Biomedical subjects

J Hallgrimsson

Publications and source records attributed to J Hallgrimsson.

17 recordsLinked to original sources

PubMed2000

Dietary cod liver oil decreases arachidonic acid in rat gastric mucosa and increases stress-induced gastric erosions.

The purpose of this study was to examine the influence of long-term feeding of dietary fat rich in either n-3 or n-6 fatty acids on the availability of arachidonic acid (20:4n-6) in major phospholipids of gastric mucosa in rats. Three groups of male Wistar rats were fed either a standard diet, a cod liver oil-enriched diet (10% by weight), or a corn oil-enriched diet (10% by weight) for 8 mon. Dietary cod liver oil significantly reduced the level of 20:4n-6 in phosphatidylcholine (PC) and in phosphatidylethanolamine (PE) of gastric mucosa. The loss of 20:4n-6 was compensated for by eicosapentaenoic acid (20:5n-3) in PC, whereas the decrease in 20:4n-6 in PE corresponded to the increase in three n-3 fatty acids: 20:5n-3, docosapentaenoic acid (22:5n-3), and docosahexaenoic acid (22:6n-3). The level of 20:5n-3 was higher than the level of 22:6n-3 both in PC and PE of mucosa in rats fed cod liver oil. Diets supplemented with corn oil increased the level of 18:2n-6 but decreased the monoene fatty acids 16:1 and 18:1n-7 in PC but not in PE of gastric mucosa. The 20:4n-6 levels of both PC and PE were markedly reduced by dietary cod liver oil, to about one-third of control levels. Similar changes were also observed in the stomach wall. Gastric erosions were observed in all rats exposed to restriction stress, but this form of stress induced twice the number of erosions in rats fed fish oil compared to control rats or rats fed corn oil. We conclude that a diet rich in fish oil altered the balance between n-6 and n-3 fatty acids in major gastric mucosal phospholipids, markedly reduced the availability of 20:4n-6, and increased the incidence of gastric erosions induced by restriction or emotional stress.

Animals↗

PubMed1998

Mapping loss of heterozygosity at chromosome 13q: loss at 13q12-q13 is associated with breast tumour progression and poor prognosis.

Several chromosome regions exhibit loss of heterozygosity (LOH) in human breast carcinoma and are thought to harbour tumour suppressor genes (TSG). At chromosome 13q, two TSGs have been identified, RB1 at 13q14 and BRCA2 at 13q12-q13. In this study, 139 sporadic breast tumours were analysed with 18 polymorphic microsatellite markers for detailed mapping of LOH at chromosome 13q and evaluation of an association with known progression factors. LOH with at least one marker was observed in 71 (51%) of the tumours analysed. The deletion mapping indicated three LOH target regions, 13q12-q13, 13q14 and 13q31-q34. LOH at chromosome 13q12-q13 was associated with low progesterone receptor content, a high S phase fraction and aneuploidy. Multivariate analysis adjusting for lymph node involvement and S phase fraction showed that patients with tumours exhibiting LOH at 13q12-q13 have a 3-4-fold increased risk of recurrence and death compared with other patients. Our results suggest there are at least three separate LOH target regions at chromosome 13q and inactivation of one or more genes at chromosome 13q12-q13 results in poor prognosis for breast cancer patients.

Aneuploidy↗

PubMed1997

Topoisomerase II alpha expression in normal, inflammatory, and neoplastic conditions of the gastric and colonic mucosa.

Topoisomerase II alpha (TP) excises and reconnects double-stranded super-coiled DNA during the replicative cell cycle. We studied the localization of TP and Ki-67 in inflammatory and neoplastic mucosal lesions of the stomach and of TP in similar conditions of the colon. TP expression was correlated with tumor stage, grade, and survival time in the colonic tumors to evaluate its potential utility as a predictive marker for clinical outcome. Forty-three sections of chronic gastritis, lesions indefinite for dysplasia, low- and high-grade dysplasia, and gastric adenocarcinomas were immunostained with antibody against TP and Ki-67. For the colon, 71 sections of normal mucosa, chronic colitis, hyperplastic polyps, adenomas, and carcinomas were examined; fresh tissue was analyzed by flow cytometry. Expression of TP in non-neoplastic gastric mucosa was maximal in neck/foveolar cells and focal in surface and deep gland cells. Increased surface and deep gland positivity was found in low-grade dysplasia and a diffuse distribution of positive cells in high-grade dysplasia and carcinoma. The Ki-67 staining pattern was similar. TP in non-neoplastic colon was restricted to the lower crypt zone; it was greatly expanded in the surface/upper crypt region in adenomas and was diffuse in carcinomas. Flow cytometric analysis revealed TP expression mainly in the S and G2/M phase, with higher labeling index in tumors. There was no correlation of TP with stage, grade, or survival times in the colonic tumors. Staining for TP and Ki-67 might help in the distinction of inflammatory and neoplastic lesions of the stomach and colon.

Antigens, Neoplasm↗

PubMed1994

Racial variation in the O-acetylation phenotype of human colonic mucosa.

