Evaluation of Current Repair Criteria for Longitudinal Barrier with Crash Damage

To protect motorists and avoid tort liability, highway agencies expend considerable resources to repair damaged longitudinal barriers, such as w-beam guardrails. With limited funding available, though, highway agencies are unable to maintain all field-installed systems in the ideal as-built condition. Instead, these agencies focus on repairing only damage that has a detrimental effect on the safety performance of the barrier. The distinction between minor damage and more severe performance-altering damage, however, is not always clear. This paper presents a critical review of current United States (US) and Canadian criteria on whether to repair damaged longitudinal barrier. Barrier repair policies were obtained via comprehensive literature review and a survey of US and Canadian transportation agencies. In an analysis of the maintenance procedures of 40 US States and 8 Canadian transportation agencies, fewer than one-third of highway agencies were found to have quantitative measures to determine when barrier repair is warranted. In addition, no engineering basis for the current US barrier repair guidelines could be found. These findings underscore the importance of the development of quantitative barrier repair guidelines based on a strong technical foundation.

Comparison of Roadside Crash Injury Metrics using Event Data Recorders

The occupant impact velocity (OIV) and acceleration severity index (ASI) are competing measures of crash severity used to assess occupant injury risk in full-scale crash tests involving roadside safety hardware, e.g. guardrail. Delta-V, or the maximum change in vehicle velocity, is the traditional metric of crash severity for real world crashes. This study compares the ability of the OIV, ASI, and delta-V to discriminate between serious and non-serious occupant injury in real world frontal collisions. Vehicle kinematics data from event data recorders (EDRs) were matched with detailed occupant injury information for 180 real world crashes. Cumulative probability of injury risk curves were generated using binary logistic regression for belted and unbelted data subsets. By comparing the available fit statistics and performing a separate ROC curve analysis, the more computationally intensive OIV and ASI were found to offer no significant predictive advantage over the simpler delta-V.

Experimental Infection of Bats with Geomyces destructans Causes White-nose Syndrome

White-nose syndrome (WNS) has caused recent catastrophic declines among multiple species of bats in eastern North America1, 2. The disease’s name derives from a visually apparent white growth of the newly discovered fungus Geomyces destructans on the skin (including the muzzle) of hibernating bats1, 3. Colonization of skin by this fungus is associated with characteristic cutaneous lesions that are the only consistent pathological finding related to WNS4. However, the role of G. destructans in WNS remains controversial because evidence to implicate the fungus as the primary cause of this disease is lacking. The debate is fuelled, in part, by the assumption that fungal infections in mammals are most commonly associated with immune system dysfunction5, 6, 7. Additionally, the recent discovery that G. destructans commonly colonizes the skin of bats of Europe, where no unusual bat mortality events have been reported8, 9, 10, has generated further speculation that the fungus is an opportunistic pathogen and that other unidentified factors are the primary cause of WNS11, 12. Here we demonstrate that exposure of healthy little brown bats (Myotis lucifugus) to pure cultures of G. destructans causes WNS. Live G. destructans was subsequently cultured from diseased bats, successfully fulfilling established criteria for the determination ofG. destructans as a primary pathogen13. We also confirmed that WNS can be transmitted from infected bats to healthy bats through direct contact. Our results provide the first direct evidence that G. destructans is the causal agent of WNS and that the recent emergence of WNS in North America may represent translocation of the fungus to a region with a naive population of animals8. Demonstration of causality is an instrumental step in elucidating the pathogenesis14 and epidemiology15 of WNS and in guiding management actions to preserve bat populations against the novel threat posed by this devastating infectious disease.

