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At least 721 records · Page 40Linked to original sources
PubMed1977

Comparative evaluation of three different commercial blood culture media for recovery of anaerobic organisms.

A comparison of three different commercial media was made to assess their recovery of anaerobic organisms from the blood stream. The three media used were the 50-ml brain heart infusion broth with added CO2 (Pfizer), the 50-ml Thiol broth with added CO2 (Difco), and the 50-ml prereduced, supplemented peptone broth in a Vacutainer tube with added CO2 (Becton-Dickinson). During a period of 17 consecutive months, 12,216 specimens of blood were processed with each broth. Aerobic or anaerobic bacteria were recovered from 913 specimens (7%). Seventy-four specimens (8%) of the total positive cultures contained anaerobic organisms. When potential contaminants were removed from the totals, 7% of the positive cultures contained anaerobic organisms and 7% of the patients with positive cultures had bacteremia with anaerobic bacteria. Of the three commercial blood culture media studied, the prereduced, supplemented peptone broth recovered more anaerobic organisms than did either the brain heart infusion or Thiol broths.

Anaerobiosis↗
PubMed1973

Ammonia production by intestinal bacteria.

Bacterial growth and the production of ammonia from urea and by deamination of peptone has been examined at various pHs in both conventional static bacterial cultures and in a continuous cultivation system. Growth occurred on primary testing of 93 out of 100 strains of aerobic Gram-negative bacteria at pH 5, and 48 out of 50 strains of Esch. coli at pH 4.6. Hydrolysis of urea by Proteus mirabilis decreased steadily from pH 7.2 to pH 5.3; below pH 5.3 little hydrolysis occurred. Ammonia production from peptones by Esch. coli decreased from pH 7.2 to pH 4.6. Considerable variation was noted in the ability of different strains to produce ammonia. Experiments with cultures containing both Esch. coli and Pr. mirabilis showed that more ammonia was produced at low pH than was produced by cultures of single organisms. At low pH reduction in the count of organisms was not found to be an essential prerequisite for reduction of ammonia formation.

Ammonia↗
PubMed1975

Lipase and esterase formation by psychrophilic and mesophilic Acinetobacter species.

Acinetobacter O16, a psychrophilic species, produced extracellular lipase (measured by hydrolysis of olive oil, tributyrin, or beta-naphthyl laurate) when grown on a complex medium (peptone plus yeast extract). Most lipase was produced during the logarithmic phase of growth. Very little cell-bound lipase was formed. These cells also produced an esterase (measured by the hydrolysis of beta-naphthyl acetate). At first, all esterase was cell bound; significant amounts appeared in the external medium late in growth. Breaking the cells did not increase cell-bound lipase activity. After breaking of the cells, most of the cell-bound lipase and esterase activity was solubilized, even after very high speed centrifugation. No appreciable amounts of these enzymes were released by osmotic shock. Lipase formation was greatly affected by nutrient conditions. Lowering either the yeast extract of the peptone content of the normal complex medium lowered or abolished lipase formation. Esterase activity was lowered to a lesser extent. Cells growing in synthetic amino acid plus vitamin medium or in acid-hydrolyzed casein produced substantial amounts of esterase but no cell-free or cell-bound lipase. However, if sodium taurocholate was added to these media, lipase was produced. Greatest production occurred if a mixture of di- and poly-peptides was also present. Taurocholate also stimulated lipase production in the normal complex medium. Adding Tween 80 or ethanol to the normal complex medium inhibited lipase production. Sodium acetate, oleic acid, olive oil, or Tween 20 added to synthetic media did not affect lipase production. The psychrophile grew more quickly at 30 degrees C than at 15 or 20 degrees C but produced more lipase at the lower temperatures. Esterase production was about the same at 20 and 30 degrees C. A mesophilic Acinetobacter species produced the same amount of lipase and esterase at 20 and 30 degrees C. The best production of lipase by the psychrophile occurred in standing cultures.

Acinetobacter↗
PubMed1979

A liquid medium for the production of Kabatiella zeae conidia.

A liquid medium, designated as Kabatiella zeae medium (KZM), containing 10.0 g of carboxymethylcellulose, 5.0 g of maltose, 1.5 g of peptone, 1.0 g of monobasic potassium phosphate, 1 L of distilled water, is described. Peptone was found to be the component most influential in stimulating sporulation. The optimum temperature for conidial production was 25 degrees C. In shake culture about 10(7) conidia/mL were produced in 5 days at room temperature (about 21 degrees C) when KZM was seeded with 4-day-old colony plugs. The optimum for conidial production was pH 5 with only a slight gradual reduction to pH 9. However, fungal development was abnormal at pH values of 4 and 5. Of the 29 isolates tested, only two did not sporulate in KZM or in any other medium. Because of the high yield of conidia in a short time, the ease of preparation and use, and its low cost, KZM is especially useful where large amounts of inoculum are needed.

