198 research outputs found
The Future of California Transportation Revenue
Stable, predictable, and adequate transportation revenues are needed if California is to plan and deliver an excellent transportation system. This report provides a brief history of transportation revenue policies and potential futures in California. It then presents projections of transportation revenue under the recently enacted Senate Bill 1, the Road Repair and Accountability Act of 2017. Those revenue projections are compared with projections of revenue should SB 1 be repealed by voters in the November 2018 election. State-generated transportation revenues will be higher under SB1 than if the act is repealed. For 2020, the mean projection is that the state will collect 6.6 billion without it, a difference of 8.6 billion with SB1 and 5.2 billion difference. The total of all state transportation revenue collected between 2018 and 2040, assuming no other revisions to transportation revenue programs during these years, will be about $100 billion less if SB 1 is repealed than if the law is retained. The final section of the report addresses public attitudes toward transportation tax and fee policies, since future any policy changes must be informed by public willingness to consider revenue increases and opinions about which taxes or fees would be most appropriate
The Impact of ZEV Adoption on California Transportation Revenue
Former California Governor Jerry Brown set an ambitious target for the state to reach five million zero-emission vehicles (ZEVs) by 2030. The policy is intended to reduce greenhouse gas emissions, but progress toward this target will also affect future state-generated transportation revenues collected from vehicle owners and operators. A central concern for policymakers is to estimate the magnitude of the revenue impact. We used a simple spreadsheet model to project future transportation revenue in California through 2040 under two scenarios. The first scenario assumes that ZEV ownership continues at its historical rate of net increase, approximately 26,000 vehicles per year (the âlow-adoption scenarioâ). The second scenario assumes that California reaches its goal of five million ZEVs by 2030 (the âhigh-adoption scenarioâ). The projections are for light duty vehicles and do not address the possibility that heavy trucks may over time also adopt alternative fuels
FITW Module Demos
This session is for representatives from partner colleges on the U. S. Department of Education FIPSE\u27s First in the World grant-funded project to develop a just-in-time, blended approach to mathematics fundamentals support in introductory STEM courses. Partner colleges are Allegheny, Bryn Mawr, Denison, Franklin & Marshall, Grinnell, Lafayette, Mills, Oberlin, Smith, St. Olaf, Vassar, and Wellesley. In this session members from the Bryn Mawr team will demonstrate the prototype modules we have developed using Khan Academy and WeBWorK materials. Our goal is to get feedback on these prototypes, partners envision implementing them to support our target courses (introductory calculus, chemistry and physics) and what kinds of features will be most useful for students, faculty, tutors and other support staff
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Inequality by Design? An Analysis of Policy Design and Inequities in Recycling Program Access
There is little research on the causal mechanisms that lead to the phenomena of certain groups being disproportionately burdened or excluded from public policy initiatives. One of the areas in which the research is characterized by numerous gaps is that of policy design and the extent to which the design of public policy initiatives affects their outcomes or successes. An example of a time in which certain groups are excluded from public policy initiatives is recycling policy, with nearly half of the population in the United States lacking equitable access to recycling. This research examines not only the extent to which policy design of public policy may contribute to exacerbated inequities in society, but more specifically looks at the extent to which and how recycling programs and recycling policies illustrate the way policy design may lead to those exacerbated inequities (in this case, referring to inequitable access to recycling programs).</p
How Will Californiaâs Electric Vehicle Policy Impact State-Generated Transportation Revenues? Projecting Scenarios through 2040
California faces unprecedented uncertainty about how much revenue the state will raise from a package of taxes on motor fuels and annual registration fees on light-duty vehicles that was established in 2017 by Senate Bill 1 (SB 1). The SB 1 taxes are by far the largest source of revenue that the State of California generates to support maintenance, operations, and improvements for state highways, and the funds also contribute substantially to local transportation and public transit budgets. To help policymakers navigate the uncertainty about future SB 1 transportation revenue, this study used spreadsheet models to project revenue from the SB 1 taxes through 2040 under a set of eight scenarios that consider a wide range of possible futures. The scenarios consider changes to revenue that could arise from implementation of Californiaâs zero-emission vehicle (ZEV) regulations, as well as potential changes in driving costs, population size, vehicle ownership rates, and trucking industry operations.
Key findings include:
âą It is impossible to project future revenues with any confidence for more than a few years into the future. By 2040, annual revenue ranges from a low of 12.15 billion.
âą The state may lose substantial revenue if the SB 1 taxes and fees are not changed and/or replaced within the coming few years. In 2027, just three years out, projected annual revenue for some scenarios drops by more than a billion dollars below 2024 revenue.
âą A fast ICE to ZEV transition would significantly reduce annual revenueâbut so could changes in VMT.
âą Fuel taxes currently provide most SB 1 revenue, but by 2040 California may rely on vehicle registration fees to provide most of the revenue.
