Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 6 de 6
Filter
Add more filters










Database
Language
Publication year range
1.
Int J Sports Med ; 37(4): 274-81, 2016 Apr.
Article in English | MEDLINE | ID: mdl-26667921

ABSTRACT

Our purpose in this study was to investigate efficient and sustainable combinations of exercise and diet-induced weight loss (DIET), in order to combat obesity in metabolic syndrome (MetS) patients. We examined the impact of aerobic interval training (AIT), followed by or concurrent to a DIET on MetS components. 36 MetS patients (54±9 years old; 33±4 BMI; 27 males and 9 females) underwent 16 weeks of AIT followed by another 16 weeks without exercise from the fall of 2013 to the spring of 2014. Participants were randomized to AIT without DIET (E CON, n=12), AIT followed by DIET (E-then-D, n=12) or AIT concurrent with DIET (E+D, n=12) groups. Body weight decreased below E CON similarly in the E-then-D and E+D groups (~5%). Training improved blood pressure and cardiorespiratory fitness (VO2peak) in all groups with no additional effect of concurrent weight loss. However, E+D improved insulin sensitivity (HOMA) and lowered plasma triglycerides and blood cholesterol below E CON and E-then-D (all P<0.05). Weight loss in E-then-D in the 16 weeks without exercise lowered HOMA to the E+D levels and maintained blood pressure at trained levels. Our data suggest that a new lifestyle combination consisting of aerobic interval training followed by weight loss diet is similar, or even more effective on improving metabolic syndrome factors than concurrent exercise plus diet.


Subject(s)
Diet, Reducing , Exercise Therapy , Metabolic Syndrome/therapy , Weight Loss , Adult , Blood Pressure , Female , Humans , Male , Middle Aged , Obesity/therapy , Oxygen Consumption , Physical Fitness
2.
Lupus ; 25(2): 137-54, 2016 Feb.
Article in English | MEDLINE | ID: mdl-26385218

ABSTRACT

Lupus is an autoimmune disease characterized by the development of antinuclear autoantibodies and immune complex-mediated tissue damage. T cells in lupus patients appear to undergo apoptosis at an increased rate, and this enhanced T cell apoptosis has been postulated to contribute to lupus pathogenesis by increasing autoantigen load. However, there is no direct evidence to support this hypothesis. In this study, we show that an Lck-cre transgene, which increases T cell apoptosis as a result of T cell-specific expression of cre recombinase, accelerates the development of autoantibodies and nephritis in lupus-prone (NZB × NZW)F1 mice. Although the enhanced T cell apoptosis in Lck-cre transgenic mice resulted in an overall decrease in the relative abundance of splenic CD4(+) and CD8(+) T cells, the proportion of activated CD4(+) T cells was increased and no significant change was observed in the relative abundance of suppressive T cells. We postulate that the Lck-cre transgene promoted lupus by enhancing T cell apoptosis, which, in conjunction with the impaired clearance of apoptotic cells in lupus-prone mice, increased the nuclear antigen load and accelerated the development of anti-nuclear autoantibodies. Furthermore, our results also underscore the importance of including cre-only controls in studies using the cre-lox system.


Subject(s)
Autoantibodies/biosynthesis , Lupus Nephritis/genetics , Lupus Nephritis/immunology , Transgenes , Alleles , Animals , Antigen-Antibody Complex/immunology , Apoptosis/genetics , Apoptosis/immunology , Autoantibodies/genetics , Disease Models, Animal , Female , Integrases/metabolism , Male , Mice , Mice, Inbred NZB , Mice, Transgenic , Sequence Analysis , T-Lymphocytes/immunology , T-Lymphocytes/pathology
3.
Mar Pollut Bull ; 58(10): 1505-13, 2009 Oct.
Article in English | MEDLINE | ID: mdl-19540535

ABSTRACT

Locating areas of seafloor contamination caused by heavy oil spills is challenging, in large part because of observational limitations in aquatic subsurface environments. Accepted methods for surveying and locating sunken oil are generally slow, labor intensive and spatially imprecise. This paper describes a method to locate seafloor contamination caused by heavy oil fractions using in situ mass spectrometry and concurrent acoustic navigation. We present results of laboratory sensitivity tests and proof-of-concept evaluations conducted at the US Coast Guard OHMSETT national oil spill response test facility. Preliminary results from a robotic seafloor contamination survey conducted in deep water using the mass spectrometer and a geo-referenced acoustic navigation system are also described. Results indicate that this technological approach can accurately localize seafloor oil contamination in real-time at spatial resolutions better than a decimeter.


Subject(s)
Disasters , Environmental Pollutants/analysis , Geologic Sediments/analysis , Mass Spectrometry/methods , Petroleum/analysis , Geography , Mass Spectrometry/instrumentation , Oceans and Seas
4.
Proc Natl Acad Sci U S A ; 103(37): 13570-4, 2006 Sep 12.
Article in English | MEDLINE | ID: mdl-16945904

ABSTRACT

Marine hydrocarbon seepage emits oil and gas, including methane ( approximately 30 Tg of CH(4) per year), to the ocean and atmosphere. Sediments from the California margin contain preserved tar, primarily formed through hydrocarbon weathering at the sea surface. We present a record of variation in the abundance of tar in sediments for the past 32,000 years, providing evidence for increases in hydrocarbon emissions before and during Termination IA [16,000 years ago (16 ka) to 14 ka] and again over Termination IB (11-10 ka). Our study provides direct evidence for increased hydrocarbon seepage associated with deglacial warming through tar abundance in marine sediments, independent of previous geochemical proxies. Climate-sensitive gas hydrates may modulate thermogenic hydrocarbon seepage during deglaciation.

5.
J Am Vet Med Assoc ; 193(2): 211-4, 1988 Jul 15.
Article in English | MEDLINE | ID: mdl-2841268

ABSTRACT

As a follow-up to an investigation of 2 dogs that died as a result of apparent toxicosis attributable to a cholecalciferol-containing rodenticide, we tested the toxicity of this product in dogs. Two groups of 2 dogs each were fed amounts of rodenticide that provided 20 and 10 mg of cholecalciferol/kg of body weight (approx one fourth and one eighth of the published LD50, respectively). All dogs developed hypercalcemia and hyperphosphatemia and then died. Major lesions were gastrointestinal hemorrhage, myocardial necrosis, and mineralization of vascular walls. Our data indicate that cholecalciferol-containing rodenticides pose a much greater hazard to dogs than was previously believed.


Subject(s)
Cholecalciferol/adverse effects , Dog Diseases/chemically induced , Rodenticides/adverse effects , Animals , Dog Diseases/pathology , Dogs , Female , Gastrointestinal Diseases/chemically induced , Gastrointestinal Diseases/pathology , Gastrointestinal Diseases/veterinary
SELECTION OF CITATIONS
SEARCH DETAIL
...