Identification of differentially expressed genes using an annealing control primer system in stage III serous ovarian carcinoma

<p>Abstract</p> <p>Background</p> <p>Most patients with ovarian cancer are diagnosed with advanced stage disease (<it>i.e</it>., stage III-IV), which is associated with a poor prognosis. Differentially expressed genes (DEGs) in stage III serous ovarian carcinoma compared to normal tissue were screened by a new differential display method, the annealing control primer (ACP) system. The potential targets for markers that could be used for diagnosis and prognosis, for stage III serous ovarian cancer, were found by cluster and survival analysis.</p> <p>Methods</p> <p>The ACP-based reverse transcriptase polymerase chain reaction (RT PCR) technique was used to identify DEGs in patients with stage III serous ovarian carcinoma. The DEGs identified by the ACP system were confirmed by quantitative real-time PCR. Cluster analysis was performed on the basis of the expression profile produced by quantitative real-time PCR and survival analysis was carried out by the Kaplan-Meier method and Cox proportional hazards multivariate model; the results of gene expression were compared between chemo-resistant and chemo-sensitive groups.</p> <p>Results</p> <p>A total of 114 DEGs were identified by the ACP-based RT PCR technique among patients with stage III serous ovarian carcinoma. The DEGs associated with an apoptosis inhibitory process tended to be up-regulated clones while the DEGs associated with immune response tended to be down-regulated clones. Cluster analysis of the gene expression profile obtained by quantitative real-time PCR revealed two contrasting groups of DEGs. That is, a group of genes including: <it>SSBP1</it>, <it>IFI6 DDT</it>, <it>IFI27</it>, <it>C11orf92</it>, <it>NFKBIA</it>, <it>TNXB</it>, <it>NEAT1 </it>and <it>TFG </it>were up-regulated while another group of genes consisting of: <it>LAMB2</it>, <it>XRCC6</it>, <it>MEF2C</it>, <it>RBM5</it>, <it>FOXP1</it>, <it>NUDCP2</it>, <it>LGALS3</it>, <it>TMEM185A</it>, and <it>C1S </it>were down-regulated in most patients. Survival analysis revealed that the up-regulated genes such as <it>DDAH2, RNase K and TCEAL2 </it>might be associated with a poor prognosis. Furthermore, the prognosis of patients with chemo-resistance was predicted to be very poor when genes such as <it>RNase K, FOXP1</it>, <it>LAMB2 </it>and <it>MRVI1 </it>were up-regulated.</p> <p>Conclusion</p> <p>The DEGs in patients with stage III serous ovarian cancer were successfully and reliably identified by the ACP-based RT PCR technique. The DEGs identified in this study might help predict the prognosis of patients with stage III serous ovarian cancer as well as suggest targets for the development of new treatment regimens.</p

Metrolab a saisi l'opportunite de l'imagerie medicale

"Le Prix Nobel de medecine a ete decerne lundi a Paul Lauterbur et Peter Mansfield, dont les recherches ont abouti au developpement de l'imagerie par resonance magnetique nucleaire (IRM).... Ces appareils ne fonctionnent correctement que si leur champ magnetique est absolument homogene. Et c'est ici qu'intervient une petite societe genevoise, Metrolab, leader mondial dans la fabrication de magnetometres RMN, qui mesurent tres exactement cette homogeneite" (1/2 page)

α-Smooth muscle actin, a differentiation marker of smooth muscle cells, is present in microfilamentous bundles of pericytes

α-Smooth muscle (α-sm) actin, an isoform typical of smooth muscle cells (SMC) and present in high amounts in vascular SMC, was demonstrated in the cytoplasm of pericytes of various rat and human organs by means of immunocytochemistry at the electron microscopic level. In SMC and pericytes, α-sm actin was localized in microfilament bundles, strengthening the assumption that it is the functional isoform in these cell types and supporting the assumption that pericytes exert contractile functions

Patterns of injury in children

Trauma is the leading cause of death for children over 1 year of age. This study was undertaken to identify the patterns of injury among children admitted to a regional pediatric trauma center. During a 34-month period, 3,472 injured children were consecutively admitted to a regional pediatric trauma center. Data were collected on medical, etiological, and financial aspects of injury. Eight subgroups were defined by mechanism of injury: motor-vehicle crash occupants, pedestrian and cycle injuries, falls, child abuse, gunshot and stab wounds, burns, poisonings, and foreign body ingestions or aspirations. Analysis of variance, Duncan\u27s multiple range test, and contingency table analysis were used to determine differences among subgroups of children. Blunt and penetrating trauma accounted for 64.3% of all admissions. The mean age of injured children was 5.5 years; 64% of the children were boys. Sixty-seven percent of the children were admitted directly from the scene of injury. One-way analysis of variance yielded significant differences in mena age, mean hospital length of stay (LOS), mean intensive care LOS, mean trauma score, mean injury severity, and mean hospital charges by mechanism of injury (P\u3c.01). The overall mortality rate was 2.4%. Child abuse, gunshot/stab wounds, and drowning had the highest mortality rates, but injuries to motorvehicle crash occupants and pedestrians accounted for the greatest number of deaths. © 1990 W.B. Saunders Company

Consensus Expert Recommendations for the Diagnosis and Management of Autosomal Recessive Polycystic Kidney Disease: Report of an International Conference

Autosomal recessive polycystic kidney disease (ARPKD; MIM 263200) is a severe, typically early onset form of cystic disease that primarily involves the kidneys and biliary tract. Phenotypic expression and age at presentation can be quite variable(1). The incidence of ARPKD is 1 in 20,000 live births(2), and its pleotropic manifestations are potentially life-threatening. Optimal care requires proper surveillance to limit morbidity and mortality, knowledgeable approaches to diagnosis and treatment, and informed strategies to optimize quality of life. Clinical management therefore is ideally directed by multidisciplinary care teams consisting of perinatologists, neonatologists, nephrologists, hepatologists, geneticists, and behavioral specialists to coordinate patient care from the perinatal period to adulthood. In May 2013, an international team of 25 multidisciplinary specialists from the US, Canada, Germany, and the United Kingdom convened in Washington, DC, to review the literature published from 1990 to 2013 and to develop recommendations for diagnosis, surveillance, and clinical management. Identification of the gene PKHD1, and the significant advances in perinatal care, imaging, medical management, and behavioral therapies over the past decade, provide the foundational elements to define diagnostic criteria and establish clinical management guidelines as the first steps towards standardizing the clinical care for ARPKD patients. The key issues discussed included recommendations regarding perinatal interventions, diagnostic criteria, genetic testing, management of renal and biliary-associated morbidities, and behavioral assessment. The meeting was funded by the National Institutes of Health and an educational grant from the Polycystic Kidney Disease Foundation. Here we summarize the discussions and provide an updated set of diagnostic, surveillance, and management recommendations for optimizing the pediatric care of patients with ARPKD. Specialist care of ARPKD-related complications including dialysis, transplantation, and management of severe portal hypertension will be addressed in a subsequent report. Given the paucity of information regarding targeted therapies in ARPKD, this topic was not addressed in this conference.