A Comparative Analysis of Alcohol in Fatal and Nonfatal Bicycling Injuries

Bicycling is the leading cause of recreational injury, resulting in more than half a million emergency department visits and about 900 deaths each year in the United States. Previous research on bicycling injury was conducted predominantly in children and focused on the effectiveness of safety helmets. Few studies have examined the role of alcohol in bicycling injuries. This study examined the magnitude of and factors related to alcohol involvement in fatal and nonfatal bicycling injuries, and tested the hypothesis that alcohol intoxication is associated with significantly increased likelihood of fatality given a serious bicycling injury. Medical examiner data on all fatally injured bicyclists aged 10 years or older from 1987 to 1994 in Maryland (fatal cases, n= 63) were compared with trauma registry data on all injured bicyclists who were treated at a regional trauma center during the same time period (nonfatal cases, n= 253) on variables related to blood alcohol concentrations (BACs), demographic characteristics, and injury circumstances. The fatal cases were more likely than the nonfatal cases to have positive BACs (30% vs. 16%, p < 0.01). and to be legally intoxicated (is., BACs ≥ 0.10%) (22% vs. 13%, p < 0.01). For both fatal and nonfatal cases, intoxication was more prevalent among victims who were male, aged 20 to 39 years, or who were injured at nighttime (7:00 PM to 6:59 AM). Bicyclists who died at the scene were four times as likely as those who died at hospitals to be legally intoxicated (35% vs. 9%, p < 0.02). Given a serious bicycling injury, intoxication was associated with significantly increased likelihood of fatality, with an adjusted odds ratio of 2.8 (95% confidence interval, 1.3 to 6.3). This increased likelihood of fatality was probably due in part to the fact that the rate of helmet use at the time of injury among the intoxicated was much lower than among the sober (vs. 31%, p < 0.05). Results indicate that alcohol plays an important role in fatal and serious bicycling injuries. Preventing intoxicated biking should be incorporated into helmet campaigns and other bicycle safety programs.     

Office treatment of the pathologic cervix

This paper discusses the office treatment of the following cervical lesions: erosions, nonspecific endocervicitis, lacerations complicated by eversion and/or erosion, cysts, polyps, stricture, stenosis, leucoplakia, endometriosis, varicosities, and “strawberry cervix.” Cervical anatomy and pathology are reviewed briefly. Accepted methods of office treatment of these lesions are discussed.     

Carbonic anhydrase,obstructive sleep apnea and hypertension: Effects of intervention

Whole blood carbonic anhydrase activity (CAa) is increased in patients with obstructive sleep apnea (OSA). Our study investigated the influence of positive airway pressure (PAP) or CA inhibitor acetazolamide (ACT) therapy on CAa, OSA and blood pressure. Thirty‐three OSA patients (21 hypertensive, body mass index (BMI) 37 ± 7 kg/m² and apnea–hypopnea index (AHI) of 47 ± 31 events/hr) were followed‐up after PAP treatment (compliance, 4.7 ± 1.5 hr/day; duration, median 6 [IQR 6,6] months) (Cohort A). A second OSA Cohort (B) contained nine hypertensive patients (BMI, 29 ± 4 kg/m²; AHI, 39 ± 20 events/hr) with 2‐week treatment of ACT, PAP or ACT + PAP in an open crossover study. CAa was assessed at baseline and at the end of each treatment period. In Cohort A, baseline CAa was higher in hypertensive, compared with normotensive, patients (1,033 ± 204 versus 861 ± 201 units, p = .028). PAP treatment reduced systolic/diastolic blood pressure but not CAa (?9 ± 11/?5 ± 7 mmHg and ?20 ± 289 units, p < .001, <.001 and .70). In Cohort B, blood pressure was reduced in both ACT‐treated groups (?10 ± 10/?5 ± 7 mmHg, p = .043 and .019; and ?5 ± 5/?13 ± 13 mmHg, p < .001 and .009). AHI was reduced in both groups: ACT only, ?17 ± 9 events/hr p = .001; and ACT + PAP, ?39 ± 19 events/hr, p < .001. PAP did not change CAa (p = .98) but activity tended to decrease after ACT with or without PAP (p = .081 and .056). CAa is elevated in hypertensive OSA patients. Long‐term PAP reduced blood pressure without affecting CAa. ACT reduced blood pressure and CAa. Increased CAa may constitute a physiological characteristic in OSA, contributing to comorbid hypertension.     

