Biomedical subjects
Publications and source records attributed to P Petit.
We report on the spontaneous disappearance of a dense round lesion from within the greater tuberosity of the humerus. The patient was treated with oral non-steroidal anti-inflammatory agents for symptoms of subacromial bursitis. Symptoms resolved in 10 days and the lesion had vanished when radiographed 3 months later. We surmise the lesion to represent intraosseous crystal deposition.
The purpose of this study was to assess the radiological findings after surgical removal of juvenile nasopharyngeal angiofibromas (JNA). The postoperative CT and MRI scans of ten patients were reviewed. The cured group included six patients. The non-controlled group included six patients with eight recurrences. Two patients belonged to both groups as they were also followed and cured after surgery for relapse. Four recurrences were asymptomatic and diagnosed by imaging. The imaging patterns were matched to the patients clinical status and endoscopic findings. In the cured group, non-enhanced residual soft tissue masses were seen in all cases. In the non-controlled group, recurrence was always demonstrated on early postoperative CT or MR as a dramatically enhanced mass. The recurrence was located in the lateral or superior aspect of the nasopharynx (n = 3), deep to the fossa of Rosenmuller (n = 4) or out of the nasopharynx (n = 1). In two cases a remaining enhanced mass disappeared spontaneously on iterated examinations. Because of numerous asymptomatic relapses, a radiological workup is recommended four months after surgery, even in patients with normal endoscopy, to rule out posterolateral or extranasopharyngeal recurrences. Spontaneous evolution of residual masses must be appreciated on iterated imaging examinations.
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1. We have previously demonstrated that adenosine-5'-O-(2-thiodiphosphate) (ADPbetaS), a potent P2Y-purinoceptor agonist, relaxed pancreatic vasculature not only through prostacyclin (PGI2) and nitric oxide (NO) release from the endothelium but also through other mechanism(s). In this study, we investigated the effects of an inhibitor of the Na+/K+ pump, of ATP-sensitive K+ (K(ATP)) channels and of small (SK(Ca)) or large (BK(Ca)) conductance Ca2+-activated K+ channels. Experiments were performed at basal tone and during the inhibition of NO synthase and cyclo-oxygenase. 2. In control conditions, ADPbetaS (15 microM) induced an initial transient vasoconstriction followed by a progressive and sustained vasodilatation. In the presence of N(omega)-nitro-L-arginine methyl ester (L-NAME, 200 microM) the transient vasoconstriction was reversed into a one minute vasodilator effect, which was then followed by a progressive and sustained vasodilatation similar to that observed with ADPbetaS alone. The addition of indomethacin (10 microM) did not significantly modify the profile of ADPbetaS-induced vasodilatation. 3. Ouabain (100 microM) decreased basal pancreatic flow rate and did not modify ADPbetaS-induced relaxation. This inhibitor of the Na+/K+ pump increased the pancreatic vasoconstriction induced by L-NAME or by the co-administration of L-NAME and indomethacin. Ouabain did not modify either the L-NAME or the L-NAME/indomethacin resistant part of the ADPbetaS vasodilatation. 4. The K(ATP) inhibitor tolbutamide (185 microM) did not significantly modify basal pancreatic flow rate and ADPbetaS-induced relaxation. This inhibitor which did not change L-NAME-induced vasoconstriction, significantly diminished the L-NAME resistant part of ADPbetaS-induced vasodilatation. Tolbutamide intensified the vasoconstriction induced by the co-administration of L-NAME and indomethacin. In contrast, the L-NAME/indomethacin resistant part of ADPbetaS vasodilatation was not changed by the closure of K(ATP). 5. The SK(Ca) inhibitor apamin (0.1 microM) did not significantly change pancreatic vascular resistance whatever the experimental conditions (in the absence or in presence of L-NAME or L-NAME/indomethacin). In the presence of L-NAME, the closure of SK(Ca) channels changed the one minute vasodilator effect of ADPbetaS into a potent vasoconstriction and thereafter modified only the beginning of the second part of the L-NAME-resistant part of the ADPbetaS-induced vasodilatation. In contrast, the L-NAME/indomethacin resistant part of ADPbetaS-induced relaxation remained unchanged in the presence of apamin. 6. Charybdotoxin (0.2 microM), an inhibitor of BK(Ca), increased pancreatic vascular resistance in the presence of L-NAME/indomethacin. In the presence of L-NAME, the closure of BK(Ca) channels reversed the one minute vasodilator effect of ADPbetaS into a potent vasoconstriction and drastically diminished the sustained vasodilatation. In contrast the L-NAME/indomethacin resistant part of ADPbetaS-induced relaxation was not modified by the presence of charybdotoxin. Under L-NAME/indomethacin/charybdotoxin/apamin infusions, ADPbetaS evoked a drastic and transient vasoconstriction reaching a maximum at the second minute, which was followed by a sustained increase in the flow rate throughout the ADPbetaS infusion. The maximal vasodilator effect of ADPbetaS observed was not modified by the addition of apamin. 7. The results suggest that the L-NAME-resistant relaxation induced by ADPbetaS in the pancreatic vascular bed involves activation of BK(Ca), K(ATP) and to a lesser extent of SK(Ca) channels, but the L-NAME/indomethacin resistant part of ADPbetaS-induced relaxation is insensitive to the closure of K(ATP), SK(Ca) and BK(Ca) channels.
