A Simple Intervention to Increase Human Papillomavirus Vaccination in a Family Medicine Practice.

Human papillomavirus (HPV) is a sexually transmitted virus that is the leading cause of cervical cancer world- wide. It is vaccine-preventable. According to the Centers for Disease Control, only 60 percent of girls have started the HPV vaccination series countrywide and only 50 percent of boys have started. South Dakota is below this national average. In an effort to assess - and improve - HPV vaccination rates in our practice a quality improvement effort was undertaken. Two interventions were implemented a month apart: the first was a mailing to the parent(s) of all patients 11-12 years of age during the time period of the intervention; the second was an in-office reminder system for both patients and physicians at the time of an office encounter. After each of the interventions, the immunization rate for one injection was significantly greater than baseline; while slightly higher than baseline, that for those receiving both injections was not statistically different for either intervention.

Acute Hemolytic Transfusion Reaction Due to Anti-Kpa Antibody.

BACKGROUND: Kpa (KEL3, Penney) is a red blood cell antigen within the Kell system, first described in 1957, that occurs in less than 2 percent of the population. Although anti-Kpa antibodies were identified in 2-5 percent of those with alloantibodies among patients requiring chronic transfusion, only five previously published case reports of anti-Kpa reactions were identified. CASE REPORT: Reported here is a case of an elderly female who experienced an acute hemolytic transfusion reaction due to this antigen. Following initiation of blood transfusion, she experienced a sudden onset of rigorous chills, accompanied by elevated temperature, tachycardia, and hypertension. Laboratory studies showed uremia, elevated creatinine, positive direct Coomb's, and low haptoglobin. Serology revealed anti-Kpa antibody. CONCLUSION: This report is only the sixth, to our knowledge, of a significant reaction attributable to anti-Kpa and only the second of an acute hemolytic reaction associated with it. It serves as a reminder of the potential of low incidence antigens causing severe reactions; this potential should be considered when evaluating acute hemolytic reaction.

Formation of the collateral circulation is regulated by vascular endothelial growth factor-A and a disintegrin and metalloprotease family members 10 and 17.

RATIONALE: The density of native (preexisting) collaterals varies widely and is a significant determinant of variation in severity of stroke, myocardial infarction, and peripheral artery disease. However, little is known about mechanisms responsible for formation of the collateral circulation in healthy tissues. OBJECTIVE: We previously found that variation in vascular endothelial growth factor (VEGF) expression causes differences in collateral density of newborn and adult mice. Herein, we sought to determine mechanisms of collaterogenesis in the embryo and the role of VEGF in this process. METHODS AND RESULTS: Pial collaterals begin forming between embryonic day 13.5 and 14.5 as sprout-like extensions from arterioles of existing cerebral artery trees. Global VEGF-A overexpressing mice (Vegf(hi/+)) formed more, and Vegf(lo/+) formed fewer, collaterals during embryogenesis, in association with differences in vascular patterning. Conditional global reduction of Vegf or Flk1 only during collaterogenesis significantly reduced collateral formation, but now without affecting vascular patterning, and the effects remained in adulthood. Endothelial-specific Vegf reduction had no effect on collaterogenesis. Endothelial-specific reduction of a disintegrin-and-metalloprotease-domain-10 (Adam10) and inhibition of γ-secretase increased collateral formation, consistent with their roles in VEGF-induced Notch1 activation and suppression of prosprouting signals. Endothelial-specific knockdown of Adam17 reduced collateral formation, consistent with its roles in endothelial cell migration and embryonic vascular stabilization, but not in activation of ligand-bound Notch1. These effects also remained in adulthood. CONCLUSIONS: Formation of pial collaterals occurs during a narrow developmental window via a sprouting angiogenesis-like mechanism, requires paracrine VEGF stimulation of fetal liver kinase 1-Notch signaling, and adult collateral number is dependent on embryonic collaterogenesis.

Chronic, low-dose prenatal exposure to methylmercury impairs motor and mnemonic function in adult C57/B6 mice.

Methylmercury (MeHg) has cytotoxic effects on animals and humans, and a major target organ for MeHg is the central nervous system (CNS). It is well known that the developing CNS is extremely vulnerable to MeHg-induced changes in comparison to the mature brain. Most studies have concentrated on the direct effects of high levels of prenatal MeHg exposure. Surprisingly, behavioral outcomes found in adult offspring exposed developmentally to the neurotoxic effects of chronic, low-dose mercury more akin to ingestion in humans are not well characterized. The objective of this study was to determine whether such exposure produces deleterious effects on behavior in adult mice, including motor/coordination abilities, overall activity and mnemonic function. Developing mouse fetuses were exposed in utero during gestational days 8-18 by giving pregnant C57Bl/6J female mice food containing MeHg at a daily dose of 0.01 mg/kg body weight. Adult mice prenatally exposed to MeHg exhibited significant deficits in motor abilities, coordination, and overall activity, as measured by rotarod, footprint analysis and open field. In addition, MeHg-exposed mice were impaired with respect to reference memory but not in a visible, cued version of the Morris water maze task. These results indicate that prenatal exposure to the lowest dose of MeHg examined to date can have long-lasting motor and cognitive consequences on adult offspring. These findings have far reaching implications related to putative safe levels of MeHg ingestion, particularly during pregnancy, and increasing rates of cognitive and psychological disorders (e.g. attention hyperactivity deficit disorder, autism) in our society.