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Biomedical subjects

P Bonnet

Publications and source records attributed to P Bonnet.

At least 55 records · Page 3Linked to original sources
PubMed1999

[Surgery, radiotherapy or hormonal therapy in the treatment of prostate cancer].

Prostatic cancer (PC) became the first diagnosed cancer in western men and is the second leading cause of cancer death in men. Wide utilisation of serum PSA and free PSA measurements, identifies patients requiring transrectalultrasonography (TRUS) and TRUS guided biopsies. Most prostatic cancers diagnosed today are locally limited and may be treated by radical surgery or radiotherapy. In case of disseminated disease, hormonal manipulations remain the treatment of choice. In that field, many new drugs have been designed to allow medical castration with less complications, especially regarding sexual potency.

Adult↗
PubMed1998

Histopathological study in B6C3F1 mice chronically exposed by inhalation to glutaraldehyde.

Glutaraldehyde vapors are irritating for the skin, eyes, nose and lungs; respiratory symptoms and headaches have been described among workers exposed to low concentrations of glutaraldehyde far below to 190 ppb. This study was initiated to determine the chronic effects in mice of inhaled glutaraldehyde vapors. B6C3F1 mice were exposed using whole-body inhalation chambers, 6 h/day, 5 days/week, for 52 and 78 weeks to 100 ppb, or to filtered air (controls). In nasal passages at the level of the vestibule, hyperplasia of the squamous epithelium lining of the dorsal wall and lateral aspect of the atrioturbinate was observed in a greater number of exposed females than in controls. Epidermal erosion and ulceration as well as squamous and inflammatory exfoliation were also seen in the nasal lumens. All these changes were dependent on the length of glutaraldehyde exposure. The present data suggest that glutaraldehyde long term exposure only led to changes in nasal passages of female mice but did not induce mortality and/or tumors in nasal passages, in all mice. These results, along with the previous subchronic inhalation study of Gross et al., 1994, demonstrates that in a long term study, chronic glutaraldehyde exposure close to the current threshold limit values induced lesions at the more anterior part of the nasal passages in mice and that they likely result from an irritation mechanism (antero-posterior gradient).

Animals↗
PubMed1998

Reading and spelling acquisition in French: the role of phonological mediation and orthographic factors.

The objective of this research was to study the development of reading and spelling in French. The two main hypotheses were that (1) phonological mediation is the primary process in the acquisition of these skills and that (2) the use of phonological mediation may allow the construction of the orthographic lexicon. In January and June, first graders (n = 57) were required to read and spell items designed to assess the variables of regularity, graphemic complexity, frequency, lexicality and analogy. The findings of the January session partially corroborated the first hypothesis as a regularity effect, but no frequency effect and no word superiority, were found both in reading and spelling. The main contradictory finding was the presence, in early reading only, of a facilitative effect of analogy. The changes in the frequency and the lexicality effects between the two sessions in reading and in spelling indicated that the children were able to rapidly construct an orthographic lexicon. However, this procedure did not entirely replace phonological mediation since a regularity effect and regularization errors were observed and increased between sessions. The second hypothesis was supported as relationships were found to exist between early phonological skills and subsequent orthographic skills. Finally, we observed that French children were using graphemes (not only letters), in the early stage of reading, and, to a lesser extent, in the early stage of spelling. The findings are discussed in the context of developmental models of reading and spelling.

Child↗
PubMed1998

The role of glutathione and cysteine conjugates in the nephrotoxicity of o-xylene in rats.

Moderate nephrotoxicity was induced in male and female rats exposed to o-xylene for 4 h at atmospheric concentrations of approximately 3000 ppm. The xylene in vivo nephrotoxicity resulted in low enzyme leakage from the kidney into the urine. This low leakage was confirmed in 24-h urine by an increase in gamma-glutamyltranspeptidase (gammaGT), N-acetyl-beta-D-glucosaminidase (NAG) and alkaline phosphatase (ALP) activities. Compared to the control, both the 24-h urine output and the glucose excretion increased in male and female rats. These increases were probably a result of damage to the renal proximal tubules. The role of the metabolic pathway of glutathione in the emergence of the renal damage observed with o-xylene was investigated in rats. Recent studies indicate that the metabolic pathway of glutathione may be a bioactivation pathway, which is responsible for nephrotoxic effects with several drugs or chemicals. The renal toxicity of three synthesized o-xylene thio-conjugates was investigated in several groups of female rats. Administration of S-(o-methylbenzyl)glutathione (i.p., 1 mmol/kg), S-(o-methylbenzyl)cysteine (per os, 1 mmol/kg) or N-acetyl-S-(o-methylbenzyl)cysteine (i.p., 0.75 mmol/kg) to female rats did not induce renal toxicity, as monitored by urinary biochemical parameters (gammaGT, NAG, ALP, glucose). The data obtained suggest that the glutathione pathway would appear to be only detoxication, and probably does not contribute to the renal toxicity of o-xylene in female rats. Thus, either another metabolic pathway or other intermediate metabolites are probably involved in the nephrotoxic action of o-xylene.

