Quenched QCD with domain wall fermions

We report on simulations of quenched QCD using domain wall fermions, where we focus on basic questions about the formalism and its ability to produce expected low energy hadronic physics for light quarks. The work reported here is on quenched $8^3 \times 32$ lattices at $\beta = 5.7$ and 5.85, using values for the length of the fifth dimension between 10 and 48. We report results for parameter choices which lead to the desired number of flavors, a study of undamped modes in the extra dimension and hadron masses.Comment: Contribution to Lattice '98. Presented by R. Mawhinney. 3 pages, 3 figure

Dynamical QCD thermodynamics with domain wall fermions

We present results from numerical simulations of full, two flavor QCD thermodynamics at N_t=4 with domain wall fermions. For the first time a numerical simulation of the full QCD phase transition displays a low temperature phase with spontaneous chiral symmetry breaking but intact flavor symmetry and a high temperature phase with the full SU(2) x SU(2) chiral flavor symmetry.Comment: LATTICE98(hightemp

The domain wall fermion chiral condensate in quenched QCD

We examine the chiral limit of domain wall fermions in quenched QCD. One expects that in a quenched simulation, exact fermion zero modes will give a divergent, 1/m behavior in the chiral condensate for sufficiently small valence quark masses. Unlike other fermion formulations, domain wall fermions clearly demonstrate this behavior.Comment: LATTICE98(spectrum), G. R. Fleming presented talk, 5 pages, 3 figures, corrected typos in printed versio

A home-based exercise intervention to increase physical activity among people living with HIV: study design of a randomized clinical trial

Background While combination antiretroviral therapy has extended the life expectancy of those infected with human immunodeficiency virus (HIV), there is a high prevalence of comorbidities that increase the risk of cardiovascular morbidity and mortality among people living with HIV/AIDS (PLWHA). The side effects associated with antiretroviral therapy (ART) lead to multiple metabolic disorders, making the management of these metabolic issues and risk of cardiovascular disease (CVD) in those treated with ART a critical issue. Clinical research trials, primarily clinical exercise, rarely include this population due to unique challenges in research methods with underserved minority populations living with a life threatening illness like HIV/AIDS. This paper describes the rationale and design of a randomized clinical trial evaluating the feasibility of a home-based exercise program designed to increase physical activity (PA) and reduce the risk of CVD in PLWHA. Methods/design PLWHA being treated with ART will be randomly assigned to one of two groups: a home-based PA intervention or standard care. All participants will receive an educational weight loss workbook and pedometer for self-monitoring of PA. Only those in the intervention group will receive additional elastic Thera-bands® for strength training and behavioral telephone based coaching. Discussion This study will evaluate the feasibility of a home-based program designed to increase PA among PLWHA. Further, it will evaluate the effectiveness of such a program to decrease modifiable risk factors for CVD as a secondary outcome. This study was funded by the NIH/NINR R21 Grant 1R21NRO11281

A fate-alternating transitional regime in contracting liquid filaments

The fate of a contracting liquid filament depends on the Ohnesorge number, the initial aspect ratio and surface perturbation. Generally, it is believed that there exists a critical aspect ratio such that longer filaments break up and shorter ones recoil into a single drop. Through computational and experimental studies, we report a transitional regime for filaments with a broad range of intermediate aspect ratios, where there exist multiple thresholds at which a novel breakup mode alternates with a no-break mode. We develop a simple model considering the superposition of capillary waves, which can predict the complicated new phase diagram. In this model, the breakup results from constructive interference between the capillary waves that originate from the ends of the filament

Targeting IκB Kinase β in Adipocyte Lineage Cells for Treatment of Obesity and Metabolic Dysfunctions

IκB kinase β (IKKβ), a central coordinator of inflammation through activation of nuclear factor-κB, has been identified as a potential therapeutic target for the treatment of obesity-associated metabolic dysfunctions. In this study, we evaluated an antisense oligonucleotide (ASO) inhibitor of IKKβ and found that IKKβ ASO ameliorated diet-induced metabolic dysfunctions in mice. Interestingly, IKKβ ASO also inhibited adipocyte differentiation and reduced adiposity in high-fat (HF)-fed mice, indicating an important role of IKKβ signaling in the regulation of adipocyte differentiation. Indeed, CRISPR/Cas9-mediated genomic deletion of IKKβ in 3T3-L1 preadipocytes blocked these cells differentiating into adipocytes. To further elucidate the role of adipose progenitor IKKβ signaling in diet-induced obesity, we generated mice that selectively lack IKKβ in the white adipose lineage and confirmed the essential role of IKKβ in mediating adipocyte differentiation in vivo. Deficiency of IKKβ decreased HF-elicited adipogenesis in addition to reducing inflammation and protected mice from diet-induced obesity and insulin resistance. Further, pharmacological inhibition of IKKβ also blocked human adipose stem cell differentiation. Our findings establish IKKβ as a pivotal regulator of adipogenesis and suggest that overnutrition-mediated IKKβ activation serves as an initial signal that triggers adipose progenitor cell differentiation in response to HF feeding. Inhibition of IKKβ with antisense therapy may represent as a novel therapeutic approach to combat obesity and metabolic dysfunctions. Stem Cells 2016;34:1883–1895

IKKβ is Essential for Adipocyte Survival and Adaptive Adipose Remodeling in Obesity

IκB kinase β (IKKβ), a central coordinator of inflammatory responses through activation of nuclear factor-κB (NF-κB), has been implicated as a critical molecular link between inflammation and metabolic disorders; however, the role of adipocyte IKKβ in obesity and related metabolic disorders remains elusive. Here we report an essential role of IKKβ in the regulation of adipose remodeling and adipocyte survival in diet-induced obesity. Targeted deletion of IKKβ in adipocytes does not affect body weight, food intake, and energy expenditure but results in an exaggerated diabetic phenotype when challenged with a high-fat diet (HFD). IKKβ-deficient mice have multiple histopathologies in visceral adipose tissue, including increased adipocyte death, amplified macrophage infiltration, and defective adaptive adipose remodeling. Deficiency of IKKβ also leads to increased adipose lipolysis, elevated plasma free fatty acid (FFA) levels, and impaired insulin signaling. Mechanistic studies demonstrated that IKKβ is a key adipocyte survival factor and that IKKβ protects murine and human adipocytes from HFD- or FFA-elicited cell death through NF-κB-dependent upregulation of antiapoptotic proteins and NF-κB-independent inactivation of proapoptotic BAD protein. Our findings establish IKKβ as critical for adipocyte survival and adaptive adipose remodeling in obesity

Metabolic Syndrome and Risk of Cancer Mortality in Men

Background—Metabolic syndrome (MetS) has been linked with an increased risk of developing cancer; however the association between MetS and cancer mortality remains less clear. Little research has focused on pre-cancer risk factors that may affect the outcome of treatment. The purpose of this study was to examine the association between MetS and all-cancer mortality in men. Methods—The participants included 33,230 men aged 20-88 years who were enrolled in the Aerobics Center Longitudinal Study and free of known cancer at baseline. Results—At baseline 28% of all the participants had MetS. During an average of 14 years followup there were a total of 685 deaths due to cancer. MetS at baseline was associated with a 56% greater age-adjusted risk in cancer mortality. Conclusion—These data show that MetS is associated with an increased risk of all-cause cancer mortality in men. Based on these findings it is evident that successful interventions should be identified to attenuate the negative effects of MetS