O-acetylated and non-O-acetylated sialoglycoproteins can be distinguished by the mPAS (mild periodic acid-Schiff) histochemical technique. Individual adults show one of three different patterns of staining of large intestinal mucosa: uniformly mPAS-positive, uniformly mPAS-negative, or mPAS-negative with scattered mPAS-positive crypts. To test our hypothesis that these variations are the result of a single autosomal gene (oat) polymorphism, we have studied the frequency of the three patterns of staining in a total of 435 adult colon specimens from six geographically separate populations: British, South African blacks, Icelanders, Japanese, Hong Kong Chinese, and Bahrainis. The distribution of the three types of staining fell into two groups. In Japanese and Chinese, uniformly mPAS-positive cases were much more frequent than uniformly mPAS-negative cases; this distribution differed significantly (chi 2, P < 0.001) from that in non-Sino-Japanese, where the uniformly mPAS-positive phenotype was much less frequently found than the uniformly mPAS-negative phenotype. In neither of the groups did the frequency of the three phenotypes differ significantly from that predicted for a single gene polymorphism by the Hardy-Weinberg law. The variation in staining patterns between populations is consistent with variation in frequency of a single polymorphic autosomal gene (oat) controlling O-acetylation of sialic acid, probably by an O-acetyl transferase enzyme. Loss of function mutation in the high acetylator gene (oata) in a colonic crypt stem cell in heterozygous individuals would account for the scattered discordant crypts. Gene frequencies for a variety of enzymes differ between the Sino-Japanese and non-Sino-Japanese races.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylation↗

PubMed1992

The prevalence of hypertrophic cardiomyopathy in men: an echocardiographic population screening study with a review of death records.

The purpose of this study was to estimate the prevalence of hypertrophic cardiomyopathy (HCM) in 3607 men from the Reykjavik study of 1979-81. Of these, 452 men had an abnormal (group A) and 3155 a normal electrocardiogram. An echocardiographic control group of 128 men was selected from cohorts with a normal electrocardiogram (group B). Until 1987, 189 deaths had occurred, 59 from group A and 130 from cohorts with a normal ECG including 4 from group B. To identify subjects with HCM, survivors of groups A and B were examined by echocardiography and by review of all autopsy data and death certificates. HCM was found in 14 subjects from group A but none in group B. Two additional cases were found at autopsy in cohorts with a normal ECG. The prevalence of HCM in men with an abnormal and normal ECG was 3.6% and 0.8%, respectively. The overall prevalence was calculated to be 1.1% with a 95% confidence interval of 0.3-3.2%. Men with HCM reported more symptoms than others in groups A and B (P < 0.05-0.001). 25% were without symptoms. Asymptomatic ventricular arrhythmias were detected by Holter monitoring in 45% of men with HCM. The total annual mortality was 1.6% compared with 0.5% in the group with a normal ECG (P < 0.001).

Adult↗

PubMed1988

Arachidonic acid level of non-esterified fatty acids and phospholipids in serum and heart muscle of patients with fatal myocardial infarction.

The relationship between non-esterified fatty acids (NEFA) in serum and heart muscle was examined in 15 patients who died of myocardial infarction (MI) and seven people who died suddenly in accidents. There was no correlation between NEFA levels of serum and non-infarcted cardiac muscle in patients with fatal MI. No significant difference was encountered in cardiac NEFA content between patients with fatal MI and people who died in accidents. The phospholipid (PL) content was significantly lower in patients with fatal MI than observed in people who died in accidents. The arachidonic acid (20:4 (n-6)) concentration of serum NEFA was significantly lower in patients with fatal MI compared to normal subjects. The cardiac NEFA and PL in patients with fatal MI contained significantly lower percentage levels of arachidonic acid compared to people who died in accidents. The results indicate that the death of the MI patients was not accompanied by elevated cardiac NEFA levels.

Adolescent↗

PubMed1976

The role of myocardial membrane lipids in the development of cardiac necrosis.

1. The fatty acid composition of cardiac membrane lipids is influenced by age, sex, diet and other factors. 2. The relative amounts of various polyunsaturated fatty acids in cardiac lipids influence markedly the development of myocardial necrosis and mortality following overstimulation with isoproterenol. 3. The availability and metabolism of arachidonic acid may play an important role in regulation of cardiac metabolism.

Adenosine Triphosphate↗

PubMed1976

Prostaglandins and polyunsaturated fatty acids in heart muscle.

1. Dietary lipids modify fatty acid composition of cardiac lipids. Polyunsaturated fatty acids replace less unsaturated fatty acids in phospholipds. 2. Mortality following isoproterenol-stimulation increase with decreasing amount of arachidonic acid in cardiac phospholipds. 3. In normal human heart muscle the ratio of essential, omega-6/nonessential, omega-3 fatty acids diminshes from age 17 to age 50 years. 4. In sudden cardiac death the ratio of prostaglandin substrate, C20:4, to prostaglandin inhibitor, C22:6, is frequently much higher than expected.

Age Factors↗

PubMed1975