DOES ECONOMIC VULNERABILITY DEPEND ON PLACE OF RESIDENCE? ASSET POVERTY ACROSS THE RURAL-URBAN CONTINUUM

This paper uses Panel Study of Income Dynamics data for 1989, 1994, and 1999 to examine why some U.S. households are asset poor; that is, why households have insufficient resources to invest in their future or to sustain household members at a basic level during times of economic disruption. The study contributes to an improved understanding of asset poverty's correlates by examining the influence of place of residence; the extant literature has focused on individual-level explanations. We estimate a random-effects logistic model of the probability that an individual is asset poor at a given point in time as a function of household-level (e.g. age, gender, race of the household head and family structure) and place-level (regional and rural-urban continuum) variables. The central finding of the paper is that place of residence is an important determinant of asset poverty, above and beyond the influence of household characteristics. We find that living in a central metropolitan county and in a nonmetropolitan area is associated with a higher risk of being asset poor, all else being equal. Implications for future research are discussed.Food Security and Poverty,

A Prediction Model for Chronic Kidney Disease Includes Periodontal Disease

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/142173/1/jper0016.pd

Predictive Values of Self‐Reported Periodontal Need: National Health and Nutrition Examination Survey III

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/142204/1/jper1551.pd

Sociodemographic characteristics and diabetes predict invalid self-reported non-smoking in a population-based study of U.S. adults

BACKGROUND: Nearly all studies reporting smoking status collect self-reported data. The objective of this study was to assess sociodemographic characteristics and selected, common smoking-related diseases as predictors of invalid reporting of non-smoking. Valid self-reported smoking may be related to the degree to which smoking is a behavior that is not tolerated by the smoker's social group. METHODS: True smoking was defined as having serum cotinine of 15+ng/ml. 1483 "true" smokers 45+ years of age with self-reported smoking and serum cotinine data from the Mobile Examination Center were identified in the third National Health and Nutrition Examination Survey. Invalid non-smoking was defined as "true" smokers self-reporting non-smoking. To assess predictors of invalid self-reported non-smoking, odds ratios (OR) and 95% confidence intervals (CI) were calculated for age, race/ethnicity-gender categories, education, income, diabetes, hypertension, and myocardial infarction. Multiple logistic regression modeling took into account the complex survey design and sample weights. RESULTS: Among smokers with diabetes, invalid non-smoking status was 15%, ranging from 0% for Mexican-American (MA) males to 22%–25% for Non-Hispanic White (NHW) males and Non-Hispanic Black (NHB) females. Among smokers without diabetes, invalid non-smoking status was 5%, ranging from 3% for MA females to 10% for NHB females. After simultaneously taking into account diabetes, education, race/ethnicity and gender, smokers with diabetes (OR(Adj )= 3.15; 95% CI: 1.35–7.34), who did not graduate from high school (OR(Adj )= 2.05; 95% CI: 1.30–3.22) and who were NHB females (OR(Adj )= 5.12; 95% CI: 1.41–18.58) were more likely to self-report as non-smokers than smokers without diabetes, who were high school graduates, and MA females, respectively. Having a history of myocardial infarction or hypertension did not predict invalid reporting of non-smoking. CONCLUSION: Validity of self-reported non-smoking may be related to the relatively slowly progressing chronic nature of diabetes, in contrast with the acute event of myocardial infarction which could be considered a more serious, major life changing event. These data also raise questions regarding the possible role of societal desirability in the validity of self-reported non-smoking, especially among smokers with diabetes, who did not graduate from high school, and who were NHB females

Clinical and Serologic Markers of Periodontal Infection and Chronic Kidney Disease

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/141492/1/jper1670.pd

Effects of Neuromuscular Electrical Stimulation Training on Skeletal Muscle Anabolic Signaling in Older Adults

