Effects of vehicle power on passenger vehicle speeds

<p><b>Objectives</b>: During the past 2 decades, there have been large increases in mean horsepower and the mean horsepower-to–vehicle weight ratio for all types of new passenger vehicles in the United States. This study examined the relationship between travel speeds and vehicle power, defined as horsepower per 100 pounds of vehicle weight.</p> <p><b>Methods</b>: Speed cameras measured travel speeds and photographed license plates and drivers of passenger vehicles traveling on roadways in Northern Virginia during daytime off-peak hours in spring 2013. The driver licensing agencies in the District of Columbia, Maryland, and Virginia provided vehicle information numbers (VINs) by matching license plate numbers with vehicle registration records and provided the age, gender, and ZIP code of the registered owner(s). VINs were decoded to obtain the curb weight and horsepower of vehicles. The study focused on 26,659 observed vehicles for which information on horsepower was available and the observed age and gender of drivers matched vehicle registration records. Log-linear regression estimated the effects of vehicle power on mean travel speeds, and logistic regression estimated the effects of vehicle power on the likelihood of a vehicle traveling over the speed limit and more than 10 mph over the limit.</p> <p><b>Results</b>: After controlling for driver characteristics, speed limit, vehicle type, and traffic volume, a 1-unit increase in vehicle power was associated with a 0.7% increase in mean speed, a 2.7% increase in the likelihood of a vehicle exceeding the speed limit by any amount, and an 11.6% increase in the likelihood of a vehicle exceeding the limit by 10 mph. All of these increases were highly significant.</p> <p><b>Conclusions</b>: Speeding persists as a major factor in crashes in the United States. There are indications that travel speeds have increased in recent years. The current findings suggest the trend toward substantially more powerful vehicles may be contributing to higher speeds. Given the strong association between travel speed and crash risk and crash severity, this is cause for concern.</p

Effects of automated speed enforcement in Montgomery County, Maryland, on vehicle speeds, public opinion, and crashes

<p><b>Objectives</b>: In May 2007, Montgomery County, Maryland, implemented an automated speed enforcement program, with cameras allowed on residential streets with speed limits of 35 mph or lower and in school zones. In 2009, the state speed camera law increased the enforcement threshold from 11 to 12 mph over the speed limit and restricted school zone enforcement hours. In 2012, the county began using a corridor approach, in which cameras were periodically moved along the length of a roadway segment. The long-term effects of the speed camera program on travel speeds, public attitudes, and crashes were evaluated.</p> <p><b>Methods</b>: Changes in travel speeds at camera sites from 6 months before the program began to 7½ years after were compared with changes in speeds at control sites in the nearby Virginia counties of Fairfax and Arlington. A telephone survey of Montgomery County drivers was conducted in Fall 2014 to examine attitudes and experiences related to automated speed enforcement. Using data on crashes during 2004–2013, logistic regression models examined the program's effects on the likelihood that a crash involved an incapacitating or fatal injury on camera-eligible roads and on potential spillover roads in Montgomery County, using crashes in Fairfax County on similar roads as controls.</p> <p><b>Results</b>: About 7½ years after the program began, speed cameras were associated with a 10% reduction in mean speeds and a 62% reduction in the likelihood that a vehicle was traveling more than 10 mph above the speed limit at camera sites. When interviewed in Fall 2014, 95% of drivers were aware of the camera program, 62% favored it, and most had received a camera ticket or knew someone else who had. The overall effect of the camera program in its modified form, including both the law change and the corridor approach, was a 39% reduction in the likelihood that a crash resulted in an incapacitating or fatal injury. Speed cameras alone were associated with a 19% reduction in the likelihood that a crash resulted in an incapacitating or fatal injury, the law change was associated with a nonsignificant 8% increase, and the corridor approach provided an additional 30% reduction over and above the cameras.</p> <p><b>Conclusions</b>: This study adds to the evidence that speed cameras can reduce speeding, which can lead to reductions in speeding-related crashes and crashes involving serious injuries or fatalities.</p

Enzyme-Catalyzed Direct Three-Component Aza-Diels–Alder Reaction Using Hen Egg White Lysozyme

The direct three-component aza-Diels–Alder reaction of aromatic aldehyde, aromatic amine, and 2-cyclohexen-1-one was catalyzed by hen egg white lysozyme for the first time. Under the optimized conditions investigated in this paper, the enzyme-catalyzed aza-Diels–Alder reaction gave yields up to 98% and stereoselectivity of <i>endo</i>/<i>exo</i> ratios up to 90:10

I_h Channels Control Feedback Regulation from Amacrine Cells to Photoreceptors

<div><p>In both vertebrates and invertebrates, photoreceptors’ output is regulated by feedback signals from interneurons that contribute to several important visual functions. Although synaptic feedback regulation of photoreceptors is known to occur in <i>Drosophila</i>, many questions about the underlying molecular mechanisms and physiological implementation remain unclear. Here, we systematically investigated these questions using a broad range of experimental methods. We isolated two <i>I_h</i> mutant fly lines that exhibit rhythmic photoreceptor depolarization without light stimulation. We discovered that I_h channels regulate glutamate release from amacrine cells by modulating calcium channel activity. Moreover, we showed that the eye-enriched kainate receptor (EKAR) is expressed in photoreceptors and receives the glutamate signal released from amacrine cells. Finally, we presented evidence that amacrine cell feedback regulation helps maintain light sensitivity in ambient light. Our findings suggest plausible molecular underpinnings and physiological effects of feedback regulation from amacrine cells to photoreceptors. These results provide new mechanistic insight into how synaptic feedback regulation can participate in network processing by modulating neural information transfer and circuit excitability.</p></div

Expression of I_h channels in ACs restores a normal ERG response.

