The effects of F strain Mycoplasma gallisepticum, Mycoplasma synoviae, and the dual infection in commercial layer hens over a 44-week laying cycle when challenged before beginning of lay. I. Egg production and selected egg quality parameters

In each of two trials, 160 commercial pullets were separated into four treatments with four replicates of 10 chickens in each treatment. Forty pullets were designated as controls and received no inoculation; 40 other pullets received F strain Mycoplasma gallisepticum (FMG); an additional 40 pullets received Mycoplasma synoviae (MS); and the final 40 pullets were inoculated with both FMG and MS (dual). Hen-day egg production, egg weight, eggshell strength, Haugh unit score, pimpling incidence, and blood/meat spot incidence were monitored and recorded in each trial through an entire laying cycle. No significant difference was observed among the treatments for hen-day egg production, egg weight, eggshell strength, or Haugh unit scores. Significant differences were observed for pimpling incidence among controls (1.63%), Mycoplasma gallisepticum (MG)-infected (2.09%), and dual-infected hens (2.41%). A significant difference in blood/meat spot incidence was observed between MG-infected hens (0.27%) and dual-infected hens (0.45%). Histopathologic examination of the ovary and all segments of the oviduct revealed no significant differences among the treatments. These results suggest that the majority of the hen reproductive tract functions similarly in FMG-vaccinated, MS-infected, or dual-infected hens as compared with Mycoplasma-clean hens.     

Acute high environmental temperature and calcium-estrogen relationship in the hen

Much is known about the effects of high environmental temperature (HT) on egg production, but very little is understood about the mechanisms that underlie them. Two experiments were conducted to examine the effects of acute heat stress on circulating estradiol, on calcium uptake by gut tissue, on bone resorption, and on the dynamic relationship between estradiol and calcium in the hen during one ovulatory cycle. In one study, hens were moved individually and randomly into a hot [HT: temperature (T) = 35 C, relative humidity (RH) = 50%; n = 18] or a control, thermoneutral (TN: T = 23 C, RH = 50%; n = 18) environment immediately after a mid-sequence oviposition and brachial vein cannulation. Blood samples (2 mL) were collected every 3 h for 21 h for ionized calcium (Ca2+) and pH determinations and from which aliquots were frozen for 17 beta-estradiol (E2), total calcium (TCa), and inorganic P analysis. Excreta and urine were assayed for TCa and hydroxyproline (OHPr), respectively. A second study was conducted to determine the effects of HT (T = 35, H = 50%, 12 h) vs TN (T = 23 C, RH = 50%, 12 h) on the ability of duodenal cells to take up calcium (CaT). Blood pH and calcium responded to HT as expected (pH increased, Ca2+ decreased, and TCa decreased) and the cyclic pattern of Ca2+ in blood was abolished. The ratio of Ca2+:TCa decreased sharply at approximately the onset of shell calcification in control hens, but in HT hens there was no clear change in the ratio of any point in the cycle. The pattern of E2 typical of hens under normal conditions was significantly depressed in plasma of HT hens. Calcium uptake by duodenal epithelial cells of HT hens was lower than in TN hens. There was a clear inverse correlation between blood Ca2+ and urine OHPr in TN hens (r2 = -73, P = 0.0021) but not in HT hens (r2 = -27, P = 0.32). In addition to alterations in acid-base balance and the status of Ca2+, diminished ability of duodenal cells to transport calcium may be a critical factor in the detrimental effects of heat stress on egg production (numbers), eggshell characteristics, and skeletal integrity often documented in the laying hen.     

NCI? What is it? What do they do?

BACKGROUND: Omeprazole, a H+/K+ ATPase inhibitor, has been shown to reduce gastric bicarbonate secretion in cats. However, there has been no study on the effect of omeprazole on bicarbonate secretion in patients with duodenal ulcer (DU). METHODS: Fifteen men with duodenal ulcer (mean age 38 years, range 22-57) were included. Baseline gastric acid output, bicarbonate secretion, and parietal and nonparietal secretions were estimated before and after omeprazole therapy (20 mg/day) for four weeks. RESULTS: Omeprazole administration did not significantly alter bicarbonate secretion (3.3 [1.2] vs 2.4 [0.4] mmol/h), though there was significant reduction in gastric acidity (44.2 [6.6] vs 20.7 [4.6] mmol/L, p < 0.01). CONCLUSION: Omeprazole reduces acid secretion but does not affect gastric bicarbonate secretion in patients with DU.     

