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Biomedical subjects

R Gross

Publications and source records attributed to R Gross.

At least 289 records · Page 16Linked to original sources
PubMed1989

The impact of improvement of water supply and sanitation facilities on diarrhea and intestinal parasites: a Brazilian experience with children in two low-income urban communities.

During the second half of 1986 the impact of the improvement of water supply and excreta disposal facilities on diarrheal diseases and intestinal parasitosis was studied in 254 children up to six years of age from two favelas (shanty towns) of Belo Horizonte, Brazil. The estimated incidence of diarrhea was 6.2 episodes/child year and the estimated period prevalence reached 31.0 episode days/child/year. The point prevalence of parasitosis was 70.7% (Ascaris lumbricoides: 55.4%, Trichuris trichiura: 19.6%, Giardia lamblia: 17.9%). The estimated prevalence of diarrhea decreased with improvement of water supply and sanitation facilities to 45% and 44% respectively, but no statistically significant impact was observed in the case of parasitosis. School education and weaning practice were found to be other important determinants of diarrhea.

Brazil↗
PubMed1989

Diabetes and impaired response of glucagon cells and vascular bed to adenosine in rat pancreas.

Previous studies have shown that adenosine, by activation of purinergic A2-receptors, stimulates glucagon secretion and increases vascular flow rate in isolated perfused pancreases from nondiabetic rats. Because alpha-cell function and blood flow control are known to be disturbed in diabetes, we investigated whether adenosine was still effective in streptozocin-induced diabetic (STZ-D) rats. Our experiments were performed on isolated perfused rat pancreases. Whereas, in normal rats, adenosine (1.65 microM) induced a 200% increase in glucagon output and a 25% rise in the pancreatic vascular flow rate, in rats diabetic for 5-6 wk, this nucleoside was ineffective on glucagon secretion, and its vasodilatory effect was strongly reduced. Long-term in vivo insulin treatment that reversed high glycemia levels was able to restore in large part both adenosine effects. In contrast, a short-term in vitro pretreatment with insulin was unable to restore the nucleoside effects. We conclude that STZ-D suppresses the stimulatory effect of adenosine on alpha-cells and strongly reduces its vasodilator properties; these abnormalities may be corrected in large part by long-term insulin treatment with normalization of glycemia.

Adenosine↗
PubMed1988

Positive regulation of pertussis toxin expression.

Although the genus Bordetella contains several closely related species, pertussis toxin (PT) is produced only by phase I Bordetella pertussis. In this work we have studied the regulation of expression of the PT operon and investigated why PT is produced by phase I and not by phase III B. pertussis despite the presence of the PT genes. We have constructed a vector for Bordetella species that contains the PT promoter fused to the coding region of the chloramphenicol acetyltransferase (CAT) gene, and we have used it to identify the regulatory elements involved in the transcription of the PT operon. Efficient transcription of these genes requires at least two features: (i) the 170-base-pair DNA sequence upstream from the start site of transcription and (ii) a trans-activating factor encoded by the vir locus. Bordetella parapertussis and Bordetella bronchiseptica, although endowed with a functional trans-activating system, do not produce PT because of mutations within their PT promoter regions. In contrast, phase III Bordetella species do not show any trans activity.

Base Sequence↗
PubMed1988

Clinical and microbiologic features of Shigella and enteroinvasive Escherichia coli infections detected by DNA hybridization.

To determine the clinical and microbiologic features of Shigella and enteroinvasive Escherichia coli (EIEC) infections, we investigated 410 children with diarrhea and 410 control children without diarrhea who were seen at Children's Hospital, Bangkok, Thailand, from January to June 1985. Shigella spp. were isolated from 96 (23%) and EIEC were isolated from 17 (4%) of 410 children with diarrhea and from 12 (3%) and 6 (1%) of 410 control children, respectively. The isolation rates of both pathogens increased with age and peaked in children 3 to 5 years old from whom Shigella spp. were isolated from 38% and EIEC were isolated from 9%. Shigella spp. were isolated from 52% and EIEC were isolated from 7% of 91 children with bloody diarrhea and from 15 and 3% of 319 children with nonbloody diarrhea. Fifteen (65%) of 23 EIEC were lactose positive, and all belonged to recognized EIEC serotypes. Among children with diarrhea, the stool blots of 76% of 17 children infected with EIEC, 45% of 96 children infected with Shigella spp., and 1% of 297 culture-negative children hybridized with the 17-kilobase EcoRI digestion fragment of pRM17, a recombinant plasmid containing DNA derived from the 140-megadalton Shigella flexneri plasmid. Although EIEC colonies can be reliably detected by DNA hybridization, detection by stool blot is less sensitive. Shigella spp. and EIEC are important causes of endemic diarrhea among children greater than 1 year old in Thailand.

Age Factors↗
PubMed1988

Effect of insulin on basal pancreaticoduodenal output of somatostatin in normal and diabetic dogs.