Neuromuscular electrical stimulation (NMES) generates involuntary muscle contraction and may be a safe and effective alternative to voluntary resistance training, which is important for those who cannot perform voluntary exercise due to age-related conditions. However, further research is needed to better understand the skeletal muscle anabolic signaling response of the mTORC1 (mammalian target of rapamycin complex 1) pathway with repeated bouts of NMES. PURPOSE: To determine changes in skeletal muscle anabolic signaling in response to a 4-week NMES intervention in older adults. METHODS: Participants (n = 7) in this clinical trial were healthy, older adults (70.4 ± 2.9 years). NMES was applied to the quadriceps muscles for 40 min/treatment, 3x/week for 4 weeks (12 sessions). On Day 1 and Day 12 of the NMES intervention, skeletal muscle biopsies were obtained from the vastus lateralis Pre-NMES and 30 minutes Post-NMES and were analyzed for phosphorylation of mammalian target of rapamycin (mTOR) and p70-S6 Kinase 1 (S6K1) anabolic signaling proteins using the SDS-PAGE Western blot technique. Phosphorylation is expressed as the ratio of phosphorylated to total protein content. Data were analyzed using paired t-tests and data are reported as mean ± SE with statistical significance set at p ≤ 0.05. RESULTS: On Day 1, phosphorylation of S6K1 increased (Pre-NMES: 0.652 ± 0.145 AU vs. Post-NMES: 0.979 ± 0.151 AU, p = 0.037) and phosphorylation of mTOR increased (Pre-NMES: 0.464 ± 0.077 AU vs. Post-NMES: 1.046 ± 0.128 AU, p = 0.006) from Pre-NMES to Post-NMES. On Day 12, phosphorylation of S6K1 increased (Pre-NMES: 0.628 ± 0.108 AU vs. Post-NMES: 1.253 ± 0.288 AU, p = 0.048) with an increasing trend for mTOR (Pre-NMES: 0.485 ± 0.044 AU vs. Post-NMES: 0.700 ± 0.154 AU, p = 0.053) from Pre-NMES to Post-NMES. Phosphorylated S6K1 and mTOR protein content were not different between Day 1 and Day 12 at Pre-NMES (p \u3e 0.05) or at Post-NMES (p \u3e 0.05). CONCLUSION: The findings of this study suggest that the anabolic signaling response to a bout of NMES remains upregulated after 4-weeks of treatment; thus, the response is not attenuated with short-term repeated bouts of NMES. Funding: Research Enhancement Program Grant to J Mettler and L Kipp; Research Accelerator Grant, Texas State University, to J Mettler

ENU Mutagenesis Reveals a Novel Phenotype of Reduced Limb Strength in Mice Lacking Fibrillin 2

Background: Fibrillins 1 (FBN1) and 2 (FBN2) are components of microfibrils, microfilaments that are present in many connective tissues, either alone or in association with elastin. Marfan's syndrome and congenital contractural arachnodactyly (CCA) result from dominant mutations in the genes FBN1 and FBN2 respectively. Patients with both conditions often present with specific muscle atrophy or weakness, yet this has not been reported in the mouse models. In the case of Fbn1, this is due to perinatal lethality of the homozygous null mice making measurements of strength difficult. In the case of Fbn2, four different mutant alleles have been described in the mouse and in all cases syndactyly was reported as the defining phenotypic feature of homozygotes.Methodology/Principal Findings: As part of a large-scale N-ethyl-N-nitrosourea (ENU) mutagenesis screen, we identified a mouse mutant, Mariusz, which exhibited muscle weakness along with hindlimb syndactyly. We identified an amber nonsense mutation in Fbn2 in this mouse mutant. Examination of a previously characterised Fbn2-null mutant, Fbn2(fp), identified a similar muscle weakness phenotype. The two Fbn2 mutant alleles complement each other confirming that the weakness is the result of a lack of Fbn2 activity. Skeletal muscle from mutants proved to be abnormal with higher than average numbers of fibres with centrally placed nuclei, an indicator that there are some regenerating muscle fibres. Physiological tests indicated that the mutant muscle produces significantly less maximal force, possibly as a result of the muscles being relatively smaller in Mariusz mice.Conclusions: These findings indicate that Fbn2 is involved in integrity of structures required for strength in limb movement. As human patients with mutations in the fibrillin genes FBN1 and FBN2 often present with muscle weakness and atrophy as a symptom, Fbn2-null mice will be a useful model for examining this aspect of the disease process further

The Grizzly, December 4, 2003

Bringing Washington to Ursinus: Congress to Campus a Success • To Give is Better than to Receive: The Season of Generosity • Saying Goodbye to the Grizzly • Opinions: Holidays Hitting you too Soon?; New Year\u27s Resolutions Through the Years; Necessary Evils of Resolutions; Intramural Sports: Not Just Fun • Final Exam Schedule • Berman Exhibit • ProTheatre Play a Success • Four Women Soccer Players Named All Conference • Men\u27s and Women\u27s Basketball off to a Good Start • Ursinus Wrestling Dominates at Home • Stanton Named Player of the Week • Steroids in Pro Sportshttps://digitalcommons.ursinus.edu/grizzlynews/1550/thumbnail.jp

Dose-dense adjuvant chemotherapy for primary breast cancer

Adjuvant chemotherapy has been proven to reduce significantly the risk for relapse and death in women with operable breast cancer. Nevertheless, the prognosis for patients presenting with extensive axillary lymph node involvement remains suboptimal. In an attempt to improve on the efficacy of existing chemotherapy, a phase III intergroup trial led by the Cancer and Leukemia Group B (CALGB 97-41) was designed, which tested a mathematical model of tumor growth based on the Norton–Simon hypothesis. This hypothesis, developed about 3 decades ago, and the kinetic model derived from it, created the basis of the concepts of dose density and sequential therapy, both of which were tested in CALGB 97-41. This large prospective randomized trial demonstrated that shortening the time interval between each chemotherapy cycle while maintaining the same dose size resulted in significant improvements in disease-free and overall survival in patients with node-positive breast carcinoma. This finding is highly relevant and has immediate implications for clinical practice