Commute Times, Food Retail Gaps, and Body Mass Index in North Carolina Counties

Introduction: The prevalence of obesity is higher in rural than in urban areas of the United States, for reasons that are not well understood. We examined correlations between percentage of rural residents, commute times, food retail gap per capita, and body mass index (BMI) among North Carolina residents. Methods: We used 2000 census data to determine each county\u27s percentage of rural residents and 1990 and 2000 census data to obtain mean county-level commute times. We obtained county-level food retail gap per capita, defined as the difference between county-level food demand and county-level food sales in 2008, from the North Carolina Department of Commerce, and BMI data from the 2007 North Carolina Behavioral Risk Factor Surveillance System. To examine county-level associations between BMI and percentage of rural residents, commute times, and food retail gap per capita, we used Pearson correlation coefficients. To examine cross-sectional associations between individual-level BMI (n=9,375) and county-level commute times and food retail gap per capita, we used multilevel regression models. Results: The percentage of rural residents was positively correlated with commute times, food retail gaps, and county-level BMI. Individual-level BMI was positively associated with county-level commute times and food retail gaps. Conclusions: Longer commute times and greater retail gaps may contribute to the rural obesity disparity. Future research should examine these relationships longitudinally and should test community-level obesity prevention

Energy Loss of Gluons, Baryons and k-Quarks in an N=4 SYM Plasma

We consider different types of external color sources that move through a strongly-coupled thermal N=4 super-Yang-Mills plasma, and calculate, via the AdS/CFT correspondence, the dissipative force (or equivalently, the rate of energy loss) they experience. A bound state of k quarks in the totally antisymmetric representation is found to feel a force with a nontrivial k-dependence. Our result for k=1 (or k=N-1) agrees at large N with the one obtained recently by Herzog et al. and Gubser, but contains in addition an infinite series of 1/N corrections. The baryon (k=N) is seen to experience no drag. Finally, a heavy gluon is found to be subject to a force which at large N is twice as large as the one experienced by a heavy quark, in accordance with gauge theory expectations.Comment: Latex 2e, 24 pages, 1 eps figure; v2: slightly amplified discussion on the relation between the drag force and the tension of a spatial Wilson loop; v3: minor changes, version to appear in JHE

Jet Quenching via Jet Collimation

The ATLAS Collaboration recently reported strong modifications of dijet properties in heavy ion collisions. In this work, we discuss to what extent these first data constrain already the microscopic mechanism underlying jet quenching. Simple kinematic arguments lead us to identify a frequency collimation mechanism via which the medium efficiently trims away the soft components of the jet parton shower. Through this mechanism, the observed dijet asymmetry can be accomodated with values of $\hat{q}\, L$ that lie in the expected order of magnitude.Comment: 6 pages, 4 figure

Early onset and novel features in a spinal and bulbar muscular atrophy patient with a 68 CAG repeat

AbstractSpinal and bulbar muscular atrophy (SBMA) is an X-linked neuromuscular disease caused by a trinucleotide (CAG) repeat expansion in the androgen receptor gene. Patients with SBMA have weakness, atrophy, and fasciculations in the bulbar and extremity muscles. Individuals with CAG repeat lengths greater than 62 have not previously been reported. We evaluated a 29year old SBMA patient with 68 CAGs who had unusually early onset and findings not seen in others with the disease. Analysis of the androgen receptor gene confirmed the repeat length of 68 CAGs in both peripheral blood and fibroblasts. Evaluation of muscle and sensory function showed deficits typical of SBMA, and in addition the patient had manifestations of autonomic dysfunction and abnormal sexual development. These findings extend the known phenotype associated with SBMA and shed new insight into the effects of the mutated androgen receptor

