Chip technology for fast serological determination of Salmonella serovars

The nucleotide sequence encoding the Salmonella plasmid virulence factor D (SpvD) was determined in 17 Salmonella strains that were different in O and H antigen patterns, animal host and geographical origin, and year of isolation. Nucleotide sequence comparison revealed the existence of at least nine spvD alleles resulting in 8 SpvD protein variants although the nucleotide sequences were highly similar (identity 98.8- 100 %)

The use of a commercial test system (SALMOTYPE ELISA) for tracing antibodies against Salmonella in the serum of pigs

The German Federal Ministry of Health and the Federal Ministry of Food, Agriculture and Forestry have resented guidelines for a program to reduce the introduction of Salmonella into meat production via slaughter pigs . These guidelines intend to determine the prevalence of Salmonella in farms raising slaughter pigs. For this, random samples are to be examined with a meat juice ELISA for the detection of Salmonella antibodies. In this study the use of two such ELISA systems was tested. In order to compare the commercially available SALMOTYPE ®meat juice ELISA with a meat juice ELISA developed by the German Federal Institute for Health Protection of Consumers and Veterinary Medicine (BgVV) test sera were examined in parallel via both systems. In these examinations the SALMOTYPE ® meat juice ELISA showed a higher sensitivity. Further experiments were carried out to analyze the practical applicability of the SALMOTYPE ®meat juice ELISA. Fo r this, 119 serum samples of slaughter pigs were examined with the SALMOTYPE ®meat juice ELISA. The advantages of this test system, which were already noticed in the comparison of the two test systems, like quick performance, ease of application and reliability of results, were confmned in these examinations

The combination of two Salmonella-antigen test systems for reliable diagnostic of Salmonellosis in stockbreeding pigs

Salmonella enterica is a facultative intracellular pathogen that is capable of causing disease in a range of hosts. The genus Salmonella covers more than 2,400 different serotypes, whereof some specific clones have become very dominant in one or more host species and have been able to spread worldwide. Nevertheless, all serotypes must be considered potential human pathogens

Hospitalizations and Costs Incurred at the Facility Level After Scale-Up of Malaria Control: Pre-Post Comparisons From Two Hospitals in Zambia

There is little evidence on the impact of malaria control on the health system, particularly at the facility level. Using retrospective, longitudinal facility-level and patient record data from two hospitals in Zambia, we report a pre-post comparison of hospital admissions and outpatient visits for malaria and estimated costs incurred for malaria admissions before and after malaria control scale-up. The results show a substantial reduction in inpatient admissions and outpatient visits for malaria at both hospitals after the scale-up, and malaria cases accounted for a smaller proportion of total hospital visits over time. Hospital spending on malaria admissions also decreased. In one hospital, malaria accounted for 11% of total hospital spending before large-scale malaria control compared with \u3c 1% after malaria control. The findings demonstrate that facility-level resources are freed up as malaria is controlled, potentially making these resources available for other diseases and conditions

The effect of modern intensive monitoring in obstetrics on infant mortality and the incidence of hypoxia and acidosis

Peer Reviewe

An 11p15 Imprinting Centre Region 2 Deletion in a Family with Beckwith Wiedemann Syndrome Provides Insights into Imprinting Control at CDKN1C

We report a three generation family with Beckwith Wiedemann syndrome (BWS) in whom we have identified a 330 kb deletion within the KCNQ1 locus, encompassing the 11p15.5 Imprinting Centre II (IC2). The deletion arose on the paternal chromosome in the first generation and was only associated with BWS when transmitted maternally to subsequent generations. The deletion on the maternal chromosome was associated with a lower median level of CDKN1C expression in the peripheral blood of affected individuals when compared to a cohort of unaffected controls (p<0.05), however was not significantly different to the expression levels in BWS cases with loss of methylation (LOM) within IC2 (p<0.78). Moreover the individual with a deletion on the paternal chromosome did not show evidence of elevated CDKN1C expression or features of Russell Silver syndrome. These observations support a model invoking the deletion of enhancer elements required for CDKN1C expression lying within or close to the imprinting centre and importantly extend and validate a single observation from an earlier study. Analysis of 94 cases with IC2 loss of methylation revealed that KCNQ1 deletion is a rare cause of loss of maternal methylation, occurring in only 3% of cases, or in 1.5% of BWS overall

Hypoxia inducible factor 1α gene (HIF-1α) splice variants: potential prognostic biomarkers in breast cancer

