36 research outputs found

    Coliform pyosalpinx as a rare complication of appendicectomy: a case report and review of the literature on best practice

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    <p>Abstract</p> <p>Introduction</p> <p>Coliform pyosalpinx is a rare entity. We report a case that occurred three months after appendicectomy for gangrenous appendicitis. There follows a literature review on best practice for the treatment of pyosalpinx.</p> <p>Case presentation</p> <p>A seventeen year old girl presented with an acute abdomen three months after an appendicectomy for gangrenous appendicitis. Intraoperative findings were bilateral pyosalpinx treated by aspiration, saline and Betadine irrigation and intravenous antibiotics.</p> <p>Conclusion</p> <p>Microbiological analysis of the pus revealed <it>Escherichia coli </it>and anaerobes. Chlamydia and Candida were not isolated. This is the first known reported case of Coliform Pyosalpinx following appendicectomy. The best treatment does not necessarily involve salpingectomy especially in women of reproductive age where fertility may become compromised.</p

    CXCR2 Signaling Protects Oligodendrocytes and Restricts Demyelination in a Mouse Model of Viral-Induced Demyelination

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    BACKGROUND: The functional role of ELR-positive CXC chemokines during viral-induced demyelination was assessed. Inoculation of the neuroattenuated JHM strain of mouse hepatitis virus (JHMV) into the CNS of susceptible mice results in an acute encephalomyelitis that evolves into a chronic demyelinating disease, modeling white matter pathology observed in the human demyelinating disease Multiple Sclerosis. METHODOLOGY/PRINCIPAL FINDINGS: JHMV infection induced the rapid and sustained expression of transcripts specific for the ELR+ chemokine ligands CXCL1 and CXCL2, as well as their binding receptor CXCR2, which was enriched within the spinal cord during chronic infection. Inhibiting CXCR2 signaling with neutralizing antiserum significantly (p<0.03) delayed clinical recovery. Moreover, CXCR2 neutralization was associated with an increase in the severity of demyelination that was independent of viral recrudescence or modulation of neuroinflammation. Rather, blocking CXCR2 was associated with increased numbers of apoptotic cells primarily within white matter tracts, suggesting that oligodendrocytes were affected. JHMV infection of enriched oligodendrocyte progenitor cell (OPC) cultures revealed that apoptosis was associated with elevated expression of cleaved caspase 3 and muted Bcl-2 expression. Inclusion of CXCL1 within JHMV infected cultures restricted caspase 3 cleavage and increased Bcl-2 expression that was associated with a significant (p<0.001) decrease in apoptosis. CXCR2 deficient oligodendrocytes were refractory to CXCL1 mediated protection from JHMV-induced apoptosis, readily activating caspase 3 and down regulating Bcl-2. CONCLUSION/SIGNIFICANCE: These findings highlight a previously unappreciated role for CXCR2 signaling in protecting oligodendrocyte lineage cells from apoptosis during inflammatory demyelination initiated by viral infection of the CNS

    Ectopic pregnancy secondary to in vitro fertilisation-embryo transfer: pathogenic mechanisms and management strategies

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    Quelle gestion des ovocytes immatures ?

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