Search PubMed⌕ Search

Biomedical subjects

M Boucher

Publications and source records attributed to M Boucher.

At least 19 recordsLinked to original sources
PubMed2006

Reduction of apoptosis in the amygdala by an A2A adenosine receptor agonist following myocardial infarction.

It has been observed that a cytokine synthesis inhibitor, pentoxifylline, prevents the apoptotic processes taking place in the amygdala following myocardial infarction. However, it is unknown if the cardioprotective effect of A(2A) adenosine receptor agonist, CGS21680, which reduces cytokine synthesis, would lead to such amygdala apoptosis regression. Thus, this study was designed to investigate whether cardioprotective A(2A) adenosine receptor activation reduces apoptosis in the amygdala following myocardial infarction. Anesthetized rats were subjected to left anterior descending coronary artery occlusion for 40 min, followed by 72 h of reperfusion. The A(2A) agonist CGS21680 (0.2 mug/kg/min i.v.) was administered continuously for 120 min, starting (1) five minutes prior to instituting reperfusion (Early) or (2) five minutes after the beginning of reperfusion (Late). After reperfusion, myocardial infarct size was determined and the amygdala was dissected from the brain. Infarct size was reduced significantly in the Early compared to the Control group (34.6 +/- 1.8% and 52.3 +/- 2.8% respectively; p < 0.05), with no difference compared to the Late group (40.1 +/- 6.1%). Apoptosis regression was documented in the amygdala of the Early group by an enhanced phosphatidylinositol 3-kinase-Akt pathway activation and Bcl-2 expression concurrently to a caspase-3 activation limitation and reduction in TUNEL-positive cells staining. On the other hand, amygdala TUNEL-positive cell numbers were not reduced in the Late group. Moreover, TNFalpha was significantly reduced in the amygdala of the Early group compared to the Control and Late groups. These results indicate that A(2A) adenosine receptor stimulation is associated with apoptosis regression in the amygdala following myocardial infarction.

Adenosine↗
PubMed2004

Ximelagatran in prevention of cardiovascular events.

Ximelagatran (Exanta (R) is the first oral anticoagulant in a new class of drugs called direct thrombin inhibitors. Two studies suggest that ximelagatran is at least as effective as warfarin in preventing stroke in high risk patients with atrial fibrillation. Ximelagatran may also reduce the rate of major cardiovascular events after a myocardial infarction, compared to placebo. Ximelagatran does not require dose adjustments or routine blood monitoring. As with warfarin, bleeding risks increase with higher doses of ximelagatran. There is, however, no specific antidote to help manage bleeding. The safety of ximelagatran will not be fully known without further evaluation and surveillance for potential liver toxicity and drug interactions.

Anticoagulants↗
PubMed2003

Immunohistochemical detection of uroplakin III, cytokeratin 7, and cytokeratin 20 in canine urothelial tumors.

Immunohistochemistry for uroplakin III (UP III), cytokeratin 7 (CK 7), and cytokeratin 20 (CK 20) using commercially available antibodies was done in normal canine urinary bladder and 72 canine urinary bladder tumors that had been fixed in formalin and embedded in paraffin. Prolonged fixation (3-28 days) did not significantly alter the immunostaining for UP III. There was moderate reduction in the intensity for CK 7 and CK 20 after 1 week of fixation. UP III was detected in superficial (umbrella) cells and some intermediate cells of the normal urinary bladder, 7 of 7 transitional cell papillomas (TCPs), 50 of 55 transitional cell carcinomas (TCCs), and 4 of 5 metastatic TCCs. Staining was typically outlined in the plasma membrane, but diffuse or focal cytoplasmic staining was also observed. Intracytoplasmic lumina were usually positive for UP III. One squamous cell carcinoma of the bladder, 4 nonepithelial bladder tumors, and 285 nonurothelial tumors from different nonurinary locations were negative for UP III. CK 7 was detected in 7 of 7 TCPs, 53 of 54 TCCs, and 5 of 5 metastatic TCCs. The staining for CK 7 was diffuse cytoplasmic. CK 20 was detected in 1 of 7 TCPs, 37 of 54 TCCs, and 1 of 5 metastatic TCCs. The staining with CK 20 was cytoplasmic and weaker than with antibodies to UP III or CK 7. There was concurrent expression of UP III, CK 7, and CK 20 in 36 of 54 TCCs. UP III is a specific and sensitive marker for canine transitional epithelial (urothelial) neoplasms, detecting 91% of TCCs. Negative results may be observed with anaplastic tumors.