Carboxymethylcellulose Sodium↗
PubMed1982

The effect of growth media upon the ultrastructure of Blastomyces dermatitidis.

The ultrastructure of yeast, intermediate transitional forms, and mycelia of Blastomyces dermatitidis cultured in brain heart infusion (BHI) was compared with that of like forms grown in leucine-glucose (LG) medium. Blastomyces dermatitidis yeasts were also grown in yeast extract - peptone (YP) medium and in glucose - yeast extract - peptone (GYP) medium, and their ultrastructures were compared with BHI-grown yeasts. Yeast, intermediate, and mycelial cells cultured in LG had more granular cytoplasm and better defined membranes than analogous BHI-grown cells. Yeasts grown in LG contained more glycogen and fewer lipid bodies and had no visible intracytoplasmic membrane systems. Some yeasts from LG cultures had bizarre shapes and structure. Intermediate and mycelial forms from LG cultures contained more glycogen and lipid bodies than analogous cells from BHI. Yeasts grown in YP had a more highly defined internal structure than BHI-grown yeasts. Some cells were doubly budded. and some were elongated. Similar elongated yeasts were found growing in GYP. Yeasts grown in GYP lacked a well-defined internal structure and had less glycogen than BHI-grown yeasts. They had no visible lipid bodies, but large vacuoles were present. Intrayeast hyphae were observed only in BHI-grown intermediate cells.

Blastomyces↗
PubMed2000

Stoichiometry of diauxic growth of a xylanase-producing Bacillus strain.

In this work, the establishment of material balances and stoichiometry of the growth of Bacillus sp. was undertaken. This strain produces high quantities of a xylanase suitable for use as bleach boost agent in chlorine-free bleaching sequences of paper pulp. As carbon dioxide plays an important role as a growth factor, bacterial growth in two fermentations, one fed with air and another fed with carbon-dioxide-enriched air, were compared. For this purpose, a method permitting the determination of the consumption of the two carbon sources, xylan and peptone, was proposed. The material balances revealed that in both cases, the bacteria first use peptone as their carbon source, and then xylan in the second part of the growth phase. The aerated culture showed diauxic growth on these two substrates, whereas carbon-dioxide-enriched air caused disappearance of the metabolic adaptation phase, and rendered biomass production more economic. The fermentation fed with air needed 30% more xylan than the fermentation fed with carbon-dioxide-enriched air for the same quantity of biomass produced.

Air↗
PubMed2004

Optimization of extracellular fungal peroxidase production by 2 Coprinus species.

Optimum culture conditions for the batch production of extracellular peroxidase by Coprinus cinereus UAMH 4103 and Coprinus sp. UAMH 10067 were explored using 2 statistical experimental designs, including 2-level, 7-factor fractional factorial design and 2-factor central composite design. Of the 7 factors examined in the screening study, the concentrations of carbon (glucose) and nitrogen (peptone or casitone) sources showed significant effects on the peroxidase production by Coprinus sp. UAMH 10067. The optimum glucose and peptone concentrations were determined as 2.7% and 0.8% for Coprinus sp. UAMH 10067, and 2.9% and 1.4% for C. cinereus UAMH 4103, respectively. Under the optimized culture condition the maximum peroxidase activity achieved in this study was 34.5 U x mL(-1) for Coprinus sp. UAMH 10067 and 68.0 U x mL(-1) for C. cinereus UAMH 4103, more than 2-fold higher than the results of previous studies.

Carbon↗
PubMed1986

Evidence for reflex adrenergic inhibition of acid secretion in the conscious rat.

In conscious gastric fistula rats, gastric distension with saline to a pressure of 7 cm caused a threefold reduction of basal gastric acid secretion. Distension with 6.25% peptone solution to the same pressure doubled basal acid secretion. The saline distension-induced inhibition was abolished by guanethidine and markedly reduced by propranolol; phentolamine was ineffective. The response to peptone was unaffected by guanethidine. The results suggest that in the rat, gastric distension at physiological pressures inhibits acid secretion by a beta-adrenergic reflex. The inhibition can be masked by concurrent chemical stimulation of the gastric mucosa by the digestion products of food.

