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1,3-Butadiene: exposure estimation, hazard characterization, and exposure-response analysis.

https://arctichealth.org/en/permalink/ahliterature186649
Source
J Toxicol Environ Health B Crit Rev. 2003 Jan-Feb;6(1):55-83
Publication Type
Article
Author
K. Hughes
M E Meek
M. Walker
R. Beauchamp
Author Affiliation
Existing Substances Division, Environmental Health Directorate, Health Canada, Environmental Health Centre, Tunney's Pasture PL0802B1, Ottawa, Ontario, Canada K1A 0L2.
Source
J Toxicol Environ Health B Crit Rev. 2003 Jan-Feb;6(1):55-83
Language
English
Publication Type
Article
Keywords
Animals
Butadienes - metabolism - toxicity
Canada - epidemiology
Carcinogens, Environmental - toxicity
Environmental Exposure
Hazardous Substances - toxicity
Humans
Mutagens - toxicity
Neoplasms - chemically induced - epidemiology
Occupational Diseases - chemically induced - epidemiology
Risk assessment
Abstract
1,3-Butadiene has been assessed as a Priority Substance under the Canadian Environmental Protection Act. The general population in Canada is exposed to 1,3-butadiene primarily through ambient air. Inhaled 1,3-butadiene is carcinogenic in both mice and rats, inducing tumors at multiple sites at all concentrations tested in all identified studies. In addition, 1,3-butadiene is genotoxic in both somatic and germ cells of rodents. It also induces adverse effects in the reproductive organs of female mice at relatively low concentrations. The greater sensitivity in mice than in rats to induction of these effects by 1,3-butadiene is likely related to species differences in metabolism to active epoxide metabolites. Exposure to 1,3-butadiene in the occupational environment has been associated with the induction of leukemia; there is also some limited evidence that 1,3-butadiene is genotoxic in exposed workers. Therefore, in view of the weight of evidence of available epidemiological and toxicological data, 1,3-butadiene is considered highly likely to be carcinogenic, and likely to be genotoxic, in humans. Estimates of the potency of butadiene to induce cancer have been derived on the basis of both epidemiological investigation and bioassays in mice and rats. Potencies to induce ovarian effects have been estimated on the basis of studies in mice. Uncertainties have been delineated, and, while there are clear species differences in metabolism, estimates of potency to induce effects are considered justifiably conservative in view of the likely variability in metabolism across the population related to genetic polymorphism for enzymes for the critical metabolic pathway.
PubMed ID
12587254 View in PubMed
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The 1 alpha-hydroxylase locus is not linked to calcium stone formation or calciuric phenotypes in French-Canadian families.