Animals↗
PubMed2001

Enhancement of the effects of a complete inhibitor of enkephalin-catabolizing enzymes, RB 101, by a cholecystokinin-B receptor antagonist in diabetic rats.

1. RB 101, a complete inhibitor of enkephalin-catabolizing enzymes, has been previously shown to produce antinociception in normal rats after systemic administration. Moreover, its coadministration with a cholecystokinin-B (CCK-B) receptor antagonist has been shown to strongly enhance its antinociceptive effect in normal rats. In this work, we determined whether RB 101 was able to reduce hyperalgesia and allodynia in diabetic rats, a model of neuropathic pain. The type of opioid receptors (mu or delta) involved was determined using naloxone and naltrindole, respectively, and the interactions between endogenous enkephalins and CCK on nociception control was investigated using coadministration of RB 101 and the CCK-B receptor antagonist CI-988. 2. RB 101 suppressed mechanical hyperalgesia (paw pressure-induced vocalization test), partially alleviated mechanical allodynia (von Frey hair test), and was ineffective in thermal allodynia (tail immersion test). The analgesic effect was completely cancelled by naloxone or naltrindole, suggesting that is requires the availability of mu- and/or delta-opioid receptors. 3. The combination of an inactive dose of CI-988 with the lowest effective dose of RB 101 resulted in a stronger increase in the vocalization threshold comparatively to RB 101 alone. 4. The present study demonstrates that the antinociception generated by RB 101 induced by elevation of extracellular levels of endogenous enkephalins, can be extended to neuropathic pain in diabetic rats and that blockade of CCK-B receptors potentiated antinociceptive effects elicited by RB 101.

Aminopeptidases↗
PubMed2001

Health-related quality of life after short segment instrumentation of lumbar burst fractures.

Management of lumbar burst fractures remains controversial. Surgical reduction/stabilization is becoming more popular; however, the functional impact of operative intervention is not clear. The purpose of this study was to assess health-related quality of life and functional outcome after posterior fixation of lumbar burst fractures with either posterolateral or intrabody bone grafting. Twenty-four subjects were included. Radiographs and computed tomography scans were evaluated for deformity (kyphosis, vertebral compression, lateral angulation, lateral body height, and canal compromise) postoperatively, at 1 year, and at final follow-up (mean 3.2 years). Patients completed the SF 36 Health Survey and the Oswestry Low Back Pain Disability Questionnaire at final follow-up. Significant improvement was noted in midsagittal diameter compromise, vertebral compression, and kyphosis. The difference observed between the respondents mean scores on the SF 36 was not significantly different from those presented as the U.S. national average (p = 0.053). Data from the Oswestry questionnaire indicated a similarly high level of function. Overall, we found posterior spinal instrumentation to correlate with positive functional outcome based on both general health (SF 36) and joint-specific outcome scales (Oswestry). Posterior instrumentation provides sound canal decompression, kyphotic reduction, and maintains vertebral height with minimal transgression and long-term sequelae. In cases of severe initial deformity and neurologic compromise, intrabody bone grafting is most certainly indicated; the additional support provided by a posterolateral graft may also prove beneficial as an adjunct.

Adolescent↗
PubMed2001

Involvement of hypogastric and pelvic nerves for conveying cystitis induced nociception in conscious rats.

