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Biomedical subjects

A Grenier

Publications and source records attributed to A Grenier.

At least 19 recordsLinked to original sources
PubMed2003

Assessment by MRI of local porosity in dough during proving. theoretical considerations and experimental validation using a spin-echo sequence.

Proving is a key stage in the development of the final structure of bread, as invasive measurements may provoke dough collapse. Therefore, better understanding and better control of the nucleation and the growth of bubbles require the development of non-invasive methods of measurement. In the present work, a non-invasive method is presented for the measurement of local dough porosity from MR image analysis. For this, a direct relation between the gray level of a voxel and its gas fraction was established in the absence of heat and mass transfer. At whole dough scale for a one-dimensional expansion, the porosity estimated from the gray level was compared with the porosity estimated from total dough volume measurements in a range of [0.10, 0.74 m(3) of gas/m(3) of dough]. For short proving times (<30 min), MR image analysis underestimated porosity by a maximum of 0.03 m(3) of gas/m(3) of dough, but otherwise the difference between the two means of measurement was within the standard error of total dough measurements (+/-0.01 m(3) of gas/m(3) of dough). Maps of local porosity in dough during proving are also presented and discussed.

Algorithms↗
PubMed2001

Oncostatin M production by blood and alveolar neutrophils during acute lung injury.

Polymorphonuclear neutrophils (PMN) are involved in the pathogenesis of acute lung injury (ALI), secreting numerous mediators such as proteases, reactive oxygen species, and cytokines. Because we had recently observed the ability of normal human PMN to degranulate and synthesize oncostatin M (OSM), an IL-6-family cytokine, we quantified OSM production ex vivo by highly purified blood and alveolar PMN from 24 ventilated patients with ALI, including some patients with severe pneumonia. Most of the patients had no detectable OSM in plasma, and OSM production by cultured blood PMN was similar to that of healthy controls. However, OSM was present in bronchoalveolar lavage (BAL) fluid supernatant, with significantly higher levels during pneumonia. In addition, alveolar OSM levels correlated with the number of PMN obtained by BAL, suggesting that PMN are an important source of OSM within the alveoli. Indeed, purified alveolar PMN from all of the patients, especially those with pneumonia, strongly produced OSM. Interestingly, in the latter patients, alveolar PMN always produced more OSM than autologous blood PMN. These results document the functional duality of PMN in ALI by showing the participation of PMN in the modulation of lung inflammation.

Aged↗
PubMed1999

Oncostatin M production and regulation by human polymorphonuclear neutrophils.

Oncostatin M (OSM) is an interleukin-6 (IL-6) family cytokine known in particular to induce the synthesis of acute-phase proteins by hepatocytes. Because human polymorphonuclear neutrophils (PMN) can secrete numerous cytokines, the potential production of OSM by PMN was investigated. Highly purified PMN were found to contain an intracellular stock of preformed OSM that was rapidly mobilized by degranulating agents such as phorbol myristate acetate and granulocyte-macrophage colony-stimulating factor (GM-CSF). Moreover, PMN produced OSM after a few hours of stimulation by various agonists. The most potent effect was observed with the combination of lipopolysaccharide and GM-CSF, which had a concentration- and time-dependent effect at both the protein and mRNA levels. Actinomycin D strongly reduced OSM mRNA induction, suggesting the involvement of gene transcription. Cycloheximide inhibited OSM protein synthesis but did not affect the release of preformed stores. In addition, OSM production was downregulated by dexamethasone, whereas IL-10 had no effect. The OSM produced by PMN was biologically active, as demonstrated by its ability to induce alpha1-acid glycoprotein synthesis by HepG2 cells. OSM secretion thus occurs through a two-step mechanism in PMN, consisting of early release of a preformed stock, followed by de novo protein synthesis. This would allow rapid and sustained OSM release to occur at inflammatory sites, and may contribute to the modulation of local inflammation.

