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S Marchand

Publications and source records attributed to S Marchand.

86 records · Page 5Linked to original sources

Age-related changes in cardiac muscarinic receptors: decreased ability of the receptor to form a high affinity agonist binding state.

Cardiac ventricular muscarinic cholinergic receptors and agonist binding properties were determined in Fischer 344 rats at 3, 12, and 24 months of age. Muscarinic receptors were determined by specific (-)-[3H]quinuclidinyl benzilate (QNB) binding, and the agonist binding properties were determined by competition assays. There were no differences in the concentration of the receptor or the dissociation constant of [3H]QNB binding among the three age groups. In cardiac membranes from 3- and 12-month-old animals, 5'-guanylyl-imidodiphosphate (Gpp(NH)p) increased by 16- to 18-fold (p less than .01) the concentration of carbachol required to inhibit [3H]QNB binding by 50% (IC50). At 24 months, however, Gpp(NH)p induced only a 2.7-fold shift in the carbachol IC50 value (p less than .01). The reduced shift was due to an increase in the carbachol IC50 value determined in the absence of Gpp(NH)p (p less than .01). There was no significant differences among the 3-, 12-, and 24-month-old animals in the half-maximal concentration of Gpp(NH)p required to produce the carbachol IC50 shift. The data indicated that with age there is a reduced ability of the muscarinic receptor to form a high affinity agonist binding state.

Aging↗

[C-reactive protein of the cerebrospinal fluid in children. A new evaluation of its diagnostic value].

The presence of C-reactive protein in the cerebrospinal fluid (CSF) has been proposed as an early indicator of bacterial meningitis in children. A commercial latex agglutination test (CR-test, Hyland) was performed in CSF obtained at first lumbar puncture in 114 children (26 neonates and 88 children aged from 1 month to 15 years) presenting with meningitis-like episodes. The CSF was regarded as normal in 41 cases; 50 had non-bacterial meningitis, and bacterial infection was diagnosed in 14 and suspected in 9. The latex agglutination test was positive in the first CSF sample from 2 neonates with bacterial meningitis, but its specificity was low (= 0.58). In older infants and children the test was positive in 18/21 cases of bacterial meningitis (sensitivity = 0.86) and negative in the 18 cases with normal CSF, as well as in 47/49 cases of non-bacterial meningitis (specificity = 0.97). The presence of C-reactive protein in CSF obtained at first lumbar puncture therefore is unreliable to distinguish between bacterial and aseptic meningitis.

Adolescent↗

Efficacy of inactivated Mycoplasma pneumoniae vaccine in man.

Inactivated Mycoplasma pneumoniae vaccine produced antibody responses that reached protective levels in most individuals. These were almost equivalent to natural infection in amount and duration, and they persisted more than a year. Adverse effects were inconsequential. At Keesler Air Force Base, Mississippi, where the annual rate of mycoplasma pneumonia varied from 20 to 50 per 1000 since 1959, protection studies were conducted in 21, 199 men in 1964-1966 and in 13, 892 men in 1969-1971. This produced a 36 percent reduction in bronchitis and a 45 percent reduction in pneumonia due to all etiologies in the frist study and 37 percent and 48 percent respectively in the second study. The protective efficacy of the second vaccine was 87 percent for acutebronchitis and 66 percent for pneumonia due to Mycoplasma pneumoniae. Persons who developed Mycoplasma pneumoniae infections in spite of vaccination did not experience more severe illnesses.

Adult↗

Kinetic parameters of amikacin in cystic fibrosis children.

35 kinetic studies have been performed, in nine CF children three to 15 years old; six kinetic studies were performed in four non-CF children, one to 12 years old. The dosage was 5 to 12.5 mg/kg, i.v. during 0.5 to 1.0 h, three to four times per day. Amikacin concentrations were measured in the plasma of all children, and in the sputum of CF-patients, by fluorescent polarization (TDX Abbott). The pharmacokinetic parameters in the plasma did not differ significantly in both groups of patients. In CF children t1/2 = 0.94 h (SD = 0.25 h), Vd (area) = 0.257 l/kg (SD = 0.06 l/kg), total body clearance = 130.7 ml/min/1.73 m2 (SD = 32.4 ml/min/1.73 m2). In non-CF children t1/2 = 0.83 h (SD = 0.15 h), Vd (area) = 0.265 l/kg (SD = 0.04 l/kg) and clearance = 155 ml/min/1.73 m2 (SD = 17.4 ml/min/1.73 m2). The parameters were not affected by the dosage of amikacin. The peak plasma concentrations ranged from 19 to 43.8 mg/l. Amikacin peak level in the sputum of CF children never reached the average MIC (4 mg/l) of Pseudomonas aeruginosa strains isolated in these patients. Amikacin concentration in the sputum reached its highest value about 2 h after the completion of i.v. infusion and was directly related to the peak plasma concentration. According to these parameters, the best dosage regimen appeared to be 7.5 to 8 mg/kg or 225 to 240 mg/m2 administered intravenously in 1.0 h, three times per day.

Adolescent↗

Targeting of acetylcholine receptor and 43 kDa rapsyn to the postsynaptic membrane in Torpedo marmorata electrocyte.

