Center for HPV Research at IUPUI

poster abstractHuman Papillomavirus (HPV) infection is highly prevalent among women and men and is associated with a number of diseases including genital warts, cervical cancers, other anogenital cancers in both men and women, and cancers of the head and neck. HPV infections are also associated with millions of dollars in annual health care costs. Two vaccines have been developed to prevent HPV infection. Both are approved for use in females ages 9 through 26, and one vaccine is approved for use in 9 to 26 year old males as well. Both vaccines are efficacious, safe, and cost-effective. Despite the great promise of HPV vaccines, vaccination rates in the U.S. are much lower than desired, with 2011 data indicating that 53% of 13-17 year old females received one or more doses and only 37% completed the 3-dose series. The ongoing medical, psychosocial, and financial costs of HPV infection indicate the need for comprehensive, cross-disciplinary research efforts coordinated with community outreach. We have established the Center for Human Papillomavirus (HPV) Research at IUPUI; which fosters cohesion and collaboration among investigators from multiple disciplines and departments at IUPUI, IU Bloomington, and University of Notre Dame pursuing HPV-related research. This group of accomplished senior faculty and promising junior scholars represents a growing synergy between basic, clinical, and social/behavioral sciences. The Center for HPV Research will provide formal infrastructure and resources for pilot research projects, and a collaborative environment for development of proposals for external funding. By capitalizing on the unique strengths of an internationally recognized faculty and IUPUI’s remarkable culture of collaborative and interdisciplinary research, we will establish a world-class center for HPV research, research training, and research translation. The overall mission of the Center for HPV Research will be to improve understanding of HPV transmission, infection, and prevention of HPV infection and its consequences

How much does weight loss affect hypertension?

Weight loss of 4 kg by diet reduces systolic and diastolic blood pressure (BP) by 4.5 and 3.2 mm Hg, respectively (SOR: A, systematic review with consistent findings). Weight loss of 1 to 1.2 kg by exercise may produce small reductions in systolic or diastolic BP (SOR: B, mixed quality of studies). Available evidence is inadequate to examine the combined effects of diet and exercise

Which detoxification regimens are effective for alcohol withdrawal syndrome?

Q: Which detoxification regimens are effective for alcohol withdrawal syndrom? Evidence based answer: Benzodiazepines remain the first-line regimen for alcohol withdrawal syndrome (AWS) and are the only class more effective than placebo for reducing seizure (strength of recommendation [SOR]: B, based on 3 medium-quality randomized controlled trials [RCTs]). Anticonvulsants are no more effective than placebo at reducing seizures (SOR: B, based on 10 moderate-quality RCTs). Gabapentin reduces withdrawal symptoms and is less sedating than benzodiazepines (SOR: B, based on 1 medium-quality RCT). Carbamazepine also reduces withdrawal symptoms (SOR: B, based on 3 RCTs). Evidence of benzodiazepine superiority to other drugs with respect to safety is lacking (SOR: A, based on a meta-analysis).Rachel Caspar, MD; Katherine Fortenberry, PhD; Jennifer Leiser, MD; Dominik Ose, DrPH, MPH (Department of Family and Preventive Medicine, University of Utah), Joan Nashelsky, MLS (Family Physicians Inquiries Network)Includes bibliographical reference

Does regular walking improve lipid levels in adults?

Q: Evidence-based answer: Minimally. Regular moderateintensity walking for a period of 4 or more weeks minimally decreased total cholesterol (TC) and low-density lipoprotein (LDL) levels by about 7 mg/dL in women with overweight or obesity (strength of recommendation [SOR]: C, systematic review and meta-analysis on disease-oriented evidence). For adults ages 40 to 65 years, regular walking for 3 or more months inconsistently affected cholesterol and triglyceride levels (SOR: C, based on 3 randomized controlled trials [RCTs] with disease-oriented evidence).Kayla Hatchell, MD; Emily Chin, DO; Brian Vukelic, MD; Katherine Fortenberry, PhD; Dominick Ose, DrPH; Eliza Taylor, MPH, BS, CHES; Rachel Goossen, MD (University of Utah), Rick Guthmann, MD, MPH (Advocate Health Care Illinois Masonic Medical Center Program)Includes bibliographical reference

