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1.
Eur Rev Med Pharmacol Sci ; 17(17): 2295-301, 2013 Sep.
Article in English | MEDLINE | ID: mdl-24065221

ABSTRACT

OBJECTIVES: Metabolic syndrome (MetS) is a cluster of metabolic abnormalities involving several cardiovascular risk factors. Carotid intima media thickness (CIMT) is an important early screening tool to assess subclinical manifestation of cardiovascular and metabolic diseases. We aimed to investigate the impact of MetS on CIMT in a large scaled community based study. METHODS: The study was conducted on 2102 participants. Carotid intima media thickness was measured in all of the participants. The study sample was divided into 4 groups; Group 1 subjects with a body mass index (BMI) < 25.0 kg/m2 [n = 499 (MetS- = 488, MetS+ = 11)], Group 2 BMI between 25.0 and 29.9 kg/m2 [n = 693 (MetS- = 559, MetS+ = 134)], Group 3 BMI between ≥ 30 kg/m2 and 39.9 kg/m2 [n = 822 (MetS- = 375, MetS+ = 477)], and Group 4 BMI ≥ 40 kg/m2 [n = 88 (MetS- = 27, MetS+ = 61)]. RESULTS: Carotid intima media thickness was higher in the individuals with MetS compared to their normal counterparts. Furthermore, the subgroup analysis showed that CIMT values in Group 1 (0.55±0.18 vs 0.82±0.70; p < 0.001), Group 2 (0.59±0.20 vs 0.68±0.18; p < 0.001) and Group 3 (0.61±0.15 vs 0.65±0.18; p < 0.001) were significantly higher in subjects with MetS compared to their normal counterparts, whereas the values were similar in Group 4 (0.62±0.13 vs 0.65±0.17; p = 0.363). CONCLUSIONS: Carotid intima media thickness of overweight, obese and normal weight individuals without MetS were lower than their counterparts with MetS. MetS had no impact on CIMT in morbid obese individuals possibly due to established insulin resistance earlier than MetS.


Subject(s)
Carotid Arteries/pathology , Carotid Intima-Media Thickness , Metabolic Syndrome/complications , Obesity/complications , Adolescent , Adult , Aged , Aged, 80 and over , Body Mass Index , Case-Control Studies , Female , Follow-Up Studies , Humans , Insulin Resistance , Male , Metabolic Syndrome/physiopathology , Middle Aged , Obesity, Morbid/complications , Overweight/complications , Prospective Studies , Risk Factors , Young Adult
2.
Br Poult Sci ; 44(3): 419-26, 2003 Jul.
Article in English | MEDLINE | ID: mdl-12964626

ABSTRACT

1. This study was conducted to determine the effects of starter and grower diets with differing crude protein (CP) and metabolisable energy (ME) concentrations on the body weight (BW), live weight gain (LWG), feed consumption (FC), feed conversion ratio (FCR), and carcase, breast+back, rump, wing, neck and abdominal fat weights of chukar partridge raised in captivity. 2. Chukar partridges were fed on starter diets containing 4 concentrations of CP (160, 200, 240, 280 g/kg) and 4 concentrations of ME (10.9, 11.7, 12.6, 13.4 MJ/kg) from hatch to 8 weeks of age; they were fed on grower diets containing 4 concentrations of CP (150, 175, 200, 225 g/kg) and 4 concentrations of ME (11.9, 12.6, 13.2, 13.8 MJ/kg) from 9 to 16 weeks of age. All diets contained at least 5.5 g/kg methionine, 15 g/kg lysine and 10 g/kg methionine+cystine. Sixteen starter and 16 grower diets were arranged in a 4 x 4 factorial design with 4 levels of CP and 4 levels of ME. Each treatment was replicated three times with each replicate consisting of 5 males and 5 females. 3. Partridges fed on a starter diet containing 160 g CP/kg were significantly lighter at 8 weeks of age than those in groups given diets containing a higher CP. However, at 16 weeks of age, the differences in BW among treatments had disappeared. Throughout, there were no significant effects of ME concentration on BW and LWG. 4. The daily mean FC for the 0 to 8 week and 0 to 16 week periods was not affected by dietary CP concentration. For the 9 to 16 week period, the partridges fed on a grower diet containing 225 g CP/kg consumed more feed than those given a diet containing 175 g CP/kg. 5. The highest FCR for the 0 to 8 week period was in partridges fed on a starter diet containing 160 g CP/kg. For the 9 to 16 week period, the lowest FCR was in partridges fed on a grower diet containing 150 g CP/kg. For the 0 to 16 week period, there was not a significant effect of dietary CP concentration on FCR. The daily mean FC and the FCR for the 0 to 8, 9 to 16 and 0 to 16 week periods decreased when the ME concentration of the starter and grower diets increased. 6. The carcase, rump and breast+back weights of the male partridges increased when the ME content of the diets increased. Weights of all carcase components of the male partridges were significantly greater than those of the carcase components of the females. 7. There were no significant interactions between CP and ME concentrations on BW, LWG, FC, FCR and carcase characteristics. 8. We conclude that the starter diet for chukar partridges raised for meat production should contain at least 200 g CP/kg, 11.7 MJ ME/kg, and the grower diet should contain 150 g CP/kg, 12.6 MJ ME/kg.


Subject(s)
Birds/growth & development , Body Composition/drug effects , Dietary Proteins/administration & dosage , Energy Intake/physiology , Meat/standards , Age Factors , Animal Feed , Animal Nutritional Physiological Phenomena , Animals , Birds/metabolism , Dose-Response Relationship, Drug , Energy Metabolism , Female , Male , Nutritional Requirements , Random Allocation , Sex Factors , Weight Gain/drug effects
3.
Cancer Res ; 61(3): 916-20, 2001 Feb 01.
Article in English | MEDLINE | ID: mdl-11221882

ABSTRACT

The role of the Jun family of proteins (c-Jun, JunB, and JunD) in oncogenesis has been extensively studied, but the distinct biological roles of each Jun protein is not known. For example, whereas c-Jun can transform primary cells in cooperation with an activated ras oncogene, JunD antagonizes ras-mediated transformation. We have discovered that two isoforms of the JunD transcription factor are ubiquitously expressed, resulting from use of an alternative translation start codon within the JunD mRNA. Here we report the first characterized functional difference between these JunD isoforms; only the full-length isoform of JunD binds to the Menin tumor suppressor protein. Furthermore, Menin suppresses transcriptional activity of the full-length but not the truncated isoform of JunD, which identifies the full-length JunD isoform as a functional target of Menin.


Subject(s)
Neoplasm Proteins/metabolism , Proto-Oncogene Proteins c-jun/metabolism , Proto-Oncogene Proteins , Animals , CHO Cells/metabolism , Cricetinae , Genes, Tumor Suppressor , Mice , Neoplasm Proteins/genetics , Phosphorylation , Point Mutation , Protein Binding , Protein Isoforms , Proto-Oncogene Proteins c-jun/antagonists & inhibitors , Proto-Oncogene Proteins c-jun/genetics , Recombinant Proteins/genetics , Recombinant Proteins/metabolism , Transcriptional Activation , Transfection
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