What’s Behind Recent Transit Ridership Trends in the Bay Area? Volume I: Overview and Analysis of Underlying Factors

Public transit ridership has been falling nationally and in California since 2014. The San Francisco Bay Area, with the state’s highest rates of transit use, had until recently resisted those trends, especially compared to Greater Los Angeles. However, in 2017 and 2018 the region lost over five percent (>27 million) of its annual riders, despite a booming economy and service increases. This report examines Bay Area transit ridership to understand the dimensions of changing transit use, its possible causes, and potential solutions. We find that: 1) the steepest ridership losses have come on buses, at off-peak times, on weekends, in non-commute directions, on outlying lines, and on operators that do not serve the region’s core employment clusters; 2) transit trips in the region are increasingly commute-focused, particularly into and out of downtown San Francisco; 3) transit commuters are increasingly non-traditional transit users, such as those with higher incomes and automobile access; 4) the growing job-housing imbalance in the Bay Area is related to rising housing costs and likely depressing transit ridership as more residents live less transit-friendly parts of the region; and 5) ridehail is substituting for some transit trips, particularly in the off-peak. Arresting falling transit use will likely require action both by transit operators (to address peak capacity constraints; improve off-peak service; ease fare payments; adopt fare structures that attract off-peak riders; and better integrate transit with new mobility options) and public policymakers in other realms (to better meter and manage private vehicle use and to increase the supply and affordability of housing near job centers)

Design, Performance, and Complexity of CRC-Aided List Decoding of Convolutional and Polar Codes for Short Messages

Motivated by the need to communicate short control messages in 5G and beyond, this paper carefully designs codes for cyclic redundancy check (CRC)-aided list decoding of tail-biting convolutional codes (TBCCs) and polar codes. Both codes send a 32-bit message using an 11-bit CRC and 512 transmitted bits. We aim to provide a careful, fair comparison of the error performance and decoding complexity of polar and TBCC techniques for a specific case. Specifically, a TBCC is designed to match the rate of a (512, 43) polar code, and optimal 11-bit CRCs for both codes are designed. The paper examines the distance spectra of the polar and TBCC codes, illuminating the different distance structures for the two code types. We consider both adaptive and non-adaptive CRC-aided list decoding schemes. For polar codes, an adaptive decoder must start with a larger list size to avoid an error floor. For rate-32/512 codes with an 11-bit CRC, the optimized CRC-TBCC design achieves a lower total failure rate than the optimized CRC-polar design. Simulations showed that the optimized CRC-TBCC design achieved significantly higher throughput than the optimized CRC-polar design, so that the TBCC solution achieved a lower total failure rate while requiring less computational complexity.Comment: First revision submitted to IEEE Transactions on Communication

The Speed of Fronts of the Reaction Diffusion Equation

We study the speed of propagation of fronts for the scalar reaction-diffusion equation $u_t = u_{xx} + f(u)$\, with $f(0) = f(1) = 0$. We give a new integral variational principle for the speed of the fronts joining the state $u=1$ to $u=0$. No assumptions are made on the reaction term $f(u)$ other than those needed to guarantee the existence of the front. Therefore our results apply to the classical case $f > 0$ in $(0,1)$, to the bistable case and to cases in which $f$ has more than one internal zero in $(0,1)$.Comment: 7 pages Revtex, 1 figure not include