https://arctichealth.org/en/permalink/ahliterature206213
Source
J Am Soc Nephrol. 1998 Mar;9(3):425-32
Publication Type
Article
Date
Mar-1998
Author
P. Scott
D. Ouimet
Y. Proulx
M L Trouvé
G. Guay
B. Gagnon
L. Valiquette
A. Bonnardeaux
Author Affiliation
Service de Néphrologie, Hôpital Maisonneuve-Rosemont, Montreal, Quebec, Canada.
Source
J Am Soc Nephrol. 1998 Mar;9(3):425-32
Date
Mar-1998
Language
English
Publication Type
Article
Keywords
25-Hydroxyvitamin D3 1-alpha-Hydroxylase - genetics - metabolism
Adult
Calcium - urine
Canada
European Continental Ancestry Group - genetics
Family Health
Female
France - ethnology
Genetic Linkage
Genetic Markers - genetics
Humans
Kidney Calculi - enzymology - genetics
Male
Middle Aged
Nuclear Family
Pedigree
Phenotype
Vitamin D - blood
Abstract
Calcium urolithiasis is often associated with increased intestinal absorption and urine excretion of calcium, and has been suggested to result from increased vitamin D production. The role of the enzyme 1 alpha-hydroxylase, the rate-limiting step in active vitamin D production, was evaluated in 36 families, including 28 sibships with at least a pair of affected sibs, using qualitative and quantitative trait linkage analyses. Sibs with a verified calcium urolithiasis passage (n = 117) had higher 24-h calciuria (P = 0.03), oxaluria (P = 0.02), fasting and postcalcium loading urine calcium/creatinine (Ca/cr) ratios (P = 0.008 and P = 0.002, respectively), and serum 1,25(OH)2 vitamin D levels (P = 0.02) compared with nonstone-forming sibs (n = 120). Markers from a 9-centiMorgan interval encompassing the VDD1 locus on chromosome 12q13-14 (putative 1 alpha-hydroxylase) were analyzed in 28 sibships (146 sib pairs) of single and recurrent stone formers and in 14 sibships (65 sib pairs) with recurrent-only (> or = 3 episodes) stone-forming sibs. Two-point and multipoint analyses did not reveal excess in alleles shared among affected sibs at the VDD1 locus. Linkage of stone formation to the VDD1 locus could be excluded, respectively, with a lambda d of 2.0 (single and recurrent stone formers) and 3.25 (recurrent stone formers). Quantitative trait analyses revealed no evidence for linkage to 24-h calciuria and oxaluria, serum 1,25(OH)2 vitamin D levels, and Ca/cr ratios. This study shows absence of linkage of the putative 1 alpha-hydroxylase locus to calcium stone formation or to quantitative traits associated with idiopathic hypercalciuria. In addition, there is coaggregation of calciuric and oxaluric phenotypes with stone formation.
PubMed ID
9513904 View in PubMed
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1H-MRS Measured Ectopic Fat in Liver and Muscle in Danish Lean and Obese Children and Adolescents.

https://arctichealth.org/en/permalink/ahliterature273208
Source
PLoS One. 2015;10(8):e0135018
Publication Type
Article
Date
2015
Author
Cilius Esmann Fonvig
Elizaveta Chabanova
Ehm Astrid Andersson
Johanne Dam Ohrt
Oluf Pedersen
Torben Hansen
Henrik S Thomsen
Jens-Christian Holm
Source
PLoS One. 2015;10(8):e0135018
Date
2015
Language
English
Publication Type
Article
Keywords
Adolescent
Anthropometry
Blood Glucose - analysis
Blood pressure
Body mass index
Body Weight
Cardiovascular Diseases - physiopathology
Child
Cross-Sectional Studies
Denmark
Dyslipidemias - blood
Fatty Liver - pathology
Female
Humans
Insulin - blood
Insulin Resistance
Intra-Abdominal Fat - pathology
Linear Models
Lipids - blood
Liver - metabolism - pathology
Male
Muscles - pathology
Overweight
Pediatric Obesity - blood - pathology
Proton Magnetic Resonance Spectroscopy
Puberty
Sex Factors
Subcutaneous Fat - pathology
Abstract
This cross sectional study aims to investigate the associations between ectopic lipid accumulation in liver and skeletal muscle and biochemical measures, estimates of insulin resistance, anthropometry, and blood pressure in lean and overweight/obese children.
Fasting plasma glucose, serum lipids, serum insulin, and expressions of insulin resistance, anthropometry, blood pressure, and magnetic resonance spectroscopy of liver and muscle fat were obtained in 327 Danish children and adolescents aged 8-18 years.
In 287 overweight/obese children, the prevalences of hepatic and muscular steatosis were 31% and 68%, respectively, whereas the prevalences in 40 lean children were 3% and 10%, respectively. A multiple regression analysis adjusted for age, sex, body mass index z-score (BMI SDS), and pubertal development showed that the OR of exhibiting dyslipidemia was 4.2 (95%CI: [1.8; 10.2], p = 0.0009) when hepatic steatosis was present. Comparing the simultaneous presence of hepatic and muscular steatosis with no presence of steatosis, the OR of exhibiting dyslipidemia was 5.8 (95%CI: [2.0; 18.6], p = 0.002). No significant associations between muscle fat and dyslipidemia, impaired fasting glucose, or blood pressure were observed. Liver and muscle fat, adjusted for age, sex, BMI SDS, and pubertal development, associated to BMI SDS and glycosylated hemoglobin, while only liver fat associated to visceral and subcutaneous adipose tissue and intramyocellular lipid associated inversely to high density lipoprotein cholesterol.
Hepatic steatosis is associated with dyslipidemia and liver and muscle fat depositions are linked to obesity-related metabolic dysfunctions, especially glycosylated hemoglobin, in children and adolescents, which suggest an increased cardiovascular disease risk.
Notes
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PubMed ID
26252778 View in PubMed
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1st European Congress on Parenteral and Enteral Nutrition, Stockholm, Sweden, September 2-5, 1979.