Platelet-derived growth factor BB mediated regulation of 12-lipoxygenase in porcine aortic smooth muscle cells

BACKGROUND & AIMS: Recently, we postulated a new concept of duodenal ulcer pathogenesis suggesting that antral Helicobacter pylori infection blocks inhibitory pathways to the gastrin and parietal cells, resulting in an increased and prolonged postprandial acid secretion. the aim of this study was to examine duodenal acid load and duodenal bulb pH after a meal before and after eradication of H. pylori. METHODS: Using a marker-dilution method and a pH electrode in the duodenal bulb, gastric emptying, acid secretion, gastrin release, duodenal acid load, and duodenal bulb pH were studied during 2 hours after peptone meals of pH 7.0 and 2.0 in 8 H. pylori-negative controls and 8 H. pylori-infected subjects before and 6 months after eradication. RESULTS: The H. pylori-infected subjects had an increased gastric emptying, gastrin release, and acid secretion, higher duodenal acid load, and lower duodenal bulb pH after the meals. These responses were normalized after eradication. CONCLUSIONS: H. pylori-infected subjects have an increased and prolonged postprandial acid secretion, partly caused by an impaired low pH inhibition of acid secretion, gastrin release, and gastric emptying, resulting in an increased duodenal acid load and a prolongation of low pH in the duodenal bulb, as a general prerequisite for the development of duodenal ulcer disease.     

Effect of proton pump inhibitor, omeprazole, on expression of rat parietal cell specific carbohydrate antigen, type 2 chain N-acetyllactosamine

The effect of a proton pump inhibitor, omeprazole, on the rat gastric mucosal expression of carbohydrate antigens was studied. Type 2 chain N-acetyllactosamine was detected specifically on the apicocanalicular cell membranes of parietal cells. Pretreatment of rats with omeprazole profoundly suppressed the antigen expression, which followed the inhibition of gastric acid secretion. When omeprazole was discontinued, the antigen was reexpressed, which preceded the restoration of acid secretion. The antigen-negative tissues became antigen-positive when they were desialylated. Gastric membrane vesicles from the normal and omeprazole-treated rats were antigen-positive and -negative, respectively. SDS-PAGE revealed that a glycoprotein with an apparent molecular weight of 64-78 kDa carried type 2 chain N-acetyllactosamine. In the omeprazole-treated rats, the same molecular weight glycoprotein was positively immunostained only after desialylation. We concluded that: (1) the expression of type 2 chain N-acetyllactosamine was closely correlated with gastric acid secretion, and (2) the inhibition of acid secretion was accompanied by the sialylation of the parietal cell membrane glycoprotein.     

Dose uniformity of ferromagnetic seed implants in tissue with discrete vasculature: a numerical study on the impact of seed characteristics and implantation techniques

There is evidence of a two-way interaction between gastric acid secretion and H. pylori-associated gastritis. Gastric acid secretion influences the density of H. pylori colonisation, its distribution within the stomach and the severity of the mucosal inflammatory response to the infection. In addition, H. pylori gastritis alters gastric acid secretion. In subjects with a predominant antral gastritis, it increases acid secretion predisposing to duodenal ulcer, whereas in others with predominant body gastritis, acid secretion is impaired and the subjects have an increased risk of gastric cancer. The two-way interaction between acid secretion and H. pylori gastritis is observed when H. pylori-positive subjects are treated with proton pump inhibitor agents. The inhibition of acid secretion induces a body gastritis and this inflammation of the body mucosa inhibits acid secretion thus augmenting the anti-secretory effect of the drug. In this article, we discuss the interaction between gastric acid secretion and H. pylori gastritis and its importance in determining disease outcome.     