The effect of insulin on basal pancreaticoduodenal output of SRIH was investigated in vivo and compared in normal and alloxan diabetic dogs. The experiments were performed on anesthetized dogs having a T-shaped catheter inserted into the pancreaticoduodenal vein just at the exit of the pancreas for blood sampling. In normal dogs, an insulin infusion (1 IU/kg for 20 min) or an iv insulin injection (0.2 IU/kg over 30 sec) produced, before any change in glycemia, an immediate reduction of the venous pancreaticoduodenal output of SRIH. Then pancreaticoduodenal output of SRIH rose close to starting values and decreased again when blood glucose level became very low. In alloxan-diabetic dogs, insulin infusion (1 IU/kg for 20 min) also induced an immediate inhibitory effect on pancreaticoduodenal SRIH output; the effect was more transient and from 20 min, unlike in normal dogs, an increase in pancreaticoduodenal output of SRIH was observed. In conclusion, exogenous insulin induces an immediate reduction in pancreaticoduodenal SRIH secretion both in normal and diabetic dogs, independently of basal blood glucose level and before any change in glycemia. In contrast, the delayed effect is different: SRIH secretion is reduced in normal dogs, whereas it is enhanced in diabetic dogs.

Animals↗
PubMed1988

Engineering bacterial toxin for the development of new vaccine against pertussis.

Bordetella pertussis is the causative agent of whooping cough. The cellular pertussis vaccine introduced in the forties is highly effective and is widely used, but its reactogenicity has led to public concern regarding its safety. The attempts to reduce the side effects associated with pertussis immunization have led to the preparation of acellular B. pertussis products: one composed of detoxified pertussis toxin (PT) and filamentous haemagglutinin (FHA), another one composed only of detoxified PT and a third vaccine composed of detoxified PT, FHA and serotypes 1, 3 of fimbriae. In our laboratories we have approached the study of pertussis toxin, the molecule present in all the proposed acellular pertussis vaccines and one of the main virulence factors of B. Pertussis, with the aim of producing new acellular pertussis vaccines by using recombinant DNA techniques.

Antibodies, Monoclonal↗
PubMed1987

Evidence for an inhibitory A1 subtype adenosine receptor on pancreatic insulin-secreting cells.

The effects of L- and D-phenylisopropyladenosine (L- and D-PIA) were studied on glucose-induced insulin secretion from the isolated perfused rat pancreas. L-PIA at the low dose of 16.5 nM inhibited insulin secretion by 50%. In contrast, D-PIA at 16.5 and 82.5 nM was ineffective. D-PIA used at a 100-fold higher concentration (1.65 microM) than L-PIA induced a similar inhibition of insulin secretion. The inhibitory effect of L-PIA was abolished by 8-phenyltheophylline (1 microM), a potent P1 purinoceptor antagonist. The present experiments provide evidence for an adenosine receptor of the A1 subtype on the insulin-secreting pancreatic cell of rats.

Animals↗
PubMed1987

In vivo study of glucose-induced somatostatin secretion: comparison in normal and alloxan-diabetic dogs.

This work was undertaken to study the effect of glucose on pancreaticoduodenal and peripheral venous somatostatin-like immunoreactivity (SLI) levels in dogs. Our experiments were performed in normal and alloxan diabetic dogs, conscious or anesthetized. The response of somatostatin was studied following intravenous (0.2 g/kg) or oral (1 g/kg) glucose administration. SLI levels were assayed in peripheral venous blood and in superior pancreaticoduodenal venous blood. An interplay of the cholinergic nervous system was challenged both after oral and intravenous glucose load by a prior administration of atropine sulfate (0.2 mg/kg i.v.). Our results show that (a) peripheral venous SLI levels do not reflect pancreatic D-cell activity in alloxan diabetic as in normal animals. (b) Increase of peripheral venous SLI level after oral glucose is under cholinergic nervous system control. (c) In alloxan diabetic dogs, the response of pancreaticoduodenal venous SLI to intravenous glucose was decreased, whereas peripheral SLI response to oral glucose was increased.

Animals↗
PubMed1987

Evolutionary relationships in the genus Bordetella.

The nucleotide sequence of the pertussis toxin operon of Bordetella pertussis, Bordetella parapertussis and Bordetella bronchiseptica, has shown that the last two species contain many common mutations and are likely to derive from a common ancestor (Aricò and Rappuoli, 1987). To elucidate further the evolutionary relationships between the Bordetella species, we have cloned and sequenced the promoter region and the gene coding for the S1 subunit of pertussis toxin from additional B. pertussis strains, such as the type strain BP 18323 and two recent clinical isolates, namely strain BP 13456 from Sweden and strain BP SA1 from Italy. While the strains BP SA1 and BP 13456 are shown to differ from the published B. pertussis sequences by only one base pair, the type strain BP 18323 contains a total of 11 base-pair substitutions. Remarkably, 9 of the 11 substitutions found in BP 18323 are also common to B. parapertussis and B. bronchiseptica, strongly suggesting that this strain derives from the same ancestor as B. parapertussis and B. bronchiseptica. Computer analysis of the sequence data allows the construction of an evolutionary 'tree' showing that the B. pertussis strains are very homogeneous and significantly distant from B. parapertussis and B. bronchiseptica. Therefore the proposed conversion from B. parapertussis to B. pertussis appears highly improbable.

