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Biomedical subjects

D Vincent

Publications and source records attributed to D Vincent.

At least 19 recordsLinked to original sources
PubMed1998

Characterization of bifidobacteria by random DNA amplification.

RAPD conditions were optimized to generate reproducible banding patterns by testing primers, thermocyclers and overall reproducibility in repeat DNA analysis and separate DNA extractions. Five primers were chosen on the basis of band intensity and distribution (between 2 and 10 bands) which clearly distinguished among strains of Bifidobacterium adolescentis, B. animalis, B. bifidum, B. breve, B. infantis and B. longum. The use of five single-primer reactions under optimized conditions improved the resolution and accuracy of the RAPD method for the characterization of dairy-related bifidobacteria. The results indicated that this method was highly reproducible in repeated analysis. Similarity between bifidobacteria strains was evaluated based on their RAPD profiles. Using a set of five primers, it was demonstrated that it may be possible to distinguish three different species of Bifidobacterium (B. breve, B. bifidum and B. adolescentis), based on similarity of the RAPD profiles to known reference strains. Furthermore, application of the RAPD technique may also be useful and faster, than traditional systematics for placement of industrial strains into specific clusters (either B. longum/infantis or B. animalis/lactis).

Animals↗
PubMed1997

Ventilation system, indoor air quality, and health outcomes in Parisian modern office workers.

A cross-sectional study was carried out to determine the effect on health of exposure to different types of ventilation, taking indoor environmental measurements (IEMs) of major contaminants and aeroallergens into account. Three buildings ventilated with heating, ventilating, and air conditioning (HVAC), fan coil units (FCUs), and natural ventilation were selected. One thousand one hundred forty-four workers answered health questionnaires. After adjusting for potential confounders, HVAC and FCU systems were related to a slightly higher risk of nonspecific symptoms (compared with natural ventilation), short-term throat irritation, work-related nasal discharge, nasal blockage on awakening, migraine, and usual coughing induced by cold air. Studying the potential effects of environmental contaminants and aeroallergens on health outcomes, taking the floor and type of ventilation into account, did not explain the observed excess of nonspecific symptoms.

Adult↗
PubMed1997

[Sanitary impact of air conditioning: what is the relation to sick building syndrome?].

Modern architecture is creating air-conditioned offices in our society. Various diseases have been associated with conditioned air exposure, and building-related diseases are distinct from sick building syndrome (SBS). Building-related diseases have a well-characterized aetiology, essentially infectious, compared to SBS, where the aetiology is not clear. This paper reviews these syndromes, their aetiologies and their discussion in order to treat and prevent their expression. Progress has been made in the conception of air-conditioning systems. Prevention of these syndromes is based on conception and cleaning of these systems, which allows the use of air-conditioning without any major sanitary problem.

Air Conditioning↗
PubMed1997

Gastro-oesophageal reflux prevalence and relationship with bronchial reactivity in asthma.

The relationship between asthma and gastro-oesophageal reflux (GER) is controversial. In an allergy department, GER prevalence was evaluated in asthmatics, with a view to judging the potential influence of GER on asthma. One hundred and five asthmatics were recruited and co-investigated for GER and lung function. Descriptive analysis was performed, patients with (GER+) and without (GER-) GER were then compared, and finally, stepwise regression analysis was used. GER prevalence was 32%. Lung parameters did not differ between GER+ and GER- patients. When restricting analysis to GER+ patients, bronchial reactivity was closely correlated to the number of reflux episodes (NRE) (r=0.983; p=0.001). When comparing patients with more than 15 reflux episodes x day(-1) (n=50), with those having less (n=43), no differences were found in lung function and GER parameters. However, there was a positive correlation between the provocative dose of methacholine causing forced expiration volume to fall 20% from the baseline and NRE in patients with NRE>15 (r=0.561; p=0.05). In conclusion, gastro-oesophageal reflux was observed in a third of the asthma patients studied. These data do not support a firm aetiological relationship between gastro-oesophageal reflux and asthma, but do suggest an association between the number of reflux episodes and bronchial hyperresponsiveness.

