Intoxication is a Significant Risk Factor for Severe Craniomaxillofacial Injuries in Standing Electric Scooter Accidents.

PURPOSE: Standing electric scooters are a relatively new mode of transportation that are becoming increasingly popular in large metropolitan areas. The purpose of this study was to characterize injury patterns and identify risk factors for craniomaxillofacial injuries in standing electric scooter accidents. METHODS: This retrospective cohort study used a Clinical Data Warehouse search engine to identify patients who sustained standing electric scooter accidents from 2017 to 2019 using the International Classification of Diseases 10th revision codes. Predictors including patient demographics, presence of intoxication, helmet use, mechanism of injury, and other noncraniomaxillofacial injuries sustained at the time of standing electric scooter injury were identified. Patients were grouped as per the presence or absence of craniomaxillofacial injuries so that risk factors could be identified for craniomaxillofacial injuries in standing electric scooter accidents. Logistic regression analysis was performed to identify potential risk factors and association for craniomaxillofacial injuries. RESULTS: The sample was composed of 165 patients with a mean age of 30.3 years and 73.9% were men. Of them, 38 (23.0%) sustained craniomaxillofacial trauma. They were ten times more likely to have been intoxicated than those who did not have craniomaxillofacial injuries (4.7 vs 52.6%). Concomitant injuries of the extremities and the craniomaxillofacial region were rare indicating that in many cases the arms and legs were not outstretched to "break the fall." The high numbers of mandibular fractures to the condylar, subcondylar, and symphyseal regions (23.8, 33.3, and 28.6%, respectively), Le Fort fractures (18.4%), and frontal sinus fractures (15.8%) indicate that falls in the anterior-posterior direction occur with the main point of impact occurring at the chin, midface, and forehead. CONCLUSIONS: Intoxication may inhibit or depress protective reflexes that leave the face and head vulnerable during standing electric scooter accidents.

Microarray analysis of Bmi-1 downstream genes in normal human oral keratinocytes.

Bmi-1 is a polycomb group oncogene highly overexpressed in premalignant and malignant oral lesions. Bmi-1 is believed to promote oral carcinogenesis in part by allowing normal cells to evade the senescence checkpoint and extending their replicative life span. To determine the mechanisms underlying the role of Bmi-1 in oral carcinogenesis, the authors performed microarray analysis in normal human oral keratinocytes, NHOK, overexpressing Bmi-1. The authors report here several potential target genes of Bmi-1.

Extramammary Paget's disease resistant to surgery and imiquimod monotherapy but responsive to imiquimod combination topical chemotherapy with 5-fluorouracil and retinoic acid: a case report.

Extramammary Paget's disease (EMPD) is an uncommon skin neoplasm that usually affects the elderly population and occurs in the genital, anorectal, or axillary areas. The recommended treatment of EMPD involves surgical excision, including Mohs micrographic surgery; however, surgery is associated with a high rate of recurrence. There have been reports of successful treatment of recurrence with monochemotherapy involving topical imiquimod 5% cream. We report a case of EMPD recurrence after surgery that was resistant to imiquimod monotherapy but that completely resolved after imiquimod was combined with topical 5-fluorouracil (5-FU) and retinoic acid. To our knowledge, this is the first reported case of imiquimod combination therapy with 5-FU and retinoic acid for the treatment of recurrent EMPD.

HPV-16 E6 oncoprotein impairs the fidelity of DNA end-joining via p53-dependent and -independent pathways.

We previously reported that the E6 oncoprotein of high-risk human papillomavirus (HPV) caused genetic instability and oncogenesis by disrupting cellular DNA repair. Here, to investigate the effect of different domains of E6 on DNA double-strand break (DSB) repair, we infected normal human oral fibroblasts (NHOF) with retroviruses expressing wild-type (wt) or mutant (mt) HPV-16 E6 and examined the cellular DNA end-joining (EJ) activity. The cells expressing E6 showed not only a diminution of error-free DNA EJ but also an increase in erroneous DNA EJ capacity if compared with cells without wt E6. Analysis of DNA EJ activities from the cells expressing mt HPV-16 E6 indicated that binding to p53 and the presence of both intact zinc finger domains of E6 are necessary for inducing the E6-mediated aberrant DNA EJ activity. Also, deletion of the PDZ binding C-terminal region reduced this activity by 50%. These findings suggest that E6 can disrupt the fidelity of DSB repair via both p53-dependent and -independent pathways and the impaired fidelity might contribute to the development of genetic instability found in HPV-associated cancer.

Normal human oral keratinocytes demonstrate abnormal DNA end joining activity during replicative senescence.

Repair of DNA double-strand breaks (DSBs) is critical for the maintenance of cellular genetic integrity. DSBs are repaired by cellular end joining activity, which could proceed with varying degrees of accuracy. Abnormal end joining may lead to an accumulation of mutations and contribute to genetic instability and cellular aging. In the present study, we compared the efficiency and accuracy of end joining activities in exponentially replicating and senescing normal human oral keratinocytes (NHOK). We developed an in vitro end joining assay utilizing a plasmid linearized with a unique EcoR I or EcoR V restriction site. The efficiency of end joining was determined by PCR with primers that could amplify the fragment containing the end joining site. The accuracy of end joining was assessed by determining whether the original EcoR I site was restored after end joining. Both replicating and senescing cultures of NHOK yielded a similar level of end joining efficiency, which was noted by the similar intensity of PCR amplification. However, the frequency of end joining errors was significantly elevated in NHOK during replicative senescence. Senescing NHOK could thus accumulate abnormal end joining products, which might contribute to cellular aging and cancer.