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Biomedical subjects

J Perrin

Publications and source records attributed to J Perrin.

At least 37 records · Page 2Linked to original sources
PubMed1993

Sensitivity of lateral hypothalamic neurons to nicotine: origin and possible correlation with nutritional effects of nicotine.

Single-unit activity was recorded extracellularly in the lateral hypothalamus of anesthetized rats. A number of neurons responded to intravenous nicotine, but most failed to respond similarly to local nicotine or systemic administration of a peripheral acting agonist. This finding suggests that these neurons respond indirectly to systemic nicotine through afferent pathways originating in central nicotinoceptive cells. The incidence of response was significantly greater in the cells sensitive to moderate changes in blood glucose. This finding suggests that the effects of peripheral nicotine on food intake and body weight are partly mediated by "glycemia-sensitive neurons" in the lateral hypothalamus.

Afferent Pathways↗
PubMed1993

Intestinal carriage of Clostridium difficile in neonate dogs.

A total of 70 puppies and their dams, distributed in 14 litters, were submitted to weekly fecal examinations for C. difficile during the first 10 weeks after birth. During the study, 94.3% of the puppies and 42.9% of the dams harboured C. difficile at least once in their feces. We calculated that 58% of the puppies carried toxigenic C. difficile at least once during the survey. In the puppies, C. difficile carriage rates ranging from 3.1% to 67.1% were observed at different moments of the observation period. In comparison, C. difficile carriage rate was 1.4% in a control group of healthy dogs more than 3 months old. Discrepancies in the toxigenic phenotype of the C. difficile strains isolated in the same litter showed that the neonate dogs were transiently infected with different strains, and that the dam is often not the source of infection with C. difficile. We could not demonstrate any pathogenicity of C. difficile for neonate dogs.

Animals↗
PubMed1993

Convergence of the Child Behavior Checklist with structured interview-based psychiatric diagnoses of ADHD children with and without comorbidity.

We evaluated the convergence of CBCL scales with the diagnosis of ADHD and comorbid disorders in 133 ADHD and 118 normal control boys, aged 6-17 years old. We evaluated the strength of association between each CBCL scale and structured-interview derived diagnoses with Total Predictive Value (TPV) and the odds-ratio (OR). Excellent convergence was found between the CBCL Attention Problems scale with the diagnosis of ADHD, between the Delinquent Behavior scale and the diagnosis of CD, and between the Anxiety/Depression scale and the diagnoses of Anxiety Disorders. These findings indicate that the CBCL could serve as a rapid and useful screening instrument to identify comorbid and non-comorbid cases of ADHD.

Adolescent↗
PubMed1993

Evidence for the independent familial transmission of attention deficit hyperactivity disorder and learning disabilities: results from a family genetic study.

OBJECTIVE: The purpose of the study was to clarify the relationship between attention deficit hyperactivity disorder and learning disabilities. METHOD: The authors assessed learning disabilities in a sample of 140 children with attention deficit hyperactivity disorder and in 120 normal comparison children. They also assessed a sample of the probands' 822 first-degree relatives. RESULTS: The risk for learning disabilities was highest among relatives of probands with both attention deficit hyperactivity disorder and learning disabilities. The two disorders did not cosegregate in families. There was nonrandom mating between spouses with attention deficit hyperactivity disorder and learning disabilities. CONCLUSIONS: The two disorders are transmitted independently in families, and their co-occurrence may be due to nonrandom mating. Attention deficit hyperactivity disorder is likely to be etiologically independent from learning disabilities.

Adult↗
PubMed1993

Induction of hprt mutations in mice after exposure to fission-spectrum neutrons or 60Co gamma rays.