The dataset for this report is available in SJSU ScholarWorks
The Impact of the COVID-19 Recovery on California Transportation Revenue: A Scenario Analysis through 2040
The COVID-19 public health emergency has affected every aspect of life in California, reducing social and economic activity. Less activity translates to less travel, and less travel leads to less revenue generated from taxes on motor fuels. As California emerges from the COVID-19 crisis and returns to more normal levels of activity, the state must plan transportation system operations and maintenance in the context of deep uncertainty regarding future revenue.
To help decision makers navigate that uncertainty, we used spreadsheet models to estimate the impacts of different economic recovery scenarios from the COVID-19 pandemic on state-generated transportation revenue. Because it is not possible to anticipate future economic conditions, travel volumes, and vehicle markets with certainty, we created six potential economic recovery scenarios and projected future transportation revenue in California through 2040 under each.
Scenarios cannot foretell which conditions will predominate in future decades, but scenario analysis helps state officials assess the impact of different economic futures and policy choices, including policies to change the rates of adoption of alternative-fueled vehicles.
Key findings include: The projections from the six scenarios demonstrate that California transportation revenue by 2040 could range widely, from as little as 10.9 billion, if the assumptions and conditions used to create particular scenarios are realized over time. The cumulative revenue raised between 2020 and 2040 varies by more than 153 billion to $195 billion. In 2020, taxes on fuels will generate roughly three-quarters of state-generated transportation revenue. By 2040, however, taxes on fuels will generate a much smaller percentage of overall revenue. For example, in four of the six scenarios they generate less than a quarter of revenues
Nutrient Sensing by Tas1R Proteins is Required for Normal Bone Resorption
Current therapies for low bone mass consist of inhibiting osteoclast activity or increasing the PTH or Wnt signaling pathways. These approaches have significant drawbacks that limit their use in specific patient populations and/or negatively impact patient compliance with therapy. Developing improved therapies requires diversifying our understanding of the mechanisms underlying postnatal bone remodeling by examining lesser-known signaling pathways. One such pathway is the taste receptor type 1 (TAS1R) family of heterotrimeric G protein-coupled receptors, which participates in monitoring energy and nutrient status. Previous work reported that global deletion of TAS1R member 3 (TAS1R3), which is a bi-functional protein that recognizes amino acids or sweet molecules when dimerized with TAS1R member 1 (TAS1R1) or TAS1R member 2 (TAS1R2), respectively, leads to increased cortical bone mass. Here, we corroborate the increased thickness of cortical bone in Tas1R3 knockout mice and confirm that Tas1R3 is expressed in the bone environment. Quantification of serum bone turnover markers indicate that this phenotype is likely due to uncoupled bone remodeling, with levels of the bone resorption marker CTx being reduced greater than 60% in Tas1R3 mutant mice; no changes were observed in levels of the bone formation marker PINP. Consistent with this, Tas1R3 and its putative signaling partner Tas1R2 are expressed in primary osteoclasts and RAW264.7 cells following RANKL-mediated differentiation. These findings suggest that osteoclast function and/or differentiation may be altered in the absence of Tas1R3 expression. To test this, we quantified bone-specific expression of Rankl and determined the Rankl:Opg ratio; no differences were observed between control and Tas1R3 knockout mice in these analyses. In vitro studies examining further downstream effectors of TAS1R2:3 in response to saccharin and receptor antagonist gurmarin are currently underway. Collectively, our findings provide the first demonstration that nutrient monitoring by TAS1R3 is essential for normal bone resorption in vivo
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Club-like cells in proliferative inflammatory atrophy of the prostate.