Effects of intravenous lansoprazole on acute gastric mucosal lesions and acid secretion

The effects of lansoprazole given intravenously on gastric mucosal lesions, gastric bleeding and acid secretion were investigated in rats in comparison with those of omeprazole, famotidine and ranitidine. Lansoprazole inhibited the formation of gastric mucosal lesions in rats induced by water-immersion stress or aspirin with ID50 values of 0.26 and 0.99 mg/kg, respectively, and also inhibited gastric bleeding induced by hemorrhagic shock or water-immersion stress with ID50 values of 0.46 and 1.22 mg/kg, respectively. Lansoprazole was more potent than omeprazole, famotidine and ranitidine in inhibiting gastric mucosal lesions and hemorrhagic shock- or stress-induced bleeding. Famotidine and ranitidine showed negligible inhibition of water-immersion stress-induced gastric bleeding. Lansoprazole strongly inhibited water-immersion stress-stimulated acid secretion in rats, whereas famotidine and ranitidine did not show a potent inhibitory effect. These results indicate that lansoprazole exerts prominent inhibitory actions against the formation of gastric mucosal lesions and gastric bleeding by inhibiting acid secretion, and they show that it is superior to histamine H2-receptor antagonists in inhibiting stress-induced gastric bleeding.     

Influence of Fusarium-infected corn and F-2 on laying hens

Diets containing either Fusarium-infected corn supplying 25 and 100 p.p.m. of F-2 (zearalenone) or purified F-2 at these levels did not adversely influence the reproductive performance of laying hens. In trial 1, no deleterious effects were observed for 20- and 36-week body weights, age at first egg, egg weight, albumen height, shell deformation, fertility or hatchability when Fusarium-infected corn was fed to 20-week-old pullets for 28 days. Percent hen-day egg production of birds fed Fusarium-infected corn supplying 25 and 100 p.p.m. of F-2 was superior (P less than or equal to 0.5) to egg production of nontreated controls. In trial 2, three replications of ten adult Leghorn hens were evaluated under five dietary treatments: (1) 16.7% protein basal; (2) basal plus Fusarium-infected corn (25 p.p.m. of F-2); (3) basal plus 25 p.p.m. of (purified) F-2; (4) basal plus Fusarium-infected corn (100 p.p.m. of F-2); (5) basal plus 100 p.p.m. of (purified) F-2. Difference between dietary treatments for 14-day pre-treatment, treatment and post-treatment periods were nonsignificant for 42- and 44-week body weights, egg production, egg weights, fertility and hatchability. Body weights of chicks from hens fed F-2 diets were not significantly different from those of chicks from hens fed the basal diet.     

Regulation of somatostatin-14 and -28 secretion by gastric acid in dogs: differential role of cholecystokinin

BACKGROUND: Prosomatostatin-derived peptides include two principle bioactive molecular forms, somatostatin 28 (S-28) and somatostatin 14 (S-14). This study examined whether there is a functional relationship between gastric acid secretion and the release of S-28 and S-14 into the circulation. METHODS: In conscious dogs with gastric and duodenal cannulas, S-28 and S-14 responses, measured after extraction of acidified plasma and separation by gel chromatography, were evaluated by administration of nutrients and acid-inducing secretagogues without and with omeprazole. RESULTS: Ingestion of a solid meal caused equivalent plasma elevations of S-28 and S-14, whereas infusions of histamine and gastrin selectively increased plasma S-14. Omeprazole decreased meal-stimulated S-28 (-67% +/- 8%; P < 0.01) and S-14 (-56 +/- 9%; P < 0.01) and abolished S-14 increases to histamine and gastrin. Intraduodenal perfusions of a liquid protein meal increased S-28 above S-14, comprising approximately 71% of total somatostatin-like immunoreactivity released, and omeprazole suppressed S-28 (-87% +/- 5%; P < 0.01) without influencing S-14. Similar responses occurred after exogenous cholecystokinin. Moreover, pretreatment of the intraduodenal protein meal with the cholecystokinin-A receptor antagonist MK-329 abolished increases of S-28 and S-14 and caused a further twofold increase of gastric acid (P < 0.025). CONCLUSIONS: In the fed state, gastric acid causes direct release of S-14 from the stomach, but the acid-dependent component of S-28 secretion requires cholecystokinin as a cofactor. Negative feedback regulation between somatostatin and gastric acid secretory responses to nutrients may include S-28 modulated, in part, by cholecystokinin.     

