372 research outputs found

    Incidence and clinicopathologic behavior of uterine cervical carcinoma in renal transplant recipients

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    <p>Abstract</p> <p>Background</p> <p>Renal allograft recipients are reported to have a higher incidence of malignancy than the general population. This single hospital-based study examined the incidence and clinicopathologic behavior of uterine cervical carcinoma in renal transplant recipients.</p> <p>Methods</p> <p>Among 453 women receiving renal transplantation from January 1990 to December 2008, 5 patients were diagnosed with cervical carcinoma. Medical records of these 5 patients were retrospectively reviewed, and clinicopathologic data were collected and analyzed.</p> <p>Results</p> <p>The incidence of cervical carcinoma in renal transplant recipients was 58.1 out of 100,000 per year, which is 3.5 times higher than in the general Korean population. The mean interval between the time of renal transplantation and the time of cervical carcinoma diagnosis was 80.7 months. After a median follow-up of 96.2 months, there was no recurrence of the disease or death. In 4 patients who were positive from human papillomavirus in situ hybridization (HPV ISH), high or probably high risk HPV DNA was detected in all. Punctate staining of HPV ISH was detected in 3 out of 4 patients.</p> <p>Conclusions</p> <p>Higher incidence of cervical carcinoma is expected in renal transplant recipients, so appropriate surveillance is needed to ensure early detection and treatment of cervical carcinoma.</p

    Adenoma malignum of the uterine cervix: report of four cases

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    Efficacy evaluation of combination vaccine of recombinant C-terminal fragments of ApxIA, ApxIIA and ApxIIIA in piglets

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    The efficacy of the combination vaccine of the individual C-terminal fragments of ApxIA, ApxIIA and ApxIIIA of Actinobacillus pleuropneumoniae (APP) was evaluated in piglets. Twenty piglets were divided equally into 2 groups (n=10). All piglets were intramuscularly primed at 4 week-of-age (0 week post prime inoculation (WPPI)) and were intramuscularly boosted at 6 week-of-age (2 WPPI). Group A piglets were inoculated with sterile PBS and group B piglets were inoculated with the combination vaccine. Concentrations of each of the C-terminal fragment-specific IgG as determined by ELISA were significantly higher in group B than in group A from 2 WPPI until the end of this study. Clinical signs were observed from only 10% of group B piglets after the challenge with the mixture of APP serotypes 1, 2 and 5 at 4 WPPI, while 50% of group A piglets were protected against APP infections. Overall, intramuscular inoculation with the vaccine candidate can efficiently protect piglets against APP infection

    Recurrent Streptococcus Pneumoniae Meningoencephalitis in a Patient With a Transethmoidal eningoencephalocele

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    We report a case of recurrent Streptococcus Pneumoniae meningoencephalitis with a transethmoidal meningoencephalocele (TEME) but without cerebrospinal fluid (CSF) leakage

    Evaluation of the pathogenicity of GJB3 and GJB6 variants associated with nonsyndromic hearing loss

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    AbstractA number of genes responsible for hearing loss are related to ion recycling and homeostasis in the inner ear. Connexins (Cx26 encoded by GJB2, Cx31 encoded by GJB3 and Cx30 encoded by GJB6) are core components of gap junctions in the inner ear. Gap junctions are intercellular communication channels and important factors that are associated with hearing loss. To date, a molecular genetics study of GJB3 and GJB6 as a causative gene for hearing loss has not been performed in Korea. This study was therefore performed to elucidate the genetic characteristics of Korean patients with nonsyndromic sensorineural hearing loss and to determine the pathological mechanism of hearing loss by analyzing the intercellular communication function of Cx30 and Cx31 variants. Sequencing analysis of the GJB3 and GJB6 genes in our population revealed a total of nine variants, including four novel variants in the two genes. Three of the novel variants (Cx31-p.V27M, Cx31-p.V43M and Cx-30-p.I248V) and two previously reported variants (Cx31-p.V84I and Cx30-p.A40V) were selected for functional studies using a pathogenicity prediction program and assessed for whether the mutations were located in a conserved region of the protein. The results of biochemical and ionic coupling tests showed that both the Cx31-p.V27M and Cx31-p.V84I variants did not function normally when each was expressed as a heterozygote with the wild-type Cx31. This study demonstrated that two variants of Cx31 were pathogenic mutations with deleterious effect. This information will be valuable in understanding the pathogenic role of GJB3 and GJB6 mutations associated with hearing loss
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