Club cells are a type of bronchiolar epithelial cell that serve a protective role in the lung and regenerate damaged lung epithelium. Single-cell RNA sequencing (scRNA-seq) of young adult human prostate and urethra identified cell populations in the prostatic urethra and collecting ducts similar in morphology and transcriptomic profile to lung club cells. We further identified club cell-like epithelial cells by scRNA-seq of prostate peripheral zone tissues. Here, we aimed to identify and spatially localize club cells in situ in the prostate, including in the peripheral zone. We performed chromogenic RNA in situ hybridization for five club cell markers (CP, LTF, MMP7, PIGR, SCGB1A1) in a series of (1) nondiseased organ donor prostate and (2) radical prostatectomy specimens from individuals with prostate cancer. We report that expression of club cell genes in the peripheral zone is associated with inflammation and limited to luminal epithelial cells classified as intermediate cells in proliferative inflammatory atrophy (PIA). Club-like cells were enriched in radical prostatectomy specimens compared to nondiseased prostates and associated with high-grade prostate cancer. We previously reported that luminal epithelial cells in PIA can rarely harbor oncogenic TMPRSS2:ERG (ERG+) gene fusions, and we now demonstrate that club cells are present in association with ERG+ PIA that is transitioning to early adenocarcinoma. Finally, prostate epithelial organoids derived from prostatectomy specimens demonstrate that club-like epithelial cells can be established in organoids and are sensitive to anti-androgen-directed treatment in vitro in terms of decreased androgen signaling gene expression signatures compared to basal or hillock cells. Overall, our study identifies a population of club-like cells in PIA and proposes that these cells play an analogous role to that of club cells in bronchiolar epithelium. Our results further suggest that inflammation drives lineage plasticity in the human prostate and that club cells in PIA may be prone to oncogenic transformation. © 2023 The Authors. The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland
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Manganese tricarbonyl complexes with asymmetric 2 2âiminopyridine ligands: toward decoupling steric and electronic 3 factors in electrocatalytic CO2 reduction
Manganese tricarbonyl bromide complexes incorporating IP
(2-(phenylimino)pyridine) derivatives, [MnBr(CO)3(IP)], are demonstrated as a new group of catalysts for CO2 reduction, which represent the first example of utilization of (phenylimino)pyridine ligands on manganese centers for this purpose. The key feature is the asymmetric structure of the redox-noninnocent ligand that permits independent tuning of its steric and electronic properties. The α-diimine ligands and five new Mn(I) compounds have been synthesized, isolated in high yields, and fully characterized, including X-ray crystallography. Their electrochemical and electrocatalytic behavior was investigated using cyclic voltammetry and UVâvisâIR spectroelectrochemistry within an OTTLE cell. Mechanistic investigations under an inert atmosphere have revealed differences in the nature of the reduction products as a function of steric bulk of the ligand. The direct ECE (electrochemicalâchemicalâelectrochemical) formation of
a five-coordinate anion [Mn(CO)3(IP)]â, a product of two-electron reduction of the parent complex, is observed in the case of the bulky DIPIMP (2-[((2,6-diisopropylphenyl)imino)methyl]pyridine), TBIMP (2-[((2-tert-butylphenyl)imino)methyl]-pyridine), and TBIEP (2-[((2-tert-butylphenyl)imino)ethyl]pyridine) derivatives. This process is replaced for the least sterically demanding IP ligand in [MnBr(CO)3(IMP)] (2-[(phenylimino)methyl]pyridine) by the stepwise formation of such a monoanion via an ECEC(E) mechanism involving also the intermediate MnâMn dimer [Mn(CO)3(IMP)]2. The complex [MnBr(CO)3(IPIMP)] (2-[((2-diisopropylphenyl)imino)methyl]pyridine), which carries a moderately electron donating, moderately bulky IP ligand, shows an intermediate behavior where both the five-coordinate anion and its dimeric precursor are jointly detected on the time scale of the spectroelectrochemical experiments. Under an atmosphere of CO2 the studied complexes, except for the DIPIMP derivative, rapidly coordinate CO2, forming stable bicarbonate intermediates, with no dimer being observed. Such behavior indicates that the CO2 binding is outcompeting another pathway: viz., the dimerization reaction between the five-coordinate anion and the neutral parent complex. The bicarbonate intermediate species undergo reduction at more negative potentials (ca. â2.2 V vs Fc/Fc+
), recovering [Mn(CO)3(IP)]â and triggering the catalytic production of CO
Loss of the nutrient sensor TAS1R3 leads to reduced bone resorption
The taste receptor type 1 (TAS1R) family of heterotrimeric G protein-coupled receptors participates in monitoring energy and nutrient status. TAS1R member 3 (TAS1R3) is a bi-functional protein that recognizes amino acids such as L-glycine and L-glutamate or sweet molecules such as sucrose and fructose when dimerized with TAS1R member 1 (TAS1R1) or TAS1R member 2 (TAS1R2), respectively. It was recently reported that deletion of TAS1R3 expression in Tas1R3 mutant mice leads to increased cortical bone mass but the underlying cellular mechanism leading to this phenotype remains unclear. Here, we independently corroborate the increased thickness of cortical bone in femurs of 20-week-old male Tas1R3 mutant mice and confirm that Tas1R3 is expressed in the bone environment. Tas1R3 is expressed in undifferentiated bone marrow stromal cells (BMSCs) in vitro and its expression is maintained during BMP2-induced osteogenic differentiation. However, levels of the bone formation marker procollagen type I N-terminal propeptide (PINP) are unchanged in the serum of 20-week-old Tas1R3 mutant mice as compared to controls. In contrast, levels of the bone resorption marker collagen type I C-telopeptide are reduced greater than 60% in Tas1R3 mutant mice. Consistent with this, Tas1R3 and its putative signaling partner Tas1R2 are expressed in primary osteoclasts and their expression levels positively correlate with differentiation status. Collectively, these findings suggest that high bone mass in Tas1R3 mutant mice is due to uncoupled bone remodeling with reduced osteoclast function and provide rationale for future experiments examining the cell-type-dependent role for TAS1R family members in nutrient sensing in postnatal bone remodeling
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