The accurate staging of ovarian cancer using 3T magnetic resonance imaging - a realistic option

Objectives: The aim of the study was to determine whether staging primary ovarian cancer using 3.0 Tesla (3T) magnetic resonance imaging (MRI) is comparable to surgical staging of the disease. Design: A retrospective study consisting of a search of the pathology database to identify women with ovarian pathology from May 2004 to January 2007. Setting: All women treated for suspected ovarian cancer in our cancer centre region. Sample: All women suspected of ovarian pathology who underwent 3T MRI prior to primary surgical intervention between May 2004 and January 2007. Methods: All women found to have ovarian pathology, both benign and malignant, were then cross checked with the magnetic resonance (MR) database to identify those who had undergone 3T MRI prior to surgery. The resulting group of women underwent comparison of the MR, surgical and histopathological findings for each individual including diagnosis of benign or malignant disease and International Federation of Gynecology and Obstetrics (FIGO) staging where appropriate. Main outcome measures: Comparisons were made between the staging accuracy of 3T MRI and surgical staging compared with histopathological findings and FIGO stage using weighted kappa. Sensitivity, specificity and accuracy were calculated for diagnosing malignant ovarian disease with 3T MRI. Results: A total of 191 women identified as having ovarian pathology underwent imaging with 3T MR and primary surgical intervention. In 19 of these women, the ovarian disease was an incidental finding. The group for which staging methods were compared consisted of 77 women of primary ovarian malignancy (20 of whom had borderline tumours). 3T MRI was able to detect ovarian malignancy with a sensitivity of 92% and a specificity of 76%. The overall accuracy in detecting malignancy with 3T MRI was 84%, with a positive predictive value of 80% and negative predictive value of 90%. Statistical analysis of the two methods of staging using weighted kappa, gave a K value of 0.926 (SE ±0.121) for surgical staging and 0.866 (SE ±0.119) for MR staging. A further analysis of the staging data for ovarian cancers alone, excluding borderline tumours resulted in a K value of 0.931 (SE ±0.136) for histopathological staging versus MR staging and 0.958 (±0.140) for histopathological stage versus surgical staging. Conclusion: Our study has shown that MRI can achieve staging of ovarian cancer comparable with the accuracy seen with surgical staging. No previous studies comparing different modalities have used the higher field strength 3T MRI. In addition, all other studies comparing radiological assessment of ovarian cancer have grouped the stages into I, II, III and IV rather than the more clinically appropriate a, b and c subgroups. © 2008 The Authors

High star formation rates as the origin of turbulence in early and modern disk galaxies

High spatial and spectral resolution observations of star formation and kinematics in early galaxies have shown that two-thirds are massive rotating disk galaxies with the remainder being less massive non-rotating objects. The line of sight averaged velocity dispersions are typically five times higher than in today's disk galaxies. This has suggested that gravitationally-unstable, gas-rich disks in the early Universe are fuelled by cold, dense accreting gas flowing along cosmic filaments and penetrating hot galactic gas halos. However these accreting flows have not been observed, and cosmic accretion cannot power the observed level of turbulence. Here we report on a new sample of rare high-velocity-dispersion disk galaxies we have discovered in the nearby Universe where cold accretion is unlikely to drive their high star-formation rates. We find that the velocity dispersion is most fundamentally correlated with their star-formation rates, and not their mass nor gas fraction, which leads to a new picture where star formation itself is the energetic driver of galaxy disk turbulence at all cosmic epochs.Comment: 9 pages, 2 figures, Supplimentary Info available at: http://pulsar.swin.edu.au/~agreen/nature/sigma_mean_arXiv.pdf. Accepted for publication in Natur

EBI2

My project this year was a great learning experience and helped me to better understand the complexity of lab work, as well as, the tools used in troubleshooting problems; including collaboration with lab researchers and professors. I learned about flow cytometry and how to analyze migration data. I also learned how to do transfections with HEK cells and how to separate B cells from a fresh sample of blood. I was thankful that I could spend time doing lab work because it’s the best teaching environment I know of in academia. I came across genuine problems and studied topics with the intent of using my knowledge to inform my research and legitimize my experiments

Determining the effect of Toll-like Receptor-7 on Systemic Lupus Erythematosus Development

Systemic Lupus Erythematosus (Lupus) is an autoimmune disease that afflicts over 250,000 citizens of the United States. Although much remains to be learned about Lupus, the information gathered so far has proven to be extremely valuable in increasing survival rates and improving the quality of life of Lupus patients. As we continue to put time and energy into Lupus research, the result will be that we will be able to combat the disease more effectively. The first step in combating Lupus is to gain knowledge about the pathogenesis and mechanisms of the disease. By further developing our knowledge, we will be able to develop new ways to prevent and treat, or lessen the symptoms of, Lupus

