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Biomedical subjects

A P Jayaraj

Publications and source records attributed to A P Jayaraj.

At least 19 recordsLinked to original sources
PubMed2001

Dietary factors in relation to the distribution of duodenal ulcer in India as assessed by studies in rats.

BACKGROUND: The prevalence of duodenal ulcer is less in the northern wheat-eating regions of India and China than in the southern rice-eating areas. METHODS AND RESULTS: Experiments were conducted on rat peptic ulcer models in which controls were fed on either known ulcerogenic rice or rice plus tapioca diets or on non-ulcerogenic stock diet. By using an ulcerogenic diet and pyloric ligation, unrefined wheat, wheat bran and their respective oils were protective against ulceration. Refined wheat, wheat germ and its oil were not protective. Freshly milled rice and unmilled rice were protective, but stored rice bran and its oil increased the ulceration. Fresh rice bran oil was not ulcerogenic, but on storage, it became ulcerogenic. By using stock diet and alcohol-induced ulceration, the findings with whole wheat oil, wheat bran and wheat germ oil were confirmed. Rats fed on the stock diet subjected to pyloric ligation developed ulcers following intragastric injection of stored rice bran oil. This ulcerogenicity was counteracted by whole wheat oil. CONCLUSION: These results suggest that the factor of diet may well explain the regional differences in the prevalence of duodenal ulceration between North and South India and China where other etiologic factors are similar.

Animals↗
PubMed2000

Duodenal ulcer prevalence: experimental evidence for the possible role of dietary lipids.

BACKGROUND AND AIMS: Mapping the geographical distribution of duodenal ulcer in relation to staple diets, and experiments on animal peptic ulcer models suggested that the lipid fraction in certain foodstuffs had a protective effect which was most marked in the lipid obtained from Horse gram (Dolichos biflorus). Lipid obtained from stored polished rice or rice bran was ulcerogenic. Further animal experiments were designed to investigate the protective and healing effects of Horse gram lipid (HGL) against peptic ulceration. METHODS: Three effects were investigated in rats: (i) the protective effect of HGL on peptic ulceration produced by using pyloric ligation in combination with South Indian diet or rice bran oil, or by cysteamine, alcohol or aspirin; (ii) the effect of HGL on mast cell degranulation in response to pyloric ligation and rice bran oil; and (iii) the healing effect of HGL on acute gastric ulceration produced by alcohol, on chronic gastric ulceration produced by topical acetic acid or on chronic duodenal ulcer following cysteamine. RESULTS: Horse gram lipid was shown to be protective and to promote ulcer healing in all the models used. Mast cell degranulation was inhibited. CONCLUSION: The experiments confirm the presence of a lipid in certain staple foods that have protective and healing properties in experimental peptic ulcer animal models. The differences in the prevalence of duodenal ulceration between different regions in some developing countries with a high prevalence of Helicobacter pylori infection might be explained by the presence or absence of protective lipids or ulcerogenic factors in the staple diet.

Acetic Acid↗
PubMed1996

Duodenal mucosal histology and histochemistry in active, treated and healed duodenal ulcer: correlation with duodenal prostaglandin E2 production.

