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1.
Eur Rev Med Pharmacol Sci ; 22(20): 7034-7038, 2018 10.
Article in English | MEDLINE | ID: mdl-30402871

ABSTRACT

OBJECTIVE: Paraquat poisoning has almost disappeared from metropolitan France following its ban from the European market ten years ago. However, due to neighboring countries still authorizing paraquat use, French Guyana seems in a different situation. Here we aimed to report a series of paraquat-poisoned patients admitted to the emergency department of the Western French Guyana Hospital in Saint-Laurent du Maroni, to raise awareness of national health authorities on this persistent major issue. PATIENTS AND METHODS: We conducted a retrospective observational study describing the clinical features, the prognostic factors and the final outcome of paraquat-poisoned patients admitted to the emergency department between January 2008 and August 2014. RESULTS: Twenty-six paraquat-poisoned patients were included in the study. The median estimated paraquat dose intentionally ingested was 105 mg/kg (interquartile range, IQR: 359). Eighteen patients were treated with the cyclophosphamide/dexamethasone combination and seventeen with N-acetylcysteine in addition to the usual supportive care. Six patients survived and twenty died within a median 36h delay after admission (IQR: 130). Death was associated with cardiovascular (65%) and respiratory (35%) failure. Based on a bivariate analysis, predictive factors of death included (p≤0.05): advanced age, higher ingested paraquat dose, altered renal function, hypokalemia, acidosis, and dark blue dithionite test, observed on hospital admission. CONCLUSIONS: Paraquat poisoning still persists in French Guyana despite its withdrawal from the market. It is possible to determine the probability of death on patient admission based on routine clinical and biological parameters. There is an urgent need to request neighboring countries to ban paraquat with the aim of eradicating this dramatically life-threatening poisoning.


Subject(s)
Paraquat/poisoning , Poisoning/therapy , Public Health , Adolescent , Adult , Child , Cyclophosphamide/administration & dosage , Emergency Service, Hospital , Female , French Guiana/epidemiology , Humans , Hypokalemia/chemically induced , Male , Poisoning/epidemiology , Retrospective Studies , Young Adult
2.
Pediatr Med Chir ; 36(3): 5, 2014 06 30.
Article in Italian | MEDLINE | ID: mdl-25573640

ABSTRACT

Breast milk has always been the best source of nourishment for newborns. However, breast milk can carry a risk of infection, as it can be contaminated with bacterial or viral pathogens. This paper reviews the risk of acquisition of varicella-zoster virus (VZV) and cytomegalovirus (CMV), herpesviruses frequently detected in breastfeeding mothers, via breast milk, focusing on the clinical consequences of this transmission and the possible strategies for preventing it. Maternal VZV infections are conditions during which breastfeeding may be temporarily contraindicated, but expressed breast milk should always be given to the infant. CMV infection acquired through breast milk rarely causes disease in healthy term newborns; an increased risk of CMV disease has been documented in preterm infants. However, the American Academy of Pediatrics (AAP) does not regard maternal CMV seropositivity as a contraindication to breastfeeding; according to the AAP, in newborns weighing less than 1500 g, the decision should be taken after weighing the benefits of breast milk against the risk of transmission of infection. The real efficacy of the different methods of inactivating CMV in breast milk should be compared in controlled clinical trials, rigorously examining the negative consequences that each of these methods can have on the immunological and nutritional properties of the milk itself, with a view to establish the best risk-benefit ratio of these strategies before they are recommended for use in clinical practice.


Subject(s)
Breast Feeding , Cytomegalovirus Infections/transmission , Herpesviridae Infections/transmission , Infectious Disease Transmission, Vertical , Milk, Human/virology , Cytomegalovirus/pathogenicity , Female , Guidelines as Topic , Herpesviridae/pathogenicity , Humans , Infant , Infant, Newborn , Infant, Premature , Infant, Premature, Diseases/virology , Pregnancy , Pregnancy Complications, Infectious/virology , Probability , Risk Assessment
3.
Pediatr Med Chir ; 35(6): 263-8, 2013.
Article in Italian | MEDLINE | ID: mdl-24620553