EBI2 Expression in Different Latency Stages and Primary B Cells

Epstein-­‐Barr Virus (EBV) causes infectious mononucleosis upon primary infection, commonly known as “mono.” Less commonly known is that EBV doesn’t get eradicated from your body after you recover from mono. EBV quietly occupies a small portion of B cells in 90% of human adults [1]. Besides mononucleosis, EBV infection is linked to cancers, lymphomas, and several autoimmune diseases [2.3]

The Influence of the IRF 5 Risk Haplotype on EBV Gene Expression in B Cells

IRF5 (interferon regulatory factor 5) is an integral protein in the innate immune response to viruses in humans. Once activated, IRF5 acts as a transcription factor which facilitates the production of inflammatory cytokines, interferons, and a host of other anti-viral agents in humans. To date, there are twelve documented splice variants of IRF5 in the human population. These variants range from minor deletions to drastic changes in the protein makeup of IRF5. A risk IRF5 haplotype is a person possessing alleles coding for these radically altered IRF5 mRNA (Kozyrev). A protective IRF5 hapolotype is a person possessing alleles coding for complete IRF5 mRNA

Characterization of Herpes Simplex Clinical Isolate

My project was focused on the identification and characterization of a clinical isolate of Herpes Simplex, the virus family responsible for cold sores and genital herpes. The virus was collected from a 48 year old female who was otherwise healthy. The patient had no previous history of genital herpes. The patient’s sexual partner was also HSV positive. The specimen was collected from a suspected infected genital tract and was submitted for analysis for Herpes simplex virus. Initial analysis using non-specific antibody tests verified that the virus was indeed a member of the herpes simplex family. Further analysis, shown in Figure 1, found the virus to be untypeable using the most common method for testing

Understanding the IRF5 Gene through Characterization of its Four Promoters

Interferon Regulatory Factor 5 (IRF5) is a transcription factor involved with the innate antiviral immune response and primarily expressed in immune cells1. This protein is responsible for the regulation of interferon activity and cytokine signaling, namely that of pro-inflammatory cytokines. These processes play major roles in autoimmune diseases. IRF5 is also involved with control of cell cycle and apoptosis upon activation2, therefore in certain cancers it can be inactivated3,4. The IRF5 gene has four different promoters for each first exon: 1A, 1B, 1C, and 1D. Each promoter is distinct, displaying unique correlations with certain proteins. However, the resulting IRF5 protein produced is identical in all cases. That means there are 4 distinct ways to turn on IRF5

Assessing the Splicing Variants of the Interferon Regulatory Factor 5 Risk Haplotype

Systemic lupus erythematosus (SLE) is an autoimmune disease which commences from the immune system producing antibodies which target the body’s own tissues and cells. There are various factors thought to be involved in the development of SLE. In this study I assessed how the splicing variants of the interferon regulatory factor (IRF5) gene are affected by a single nucleotide polymorphism (SNP) associated with risk for systemic lupus erythematosus (SLE). Through this assessment I hoped to more fully determine the mechanisms through which this risk allele affects the development of SLE. IRF5 is a cytoplasmic transcription factor gene responsible for interferon production. Polymorphisms of IRF5 are genetically associated with SLE (2). A trait of SLE patients is the presence of elevated levels of interferon (proteins that are invaluable in the immune systems response to viral infection) (3). Previous research has shown that the risk of SLE is strongly associated with the single-nucleotide polymorphism (SNP) rs2004640 “T” allele in IRF5. This has been confirmed multiple times across many ethnicities (4). This specific allele creates a novel splice acceptor site in the RNA. My research focused on obtaining data on how the systemic lupus IRF5 risk haplotype affects the cells of the immune system by assessing its splicing variants through PCR and DNA sequencing

IRF7 expression in B cells infected with EBV

Systemic lupus erythematosus, commonly known simply as lupus, is an incurable autoimmune disorder that can cause inflammation and tissue damage in virtually any part of the body. Many studies have shown a correlation between lupus diagnosis and positive infection with Epstein-Barr Virus (EBV). Scientists currently estimate that greater than 90% of the adult US population is infected with this human herpesvirus, probably because it is easily transferred through saliva. Although we do not entirely understand how it contributes to lupus it is apparent there is a link between the two. Other research has shown that EBV may also play a role in infectious mononucleosis, and certain types of cancer, such as Hodgkin’s lymphoma and Burkitt’s lymphoma. It is important to note that many of the people who test positive for EBV infection exhibit no signs or symptoms associated with these illnesses. Genetics and environmental factors, as well as EBV, are believed to play an important role in whether or not a particular disease develops