<ORIGINAL>Quantification of Porphyromonas gingivalis by real time PCR : new primers targeting the rgpA and rgpB gene encoding RGP

We designed new primers for the quantification of Porphyromonas gingivalis by real time PCR. The new primer set targeted the rgpA and rgpB genes that encode arginine specific cysteine proteinase (Arggingipain or Rgp), one of the putative pathogenic factors of P. gingivalis. The PCR product obtained using our primers showed no by-products by melting curve analysis. The PCR product sequence showed no significant matches to other sequences by BLAST searching of genetic databases except for matches to P. gingivalis rgpA and rgpB sequence, and could not be amplified from template derived from other oral bacteria apart from P. gingivalis. Therefore, we concluded that our primers were specific for P. gingivalis rgpA and rgpB, and could be used to quantity from 10^3 to 10^7 P. gingivalis cells when applied to real time PCR

Distribution and Endocrine Morphology of Polypeptide YY (PYY) Containing Cells in the Human Gut

Using human materials, the distribution of PYY containing cells was determined by immunocytochemical methods and discussion was made on their morphological endocrinology. PYY cells were fairly numerous in the lower gastrointestinal tract of man, particularly in the colon and rectum. The cells were also present in the pancreas and duodenum but quite rarely. PYY cells were not observed at all in the lower part of the esophagus, stomach and gall bladder. Their peculiar and characteristic shapes as well as distribution suggest that PYY may have some action (probably specific) on the function of the distal gastrointestinal tract

Preventive Effect of Proglumide on Erosive Gastritis in the Rat

The purpose of this study is to determine whether or not proglumide has a preventive effect on the erosive gastritis induced by sodium salt of taurocholic acid (TCA) in the rat. Its effect on the formation of gastric erosions, serum gastrin levels and secretion of acid and pepsin were also studied. The rats were given standard feed containing 0.25% proglumide and water containing 5mM TCA (experimental E group). The control rats were given standard feed and water containing 5mM TCA (TCA group). All rats were killed at the end of the 3 months. The tissue specimens of the resected gastric mucosa were stained with hematoxylin eosin for histopathology and with azan for evaluation of fibrous ploriferation. From microscopic observation of the stained specimens, the following results were obtained. TCA-group showed long mucosal surface injury (erosion), inflammatory cell infiltration, a reduction in the number of parietal cells, a decrease of mucosal thickness, and proliferation of collagenous fiber. In contrast, in the E group, these morphological and morphoquantitative changes were significantly small. The length of erosion and inflammatory cell infiltration were significantly reduced in the E group when compared with the TCA group. Furthermore, mucosal thickness was almost normal and fibrous proliferation was significantly scarce in the E group. Proglumide had an insignificant effect on pH on the mucosa, volume and pH of gastric juice, serum gastrin levels and tetragastrin-induced secretion of acid and pepsin. It is, thus, evident that proglumide has a preventive effect on the induction of erosive gastritis caused by TCA in the rats. Since it is difficult to explain its mechanism for the prevention of gastritis from only the already known facts that it has protective action on gastric mucosa and an inhibitory effect on secretion of acid and pepsin, unknown mechanisms are suspected to be involved

Endocrine Profile in Rats with Postgastrectomy Malabsorption: a Pilot Study

Abnormal endocrine profile, especially in the enteropancreatic axis, was described in rats with malnutrition caused by malabsorption after total gastrectomy. Insulin, substance P and motilin concentrations at the fasting condition were significantly elevated in malnutritious rats after total gastrectomy when compared to those in control rats. A significant elevation of pancreatic glucagon and motilin was noted after intraduodenal fat administration in malnutritious rats. These data suggest that these peptides of many humoral factors may thus cause abnormal enteropancreatic axis and consequent malnutrition

Induction of Experimental Atrophic Gastritis by N-Methyl-N'-Nitro-N-Nitrosoguanidine or Taurocholic Acid in Donryu Rats

The morphology of the rat (Donryu) gastric mucosa was examined by light microscopy after administration of N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) or taurocholic acid (TCA), a component of bile acids. MNNG was given to rats ad libitum from light-sealed bottles for 5 months and deionized water was given freely for 6 months thereafter. TCA was administered to rats freely for 11 months. Deionized water was given to rats as control (non-treated rats). Rats treated with MNNG or TCA and control rats were killed at 11 months after the beginning of the experiment. Using 3 micron tissue samples taken from the area of the gastric mucosa designated before the experiment, hematoxylin and eosin and azan stain were made for histopathological evaluation and fibrosis. Marked atrophic changes, such as reduction in the number of parietal cells, shortened mucosa! length, inflammaotry cell infiltration, and proliferation of fibrosis, were present in the gastric mucosa of rats treated with MNNG as well as TCA. These findings were typical for atrophic gastritis. Such atrophic changes were slight in the gastric mucosa of the control rats. The frequency of tumourous lesions was very low in MNNG-treated rats. We have concluded on the basis of the present data that MNNG as well as TCA can induce atrophic gastritis in Donryu rats

Existence of VIP and PHI-Like Immunoreactivities in the Amphibian Gut

The present paper provides the first definitive evidence on the presence and possible co-existence of VIP- and PHI-like peptides in the peripheral nervous system of the amphibian (bullfrog) gut wall. The possibility of co-existence of the peptides suggests that VIP- and PHI-like peptide may be synthesized from the same precursor protein in the amphibian

Gastrin and Somatostatin in Patients with Hyperchlorhydric Duodenal Ulcer

Hormonal and morphological studies were conducted to ascertain the role played by gastrin and somatostatin in the pathophysiology of duodenal ulcer, in particular hyperchlorhydric duodenal ulcer, using 35 patients with duodenal ulcer, of whom 15 were hyperchlorhydric and 20 were normochlorhydric. Twenty normal subjects with normochlorhydria were used as a control. In patients with hyperchlorhydric duodenal ulcer following significant findings were observed: 1. Basal and stimulated hyperchlorhydria, 2. Parietal cell hyperplasia, 3. Basal hypergastrinemia, 4. Increased concentration of gastrin and large number of G cells (G cell hyperplasia) in the antral mucosa. 5. Mucosal concentration of somatostatin and D cells in the antrum was reduced, but the former in patients with hyperchlorhydric duodenal ulcer was not different from that in patients with normoacidic duodenal ulcer. 6. A significant correlation in mucosal concentration was demonstrated between gastrin and somatostatin in control subjects but not in patients with duodenal ulcer. 7. There was a significant correlation in maximal acidity in gastric secretion and mucosal concentration of antral somatostatin in control subjects but not in patients with duodenal ulcer. 8. Concentration of plasma somatostatin in patients with duodenal ulcer was not different from that in control subjects. These findings indicate that gastrin and somatostatin may participate in the pathophysiology of duodenal ulcer, at least in the subgroup of duodenal ulcer associated with hyperchlorhydria, and the subgroup of duodenal ulcer may be an endocrine disorder

Cryptococcus gattii Genotype VGIIa Infection in Man, Japan, 2007

We report a patient in Japan infected with Cryptococcus gattii genotype VGIIa who had no recent history of travel to disease-endemic areas. This strain was identical to the Vancouver Island outbreak strain R265. Our results suggest that this virulent strain has spread to regions outside North America