Objectives: To investigate whether daily bathing with a soap-like solution of 4% chlorhexidine (CHG) followed by water rinsing (CHGwr) would decrease the incidence of hospital-acquired infections (HAI) in intensive care settings. Methods: Randomized, controlled trial; infectious diseases specialists were blinded to the intervention status. All patients admitted to the Intensive Care Unit (ICU) and to the Post-operative Cardiosurgical Intensive Care Unit (PC-ICU) of the University Hospital of Perugia were enrolled and randomized to the intervention arm (daily bathing with 4% CHGwr) or to the control arm (daily bathing with standard soap). The incidence rate of acquisition of HAI was compared between the two arms as primary outcome. We also evaluated the incidence of bloodstream infections (BSI), central-line-associated BSI (CLABSI), ventilator-associated pneumonia (VAP) and catheter-associated urinary tract infections (CAUTI), and 4% CHGwr safety. Results: In all, 449 individuals were enrolled, 226 in treatment arm and 223 in control arm. Thirty-four individuals of the 226 (15%) and 57 (25.6%) suffered from at least an HAI in the intervention and control arms, respectively (p 0.008); 23.2 and 40.9 infections/1000 patient-days were detected in the intervention arm and control arm, respectively (p 0.037). The incidence of all bloodstream infections (BSI plus CABSI) was significantly reduced in the intervention arm (9.2 versus 22.6 infections/1000 patient-days, p 0.027); no differences were observed in the mortality between the two arms. Conclusions: Daily bathing with 4% CHGwr significantly reduced HAI incidence in intensive care settings.

The median OS following standard temozolomide treatment concurrent with and adjuvant to radiotherapy given to (72.8% of) patients aged ≤70 years is consistent with findings reported from randomized phase III trials. The volume and expertise of the treatment center should be further investigated as a prognostic factor.

No abstract

Abstract. We previously described a cohort of grade II oligodendroglioma (OII) patients, in whom the loss of heterozygosity (LOH) 19q was present in the subgroup at a higher risk of relapse. In this study, we evaluated the CpG methylation of the putative tumor suppressor epithelial membrane protein 3 (EMP3, 19q13.3) gene promoter in the same OII cohort, to investigate whether a correlation could be found between EMP3 cytogenetic and epigenetic loss and higher risk of relapse. Twenty-three tumor samples from OII patients were collected over a period of 10 years. Seventeen glioblastoma (GBM) samples (2 of which were relapses) were collected from 15 patients. The EMP3, O 6 -methylguanine methyltransferase (MGMT) and cyclooxygenase 2 (COX2) promoter methylation, evaluated by methylation-specific PCR, and the isocitrate dehydrogenase 1 (IDH1) mutation, identified by sequencing, were compared between the OII and GBM histotypes. The EMP3 promoter methylation was correlated with the analysis of LOH 19q, performed by microsatellite amplification, in OII patients. Disease progression-free interval was evaluated in the OII patients with the EMP3 methylation with either LOH 19q or conserved chromosome 19 arms. The EMP3 and MGMT promoter methylation was more frequent in OII than in GBM patients, and the IDH1 mutation was absent in GBM. The COX2 promoter was unmethylated in both histotypes. Both LOH +/-19q OII patients showed EMP3 hypermethylation. Concomitant LOH 19q and EMP3 gene promoter methylation was observed in the OII patients at a higher risk of relapse. Our results suggest that a total (cytogenetic and epigenetic) functional loss of both EMP3 alleles accounts for the reduced disease progression-free interval in OII patients. Although the small sample size limits the strength of this study, our results support testing this hypothesis in larger cohorts of patients, considering the methylation of the EMP3 gene promoter together with LOH 19q as an indication for treatment with adjuvant therapy ab initio in order to improve the overall survival of OII patients.

equilibrium between the h/A3 genes is "back lit" by a strong selective force originating approximately 400 generations ago.The "reconstructed' location of the h-allele remarkably corresponds to the calculation that in 400 generations a biological fitness 1% greater than average would produce a change in frequency of the gene for adult lactase persistence from 0.05 (in lactase intolerant populations) to 0.60 in tolerant populations [ 121. Prior to the domestication of animals and the invention of dairying, lactose was not available to adults in significant quantities. Therefore, adult man, like other adult mammals, was naturally lactase deficient. Dairying cultures tended to select for adult lactose tolerance. The milk is a poor source of iron and may actually inhibit absorption of the metal. A separate, and easily disproved, argument for selection would be a proposition that the frequency of the h-allele should be high in populations depending on milk and cereals in their diet. The higher the proportion of lactose tolerance in the population, the higher the frequency of the h-allele in it. So far unsuspected, the evolutionary rivalry between the h-allele and the gene for lactase persistence is likely. It would suggest that these genes coevolved and probably originated some 400 generations ago. In conclusion, the h-allele evolved as an evolutionary rehabilitation of iron carency in farming and pastoralist populations. Its location is approximately 401 kb centromeric from the HLA A genes. REFERENCES 1 . Edwards CQ, Griffen LM, Dadone MM, Skolnick MH, Kushner JP: Mapping the locus for hereditary hemochromatosis: Localization between HLA-B and HLA-A. Am J Hum Genet 38:805-811, 1986. 2. Cox TM: Prevalence of the hemochromatosis gene. N Engl J Med 302695496, 1980. 3. JankoviC GM, coloviC MD, PetroviC MD, SuvajdiiC N, BogdanoviC G , Rado-vanEeviC R, TomaSeviC R, Trpinac D P Selective advantage for females with h-allele? Eur J Haematol43:265-266, 1989. 4. JankoviC GM, PetroviC MD, colovii. MD, MiloSeviC R, JanoSevii. S, Trpinac D P Increased transplacental and breast milk iron delivery in hereditary hemochromatosis. Am J Hematol 38:153-155, 1991.