Inner Ear Complications in Children and Adolescents with Sickle Cell Disease.

Hearing impairment is a reported complication of sickle cell disease, yet inner ear pathology is not fully understood. The study purpose was to examine the patterns of inner ear involvement in patients with sickle cell disease by magnetic resonance imaging (MRI) and to assess its association with auditory functions. A cross-sectional study included 22 children with sickle cell disease examined for inner ear pathology by audiogram, MRI inner ear and transcranial Doppler (TCD) with revision of their hospital records for transfusion, chelation and hydroxyurea (HU) therapy. Abnormal MRI in the form of intrinsic T1 hyperintensity within the lumen of inner ear structures and cochlear neuropathy was found in five (22.7%) patients; left middle cerebral artery (MCA) flow velocity was higher in patients with abnormal MRI (83.4 ± 5.3 cm/sec) compared to normal MRI (68.2 ± 11.1 cm/sec) (p = 0.015), however, none of the patients had TCD of >170 cm/sec. There was no significant difference between patients with normal and abnormal MRI as regards hearing level and speech audiometry. Sensorineural hearing loss (SNHL) was present in two (9.1%) and conductive hearing loss (CHL) in two (9.1%) patients. There was a significant negative correlation between right ear mean hearing level and right MCA flow velocity and significant negative correlation between left ear mean hearing level and basilar artery (BA) flow velocity. We concluded that inner ear pathology is not uncommon in asymptomatic patients with sickle cell anemia, yet it did not correlate with hearing impairment and may occur with normal TCD results.

Healthcare-associated Gram-negative bloodstream infections: antibiotic resistance and predictors of mortality.

This article describes the prevalence of antibiotic resistance and predictors of mortality for healthcare-associated (HA) Gram-negative bloodstream infections (GN-BSI). In total, 831 cases of HA GN-BSI from 17 intensive care units in different centres in Turkey were included; the all-cause mortality rate was 44%. Carbapenem resistance in Klebsiella pneumoniae was 38%, and the colistin resistance rate was 6%. Multi-variate analysis showed that age >70 years [odds ratio (OR) 2, 95% confidence interval (CI) 1.22-3.51], central venous catheter use (OR 2.1, 95% CI 1.09-4.07), ventilator-associated pneumonia (OR 1.9, 95% CI 1.1-3.16), carbapenem resistance (OR 1.8, 95% CI 1.11-2.95) and APACHE II score (OR 1.1, 95% CI 1.07-1.13) were significantly associated with mortality.

Antimicrobial susceptibilities of uropathogen Escherichia coli in renal transplant recipients: dramatic increase in ciprofloxacin resistance.

The urinary tract is the most common site of bacterial infections in renal transplant recipients. The management of urinary tract infections (UTI) in renal transplant recipients is becoming more difficult because of drug-resistant bacteria. The antimicrobial susceptibilities of uropathogen bacteria isolated from 398 patients who underwent renal transplantation between 2007 and 2011 were obtained from medical records. At least 1 UTI episode was diagnosed in 172 (43.2%) patients. Among the 703 bacteria isolated from these patients, Exherichia coli the most common pathogen, was isolated from 407/703 episodes (57.8%). Ciprofloxacin, co-trimoxazole, ceftriaxone, and gentamicin resistance rates were 59.4%, 85.7%, 40.7%, and 36.6%, respectively. Ninty six of 407 E. coli isolates (23.5%) were ESBL positive. Analysis of resistance rates in our center demonstrated ciprofloxacin resistance rate in uropathogenic E. coli to have increased gradually from 30.4% in 2003, 41.3% in 2007, and 59.4% in 2012. Instutional data regarding the etiologic agents and antimicrobial susceptibility results are important for proper management of patients with UTI.

The cloning and characterization of the CDC50 gene family in Saccharomyces cerevisiae.

We have cloned a gene that complements the cold-sensitive growth of cdc50-1 mutant strain of Saccharomyces cerevisiae at 14 degrees C. The CDC50 gene was found to be identical to YCR094w on chromosome III and contains 1173 nucleotides encoding 391 amino acids. We found a missense mutation at the first initiation codon of cdc50-1. The disruption of the CDC50 gene revealed that it is not essential for growth, but the disruptant caused the same cold-sensitive phenotype as cdc50-1, suggesting that the cdc50-1 is a null mutation resulted from the mutation in the first codon. The cdc50-1 mutant arrests at START in G1 phase at the non-permissive temperature. The CDC50 gene product has strong structural similarity to two other proteins in Saccharomyces cerevisiae encoded by YNR048w and YNL323w. The over-expression of either YNR048w or YNL323w suppressed the cdc50-1 mutant and the double disruption of either CDC50 and YNR048w or CDC50 and YNL323w resulted in a severe slow-growth phenotype. We conclude that these three genes constitute a family with redundant function. We also found that the CDC39 gene was a multicopy suppressor of cdc50-1 mutation, suggesting that the CDC50 family is involved in regulation of transcription via CDC39.