35 research outputs found

    The first clinical case due to AP92 like strain of Crimean-Congo Hemorrhagic Fever virus and a field survey

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    <p>Abstract</p> <p>Background</p> <p>Crimean-Congo Hemorrhagic Fever (CCHF) is a fatal infection, but no clinical case due to AP92 strain was reported. We described the first clinical case due to AP92 like CCHFV.</p> <p>Methods</p> <p>A case infected by a AP92 like CCHFV was detected in Balkanian part of Turkey. Diagnosis was confirmed by RT-PCR and sequencing. A human serologic and tick survey studies were performed in the region, where the case detected.</p> <p>Results</p> <p>Thirty eight individuals out of 741 were found to be anti CCHFV IgM positive. The attack rate for overall CCHFV was calculated as 5.2%. In univariate analyses, CCHFV IgM positivity was found to be associated with the age (p < 0.001), male gender (p = 0.001), agricultural activity (p = 0.036), and history of tick bite (p = 0.014). In multivariate analysis, older age (OR: 1.03, CI:1.01–1.05, p < 0.001), male gender were found to be the risk factors (OR: 2.5, CI:1.15–5.63, p = 0.020) for CCHFV infection.</p> <p>Conclusion</p> <p>This is the first human case with AP92 like CCHFV infection. Furthermore, this is the first report of AP92 like strain in Turkey. In the region, elderly males carry the highest risk for CCHFV infection.</p

    Imported Crimean-Congo hemorrhagic fever cases in Istanbul

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    We described a series of imported cases of Crimean-Congo Hemorrhagic Fever (CCHF) in Istanbul and investigated the genetic diversity of the virus. All the suspected cases of CCHF, who were applied to the health centers in Istanbul, were screened for CCHF virus (CCHFv) infection by using semi-nested Polymerase Chain Reaction (PCR) following RT-PCR. Simultaneous blood samples were also sent to the national reference laboratory in Ankara for serologic investigation. In 10 out of 91 patients, CCHFv was detected by PCR, and among 9 out of 10, anti-CCHFv IgM antibodies were also positive. Clinical features were characterized by fever, myalgia, and hemorrhage. The levels of liver enzymes, creatinine phosphokinase, and lactate dehydrogenase were elevated, and bleeding markers were prolonged. All the cases were treated with ribavirin. There was no fatal case. All the strains clustered within the same group as other Europe/Turkey isolates

    K+ channel openers restore verapamil-inhibited lung fluid resolution and transepithelial ion transport

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    <p>Abstract</p> <p>Background</p> <p>Lung epithelial Na<sup>+ </sup>channels (ENaC) are regulated by cell Ca<sup>2+ </sup>signal, which may contribute to calcium antagonist-induced noncardiogenic lung edema. Although K<sup>+ </sup>channel modulators regulate ENaC activity in normal lungs, the therapeutical relevance and the underlying mechanisms have not been completely explored. We hypothesized that K<sup>+ </sup>channel openers may restore calcium channel blocker-inhibited alveolar fluid clearance (AFC) by up-regulating both apical and basolateral ion transport.</p> <p>Methods</p> <p>Verapamil-induced depression of heterologously expressed human αβγ ENaC in <it>Xenopus </it>oocytes, apical and basolateral ion transport in monolayers of human lung epithelial cells (H441), and <it>in vivo </it>alveolar fluid clearance were measured, respectively, using the two-electrode voltage clamp, Ussing chamber, and BSA protein assays. Ca<sup>2+ </sup>signal in H441 cells was analyzed using Fluo 4AM.</p> <p>Results</p> <p>The rate of <it>in vivo </it>AFC was reduced significantly (40.6 ± 6.3% of control, <it>P </it>< 0.05, n = 12) in mice intratracheally administrated verapamil. K<sub>Ca3.1 </sub>(1-EBIO) and K<sub>ATP </sub>(minoxidil) channel openers significantly recovered AFC. In addition to short-circuit current (Isc) in intact H441 monolayers, both apical and basolateral Isc levels were reduced by verapamil in permeabilized monolayers. Moreover, verapamil significantly altered Ca<sup>2+ </sup>signal evoked by ionomycin in H441 cells. Depletion of cytosolic Ca<sup>2+ </sup>in αβγ ENaC-expressing oocytes completely abolished verapamil-induced inhibition. Intriguingly, K<sub>V </sub>(pyrithione-Na), K <sub>Ca3.1 </sub>(1-EBIO), and K<sub>ATP </sub>(minoxidil) channel openers almost completely restored the verapamil-induced decrease in Isc levels by diversely up-regulating apical and basolateral Na<sup>+ </sup>and K<sup>+ </sup>transport pathways.</p> <p>Conclusions</p> <p>Our observations demonstrate that K<sup>+ </sup>channel openers are capable of rescuing reduced vectorial Na<sup>+ </sup>transport across lung epithelial cells with impaired Ca<sup>2+ </sup>signal.</p

    Unilateral Abducens Nerve Palsy with Ipsilateral Horner’s Syndrome as an Initial Manifestation of Recurrent Nasopharyngeal Carcinoma

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    ###EgeUn###A 62-year-old man was admitted to our clinic with a two-week history of double vision. Neuro-ophthalmological examination showed a left abducens nerve palsy with an ipsilateral Horner’s syndrome. Neuro-imaging identified recurrent nasopharyngeal carcinoma explaining the clinical findings. Co-existence of unilateral abducens nerve palsy and ipsilateral Horner’s syndrome is very rare and localises to the posterior cavernous sinus. Therefore, clinicians should be aware of this rare co-existence and perform appropriate neuro-imaging to clarify the underlying aetiology. © 2019, © 2019 Taylor & Francis Group, LLC
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