Adenine nucleotides have been shown to stimulate insulin secretion by acting on P2 receptors of the P2Y type. Since there have been some discrepancies in the insulin response of different analogues of ATP and ADP, we investigated whether two different types of P2 receptors exist on pancreatic B cells. The effects of alpha,beta-methylene ATP, which is more specific for the P2X subtype, were studied in vitro in pancreatic islets and isolated perfused pancreas from rats, in comparison with the potent P2Y receptor agonist ADPbetaS. In isolated islets, incubated with a slightly stimulating glucose concentration (8.3 mM), alpha,beta-me ATP (200 microM) and ADPbetaS (50 microM) similarly stimulated insulin secretion; by contrast, under a non stimulating glucose concentration (3 mM), alpha,beta-me ATP was still effective whereas ADPbetaS was not. In the same way, in islets perifused with 3 mM glucose, alpha,beta-me ATP but not ADPbetaS induced a partial but significant reduction in the peak 86Rb efflux induced by the ATP-dependent potassium channel opener diazoxide. In the isolated pancreas, perfused with a non stimulating glucose concentration (4.2 mM), ADPbetaS and alpha,beta-me ATP (5-50 microM), administered for 10 min, induced an immediate, transient and concentration-dependent increase in the insulin secretion; their relative potency was not significantly different. In contrast, with a slightly stimulating glucose concentration (8.3 mM), ADPbetaS was previously shown to be 100 fold more potent than alpha,beta-me ATP. Furthermore, at 4.2 mM glucose a second administration of alpha,beta-me ATP was ineffective. In the same way, ADPbetaS was also able to desensitize its own insulin response. At 3 mM glucose, alpha,beta-me ATP as well as ADPbetaS (50 microM) induced a transient stimulation of insulin secretion and down regulated the action of each other. These results give evidence that pancreatic B cells, in addition to P2Y receptors, which potentiate glucose-induced insulin secretion, are provided with P2X receptors, which transiently stimulate insulin release at low non-stimulating glucose concentration and slightly affect the potassium conductance of the membrane.
Experimentally, desflurane causes a moderate positive inotropic effect and a transient increase in arterial pressure with rapid increases in concentration compared with isoflurane. We used a continuous oesophageal aortic blood flow echo Doppler device to study the myocardial effects of equi-anaesthetic concentrations of isoflurane and desflurane in 32 healthy patients undergoing superficial surgery. After induction of anaesthesia with midazolam, etomidate and fentanyl general anaesthesia was maintained in 16 patients with 0.6% end-expired concentration of isoflurane and in 16 patients with 3% end expired concentration of desflurane. Isoflurane induced a rapid decrease in aortic blood flow (ABF) which remained almost stable whereas desflurane induced an early, moderate and transient increase in ABF (1 min after introduction of the halogenated agent, mean ABF was 107 (SD 3)% in the desflurane group vs 95 (9)% in isoflurane group compared with control values before introduction of the inhalation agent; P = 0.005), followed by a marked secondary decrease in ABF. The maximal decrease in ABF reached 71 (15)% of its initial value in the desflurane group compared with 80 (14)% in the isoflurane group (ns). Neither agent caused significant changes in other variables except for PE'CO2 which decreased in both groups. Continuous ABF echo-Doppler monitoring demonstrated an early transient positive inotropic effect of desflurane.
