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Oxygen consumption, thermal conductance and body temperature of Meriones unguiculatus (Milne-Edwards, 1867) were measured at a temperature range from 5 to 40°C. The lowest mean metabolic rate tBMR) was 2.13 ± 0.14 ml02 g~ 1 h , which is higher than the predicted values based on their body mass. The thermal neutral zone (TNZ) was 26 to 38°C. Mean body temperature below the TNZ was 38.4 ± 0.5°C. Mean thermal conductance below the TNZ was 0.179 ± 0.037 ml02 g-1 • h-1 • °C which is also higher than predicted values based on their body mass. Thermoregulatory characteristics of Mongolian gerbils are very different from that found in arid-adapted small mammals. The extreme severe climate perhaps is the main selective force faced by Mongolian gerbils during their evolution with their macroenvironments.
This study examined the effects of indomethacin and rofecoxib on normal and Helicobacter pylori (H. pylori)-infected gastric mucosa of Mongolian (M.) gerbils. M. gerbils (6-wk-old) were orally administered H. pylori (ATCC43504, 2×108 CFU/ml) after fasting for 24 hours. Beginning 3 mo after inoculation, indomethacin (2 mg/kg, s.c) or rofecoxib (10 mg/kg, p.o.) was administered once daily for 2 wk to the gerbils. At autopsy, gastric mucosal ulcer area, myeroperoxidase (MPO) activity, prostaglandin (PG) E2 synthesis, and H. pylori viability were determined. Histamine-stimulated gastric acid secretion was measured with the acute gastric fistula method. Histological study was performed with H&E staining. H. pylori infection caused severe mucosal damage and production of lymphoid follicles in the gastric submucosa. In H. pylori-infected gerbils, indomethacin aggravated the gastric mucosal damage induced by H. pylori infection. Furthermore, indomethacin by itself induced gastric ulcers at an incidence of 6/10. In contrast, rofecoxib did not aggravate the H. pylori-induced mucosal damage. Indomethacin and rofeocoxib significantly reduced H. pylori viability. MPO activity was significantly increased in H. pylori-infected gerbils compared with H. pylori-uninfected gerbils. Indomethacin and rofecoxib reduced MPO activity in H. pylori-infected gerbils. PGE2 synthesis was markedly increased in H. pylori-infected gerbils (approximately 3-times) compared with the normal gerbils. Indomethacin significantly inhibited PGE2 synthesis in the gastric mucosa, both in normal and H. pylori-infected gerbils. Rofecoxib did not reduce PGE2 synthesis in normal gerbils, however, PGE2 synthesis was reduced to normal levels in H. pylori-infected gerbils. In H. pylori-infected gerbils, histamine-stimulated gastric acid secretion was reduced compared with normal gerbils. Indomethacin significantly increased histamine-stimulated gastric acid secretion and rofecoxib tended to increase secretion in H. pylori-infected gerbils. It was concluded that indomethacin enhances development of gastric mucosal damage in normal gerbils and aggravates H. pylori-induced gastric damage, resulting in gastric ulcers. Rofecoxib did not induce gastric damage in normal gerbils and did not aggravate damage in H. pylori-infected gerbils, suggesting that rofecoxib is less damaging to the stomach than indomethacin.
Preliminary study of memory processes in Mongolian gerbil (Meriones unguiculatus). Mongolian gerbil (Meriones unguiculatus) a small rodent living in the wild steppes of Mongolia was discovered in 1866 and it is becoming increasingly popular as a pet. The present work is an introduction to describe the behavior of this species and to investigate the influence of gender and age on memory process. 40 gerbils divided into four study groups (young males, young females, adult males, adult females) were twice tested in a modified version of the Lashley III maze (repeat after a week). Using statistical tests memory parameters, the activity of animals and behavior associated with the level of stress were analyzed. Conducted observations and calculations performed showed no difference between the groups (p > 0.05), which leads to the conclusion that in Mongolian gerbils age and sex have no effect on memory.