The histone deacetylase inhibitor trichostatin a has genotoxic effects in human lymphoblasts in vitro.

Histone deacetylase inhibitors (HDACi) are a class of putative chemotherapeutic agents for which the mechanism of toxicity has not been fully identified. To explore the possibility that HDACi are genotoxic, human TK6 lymphoblastoid cells were exposed to trichostatin A (TSA) and genetic damage was measured. TSA caused a dose-dependent increase of G1-arrested cells at 24 h that correlated with increasing levels of p21 and apoptosis. Significantly elevated frequencies of structural chromosomal aberrations in cells exposed to TSA were observed using both the kinetochore-antibody micronucleus assay and nonbanding metaphase chromosome analysis. Increased tail intensities, indicative of elevated levels of DNA damage, were observed using the alkaline comet assay. Elevated levels of phosphorylated histone gammaH2AX protein were observed as early as 3 h following TSA exposure and peaked at 12 h for 200nM TSA. Significant levels of aneuploidy at the 200nM TSA dose were observed using metaphase analysis, but interestingly, kinetochore-positive micronuclei were not detected at any dose using the kinetochore micronucleus assay, suggesting that TSA induces aneuploidy via a nondisjunction event rather than chromosome lagging. Increases in chromosomal loss and breakage were observed using simultaneous FISH metaphase analysis of chromosomes 5, 7, 8, and 21, consistent with data obtained from the micronucleus and metaphase chromosome analyses. We conclude that TSA is both a clastogen and aneugen in the TK6 cell line and propose that the observed cytostatic and apoptotic properties of TSA may partially be due to this genotoxicity.     

African American Children: A Culturally Sensitive Model for Group Practice

This article describes a time-limited group model based on culturally sensitive practice for African American children ages 8-12. This group model: (1) discusses the role of the social work professional in providing culturally sensitive treatment; (2) introduces this specific model for practice in the short-term treatment setting; and (3) provides specific intervention suggestions for implementation of children's group therapy in a culturally sensitive milieu.     

Nicotinic acetylcholine receptor-mediated stimulation of endothelial cells results in the arrest of haematopoietic progenitor cells on endothelium

The function of endothelial cells that contribute to the regulation of haematopoietic stem/progenitor cells (HSPC) migration from peripheral blood into bone marrow can be influenced by extrinsic factors including nicotine. Therefore, the effect of nicotine on HSPC extravasation was studied. Using a parallel laminar flow chamber, we demonstrated an increase in the number of HSPC adhering to the nicotine-exposed endothelium under conditions of physiological shear stress in vitro. Nicotine-induced adhesion of HSPC was inhibited by mecamylamine, a non-selective nicotinic acetylcholine receptor (nAchR) antagonist. The enhanced adhesive interactions of HSPC with nicotine-exposed endothelial monolayers coincided with the nicotine-induced activation of endothelial cells. Nicotine induced fast cytoskeletal reorganization and formation of filopodia in endothelial cells through interaction with the non-neuronal nAchR expressed by these cells. In addition, nicotine treatment stimulated rapid phosphorylation of Erk1/2 and p-38 in endothelial cells. Finally, nicotine inhibited the stroma derived factor-1-mediated transendothelial migration of HSPC. Decreased migration of HSPC correlated with diminished matrix metalloproteinase-9 activity secreted by bone marrow cells and decreased expression of CD44 on the surface of endothelial cells. Overall, our data suggest that exposure to nicotine causes endothelial cell dysfunction and leads to the pathological arrest of HSPC on endothelium, interfering with their proper migration process.