Administration, Inhalation↗
PubMed1998

Intracellular acidosis differentially regulates KV channels in coronary and pulmonary vascular muscle.

Decreases in intracellular pH (pHi) potently dilate coronary resistance arteries but constrict small pulmonary arteries. To define the ionic mechanisms of these responses, this study investigated whether acute decreases in pHi differentially regulate K+ currents in single vascular smooth muscle (VSM) cells isolated from rat coronary and pulmonary resistance arteries. In patch-clamp studies, whole cell K+ currents were elicited by 10-mV depolarizing steps between -60 and 0 mV in VSM cells obtained from 50- to 150-micrometers-OD arterial branches, and pHi was lowered by altering the NH4Cl gradient across the cell membrane. Progressively lowering pHi from calculated values of 7.0 to 6.7 and 6.4 increased the peak amplitude of K+ current in coronary VSM cells by 15 +/- 5 and 23 +/- 3% but reduced K+ current in pulmonary VSM cells by 18 +/- 3 and 21 +/- 3%, respectively. These changes were reversed by returning cells to the control pHi of 7.0 and were eliminated by dialyzing cells with pipette solution containing 50 mmol/l HEPES to buffer NH4Cl-induced changes in pHi. Pharmacological block of ATP-sensitive K+ channels and Ca2+-activated K+ channels by 1 micromol/l glibenclamide and 100 nmol/l iberiotoxin, respectively, did not prevent changes in K+ current levels induced by acidotic pHi. However, block of voltage-gated K+ channels by 3 mmol/l 4-aminopyridine abolished acidosis-induced changes in K+ current amplitudes in both VSM cell types. Interestingly, alpha-dendrotoxin (100 nmol/l), which blocks only select subtypes of voltage-gated K+ channels, abolished the acidosis-induced decrease in K+ current in pulmonary VSM cells but did not affect the acidosis-induced increase in K+ current observed in coronary VSM cells. These findings suggest that opposing, tissue-specific effects of pHi on distinct subtypes of voltage-gated K+ channels in coronary and pulmonary VSM membranes may differentially regulate vascular reactivity in these two circulations under conditions of acidotic stress.

4-Aminopyridine↗
PubMed1998

Spontaneous transient outward currents and delayed rectifier K+ current: effects of hypoxia.

Single smooth muscle cells of rabbit intrapulmonary artery were voltage clamped using the perforated-patch configuration of the patch-clamp technique. We observed spontaneous transient outward currents (STOCs) and a steady-state outward current. Because STOCs were tetraethylammonium sensitive and activated by Ca2+ influx, they were believed to represent activation of Ca2+-activated K+ channels. The steady-state outward current, which was sensitive to 4-aminopyridine, was the delayed rectifier K+ current. In cells voltage clamped at 0 mV, we found that STOCs were not randomly distributed in amplitude but were composed of multiples of 1.57 +/- 0.56 pA/pF. The mean frequency of STOCs was 5.51 +/- 3.49 Hz. Ryanodine (10 microM), caffeine (5 mM), thapsigargin (200 nM), and hypoxia (PO2 = 10 mmHg) decreased STOCs. The effect of hypoxia on STOCs was partially reversible only if the experiment was conducted in the presence of thapsigargin. Hypoxia and thapsigargin decrease steady-state outward current. Thapsigargin and removal of external Ca2+ abolished the effect of hypoxia, suggesting that hypoxia decreases steady-state outward current by a Ca2+-dependent mechanism.

4-Aminopyridine↗
PubMed1998

[Antegrade scrotal embolization of varicocele: results].