PPIP5K2 and PCSK1 are Candidate Genetic Contributors to Familial Keratoconus

Keratoconus (KC) is the most common corneal ectatic disorder affecting >300,000 people in the US. KC normally has its onset in adolescence, progressively worsening through the third to fourth decades of life. KC patients report significant impaired vision-related quality of life. Genetic factors play an important role in KC pathogenesis. To identify novel genes in familial KC patients, we performed whole exome and genome sequencing in a four-generation family. We identified potential variants in the PPIP5K2 and PCSK1 genes. Using in vitro cellular model and in vivo gene-trap mouse model, we found critical evidence to support the role of PPIP5K2 in normal corneal function and KC pathogenesis. The gene-trap mouse showed irregular corneal surfaces and pathological corneal thinning resembling KC. For the first time, we have integrated corneal tomography and pachymetry mapping into characterization of mouse corneal phenotypes which could be widely implemented in basic and translational research for KC diagnosis and therapy in the future

One-carbon metabolism in cancer

Cells require one-carbon units for nucleotide synthesis, methylation and reductive metabolism, and these pathways support the high proliferative rate of cancer cells. As such, anti-folates, drugs that target one-carbon metabolism, have long been used in the treatment of cancer. Amino acids, such as serine are a major one-carbon source, and cancer cells are particularly susceptible to deprivation of one-carbon units by serine restriction or inhibition of de novo serine synthesis. Recent work has also begun to decipher the specific pathways and sub-cellular compartments that are important for one-carbon metabolism in cancer cells. In this review we summarise the historical understanding of one-carbon metabolism in cancer, describe the recent findings regarding the generation and usage of one-carbon units and explore possible future therapeutics that could exploit the dependency of cancer cells on one-carbon metabolism

Hematopoietic Cell Transplantation in Patients With Primary Immune Regulatory Disorders (PIRD): A Primary Immune Deficiency Treatment Consortium (PIDTC) Survey.

Primary Immune Regulatory Disorders (PIRD) are an expanding group of diseases caused by gene defects in several different immune pathways, such as regulatory T cell function. Patients with PIRD develop clinical manifestations associated with diminished and exaggerated immune responses. Management of these patients is complicated; oftentimes immunosuppressive therapies are insufficient, and patients may require hematopoietic cell transplant (HCT) for treatment. Analysis of HCT data in PIRD patients have previously focused on a single gene defect. This study surveyed transplanted patients with a phenotypic clinical picture consistent with PIRD treated in 33 Primary Immune Deficiency Treatment Consortium centers and European centers. Our data showed that PIRD patients often had immunodeficient and autoimmune features affecting multiple organ systems. Transplantation resulted in resolution of disease manifestations in more than half of the patients with an overall 5-years survival of 67%. This study, the first to encompass disorders across the PIRD spectrum, highlights the need for further research in PIRD management

Arsenic Trioxide Modulates DNA Synthesis and Apoptosis in Lung Carcinoma Cells

Arsenic trioxide, the trade name Trisenox, is a drug used to treat acute promyleocytic leukemia (APL). Studies have demonstrated that arsenic trioxide slows cancer cells growth. Although arsenic influences numerous signal-transduction pathways, cell-cycle progression, and/or apoptosis, its apoptotic mechanisms are complex and not entirely delineated. The primary objective of this research was to evaluate the effects of arsenic trioxide on DNA synthesis and to determine whether arsenic-induced apoptosis is mediated via caspase activation, p38 mitogen–activated protein kinase (MAPK), and cell cycle arrest. To achieve this goal, lung cancer cells (A549) were exposed to various concentrations (0, 2, 4, 6, 8, and 10 μg/mL) of arsenic trioxide for 48 h. The effect of arsenic trioxide on DNA synthesis was determined by the [3H]thymidine incorporation assay. Apoptosis was determined by the caspase-3 fluorescein isothiocyanate (FITC) assay, p38 MAP kinase activity was determined by an immunoblot assay, and cell-cycle analysis was evaluated by the propidium iodide assay. The [3H]thymidine-incorporation assay revealed a dose-related cytotoxic response at high levels of exposure. Furthermore, arsenic trioxide modulated caspase 3 activity and induced p38 MAP kinase activation in A549 cells. However, cell-cycle studies showed no statistically significant differences in DNA content at subG1 check point between control and arsenic trioxide treated cells

Bowel function, sexual function, and symptoms of pelvic organ prolapse in women with and without urinary incontinence

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/146399/1/nau23587_am.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/146399/2/nau23587.pd