Mechanism of inhibition of H+, K(+)-ATPase by sodium 2-[[4-(3- methoxypropoxy)-3-methylpyridin-2-yl]methylsulfinyl]-1H-benzimidazole (E3810)

Sodium 2-[[4-(3-methoxypropoxy)-3-methylpyridin-2-yl]methylsulfinyl ]- 1H-benzimidazole (E3810) and omeprazole inhibit gastric acid secretion through inhibition of the activity of H+, K(+)-ATPase present in parietal cell membrane vesicles, by chemical modification of SH groups in the enzyme molecule. In order to clarify the mechanism of the chemical modification, reaction products of E3810 and omeprazole with 2-mercaptoethanol under acidic conditions (pH 3, 4, 5, 6) were isolated by HPLC, and subjected to structural analysis by UV, 1H-NMR and mass spectrometry. E3810 and omeprazole appeared to undergo two kinds of reactions, affording disulfide-type products (type I reaction) and sulfide-type products (type II reaction). The rates of these reactions were determined by HPLC, and the stability of the products in the presence and absence of glutathione was investigated. In the case of E3810, type I reaction was found to proceed faster than type II reaction at every pH value studied. The type I reaction of E3810 was faster than that of omeprazole. The rate of type I reaction decreased at pH 5 and 6, especially for omeprazole, and the contribution of type II reaction increased as the pH of the reaction mixture was increased. The sulfide-type modification products were stable, whereas the formation of the disulfide-type modification products was reversed by the action of endogenous SH compounds such as glutathione. These results suggest that higher inhibitory activity of E3810 against gastric acid secretion and faster recovery of the enzyme activity after inhibition by E3810 can be expected, as compared with those of omeprazole.     

Fibrinolytic components in nasal mucosa and nasal secretion

Effects of a newly synthesized antiulcer agent, YJA20379-4, on gastric proton pump (H+/K+-ATPase) activity, Helicobacter pylori (H. pylori) growth, gastric acid secretion, and gastro-duodenal lesions, were examined in comparison with those of omeprazole. YJA20379-4 markedly inhibited the H+/K+-ATPase activity in a concentration-dependent manner and the inhibitory effect was increased under a weak acidic condition; the IC50 values were 32 and 81 microM at pH 6.4 and 7.4, respectively. The inhibition was completely antagonized by 0.5 mM dithiothreitol (DTT). In addition, YJA20379-4 showed a significant anti-H. pylori activity determined by the agar dilution method. The value of minimum inhibitory concentration (MIC, 3.9-11.7 microg/ml) was at least 3 times more potent than that of omeprazole. In pylorus ligated rats, YJA20379-4 inhibited basal gastric acid secretion when administered by the intraduodenal route (ED50: 23.6 mg/kg). In experimental ulcer models, YJA20379-4 administered by the oral route dose-dependently prevented the development of gastro-duodenal lesions in rats. Moreover, repeated administration of YJA20379-4 promoted the healing of gastric ulcers induced by acetic acid. On the basis of the data obtained, it is suggested that YJA20379-4 has a wide spectrum of antiulcer activities, and its mode of antiulcer actions is dependent on the inhibition of H+/K+-ATPase activity and H. pylori growth and the enhancement of a mucosal defense. Thus, YJA20379-4 might prove to be a beneficial therapy for gastritis and peptic ulcer diseases.     

