaluated by routine histologic stains and immunocytochemical stains for insulin, glucagon, and somatostatin. Semiquantitative assessment of the degree of exocrine pancreatic atrophy and of two endocrine features (diffuse endocrine proliferation and ductoendocrine proliferation) was performed for each pancreas. Quantitative determination of the cell composition was carried out in three kinds of islets (parenchymal, sclerosis, and newly formed). The mean percentages of the insulin-producing B cells were significantly lower in the parenchymal (44.5%) and new (34.3%) islets of diabetic patients than in the controls (67.8%) and parenchymal (59.4%) islets of nondiabetic patients. The mean percentages of glucagon-producing A cells revealed significant increases in the parenchymal (43.0%) and new (55.7%) islets of diabetic patients as compared with the controls (24.3%) and parenchymal (32.2%) islets of nondiabetic patients. The mean percentage of somatostatin-producing D cells was significantly increased in the parenchymal islets (12.4%) of diabetic patients as compared with the parenchymal islets (8.2%) of nondiabetic patients and controls (7.5%). These findings correlate with clinical data of frequent DM in CP, but are partly in contrast with previous immunohistochemical analysis findings in CP.

Adult↗
PubMed1989

[Changes in chronic pancreatitis. Functional, structural and histological studies].

Pancreatic function, structural changes in comparison with morphologic (histological) ones were studied in 22 patients suffering from chronic pancreatitis. Gravity of functional and structural damages--apart from minor differences--showed close cinnection with the severity of tissue alterations. In half of the cases, combination of tissue signs of obstructive and calcificating pancreatitis were observed, so it is considered gratuitous to separate sharply the two forms of chronic pancreatitis.

Adult↗
PubMed1989

[Morphologic and biochemical changes in acute experimental interstitial pancreatitis].

Repeated subcutaneous injections of cholecystokinin-octapeptide has brought about an acute interstitial pancreatitis in rats. The aim of the experiment was the study of histological and biochemical alterations with special regard to regeneration phenomena. The treatment was carried out for 1 (group 1), 3,5 and 7 (group 2) days. Morphological alterations were more pronounced in group 2 than in group 1, but the pathological process was principally similar in both groups. Lowest values of pancreatic weight, protein and DNA content were attained in both groups at day 5. After this, protein and DNA started to increase. Hyperstimulation with CCK-OP on day 5 did not increase the degree of pancreas damage, nor did it prevent morphological and functional regeneration. The reason of this may be the decreased CCK-OP sensitivity of pancreatic acinar cells and/or the increased CCK-OP tolerance of newly formed acinar cells.

Acute Disease↗
PubMed1988

The anti-CCK effect of glutaramic acid derivatives in anesthetized and conscious rats.

The effects of specific gastrin-cholecystokinin (CCK) receptor blockers (proglumide and a new, more potent product of Rotta Research Laboratorium, CR-1392) on pancreatic secretion were studied. Proglumide and CR-1392 caused a rightward and parallel shift, respectively, in the dose-response curve of CCK8 stimulated pancreatic protein secretion in anesthetized rats, demonstrating a competitive-like mechanism of inhibition. The mean PA2 values, demonstrating the 50% inhibitory dose of proglumide and CR-1392 were 3.7 and 5.7, respectively; i.e., CR-1392 proved to be about 100 times more potent than proglumide. In conscious rats, protein output and the volume of pancreatic juice were significantly decreased for about 2 h in response to 150 mg/kg of proglumide or 3 mg/kg of CR-1392 administered s.c. during diversion of pancreatic juice, demonstrating inhibition of endogenous CCK by glutaramic acid derivatives. Indeed, during reintroduction of precollected pancreatic juice into the duodenum, when the release of CCK is known to be almost totally eliminated, pancreatic secretion was not significantly modified by the same doses.

Anesthesia↗
PubMed1988

Replacement therapy in pancreatic insufficiency with a new pancreatin preparation respecting the physiological ratio of lipase/trypsin activity.

An open, intraindividually controlled study with two doses of Creon (5 X 2 and 5 X 3 capsules/day) was performed in 15 patients suffering from severe pancreatic steatorrhea. A diet containing 70 g of fat/day was offered and the means of 3-day fat loss of daily collected stools were measured in the last 3 days of 5-day equilibration periods with and without replacement therapy. After these short-term periods, patients were treated with 5 X 2 capsules of Creon for 3 months at home, and fat loss was then measured as previously on a 70 g fat/day diet. Stool weight and stool frequency significantly decreased already during the short-term periods. The fat loss decreased dose-dependently during the short periods, more after 5 X 3 capsules/day than after 5 X 2 capsules/day. However, after 3-month replacement therapy the effect of 5 X 2 capsules of Creon was similar (16.5%), possibly because of improved intes-tinal function. Weight increases and patients' appraisal were also favorable. The excellent results with Creon treatment were attributed to a better lipase/trypsin ratio of the pancreatin pre-aration which, together with the favorable galenic properties, can diminish proteolytic inactivation of lipase during passage through the gastrointestinal tract.

Adult↗
PubMed1987

Functional impairment of the sacroiliac joint after total hip replacement.

