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Portland, OR, United States

Waterman E.H.,OHSU | Pruett D.,Oregon Health And Science University | Caughey A.B.,Oregon Health And Science University
Obstetrical and Gynecological Survey | Year: 2013

Fetal alcohol exposure is the leading preventable cause of birth and developmental defects in the United States. Despite a growing body of knowledge about the spectrum of disorders resulting from fetal alcohol exposure, 1 in 9 pregnant women continues to drink alcohol during pregnancy, and a small percentage of pregnant women continues to binge drink. Health care providers do not consistently screen pregnant women for alcohol use, nor do health professionals necessarily know how to counsel pregnant women effectively about the risks of fetal alcohol exposure. In this article, we review the epidemiology of fetal alcohol exposure and discuss current strategies for screening and prevention of fetal alcohol exposure. We also explore the multiple barriers that exist toward reducing alcohol-exposed pregnancies from the patient, provider, and systems perspectives. Finally, we make recommendations for improved clinical and public health strategies to eliminate fetal alcohol exposure in the United States.Target Audience: Obstetricians and gynecologists, family physiciansLearning Objectives: After completing this CME activity, physicians should be better able to describe rates of fetal alcohol exposure in the United States, describe the demographic characteristics of women at highest risk for fetal alcohol exposure, counsel patients appropriately regarding the risk of poor fetal outcomes in association with fetal alcohol exposure, and understand the barriers to effective counseling about fetal alcohol exposure. Copyright © 2013 Lippincott Williams & Wilkins. Source

Angelos P.,Oregon Health And Science University | Wang T.,OHSU
Facial Plastic Surgery | Year: 2012

Secondary or revision rhinoplasty for the cleft nasal deformity represents one of the most challenging problems in rhinoplasty surgery. The secondary nasal deformity of the unilateral cleft lip involves a retrodisplaced dome of the ipsilateral nasal tip, hooding of the alar rim, a secondary alar-columellar web, and other deficiencies. This article discusses techniques to achieve the best possible outcome for patients with cleft nasal deformities. We emphasize the importance of early intervention by way of primary cleft rhinoplasty and highlight the typical challenges presented in delayed (secondary) or revision cleft rhinoplasty. We describe how the sliding flap cheilorhinoplasty effectively corrects these deformities using a laterally based chondrocutaneous flap via an open rhinoplasty approach. Columellar struts and shield grafts are some of the techniques combined with this approach to produce optimal results. Copyright © 2012 by Thieme Medical Publishers, Inc. Source

Genta R.M.,Miraca Life science Research Institute | Sonnenberg A.,OHSU
Alimentary Pharmacology and Therapeutics | Year: 2015

Results Of 895 323 patients, 10.6% had Hp-gastritis and 1.5% Helicobacter-negative gastritis. Hp-gastritis, but not Helicobacter-negative gastritis, was more common in males than females (OR 1.17, 95% CI: 1.16-1.19). While Hp-gastritis was more prevalent in high than in low-prevalence areas (OR 3.65, 95% CI: 3.57-3.74), Helicobacter-negative gastritis was only minimally affected by the underlying H. pylori prevalence (1.7% vs. 1.5%). The age-specific prevalence of Hp-gastritis peaked in the 4th to 5th decades; Helicobacter-negative gastritis exhibited a low and relatively flat pattern. The geographic distribution of H. pylori-positive and -negative gastritis showed no significant correlation. Intestinal metaplasia was found in 13.0% of patients with Hp-gastritis and in 6.1% of those with Helicobacter-negative gastritis (OR 0.43, 95% CI: 0.40-0.47). Conclusion These data suggest that Helicobacter-negative gastritis is, in the vast majority of cases, a nosologically and epidemiologically distinct entity that deserves further investigation.Background Helicobacter-negative gastritis is diagnosed when no organisms are detected in a gastric mucosa with typical features of Helicobacter gastritis (Hp-gastritis). If Helicobacter-negative gastritis consisted mostly of 'missed' Helicobacter infections, its prevalence should represent a constant percentage of these infections in a population, and their clinico-epidemiological features would overlap.Aim To compare the epidemiologic patterns of Hp-positive and Hp-negative gastritis.Methods From a pathology database, we extracted demographic, clinical and histopathological data from patients with gastric biopsies (1.2008-12.2013). We allocated patients to high (≥12%) and low (≤6%) H. pylori prevalence regions defined by ZIP code-based data. The prevalence of H. pylori-positive and -negative gastritis by sex, age and state were expressed as a per cent of the total study population stratified accordingly. © 2014 John Wiley & Sons Ltd. Source