Assessment of Olfactory Processing in Parkinson’s Disease Patients

Background: Hyposmia is an early symptom of Parkinson’s Disease (PD) that often predates motor symptoms by years. Hyposmia has been shown to have a more consistent link to idiopathic PD than to other movement disorders. Olfaction has the potential to be used as a biomarker for PD, either through clinical evaluation or imaging. Objectives: This study uses functional magnetic resonance imaging (fMRI) to assess differences in olfaction pathways between anosmic early PD patients and age and gender-matched controls. Methods: 12 PD patients and 12 age- and gender-matched control subjects were recruited from the subject panel of a previous UMMS study on olfaction and PD. All PD patients were determined to be anosmic, and all controls were determined to have normal olfaction for their age and gender. All subjects underwent fMRI including periods with and without odorant exposure. Statistical analysis was performed using SPM8, using a general linear model to calculate BOLD signal changes for each scent relative to room air. A random effect model was used to infer general population effects. Results: Control subjects showed significant activation in the piriform cortex, anterior olfactory nucleus, insula, hippocampus and temporal lobe, all regions associated with olfactory processing. Relative to control subjects, PD patients showed no significant BOLD activation in the olfactory pathways of the brain. In response to a citrus scent, PD patients showed activation in the superior and middle frontal lobe, as well as the cingulate gyrus. In response to a cinnamon scent, PD patients showed significant activation in the precuneus and paracentral lobule as well as lower levels of activation in the frontal lobe. PD patients showed no significant areas of activation in response to a mint scent. Conclusion: Our results suggest that anosmic PD patients do not show activation of the olfactory pathways in the brain on exposure to these odorants. Taken together with previous studies, this suggests that BOLD activation in these regions of the brain can reflect clinical olfactory capability. In addition, PD patients show areas of increased activation, particularly in the frontal lobe. These distinct patterns of BOLD activation allow us to consider the feasibility of fMRI as a biomarker for diagnosis and evaluation of PD

Infection control and the prevalence, management and outcomes of SARS-CoV-2 infections in mental health wards in London, UK: lessons learned from wave 1 to wave 2

Background: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) disease (COVID-19) has high morbidity and mortality in older adults and people with dementia. Infection control and prevention measures potentially reduce transmission within hospitals. Aims: We aimed to replicate our earlier study of London mental health in-patients to examine changes in clinical guidance and practice and associated COVID-19 prevalence and outcomes between COVID-19 waves 1 and 2 (1 March to 30 April 2020 and 14 December 2020 to 15 February 2021). Method: We collected the 2 month period prevalence of wave 2 of COVID-19 in older (≥65 years) in-patients and those with dementia, as well as patients’ characteristics, management and outcomes, including vaccinations. We compared these results with those of our wave 1 study. Results: Sites reported that routine testing and personal protective equipment were available, and routine patient isolation on admission occurred throughout wave 2. COVID-19 infection occurred in 91/358 (25%; 95% CI 21–30%) v. 131/344, (38%; 95% CI 33–43%) P < 0.001 in wave 1. Hospitals identified more asymptomatic carriers (26/91; 29% v. 16/130; 12%) and fewer deaths (12/91; 13% v. 19/131; 15%; odds ratio = 0.92; 0.37–1.81) compared with wave 1. The patient vaccination uptake rate was 49/58 (85%). Conclusions: Patients in psychiatric in-patient settings, mostly admitted without known SARS-CoV-2 infection, had a high risk of infection compared with people in the community but lower than that during wave 1. Availability of infection control measures in line with a policy of parity of esteem between mental and physical health appears to have lowered within-hospital COVID-19 infections and deaths. Cautious management of vulnerable patient groups including mental health patients may reduce the future impact of COVID-19

Non-leftmost Unfolding in Partial Evaluation of Logic Programs with Impure Predicates

Abstract. Partial evaluation of logic programs which contain impure predicates poses non-trivial challenges. Impure predicates include those which produce side-effects, raise errors (or exceptions), and those whose truth value varies according to the degree of instantiation of arguments 4. In particular, non-leftmost unfolding steps can produce incorrect results since the independence of the computation rule no longer holds in the presence of impure predicates. Existing proposals allow non-leftmost unfolding steps, but at the cost of accuracy: bindings and failure are not propagated backwards to predicates which are potentially impure. In this work we propose a partial evaluation scheme which substantially reduces the situations in which such backpropagation has to be avoided. With this aim, our partial evaluator takes into account the information about purity of predicates expressed in terms of assertions. This allows achieving some optimizations which are not feasible using existing partial evaluation techniques. We argue that our proposal goes beyond existing ones in that it is a) accurate, since the classification of pure vs impure is done at the level of atoms instead of predicates, b) extensible, as the information about purity can be added to programs using assertions without having to modify the partial evaluator itself, and c) automatic, since (backwards) analysis can be used to automatically infer the required assertions. Our approach has been implemented in the context of CiaoPP, the abstract interpretation-based preprocessor of the Ciao logic programming system.