In this study we have investigated the intracellular routing of two major components of the postsynaptic membrane in Torpedo electrocytes, the nicotinic acetylcholine receptor and the extrinsic 43 kDa protein rapsyn, and of a protein from the non-innervated membrane, the Na+,K+ ATPase. We isolated subpopulations of post-Golgi vesicles (PGVs) enriched either in AChR or in Na+,K+ ATPase. Rapsyn was associated to AChR-containing PGVs suggesting that both AChR and rapsyn are targeted to intracellular organelles in the secretory pathway before delivery to the postsynaptic membrane. In vitro assays further show that rapsyn-containing PVGs do bind more efficiently to microtubules compared to Na+,K+ ATPase-enriched PVGs. These data provide evidence in favor of the contribution of the secretory pathway to the delivery of synaptic components.

Animals↗

Post-transplantation polyomavirus infections.

Increasing attention has been recently accorded to BK and JC viruses (BKV and JCV). Both these human polyomavirus (HPV) are members of the papovavirus family which includes the simian virus SV 40. BKV and JCV infect more than 60% of the population worldwide. After primary infection, they remain harboured in the kidneys and may become reactivated in situations of immune impairment. HPV were first described in 1971. BKV was isolated in a renal transplant patient with ureteral stricture and JCV in a patient with progressive multifocal leukoencephalopathy (PML). BKV was known to be involved in post-bone marrow transplantation (BMT) hemorrhagic cystitis. In renal transplantation, BKV and JCV were initially found in the post-transplant ureteric stricture and PML. They are now recognised as a possible cause of transplant interstitial nephritis, mimicking rejection (satisfying the Banff criteria for acute rejection) or drug toxicity. In HPV nephritis there is a mixed interstitial inflammatory infiltrate with focal tubular injury; the tubular epithelium shows marked anisonucleosis, nuclear atypia and basophilic or amphophilic intranuclear inclusions. Tubulitis is frequent. DNA hybridisation or gene amplification by polymerase chain reaction usually demonstrate HPV. Although histology with viral nucleic acid detection may be helpful in differentiating viral infection and rejection, confusion between these complications may lead to either anti-rejection therapy, with the risk of over-immunosuppression, or reduction of immunosuppression, with the risk of graft loss. Confusion may also arise with inclusions of other viruses, such as cytomegalovirus, herpes virus and adenovirus. Reactivation of BKV and JCV infection was demonstrated in respectively 22.2% and 10.9% of renal transplant recipients and 55% and 6.7% of BMT patients. Unfortunately, no routine screening is available for these viruses, so this complication is probably underestimated. No specific therapy of HPV infection is currently available.

Bone Marrow Transplantation↗

Ciprofloxacin pharmacokinetics in young cystic fibrosis patients after repeated oral doses.

Until recently, only compassionate use of ciprofloxacin in children with cystic fibrosis was possible despite limited pharmacokinetic data. We studied five subjects with cystic fibrosis and exacerbation of pulmonary infection. A 15 mg/kg b.i.d. regimen of oral ciprofloxacin was administered. On the 15th day, eight blood samples were collected and plasma concentrations were measured by HPLC. The actual dose administered ranged from 10 to 14 mg/kg b.i.d., due to the fixed-dosage formulation. Corresponding AUC0-12 ranged from 8.2 to 11.9 mg.h/L. Plasma concentrations were maintained above individual MICs for a median time of 12.7 h over 24 h. The median area under the inhibitory curve was 52.8, which is about half the proposed target value for ciprofloxacin in pulmonary infections with Gram-negative bacteria such as Pseudomonas aeruginosa. A higher dose, administered from a specific formulation to ensure precise dosing, must be given in order to obtain adequate concentrations in cystic fibrosis children.

Administration, Oral↗

Incidence and consequences of post-transplantation lymphoproliferative disorders.

Post-transplant lymphoproliferative disorder (PTLD) is a recognized severe complication arising in allograft recipients treated with immunosuppressive drugs. Although not common, PTLD is one of the most frequent tumours among graft recipients, comprising 15-25% of neoplasms, compared with 5% in the general population. The introduction of cyclosporin A (CyA) in the early 1980's and the very potent new immunosuppressants such as anti-CD3 monoclonal OKT3 and FK506 have been associated with a significant rise in the incidence of PTLD and with their earlier presentation. The incidence of this malignancy varies with the organ transplanted (1-2% of renal transplant recipients) and with the nature and severity of the accompanying immunosuppressive regimen. While the precise etiology of PTLD is still unclear, significant advances have been made recently in the understanding of its pathogenesis. Most PTLD tumour cells present an activated B-cell phenotype and an unrestricted pattern of latent EBV gene products. It is generally accepted that Epstein-Barr virus (EBV) infection or reactivation and intensive anti-T lymphocyte regimens play a major role in the genesis of PTLD. They include a spectrum of EBV-related disorders ranging from lymphoid hyperplasia to frank malignant non-Hodgkin's lymphoma. Although different therapeutic attempts have been proposed, optimal treatment remains elusive. The mortality rate for monoclonal lymphomas was reported to be as high as 80%. Infusion of anti-B monoclonal antibodies seems to be a promising modality. Different preventive approaches have been proposed, including EBV sero-negative donor/recipient matching and careful monitoring of EBV infection. Cautious use of anti-rejection treatment in combination with prophylactic antiviral therapy is recommended.

Humans↗