Purpose: To investigate differences in mortality of intensive care unit (ICU)

We report a novel locus responsible for postlingual progressive sensorineural hearing loss (designated DFNA9) that maps to chromosome 14q12-13. A large kindred with autosomal dominant transmission of non-syndromic hearing loss was clinically studied. Hearing in affected individuals deteriorated at approximately 20 years of age and progressed to anacusis in the fifth decade. A random genome-wide search using polymorphic short tandem repeats demonstrated linkage with D14S121 (maximum two point LOD score = 6.19, theta = 0). Haplotype analysis of recombination events defined a 9 cM disease interval, between D14S252 and D14S49.

The extensive dissemination of imipenem-resistant A. baumannii clonal strains causing episodes of bacteremia and/or sepsis resulted from modes of transmission via multiple contaminated surfaces and objects and transiently colonized HCWs' hands. Closure of the ICU and its meticulous environmental decontamination led to the successful control of the outbreak.

The pathogenic role of immune-mediated mechanisms in chronic hepatitis C virus (HCV) infection has not yet been elucidated. In this study, we report different cytokine expression profiles from hemodialysis (HD) and non-HD HCV (+) patients. IL-1beta, IL-2, IL-4, IL-6, TNF-alpha, and TGF-beta1 serum levels, and liver biochemical parameters were determined in 85 individuals (41 HD patients and 44 non-HD patients). Screening for HCV RNA and anti-HCV antibodies was performed using qualitative and quantitative reverse transcription polymerase chain reaction (RT-PCR), and standardized enzyme-linked immunosorbent assay (ELISA) and recombinant immunoblot assay (RIBA) methods, respectively. IL-4 and IL-1beta demonstrated decreased serum levels in non-HD HCV carriers compared with healthy controls. Both T helper (Th) 1 and Th2 lymphocytes were highly associated with chronic HCV infection, as indicated by the increased IL-2, IL-4, and IL-6 cytokine circulating levels in all chronic active hepatitis (CAH) patients examined. An enhanced Th2 response (IL-4 and IL-6) coupled with increased TNF-alpha and IL-1beta serum levels was reported in HD HCV (-) patients. In conclusion, our data show that a virus-induced Th2 and IL-1beta immunosuppression is an early event in HCV-related chronicity. Long-term HD specifically exerts a chronic effect on IL-6, IL-1beta, and TNF-alpha serum circulating levels. Irrespective of the HD status, HCV viremia, and liver biochemistry parameters, both Th1 and Th2 responses are highly associated with chronic HCV infection.

Loss of E (epithelial)-cadherin expression has been previously documented in sporadic colorectal carcinomas (SCRCs), but not as a consequence of mutations or allelic loss. In this study, the methylation status of the E-cadherin promoter was examined by utilizing the methylation-specific polymerase chain reaction (MSP) assay in 63 primary SCRCs and paired adjacent normal tissues. This was correlated with E-cadherin expression at both the RNA and the protein levels using multiplex reverse transcription (RT)-PCR and immunohistochemistry (IHC), respectively. Data were associated with the patients' clinicopathological features. Methylated alleles were present in 34/61 (56%) of the samples examined. Decreased E-cadherin mRNA expression was demonstrated in 29/61 carcinomas (47.5%) and was significantly associated with lymph node (LN) metastases (p = 0.03, Kruskal-Wallis) and tumour stages Astler-Coller B1 and B2 (p = 0.01, chi(2)). E-cadherin IHC expression was significantly associated with the absence of LN metastases (p = 0.01, chi(2)) and tumour stages Astler-Coller B1 and B2 (p = 0.002, Kruskal-Wallis) in 28/63 (44.4%) of the samples examined. Twenty-three out of 29 (79.3%) samples with decreased mRNA expression and 20/33 (60.6%) with detected protein expression revealed methylated (p = 0.03, Kruskal-Wallis) and unmethylated (p = 0.01, Kruskal-Wallis) alleles, respectively. In agreement with previous work demonstrating that somatic mutations and loss of heterozygosity of the E-cadherin gene are rare or absent in the majority of SCRCs studied so far, this study reports a consistent and uniform decrease or absence of E-cadherin expression, associated with aberrant methylation, in the majority of carcinomas examined, suggesting an epigenetically mediated loss of E-cadherin function in these carcinomas.