Adult↗
PubMed1997

[Relationship of asthma to gastroesophageal reflux].

A relationship between asthma and gastro-oesophegal reflux (RGO) has been suspected for a long time but never proved. Many studies have shown improvement of asthma by treatment of RGO. The predictive factors of this improvement are unknown. After a short description of the epidemiology of RGO, in general and asthmatic populations, the mechanisms that link the two pathologies have been evaluated, the first consideration being the relationship between bronchial reactivity and RGO, to suggest a practical procedure for asthmatics, with regard to RGO. For therapy, inhibitors of the proton pump arise naturally.

Adult↗
PubMed1996

Quantitating immunosuppression. Estimating the 50% inhibitory concentration for in vivo cyclosporine in mice.

Cyclosporine (CsA) blocks T cell responses in vitro by inhibiting the phosphatase activity of calcineurin (CN) and thus preventing the activation of cytokine transcription. In the study presented here, we measured the extent of inhibition of these functions in the tissues of CsA-fed mice. Mice fed increasing doses of CsA were assessed for CsA blood and tissue levels, spleen cell CN activity, ex vivo spleen cell cytokine induction by A23187, and in vivo interferon-gamma induction during an allogeneic response. The CN activity of spleen homogenates and cell suspensions and the ex vivo cytokine responses of spleen cells from CsA-treated mice were inhibited with a 50% inhibitory concentration (IC50) greater than 300 microg/L. The in vivo interferon-gamma response to an allogeneic ascites tumor was also inhibited by CsA treatment, with IC50s between 517 and 886 microg/L. The true IC50 for CsA in vivo may be even higher, as CsA levels in spleen and kidney were 4-fold higher than concomitant blood levels. We conclude that inhibition of CN activity by systemically administered CsA leads to a parallel reduction in cytokine gene induction in response to an allogeneic stimulus. In light of our previous clinical findings that therapeutic levels of CsA in renal transplant patients were associated with only partial inhibition of CN activity, these current results support the concept that partial CN inhibition can account for both the immunosuppression and the immunocompetence of CsA-treated patients.

Animals↗
PubMed1996

Effect of recombinant human insulin-like growth factor-1 on the inflammatory response to acute renal injury.

Renal ischemic injury evokes an inflammatory response with increased cytokine and major histocompatibility complex (MHC) expression and a mild interstitial infiltrate. This "injury response" could contribute to the tendency of ischemically injured renal transplants to reject. The studies presented here evaluated the ability of recombinant human insulin-like growth factor-1 (rhlGF-1) given after renal injury to prevent renal inflammation. The left renal pedicle of CBA and BALB/c mice was clamped for 60 min, and rhlGF-1 (25, 50, 100 micrograms) was administered sc at 2, 24, 48, 72, and 96 h after reflow. Cytokine and MHC expression was monitored in the injured kidney, compared with the contralateral kidney. In untreated mice, a single episode of injury induced the expression of MHC mRNA and products and tumor necrosis factor-alpha (TNF-alpha) mRNA, and depressed preproepidermal growth factor (ppEGF) mRNA, for up to 5 wk. With immunohistology, epithelial Class I and II MHC expression was shown to be increased for 2 wk, and Class II positive interstitial cells were shown to be increased for up to 5 wk. The ischemically injured kidneys from mice treated with rhlGF-1 and examined at 5 days showed a dose-dependent normalization of all of the changes of the injury response. This included prevention of the increased expression of MHC and cytokines and the Class II positive interstitial cells, and restoration of ppEGF mRNA. Thus the complex and long-lasting increase in proinflammatory cytokines and MHC expression that follow renal ischemia can be interrupted by treatment with rhlGF-1 beginning 2 h after the injury. This therapy may have applications to the injury response in renal transplants.