The effects of exposure to fission-spectrum neutrons and 60Co gamma rays on mutation induction in B6CF1 mice were investigated. Mutation induction was measured at the hypoxanthine-phosphoribosyl-transferase (hprt) locus in splenic lymphocytes at 56 days after whole-body irradiation. Lymphocytes were cultured 12-16 days in round-bottomed, 96-microwell plates in the presence of 5 x 10(4) feeder cells (syngeneic lymphocytes irradiated with 50 Gy gamma rays). The selective agent used as 6-thioguanine at a concentration of 2.5 micrograms/ml. Animals were exposed to either single doses of neutrons (1.5 Gy) or photons (7.5 Gy) or fractionated doses delivered over 2 weeks of neutrons (0.25 Gy x 6, total 1.5 Gy) or photons (1.5 Gy x 6, total 9.0 Gy). The frequency of hprt mutant induction by fission-spectrum neutrons delivered in a 1.5-Gy single dose compared to a 7.5-Gy single dose of 60Co photons was approximately the same, i.e., 5.98 x 10(-5) +/- 1.51 x 10(-5) (SE) vs. 5.56 x 10(-5) +/- 3.09 x 10(-5) (SE), respectively (Student's two-tailed t test, P = 0.8997). Multiple doses of neutrons gave rise to slightly higher mutant frequencies compared to photons even though the ratio of total doses of neutrons to photons was increased from 5 to 6, i.e., 8.71 x 10(-5) +/- 5.39 x 10(-5) (SE), total dose 1.5 Gy, vs 2.30 x 10(-5) +/- 9.07 x 10(-6) (SE), total dose 9.0 Gy, respectively (Student's two-tailed t test, P = 0.3330). These results suggest that the relative differences in magnitude in radiation-induced genotoxic effects between fission-spectrum neutrons and 60Co gamma rays increase when the comparisons are made between fractionated rather than single-dose exposure regimens.

Animals↗
PubMed1992

Antimutagenic effects of radioprotector WR-2721 against fission-spectrum neurons and 60Co gamma-rays in mice.

The antimutagenic effects of the radiation protective agent, S-2-(3-aminopropylamino)ethylphosphorothioic acid (WR-2721), were studied against fission-spectrum-neutron- and 60Co-gamma-ray-induced mutagenesis in mice. Mutagenesis at the hypoxanthine-guanine phosphoribosyl transferase (hprt) locus was measured 56 days following whole-body irradiation with JANUS neutrons (single doses, 50-150 cGy) or 60Co photons (single doses, 250-750 cGy). Splenic T lymphocytes from B6CF1 mice were grown in round-bottomed 96-microwell culture plates with or without the selective agent 6-thioguanine (6-TG). The mutant frequency, as a result of exposure to neutrons or 60Co photons, increased 100-fold with dose. Doses of 150 cGy neutrons and 750 cGy 60Co photons were equally mutagenic. When animals were injected with WR-2721 at a dose of 400 mg/kg body weight, i.p., 30 min before whole-body irradiation with JANUS neutrons or 60Co photons, mutant frequencies were significantly reduced at all radiation doses (i.e. protection factors of 1.4 and 2.4, respectively). Thus, the aminothiols are effective antimutagens. A novel clinical application of these compounds could be in their use to protect against radiation- and/or chemotherapy-induced genotoxic damage to normal cells.

Amifostine↗
PubMed1992

The radioprotector WR-2721 reduces neutron-induced mutations at the hypoxanthine-guanine phosphoribosyl transferase locus in mouse splenocytes when administered prior to or following irradiation.

An in vitro T-lymphocyte cloning technique has been applied to study the effects of JANUS fission-spectrum neutron irradiation and the radioprotector S-2-(3-aminopropylamino) ethylphosphorothioic acid (WR-2721) on the subsequent development of somatic mutations at the hypoxanthine-guanine phosphoribosyl transferase (hprt) locus in hybrid B6CF1 male mice. In control studies performed to establish an in vitro cloning technique, the mutant frequencies of splenic T-lymphocytes, as a result of exposure to a 100 cGy dose of neutrons, increased with time from a control level of 9 x 10(-7) to a maximum value of 1.7 x 10(-5) at 56 days following irradiation. Between 56 and 150 days after irradiation, mutant frequencies were observed to plateau and remain stable. All subsequent determinations were performed at 56 days following the experimental treatment of animals. WR-2721 at a dose of 400 mg/kg was effective in protecting against the induction of hprt mutants (i.e. a mutant frequency reduction factor, MFRF) following the largest dose of neutrons used (i.e. 150 cGy), whether it was administered i.p. 30 min before, 5 min after, 3 h after, or three times at 3, 24, and 48 h after, as evidenced by MFRFs of 6.0, 6.6, 4.8 and 5.8 respectively. The antimutagenic effectiveness of WR-2721 administered 30 min prior to irradiation was unaffected, even when the dose was reduced to 200 mg/kg, MFRF = 7.0; 100 mg/kg, MFRF = 3.8; and 50 mg/kg, MFRF = 8.9. These findings confirm our earlier report using the radioprotector N-(2-mercaptoethyl)-1,3-diaminopropane (WR-1065) under in vitro conditions, and demonstrate that these agents can be used as effective antimutagens even when they are administered up to 3 h following radiation exposure.