UNLABELLED: Cardiovascular changes due to pneumoperitoneum during laparoscopic surgery are established in adult patients, but not known in infants. We investigated the hemodynamic effects of laparoscopy during general anesthesia in 12 ASA physical status I infants by using noninvasive continuous esophageal aortic blood flow (ABF) echo-Doppler monitoring. During the laparoscopic procedure, intraabdominal pressure was maintained automatically at 10 mm Hg by a CO2 insufflator, and minute ventilation was adjusted to avoid hypercapnia. Hemodynamic changes were continuously recorded on soft magnetic support and assessed at three time intervals: t0 (after the initiation of anesthesia), t1 (5 min after peritoneal insufflation), and t2 (5 min after exsufflation). The induction of pneumoperitoneum resulted in a significant decrease in ABF and stroke volume, and in a significant increase in systemic vascular resistance, compared with control values: 67% +/- 9% (P < 0.001), 68% +/- 10% (P < 0.001), and 162% +/- 34% (P < 0.001), respectively. These changes were completely reversed after peritoneal exsufflation. Pneumoperitoneum caused no significant changes in mean arterial pressure or in end-tidal CO2 pressure. These findings demonstrate that laparoscopy is associated with hemodynamic changes without clinically deleterious consequences in healthy infants during a short duration of pneumoperitoneum. IMPLICATIONS: The peritoneal insufflation achieved during laparoscopic surgery is associated with cardiovascular impairments (decrease in cardiac performance and increase in vascular resistance). We found that these changes had no clinically deleterious effects in healthy infants.
We describe the case of a seriously burned infant who suffered from a deep burn covering approximately 30% of his total body surface area. Because invasive hemodynamic monitoring is usually not suggested in infants, hemodynamic profile can be misunderstood. We tested a new echo-Doppler device to determine hemodynamic variation using a small esophageal probe specifically designed for newborns and infants. The aortic flowmeter was connected with satellite devices to obtain the hemodynamic profile, including aortic blood flow (ABF), preejection period, left ventricular ejection time, mean arterial pressure, heart rate, calculated stroke volume, calculated total systemic vascular resistance (TSVR), and end-tidal CO2 pressure. The positioning of the probe was easily obtained at each time. The hemodynamic management initially exhibited a hypovolemic status followed by a hyperdynamic profile, as suggested by a gradually increased ABF, which seemed similar to the variations currently reported in adult burn patients. Concurrent with hemodynamic determinations, plasma samples were drawn to measure interleukin-6 (IL-6), interleukin-1beta(IL-1beta), and tumor necrosis factor-alpha(TNF-alpha)levels. A consistent peak of IL-6 occurred simultaneously with the drop in TSVR. In contrast, no marked modifications were observed with IL-1beta and TNF-alpha. The same circulating cytokines moved alike in burned adults; IL-6 could partly explain the mechanisms of hemodynamic variation through the systemic inflammatory response syndrome. On the other hand, the echo-Doppler device could provide valuable noninvasive findings, allowing early improvement in resuscitation during the acute phase of critically burned infants and children.
The dibenzoxazepine neuroleptic loxapine, its N-demethylated metabolite amoxapine, and their 7- and 8-hydroxymetabolites were measured simultaneously in plasma by reversed-phase high-performance chromatographic method. An original liquid-liquid extraction procedure was performed, consisting in coextraction of the substances together with a water-miscible solvent (acetonitrile) by a non-water-miscible solvent (toluene). The substances were separated on a 5-microm CN 25-cm column, and eluted with a mobile phase consisting of acetonitrile-acetic acid 0.5 N (30:70) and hexylamine (0.05%). They were detected by ultraviolet spectrophotometry at 310 nm. Clozapine was used as internal standard. Linearity was demonstrated in the range of 10 to 250 microg/l, and detection limits were found to be 3.5 to 6.3 microg/l according to the substance. Within-day repeatability ranged from 2.7% to 6.5%, and between-day reproducibility ranged from 0.9% to 20.2%. The extraction procedure provided a mean absolute recovery of 51.1% (range, 40.7% to 58.6%) with a mean coefficient of variation of 4.2%. This technique was applied to the concurrent determination of plasma concentrations of the compounds in 10 patients administered loxapine 75 to 600 mg daily. Steady state plasma levels of loxapine were significantly correlated with oral doses (n = 10, r = 0.858, p < 0.002). In conclusion, the method proved to be a convenient and reproducible procedure allowing the simultaneous measurement of loxapine, amoxapine, and their metabolites in patients.