Amino Acid Sequence↗
PubMed1987

Epinephrine potentiates adenosine-stimulating effect on glucagon secretion.

The aim of the present work is to investigate a possible interaction on glucagon secretion between adenosine, a compound released by tissues in energy-deficient states, and epinephrine, the hormone of stress largely implicated in such conditions. The study was performed using the isolated perfused rat pancreas in presence of a physiological glucose concentration (5 mM). Epinephrine administered at a low concentration (0.01 microM) was ineffective on glucagon secretion, and adenosine at 1.65 microM was previously shown to be moderately stimulating. This nucleoside alone induced a transient increase of glucagon secretion rate that peaked at 300% of basal value at 2 min; in presence of epinephrine (ineffective per se) the rise induced by the nucleoside alone was doubled. This potentiating effect was not observed with the neurotransmitter norepinephrine at the dose tested. Propranolol (1 microM) did not alter the potentiating effect of epinephrine but this effect was completely suppressed by the alpha-blocker, phenoxybenzamine (6 microM). In conclusion epinephrine potentiates an adenosine-stimulating effect on glucagon secretion; this effect seems more specific for the adrenal medulla hormone epinephrine, since norepinephrine at the same dose is ineffective; it is mediated via alpha-adrenergic receptors. It is attractive to speculate that epinephrine and adenosine act in potentiating synergism on glucagon secretion; this might be of physiological importance during stressful energy-deficient situations.

Adenosine↗
PubMed1987

Alpha 2-adrenergic potentiation of adenosine-stimulating effect on glucagon secretion.

Previous studies from our laboratory showed 1) that adenosine (1.65 microM), a substance released by tissues in energy-deficient states, stimulated glucagon secretion by activation of A2 purinergic receptors, and 2) that this effect was potentiated by a low substimulating concentration of epinephrine through activation of alpha-adrenergic receptors. The present work was undertaken to assess the subtype of alpha-adrenergic receptor involved in this potentiation. Therefore, we used adrenergic blockers and agonist drugs more specific for alpha 1- or alpha 2-adrenergic receptors. The potentiating effect of epinephrine (0.01 microM) on glucagon secretion induced by adenosine (1.65 microM) was not prevented by an alpha 1-adrenergic blocker, prazosine (6 microM), but was suppressed by an alpha 2-adrenergic blocker, yohimbine (0.6 microM). The implication of alpha 2-adrenergic receptors in the potentiating effect was confirmed by the use of selective alpha 1- or alpha 2-adrenergic agonist drugs. Indeed, clonidine (0.01 microM), an alpha 2-agonist, ineffective per se, potentiated, whereas phenylephrine (0.01 microM), an alpha 1-agonist, had no effect on glucagon secretion induced by adenosine. We conclude that the potentiation by epinephrine of adenosine-induced glucagon secretion is mediated by alpha 2-adrenergic receptor activation. A potentiation between the effects of A2 purinergic and alpha 2-adrenergic agonists may be of physiological relevance in stressful energy-deficient states, when an increase in glucagon secretion is necessary.

Adenosine↗
PubMed1987

Glucose, beta adrenergic effects, and pancreatic endocrine function in the isolated perfused duck pancreas.

Duck isolated perfused pancreas was used to assess glucose, adrenergic mediated effects and pancreatic function interrelationships. A moderate physiological 50% increase in glucose level, corresponding closely to the difference observed between 24-h-fasted and fed animals, induced a significant decrease of pancreatic glucagon not due to a rise in somatostatin secretion. The great responsiveness of the A cell was still found after glucagon stimulation by catecholamines or beta adrenergic agonism. Insulin was irresponsive to the glucose load we used, suggesting that glucose-induced glucagon suppression was also insulin independent. As far as the D cell was concerned, glucose had no effect on pancreatic somatostatin output; however, an interesting finding was that beta adrenergic agonism has a permissive effect on D cell responsiveness to the nutriment.

Animals↗
PubMed1987

[Potentiating synergism between alpha, beta-methylene ADP and acetylcholine on the secretion of insulin from the isolated pancreas of the newborn dog].

A possible interaction between alpha,beta-methylene ADP, a stable analogue of ADP, and acetylcholine, was studied on insulin secretion from isolated new-born dog pancreas, perfused in the presence of a non stimulating glucose concentration (4.2 mM). alpha,beta-methylene ADP alone (16.5 microM) and acetylcholine alone (0.5 microM) induced a comparable increment of insulin secretion. When the two substances were simultaneously infused, the increment of secretion was significantly higher than the sum of the increments induced by alpha,beta-methylene ADP and acetylcholine infused separately (p less than 0.005). Our results show a potentiating synergism between alpha,beta-methylene ADP and acetylcholine, on insulin secretion, alpha,beta-methylene ADP acting via a P2 purinoceptor and acetylcholine via a muscarinic receptor. Similar results were previously obtained on the rat pancreas.

Acetylcholine↗