Amifostine↗
PubMed1992

Influence of the transport on the outcome of the bacteriological analysis of dog urine comparison of three transport tubes.

A sterile plastic tube, a boric acid-glycerol-sodium formate tube and a dip-slide tube were compared for transport of dog urine for bacteriological examination under practice conditions, at ambient temperature. In a first part, 50 dog urine samples were cultured on agar plates and on a dip-slide kit within 2 h after collection and after storage at 20 degrees C in a sterile tube and in a boric acid tube for 24 h and 48 h. Culture of the samples stored in the boric acid tube and culture on the dip-slide yielded results which correlated very well with those of the culture of fresh urine. However, culture of the samples stored in the sterile tube yielded up to 65% false positive results. In a second part, a comparison was drawn with culture results of 100 dog urine specimens collected by different practitioners and simultaneously mailed to our laboratory in a sterile tube, in a boric acid tube and in a dip-slide kit. Samples sent in the boric acid and in the dip-slide tube showed comparable culture results. Culture of the samples sent in the plastic tube yielded 53% false positive results in comparison with those of the samples preserved in boric acid.

Animals↗
PubMed1991

Sensitivity of lateral hypothalamic neurons to glycemic level: possible involvement of an indirect adrenergic mechanism.

Most of the lateral hypothalamic neurons responding to moderate changes in blood glucose fail to be affected by direct glucose applications. Therefore their sensitivity to glycemic level must be mediated by an indirect mechanism. In order to test whether adrenergic afferents might be involved, the activity of lateral hypothalamic neurons was recorded during hyperglycemia and local glucose and epinephrine microiontophoresis. A majority of the recorded cells sensitive to local epinephrine responded to this substance with a decrease in activity. While no consistent correspondence was found between the responses of the same cells to local glucose and epinephrine ejections, almost all the neurons sensitive to glycemic alterations responded in the same direction to hyperglycemia and iontophorised epinephrine. These results support the view that the activity of lateral hypothalamic cells can be modulated in relation to changes in glycemic level through adrenergic signals released by some neurons which are sensitive to the blood glucose. The possible localization in the solitary tract area of such neurons projecting to the lateral hypothalamus is discussed.

Animals↗
PubMed1990

Local versus indirect action of glucose on the lateral hypothalamic neurons sensitive to glycemic level.

The neuronal activity in the lateral hypothalamus may be affected by moderate changes in blood glucose. The present study aimed to specify the direct or indirect origin of this sensitivity to glycemia, by recording the unit responses in this area to both local glucose application (by means of microelectrophoresis) and hyperglycemia (induced by an IV glucose injection). The activity of approximately 25% of the recorded LHA neurons was modified by topically ejected glucose. However, a large majority of these neurons sensitive to local glucose failed to respond to hyperglycemia. Conversely, only 1/3 of the glycemia-sensitive cells responded in the same direction to systemic and local glucose administration. Therefore, the response to IV glucose of the other 2/3 glycemia-sensitive cells could not result from the direct action of glucose molecules on these neurons, but probably involved an indirect afferent pathway conveying the glycemic cues from some central or peripheral glucose sensors to the cell under investigation.

Animals↗
PubMed1990

Global breast attenuation:control group and benign breast diseases.

This paper deals with the estimation of the slope of attenuation in human breast tissue. The measurement is done in the reflection mode with a short time Fourier analysis. All important factors such as diffraction effect, tissue depth and specular reflectors are taken into account. A population of 49 normal women shows large inter-individual variations of the attenuation coefficient. A multiple linear regression allows correlation of this variation with the duration of the woman's genital life and pregnancies. A preliminary study is done on 10 benign diffuse breast diseases and shows a weak correlation with the type of the breast: normal or pathological. The utility of the quantification is discussed for one case of large fibrocystic disease.

Adult↗
PubMed1989

Cloning and expression of a cohemolysin, the CAMP factor of Actinobacillus pleuropneumoniae.