Animals↗
PubMed1988

Action of the cholecystokinin antagonist L364,718 on gastric emptying in the rat.

Cholecystokinin (CCK) is a potent inhibitor of gastric emptying. We have examined the effects of a novel potent peripheral CCK receptor antagonist (L364,718) on the action of endogenous and exogenous CCK octapeptide (CCK-8) on gastric emptying in the rat. In conscious gastric fistula rats, the recovery of liquid test meals of 3.0 ml (containing phenol red as a dilution marker) was determined over periods up to 8 min. Compared with saline, gastric emptying of solutions of peptone (4.5%), 50 mM HCl, and hyperosmolal saline was significantly delayed. The emptying of saline was also delayed by intravenous infusion of CCK-8 (400 pmol.kg-1.h-1). The CCK antagonist L364,718 reversed the effect of peptone in a dose-dependent manner and inhibited the response to exogenous CCK, but the emptying of physiological saline, 50 mM HCl, or hyperosmolal saline remained unchanged. A protease inhibitor (FOY-305) that is thought to release endogenous CCK by inhibiting negative feedback control by luminal proteases also delayed emptying, and this response was inhibited by L364,718. We conclude that CCK has a physiological role in the mediation of the effect of proteins on gastric emptying in the rat.

Animals↗
PubMed1991

Hormonal control of avian pancreas by gastrin-releasing peptide from the proventriculus.

Endocrine cells in the acid-secreting part of the avian stomach, the proventriculus, contain two forms of gastrin-releasing peptide (GRP) of 27 and 6 residues, respectively. We have examined the actions of exogenous GRP-27 and GRP-6 and endogenously released GRP in the control of pancreatic secretion in urethan-anesthetized turkeys. Chicken GRP-27 and the structurally related amphibian peptide bombesin were potent stimulants of fluid and protein output from the pancreas (at 6-100 pmol/kg, iv). GRP-6 had no significant effect at doses up to 1,000 times higher. A bombesin antagonist, (CH3)2-CHCO-[D-Ala24]GRP-20--26-NHCH3, inhibited the action of exogenous chicken GRP-27 but did not inhibit intravenous cholecystokinin octapeptide (CCK-8). Distension of the proventriculus with a solution of peptone produced an increase in the flow of pancreatic juice and an increase in protein output, which was not reduced by atropine. The bombesin antagonist produced a reversible inhibition of this response. A CCK-gastrin antagonist, BOC-beta-Ala-Trp-Leu-Asp-O(CH2)2- phenyl(4F), which inhibited the action of exogenous CCK, had no effect on the pancreatic response to exogenous GRP-27 or to distension of the proventriculus with peptone. We suggest that protein-rich solutions in the proventriculus release GRP, which in turn acts directly on the pancreas to stimulate enzyme secretion.

Amino Acid Sequence↗
PubMed1993

Duodenal lipid inhibits gastric acid secretion by vagal, capsaicin-sensitive afferent pathways in rats.

Neural and endocrine pathways mediate the inhibitory effects of intestinal fat on gastric acid secretion. To study whether vagal and/or spinal afferent nerves contribute to the neural component of the enterogastric reflex, the sensory neurotoxin capsaicin was applied topically either to the vagus nerves bilaterally or to the celiac-superior mesenteric ganglia in rats with chronic gastric and duodenal fistulas. In lightly restrained, awake rats acid secretion was stimulated for 2 h by continuous intragastric perfusion with 8% peptone and was measured by extragastric titration to pH 5.5. Duodenal lipid perfusion (0-20%) during the 2nd h caused inhibition of peptone-stimulated acid output. Acid output was inhibited by 81% during 5% lipid perfusion of the duodenum and was restored after capsaicin treatment of the vagus nerves. In contrast, capsaicin treatment of the celiac ganglion did not alter the acid inhibitory response to any dose of intestinal lipid. Basal and maximum acid outputs were not significantly different among rats treated by either method with capsaicin. The neural component of the enterogastric reflex in awake rats is mediated in part by a capsaicin-sensitive, vagal-afferent neural reflex.

Afferent Pathways↗
PubMed1999

Intestinal fat-induced inhibition of meal-stimulated gastric acid secretion depends on CCK but not peptide YY.