PURPOSE: We determined the sites of the antinociceptive action of morphine in the experimental model of cyclophosphamide induced cystitis and investigated the afferent nerve fibers involved in nociception transmission originating from the bladder. MATERIALS AND METHODS: Cyclophosphamide (200 mg./kg.) given intraperitoneally was used to induce cystitis in male rats and their behavior was observed and scored. The effect of 2 mg./kg. systemic morphine given intravenously on cyclophosphamide induced behavioral modifications was tested when administered alone and after 100 microg. naloxone per rat given intrathecally at the L1 to L2 or L6 to S1 level. The spinal antinociceptive effect of morphine was also tested when administered intrathecally alone at 10, 100 and 200 microg. per rat at L1 to L2, alone at 100 microg. per rat at L1 to L2 or L6 to S1, alone at 100 microg. per rat at L1 to L2 and L6 to S1 simultaneously, alone at 200 microg. per rat at L1 to L2 and after 100 microg. naloxone per rat given intrathecally at L6 to S1 at 100 microg. per rat at L1 to L2. RESULTS: Cyclophosphamide induced marked modifications in the behavior of the rats, including a decreased breathing rate, eye closing and specific postures. Morphine given intravenously reversed these behavioral disorders and this reversal was completely prevented by pretreatment with intrathecal naloxone. A dose of 100 microg. per rat given intrathecally also reversed these behavioral disorders by about 25% at the L1 to L2 and L6 to S1 levels. In addition, a dose of 100 microg. morphine per rat administered intrathecally and simultaneously at L1 to L2 and L6 to S1 produced an effect equal to the sum of those observed when administered separately, that is about 50%, whereas morphine at an intrathecal dose of 200 microg. at L1 to L2 produced the same effect as 100 microg. given intrathecally at the same level or at L6 to S1 (25%). Also, 100 microg. naloxone per rat administered intrathecally at L6 to S1 prevented the effect of 100 microg. morphine at L1 to L2. CONCLUSIONS: These results confirm the previously reported antinociceptive effect of systemic morphine in this model of cyclophosphamide cystitis, suggest that this antinociceptive action is completely located at the spinal site and most importantly demonstrate by the pharmacological approach and behavioral analysis that nociceptive sensations originating from the bladder are conveyed by hypogastric and pelvic nerves in this cyclophosphamide cystitis model in the conscious rat.

Animals↗
PubMed2001

Tacrolimus ointment for the treatment of atopic dermatitis.

(1) Atopic dermatitis (AD) is a chronic dermatological condition characterized by pruritus (itchiness) and rash. Topical corticosteroids are the mainstay of pharmacotherapy. (2) Tacrolimus ointment is a new topical anti-inflammatory agent available in Canada through the Special Access Program. (3) It is approved as a second line agent for short or long term intermittent treatment of moderate to severe AD. (4) Clinical trials suggest it is both effective and safe, but comparative studies with corticosteroids and long-term information are limited.

Canada↗
PubMed2000

Evidence for an involvement of tachykinins in allodynia in streptozocin-induced diabetic rats.

A better knowledge of the pathophysiology of chronic pain could help to improve the treatment of patients with such syndrome. The aim of the present work was to elucidate the possible involvement of spinal substance P and neurokinin A in the mechanical and thermal allodynia observed in streptozocin-induced diabetic rats. A tachykinin NK(1) receptor antagonist, RP-67,580 ((3aR,7aR) -7, 7-diphenyl-2-(1-imino-2(2-methoxy phenyl)-ethyl) perhydroisoindol-4-one hydrochloride), a tachykinin NK(2) receptor antagonist, SR-48,968 ((S)-N-methyl (4-(acetylamino-4phenylpiperidino)-2-(3, 4-dichlorophenyl) butyl) benzamide) and their respective enantiomers were intrathecally administered 4 weeks after the induction of diabetes. Mechanical and thermal allodynia were evaluated before and up to 60 min after injection. The tachykinin receptor antagonists at the highest doses (10 and 25 microgram) significantly reduced allodynia, their enantiomers being inactive. Both of these data suggest the involvement of substance P and neurokinin A in the neuropathy-induced allodynia and offer a novel hypothesis to treat chronic pain due to diabetes.

Analgesics↗
PubMed2000

Potentiation of morphine and clomipramine analgesia by cholecystokinin -B antagonist CI-988 in diabetic rats.

The aim of this study was to determine the influence of an intrathecally injected cholecystokinin-B (CCK-B) receptor antagonist, CI-988, on the analgesic effect of morphine and clomipramine in diabetic rats. Administered alone, morphine (0.1 mg/kg, i.v.) and clomipramine (3 mg/kg, i.v.) have respectively no effect and only a slight effect on vocalization thresholds to paw pressure in diabetic rats, but, when coadministered with CI-988 (0.1 microg/rat, i.t.), an appreciable antinociceptive effect was observed. This suggests that a spinal blockade of cholecystokininergic system increases the analgesia induced by morphine or clomipramine. A CCK-B receptor antagonist could thus be used to lower dosages of morphine or antidepressant drugs in the management of neuropathic pain in humans, and thereby reduce their side effects.