https://arctichealth.org/en/permalink/ahliterature62432
Source
Acta Chir Scand Suppl. 1980;498:1-160
Publication Type
Article
Date
1980
Source
Acta Chir Scand Suppl. 1980;498:1-160
Date
1980
Language
English
Publication Type
Article
Keywords
Animals
Humans
Metabolism
Nutrition
Parenteral Nutrition
Parenteral Nutrition, Total
PubMed ID
6776724 View in PubMed
Less detail

1st European Congress on Parenteral and Enteral Nutrition. Stockholm, Sweden. September 2--5, 1979.

https://arctichealth.org/en/permalink/ahliterature62440
Source
JPEN J Parenter Enteral Nutr. 1979 Jul-Aug;3(4):289-316
Publication Type
Conference/Meeting Material
Source
JPEN J Parenter Enteral Nutr. 1979 Jul-Aug;3(4):289-316
Language
English
Publication Type
Conference/Meeting Material
Keywords
Congresses
Enteral Nutrition
Europe
Humans
Metabolism
Nutrition
Parenteral Nutrition
Sweden
PubMed ID
39184 View in PubMed
Less detail

A 1-year randomized study to evaluate the effects of a dose reduction in oral contraceptives on lipids and carbohydrate metabolism: 20 microg ethinyl estradiol combined with 100 microg levonorgestrel.

https://arctichealth.org/en/permalink/ahliterature176202
Source
Contraception. 2005 Feb;71(2):111-7
Publication Type
Article
Date
Feb-2005
Author
Sven O Skouby
Jan Endrikat
Bernd Düsterberg
Werner Schmidt
Christoph Gerlinger
Jens Wessel
Henri Goldstein
Joergen Jespersen
Author Affiliation
Department of Obstetrics and Gynecology, Frederiksberg Hospital, University of Copenhagen, DK 2000 Copenhagen F, Denmark. sven.skouby@fh.hosp.dk
Source
Contraception. 2005 Feb;71(2):111-7
Date
Feb-2005
Language
English
Publication Type
Article
Keywords
Adult
Blood Glucose - metabolism
C-Peptide - blood
Carbohydrate Metabolism - drug effects
Cholesterol, HDL - blood
Cholesterol, LDL - blood
Contraceptive Agents, Female - administration & dosage - pharmacology
Contraceptives, Oral, Combined - administration & dosage - pharmacology
Denmark
Dose-Response Relationship, Drug
Ethinyl Estradiol - administration & dosage - pharmacology
Fatty Acids, Nonesterified - blood
Female
Humans
Insulin - blood
Levonorgestrel - administration & dosage - pharmacology
Lipid Metabolism - drug effects
Prospective Studies
Time Factors
Treatment Outcome
Triglycerides - blood
Abstract
To evaluate the impact on lipid and carbohydrate variables of a combined one-third ethinyl estradiol (EE)/levonorgestrel (LNG) dose reduction in oral contraceptives.
In an open-label, randomized study, a dose-reduced oral contraceptive containing 20 microg EE and 100 microg LNG (20 EE/100 LNG) was compared with a reference preparation containing 30 microg EE and 150 microg LNG (30 EE/150 LNG). One-year data from 48 volunteers were obtained.
We found a decrease of HDL2 cholesterol and increases of low-density lipoprotein cholesterol, very low-density lipoprotein cholesterol and total triglycerides in both treatment groups from baseline to the 13th treatment cycle. Although for four of six variables, the changes in the 20 EE group were lower compared with the 30 EE group, none of the differences between the two treatments were statistically significant. The median values for the fasting levels of insulin, C-peptide and free fatty acids slightly increased or remained unchanged while the fasting glucose levels slightly decreased after 13 treatment cycles. While the glucose area under the curve (AUC) (0-3 h) was similar in both groups during the OGTT, the insulin AUC(0-3 h) was less increased in the 20 EE/100 LNG group compared with the 30 EE/150 LNG group. None of the differences between the treatment groups for any of the carbohydrate metabolism variables were statistically significant at any time point. Both study treatments were safe and well tolerated by the volunteers.
Similar effects on the lipid and carbohydrate profiles were found for both preparations. The balanced one-third EE dose reduction in this new oral contraceptive caused slightly lower, but insignificant, changes in the lipid and carbohydrate variables compared with the reference treatment.
PubMed ID
15707560 View in PubMed
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2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) poisoning in Victor Yushchenko: identification and measurement of TCDD metabolites.