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Gastric cancer and Helicobacter pylori infection

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The Nobel prize in Physiology and Medicine in 2005 was presented to Barry Marshall and Robin Warren for their discovery of Helicobacter pylori (Hp), but only the involvement of this germ in gastritis and peptic ulcer has been mentioned in the award sentence, while numerous epidemiological, clinical and experimental studies and reports emphasized the crucial role of Hp in pathogenesis of gastric cancer (GC). This review is based on the old concept proposed by P. Correa much before the discovery of spiral bacteria in the stomach, postulating the cascade of mucosal changes from acute/chronic gastritis into the atrophic gastritis with intestinal metaplasia and finally to dysplasia and GC. It is now widely accepted view that Hp infection is the major initiator of the inflammatory and atrophic changes in gastric mucosa accompanied by an over-expression of certain growth factors such as gastrin as well as of cyclooxygenase-2 (COX-2) and anti-apoptotic proteins including survivin and B-cl2, leading to proliferation of mutated atrophic cells, excessive angiogenesis, inhibition of apoptosis and formation of gastric tumour. All the morphological and biochemical changes associated with the transformation of mucosal cells into the cancer cells can be traced in excellent experimental model of gastric cancerogenesis induced by infection of Hp in Mongolian gerbils. Since the eradication therapy was proved in several prospective clinical trials to greatly reduce the incidence of GC and this was confirmed on the gerbil model of Hp-induced GC, it has been postulated; a) that Hp is the major causal factor in pathogenesis of GC and b) that the only rational approach in attempt to reduce the occurrence of GC is the global eradication of Hp.
Using stained acryl latex injected techniques the arteries of the base of the brain in the Mongolian gerbil (Meriones unguiculatus) were studied. The brain of the Mongolian gerbil is supplied with blood by even internal carotid arteries and odd basilar artery. The branches of the internal carotid arteries supply the forebrain and interbrain. They form the arterial circle at the base of the brain. The basilar artery is a source of blood for the midbrain and hindbrain. In this species, except one case, the opened type at the back side of arterial circle was found. The posterior communicating arteries between basilar artery and internal carotid arteries were not observed.
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In this study we investigated the potential neuroprotective effect of 2-oxoglutarate (2-OG) on the hippocampus in the transient vessel occlusion ischemia model in the Mongolian gerbil. The morphological and biochemical studies were performed at 7 days after occlusion of carotid arteries. The acute reduction of NeuN-positive neurons in the CA1 pyramidal layer of the hippocampus was accompanied by increased staining intensity for GFAP-positive astrocytes, indicative of glial reaction. The neuron death in the CA1 area coincided with a strong 2.4 fold decrease in the membrane forms of neuronal cell adhesion molecules and elevated levels of astrocyte-specific proteins (soluble GFAP to 2,6 times; filament GFAP to 1,5 times; calcium-binding protein S-100b to 1,6 times). Treatment with 2-oxoglutarate (2.28 g/l drinking water) for between 7 and 21 days attenuated the neuronal death and reactive astrogliosis in this model of experimental ischemia by 20-50%. Our results suggest that 2-OG may prevent the disturbances of neural cells that usually take place during ischemic pathology.
The impact of in vitro isolation and molecular characterisation of Neospora caninum as well as sequence analyses was studied. The brain homogenate of a naturally Neospora-infected dairy cow (positive in ELISA and Western blot) was intraperitoneally inoculated into Mongolian gerbils (Meriones unguiculatus). The brain of gerbils on day 60 post-inoculation was homogenized, and, after trypsin-digestion, cultured on Vero cells. Neospora-like tachyzoites were first observed after 77 days of cultivation. The parasite was confirmed by polymerase chain reaction (PCR) using Neospora-specific primers Np21 and Np6. The PCR product of the first Slovak isolate (NC-SKB1) was subsequently sequenced and published in GenBank under accession number GU300774. Sequencing and BLAST search identified the isolate as N. caninum.