An original and reliable technique to culture growth plate chondrocytes was developed to obtain an abundant amount of mature and functional chondrocytes. Growth plates were provided from the epiphysis of 3-week-old rabbits. Isolation of the chondrocytes was optimized by the use of trypsin and collagenase. The culture was realized according to the following conditions: seeding at 20,000 or 30,000/cm2 on type I collagen substrate and in Ham F-12 medium without a supplementation of glucose or growth factors. After 7 days of culture, the implantation was to be carried out. Different implantation substrates were evaluated in vivo. Agar turned out to be the only substrate to provide strong and healthy chondrocytes 21 days after the grafting. Then implantation was tested on large iliac resections in rabbits to check whether an enchondral ossification occurred with the culture. Poor results were obtained because of an early disappearance of the cultured chondrocytes. In an other experimentation, the culture was implanted into surgically created defects in the growth plate area. In this case, the culture did produce an epiphysiodesis. However, the 6-week postoperative histological examination showed that the implant remained viable, continued to maintain a proteoglycanrich matrix, and began to organize in ordered columns of mature chondrocytes.
The authors have analyzed a retrospective series of 27 aneurysmal bone cysts (ABCs) in children and adolescents. The average age at diagnosis was 10 years (range: 3 years 7 months to 16 years), with a mean follow-up of 5 years (range: 1 month to 13 years 9 months). Pathologic fractures (8 cases) and pain (8 cases) were the main reasons for consultation. Of five spinal ABC patients, four presented with neurologic involvement. Although conventional radiology is useful for diagnosing ABCs, magnetic resonance imaging (MRI) is nevertheless the most important technique for checking the extent of the lesions. However, the diagnosis still must be based on the pathologic laboratory findings, even though this is sometimes difficult because of associated lesions. In lesions of the long bones, recurrence was observed after curettage in 5 of 12 cases. For this reason, simple resection or resection with reconstruction is recommended rather than curettage whenever possible. When an ABC is in contact with the growth plate in young children, blunt curettage should be performed to preserve the child's growth potential. Subsequent recurrence usually is easier to treat than an epiphysiodesis bridge and its consequences. The surgical procedures used to preserve the growth plate are described, along with methods of bone construction after surgery.
BACKGROUND: In paediatric healthy patients and in real peroperative conditions, the cardiovascular effects of isoflurane have been poorly described. METHODS: We have evaluated the myocardial effects of 1% end-expired concentration (EEC) of isoflurane in 25 healthy infants or small children undergoing superficial surgical therapy for small burns with a continuous aortic blood flow echo-Doppler device. Aortic blood flow (ABF) was measured with a small oesophageal probe specially designed for infants. The aortic flowmeter was connected with satellite devices to visualize the haemodynamic profile variations during the isoflurane inhalation period. RESULTS: Isoflurane significantly decreased ABF and increased pre-ejection period/left ventricular ejection time (PEP/LVET), when compared with control values previously recorded 5 min after induction with halothane-fentanyl and atracurium (respectively, 80 +/- 7%, mean +/- SD; P < 0.001 and 111 +/- 11%; P = 0.017, 5 min after EEC of isoflurane reached 1%, then respectively, 75 +/- 12%; P < 0.001 and 119 +/- 16%; P < 0.001, at the end of the isoflurane inhalation period). These variations reversed to a great extent when isoflurane was switched off (97 +/- 17% for ABF; P = 0.08 and 105 +/- 12% for PEP/LVET; P = 0.75). Among the usual parameters, 1% EEC of isoflurane caused no significant changes in heart rate, moderately decreased mean arterial pressure (successively, 88 +/- 12%; P = 0.045 and 87 +/- 19%; P = 0.049), but belatedly decreased end-tidal CO2 pressure (87 +/- 11% at the end of the inhalation period (P < 0.001) which persisted 5 min after isoflurane was turned off (90 +/- 11%; P < 0.001)). CONCLUSIONS: These findings suggest that isoflurane can transiently depress cardiac function in healthy infants.