Cells, Cultured↗
PubMed1997

Simple epithelium keratins are required for maintenance of hepatocyte integrity.

Keratin 8 (K8)-deficient adult mice develop a severe disease of the gastrointestinal tract characterized mainly by colorectal hyperplasia and inflammation. Given that hepatocytes contain K8/K18 heteropolymers only, this animal model was used to assess the contribution of these simple epithelium keratins to hepatocyte structural and functional integrity. Homozygous mutant (HMZ), heterozygous, and wild-type (WT) mice were examined for hepatocyte structural and metabolic features and their survival to partial hepatectomy. Except for the presence of few necrotic foci, no other tissular or cellular alterations were observed in nonhepatectomized HMZ mouse livers; glycogen and lipid peroxidation levels were essentially normal, but a small reduction in bile flow was observed. In response to a single pentobarbital injection, HMZ mice had longer sleeping times than heterozygous and WT mice. After a two-thirds partial hepatectomy under pentobarbital anesthesia, all HMZ mice died within a few hours, whereas those anesthetized with ether survived for 1 to 2 days. One hour after hepatectomy after pentobarbital anesthesia, many hepatocytes contained erythrocytes and large vacuoles in the cytoplasm, which suggests damage at the plasma membrane level in response to a sudden increase in portal blood flow. In line with these findings, an uptake of trypan blue by HMZ but not WT mouse hepatocytes was observed during a 10 ml/minute perfusion via the portal vein with a dye-supplemented buffer. Subsequent cellular dispersion led to viable WT mouse hepatocytes but largely nonviable HMZ mouse hepatocytes. Better viability was obtained at lower perfusion rates. Partially hepatectomized heterozygous mice developed liver steatosis, a condition that was not associated with a change in K8 content but perhaps linked to the presence of the neo gene. Transgenic HMZ mouse rescue experiments with a full-length K8 gene confirmed that the phenotypic alterations observed in partially hepatectomized HMZ mice were caused by the disruption of the K8 gene. Taken together, these findings demonstrate that simple epithelium keratins are essential for the maintenance of hepatocyte structural and functional integrity.

Animals↗
PubMed1996

A case of tyrosinaemia type I with normal level of succinylacetone in the amniotic fluid.

Prenatal diagnosis of tyrosinaemia type I can be achieved in cultured amniotic cells and in chorionic villus material by testing the activity of fumarylacetoacetate hydrolase and by DNA analysis, and in amniotic fluid by succinylacetone measurement. This specific metabolite can be measured either by gas chromatography-mass spectrometry or by delta-aminolevulinate dehydratase inhibition assay. In a series of 65 at-risk cases tested with the enzyme inhibition assay, one case out of the 18 with the disease had a normal level of succinylacetone. This case is presented.

Amino Acid Metabolism, Inborn Errors↗
PubMed1995

Polyomavirus middle T selective action on cytokeratin 14 gene expression in liver nonparenchymal epithelial cells.

We reported recently that liver nonparenchymal epithelial cells (LECs) constitute a small population of cells scattered throughout biliary structures and the Glisson's capsule, containing the unusual cytokeratin (CK) pair CK8/CK14 (Blouin et al., Differentiation, 1992, 52, 45). The transfection of polyomavirus middle T oncogene (MT) into the LEC line T51B leads to the loss of their CKs, due to a down-regulation of CK14 gene expression (Royal et al., Cell Growth Differ., 1992, 3, 589). In the present work, we examined CK gene expression at both mRNA and protein levels following polyomavirus small T oncogene (ST), MT, or large T oncogene (LT) transfection of T51B cells, MT transfection of rat hepatic cell lines containing different subsets of CKs, and MT transfection of rat keratinocytes. Immunofluorescence staining revealed that MT indeed induced an inhibition of CK14 gene expression and a loss of CK8/CK14 intermediate filaments (IFs) in liver cells, whereas ST and LT had no effect. Moreover, CK14 was the only CK gene whose expression was inhibited in MT-containing hepatic cells, in the sense that the expression of the CK7, CK8, CK18, and CK19 genes was not affected. Two-dimensional SDS-PAGE of the Triton-resistant cytoskeletal proteins and Northern blotting of the CK mRNA content confirmed these findings. The transfer of the MT oncogene into the keratinocytes did not result in the loss of CK5/CK14 IFs nor the inhibition of CK14 gene expression. These results show that the polyomavirus oncogene action on CK gene expression is restricted to an MT effect on CK14 in rat LECs.