Fat in small intestine decreases meal-stimulated gastric acid secretion and slows gastric emptying. CCK is a mediator of this inhibitory effect (an enterogastrone). Because intravenously administered peptide YY (PYY) inhibits acid secretion, endogenous PYY released by fat may also be an enterogastrone. Four dogs were equipped with gastric, duodenal, and midgut fistulas. PYY antibody (anti-PYY) at a dose of 0.5 mg/kg or CCK-A receptor antagonist (devazepide) at a dose of 0.1 mg/kg was administered alone or in combination 10 min before the proximal half of the gut was perfused with 60 mM oleate or buffer. Acid secretion and gastric emptying were measured. We found that 1) peptone-induced gastric acid secretion was inhibited by intestinal fat (P < 0.0001), 2) inhibition of acid secretion by intestinal fat was reversed by CCK-A receptor antagonist (P < 0.0001) but not by anti-PYY, and 3) slowing of gastric emptying by fat was reversed by CCK-A antagonist (P < 0. 05) but not by anti-PYY. We concluded that inhibition of peptone meal-induced gastric acid secretion and slowing of gastric emptying by intestinal fat depended on CCK but not on circulating PYY.

Animals↗
PubMed2001

Acid inhibition by intestinal nutrients mediated by CCK-A receptors but not plasma CCK.

We examined the role of CCK-A receptors in acid inhibition by intestinal nutrients. Gastric acid and plasma CCK and gastrin levels were measured in rats with gastric and duodenal fistulas during intragastric 8% peptone and duodenal perfusion with saline, complete liquid diet (CLD; 20% carbohydrate, 6% fat, and 5% protein), and the individual components of CLD. Acid output was significantly inhibited (50-60%) by CLD, lipid, and dextrose. Plasma CCK was significantly increased by CLD (from 2.6 +/- 0.3 to 4.8 +/- 0.5 pM) and lipid (4.6 +/- 0.5 pM). CCK levels 50-fold higher (218 +/- 33 pM) were required to achieve similar acid inhibition by exogenous CCK-8 (10 nmol x kg(-1) x h(-1) iv). Intestinal soybean trypsin inhibitor elevated CCK (10.9 +/- 2.5 pM) without inhibiting acid secretion. The CCK-A antagonist MK-329 (1 mg/kg iv) reversed acid inhibition caused by CLD, lipid, and dextrose. Peptone-stimulated gastrin (21.7 +/- 1.9 pM) was significantly inhibited by CLD (14.5 +/- 3.6 pM), lipid (12.3 +/- 2.2 pM), and dextrose (11.9 +/- 1.5 pM). Lipid and carbohydrate inhibit acid secretion by activating CCK-A receptors but not by altering plasma CCK concentrations.

Animals↗
PubMed2003

Effects of peripheral CCK receptor blockade on food intake in rats.

Type A cholecystokinin receptor (CCKAR) antagonists differing in blood-brain barrier permeability were used to test the hypothesis that satiety is mediated, in part, by CCK action at CCKARs located peripheral to the blood-brain barrier. At dark onset, non-food-deprived rats received a bolus injection of devazepide (2.5 micromol/kg iv), a 3-h infusion of A-70104 (1 or 3 micromol x kg-1 x h-1 iv), or vehicle either alone or coadministered with a 3-h infusion of CCK-8 (10 nmol x kg-1 x h-1 iv) or a 2-h intragastric infusion of peptone (1 g/h). Food intake was determined from continuous computer recordings of changes in food bowl weight. Devazepide penetrates the blood-brain barrier; A-70104, the dicyclohexylammonium salt of Nalpha-3-quinolinoyl-d-Glu-N,N-dipentylamide (A-65186), does not. CCK-8 inhibited 3-h food intake by more than 50% and both A-70104 and devazepide abolished this response. A-70104 and devazepide stimulated food intake and similarly attenuated the anorexic response to intragastric infusion of peptone. Thus endogenous CCK appears to act, in part, at CCKARs peripheral to the blood-brain barrier to inhibit food intake.

Animals↗
PubMed2002

Effects of peripheral CCK receptor blockade on gastric emptying in rats.