Fifty patients who underwent total hip replacement were examined within 3 months by two independent investigators with respect to functional impairment of the sacroiliac joint. Several well-defined clinical tests were used, e.g. spine test, standing flexion test, Menell's sign, tenderness of the sacroiliac joint. The results of both investigators were comparable, with corresponding results in 94 per cent. Nearly 30 per cent of the patients showed functional impairment of one sacroiliac joint. This finding may partly cause the gluteal or low back pains which are reported by patients after hip replacement.

Aged↗
PubMed1986

Complex evaluation of secretin-pancreozymin test data by multivariate statistical pattern recognition methods.

Complex evaluation of secretin-pancreozymin test data with multivariate statistical methods was performed in patients with pancreatic insufficiency and in controls. The centroid, the nearest neighbour methods and the linear discriminant analysis led to the correct diagnosis in 84, 77 and 92%, respectively, when the overall responses to synthetic secretin plus cholecystokinin-octapeptide were evaluated. Results of individual stimulations were less precise. The linear discriminant analysis also successfully separated the patients with mild chronic pancreatitis from the healthy subjects, and seems to provide a useful support in medical diagnosis, particularly in controversial cases.

Cholecystokinin↗
PubMed1986

Inactivation of cholecystokinin octapeptide by normal and cirrhotic liver in rats.

In anesthetized rats, a marked decrease in CCK-OP activity and, to a far lesser extent, in the pancreatic secretory effect of CCK-33 were found after portal administration, compared to the femoral route. Changes in the biological activity of CCK-OP were further investigated after 30 min incubation with different subcellular liver fractions (1000 X g, 12,000 X g, microsomal fraction with or without NADPH). All the subcellular liver fractions caused an approximately 70% decrease in the CCK-effect, as calculated from dose-response relationships. The inactivation of CCK-OP after incubation with microsomal fractions of thioacetamide (TAA)-induced cirrhotic liver did not differ from that of control rats. The CCK-OP dose-response curves were similar in cirrhotic and control rats, but the pancreatic secretion was sustained to a greater extent and the inhibitory effect of supramaximal stimulation was delayed in cirrhotic rats. It was concluded that CCK-OP can be inactivated by liver proteins present in microsomal fractions, by a NADPH-independent mechanism. This inactivation did not diminish in liver cirrhosis. There were no changes in CCK-OP elimination in cirrhotic rats in vivo, thus pancreatic hypertrophy in experimental cirrhosis must be explained by other mechanisms.

Animals↗
PubMed1986

Effect of atropine on pancreatic secretion in conscious rats.

The effect of atropine on exocrine pancreatic secretion was investigated in conscious rats. Intravenous atropine infusion decreased nonstimulated protein secretion during recirculation of pancreatic juice into the duodenum D50 = 15-20 micrograms/kg/h. The maximum inhibition from protein secretion (-89%) was obtained with 600 micrograms/kg/h. With larger doses, the inhibition was less. The response to secretin and cholecystokinin-pancreozymin was not significantly modified by atropine. When pancreatic juice was diverted during the course of an intravenous atropine infusion, the first 1-hour peak of protein output was significantly decreased, but the following 2-hour period was increased, the sum of these 2 periods being similar in both conditions. The response to soybean trypsin inhibitor during recirculation was decreased as well as the first peak after diversion. During atropine infusion fluid secretion decreased more powerfully after 1 h diversion and after soybean trypsin inhibitor than during recirculation of pancreatic juice. It is suggested that during recirculation of pancreatic juice nonstimulated protein secretion is mostly (89%), and water secretion is partially controlled by cholinergic mechanisms. After soybean trypsin inhibitor stimulus and during the early phase following juice diversion protein secretion seems to be partly under the control of cholinergic mechanisms. However, during the latter phase following diversion, it is not so. Parasympathetic stimulation appears also to play a significant, although less important, role in fluid secretion.

Animals↗
PubMed1986

Effects of somatostatin on basal and stimulated pancreatic secretion in conscious rat.

The effects of somatostatin on pancreatic secretion were studied in conscious rats during diversion and recirculation of pancreatic juice. Pancreatic secretion was significantly inhibited by low doses (2 micrograms/kg/h) of somatostatin during diversion of pancreatic juice. The inhibitory effect was more marked on bicarbonate and protein output than on volume, while in bicarbonate and protein output a rebound effect was observed. These data suggest a combined inhibitory effect of somatostatin on endogenous CCK release and cholinergic mechanisms. During recirculation of pancreatic juice there was no rebound effect, thus only the inhibition of cholinergic mechanisms seems to be involved in the inhibitory effect of somatostatin. During recirculation, CCK-OP-stimulated bicarbonate and protein secretion was strongly inhibited by somatostatin. Even water secretion not stimulated by CCK-OP was significantly inhibited demonstrating a supplementary inhibitory effect on basal cholinergic mechanisms. Somatostatin decreased only slightly the synthetic secretin-stimulated water and bicarbonate secretion. The more effective inhibition of protein output was explained by an additive effect of somatostatin on basal cholinergic tone.

Animals↗