We investigated whether impaired duodenal mucosal prostaglandin E2 (PGE2) production previously observed in duodenal ulcer (DU) was a primary pathophysiological abnormality or secondary to mucosal architectural changes that accompany ulceration. One hundred patients were studied: at endoscopy, paired duodenal biopsies were taken in patients with normal endoscopies and from the ulcer edge or scar and background mucosa in active or healed DU. One of the pair of biopsies was used to estimate PGE2 synthesis ability, the other was processed for histology and histochemistry. The following features graded: goblet cell numbers and staining with Periodic acid-Schiff reagent (PAS), epithelial staining with PAS, villous atrophy, columnar cell height, inflammatory cell infiltrate and micro-erosions and gastric metaplasia taken as a whole. Patients were found to have normal endoscopy (n = 31), active untreated DU (n = 20) active DU on treatment with either cimetidine or ranitidine (n = 13), healed DU on maintenance treatment (n = 27) and healed DU off treatment (n = 9). Active duodenal ulceration was found to be associated with decreased numbers of goblet cells, loss and blunting of villi, increased columnar cell height, increased epithelial cell PAS staining and with gastric metaplasia. After healing, only villous blunting remained. These changes were present, but less marked, at sites removed from the ulcer and were not apparent in the patient groups with healed ulcers. A strong correlation between overall gastric metaplasia and epithelial cell PAS staining and the reduced ability to synthesize PGE2 (P < 0.001) was only apparent when biopsies from all patients were grouped together, but not within individual patient subgroups. There was no consistent correlation between PGE2 generation and individual parameters of pathological change in duodenum. We conclude that, although inflammatory and mucosal changes may contribute, the evidence suggests that the impaired PGE2 generation in DU disease is, to a large extent, independent of histological and histochemical features.

Analysis of Variance↗
PubMed1989

Differences in mucosal appearances and in relapse rates in duodenal ulceration treated with sucralfate or cimetidine.

A total of 46 patients with duodenal ulcer were randomly assigned, without the knowledge of the investigators, to treatment with cimetidine 200 mg three times daily and 400 mg at night or sucralfate 1 g four times daily followed by one year of maintenance treatment with cimetidine 400 mg at night or sucralfate 1 g twice daily, respectively, in those patients with healed ulcers. The endoscopic healing rates and relapse rates during the maintenance period were similar, four relapses occurring in each group. All four relapses in the sucralfate group occurred at 12 months and only two were symptomatic. All the cimetidine relapses were symptomatic, two occurring at six months, one at nine months, and one at 12 months. Following the one year maintenance period, 13 cimetidine patients and 11 sucralfate patients were followed up for 36 months. During the first two years, nine of 13 (69 percent) cimetidine-treated and two of 11 (18 percent) sucralfate-treated patients had relapses. During the third year, three more sucralfate-treated patients and one more cimetidine-treated patient had relapses, making a total of 10 of 13 (77 percent) and five of 11 (45 percent) in the cimetidine and sucralfate groups, respectively. Duodenal biopsy specimens obtained before and after healing and after one year of maintenance were examined by light and electron microscopy. The sucralfate group showed greater improvement after one year of maintenance therapy than did the cimetidine group, although the appearances in either group were not predictive of subsequent relapse. The results show that relapses are less frequent and occur later after sucralfate therapy and also that the morphologic appearances are more normal after treatment with sucralfate than after treatment with cimetidine.

Adolescent↗
PubMed1989

Comparison of relapse rates and of mucosal abnormalities after healing of duodenal ulceration and after one year's maintenance with cimetidine or sucralfate: a light and electron microscopy study.

Forty six patients with endoscopically diagnosed duodenal ulceration were randomly allocated to treatment with either sucralfate 1 g qds (n = 24) or cimetidine 200 mg tds and 400 mg nocte (n = 22). When the ulcers healed, a maintenance dose of sucralfate 1 g bd or cimetidine 400 mg nocte was given for one year (or until relapse if earlier). Biopsies of duodenal mucosa adjacent to ulcer sites for light and electron microscopy were obtained before and after healing and again after one year's maintenance if the ulcer remained healed. Duodenal biopsies were also taken from 20 age and sex matched controls. Rates of healing and relapse during maintenance did not differ between the two treatments, although relapses occurred earlier with cimetidine. In the three year post-maintenance follow up period 10/13 cimetidine patients relapsed compared with four of 11 sucralfate patients (p less than 0.05), the relapses occurring significantly earlier in the cimetidine treated patients (p less than 0.05). Mucosal biopsies from both treatment groups still showed considerable abnormalities after healing. During maintenance, however, the sucralfate scores fell significantly (p less than 0.02) to near control levels unlike the cimetidine scores which remained raised at pretreatment values. The histological and ultrastructural changes were not predictive of later relapse. These findings favour the use of sucralfate in preference to cimetidine for maintenance treatment in the prevention of relapse of healed duodenal ulcers.