Authors of medical diagnostic literature frequently report sensitivity and specificity as measures of the quality of an evaluative study. However, these representations are easily misinterpreted by clinicians to be indicative of the prospective value of a test as predictive of the presence (positive predictive value, PPV) or absence of disease (negative predictive value, NPV). Although these phenomena are related, the mathematical expression and, therefore, the conclusions are more complex. Using algebraic methods, we derived simplified formulas to determine PPV, NPV, and accuracy (A). These general terms were solved by constraining individual variables, resulting in the development of curves that may be used routinely to analyze medical diagnostic literature. Equations for PPV, NPV, and A were generated by using sensitivity, specificity, and incidence/prevalence as the dependent variables. These equations have been employed to generate representative graphs of PPV, NPV, and A and to clarify trends in these features with respect to commonly reported data. These simplified equations allow clinicians to determine the utility of diagnostic studies in prospect, despite having only sensitivity, specificity, and incidence or prevalence of disease. Source

News Article
Site: http://www.nature.com/nature/current_issue/

Louis Picker is not afraid to break with convention. Trained as a pathologist, he was on the front line when the AIDS epidemic emerged in the 1980s. He is now combining his interests in immunology and viruses to pursue an unusual HIV vaccine at Oregon Health and Science University (OHSU) in Portland — a project that was considered a fool's errand by many when he began. How did you get started in research? I had always wanted to be a scientist. I started an MD–PhD programme at the University of California, San Francisco, but found it much too slow, rigid and hierarchical. I left that programme, but did a year of research there. Ultimately, I decided to become a pathologist specializing in immunology. It's astonishing how much biology you can learn from looking at hundreds of biopsy slides and by performing autopsies every day. I got a feel for the immune system that you couldn't get by doing graduate research on a mouse. I was a pathology resident at Beth Israel Hospital in Boston, Massachusetts. The devastation left by AIDS stuck with me. I decided to learn more about the disease so that I could do something about it one day. I had the opportunity to move into HIV research in the mid-1990s and haven't looked back since. What led you to HIV-vaccine research? Early in my career, I worked on a flow-cytometry-based assay to measure specific T-cell responses to viral infection in humans. I chose to work with cytomegalovirus (CMV), a virus that infects around 50% of adults in the United States and triggers a T-cell response that lasts throughout a person's lifetime. These factors enabled me to test the specificity of the assay. After studying CMV-specific T cells, I hypothesized that CMV could be exploited to create a vaccine that stimulates an immediate immune response to a variety of pathogens. By incorporating bits of HIV into the vaccine, we could prime T cells to hit the intruding virus early and hard. Our data in non-human primate models show that the vaccine stops infection with the simian counterpart of HIV in slightly more than half of recipients. What does the next year hold for you? We will move into clinical trials with our potential HIV vaccine. We are also exploring the use of unconventional viral vectors to manipulate the immune system against tuberculosis, malaria, hepatitis B and cancer at a level heretofore unappreciated. Why did you choose research over more-lucrative private practice? I knew that if I wanted to make a difference — and to pursue the CMV-based vaccine while others focused on conventional antibody-led approaches — I had to do lab-based experiments. As a pathologist, I would never have had access to patients. The best way to do relevant science was to test my ideas in a non-human primate model. The job I took at the OHSU was one of two possibilities I had at the time to do that type of work. How easy was it to pursue your idea? I was fortunate to have negotiated a start-up package at the OHSU that gave me the leeway to gamble. Either I'd make it or break it. I was warmly welcomed by researchers in the HIV field, which I appreciated. But it took me a while to feel that I fit in. Self-doubt was a powerful driver for me. How risky was your decision? To be honest, it helped that I had an MD. I knew I would always be able to get a job as a physician, so the degree allowed me a little more freedom in the early years. In the first crucial years while I was establishing myself, I figured I could always return to pathology. Most people with PhDs don't have that option. You have to be a little bit of a lunatic. But your out-of-the-box thinking also has to be right. This interview has been edited for length and clarity.

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