<p>Abstract</p> <p>Background</p> <p>Hypoxia-inducible factor 1 (HIF-1) is a master transcriptional regulator of genes regulating oxygen homeostasis. The HIF-1 protein is composed of two HIF-1α and HIF-1β/aryl hydrocarbon receptor nuclear translocator (ARNT) subunits. The prognostic relevance of HIF-1α protein overexpression has been shown in breast cancer. The impact of HIF-1α alternative splice variant expression on breast cancer prognosis in terms of metastasis risk is not well known.</p> <p>Methods</p> <p>Using real-time quantitative reverse transcription PCR assays, we measured mRNA concentrations of total <it>HIF-1α </it>and 4 variants in breast tissue specimens in a series of 29 normal tissues or benign lesions (normal/benign) and 53 primary carcinomas. In breast cancers <it>HIF-1α </it>splice variant levels were compared to clinicopathological parameters including tumour microvessel density and metastasis-free survival.</p> <p>Results</p> <p><it>HIF-1α </it>isoforms containing a three base pairs TAG insertion between exon 1 and exon 2 (designated <it>HIF-1α</it>^<it>TAG</it>) and <it>HIF-1α</it>^{<it>736 </it>}mRNAs were found expressed at higher levels in oestrogen receptor (OR)-negative carcinomas compared to normal/benign tissues (<it>P </it>= 0.009 and <it>P </it>= 0.004 respectively). In breast carcinoma specimens, lymph node status was significantly associated with <it>HIF-1α</it>^{<it>TAG </it>}mRNA levels (<it>P </it>= 0.037). Significant statistical association was found between tumour grade and <it>HIF-1α</it>^{<it>TAG </it>}(<it>P </it>= 0.048), and total <it>HIF-1α </it>(<it>P </it>= 0.048) mRNA levels. <it>HIF-1α</it>^{<it>TAG </it>}mRNA levels were also inversely correlated with both oestrogen and progesterone receptor status (<it>P </it>= 0.005 and <it>P </it>= 0.033 respectively). Univariate analysis showed that high <it>HIF-1α</it>^{<it>TAG </it>}mRNA levels correlated with shortened metastasis free survival (<it>P </it>= 0.01).</p> <p>Conclusions</p> <p>Our results show for the first time that mRNA expression of a <it>HIF-1α</it>^{<it>TAG </it>}splice variant reflects a stage of breast cancer progression and is associated with a worse prognosis.</p> <p>See commentary: <url>http://www.biomedcentral.com/1741-7015/8/45</url></p

EVI1 activation in blast crisis CML due to juxtaposition to the rare 17q22 partner region as part of a 4-way variant translocation t(9;22)

<p>Abstract</p> <p>Background</p> <p>Variant translocations t(9;22) occur in 5 to 10% of newly diagnosed CMLs and additional genetic changes are present in 60–80% of patients in blast crisis (BC). Here, we report on a CML patient in blast crisis presenting with a four-way variant t(9;22) rearrangement involving the <it>EVI1 </it>locus.</p> <p>Methods</p> <p>Dual-colour Fluorescence In Situ Hybridisation was performed to unravel the different cytogenetic aberrations. Expression levels of <it>EVI1 </it>and <it>BCR/ABL1 </it>were investigated using real-time quantitative RT-PCR.</p> <p>Results</p> <p>In this paper we identified a patient with a complex 4-way t(3;9;17;22) which, in addition to <it>BCR/ABL1 </it>gene fusion, also resulted in <it>EVI1 </it>rearrangement and overexpression.</p> <p>Conclusion</p> <p>This report illustrates how a variant t(9;22) translocation can specifically target a second oncogene most likely contributing to the more aggressive phenotype of the disease. Molecular analysis of such variants is thus warranted to understand the phenotypic consequences and to open the way for combined molecular therapies in order to tackle the secondary oncogenic effect which is unresponsive to imatinib treatment.</p

Relationship of an hRAD54 gene polymorphism (2290 C/T) in an Ecuadorian population with chronic myelogenous leukemia

The hRAD54 gene is a key member of the RAD52 epistasis group involved in repair of double-strand breaks (DSB) by homologous recombination (HR). Thus, alterations of the normal function of these genes could generate genetic instability, shifting the normal process of the cell cycle, leading the cells to develop into cancer. In this work we analyzed exon 18 of the hRAD54 gene, which has been previously reported by our group to carry a silent polymorphism, 2290 C/T (Ala730Ala), associated to meningiomas. We performed a PCR-SSCP method to detect the polymorphism in 239 samples including leukemia and normal control population. The results revealed that the 2290 C/T polymorphism has frequencies of 0.1 for the leukemia and 0.1 for the control group. These frequencies show no statistical differences. Additionally, we dissected the leukemia group in chronic myelogenous leukemia (CML) and acute lymphoblastic leukemia (ALL) to evaluate the polymorphism. The frequencies found in these subgroups were 0.14 for CML and 0.05 for ALL. We found statistically significant differences between CML patients and the control group (p < 0.05) but we did not find significant differences between ALL and the control group (p > 0.05). These results suggest a possible link between the 2290 C/T polymorphism of the hRAD54 gene and CML

CCN3: a key growth regulator in Chronic Myeloid Leukaemia

Chronic Myeloid Leukaemia (CML) is characterized by expression of the constitutively active Bcr-Abl tyrosine kinase. We have shown previously that the negative growth regulator, CCN3, is down-regulated as a result of Bcr-Abl kinase activity and that CCN3 has a reciprocal relationship of expression with BCR-ABL. We now show that CCN3 confers growth regulation in CML cells by causing growth inhibition and regaining sensitivity to the induction of apoptosis. The mode of CCN3 induced growth regulation was investigated in K562 CML cells using gene transfection and treatment with recombinant CCN3. Both strategies showed CCN3 regulated CML cell growth by reducing colony formation capacity, increasing apoptosis and reducing ERK phosphorylation. K562 cells stably transfected to express CCN3 showed enhanced apoptosis in response to treatment with the tyrosine kinase inhibitor, imatinib. Whilst CCN3 expression was low or undetectable in CML stem cells, primary CD34+ CML progenitors were responsive to treatment with recombinant CCN3. This study shows that CCN3 is an important growth regulator in haematopoiesis, abrogation of CCN3 expression enhances BCR-ABL dependent leukaemogenesis. CCN3 restores growth regulation, regains sensitivity to the induction of apoptosis and enhances imatinib cell kill in CML cells. CCN3 may provide an additional therapeutic strategy in the management of CML