Adolescent↗
PubMed1988

The protective effect of Meciadanol (O-methyl-3(+)-catechin) on experimental ulceration.

Meciadanol, (O-methyl-3(+)-catechin), a histidine decarboxylase inhibitor was shown to have a marked protective action against experimental peptic ulceration in three rat models. The three methods used to induce ulceration were the instillation of absolute alcohol, pyloric ligation following an ulcerogenic South Indian diet and the instillation of rice bran oil into the stomach after pyloric ligation. Meciadanol was shown to reduce incidence, numbers and areas of ulceration and protected mast cells against degranulation and to preserve a normal vascular patterns. Furthermore, Meciadanol reduced gastric acid output and concentration in the pylorus ligation model. These results indicate that Meciadanol may be useful for the treatment of peptic ulcers in humans.

Animals↗
PubMed1988

Alpha-1-antitrypsin hepatic cell globules in autotransplanted liver of rats.

The autotransplantation of liver into the subcutaneous tissues in rats and hamsters resulted in the development of periodic acid Schiffs staining positive granules, which were resistant to diastase digestion. These granules were confirmed as alpha-1-antitrypsin by immunohistochemical staining. The appearance of the alpha-1-antitrypsin containing hepatic granules is comparable to those seen in the liver of humans with genetically determined alpha-1-antitrypsin deficiency.

Animals↗
PubMed1988

An investigation into the mechanism of collagenolytic activity in colonic mucosa by a tissue culture method.

The process of collagenolysis and the source of collagenase liberated from different cell types in the colonic mucosa has been investigated by the lysis of collagen gels in vitro. The reconstituted collagen gel strongly reacted to periodic acid Schiff (PAS) when stained with combined alcian blue-PAS, indicating the presence of glycoprotein with neutral sugars in the collagen gel. Colonic explants of rabbits produced visible collagenolysis. An area of alcian blue stained gel was seen replacing the usual PAS staining around the area of the lysis. Several histochemical methods revealed that the columnar cells had multiplied with high enzymatic activity and penetrated the collagen gel where collagenolysis took place. The action of several proteolytic enzymes on collagen gel showed that ficin caused lytic activity, even though collagen is resistant to most proteolytic enzymes. Papain, pepsin and trypsin altered composition of collagen gel from neutral mucopolysaccharide to acid mucopolysaccharide. Collagenase and pronase at low concentration were found to cause extensive collagenolysis. The synthesis and breakdown of collagen is a desirable balanced process in the remodelling of connective tissue. This dynamic equilibrium may be achieved through the subtle interplay of cells liberating and inhibiting collagenase.

Alcian Blue↗
PubMed1987

The ulcerogenic and protective action of rice and rice fractions in experimental peptic ulceration.

The ulcerogenic and protective effects of various rice fractions in the diet were studied in the pylorus ligated ulcer model in the rat. Oil present in rice and particularly rice bran becomes ulcerogenic on storage and in this model results in a significant increase in the median (range) numbers of ulcers from six (one to ten) to nine (six to 15) (P less than 0.05). The ulcerogenic effect of stored rice bran oil was reversed by cysteine which significantly reduced the ulcer incidence from 100% to 60% (P less than 0.005) and the numbers of ulcers from 26 (six to 70) to one (zero to four) (P less than 0.001). Fresh rice bran significantly reduced the numbers of ulcers from six (one to ten) to one (one to four) (P less than 0.05). Similarly, unmilled rice and freshly milled newly harvested rice was also shown to be protective in this model by significantly reducing the ulcer incidence from 87.5% to 50% and 0% respectively (P values less than 0.025) and the numbers of ulcers from three (zero to 17) to one (zero to one) and zero (zero to zero) respectively (P values less than 0.001). These results could in part explain the geographical distribution of duodenal ulceration, where the incidence is high in all the rice eating areas of the world, and provide a plausible hypothesis to explain the mechanism of dietary ulcerogenesis.

Animals↗