Animals↗
PubMed1995

[Neurological follow-up of newborn infants at risk for cerebral palsy].

BACKGROUND: Traditional neurological examination of newborns at risk for cerebral palsy (CP) is based on periodic assessment of normal milestones so that the diagnosis of CP can be very late. A complementary neuromotor evaluation based on two motor series has been proposed in order to make possible an early affirmation of integrity of motor paths. POPULATION AND METHODS: Eight hundred and seventy three infants including 371 preterms had been admitted to a neonatal intensive care unit from 1990 to 1992. Then, they were examined as outpatients by a multidisciplinary team. They were especially tested for lateral support on right and left superior limbs, alternately, and for lateral abduction reaction of each hip. RESULTS: Absence of manifestations of CP was noted in 87% of infants with a corrected age of 4 months; a correct prediction of future normal walking was made for all babies. Both tests could not be correctly performed by those babies who lately developed manifestations of CP. CONCLUSIONS: These two simple tests appear to be accurate to early predict normality.

Cerebral Palsy↗
PubMed1995

[Complementary neuromotor examination of infants at risk for sequelae.Why? How?].

In many cases the traditional neurological examination of high risk newborns for neurological problems secondary to perinatal difficulties does not identify easily the absence or the presence of cerebral palsy before walking. To help the neuromoteur follow up in these children, the authors suggest a complementary neuromotor examination that is successful only in normal infants. This examination is done in front of a mirror in the presence of the parents in order to increase the attention of the child, whose participation is necessary for a successful examination. Two motor responses are evaluated: the lateral support on, alternately, right and left superior limbs, and the lateral abduction reaction of the hip of each limb. When normal these two motor responses allow an early affirmation of integrity of motor paths if the examination is performed under carefully controlled conditions.

Cerebral Palsy↗
PubMed1992

Cytokeratin 14 expression in rat liver cells in culture and localization in vivo.

Rat liver epithelial cells (LECs) are non-parenchymal proliferating cells that readily emerge in primary culture and can be established as cell lines, but their in vivo cell(s) of origin is unclear. We reported recently some evidence indicating that the LEC line, T51B, contains two cytokeratins (CKs) equivalent to human CK8 and CK14 respectively. T51B cells also contain vimentin assembled as a network of intermediate filaments distinct from that of the CKs. In the present study, we examined the expression of CK14 gene in various LEC preparations and a Triton-resistant rat skin cytoskeletal fraction, and then assessed its usefulness as an LEC specific marker in the liver. Northern and Western blot analyses with cDNAs and antibodies for CK8, CK14, CK18 and vimentin confirmed that rat hepatocytes express CK8 and CK18 genes only, whereas T51B cells express CK8, CK14 and vimentin genes in the absence of CK18. CK14 was also present in LECs derived as primary from embryonic-day 12 rat liver and secondary cultures from 4-day-old rat liver. Primary cultures of oval cells isolated from 3'-methyl-4-dimethylaminoazobenzene (3'-Me-DAB) treated rat liver (an enriched source of biliary epithelial cells) contained CK14 mRNAs which were slightly shorter than those in LECs. The analyses of CK5 (the usual partner of CK14) gene expression using specific cDNA and antibody clearly demonstrated its absence in LECs. In situ double immunolocalization analyses by laser scanning confocal microscopy showed that CK14 was not present in hepatocytes (HES6+ cells) and was expressed in some biliary epithelial (BDS7+ cells). CK14-positive cells were also found in the Glisson's capsule. However, CK14-positive cells of the portal region were vimentin negative, whereas those of the Glisson's capsule were vimentin positive. Our results suggest that CK14 gene expression is part of the differentiation program of two types of LECs and that this differential CK14 gene expression can be used as a new means to type LECs in culture and in vivo.