The aim of this study is to judge the effectiveness of the new treatment of varicoceles, introduced in 1987 by Tauber: the antegradal scrotal sclerotherapy of varicoceles. From february 1996 to april 1998, we have realised 150 antegrade embolisations of varicoceles. The study is lead on 75 patients with mean time follow-up of 12 months. Patient's mean age is 20 years. 85% of patients had a grade 3 left varicocele and 15% a grade 2 left varicocele. The criterium of success rests on the lack of veinous flow-back during clinical examination, which is than confirmed by doppler-ultrasound. Clinical success is obtained in 87% of the cases and the doppler control is normal in 80% of the cases. We have 9% of minor complications, and no major complication. The number of failures in our study is higher than in Tauber' study, but is the same as those described in the other procedures of treatment of varicocele. On the other hand the surgical procedure is simple and the morbidity is low.

Adolescent↗
PubMed1998

[Transplantation of a kidney harvested laparoscopically from a related living donor].

Transplantation of kidney grafts harvested in living donors has demonstrated better results than grafts harvested from brain dead donors. Recently, laparoscopic live donor nephrectomy has been introduced to reduce the live procurement morbidity. In 1997, we performed two laparoscopic live donor nephrectomy and we report the first case of this program in this paper.

Adolescent↗
PubMed1997

Role of tachykinins and neutral endopeptidase in toluene diisocyanate-induced bronchial hyperresponsiveness in guinea pigs.

The role of tachykinins in toluene diisocyanate (TDI)-induced non-specific bronchial hyperreactivity (NSBH) in guinea pigs was investigated, and it was determined whether or not the activity of airway neutral endopeptidase (NEP) was inhibited in conditions where a bronchial hyperreactivity to acetylcholine (ACh) was observed. Exposures to 3 ppm TDI for 1 h, or to 0.029 ppm for 8 weeks caused a significant bronchial hyperreactivity to ACh. The depletion of tachykinins by a pretreatment with capsaicin (140 mg/kg) eliminated the TDI-induced airway hyperresponsiveness in both patterns of exposure to TDI. Capsaicin treatment had no effect on the response to ACh in guinea-pigs exposed to air (controls). Bronchial NEP activity determined by histoenzymology was significantly less 4 and 24 h after the end of a 1-h exposure to 3 ppm TDI than after exposure to air. Bronchial NEP activity evaluated 24 h after the end of a 48-h exposure to 0.116 ppm TDI, or a 1-week exposure to 0.050 ppm TDI was not significantly different from those of controls exposed to air, whereas in the same conditions of exposure a NSBH is observed in guinea-pigs. These data suggest that tachykinins released from C-fibers upon acute or repeated exposures to high or low concentrations of TDI, respectively, play an essential role in the observed bronchial hyperreactivity, and that the inhibition of NEP by TDI cannot completely account for the observed airway hyperreactivity.

Animals↗
PubMed1997

TDI inhalation in guinea-pigs involves migration of dendritic cells.

Toluene diisocyanate (TDI) can cause occupational asthma, but the mechanism underlying sensitization to this chemical compound remains controversial. The present study aims to investigate whether tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) liberated in the lungs after TDI inhalation can contribute to the migration of dendritic cells from respiratory airways towards lung associated lymph nodes for presentation of TDI hapten. Exposure was studied in two modes: (1) acute exposure (experiment no. 1, 2 and 3) where animals were exposed to 2.962, 1.060, and 1.076 ppm TDI for 1, 4, and two periods of 4 h, respectively; (2) subacute exposure (experiment no. 4, 5 and 6) where animals were exposed to 0.066, 0.110, and 0.999 ppm TDI for 48 h for the two lower doses and 5 days for the highest dose. Depending on the modes of exposure, two to four post exposure times were selected. After acute exposure to 2.962 ppm TDI for 1 h, the increase in TNF-alpha and IL-6 levels in bronchoalveolar lavage (BAL) fluid was observed immediately at the end of inhalation exposure, whereas the maximum number of dendritic cells and total cells occurred at post exposure times of 48 h and 5 days, respectively. In two other acute exposures, the peak increases in TNF-alpha, IL-6 and total cell numbers were observed at 48 h post exposure time, whereas the peak increase in dendritic cells occurred at 24 h. After subacute exposure to 48 h TDI, where TDI concentrations were relatively low (0.006 or 0.110 ppm), a parallel increase in TNF-alpha and IL-6 levels, dendritic and total cell numbers were observed at 0 h post exposure time. This phenomenon was also apparent at 24 h post exposure time when the animals had been exposed to 1.999 ppm TDI for 5 days. From these results, we can conclude that dendritic cells could play a key role as antigen presenting cells in the development of TDI-induced respiratory sensitization, and that their migration toward lung-associated lymph nodes is probably conditioned by cytokine release in their micro-environment. Future work must delineate whether TNF-alpha and IL-6 are solely responsible for the migration of dendritic cells after TDI inhalation, for example by using antibodies to neutralize these cytokines.