The genetic determinant of the cohemolysin which is responsible for the CAMP phenomenon, a cohemolysis, of Actinobacillus pleuropneumoniae was cloned in Escherichia coli. Total DNA from the A. pleuropneumoniae serotype 1 type strain 4074 was used to construct a gene library in plasmid pUC18 in E. coli JM83. A total of 10,500 clones containing recombinant plasmids have been screened for hemolysis on blood plates. Fifty-five clones which showed a weak hemolytic response after 24 to 48 h of incubation were screened for the CAMP reaction with Staphylococcus aureus. This led to the identification of one clone which showed a positive CAMP reaction. Immunoblot analysis revealed that the recombinant strain expressed a protein with a molecular mass of 27,000 daltons, similar in size to the CAMP protein of the group B streptococci. Rabbit antibodies against the CAMP+ clone neutralized the CAMP reaction mediated by the E. coli strain containing the cloned CAMP gene as well as that of A. pleuropneumoniae. Antibodies raised against the cloned CAMP cohemolysin cross-reacted with Streptococcus agalactiae protein B. We designate the 27,000-dalton molecule CAMP factor protein and name its corresponding gene cfp.

Actinobacillus↗
PubMed1988

Cell cycle redistribution of cultured cells after treatment with chemical radiation protectors.

The effect of two radioprotective agents (WR-1065 and WR-151326) was tested for their ability to modify cell cycle progression. Each protector was administered at a concentration of 4 mmol to exponentially growing cultures of V79 cells for periods of time up to 3 h. Under these conditions no cell toxicity was observed. At selected times up to and after removal of the protector, aliquots of cells were removed, counted and fixed in cold 70% ethanol. The cells were stained with DAPI in a 0.1% citrate solution and DNA histograms were obtained using a PARTEC PAS-II flow cytometer. The coefficient of variation of the G1 peaks obtained for unperturbed cell samples routinely ranged from 1.5 to 2.5%. During exposure, both radioprotectors effectively perturbed cell cycle progression, as characterized by a build-up of cells in S and G2 phases. After the protectors were removed, cells began to redistribute throughout the cell cycle. Twelve hours were required before cells exposed to WR-1065 approached levels commensurable with controls. In contrast, cells treated with WR-151236 required about 24 h to redistribute to control levels. These data demonstrate that different thiol-containing radioprotective compounds can differentially affect the progression and redistribution of exposed cells.

Animals↗
PubMed1987

Detection of Duchenne muscular dystrophy carriers: quantitative echography and creatine kinasemia.

Data obtained from simultaneous determinations of serum creatine-kinase levels and estimation of ultrasound attenuation values in muscles greatly improved the detection of obligate carriers of Duchenne muscular dystrophy than when only one of these methods was employed alone. Eleven carriers out of 19 had a high creatine-kinasemia level and nine carriers out of 19 had a high (abnormal) attenuation value. Because of the limited overlapping between the two parameters studied, we were able to recognize 17 obligate carriers out of the 19. This indicates that the parameters studied concern different features of the disease, and the practical and theoretical considerations are discussed. The techniques are discussed together with molecular genetic investigations.

Adult↗
PubMed1987

Optimal precision in ultrasound attenuation estimation and application to the detection of Duchenne muscular dystrophy carriers.

This paper deals with the measurement of the attenuation of ultrasound in muscle and its application to the detection of Duchenne Muscular Dystrophy (DMD) carriers. The precision obtained when measuring the attenuation is an important parameter to be considered. A statistical approach is taken on simulated data and compared to in vivo results. The results allow discussion for the minimum tissue volume needed for the estimation. Variations in muscle attenuation between normals were obtained from studies on 27 volunteers. These attenuation values were compared to those obtained from 19 carriers of DMD. Attenuation appears to be a potential clinical indicator of DMD carriers.

Biometry↗
PubMed1987

Diffraction correction for focused transducers in attenuation measurements in vivo.

Diffraction effects are a cause of error when estimating the frequency dependent attenuation of ultrasound in biological tissues in the reflection mode. Comparison of attenuation values estimated in vivo by different investigators using different types of transducers makes calibration and correction for diffraction necessary. In this paper, we present experimental results for in vivo calibration and correction for the diffraction effect for focused transducers. We also study numerically the diffraction filter in a time-frequency representation, and show that for a focused probe, there is a region in the time-frequency domain where the frequency slope of the diffraction filter does not vary with time. The main consequence for in vivo estimation is that for a given probe, it is possible to select both the distance between the region of interest and the probe, and the frequency limits, such that the attenuation thus estimated is unbiased by the diffraction effect. This result, obtained by numerical calculations, is confirmed by experimental calibration of a foam phantom and in vivo muscle.

Acoustics↗