In-depth analysis of the J.A.C.K. model

The Texas Transportation Commission (���the Commission���) is responsible for planning and making policies for the location, construction, and maintenance of a comprehensive system of highways and public roads in Texas. In order for the Commission to carry out its legislative mandate, the Texas Constitution requires that most revenue generated by motor vehicle registration fees and motor fuel taxes be used for constructing and maintaining public roadways and other designated purposes. The Texas Department of Transportation (TxDOT) assists the Commission in executing state transportation policy. It is the responsibility of the legislature to appropriate money for TxDOT���s operation and maintenance expenses. All money authorized to be appropriated for TxDOT���s operations must come from the State Highway Fund (also known as Fund 6, Fund 006, or Fund 0006). The Commission can then use the balance in the fund to fulfill its responsibilities. However, the value of the revenue received in Fund 6 is not keeping pace with growing demand for transportation infrastructure in Texas. Additionally, diversion of revenue to nontransportation uses now exceeds $600 million per year. As shown in Figure 1.1, revenues and expenditures of the State Highway Fund per vehicle mile traveled (VMT) in Texas have remained almost flat since 1993. In the meantime, construction cost inflation has gone up more than 100%, effectively halving the value of expenditure.

Evaluation of TxDOT���s J.A.C.K. model for revenue and expenditure projections

This research report documents work conducted by the Center for Transportation (CTR) at The University of Texas at Austin in analyzing the Joint Analysis using the Combined Knowledge (J.A.C.K.) program. This program was developed by the Texas Department of Transportation (TxDOT) to make projections of revenues and expenditures. This research effort was to span from September 2008 to August 2009, but the bulk of the work was completed and presented by December 2008. J.A.C.K. was subsequently renamed TRENDS, but for consistency with the scope of work, the original name is used throughout this report.

Review of the under the limit drink driving rehabilitation program

The combination of alcohol and driving is a major health and economic burden to most communities in industrialised countries. The total cost of crashes for Australia in 1996 was estimated at approximately 15 billion dollars and the costs for fatal crashes were about 3 billion dollars (BTE, 2000). According to the Bureau of Infrastructure, Transport and Regional Development and Local Government (2009; BITRDLG) the overall cost of road fatality crashes for 2006 $3.87 billion, with a single fatal crash costing an estimated $2.67 million. A major contributing factor to crashes involving serious injury is alcohol intoxication while driving. It is a well documented fact that consumption of liquor impairs judgment of speed, distance and increases involvement in higher risk behaviours (Waller, Hansen, Stutts, & Popkin, 1986a; Waller et al., 1986b). Waller et al. (1986a; b) asserts that liquor impairs psychomotor function and therefore renders the driver impaired in a crisis situation. This impairment includes; vision (degraded), information processing (slowed), steering, and performing two tasks at once in congested traffic (Moskowitz & Burns, 1990). As BAC levels increase the risk of crashing and fatality increase exponentially (Department of Transport and Main Roads, 2009; DTMR). According to Compton et al. (2002) as cited in the Department of Transport and Main Roads (2009), crash risk based on probability, is five times higher when the BAC is 0.10 compared to a BAC of 0.00. The type of injury patterns sustained also tends to be more severe when liquor is involved, especially with injuries to the brain (Waller et al., 1986b). Single and Rohl (1997) reported that 30% of all fatal crashes in Australia where alcohol involvement was known were associated with Breadth Analysis Content (BAC) above the legal limit of 0.05gms/100ml. Alcohol related crashes therefore contributes to a third of the total cost of fatal crashes (i.e. $1 billion annually) and crashes where alcohol is involved are more likely to result in death or serious injury (ARRB Transport Research, 1999). It is a major concern that a drug capable of impairment such as is the most available and popular drug in Australia (Australian Institute of Health and Welfare, 2007; AIHW). According to the AIHW (2007) 89.9% of the approximately 25,000 Australians over the age of 14 surveyed had consumed at some point in time, and 82.9% had consumed liquor in the previous year. This study found that 12.1% of individuals admitted to driving a motor vehicle whilst intoxicated. In general males consumed more liquor in all age groups. In Queensland there were 21503 road crashes in 2001, involving 324 fatalities and the largest contributing factor was alcohol and or drugs (Road Traffic Report, 2001). 23438 road crashes in 2004, involving 289 fatalities and the largest contributing factor was alcohol and or drugs (DTMR, 2009). Although a number of measures such as random breath testing have been effective in reducing the road toll (Watson, Fraine & Mitchell, 1995) the recidivist drink driver remains a serious problem. These findings were later supported with research by Leal, King, and Lewis (2006). This Queensland study found that of the 24661 drink drivers intercepted in 2004, 3679 (14.9%) were recidivists with multiple drink driving convictions in the previous three years covered (Leal et al., 2006). The legal definition of the term ���recidivist��� is consistent with the Transport Operations (Road Use Management) Act (1995) and is assigned to individuals who have been charged with multiple drink driving offences in the previous five years. In Australia relatively little attention has been given to prevention programs that target high-risk repeat drink drivers. However, over the last ten years a rehabilitation program specifically designed to reduce recidivism among repeat drink drivers has been operating in Queensland. The program, formally known as the ���Under the Limit��� drink driving rehabilitation program (UTL) was designed and implemented by the research team at the Centre for Accident Research and Road Safety in Queensland with funding from the Federal Office of Road Safety and the Institute of Criminology (see Sheehan, Schonfeld & Davey, 1995). By 2009 over 8500 drink-drivering offenders had been referred to the program (Australian Institute of Crime, 2009).