Animals↗
PubMed1997

RNase activity prevents the growth of a fungal pathogen in tobacco leaves and increases upon induction of systemic acquired resistance with elicitin.

The hypersensitive response and systemic acquired resistance (SAR) can be induced in tobacco (Nicotiana tabacum L.) plants by cryptogein, an elicitin secreted by Phytophthora cryptogea. Stem application of cryptogein leads to the establishment of acquired resistance to subsequent leaf infection with Phytophthora parasitica var nicotianae, the agent of the tobacco black shank disease. We have studied early events that occur after the infection and show here that a tobacco gene encoding the extracellular S-like RNase NE is expressed in response to inoculation with the pathogenic fungus. Upon induction of SAR with cryptogein, the accumulation of NE transcripts coincided with a rapid induction of RNase activity and with the increase in the activity of at least two different extracellular RNases. Moreover, exogenous application of RNase activity in the extracellular space of leaves led to a reduction of the fungus development by up to 90%, independently of any cryptogein treatment and in the absence of apparent necrosis. These results indicate that the up-regulation of apoplastic RNase activity after inoculation could contribute to the control of fungal invasion in plants induced to SAR with cryptogein.

Algal Proteins↗
PubMed1997

Hypoxia enhances agonist-induced pulmonary arterial contraction by increasing calcium sequestration.

The effects of hypoxia on norepinephrine-induced contraction to explain why rabbit pulmonary arteries must be precontracted to observe a hypoxic response were studied. A force transducer was used to record the tone of isolated rabbit intrapulmonary artery rings placed in an organ chamber perfused with a physiological solution at 37 degrees C. Norepinephrine (10(-7) M) induced a phasic followed by a tonic contraction, and hypoxia increased the former and decreased the latter. Removal of external calcium (zero calcium solution) abolished the tonic contraction but left the phasic contraction intact. In the zero calcium solution, hypoxia increased the amplitude of the phasic contraction (9.8 +/- 7.4 vs. 13.3 +/- 11.9 mN) and decreased the 50% relaxation time (59 +/- 38 vs. 48 +/- 22 s). Hypoxia also increased the caffeine (5 mM)-induced contraction. This hypoxic increase in amplitude was abolished by ryanodine (100 microM). The hypoxic decrease in the 50% relaxation time was reduced by cyclopiazonic acid (1-10 microM). Therefore, hypoxia increases the reuptake of calcium by calcium pumps sensitive to cyclopiazonic acid in the caffeine- and ryanodine-sensitive stores.

Animals↗
PubMed1996

Bronchial responsiveness and inflammation in guinea-pigs exposed to toluene diisocyanate: a study on single and repeated exposure.

The question of whether or not toluene diisocyanate (TDI)-induced airway hyperresponsiveness in the guinea-pig is accompanied by neutrophil influx into bronchoalveolar lavage fluid (BALF) was addressed. Two modes of exposure were studied; (1) acute exposures where animals were exposed to 3 ppm TDI for 1 h and experiments were carried out 30 min, 4 h, 24 h, 48 h and 1 week after the TDI exposures; (2) subacute exposures where animals were exposed to 0.080 and 0.046 ppm TDI for 48 h 1 week, respectively, and experiments were carried out 24 h after the TDI exposures. The changes in airway responsiveness to increasing doses of intravenous acetylcholine (ACh) in anaesthetized and tracheotomized spontaneously breathing guinea-pigs were examined. In order to elucidate the possible relationships of airway responsiveness to cellular infiltration, bronchoalveolar lavage was performed in additional group of guinea-pigs exposed to the same conditions. After acute exposure to 3 ppm TDI, increased bronchial responsiveness was evident within 30 min, lasted 48 h, but had vanished 1 week after the exposure. An influx of neutrophils occurred into the BALF within 1 h after exposure. The influx of neutrophil into BALF lasted 48 h and vanished 1 week after the end of exposure. After 48 h of exposure to TDI at 0.080 ppm, or 0.046 ppm for 1 week, increased bronchial responsiveness was evident 24 h after the end of the both modes of exposure, but no influx of neutrophils was observed into the BALF. It was concluded that even though the neutrophil influx and hyperresponsiveness evolve in the same way after acute exposure to a high concentration of TDI (3 ppm), this is not the case after subchronic exposure to low concentrations of TDI, where a bronchial hyperresponsiveness is observed without detectable neutrophil influx.

Acetylcholine↗