Results for contributor translation from Arabic to English

contributor laurence edward sigler.
contributor laurence edward sigler.

(symonds was a major contributor).
(symonds was a major contributor).

- contributor and editor for chapter 8: c. reichert
— contributor and editor for chapter 8: c. reichert

contributor to the development of the southern african higher educational
the beneficiary impact study, an evaluation of the land management and conservation project of the government of lesotho, in world bank report no. 15186, southern africa department, agriculture and environment division, p. 42, december 1995.

contributor to the proceedings of the american society of international law, 1966, 1981.
contributor to the proceedings of the american society of international law, 1966, 1981.

united nations publication e.93.v.16, new york (contributor).
united nations publication e.93.v.16, new york (contributor).

responding to health emergencies and disasters, article contributor “who's who?
responding to health emergencies and disasters, article contributor “who's who?

the following provides a synopsis of some of the seminars and workshops which ohchr has been a contributor to:
the following provides a synopsis of some of the seminars and workshops which ohchr has been a contributor to:

lord bonomy is a regular contributor to conferences on international child abduction and to judicial seminars on the role of the judge at the deutsche richterakademie.
lord bonomy is a regular contributor to conferences on international child abduction and to judicial seminars on the role of the judge at the deutsche richterakademie.

addressing rape in the legal system, a multidisciplinary training manual contributor, women's legal bureau, 2005.
addressing rape in the legal system, a multidisciplinary training manual contributor, women's legal bureau, 2005.

• co-editor with theodor hanf and contributor: lebanon in limbo, nomos, baden-baden, 2003.
* co-editor with theodor hanf and contributor: lebanon in limbo, nomos, baden-baden, 2003.