ABSTRACT

Outbreaks of nosocomial pathogens are one of the most relevant problems in Neonatal Intensive Care Unit (NICU). Many factors contribute to the onset of an epidemic, including virulence of the pathogen and vulnerability of the infants hospitalized in NICU. Outbreaks are often caused by multidrug-resistant organisms (MDROs). MDROs are defined as microorganisms, predominantly bacteria, that are resistant to one or more classes of antimicrobial agents. MDROs, including methicillin-resistant Staphylococcus aureus (MRSA), vancomycin-resistant enterococci (VRE) and certain gram-negative bacilli (GNB), have important infection control implications. Once MDROs are introduced into a healthcare setting, transmission and persistence of the resistant strain is determined by the availability of vulnerable patients, selective pressure exerted by antimicrobial use, increased potential for transmission from larger numbers of infected or colonized patients ("colonization pressure"), and the impact of adherence to prevention efforts. Often, routine infection control measures are not enough to contain outbreaks, and additional control measures are needed, including implementation of hand hygiene, cohorting of infected/colonized infants, neonatal surveillance cultures, screening of healthcare workers and decolonization of neonates and/or healthcare workers in selected cases. In this review, we report the practices we developed in our NICU to contain an epidemic. These recommendations reflect the experience of the group, as well as the findings of the current literature.


Subject(s)
Cross Infection/prevention & control , Disease Outbreaks/prevention & control , Gram-Positive Bacterial Infections/prevention & control , Intensive Care Units, Neonatal , Methicillin-Resistant Staphylococcus aureus , Vancomycin Resistance , Cross Infection/epidemiology , Cross Infection/microbiology , Drug Resistance, Multiple, Bacterial , Humans , Infection Control/methods , Italy/epidemiology , Population Surveillance/methods , Practice Guidelines as Topic , Risk Assessment , Risk Factors
4.
Cytotherapy ; 10(1): 54-68, 2008.
Article in English | MEDLINE | ID: mdl-18202975

ABSTRACT

BACKGROUND: Multipotent mesenchymal stromal cells (MSC) are of interest for their potential to repair bone and cartilage, and also their immunosuppressive properties. Umbilical cord blood (UCB) is reported to contain MSC, and therefore may be a useful source of these cells for clinical applications. METHODS: We evaluated protocols for isolating MSC from UCB and characterized the surface phenotype, differentiation potential and immunoregulatory properties of the cells obtained. RESULTS: Ten of 25 UCB units processed yielded MSC-like colonies, with depletion of lineage+ cells providing a higher efficiency. Only two of the cultures could be expanded satisfactorily; the remainder failed to proliferate. One culture generated transformed lines that were grossly aneuploid, had up-regulated TERT transcripts and had lost CD90 expression and the capacity to differentiate. The two propagated UCB-MSC lines were similar to those from bone marrow but were not identical to each other, with differences seen in expression of surface markers and cytoskeletal proteins. Both underwent osteogenesis, but at different rates and to different degrees, while neither generated adipocytes. When added as a third party to a mixed lymphocyte culture, both suppressed proliferation. DISCUSSION: MSC-like cells can be isolated from UCB, but at low efficiencies, and they exhibit a variety of morphologies, growth rates and differentiation potentials and can transform in culture.


Subject(s)
Fetal Blood/cytology , Mesenchymal Stem Cells/cytology , Stromal Cells/cytology , Autoantibodies/metabolism , Cell Culture Techniques , Cell Differentiation/immunology , Cell Lineage , Female , Flow Cytometry , Humans , Immunohistochemistry , Immunophenotyping , Infant, Newborn , Intermediate Filament Proteins/metabolism , Karyotyping , Leukocytes, Mononuclear/cytology , Leukocytes, Mononuclear/immunology , Leukocytes, Mononuclear/metabolism , Mesenchymal Stem Cells/immunology , Mesenchymal Stem Cells/metabolism , Nerve Tissue Proteins/metabolism , Nestin , Pregnancy , RNA, Messenger/genetics , RNA, Messenger/metabolism , Reverse Transcriptase Polymerase Chain Reaction , Stromal Cells/immunology , Stromal Cells/metabolism , Vimentin/metabolism
5.
Neuropathol Appl Neurobiol ; 31(5): 491-502, 2005 Oct.
Article in English | MEDLINE | ID: mdl-16150120