Aging impairs the osteocytic regulation of collagen integrity and bone quality

Poor bone quality is a major factor in skeletal fragility in elderly individuals. The molecular mechanisms that establish and maintain bone quality, independent of bone mass, are unknown but are thought to be primarily determined by osteocytes. We hypothesize that the age-related decline in bone quality results from the suppression of osteocyte perilacunar/canalicular remodeling (PLR), which maintains bone material properties. We examined bones from young and aged mice with osteocyte-intrinsic repression of TGFβ signaling (TβRI

Celecoxib exerts protective effects in the vascular endothelium via COX-2-independent activation of AMPK-CREB-Nrf2 signalling

Although concern remains about the athero-thrombotic risk posed by cyclo-oxygenase (COX)-2-selective inhibitors, recent data implicates rofecoxib, while celecoxib appears equivalent to NSAIDs naproxen and ibuprofen. We investigated the hypothesis that celecoxib activates AMP kinase (AMPK) signalling to enhance vascular endothelial protection. In human arterial and venous endothelial cells (EC), and in contrast to ibuprofen and naproxen, celecoxib induced the protective protein heme oxygenase-1 (HO-1). Celecoxib derivative 2,5-dimethyl-celecoxib (DMC) which lacks COX-2 inhibition also upregulated HO-1, implicating a COX-2-independent mechanism. Celecoxib activated AMPKα(Thr172) and CREB-1(Ser133) phosphorylation leading to Nrf2 nuclear translocation. Importantly, these responses were not reproduced by ibuprofen or naproxen, while AMPKα silencing abrogated celecoxib-mediated CREB and Nrf2 activation. Moreover, celecoxib induced H-ferritin via the same pathway, and increased HO-1 and H-ferritin in the aortic endothelium of mice fed celecoxib (1000 ppm) or control chow. Functionally, celecoxib inhibited TNF-α-induced NF-κB p65(Ser536) phosphorylation by activating AMPK. This attenuated VCAM-1 upregulation via induction of HO-1, a response reproduced by DMC but not ibuprofen or naproxen. Similarly, celecoxib prevented IL-1β-mediated induction of IL-6. Celecoxib enhances vascular protection via AMPK-CREB-Nrf2 signalling, a mechanism which may mitigate cardiovascular risk in patients prescribed celecoxib. Understanding NSAID heterogeneity and COX-2-independent signalling will ultimately lead to safer anti-inflammatory drugs

The Expression and Localization of N-Myc Downstream-Regulated Gene 1 in Human Trophoblasts

The protein N-Myc downstream-regulated gene 1 (NDRG1) is implicated in the regulation of cell proliferation, differentiation, and cellular stress response. NDRG1 is expressed in primary human trophoblasts, where it promotes cell viability and resistance to hypoxic injury. The mechanism of action of NDRG1 remains unknown. To gain further insight into the intracellular action of NDRG1, we analyzed the expression pattern and cellular localization of endogenous NDRG1 and transfected Myc-tagged NDRG1 in human trophoblasts exposed to diverse injuries. In standard conditions, NDRG1 was diffusely expressed in the cytoplasm at a low level. Hypoxia or the hypoxia mimetic cobalt chloride, but not serum deprivation, ultraviolet (UV) light, or ionizing radiation, induced the expression of NDRG1 in human trophoblasts and the redistribution of NDRG1 into the nucleus and cytoplasmic membranes associated with the endoplasmic reticulum (ER) and microtubules. Mutation of the phosphopantetheine attachment site (PPAS) within NDRG1 abrogated this pattern of redistribution. Our results shed new light on the impact of cell injury on NDRG1 expression patterns, and suggest that the PPAS domain plays a key role in NDRG1's subcellular distribution. © 2013 Shi et al