Analgesia↗
PubMed2000

Double-blind, randomized, controlled trial of atosiban and ritodrine in the treatment of preterm labor: a multicenter effectiveness and safety study.

OBJECTIVE: This study was undertaken to compare the efficacy and safety of intravenous administration of atosiban versus ritodrine for the treatment of preterm labor. STUDY DESIGN: Women with preterm labor and intact membranes diagnosed at 23 to 33 gestational weeks (n = 247) were randomly assigned to treatment arms and received atosiban (6.75 mg intravenous bolus, 300 microg/min for 3 hours, then 100 microg/min intravenously) or ritodrine (0.10-0.35 mg/min intravenously) for as long as 18 hours. Tocolytic effectiveness was assessed in terms of the numbers of women who had not been delivered after 48 hours and after 7 days. Safety was assessed in terms of maternal side effects and neonatal morbidity. Secondary outcomes included mean gestational age at delivery and mean birth weight. An intent-to-treat analysis was performed with the Cochran-Mantel-Haenszel test. RESULTS: The proportion of women who had not been delivered at 48 hours was 84.9% (n = 107) in the atosiban group and 86.8% (n = 105) in the ritodrine group. At 7 days 92 women had still not been delivered in both the atosiban (73.0%) and ritodrine (76.0%) groups. Neither of these differences was statistically significant. The incidence of maternal cardiovascular side effects was substantially lower in the atosiban group (4.0% vs 84.3%, P <.001). In addition, intravenous therapy was terminated more frequently as a result of maternal adverse events in the ritodrine group (29.8%) than in the atosiban group (0.8%). The overall occurrences of fetal adverse events in the two treatment groups were comparable. Neonatal morbidity was similar between the treatment groups after adjustment for unbalanced enrollment of women with multiple pregnancies and for gestational ages within treatment groups. CONCLUSION: Atosiban was comparable in clinical effectiveness to conventional ritodrine therapy but was better tolerated than ritodrine, with no evidence of significant maternal or fetal adverse events. Neonatal morbidity, which was similar between the two treatment arms, was apparently related to the gestational age of the infant rather than to the exposure to either tocolytic agent.

Adult↗
PubMed2000

Cyclophosphamide-induced cystitis in freely-moving conscious rats: behavioral approach to a new model of visceral pain.

PURPOSE: To develop a model of visceral pain in rats using a behavioral approach. Cyclophosphamide (CP), an antitumoral agent known to produce toxic effects on the bladder wall through its main toxic metabolite acrolein, was used to induce cystitis. MATERIALS AND METHODS: CP was administered at doses of 50, 100 and 200 mg./kg. i.p. to male rats, and their behavior observed and scored. The effects of morphine (0.5 to 4 mg./kg. i.v.) on CP-induced behavioral modifications were tested administered alone and after naloxone (1 mg./kg. s.c.). In addition, 90 minutes after CP injection, that is, at the time of administration of morphine, the bladder was removed in some rats for histological examination. Finally, to show that the bladder is essential for the CP-induced behavioral modifications, female rats also received CP at doses of 200 mg./kg. i.p. and of 20 mg. by the intravesical route, and acrolein at doses of 0.5 mg. by the intravesical route and of 5 mg./kg. i.v. RESULTS: CP dose-relatedly induced marked behavioral modifications in male rats: breathing rate decrease, closing of the eyes and occurrence of specific postures. Morphine dose-dependently reversed these behavioral disorders. A dose of 0.5 mg./kg. produced a reduction of almost 50% of the behavioral score induced by CP 200 mg./kg. This effect was completely prevented by pretreatment with naloxone. At the time of administration of morphine, histological modifications of the bladder wall, such as chorionic and muscle layer edema, were observed. In female rats, CP 200 mg./kg. i.p. produced the same marked behavioral modifications as those observed in male rats. Administered at the dose of 20 mg. intravesically, CP did not produce any behavioral effects, whereas acrolein at 0.5 mg. intravesically induced behavioral modifications identical to those under CP 200 mg./kg. i.p., with the same maximal levels. Conversely, acrolein 5 mg./kg. i.v. did not produce any behavioral effects at all. CONCLUSIONS: Overall, these results indicate that this experimental model of CP-induced cystitis may be an interesting new behavioral model of inflammatory visceral pain, allowing a better understanding of these painful syndromes and thus a better therapeutic approach to them.

