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Supplemental Digital Content is available in the text, Intermittent catheterization is an effective bladder management strategy for patients with incomplete bladder emptying. For self-catheterization, sufficient hand function in both hands is necessary. We have developed a novel automatic urinary catheterization device to induce self-IC for patients with bladder dysfunction and upper extremity disability. The aim of this study was to investigate the feasibility of this novel automatic catheterization device. This study was performed using 4 fresh cadavers. First, 400 mL of normal saline was filled into the cadaver bladder. Then, the catheter was inserted using the newly developed device. The catheter insertion was performed 3 times for each cadaver, with the penis positioned at 45°, 90°, and 135°, respectively. A transrectal ultrasonography was performed during the catheterization. We evaluated whether the catheter was successfully inserted into the bladder at each position of penis and whether the urethrovesical junction was injured when inserting the catheter. We also measured the volume of normal saline evacuated from the bladder after successful catheterization. With the penis positioned at 45° and 90°, catheter insertion was successful without any damage to the urethrovesical junction. However, when the penis was at 135°, the catheter could not be inserted into the bladder. When the automatic catheter insertion was successful, the bladder was successfully emptied. On average, 81.56 ± 3.26% of normal saline was discharged from the bladder and 11.13 ± 2.09% was remained. The newly developed automatic urinary catheterization device could insert the catheter effectively and safely. This device would be a useful tool for the urinary catheterization of bladder dysfunction patients with upper extremity disability.

The incidence of community-onset bacteremia caused by extended-spectrum-β-lactamase (ESBL) producers is increasing. The adverse effects of ESBL production on patient outcome have been recognized and this antimicrobial resistance has significant implications in the delay of appropriate therapy. However, a simple scoring algorithm that can easily, inexpensively, and accurately be applied to clinical settings was lacking. Thus, we established a predictive scoring algorithm for identifying patients at the risk of ESBL-producer infections among patients with community-onset monomicrobial Enterobacteriaceae bacteremia (CoMEB). In a retrospective cohort, multicenter study, adults with CoMEB in the emergency department (ED) were recruited during January 2008 to December 2013. ESBL producers were determined based on ESBL phenotype. Clinical information was obtained from chart records. Of the total 1141 adults with CoMEB, 65 (5.7%) caused by ESBL producers were identified. Four independent multivariate predictors of ESBL-producer bacteremia with high odds ratios (ORs)—recent antimicrobial use (OR, 15.29), recent invasive procedures (OR, 12.33), nursing home residents (OR, 27.77), and frequent ED user (OR, 9.98)—were each assigned +1 point to obtain the CoMEB-ESBL score. Using the proposed scoring algorithm, a cut-off value of +2 yielded a high sensitivity (84.6%) and an acceptable specificity (92.5%); the area under the receiver operating characteristic curve was 0.92. In conclusion, this simple scoring algorithm can be used to identify CoMEB patients with a high ESBL-producer infection risk. Of note, frequent ED user was firstly demonstrated to be a crucial predictor in predicting ESBL-producer infections. ED clinicians should consider adequate empirical therapy with coverage of these pathogens for patients with risk factors.

Wnt/β-catenin signaling pathway is thought to be implicated in the development of arterial stiffness and vascular calcification. As a Wnt signaling pathway inhibitor, it is interesting to investigate whether sclerostin or dickkopf-1 (DKK1) level is correlated with arterial stiffness in renal transplant (RT) recipients. Fasting blood samples were obtained for biochemical data, sclerostin, DKK1, and osteoprotegerin (OPG) determinations. In this study, we applied automatic pulse wave analyzer (VaSera VS-1000) to measure brachial-ankle pulse wave velocity and either sides of brachial-ankle pulse wave velocity value, which greater than 14.0 m/s was determined as high arterial stiffness. Among 68 RT recipients, 30 patients (44.1%) were in the high arterial stiffness group. Compared with patients in the low arterial stiffness group, patients in the high arterial stiffness group had higher prevalence of hypertension (P = 0.002), diabetes (P

Supplemental Digital Content is available in the text, Auditory neuropathy spectrum disorder (ANSD) is a sensorineural hearing disorder caused by dysfunction of auditory neural conduction. ANSD has a heterogeneous etiology, including genetic factors; the response to cochlear implantation significantly varies depending on the etiology. The results of timely cochlear implantation for OTOF-related ANSD (DFNB9) have been reported to be good. Therefore, identifying the causative gene of ANSD, especially OTOF, is an important issue to rehabilitate these patients. Six sporadic ANSD subjects without anatomical abnormality of the cochlear nerve, including the 4 subjects that were previously reported to be without detectable OTOF mutation, were included. We performed targeted resequencing (TRS) of known deafness genes and multiphasic bioinformatics analyses of the data that ensured detection of capture failure and structural variations. Exclusion of SNP was also double checked. The TRS data previously obtained from 2 subjects were reanalyzed. Through this study, we detected 2 mutant alleles of OTOF from 5 (83.3%) of 6 ANSD subjects. All of the 5 subjects carried at least 1 mutant allele carrying p.R1939Q. This variant was categorized as a simple SNP (rs201326023) in the database and it resided in the exon with frequent capture failures, which previously led to exclusion of this variant from eligible candidacy mistakenly. In addition, we detected a structural variation within OTOF from a previously undiagnosed ANSD subject, which was the second structural variation reported in DFNB9 subjects to date. We identify a strong etiologic homogeneity of prelingual ANSD in case of the anatomically normal cochlear nerve in Koreans and now report DFNB9 as the single overwhelming cause. Multiphasic analysis of TRS data ensuring detection of capture failure and structural variations would be expected to reveal DFNB9 from a substantial portion of previously undiagnosed ANSD subjects in Koreans. Based on our results, we propose a novel strategy that incorporates imaging studies, prevalent mutation screening and multiphasic analysis of TRS data in a stepwise manner to correctly detect DFNB9 in Koreans.