https://arctichealth.org/en/permalink/ahliterature95137
Source
Lancet. 2009 Oct 3;374(9696):1179-85
Publication Type
Article
Date
Oct-3-2009
Author
Sorg O.
Zennegg M.
Schmid P.
Fedosyuk R.
Valikhnovskyi R.
Gaide O.
Kniazevych V.
Saurat J-H
Author Affiliation
Dermato-Toxicology, Swiss Centre for Applied Human Toxicology, and Department of Dermatology, University Hospital, Geneva, Switzerland.
Source
Lancet. 2009 Oct 3;374(9696):1179-85
Date
Oct-3-2009
Language
English
Publication Type
Article
Keywords
Adipose Tissue - chemistry
Biopsy
Drug Residues - analysis - metabolism
Fatal Outcome
Feces - chemistry
Forensic Medicine - methods
Half-Life
Homicide
Humans
Male
Middle Aged
Politics
Substance Abuse Detection - methods
Sweat - chemistry
Tetrachlorodibenzodioxin - analysis - chemistry - metabolism - poisoning
Time Factors
Ukraine
Abstract
BACKGROUND: 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) has a long half-life of 5-10 years in human beings as a result of its high lipophilicity, and little or no metabolism. We monitored TCDD, its form, distribution, and elimination in Victor Yushchenko after he presented with severe poisoning. METHODS: In late December, 2004, a patient presented with TCDD poisoning; the levels in his blood serum (108000 pg/g lipid weight) were more than 50 000-fold greater than those in the general population. We identified TCDD and its metabolites, and monitored their levels for 3 years using gas chromatography and high-resolution mass spectrometry in samples of blood serum, adipose tissue, faeces, skin, urine, and sweat, after they were extracted and cleaned with different organic solvents. FINDINGS: The amount of unmodified TCDD in the samples that were analysed accounted for about 60% of TCDD eliminated from the body during the same period. Two TCDD metabolites-2,3,7-trichloro-8-hydroxydibenzo-p-dioxin and 1,3,7,8-tetrachloro-2-hydroxydibenzo-p-dioxin-were identified in the faeces, blood serum, and urine. The faeces contained the highest concentration of TCDD metabolites, and were the main route of elimination. Altogether, the different routes of elimination of TCDD and its metabolites accounted for 98% of the loss of the toxin from the body. The half-life of TCDD in our patient was 15.4 months. INTERPRETATION: This case of poisoning with TCDD suggests that the design of methods for routine assessment of TCDD metabolites in human beings should be a main aim of TCDD research in the metabolomic era. FUNDING: University of Geneva Dermatology Fund, and Swiss Centre for Applied Human Toxicology.
Notes
Comment In: Lancet. 2009 Oct 3;374(9696):1131-219660808
PubMed ID
19660807 View in PubMed
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2,8-dihydroxyadeninuria: are there no cases in Scandinavia?

