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S Makimoto

Publications and source records attributed to S Makimoto.

11 recordsLinked to original sources

Effect of Helicobacter pylori eradication on gastric mucosal phospholipid content and its fatty acid composition.

BACKGROUND AND AIMS: Whether Helicobacter pylori eradication alters gastric mucosal phospholipid contents and their fatty acid composition remains unclear. The aim of the present study was to clarify the effect of H. pylori eradication on gastric mucosal phosphatidylcholine (PC) content and its fatty acid composition. METHODS: Endoscopic biopsy specimens were taken from the antrum and body of each of 19 asymtomatic male volunteers for detection of H. pylori, histopathological assessment of gastritis, phospholipid determination and fatty acid analysis. All the subjects with H. pylori infection were treated with eradication therapy. Endoscopy and tissue sampling were repeated again 1 and 6 months after all treatment. RESULTS: In eight subjects, H. pylori infection was evident and was successfully eradicated. Pretreatment degrees of lymphocytes and plasma cells (inflammation) and polymorphonuclear neutrophils (activity) were greater in H. pylori-positive subjects compared with H. pylori-negative subjects (P<0.001), whereas the degree of inflammation decreased (P<0.001), and neutrophils had completely disappeared at 6 months after eradication. Moreover, the gastric mucosal PC contents at the antrum and body were unchanged within 1 month after cessation of treatment, but increased at 6 months after eradication (P<0.05). At 6 months after cessation of treatment, H. pylori-eradicated subjects had an increase (+30% at antrum, +18% at body) in linoleic acid composition and a decrease (-37%, -43%) in arachidonic acid composition of PC at the antrum and body, respectively. CONCLUSIONS: These findings suggest that H. pylori eradication reduces the production of various eicosanoids, resulting in the normalization of gastric mucosal PC content and its fatty acid composition, which may consequently cause the gastric mucosal hydrophobicity to be normalized.

Adult↗

Helicobacter pylori alters n-6 fatty acid metabolism and prostaglandin E2 synthesis in rat gastric mucosal cells.

BACKGROUND AND AIMS: Little is known about whether Helicobacter pylori infection alters fatty acid metabolism in gastric mucosal cells. By using cultured rat gastric mucosal cells (RGM-1), we investigated the effect of H. pylori broth culture filtrates on this point. Furthermore, our study aimed to find out whether n-6 long chain polyunsaturated fatty acids from linoleic acid are formed in RGM-1 cells. METHODS: Rat gastric mucosal cells were incubated with 10, 20 and 40 microg/mL of linoleic acid or medium alone. Phosphatidylcholine content extracted from whole RGM-1 cells was quantitated by using a densitometer, and its fatty acid composition was analyzed by using gas chromatography. Prostaglandin E2 concentration in the culture medium was measured by using radioimmunoassay. The expression of cyclooxygenase (COX)-1 and COX-2 was examined by using reverse transcription-polymerase chain reaction. In addition, after incubation with [1-14C] linoleic acid, radioactivities of both linoleic acid and arachidonic acid components of the PC fraction were counted. The effects of H. pylori broth culture filtrates on PC content, its fatty acid composition and prostaglandin (PG)E2 synthesis were also assessed. RESULTS: Linoleic acid addition caused an increase in the composition of arachidonic acid, as well as linoleic acid, and also in PGE2 concentration. Cyclo-oxygenase-2 expression was induced in RGM-1 cells by the addition of linoleic acid. In addition, [1-14C] linoleic acid added to the culture medium was converted to [1-14C] arachidonic acid in RGM-1 cells. Helicobacter pylori broth culture filtrates decreased linoleic acid composition and increased arachidonic acid composition. Moreover, after incubation with H. pylori broth culture filtrates, PGE2 concentrations were higher than that of the controls. CONCLUSIONS: These findings suggest the presence of fatty acid elongase and Delta5- and Delta6-desaturases synthesize arachidonic acid from linoleic acid in RGM-1 cells. Thus, H. pylori infection may enhance PGE2 synthesis and accelerate n-6 fatty acid metabolism in gastric mucosal cells, which could make the gastric mucosal barrier more fragile.

Animals↗

[Reproducibility and validity of a semi-quantitative food frequency questionnaire].

The reproducibility and relative validity of a semi-quantitative food frequency questionnaire (FFQ) were evaluated. Subjects were 72 (36 men and 36 women) residents of N island, Shimane Prefecture in Japan, aged 50-76 years. The questionnaire was administered twice at an interval of one week (FFQ1, FFQ2), and 7-day weighing diet records were collected during that period. This protocol was conducted in summer and winter. The mean intakes for 11 nutrients calculated from the FFQ1 and FFQ2 were similar and, those from the FFQ1 were smaller than those from the diet records for all but fat and vitamin C. Pearson correlation coefficients assessing reproducibility between nutrient intakes from FFQ1 and FFQ2 ranged from 0.59 for vitamin C to 0.90 for carbohydrate. Validity was measured by comparing nutrient intakes from FFQ1 with those from the 7-day diet record, and Pearson correlation coefficients ranged from 0.15 for iron to more than 0.35 for total energy and macronutrients. These correlation coefficients showed slight difference by gender or age group, but did not vary materially between seasons. These data indicate that this questionnaire is reproducible but has some problems in validity.