Acrolein↗
PubMed1999

Reduction of caveolin 1 gene expression in lung carcinoma cell lines.

Caveolae are plasma membrane microdomains that have been implicated in organizing and concentrating certain signaling molecules. Caveolins, constitute the main structural proteins of caveolae. Caveolae are abundant in terminally differentiated cell types. However, caveolin-1 is down-regulated in transformed cells and may have a potential tumor suppressor activity. In the lung, caveolae are present in the endothelium, smooth muscle cells, fibroblasts as well as in type I pneumocytes. The presence of caveolae and caveolin expression in the bronchial epithelium, although probable, has not been investigated in human. We were interested to see if the bronchial epithelia express caveolins and if this expression was modified in cancer cells. We thus tested for caveolin-1 and -2 expression several bronchial epithelial primary cell lines as well as eight lung cancer cell lines and one larynx tumor cell line. Both caveolin-1 and -2 are expressed in all normal bronchial cell lines. With the exception of Calu-1 cell line, all cancer cell lines showed very low or no expression of caveolin-1 while caveolin-2 expression was similar to the one observed in normal bronchial epithelial cells.

Caveolin 1↗
PubMed1999

Tau-mediated process outgrowth is differentially altered by the expression of MAP2b and MAP2c in Sf9 cells.

It is well documented that the MAPs, MAP2 and tau, play pivotal roles in neurite outgrowth. Several isoforms of MAP2 and tau are coexpressed in neurons, suggesting that the pattern of neurite outgrowth results from a functional equilibrium among these isoforms. In the present study, by coexpressing two of these MAPs at the same time in Sf9 cells, we demonstrated that tau-mediated process outgrowth is affected differently by MAP2b and MAP2c. MAP2b impairs tau ability to induce process outgrowth. Tau affects MAP2c capacity to induce the formation of multiple processes. There is evidence that actin microfilaments (F-actin) are involved in the elaboration of tau-mediated process outgrowth in Sf9 cells. We compared the effects of MAP2b and MAP2c with the effects of tau on F-actin distribution and stability in Sf9 cells. In MAP2b- and MAP2c-expressing cells with processes, F-actin was redistributed. However, in MAP2b-expressing cells without processes, the distribution of F-actin appears to be similar to the one in wild-type infected cells. Collectively, these results indicate that MAP2b could impair the ability of MAP2c and tau to redistribute F-actin in Sf9 cells, thereby decreasing their capacity to induce process formation. Furthermore, MAP2b and MAP2c patterns of process outgrowth were differentially modified by depolymerization of F-actin by cytochalasin D (CD). As previously reported for tau-expressing cells, the MAP2b-expressing cells developed a higher number of processes per cell and a higher number of cells presented processes in the presence of CD. However, the number of cells with multiple processes was lower in MAP2b-expressing cells than in tau-expressing cells treated with CD at 24 h postinfection. This suggests that MAP2b exerts an effect on F-actin stability at an earlier stage of infection than tau. MAP2c had also some stabilizing effects on F-actin at an early stage of infection, since the percentage of cells presenting one process was similar to the nontreated cells. Therefore, MAP2b seems to have less capacity than MAP2c to redistribute F-actin but, nonetheless, both of these MAP2 isoforms exert a stabilizing effect on F-actin at an early stage of infection. Finally, by modifying phosphorylation we showed that MAP2c capacity to induce multiple processes is related to protein phosphorylation in Sf9 cells. Therefore, the differential effect of MAP2c and MAP2b on process outgrowth seems also to depend on protein phosphorylation.

Actins↗
PubMed1999

Effects of quinidine, verapamil, nifedipine and ouabain on hysteresis in atrial refractoriness in the conscious dog: an approach to ionic mechanisms.

