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1.
J Trauma ; 53(6): 1078-86; discussion 1086-7, 2002 Dec.
Article in English | MEDLINE | ID: mdl-12478032

ABSTRACT

BACKGROUND: On July 1, 1997, Arkansas became the first state in 14 years to repeal their adult helmet law. We examined the clinical and financial impact of this repeal. METHODS: A 6-year retrospective review was conducted of the University of Arkansas for Medical Sciences trauma registry including the 3 years before and the 3 years after the repeal of the helmet law. A head and neck Abbreviated Injury Scale (AIS) score >or= 3 was considered severe. All patients admitted to the hospital or who died in the emergency department were included in the study. The database of the Arkansas Highway and Transportation Department was also used to determine the number of crashes and fatalities occurring statewide (1995-1999). RESULTS: Although total and fatal crashes in Arkansas were not significantly different (1995-1996 vs. 1998-1999), nonhelmeted deaths at the scene of a crash significantly increased from 19 of 48 (39.6%) (1995-1996) to 40 of 53 (75.5%) (1998-1999) (p < 0.0001). Before repeal, 25% of nonfatal crash admissions were nonhelmeted (18 of 73). This significantly increased to 54% (52 of 96, p< 0.001) after repeal. Overall, patients who were nonhelmeted had significantly higher AIS scores for head and neck, significantly more severe head injuries (AIS score >or= 3), 47% (33 of 70) versus 20% (20 of 99), and significantly longer length of intensive care unit stay. Financially, patients without helmets had significantly higher unreimbursed charges compared with their helmeted counterparts, resulting in a total of 982,560 dollars of additional potentially lost revenue over the length of the study. CONCLUSION: Repeal of the mandatory helmet law was associated with an increase in the nonhelmeted crash scene fatality rate. After the repeal, there was a disproportionately higher admission rate for nonhelmeted motorcycle crash survivors. These patients had an increased use of hospital resources and poorer reimbursement of charges compared with their helmeted counterparts. This resulted in significantly higher unreimbursed charges. States considering repeal of their mandatory adult helmet laws should consider the potential negative financial impact on their health care system and the increased morbidity associated with nonhelmeted motorcycle riders involved in a crash.


Subject(s)
Accidents, Traffic/prevention & control , Craniocerebral Trauma/mortality , Craniocerebral Trauma/prevention & control , Head Protective Devices/standards , Motorcycles/legislation & jurisprudence , Adolescent , Adult , Age Distribution , Analysis of Variance , Arkansas/epidemiology , Craniocerebral Trauma/diagnosis , Female , Head Protective Devices/statistics & numerical data , Humans , Incidence , Injury Severity Score , Legislation as Topic , Male , Middle Aged , Probability , Registries , Retrospective Studies , Risk Factors , Sex Distribution , Statistics, Nonparametric , Survival Analysis
2.
Mol Cancer Res ; 1(1): 25-31, 2002 Nov.
Article in English | MEDLINE | ID: mdl-12496366

ABSTRACT

Human papillomaviruses (HPVs) are found in trophoblasts of spontaneous abortions and replicate in these cells in culture. We used recombinant adeno-associated viruses (rAAV) to introduce the HPV-16 E6 and E7 oncogenes into 3A trophoblasts. AAV/E7/Neo-infected 3A trophoblasts died rapidly, but AAV/E6/Neo- and AAV/E6-E7/Neo-infected cells grew more rapidly than AAV/Neo-infected 3A cells and parental 3A. After G418 selection, the resulting E6-E7/3A and E6/3A cell lines were found to be highly defective for binding RL95 and HEC endometrial cells compared to Neo/3A and parental 3A. Serum requirements and soft agar colony formation analysis showed that E6-E7/3A had the most malignant phenotype, followed by E6/3A, with parental 3A cells having the lowest. E6/3A and E6-E7/3A were also immortal. Thus, HPV-16 oncogene expression may lead to outright trophoblast death, defective endometrial cell recognition, or a malignant phenotype. Any of these changes might lead to disruption/dysfunction of the trophoblast layer/gestational loss.


Subject(s)
DNA-Binding Proteins , Endometrium/cytology , Oncogene Proteins, Viral/pharmacology , Repressor Proteins , Trophoblasts/virology , Apoptosis , Cell Adhesion , Cell Differentiation , Cell Division , Cell Line , Cell Survival , Endometrium/metabolism , Female , Humans , Oncogene Proteins, Viral/genetics , Phenotype , Transduction, Genetic , Trophoblasts/metabolism
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