We report the characterization of a new insulinotropic compound, 4-hydroxyisoleucine. This amino acid has been extracted and purified from fenugreek seeds, which are known in traditional medicine for their antidiabetic properties. 4-Hydroxyisoleucine increases glucose-induced insulin release, in the concentration range of 100 micromol/l to 1 mmol/l, through a direct effect on isolated islets of Langerhans from both rats and humans. The stimulating effect of 4-hydroxyisoleucine was strictly glucose dependent; indeed, ineffective at low (3 mmol/l) or basal (5 mmol/l) glucose concentrations, the amino acid potentiated the insulin secretion induced by supranormal (6.6-16.7 mmol/l) concentrations of glucose. In addition, in the isolated perfused rat pancreas, we could show 1) that the pattern of insulin secretion induced by 4-hydroxyisoleucine was biphasic, 2) that this effect occurred in the absence of any change in pancreatic alpha- and delta-cell activity, and 3) that the more glucose concentration was increased, the more insulin response was amplified. Moreover, 4-hydroxyisoleucine did not interact with other agonists of insulin secretion (leucine, arginine, tolbutamide, glyceraldehyde). Therefore, we conclude that 4-hydroxyisoleucine insulinotropic activity might, at least in part, account for fenugreek seeds' antidiabetic properties. This secretagogue may be considered as a novel drug with potential interest for the treatment of NIDDM.
We report on a patient with neurosensory deafness, cataract and moderate mental retardation showing a constitutional mosaicism with the predominant cell line consisting of a 45,XY,-13,-15,+t(13;15) translocation of the Robertsonian type. By means of fluorescence in situ hybridization (FISH) using a panel of acrocentric pericentromeric probes and various banding techniques, the breakpoints in the translocation were determined at 13q12.1 and 15p13 respectively. Five other cell lines were present, at low percentage, one of them showing a t(13;15) tandem translocation. Interstitial telomeric sequences could be detected at the translocation fusion sites in both the Robertsonian and tandem translocations. The mosaicism appears therefore to be a consequence of chromosomal instability involving the t(13;15) fusion region of the predominant cell line, and related to the presence of interstitial telomeric sequences. The present observation suggests that in the pericentromeric 13q12 region, a gene involved in neurosensory deafness may be located.
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We present here a 6-year-old girl with the clinical signs of Wolf-Hirschhorn syndrome (WHS). Only after FISH studies the suspected 4p16.3 deletion could be confirmed. FISH studies in the mother showed that she was carrier of a balanced/unbalanced mosaicism with a 4p/16p translocation in 60% of the cells, and 4p16.3 deletion in 40% of the cells.
Localization by FISH of centric fission breakpoints in a de novo trisomy 9p patient with i(9p) and t(9q;11p): In this report we present a 38 year-old, severely mentally retarded female with 9p trisomy due to isochromosome 9p, i(9p), formation and translocation of the long arm of the rearranged chromosome 9 onto the telomere region of the short arm of chromosome 11: karyotype: 46, XX, -9, -11, +i(9p), +der(11) t(9;11) (q12;p15.5). C-banding showed that the i(9p) was monocentric and that der(11) had an additional C-band at the t(9q;11p) junction. The centric rearrangements were further identified by fluorescence in situ hybridisation (FISH) using a panel of chromosome 9 (peri)centric DNA probes. Analysis with probe pG-Xbal 1/340 (locus D4Z1), detecting the satellite subfamily at the centromeres of chromosomes 4 and 9, revealed small signals at the primary constriction of i(9p) but no signals at the breakpoint junction of the t(9q;11p). Further analysis using respectively chromosome 9 classical satellite probe (locus D9Z1), that consists of beta satellite sequences and pHuR98 probe (locus D9Z3) which detects satellite 3 DNA, localized to the 9qh region, both revealed translocation of these DNA sequences to the breakpoint of the t(9;11) junction. By using a 3'biotinylated oligonucleotide (TTAGGG)7 probe, no evidence was found for the presence of interstitial telomeric repeats at the t(9q;11p) breakpoint junction indicating that this derivative chromosome is the result of a reciprocal translocation with loss of telomeric regions including terminal 11p15.5-->pter. Our results provide evidence that the misdivision process that occurs on the chromosome 9 centric region results either from breakage in the alphoid DNA arrays or at the junction between alphoid and DNA regions.
We report an atypical presentation of Mycoplasma pneumoniae infection observed in a patient with primary hypogamma-globulinemia. Pulmonary miliary was combined with sternal and femoral osteomyelitis. These unusual CT findings could be explained by immunodeficiency with impaired antibody response.