Fatty liver-hemorrhagic syndrome observed in commercial layers fed diets containing chelated minerals

This study was originally conducted to determine the effect of various chloride levels and consumption of chelated versus non-chelated minerals on egg production and eggshell breaking strength. However, the focus of this report changed after fatty liver-hemorrhagic syndrome (FLHS) was observed in hens that consumed diets containing chelated minerals. No FLHS was observed in hens that consumed a diet that contained non-chelated minerals. Four hundred thirty-two 35-week-old commercial laying hens were housed in individual cages in groups of nine hens each. The treatments were factorially arranged (3 x 2) such that six experimental diets differing in chloride levels and in source of minerals were fed for six 28-day laying periods. A significantly higher mortality attributed to FLHS was observed in hens that consumed the diets having chelated minerals as compared with hens that consumed the diets with non-chelated minerals. No difference in mortality was observed among the hens fed the various chloride diets.     

Inhibition of gastric mucosal prostaglandin synthetase activity by mercaptomethylimidazole, an inducer of gastric acid secretion--plausible involvement of endogenous H2O2

We have reported earlier that mercaptomethylimidazole (MMI), an antithyroid drug of thionamide group, induces gastric acid secretion at least partially through the liberation of histamine, sensitive to cimetidine. Now, we show that the drug has a significant inhibitory effect on the cyclooxygenase and peroxidase activity of the prostaglandin (PG) synthetase of the gastric mucosal microsomal preparation. The effect can also be mimicked by low concentrations of H2O2. While studying the possible intracellular effect of MMI on acid secretion, a cell fraction (F3) enriched in parietal cell was isolated by controlled digestion of the mucosa with protease. This cell fraction is activated by MMI as measured by increased O2 consumption. The activation is sensitive to omeprazole, a proton-pump inhibitor, indicating that the activation is due to increased acid secretion by MMI. MMI was also found to directly inhibit the peroxidase activity of the F3 cell fraction and may thus increase the intracellular level of H2O2. The cyclooxygenase activity of the PG synthetase of the F3 cell fraction is also inhibited by MMI and the effect can be reproduced by low concentrations of H2O2. Both MMI and H2O2 can also inhibit the peroxidase activity of the PG synthetase. We suggest that in addition to the activation of the parietal cell by MMI possibly through endogenous H2O2, MMI induces acid secretion in vivo by inactivating the PG synthetase thereby inhibiting the biosynthesis of PG and removing its inhibitory influence on acid secretion so that the histamine released by MMI can stimulate acid secretion with maximum efficiency.     

The dynamics of pAL2-1 homologous linear plasmids in Podospora anserina

We have investigated the properties of the newly synthesized proton-pump inhibitor, 3-butyryl-8-methoxy-4-[(2-thiophenyl)amino]quinoline (YJA20379-6), on gastric mucosal proton-pump (H+/K+-ATPase) activity, gastric acid secretion and gastroduodenal lesions in experimental rats. YJA20379-6 markedly inhibited H+/K+-ATPase activity in rabbit isolated gastric mucosal microsomes, confirming its classification as a proton-pump inhibitor. The inhibitory efficacy of YJA20379-6 on the proton pump was approximately 14-times higher than that of omeprazole at pH 7.4. YJA20379-6 given intraduodenally had a potent inhibitory effect on gastric secretion in pylorus-ligated rats (ED50 22.9 mg kg(-1)) but was less active than omeprazole. Pretreatment of rats with YJA20379-6 dose-dependently protected the gastric mucosa from damage induced by water-immersion stress, indomethacin and absolute ethanol, and the duodenal mucosa from damage induced by mepirizole. Repeated administration of YJA20379-6 also dose-dependently accelerated the spontaneous healing of acetic acid-induced gastric ulcers. These results suggest that YJA20379-6 has potent anti-secretory and anti-ulcer effects which are exerted by suppression of H+/K+-ATPase activity in gastric parietal cells. YJA20379-6 might be useful for the clinical treatment of peptic ulcer diseases.     