Animals↗
PubMed1996

[Crossed aphasia disclosed by central auditory disorder].

A 80-year-old woman, right-handed, suddenly felt the impression to be deaf. Besides, she presented language disorders of aphasic type relating to a sensorial transcortical aphasia. The case meets the diagnostic criteria for crossed aphasia. The magnetic resonance imaging showed a right temporo-parietal infarct. There was no sensorial or peripheral auditive disorder and no auditory agnosia of non verbal modality. During the evolution, the aphasic symptoms diminished partially and the subjective auditory deficit of the left ear continued. The integrated auditory evaluation (neuroacoustic test, study of auditory gnosia, dichotic listening test, evoked cortical auditory potentials) allowed the evidence of the characteristic disturbances of a right hemianacousia: loss of left hear in dichotic audition, decrease of amplitude of evoked right cortical auditory potentials. In the light of theories concerning auditory integration, one can explain this evolution. The initial aphasic comprehension disturbance expresses the alteration of the linguistic treatment of auditory information of the dominant hemisphere, here the right hemisphere. Subsequently, the linguistic disturbance regresses largely, letting persist the change of general auditory treatment. The representation of this general auditory treatment is hemispheric bilateral, the only right hemispheric damage shall result in hemianacousia.

Aged↗
PubMed1995

Acute renal injury in the interferon-gamma gene knockout mouse: effect on cytokine gene expression.

We studied major histocompatibility complex (MHC) and cytokine mRNA induction after renal injury in the absence of interferon-gamma (IFN-gamma) using IFN-gamma gene knockout (GKO) mice. The left renal pedicle of normal (wild-type) and GKO BALB/c mice was clamped for 60 minutes; cytokine and MHC mRNA expression were monitored in the injured kidney and compared to the contralateral control kidney. After a single episode of ischemic injury, the expression of mRNA for MHC class I and II, interleukin-2, interleukin-10, granulocyte-macrophage colony-stimulating factor, tumor necrosis factor-alpha, and transforming growth factor-beta 1 was increased in wild-type and GKO mice, whereas preproepidermal growth factor (ppEGF) was reduced. IFN-gamma expression was induced in wild-type mice but absent in the GKO mice. Therefore, local injury was equally effective in both wild-type and GKO mice with equivalent cytokine and MHC mRNA induction, proving that local tissue injury can induce MHC expression by non-IFN-gamma factors.

Animals↗
PubMed1995

Disturbed MHC regulation in the IFN-gamma knockout mouse. Evidence for three states of MHC expression with distinct roles for IFN-gamma.

We compared the expression of MHC class I and II products in tissues of IFN-gamma knockout (GKO) vs normal (wild-type) BALB/c mice. We studied expression in the basal state, after local tissue injury, after stimuli that induce systemic MHC expression (allogeneic cells, oxazolone skin painting, or LPS), and after rIFN-gamma. Basal class II expression in interstitial cells was not reduced in GKO mice. However, GKO mice had less basal class I expression in kidney, liver, heart, and arterial endothelium than wild-type mice. Local renal ischemic injury increased class I and II expression in kidney tubules of both GKO and wild-type mice, but induction in GKO was less than in wild-type. Potent inflammatory stimuli increased systemic MHC class I and II markedly in kidney, liver, and heart of wild-type mice, but induced no increase in GKO mice. rIFN-gamma induced class I and II equally in GKO and wild-type mice. Thus, three states of MHC expression can be defined that differ in their dependencies on IFN-gamma: basal, locally induced, and systemically induced. Basal class II expression in interstitial cells is IFN-gamma independent, but basal class I expression, particularly in arterial endothelium, is partially dependent on IFN-gamma. The local increase in MHC class I and II in parenchymal cells in response to injury reflects both IFN-gamma and a non-IFN-gamma factor. Systemic MHC class I and II induction is almost exclusively due to IFN-gamma.

Animals↗