Characterization of Defects in Ion Transport and Tissue Development in Cystic Fibrosis Transmembrane Conductance Regulator (CFTR)-Knockout Rats

Animal models for cystic fibrosis (CF) have contributed significantly to our understanding of disease pathogenesis. Here we describe development and characterization of the first cystic fibrosis rat, in which the cystic fibrosis transmembrane conductance regulator gene (CFTR) was knocked out using a pair of zinc finger endonucleases (ZFN). The disrupted Cftr gene carries a 16 base pair deletion in exon 3, resulting in loss of CFTR protein expression. Breeding of heterozygous (CFTR+/−) rats resulted in Mendelian distribution of wild-type, heterozygous, and homozygous (CFTR−/−) pups. Nasal potential difference and transepithelial short circuit current measurements established a robust CF bioelectric phenotype, similar in many respects to that seen in CF patients. Young CFTR−/− rats exhibited histological abnormalities in the ileum and increased intracellular mucus in the proximal nasal septa. By six weeks of age, CFTR−/− males lacked the vas deferens bilaterally. Airway surface liquid and periciliary liquid depth were reduced, and submucosal gland size was abnormal in CFTR−/− animals. Use of ZFN based gene disruption successfully generated a CF animal model that recapitulates many aspects of human disease, and may be useful for modeling other CF genotypes, including CFTR processing defects, premature truncation alleles, and channel gating abnormalities

City of Hitchcock Comprehensive Plan 2020-2040

Hitchcock is a small town located in Galveston County (Figure 1.1), nestled up on the Texas Gulf Coast. It lies about 40 miles south-east of Houston. The boundaries of the city encloses an area of land of 60.46 sq. miles, an area of water of 31.64 sq. miles at an elevation just 16 feet above sea level. Hitchcock has more undeveloped land (~90% of total area) than the county combined. Its strategic location gives it a driving force of opportunities in the Houston-Galveston Region.The guiding principles for this planning process were Hitchcock’s vision statement and its corresponding goals, which were crafted by the task force. The goals focus on factors of growth and development including public participation, development considerations, transportation, community facilities, economic development, parks, and housing and social vulnerabilityTexas Target Communitie

Hypofibrinolysis in diabetes: a therapeutic target for the reduction of cardiovascular risk

An enhanced thrombotic environment and premature atherosclerosis are key factors for the increased cardiovascular risk in diabetes. The occlusive vascular thrombus, formed secondary to interactions between platelets and coagulation proteins, is composed of a skeleton of fibrin fibres with cellular elements embedded in this network. Diabetes is characterised by quantitative and qualitative changes in coagulation proteins, which collectively increase resistance to fibrinolysis, consequently augmenting thrombosis risk. Current long-term therapies to prevent arterial occlusion in diabetes are focussed on anti-platelet agents, a strategy that fails to address the contribution of coagulation proteins to the enhanced thrombotic milieu. Moreover, antiplatelet treatment is associated with bleeding complications, particularly with newer agents and more aggressive combination therapies, questioning the safety of this approach. Therefore, to safely control thrombosis risk in diabetes, an alternative approach is required with the fibrin network representing a credible therapeutic target. In the current review, we address diabetes-specific mechanistic pathways responsible for hypofibrinolysis including the role of clot structure, defects in the fibrinolytic system and increased incorporation of anti-fibrinolytic proteins into the clot. Future anti-thrombotic therapeutic options are discussed with special emphasis on the potential advantages of modulating incorporation of the anti-fibrinolytic proteins into fibrin networks. This latter approach carries theoretical advantages, including specificity for diabetes, ability to target a particular protein with a possible favourable risk of bleeding. The development of alternative treatment strategies to better control residual thrombosis risk in diabetes will help to reduce vascular events, which remain the main cause of mortality in this condition