Amino Acid Sequence↗
PubMed1991

Temperature-dependent immunoreactive assay to screen for digoxin-like immunoreactive factor(s).

Endogenous circulating digoxin-like immunoreactive factors (DLIF) are known to cross-react with antibodies to digoxin and to inhibit Na+/K(+)-transporting ATPase (Na+K+ATPase; EC 3.6.1.37). Moreover, increasing the immunoassay temperature from 4 to 37 degrees C markedly decreases DLIF from human cord serum. We tested several compounds, including hormonal steroids, bile salts, lipids, and methionine-enkephalin, for their ability to cross-react with two commercially available 125I digoxin RIAs, to inhibit porcine Na+K+ATPase, and to see whether they present the same incubation temperature dependence as human cord serum. Except for methionine-enkephalin, all compounds were inhibitors of Na+K+ATPase in the range of 1-10 mmol/L. Progesterone exhibited the highest cross-reactivity in the two RIAs. The apparent digoxin immunoreactivity for the majority of the cross-reacting steroids, bile salts, and linoleic acid was markedly decreased by increasing the incubation temperature from 4 to 37 degrees C, whereas estriol, pregnanediol, and nonspecific compounds (e.g., ethanol, human serum albumin) did not appear to be temperature-sensitive. Both lysophosphatidyl lipids gave an increased apparent digoxin concentration with increasing incubation temperature. Our data suggest that numerous weakly cross-reactive compounds can parallel the response of human cord serum. However, the temperature-dependent effect could be an additional criterion for identifying DLIF.

Antibodies↗
PubMed1990

Neurologic crises in hereditary tyrosinemia.

Hereditary tyrosinemia results from an inborn error in the final step of tyrosine metabolism. The disease is known to cause acute and chronic liver failure, renal Fanconi's syndrome, and hepatocellular carcinoma. Neurologic manifestations have been reported but not emphasized as a common problem. In this paper, we describe neurologic crises that occurred among children identified as having tyrosinemia on neonatal screening since 1970. Of the 48 children with tyrosinemia, 20 (42 percent) had neurologic crises that began at a mean age of one year and led to 104 hospital admissions. These abrupt episodes of peripheral neuropathy were characterized by severe pain with extensor hypertonia (in 75 percent), vomiting or paralytic ileus (69 percent), muscle weakness (29 percent), and self-mutilation (8 percent). Eight children required mechanical ventilation because of paralysis, and 14 of the 20 children have died. Between crises, most survivors regained normal function. We found no reliable biochemical marker for the crises (those we evaluated included blood levels of tyrosine, succinylacetone, and hepatic aminotransferases). Urinary excretion of delta-aminolevulinic acid, a neurotoxic intermediate of porphyrin biosynthesis, was elevated during crises but also during the asymptomatic periods. Electrophysiologic studies in seven patients and neuromuscular biopsies in three patients showed axonal degeneration and secondary demyelination. We conclude that episodes of acute, severe peripheral neuropathy are common in hereditary tyrosinemia and resemble the crises of the neuropathic porphyrias.

Acute Disease↗
PubMed1990

Fumarylacetoacetase measurement as a mass-screening procedure for hereditary tyrosinemia type I.