<p>(<b>A</b>) Expression of I_h channels in ACs suppresses ERG baseline oscillation. I_h channels were expressed using anatomically restricted GAL4 drivers. Flies possessed one copy of the indicated drivers. (<b>B</b>) The fraction of flies that exhibit the ERG oscillation phenotype in each genotype. The number of recorded flies for each genotype is listed. (<b>C</b>) Expression of I_h channels in <i>I</i>_<i>h</i> mutant (top) and <i>I</i>_<i>h</i>;<i>Lai-GAL4/UAS—I</i>_<i>h</i> (bottom) flies. Dissected whole brains were stained with anti-I_h (green) and anti-24B10 (red) antibodies. L, lamina; M, medulla. (<b>D</b>) Intracellular recordings of photoreceptors show that I_h channels expression in ACs suppresses rhythmical depolarization without light stimulation. The fractions of photoreceptors that exhibit rhythmic depolarization are presented in the right panel, and the numbers of recorded photoreceptors for each genotype are listed.</p

Identification of glutamate receptor that mediates retrograde glutamate signaling from ACs to photoreceptors.

<p>(<b>A</b>) ERG traces of flies with iGluR depletion in photoreceptors. Photoreceptor-specific Rh1-GAL4 was used for iGluR screening. (<b>B</b>) Fractions of flies exhibit ERG oscillation phenotype and the numbers of recorded flies are presented.</p

Blocking synaptic glutamate release from ACs suppresses the rhythmic depolarization in <i>I</i>_h mutant photoreceptors.

<p>(<b>A</b>) Ultrastructure of lamina cross-sections in wild-type and <i>I</i>_<i>h</i> mutant flies. The left panel shows the organization of the columnar neurons with synaptic connections in the lamina. Photoreceptor cells are shown in gray, L1–L2 neurons in black, and ACs in red. These neurons are present in all lamina columns, and single example profiles are shown arrayed across the lamina. The middle and the right panels show EM images of lamina cross-sections in wild-type and <i>I</i>_<i>h</i> mutant flies, respectively. Photoreceptor axons are colored in yellow and AC processes in blue. (<b>B</b>) Intracellular recording traces of <i>I</i>_<i>h</i> mutant flies with expression of TeTxLC using <i>L1L2-GAL4</i> and <i>Lai-GAL4</i> drivers. The fractions of photoreceptors that exhibit rhythmic depolarization are presented in the middle panel, and the time (t_3/4) required for a 3/4 recovery from the responses upon stimulation cessation is shown in the right panel. The numbers of recorded flies are listed. (<b>C</b>) Inactivation of ACs via ectopic expression of dORK^ΔC suppresses rhythmical depolarization in <i>I</i>_<i>h</i> mutant flies. The fractions of flies that exhibit ERG oscillation phenotype and the numbers of recorded flies are presented in the right panel. An ERG trace of flies expressing dORK^ΔC in wild-type ACs is also presented. (<b>D</b>) Intracellular recording traces of <i>I</i>_<i>h</i> mutant flies expressing <i>UAS-vGluT-RNAi</i> using different drivers. The fractions of photoreceptors that exhibit rhythmical depolarization are presented in the middle panel, and the time (t_3/4) required for a 3/4 recovery from the responses upon stimulation cessation are shown in the right panel. The number of recorded flies for each genotype is listed.</p

RNAi lines used for iGluR screening.

<p>RNAi lines used for iGluR screening.</p

<i>I</i>_h mutant photoreceptors undergo rhythmic depolarization without light stimulation.

<p>(<b>A</b>) Intracellular recording traces of wild-type and <i>I</i>_<i>h</i> mutant photoreceptors. For intracellular recording traces, event markers represent 5-s orange light pulses, and scale bars are 5 mV. Measurements of the amplitude (Am), frequency (Fr), rise time (R_t), and decay time (D_t) of rhythmic depolarization are provided at the top. (<b>B</b>) The fraction of photoreceptors (R-cells) that exhibit oscillation phenotype. The numbers of photoreceptors recorded for each genotype are listed. (<b>C</b>) Measurement of the amplitude of light-induced depolarization (middle) and the time (t_3/4) required for a 3/4 recovery from the responses upon stimulation cessation (right). <i>n</i> = 10.</p

<i>I</i>_h mutant lines exhibit ERG baseline oscillation.

<p>(<b>A</b>) Annotated transcriptions of the <i>I</i>_<i>h</i> gene. Two <i>piggyBac</i> insertion sites are marked with triangles. The RNAi recognized site and coding region used for antibody generation are labeled at the top. (<b>B</b>) <i>I</i>_<i>h</i> mutant lines exhibit ERG baseline oscillation. For ERG traces throughout all figures, event markers represent 5-s orange light pulses, and scale bars are 5 mV. (<b>C</b>) Fraction of flies that exhibit the ERG oscillation phenotype in each genotype. The numbers of recorded flies for each genotype are listed. (<b>D</b>) RT-PCR shows <i>I</i>_<i>h</i> mRNAs are transcripted in wild-type flies but are absent in <i>I</i>_<i>h</i> mutant flies. Primer pair CACGCGACCAATCTCATCC/ TCATGGAGTGTTACCCTCG, which can amplify all transcriptional variants, was used in RT-PCR analysis. The tubulin gene was used as a loading control. (<b>E</b>) Western blotting revealed four major I_h channel variants (indicated by arrows) expressed in wild-type flies but absent in <i>I</i>_<i>h</i> mutant flies. Note that the low-intensity bands presented in <i>I</i>_<i>h</i> mutant flies are nonspecific.</p