Secondary collisions revisited: real-world crash data and relationship to crash test criteria

Objectives: Previous research conducted in the late 1980s suggested that vehicle impacts following an initial barrier collision increase severe occupant injury risk. Now over 25years old, the data are no longer representative of the currently installed barriers or the present US vehicle fleet. The purpose of this study is to provide a present-day assessment of secondary collisions and to determine if current full-scale barrier crash testing criteria provide an indication of secondary collision risk for real-world barrier crashes. Methods: To characterize secondary collisions, 1,363 (596,331 weighted) real-world barrier midsection impacts selected from 13years (1997-2009) of in-depth crash data available through the National Automotive Sampling System (NASS) / Crashworthiness Data System (CDS) were analyzed. Scene diagram and available scene photographs were used to determine roadside and barrier specific variables unavailable in NASS/CDS. Binary logistic regression models were developed for second event occurrence and resulting driver injury. To investigate current secondary collision crash test criteria, 24 full-scale crash test reports were obtained for common non-proprietary US barriers, and the risk of secondary collisions was determined using recommended evaluation criteria from National Cooperative Highway Research Program (NCHRP) Report 350. Results: Secondary collisions were found to occur in approximately two thirds of crashes where a barrier is the first object struck. Barrier lateral stiffness, post-impact vehicle trajectory, vehicle type, and pre-impact tracking conditions were found to be statistically significant contributors to secondary event occurrence. The presence of a second event was found to increase the likelihood of a serious driver injury by a factor of 7 compared to cases with no second event present. The NCHRP Report 350 exit angle criterion was found to underestimate the risk of secondary collisions in real-world barrier crashes. Conclusions: Consistent with previous research, collisions following a barrier impact are not an infrequent event and substantially increase driver injury risk. The results suggest that using exit-angle based crash test criteria alone to assess secondary collision risk is not sufficient to predict second collision occurrence for real-world barrier crashes.

Eutrophication causes speciation reversal in whitefish adaptive radiations

Species diversity can be lost through two different but potentially interacting extinction processes: demographic decline and speciation reversal through introgressive hybridization. To investigate the relative contribution of these processes, we analysed historical and contemporary data of replicate whitefish radiations from 17 pre-alpine European lakes and reconstructed changes in genetic species differentiation through time using historical samples. Here we provide evidence that species diversity evolved in response to ecological opportunity, and that eutrophication, by diminishing this opportunity, has driven extinctions through speciation reversal and demographic decline. Across the radiations, the magnitude of eutrophication explains the pattern of species loss and levels of genetic and functional distinctiveness among remaining species. We argue that extinction by speciation reversal may be more widespread than currently appreciated. Preventing such extinctions will require that conservation efforts not only target existing species but identify and protect the ecological and evolutionary processes that generate and maintain species.

Experimental subarachnoid hemorrhage causes early and long-lasting microarterial constriction and microthrombosis: an in-vivo microscopy study

Early brain injury (EBI) after subarachnoid hemorrhage (SAH) is characterized by a severe, cerebral perfusion pressure (CPP)-independent reduction in cerebral blood flow suggesting alterations on the level of cerebral microvessels. Therefore, we aimed to use in-vivo imaging to investigate the cerebral microcirculation after experimental SAH. Subarachnoid hemorrhage was induced in C57/BL6 mice by endovascular perforation. Pial arterioles and venules (10 to 80 μm diameter) were examined using in-vivo fluorescence microscopy, 3, 6, and 72 hours after SAH. Venular diameter or flow was not affected by SAH, while >70% of arterioles constricted by 22% to 33% up to 3 days after hemorrhage (P<0.05 versus sham). The smaller the investigated arterioles, the more pronounced the constriction (r(2)=0.92, P<0.04). Approximately 30% of constricted arterioles were occluded by microthrombi and the frequency of arteriolar microthrombosis correlated with the degree of constriction (r(2)=0.93, P<0.03). The current study demonstrates that SAH induces microarterial constrictions and microthrombosis in vivo. These findings may explain the early CPP-independent decrease in cerebral blood flow after SAH and may therefore serve as novel targets for the treatment of early perfusion deficits after SAH.

A novel GH-1 gene mutation (GH-P59L) causes partial GH deficiency type II combined with bioinactive GH syndrome

Despite the differences in the main characteristics between the autosomal dominant form of GH deficiency (IGHD II) and the bioinactive GH syndrome, a common feature of both is their impact on linear growth leading to short stature in all affected patients.