metabolic variables and basal substrate kinetics basal glucose and fatty acid kinetics. basal glucose and palmitate kinetics were not different between matched subjects within any of the 2 groups (table 2). insulin sensitivity. hepatic (fig. 1a), skeletal muscle (fig. 1b), and adipose tissue (fig. 1c) insulin sensitivity was lower in subjects with high than in those with normal ihtg content. however, no differences in insulin sensitivity measures were observed between subjects with low or high vat volume, when matched on ihtg content (fig. 1). fig. 1. fig. 1. hepatic (a), skeletal muscle (b), and adipose tissue (c) insulin sensitivity in subjects matched on visceral adipose tissue (vat) volume with either normal or high intrahepatic triglyceride (ihtg) content and subjects matched on ihtg content who had either ... vldl-tg kinetics. hepatic vldl-tg secretion rate was almost double in subjects with high than in those with normal ihtg content (23 ± 2 and 12 ± 1 μmol/min, respectively; p 10% of liver volume) (n = 10) or normal (≤5.5% of liver volume) (n = 10) ihtg content (table 1) (41). the range in vat volume was similar in both the normal (vat volume: 689–3,088 cm3) and the high (vat volume: 638–2,702 cm3) ihtg groups. each subject with normal ihtg and a given vat volume was matched with a subject from the high ihtg group on vat (within ≈20% of vat volume of the normal ihtg group). group 2 subjects (n = 20) were matched on ihtg content and had either low (n = 10) or high (n = 10) vat volume (table 1). subjects were separated into low and high vat volume groups by using the median value of all subjects (1,100 cm3) as the cut point for low and high vat volumes. subjects within groups were matched on age, sex, bmi, and percentage of body fat. we did not have knowledge of any outcome measures when the matches were performed. all subjects completed a comprehensive medical evaluation, which included a 2-h oral glucose tolerance test. no subject had any history or evidence of liver disease other than nafld, took medications that can affect metabolism or cause hepatic abnormalities, consumed >20 g/day of alcohol, or had diabetes. subjects gave their written informed consent before participating in this study, which was approved by the human research protection office of washington university school of medicine, st. louis, mo. body composition analyses. body fat mass (fm) and fat-free mass (ffm) were determined by using dual-energy x-ray absorptiometry (delphi-w densitometer, hologic). intraabdominal and abdominal s.c. adipose tissue volumes were quantified by magnetic resonance imaging (siemens; analyze 7.0 software, mayo foundation) (9) and ihtg content was measured by using proton magnetic resonance spectroscopy (siemens) as we have previously described (42). hyperinsulinemic–euglycemic clamp procedure. subjects were admitted to the intensive research unit at washington university school of medicine on the evening before the clamp procedure. at 0500 hours the following morning, after subjects fasted for 12 h overnight, a 2-stage hyperinsulinemic–euglycemic clamp procedure was started and continued for 9 h. insulin was infused at a rate of 20 mu·m−2 body-surface area (bsa)·min−1 during stage 1 (3–6 h) and at a rate of 50 mu·m−2 bsa·min−1 during stage 2 (6–9 h) of the clamp procedure (9, 43). [6,6-2h2]glucose, [2,2-2h2]palmitate, and 20% dextrose enriched to 2.5% with [6,6-2h2]glucose were infused to determine hepatic, skeletal muscle, and adipose tissue insulin sensitivity. tissue samples were obtained from s.c. abdominal adipose tissue and from the quadriceps femoris muscle 60 min after starting the glucose tracer infusion during the basal stage. a detailed description of the infusion protocol and of collection of tissues and blood samples is available in supporting information (si) materials and methods. vldl-tg kinetics study. one week after the hyperinsulinemic–euglycemic clamp procedure, subjects were readmitted to the intensive research unit on the evening before the vldl kinetics study. at 0600 hours the following morning, after subjects fasted for 12 h overnight, a bolus of [1,1,2,3,3-2h5]glycerol was injected, and a constant infusion of 2,2-2h2]palmitate was started and main
metabolic variables and basal substrate kinetics basal glucose and fatty acid kinetics. basal glucose and palmitate kinetics were not different between matched subjects within any of the 2 groups (table 2). insulin sensitivity. hepatic (fig. 1a), skeletal muscle (fig. 1b), and adipose tissue (fig. 1c) insulin sensitivity was lower in subjects with high than in those with normal ihtg content. however, no differences in insulin sensitivity measures were observed between subjects with low or high vat volume, when matched on ihtg content (fig. 1). fig. 1. fig. 1. hepatic (a), skeletal muscle (b), and adipose tissue (c) insulin sensitivity in subjects matched on visceral adipose tissue (vat) volume with either normal or high intrahepatic triglyceride (ihtg) content and subjects matched on ihtg content who had either ... vldl-tg kinetics. hepatic vldl-tg secretion rate was almost double in subjects with high than in those with normal ihtg content (23 ± 2 and 12 ± 1 μmol/min, respectively; p 10% of liver volume) (n = 10) or normal (≤5.5% of liver volume) (n = 10) ihtg content (table 1) (41). the range in vat volume was similar in both the normal (vat volume: 689–3,088 cm3) and the high (vat volume: 638–2,702 cm3) ihtg groups. each subject with normal ihtg and a given vat volume was matched with a subject from the high ihtg group on vat (within ≈20% of vat volume of the normal ihtg group). group 2 subjects (n = 20) were matched on ihtg content and had either low (n = 10) or high (n = 10) vat volume (table 1). subjects were separated into low and high vat volume groups by using the median value of all subjects (1,100 cm3) as the cut point for low and high vat volumes. subjects within groups were matched on age, sex, bmi, and percentage of body fat. we did not have knowledge of any outcome measures when the matches were performed. all subjects completed a comprehensive medical evaluation, which included a 2-h oral glucose tolerance test. no subject had any history or evidence of liver disease other than nafld, took medications that can affect metabolism or cause hepatic abnormalities, consumed >20 g/day of alcohol, or had diabetes. subjects gave their written informed consent before participating in this study, which was approved by the human research protection office of washington university school of medicine, st. louis, mo. body composition analyses. body fat mass (fm) and fat-free mass (ffm) were determined by using dual-energy x-ray absorptiometry (delphi-w densitometer, hologic). intraabdominal and abdominal s.c. adipose tissue volumes were quantified by magnetic resonance imaging (siemens; analyze 7.0 software, mayo foundation) (9) and ihtg content was measured by using proton magnetic resonance spectroscopy (siemens) as we have previously described (42). hyperinsulinemic–euglycemic clamp procedure. subjects were admitted to the intensive research unit at washington university school of medicine on the evening before the clamp procedure. at 0500 hours the following morning, after subjects fasted for 12 h overnight, a 2-stage hyperinsulinemic–euglycemic clamp procedure was started and continued for 9 h. insulin was infused at a rate of 20 mu·m−2 body-surface area (bsa)·min−1 during stage 1 (3–6 h) and at a rate of 50 mu·m−2 bsa·min−1 during stage 2 (6–9 h) of the clamp procedure (9, 43). [6,6-2h2]glucose, [2,2-2h2]palmitate, and 20% dextrose enriched to 2.5% with [6,6-2h2]glucose were infused to determine hepatic, skeletal muscle, and adipose tissue insulin sensitivity. tissue samples were obtained from s.c. abdominal adipose tissue and from the quadriceps femoris muscle 60 min after starting the glucose tracer infusion during the basal stage. a detailed description of the infusion protocol and of collection of tissues and blood samples is available in supporting information (si) materials and methods. vldl-tg kinetics study. one week after the hyperinsulinemic–euglycemic clamp procedure, subjects were readmitted to the intensive research unit on the evening before the vldl kinetics study. at 0600 hours the following morning, after subjects fasted for 12 h overnight, a bolus of [1,1,2,3,3-2h5]glycerol was injected, and a constant infusion of 2,2-2h2]palmitate was started and main