1. This work determines the effects of quinidine, verapamil, nifedipine and ouabain on the hysteresis of the atrial effective refractory period (AERP) in the conscious dog. 2. AERP was always longer in the increasing phase than in the decreasing phase of the extrastimulus method, thus demonstrating the existence of AERP hysteresis. Calculated as the difference between the two values, hysteresis was between 8+/-0.8 and 11+/-1.0 msec. 3. Quinidine increased hysteresis from 9+/-0.7 to 13+/-0.7 msec, whereas verapamil decreased it from 10+/-0.9 to 5+/-0.5 msec and nifedipine did not affect it. Ouabain also lengthened hysteresis from 8+/-0.8 to 11+/-1.2 msec. 4. Thus, these results confirm the existence of a hysteresis phenomenon in the AERP in the conscious dog and are evidence that the fast sodium and slow calcium specific membrane currents participate in this phenomenon.

Animals↗
PubMed1998

Comparison of polymerase chain reaction assay with culture for detection of genital mycoplasmas in perinatal infections.

The polymerase chain reaction (PCR) technique was compared with culture for the detection of Ureaplasma urealyticum, Mycoplasma hominis, and Mycoplasma genitalium in clinical samples (vaginal secretions, throat and endotracheal secretions, and skin swabs) obtained from 47 high-risk pregnant women peripartum and eight newborn infants. Detection using PCR with homologous primers was highly specific, as a product with the expected length was consistently amplified with homologous but not with heterologous species. The limit of detection of the PCR assay was 10 color-changing units (CCU) of Mycoplasma strains. The PCR technique facilitated detection of Ureaplasma urealyticum DNA in 31 of 55 patients studied, of Mycoplasma hominis in seven samples, and of Mycoplasma genitalium in two samples. Four PCR-positive patients yielded culture-negative results. In one case a culture-positive sample was negative by PCR. The results show that PCR is a valuable tool for rapid detection of genital mycoplasmas in clinical samples. It is fast, sensitive, specific, and easy to perform, requiring minimal preparation of the clinical sample.

Base Sequence↗
PubMed1998

Patterns of visits to hospital-based emergency rooms.

What are the functions of hospital emergency care in our society? How are these functions associated with the characteristics of emergency room users, their environment and with other available medical resources? To answer these questions, an ecological conceptual framework has been developed, along with a procedure which clearly distinguishes between the sources of individual variation (user characteristics) and ecological variation (the users' environment and available medical resources). Four different functions have been identified: (1) care of critical or urgent cases requiring treatment only available in a hospital, (2) care of urgent cases requiring treatment also available elsewhere than in a hospital, (3) care of non-urgent cases requiring treatment only available in a hospital and (4) care of non-urgent cases requiring treatment also available elsewhere than in a hospital. The ecological units selected for this study do not differ statistically with regard to the frequency with which emergency rooms are used for these four functions. However, certain individual factors predicting frequency of utilization do differ depending on the unit; for example, patient health status is not uniformly related to the use of emergency rooms for non-urgent reasons in all units. This association is particularly weak in socio-economically deprived units and more significant at higher socio-economic levels.

Adolescent↗
PubMed1998

Cardiac anticholinergic effects of procainamide and its N-acetylated metabolite: experimental pharmacological and radioligand binding studies.

1. The cardiac anticholinergic effects of procainamide (1 mg kg(-1) min(-1)) and its N-acetylated metabolite (NAPA) at equimolar dose (1.16 mg kg(-1) min(-1)) were studied using in vivo experimental pharmacological and in vitro radioligand binding studies. 2. Procainamide and NAPA progressively reduced vagal stimulation-induced bradycardia in chloralose-anaesthetized dogs. As indicated by the ED50, the vagolytic activity of NAPA is 1.5-2.0 times weaker than that of procainamide. Both drugs increased heart rate, with lowering of mean blood pressure during the second part of procainamide infusion, but not during NAPA infusion. 3. Binding studies on rat heart membranes yielded Ki values that were 1.5 times higher for NAPA than for procainamide. 4. These results show that NAPA exerts a weaker cardiac vagolytic action than procainamide, which is probably linked to a lower ability to bind to cardiac muscarinic receptors.

Acecainide↗