Aetiology of in-hospital cardiac arrest on general wards

Aim: Aetiology of in-hospital cardiac arrests (IHCAs) on general wards has not been studied. We aimed to determine the underlying causes for IHCAs by the means of autopsy records and clinical judgement of the treating consultants. Furthermore, we investigated whether aetiology and preceding vital dysfunctions are associated with long-term survival. Design and setting: Prospective observational study between 2009-2011 including 279 adult IHCA patients attended by medical emergency team in a Finnish university hospital's general wards. Results: The median age of the patients was 72 (64, 80) years, 185 (66%) were male, 178 (64%) of events were monitored/witnessed, first rhythm was shockable in 42 (15%) cases and 53 (19%) patients survived six months. Aetiology was determined as cardiac in 141 events, 73 of which were due to acute myocardial infarction. There were 138 non-cardiac IHCAs; most common causes were pneumonia (39) and exsanguination (16). No statistical difference was observed in the incidence of objective vital dysfunctions preceding the event between the cardiac and non-cardiac groups (40% vs. 44%, p = 0.448). Subjective antecedents were more common in the cardiac cohort (47% vs. 32%, p = 0.022), chest pain being an example (11% vs. 0.7%, p <0.001). Reviewing all 279 IHCAs, only shockable primary rhythm, monitored/witnessed event and low comorbidity score were independently associated with 180-day survival. Conclusions: Cardiac aetiology underlies half of the IHCAs on general wards. Both objective and subjective antecedents are common. However, neither the cardiac aetiology nor the absence of preceding deterioration of vital signs were factors independently associated with a favourable outcome. (C) 2016 Elsevier Ireland Ltd. All rights reserved.Peer reviewe

Excited states in the twisted XXZ spin chain

We compute the finite size spectrum for the spin 1/2 XXZ chain with twisted boundary conditions, for anisotropy in the regime $0< \gamma <\pi/2$, and arbitrary twist $\theta$. The string hypothesis is employed for treating complex excitations. The Bethe Ansatz equtions are solved within a coupled non-linear integral equation approach, with one equation for each type of string. The root-of-unity quantum group invariant periodic chain reduces to the XXZ_1/2 chain with a set of twist boundary conditions ($\pi/\gamma\in Z$, $\theta$ an integer multiple of $\gamma$). For this model, the restricted Hilbert space corresponds to an unitary conformal field theory, and we recover all primary states in the Kac table in terms of states with specific twist and strings.Comment: 16 pages, Latex; added discussion on quantum group invariance and arbitrary magnon numbe

Comparison of Variable-Number Tandem-Repeat Markers typing and IS1245 Restriction Fragment Length Polymorphism fingerprinting of Mycobacterium avium subsp hominissuis from human and porcine origins

Peer reviewe

Variation in RNA expression and genomic DNA content acquired during cell culture

Specific chromosomal abnormalities are increasingly recognised to be associated with particular tumour subtypes. These cytogenetic abnormalities define the sites of specific genes, the alteration of which is implicated in the neoplastic process. We used comparative genomic hybridisation (CGH) to examine DNA from different breast and ovarian cancer cell lines for variations in DNA sequence copy number compared with the same normal control. We also compared different sources of the MCF7 breast line by both CGH and cDNA expression arrays. Some of the differences between the subcultures were extensive and involved large regions of the chromosome. Differences between the four subcultures were observed for gains of 2q, 5p, 5q, 6q, 7p, 7q, 9q, 10p, 11q, 13q, 14c, 16q, 18p and 20p, and losses of 4q, 5p, 5q, 6q, 7q, 8p, 11p, 11q, 12q, 13q, 15q, 19p, 19q, 20p, 21q, 22q and Xp. However, few variations were found between two subcultures examined, 5 months apart, from the same initial source. The RNA arrays also demonstrated considerable variation between the three different subcultures, with only 43% of genes expressed at the same levels in all three. Moreover, the patterns of the expressed genes did not always reflect our observed CGH aberrations. These results demonstrate extensive genomic instability and variation in RNA expression during subculture and provide supportive data for evidence that cell lines do evolve in culture, thereby weakening the direct relevance of such cultures as models of human cancer. This work also reinforces the concern that comparisons of published analyses of cultures of the same name may be dangerous

Human BCAS3 Expression in Embryonic Stem Cells and Vascular Precursors Suggests a Role in Human Embryogenesis and Tumor Angiogenesis

Cancer is often associated with multiple and progressive genetic alterations in genes that are important for normal development. BCAS3 (Breast Cancer Amplified Sequence 3) is a gene of unknown function on human chromosome 17q23, a region associated with breakpoints of several neoplasms. The normal expression pattern of BCAS3 has not been studied, though it is implicated in breast cancer progression. Rudhira, a murine WD40 domain protein that is 98% identical to BCAS3 is expressed in embryonic stem (ES) cells, erythropoiesis and angiogenesis. This suggests that BCAS3 expression also may not be restricted to mammary tissue and may have important roles in other normal as well as malignant tissues. We show that BCAS3 is also expressed in human ES cells and during their differentiation into blood vascular precursors. We find that BCAS3 is aberrantly expressed in malignant human brain lesions. In glioblastoma, hemangiopericytoma and brain abscess we note high levels of BCAS3 expression in tumor cells and some blood vessels. BCAS3 may be associated with multiple cancerous and rapidly proliferating cells and hence the expression, function and regulation of this gene merits further investigation. We suggest that BCAS3 is mis-expressed in brain tumors and could serve as a human ES cell and tumor marker

Genomic profiling of CHEK2*1100delC-mutated breast carcinomas

Background: CHEK2*1100delC is a moderate-risk breast cancer susceptibility allele with a high prevalence in the Netherlands. We performed copy number and gene expression profiling to investigate whether CHEK2*1100delC breast cancers harbor characteristic genomic aberrations, as seen for BRCA1 mutated breast cancers. Methods: We performed high-resolution SNP array and gene expression profiling of 120 familial breast carcinomas selected from a larger cohort of 155 familial breast tumors, including BRCA1, BRCA2, and CHEK2 mutant tumors. Gene expression analyses based on a mRNA immune signature was used to identify samples with relative low amounts of tumor infiltrating lymphocytes (TILs), which were previously found to disturb tumor copy number and LOH (loss of heterozygosity) profiling. We specifically compared the genomic and gene expression profiles of CHEK2*1100delC breast cancers (n = 14) with BRCAX (familial non-BRCA1/BRCA2/CHEK2*1100delC mutated) breast cancers (n = 34) of the luminal intrinsic subtypes for which both SNP-array and gene expression data is available. Results: High amounts of TILs were found in a relatively small number of luminal breast cancers as compared to breast cancers of the basal-like subtype. As expected, the