Vagal and hormonal influences on gastric secretion in duodenal ulcer disease

Current concepts on the pathophysiology of gastric hypersecretion in duodenal ulcer disease have been presented and the role of vagal nerves and gastrointestinal hormones particularly gastrin has been discussed. Duodenal ulcer patients form a heterogenous group with regard to the gastric acid and pepsin secretion and gastrin release. They may differ from healthy subjects by several wall defined defects including an increased mass of parietal and peptic cells, increased capacity to secrete acid and pepsin, increased vagal drive to the parietal cells, hyperreactivity of antrum, decreased effectiveness of antral and duodenal autoregulatory mechanisms, defective release of secretin, increased gastric emptying and defective removal of gastric acid load from the duodenum. Very little is known what proportion of duodenal ulcer patients suffer from various pathologic disturbences and what are the mechanisms underlying these changes.     

Once-daily gentamicin therapy for experimental Escherichia coli meningitis

BACKGROUND: Eradication of Helicobacter pylori by antibiotics in combination with gastric acid inhibition can result in overgrowth of non-H. pylori bacterial flora. This may confound the histological detection of H. pylori at eradication control if non-specific staining methods are used. OBJECTIVE AND METHODS: In 18 patients treated with amoxycillin (2 weeks) and omeprazole (6 weeks), endoscopically obtained gastric juice was cultured and two biopsies of corpus, antrum and duodenum were taken before and after eradication therapy (with gastric acid inhibition still going on) for culture and for histology to assess the intragastric bacterial flora. By histology, modified Giemsa (MG) and an H. pylori-specific immunohistochemical stain (IMM) were evaluated. RESULTS: Median pH of gastric juice was 1.5 (n = 18) before and 7 (n = 17) after eradication therapy, when patients were still on omeprazole. After therapy, culture showed a significant decrease (P < 0.05) in mean amount of H. pylori in corpus, antral and duodenal biopsies and a significant increase of non-H. pylori flora (P < 0.05) in gastric juice, corpus, antral and duodenal mucosa. With culture as a standard, 16 and 4 biopsy specimens were scored falsely positive for H. pylori by MG and IMM, respectively, and H. pylori was not detected in 23 and 13 biopsy specimens when culture was H. pylori-positive. CONCLUSION: Because of the possible presence of non-H. pylori flora after eradication therapy, the use of IMM is recommended in this situation for the histological detection of H. pylori, especially in those patients with ongoing gastric acid inhibitory therapy.     

Evidence that vitamin A is not required for the biosynthesis of ovalbumin in chicks

Four-day-old pullets fed a vitamin A-deficient diet were stimulated daily with 1 mg 17beta-estradiol-3-benzoate/day for 6 to 19 days. The onset of vitamin A deficiency had no effect on oviduct growth in these chicks; even though vitamin A-deficient chicks showed a severe decline in growth rate while controls (fed the same diet supplemented with retinyl palmitate) continued to grow, estrogen stimulated resulted in similar oviduct size. Ovalbumin concentrations of estrogen-stimulated chicks were determined by immunoprecipitation of the soluble protein supernatant fraction of oviduct. The concentration of ovalbumin in oviducts of chicks fed a vitamin A-supplemented diet was similar in the concentration in oviducts of chicks fed a vitamin A-deficient diet. The incorporation of [3H]glucosamine and 14C-amino acids into immunoprecipitable ovalbumin, following the in vitro incubation of minced oviduct, indicated that ovalbumin synthesis was not affected by vitamin A deficiency. The specific activity of incorporated [3H]glucosamine, the 14C-amino acid incorporation into ovalbumin, the relative rate of ovalbumin synthesis, and the relative effiency of [3H]glucosamine incorporation into ovalbumin were each similar between the two diet groups. The relative efficiency of [3H]glucosamine incorporation into sodium dodecyl sulfate and dithiothreitol extractable membranous proteins of oviduct was not affect by vitamin A deficiency.     