https://arctichealth.org/en/permalink/ahliterature175743
Source
Scand J Urol Nephrol. 2005;39(1):82-6
Publication Type
Article
Date
2005
Author
Margret Arnadottir
Thröstur Laxdal
Bergljot Halldorsdottir
Author Affiliation
Department of Internal Medicine, Landspitali University Hospital Hringbraut, Reykjavik, Iceland. margarn@landspitali.is
Source
Scand J Urol Nephrol. 2005;39(1):82-6
Date
2005
Language
English
Publication Type
Article
Keywords
Adenine - analogs & derivatives - metabolism - urine
Adenine Phosphoribosyltransferase - deficiency - genetics
Heterozygote
Homozygote
Humans
Mutation
Renal Insufficiency - etiology
Scandinavia - epidemiology
Urinary Calculi - etiology - urine
Abstract
Homozygosity or mixed heterozygosity for mutations in the adenine phosphoribosyltransferase gene cause enzyme deficiency directing adenine through an alternative metabolic pathway. This results in the production of 2,8-dihydroxyadenine, which is actively secreted into the urine. 2,8-dihydroxyadenine is insoluble at physiological urinary pH but as marked supersaturation is possible the manifestations differ: there may be minimal consequences, there may be infiltration of the tubulointerstitial tissue with acute or chronic damage or there may be stone formation in the urinary tract. Effective treatment can be offered and therefore the prognosis depends upon the renal function at diagnosis. Treatment consists of adequate fluid intake, a low-purine diet and administration of allopurinol. Urinary 2,8-dihydroxyadenine crystals are easily recognized under a microscope. The diagnosis of 2,8-dihydroxyadeninuria can be confirmed by estimation of adenine phosphoribosyltransferase activity in erythrocyte lysates. More than 300 cases of 2,8-dihydroxyadeninuria have been diagnosed worldwide, most of them in Japan, France and Iceland. One case has been reported in Finland but there have been no reports from the Scandinavian peninsula or from Denmark. The relevant mutations may be very rare in these countries but underdiagnosis is also possible.
PubMed ID
15764278 View in PubMed
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2B or not to be--the 45-year saga of the Montreal Platelet Syndrome.

https://arctichealth.org/en/permalink/ahliterature140851
Source
Thromb Haemost. 2010 Nov;104(5):903-10
Publication Type
Article
Date
Nov-2010
Author
Man-Chiu Poon
Margaret L Rand
Shannon C Jackson
Author Affiliation
Division of Hematology and Hematologic Malignancies, Department of Medicine, University of Calgary, Calgary, Alberta, Canada. mcpoon@ucalgary.ca
Source
Thromb Haemost. 2010 Nov;104(5):903-10
Date
Nov-2010
Language
English
Publication Type
Article
Keywords
Blood Coagulation - genetics
Blood Coagulation Tests - history
Blood Platelet Disorders - blood - genetics - history
Blood Platelets - metabolism - pathology
Canada
Genetic Predisposition to Disease
History, 20th Century
Humans
Mutation
Pedigree
Phenotype
Platelet Function Tests - history
Syndrome
von Willebrand Disease, Type 2 - blood - genetics - history
von Willebrand Factor - genetics - history
Abstract
Over 45 years ago, Montreal Platelet Syndrome was first described as a rare inherited platelet disorder characterised by macrothrombocytopenia with spontaneous platelet clumping, abnormal platelet shape change upon stimulation and a defect in platelet calpain. This syndrome has now been reclassified as type 2B von Willebrand disease with the V1316M VWF mutation in the only kindred ever reported. We herein revisit the historical platelet characteristics originally described in Montreal Platelet Syndrome in light of the new diagnosis. This paper will review the 45-year saga of Montreal Platelet Syndrome, a story that highlights the value of revisiting a rare diagnosis to look for a more common explanation.
PubMed ID
20838735 View in PubMed
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13719 records – page 1 of 1372.