Cholesterol enhances phospholipid-dependent activated protein C anticoagulant activity

The influence of cholesterol on activated protein C (APC) anticoagulant activity in plasma and on factor Va inactivation was investigated. Anticoagulant and procoagulant activities of phosphatidylcholine/phosphatidylserine (PC/PS) vesicles containing cholesterol were assessed in the presence and absence of APC using factor Xa-1-stage clotting and factor Va inactivation assays. Cholesterol at approximate physiological membrane levels (30%) in PC/PS (60%/10% w/w) vesicles prolonged the factor Xa-1-stage clotting time dose-dependently in the presence of APC but not in the absence of APC. APC-mediated cleavage of purified recombinant factor Va variants that were modified at specific APC cleavage sites (Q306/Q679-factor Va; Q506/Q679-factor Va) was studied to define the effects of cholesterol on APC cleavage at R506 and R306. When compared to control PC/PS vesicles, cholesterol in PC/PS vesicles enhanced factor Va inactivation and the rate of APC cleavage at both R506 and R306. Cholesterol also enhanced APC cleavage rates at R306 in the presence of the APC cofactor, protein S. In summary, APC anticoagulant activity in plasma and factor Va inactivation as a result of cleavages at R506 and R306 by APC is markedly enhanced by cholesterol in phospholipid vesicles. These results suggest that cholesterol in a membrane surface may selectively enhance APC activities. �� 2005 International Society on Thrombosis and Haemostasis.

Categorisation of activities of daily living of lower limb amputees during short-term use of a portable kinetic recording system : a preliminary study

The purpose of this preliminary study was to determine the relevance of the categorization of the load regime data to assess the functional output and usage of the prosthesis of lower limb amputees. The objectives were a) to introduce a categorization of load regime, b) to present some descriptors of each activity, and c) to report the results for a case. The load applied on the osseointegrated fixation of one transfemoral amputee was recorded using a portable kinetic system for 5 hours. The periods of directional locomotion, localized locomotion, and stationary loading occurred 44%, 34%, and 22% of recording time and each accounted for 51%, 38%, and 12% of the duration of the periods of activity, respectively. The absolute maximum force during directional locomotion, localized locomotion, and stationary loading was 19%, 15%, and 8% of the body weight on the anteroposterior axis, 20%, 19%, and 12% on the mediolateral axis, and 121%, 106%, and 99% on the long axis. A total of 2,783 gait cycles were recorded. Approximately 10% more gait cycles and 50% more of the total impulse than conventional analyses were identified. The proposed categorization and apparatus have the potential to complement conventional instruments, particularly for difficult cases.

Natural convection in a triangular enclosure subject to periodic thermal forcing

The effects of periodic thermal forcing on the flow field and heat transfer through an attic space are examined numerically in this paper. We consider the case with a fixed aspect ratio of 0.5 and a fixed Grashof number of 1.33��106. The numerical results reveal that, during the daytime, the flow is stratified; whereas at the night-time, the flow becomes unstable. A number of regular plumes and vortices are observed in the contours of isotherms and stream functions respectively. Moreover, the flow appears to be symmetric during the daytime, and becomes asymmetric at the night-time. It is also found that the flow is weaker during the daytime than that at the night-time in the present case, and the calculated heat transfer rate at the night-time is approximately three times greater than the heat transfer rate during the daytime.

Gonadotropin-induced ovarian cancer cell migration and proliferation require extracellular signal-regulated kinase 1/2 activation regulated by calcium and protein kinase C��

The gonadotropin hypothesis proposes that elevated serum gonadotropin levels may increase the risk of epithelial ovarian cancer (EOC). We have studied the effect of treating EOC cell lines (OV207 and OVCAR-3) with FSH or LH. Both gonadotropins activated the mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase 1/2 (ERK1/2) pathway and increased cell migration that was inhibited by the MAPK 1 inhibitor PD98059. Both extra- and intracellular calcium ion signalling were implicated in gonadotropin-induced ERK1/2 activation as treatment with either the calcium chelator EGTA or an inhibitor of intracellular calcium release, dantrolene, inhibited gonadotropin-induced ERK1/2 activation. Verapamil was also inhibitory, indicating that gonadotropins activate calcium influx via L-type voltage-dependent calcium channels. The cAMP/protein kinase A (PKA) pathway was not involved in the mediation of gonadotropin action in these cells as gonadotropins did not increase intracellular cAMP formation and inhibition of PKA did not affect gonadotropin-induced phosphorylation of ERK1/2. Activation of ERK1/2 was inhibited by the protein kinase C (PKC) inhibitor GF 109203X as well as by the PKC�� inhibitor rottlerin, and downregulation of PKC�� was inhibited by small interfering RNA (siRNA), highlighting the importance of PKC�� in the gonadotropin signalling cascade. Furthermore, in addition to inhibition by PD98059, gonadotropin-induced ovarian cancer cell migration was also inhibited by verapamil, GF 109203X and rottlerin. Similarly, gonadotropin-induced proliferation was inhibited by PD98059, verapamil, GF 109203X and PKC�� siRNA. Taken together, these results demonstrate that gonadotropins induce both ovarian cancer cell migration and proliferation by activation of ERK1/2 signalling in a calcium- and PKC��-dependent manner.