Gastric Helicobacter pylori (Hp) infection in Mongolian gerbils is an established experimental model of gastric carcinogenesis resulting from the long-term Hp infection but functional aspects accompanying this Hp-induced progression from gastritis to the cancer, especially changes in gastric acid secretion, gastric blood flow (GBF) and gastrin-somatostatin link have been little studied. It is unclear whether Hp eradication therapy alters the functional and the histopathological changes in this animal model of Hp-infection. We examined the effects of intragastric (i.g.) inoculation of Mongolian gerbils with Hp strain (cagA+ vacA+, 5x106 CFU/ml) that had been isolated from a patient with gastric ulcer as compared to those induced by vehicle (saline) in gerbils with or without gastric fistula (GF) at 1, 2, 4, 6, 9, 12 and 30 wks upon gastric inoculation with this bacteria. An attempt was made to evaluate the influence of anti-Hp triple therapy with omeprazole, amoxicillin and tinidazol on gastric Hp-infection and Hp-induced functional impairment of the gastric mucosa. Gastric mucosal biopsy specimens were taken for the assessment of the morphological changes and the presence of Hp infection using rapid urease test (CLO-test) and the density of Hp-colonization were assessed by counting of the number of bacterial colonies per plate. Gastric blood flow (GBF) was measured by H2-gas clearance technique and the venous blood and the gastric content were collected for the measurement of plasma gastrin levels and the gastric luminal somatostatin level by radioimmunoassay (RIA). The Hp in gastric mucosa was detected in all animals by culture and rapid urease test at various periods upon Hp inoculation. Basal gastric acid in non-infected conscious gerbils with GF reached the level of about 28±4 µmol/h and this was reduced by over 50% immediately upon the Hp-inoculation and persisted for time intervals tested up to 30 wk. Early lesions were seen 4 wks after the Hp-inoculation and consisted of chronic gastritis with thickened gastric mucosal foldings and elongated interfoveolar ridges. Edema and congestion as well as significant mucosal inflammatory infiltration with lymphoid infiltrate in lamina propria of the mucosa occurred in all infected gerbils. Adenomatous hyperplasia with cellular atypia was observed at 12 wk upon Hp-inoculation together with increased mitotic activity and numerous apoptotic bodies formation, while lamina propria was reduced leaving dilated atypical gastric gland situated "back-to-back". This glandular atypia failed to show lamina propria or submucosa infiltration corresponding to gastric intraepithelial neoplasia. The GBF in Hp-infected gerbils was significantly lower, and a 6-7 fold increase in plasma gastrin levels combined with a significant fall in gastric luminal somatostatin contents observed at all tested periods as compared to vehicle-controls and these effects were counteracted by anti-Hp triple therapy. We conclude that: 1). Hp-infection in Mongolian gerbils in early stages before adenocarcinoma formation results in the development of typical functional and pathological changes such as suppression of gastric secretion and impairment of both, gastric mucosal microcirculation and gastrin-somatostatin link, and 2). this deleterious influence of Hp on gastric morphology and gastric functions is greatly attenuated in gerbils treated with Hp-eradication therapy.
Four groups of gerbils, each consisting of nine animals, were inoculated with 10⁵ viable cysts of four Giardia isolates obtained from human and from zoo animals. The infected and control gerbils were killed on 7 and 21 day post infection and on 21 day post patent period of infection. This study showed that Giardia isolates recovered from different host species have various potency of inducing changes in the jejunum of gerbils and that the primary host imprinting on Giardia isolate may play an important role in the parasite’s behaviour in other host species. The earliest significant changes were observed in the jejunum of gerbils infected with Giardia obtained from a symptomatic patient. Noteworthy changes were found in the 3 week of infection: (1) the jejunal villi were shortened in gerbils infected with human Giardia isolates, and were elongated in animals infected with rodents Giardia isolates; (2) Giardia obtained from an asymptomatic person induced statistically significant changes in all the parameters of the gerbils’ jejunum except infiltration of the lamina propria; (3) although diarrhoea occurred in gerbils infected with Giardia from a cuis, there were no significant changes except the elongation of the villi and infiltration of lamina propria. The four Giardia isolates induced various mucosal mast cells responses in gerbils. Despite the three- weaks-earlier spontaneous ceasing of the infection caused by animal Giardia isolates, the changes in the jejunum persisted.
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