Fluorometric quantitative tyrosine determination on dried-blood spots is the primary neonatal screening test used for tyrosinemia type I (HT) in the province of Quebec. Succinylacetone determination on these same spots is used as the complementary test when the tyrosine level is higher than a given threshold. This procedure has proved to be less discriminant over the past few years because of changes in newborn feeding and because of early discharge of newborns from the nursery. We have developed an enzyme-linked immunosorbent assay (ELISA) to measure the deficient enzyme in HT in dried-blood spots. Fumarylacetoacetase (FAH) (E.C.3.7.1.2) was measured retrospectively by an ELISA on 25 dried-blood samples from proven patients with HT and prospectively in 72,000 specimens received in the neonatal screening program. In this pilot project, FAH was measured first, and, if necessary, succinylacetone was determined as the complementary test. All 25 samples from proven patients and specimens from four other patients detected in the pilot study have shown almost complete absence of FAH in dried-blood samples. At a cutoff level of 12.5% of normal adult blood spotted on the same type of paper, only 30 other cases disclosed FAH levels low enough to warrant succinylacetone measurement but had no detectable succinylacetone. The false-positive rate is thus 1:2,400 with this primary ELISA. However, blood transfusion in newborns prior to blood collection on filter paper may yield false-negative tests, since FAH is present in erythrocytes of normal donors.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Metabolism, Inborn Errors↗
PubMed1990

Oral loading of homogentisic acid in controls and in obligate heterozygotes for hereditary tyrosinemia type I.

Homogentisic acid (HGA) (50 mg/kg) was given orally to 22 obligate heterozygotes for hereditary tyrosinemia type 1 (HT) and to 11 controls. After 1 h the mean +/- standard error (SE) plasma level of HGA was 30.42 +/- 1.41 micrograms/ml in carriers and 19.29 +/- 1.62 in controls. Mean +/- SE fasting delta-amino-levulinate dehydratase (delta-ALD) was 40.05 +/- 1.79 m microM/min/g Hb in carriers, much lower than the 60.81 +/- 5.11 found in controls. After 3 h this difference in levels of delta-ALD remained, with mean +/- SE values of 25.70 +/- 2.89 m microM/min/g Hb in carriers, compared with 48.83 +/- 5.37 in controls. Three-hour mean +/- SE excretion of fumarylacetone "equivalent" [FAc] in urine in carriers, 51.597 +/- 5.580 micrograms/mg/creatinine, was significantly higher than the 27.941 +/- 5.916 in controls. Three-hour excretion of succinylacetone "equivalent" [SAc] was also significantly higher in the urine of carriers. FAc in 3-h urine was identified by thin-layer chromatography and confirmed by gas chromatography/mass spectrometry. Multivariate stepwise discriminant analysis showed that the inclusion order of significant variables was as follows: HGA levels at 1 hr, fasting level of delta-ALD, residual level of HGA at 3 h, and 3-h excretion of [FAc]. Non-significant variables were HGA tolerance, levels of delta-ALD at 3 h, sex, and 3-h excretion of [SAc].(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Metabolism, Inborn Errors↗
PubMed1989

Prospective ascertainment of complete and partial serum biotinidase deficiency in the newborn.

We screened 163,000 newborn filter-paper blood samples for serum biotinidase deficiency (McKusick 25326) and found 15 probands: three had complete deficiency (incidence 18.4 cases per million live births, 95% confidence interval 4-54 cases per million); the others had partial deficiency. The positive predictive value of the test for either form of biotinidase deficiency was 9.86%. We found seasonal variation in biotinidase activity in filter-paper blood samples. The cost per test was Can.$0.27 (1987 dollar value) and per case of complete deficiency ascertained, $15,500. Family studies indicated that complete serum biotinidase deficiency is a homozygous phenotype and partial deficiency is the heterozygous form. Homozygous cases were treated with biotin and have shown no clinical manifestations (55 patient-months of observation). None of the heterozygotes (n = 42, age 3 months - 62 years) has clinical manifestations. The number of heterozygotes found by screening was much less than predicted probably because the screening test detects mainly the samples with very low (outlier) biotinidase activity. The variant allele(s) for biotinidase deficiency was more common in French Canadians than in other ethnic groups in Quebec; there was no evidence of regional clustering or founder effect.

Amidohydrolases↗