ABSTRACT

We have previously demonstrated that amyloid beta (Abeta) peptide is acutely toxic to retinal neurones in vivo and that this toxicity is mediated by an indirect mechanism. We have now extended these studies to look at the chronic effect of intravitreal injection of Abeta peptides on retinal ganglion cells (RGC), the projection neurones of the retina and the glial cell response. 5 months after injection of Abeta1-42 or Abeta42-1 there was no significant reduction in RGC densities but there was a significant reduction in the retinal surface area after both peptides. Phosphate-buffered saline (PBS) injection had no effect on retinal size or RGC density. There was a pronounced reduction in the number of large RGCs with a concomitant significant increase in medium and small RGCs. There was no change in cell sizes 5 months after injection with PBS. At 5 months after injection of both peptides, there was marked activation of Muller glial cells and microglia. There was also expression of the major histocompatibility complex (MHC) class II molecule on some of the microglial cells but we saw no evidence of T-cell infiltration into the injected retinas. In order to elucidate potential toxic mechanisms, we have looked at levels of glutamine synthetase and nitric oxide synthase. As early as 2 days after injection we noted that activation of Muller glia was associated with a decrease in glutamine synthetase immuno-reactivity but there was no detectable expression of inducible nitric oxide synthase in any retinal cells. These results suggest that chronic activation of glial cells induced by Abeta peptides may result in chronic atrophy of projection neurones in the rat retina.


Subject(s)
Amyloid beta-Peptides/pharmacology , Nerve Degeneration/chemically induced , Neuroglia/drug effects , Retinal Ganglion Cells/drug effects , Retinal Ganglion Cells/pathology , Animals , Blotting, Western , Cell Size , Female , Glutamate-Ammonia Ligase/drug effects , Glutamate-Ammonia Ligase/metabolism , Immunohistochemistry , Microinjections , Nerve Degeneration/pathology , Nitric Oxide Synthase/drug effects , Nitric Oxide Synthase/metabolism , Rats , Rats, Sprague-Dawley
6.
Biochem J ; 349(Pt 1): 299-308, 2000 Jul 01.
Article in English | MEDLINE | ID: mdl-10861242

ABSTRACT

A novel ELISA has been developed which detects oligomerization of beta-amyloid (A beta). Oligomerization, fibrillization and neurotoxicity of native A beta associated with Alzheimer's disease (AD) type has been compared with E22Q A beta (amyloid beta-protein containing residues 1--40 with the native Glu at residue 22 changed to Gln) implicated in Dutch cerebral haemorrhage disease. Solutions of A beta rapidly yield soluble oligomers in a concentration-dependent manner, which are detected by the ELISA, and by size-exclusion gel chromatography. Conformational changes from disordered to beta-sheet occur more slowly than oligomerization, and fibrils are produced after prolonged incubation. The E22Q A beta oligomerizes, changes conformation and fibrillizes more rapidly than the native form and produces shorter stubbier fibrils. Aged fibrillar preparations of E22Q A beta are more potent than aged fibrils of native A beta in inducing apoptotic changes and toxic responses in human neuroblastoma cell lines, whereas low-molecular-mass oligomers in briefly incubated solutions are much less potent. The differences in the rates of oligomerization of the two A beta forms, their conformational behaviour over a range of pH values, and NMR data reported elsewhere, are consistent with a molecular model of oligomerization in which strands of A beta monomers initially overcome charge repulsion to form dimers in parallel beta-sheet arrangement, stabilized by intramolecular hydrophobic interactions, with amino acids of adjacent chains in register.


Subject(s)
Alzheimer Disease/metabolism , Amyloid beta-Peptides/chemistry , Cerebral Hemorrhage/metabolism , Enzyme-Linked Immunosorbent Assay/methods , Apoptosis , Biotinylation , Chromatography, Gel , Circular Dichroism , Dimerization , Dose-Response Relationship, Drug , Humans , Hydrogen-Ion Concentration , Kinetics , Magnetic Resonance Spectroscopy , Microscopy, Electron , Models, Molecular , Mutation , Phenotype , Protein Conformation , Time Factors , Tumor Cells, Cultured
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