Type A CCK receptor (CCKAR) antagonists differing in blood-brain barrier permeability [devazepide penetrates; the dicyclohexylammonium salt of Nalpha-3-quinolinoyl-d-Glu-N,N-dipentylamide (A-70104) does not] were used to test the hypothesis that duodenal nutrient-induced inhibition of gastric emptying is mediated by CCKARs located peripheral to the blood-brain barrier. Rats received A-70104 (700 or 3,000 nmol. kg(-1). h(-1) iv) or devazepide (2.5 micromol/kg iv) and either a 15-min intravenous infusion of CCK-8 (3 nmol. kg(-1). h(-1)) or duodenal infusion of casein, peptone, Intralipid, or maltose. Gastric emptying of saline was measured during the last 5 min of each infusion. A-70104 and devazepide abolished the gastric emptying response to a maximal inhibitory dose of CCK-8. Each of the macronutrients inhibited gastric emptying. A-70104 and devazepide attenuated inhibitory responses to each macronutrient. Intravenous injection of a CCK antibody to immunoneutralize circulating CCK had no effect on peptone or Intralipid-induced responses. Thus endogenous CCK appears to act in part by a paracrine or neurocrine mechanism at CCKARs peripheral to the blood-brain barrier to inhibit gastric emptying.

Animals↗
PubMed2003

Abdominal vagal mediation of the satiety effects of CCK in rats.

CCK type 1 (CCK1) receptor antagonists differing in blood-brain barrier permeability were used to test the hypothesis that satiety is mediated in part by CCK action at CCK1 receptors on vagal sensory nerves innervating the small intestine. Devazepide penetrates the blood-brain barrier; A-70104, the dicyclohexylammonium salt of N alpha-3-quinolinoyl-D-Glu-N,N-dipentylamide, does not. At dark onset, non-food-deprived control rats and rats with subdiaphragmatic vagotomies received a bolus injection of devazepide (2.5 micromol/kg i.v.) or a 3-h infusion of A-70104 (3 micromol.kg(-1).h(-1) i.v.) either alone or coadministered with a 2-h intragastric infusion of peptone (0.75 or 1 g/h). Food intake was determined from continuous computer recordings of changes in food bowl weight. In control rats both antagonists stimulated food intake and attenuated the anorexic response to intragastric infusion of peptone. In contrast, only devazepide was effective in stimulating food intake in vagotomized rats. Thus endogenous CCK appears to act both at CCK1 receptors beyond the blood-brain barrier and by a CCK1 receptor-mediated mechanism involving abdominal vagal nerves to inhibit food intake.

Abdomen↗
PubMed1998

Load-sensitive rat gastric vagal afferents encode volume but not gastric nutrients.

To assess nutrient sensitivity in a population of gastric load-sensitive vagal afferents, their neurophysiological activity was examined in anesthetized rats with inflated pyloric cuffs after gastric infusion of a range of volumes of nutrient and equiosmotic saline solutions. Responses to physiological saline loads (1, 2, 4, and 8 ml) were compared with responses elicited by the same volume range of carbohydrate (12.5% glucose), protein (12.5% peptone), and equiosmotic hypertonic (750 mosM) saline. The threshold load volume of physiological saline required to increase gastric vagal afferent activity was 1 ml. Thereafter, there was a dose-dependent relationship between increasing gastric volume and firing rate and between gastric volume and pressure. The dose-response relationships elicited by glucose, peptone, and equiosmotic hypertonic saline loads did not differ from those elicited by physiological saline loads. These data identify a population of gastric load-sensitive vagal afferents unresponsive to the chemical composition of gastric contents and are consistent with a role for vagal gastric volume signals but not gastric nutrient content in the negative feedback control of ingestion.

Afferent Pathways↗
PubMed1999

Gut vagal afferent lesions increase meal size but do not block gastric preload-induced feeding suppression.

Subdiaphragmatic vagal afferent (SVA) signals arising from gut sites may provide critical feedback for the control of food intake within a meal. To evaluate the role of SVAs in both spontaneous and scheduled meals, food intake was assessed in two paradigms in male Sprague-Dawley rats. In the first study, control (Con) rats (n = 6) and rats with subdiaphragmatic vagal deafferentation (SDA) (n = 7) had 12-h nightly access to Ensure liquid diet (1 kcal/ml). SDA rats had larger and fewer meals and maintained initial rapid rates of licking, yet total numbers of licks were unaffected. In the second study, Con (n = 8) and SDA (n = 7) rats had scheduled access to 12. 5% liquid glucose after overnight food deprivation. Glucose intake was assessed after 5-ml gastric preloads of 0.9% saline or glucose, peptone, and Intralipid solutions at three concentrations (0.5, 1, and 2 kcal/ml). Glucose and peptone preloads suppressed intake similarly in Con and SDA rats, whereas Intralipid was ineffective. These results suggest that meal-related SVA signals 1) are not critical in determining preload-induced feeding suppression after deprivation, yet 2) contribute to satiety during spontaneous meals.

Administration, Oral↗