Aged↗

Effect of pressure on the mechanism of hydrolysis of maltotetraose, maltopentaose, and maltohexose catalyzed by porcine pancreatic alpha-amylase.

Pressure effects on the time course of the products' composition accompanying the hydrolysis of maltooligosaccharides [maltotetraose (G4) maltopentaose (G5), and maltohexaose (G6)] catalyzed by porcine pancreatic alpha-amylase (PPA) were measured up to 300MPa at 30 degrees C. The composition of products, glucose (G ), maltose (G2), and maltotriose (G3), for the hydrolysis of G4, and G5 substrates changed a little by compression. But for G6 substrate, pressure induced some changes in the composition of products, G2, G3, and G4, respectively. From the pressure dependence of the observed rate constants on PPA catalyzed hydrolysis of G6, the volume difference between two kinds of Michaelis complexes of alpha-amylase-G6 is about 5.4 cm3/mol. The mechanism of an interesting pressure-induced reaction catalyzed by PPA is discussed in the terms of the reaction volumes.

Animals↗

Volatile anesthetics-induced activation phenomena of alpha-chymotrypsin-catalyzed hydrolysis.

The rates of hydrolysis of p-nitrophenyl acetate (pNPA), p-nitrophenyl propionate (pNPP), p-nitrophenyl butanate (pNPB), and p-nitrophenyl valerate (pNPV) catalyzed by alpha-chymotrypsin (alpha-CHT) were measured with and without volatile anesthetics at 25.0 degrees C. Halothane activated the hydrolysis of pNPA and pNPP, meanwhile inhibited that of pNPB and pNPV. The activation phenomena were explained by the existence of a 1:1 enzyme-anesthetics complex and the opening of an activated pathway. The rate constant of pNPA hydrolysis catalyzed by alpha-CHT of the activated pathway kA by halothane was 0.269 s-1, whereas that of the normal pathway was k0 0.093 s-1. The free energy of activation was stabilized at 0.64 kcal/mol by halothane. The mechanisms of the activation and inhibition are discussed in terms of the molecular size of the substrate and anesthetics.

Anesthetics↗

Pressure effects on substrate activation phenomena in the alpha-chymotrypsin-catalyzed hydrolysis of p-nitrophenyl acetate.

With and without p-chlorophenol as an activator, the rates of hydrolysis of p-nitrophenyl acetate catalyzed by alpha-chymotrypsin were measured at pressures up to 2 kbar at 25 degrees C. From the pressure dependence of the rate constant (kcat)A and (kcat)0 of the product formation with and without an activator, the activation volumes (delta V not equal to cat)A and (delta not equal to cat)0 were +2 and -6 +/- 1 cm3.mol-1. From the pressure dependence of the equilibrium constant (KA) of incorporation of p-chlorophenol into the enzyme, the volume change (delta VA) was -10 +/- 1 cm3.mol-1. The mechanisms of the substrate activation are discussed in terms of the activation and reaction volumes.

Atmospheric Pressure↗

Effect of pressure on the pre-steady-state kinetics of the hydrolysis of anilide substrates catalyzed by alpha-chymotrypsin.

The pre-steady-state of the hydrolysis of succinyl-L-alanyl-L-alanine p-nitroanilide (SA2pNA) and succinyl-L-alanine p-nitroanilide (SApNA) catalyzed by alpha-chymotrypsin in Tris buffer solution was measured up to 1.5 kbar at 25 degrees C. The pressure dependence of the formation of tetrahedral intermediate from the Michaelis complex on the rate constant (k1) gave activation volumes, delta V1 not equal to, of -33 +/- 2 cm3 X mol-1 for SA2pNA and -30 +/- 2 cm3 X mol-1 for SApNA. The reaction mechanism of alpha-chymotrypsin is discussed in terms of the activation volumes.

Alanine↗

Epidermoid cyst originating from an intrapancreatic accessory spleen.

Pancreatectomy in a 45-year-old woman showed, after pathologic analysis, an epidermoid cyst originating from an intrapancreatic accessory spleen. This mass consisted of parenchymal and cystic components. It is important to note the relation between the splenic parenchyma and the parenchymal component of the mass for the differential diagnosis of a cystic mass in the pancreatic tail.

Choristoma↗