Developmental regulation of gastric somatostatin secretion in the sheep

Gastric somatostatin (SRIF) regulates gastric acidity by inhibiting gastric acid and gastrin secretion. SRIF secretion is increased by gastric acidity and also directly by regulators of gastric acid secretion such as gastrin. This direct effect has not been described in the developing animal, nor have the roles of intermediaries such as histamine and gastric acidity been defined. The present study aimed to establish the regulatory role of gastrin and histamine during development on SRIF secretion and also to determine whether the effects of gastrin and histamine are independent of gastric pH. Pentagastrin and histamine were infused on separate occasions into fetal sheep, newborn lambs, and 28-day-old lambs. To determine the roles of endogenous histamine and gastric pH, ranitidine (a histamine-2 receptor antagonist) and omeprazole (a H+/K+ ATPase inhibitor) were coinfused with the agonists. Plasma SRIF and gastrin concentrations were measured by RIA. Pentagastrin stimulated SRIF secretion in the fetus after 131 days of gestation (term is 147 days), whereas stimulation by histamine was effective only after birth. The SRIF stimulatory effect of pentagastrin in 28-day-old lambs was abolished by ranitidine, which also reduced this effect in the adult sheep. This inhibitory effect of ranitidine was shown to be a result of blockade of stimulatory H2 receptors, because in the adult blockade of acid secretion with omeprazole failed to attenuate the response of histamine. These results indicate that in the fetus, gastrin receptors, but not histamine receptors, are functionally involved in the stimulation of SRIF secretion. After birth, both gastrin and histamine stimulate SRIF, but the effect of gastrin is mediated at least in part by the release of endogenous histamine. These responses occur independently of changes in gastric acidity, supporting the concept of a direct negative feedback between SRIF and gastrin.     

Postprandial biliary and pancreatic secretion during profound inhibition of gastric secretion in humans

This study assessed the effect of profound inhibition of gastric secretion by an H2 antagonist on postprandial gastric emptying of acid and chyme, and on bile acid and pancreatic enzyme secretion under physiological conditions in humans. Six subjects were studied before and while they were given famotidine (40 mg). This study combined a continuous intestinal perfusion technique using 14C-polyethylene glycol (14C-PEG) as duodenal recovery marker, with intermittent sampling of gastric content using PEG 4000 as meal marker. During the three hour study, the area under the curve for gastric acid output decreased from mean (SEM) 88.9 (7.6) mmol for those not receiving treatment, to 21.2 (2.7) mmol for subjects receiving famotidine (p < 0.01). The corresponding values for the rate of acid delivery into the duodenum decreased from 65.2 (11.9) to 16.6 (2.9) mmol (p < 0.05), and those for the rate of gastric emptying of chyme remained unchanged for the group receiving no treatment and during famotidine (1040 (200) v 985 (160) ml respectively, NS). Duodenal bile acid and trypsin output remained unchanged (area under the curve, 457 (128) v 373 (86) umol/kg and 5022 (565) v 5058 (400) IU/kg respectively, NS) receiving no treatment and during famotidine. It is concluded that profound inhibition of postprandial gastric acid secretion by anti-secretory drugs is not accompanied by changes in biliary and pancreatic secretion, mainly because the gastric emptying of chyme is unaffected.     

Effects of dietary L-carnitine on the performance and egg quality of laying hens from 65-73 weeks of age

The effects of L-carnitine supplementation (50-500 mg/kg diet) of a practical layer diet, based on maize, soyabean and wheat, on the performance of laying hens and some indices of egg quality were studied for 8 weeks, using 65-week-old hens kept in cages. Albumen quality (albumen height and Haugh (1937) unit score) was improved, while yolk index and yolk colour score were not affected by dietary L-carnitine. The percentage of egg-white increased and that of egg yolk decreased in response to dietary supplementation of L-carnitine. Dietary L-carnitine did not influence laying performance (egg production rate, mean egg weight, daily feed intake, daily egg mas and feed conversion) or external egg quality measured by egg weight, egg-shape index or by eggshell quality, either measured directly as shell breaking strength or indirectly as shell weight, shell thickness or shell weight per unit surface area. Based on the results of the present study, L-carnitine had a beneficial effect on albumen quality and could modify the components of the edible part of the egg, during the late laying period.