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L Berglund

Publications and source records attributed to L Berglund.

At least 109 records · Page 6Linked to original sources

Primary structure of EPV20, a secretory glycoprotein containing a previously uncharacterized type of domain.

A 20-kDa glycoprotein, EPV20, was isolated from bovine milk and characterized. The primary structure was determined by cDNA and protein sequencing combined with mass spectrometry. EPV20 is a 130-residue polypeptide synthesized with a 19-residue signal peptide. The function of EPV20 is unknown, but it displays 79% sequence similarity to a putative protein deduced from a human testis cDNA sequence designated HE1 (human epididymis clone 1) (Kirchhoff, C., 1992. EMBL/GeneBank/DDBJ Databases, accession number X67698). Northern blot analysis showed the bovine EPV20 to be expressed in kidney, spleen, liver and mammary gland, but remarkably not in bovine testis. The six Cys residues of EPV20 were found to be disulfide-linked in a 1-6, 2-3 and 4 5 pattern. This disulfide arrangement has been observed in other proteins, e.g. in human prostatic acid phosphatase, but the spacing between the cystines differs. Therefore, EPV20 represents a new structure among the large group of proteins containing domains with three disulfide bonds.

Amino Acid Sequence↗

Studies of the genetic variability of the coding region of the hepatocyte nuclear factor-4alpha in Caucasians with maturity onset NIDDM.

Mutations in the hepatocyte nuclear factor-4alpha (HNF-4alpha) gene cause the type 1 form of maturity onset diabetes of the young (MODY1). To address the question of whether genetic variability of HNF-4alpha is associated with late onset non-insulin-dependent diabetes mellitus (NIDDM) we have sequenced the coding region and intron/exon boundaries of the gene in 36 randomly recruited Danish NIDDM patients. Two nucleotide substitutions that changed the sequence of HNF-4alpha were identified: Thr/Ile130, which has been reported previously and a novel Val/Met255. The Val/Met 255 mutation was found in 4 of 477 Danish NIDDM patients and in none of 217 glucose tolerant control subjects; thus it cannot be excluded that this mutation may have an impact on NIDDM susceptibility. Among 509 NIDDM patients the allelic frequency of the Thr/Ile130 variant was 4.7% (95% confidence interval: 3.4-6.0%) compared to 1.9% (0.7-3.1%) among 239 control subjects (p = 0.008). However, in a population sample of 942 Swedish men with an average age of 70 years the allelic frequency of the variant was similar in 246 men with either impaired glucose tolerance (5.6% [2.6-8.6%]) or NIDDM (5.4% [2.7-8.1%]) as compared to 666 glucose tolerant men (5.1% [3.9-6.3%]). Also in a population sample of 369 young healthy Danes the prevalence of the codon 130 variant (4.7% [3.2-6.2%]) was similar to what was found in Swedish Caucasians. Thus, the allelic frequency of the Thr/Ile130 variant among the control subjects in the Danish case-control study deviates from the prevalence in the two other studies which is why we consider the significant association between the codon 130 variant and NIDDM an incidental finding. In glucose tolerant subjects the codon 130 variant in its heterozygous form had no major effect on glucose-induced insulin and C-peptide release although a tendency to a lower insulin secretion during an oral glucose tolerance test was seen in middle-aged subjects. In conclusion, variability in the coding region of the HNF-4alpha gene is not a common cause of NIDDM among whites of Danish ancestry. However, a Val/Met255 mutation was found exclusively in NIDDM patients (0.8% of cases) and functional as well as family segregation studies are needed to determine whether this HNF-4alpha variant is a NIDDM causing mutation.

Aged↗

On the interrelationship between hepatic carnitine, fatty acid oxidation, and triglyceride biosynthesis in nephrosis.

The nephrotic syndrome is associated with disturbances in plasma lipid pattern and metabolism. However, the reason for these perturbations is poorly understood. In the present study, we have investigated hepatic triglyceride metabolism in puromycin aminonucleoside-induced nephrotic syndrome in rats. Nephrotic rats displayed a 70% increase in hepatic triglyceride levels compared to controls (16.9 +/- 1.6 vs. 9.8 +/- 0.6 mumol/g liver; means +/- SEM, P < 0.01). The capacity for hepatic mitochondrial beta-oxidation of fatty acids was substantially elevated (80%). This was associated with a rise in the liver content of the fatty acid carrier carnitine (1.24 +/- 0.06 vs. 0.85 +/- 0.07 mumol/g dry weight, P < 0.05). A positive correlation between the levels of acetylcarnitine and acetyl-CoA was found in normal as well as in nephrotic rats, implying that carnitine plays an important role as an acetyl group acceptor in the liver under normo- and hyperlipidemic conditions. Changes in carnitine levels seem to be tightly coupled to the rate of fatty acid oxidation. There was a significant elevation in the activity of phosphatidate phosphohydrolase (E.C. 3.1.3.4) in liver microsomes from nephrotic rats (1.07 +/- 0.09 vs. 0.81 +/- 0.04 nmol/min.mg protein, P < 0.02). Hepatic very low density lipoprotein (VLDL)-triglyceride secretion rate was 18% higher in nephrotic rats than in controls. The results demonstrate a deranged hepatic triglyceride metabolism in nephrosis, with an increased hepatic triglyceride biosynthesis, a sizable accumulation of hepatic triglycerides, and only a modest increase in VLDL triglyceride secretion. In addition, mitochondrial beta-oxidation of fatty acids was enhanced, associated with an increased availability of carnitine.

Acetyl Coenzyme A↗

Bone loss in elderly women prevented by ultralow doses of parenteral 17beta-estradiol.

OBJECTIVES: Our purpose was to assess whether an ultralow dose of parental estradiol, aimed for treatment of vaginal atrophy, affects bone metabolism and bone density. STUDY DESIGN: Thirty healthy women > or = 60 years old were randomly assigned to a 6-month treatment with either an ultralow dose of parenteral estradiol (7.5 microg/24 hours) delivered by vaginal rings or no treatment in the proportion 2:1. RESULTS: Forearm bone density increased in estradiol users by 2.1% (95% confidence interval 0.4 to 3.8, p = 0.008), contrasting to a decrease in nonusers of -2.7% (95% confidence interval -5.9 to 0.4, p = 0.077). In analysis of variance the changes in the two study groups differed significantly (p = 0.0004). Consistently, serum alkaline phosphatases, bone-specific alkaline phosphatases, and osteocalcin concentrations decreased in the treatment group (8%, p = 0.019; 14%, p = 0.0006; and 9%, p = 0.02, respectively), suggesting reduced bone turnover. No significant changes were found in nonusers. CONCLUSION: Ultralow doses of estradiol may potentially prevent bone loss in women > or = 60 years old.

Administration, Intravaginal↗

Cardiovascular prognosis in relation to apolipoproteins and other lipid parameters in patients with stable angina pectoris treated with verapamil or metoprolol: results from the Angina Prognosis Study in Stockholm (APSIS).

Relationships between apolipoproteins and other lipid parameters and cardiovascular (CV) prognosis were evaluated in the Angina Prognosis Study In Stockholm (APSIS). Out of 809 patients with stable angina pectoris, lipid variables were obtained in 786 patients at baseline, and after one month's double-blind treatment with metoprolol or verapamil, to evaluate treatment effects on these lipid variables. During a median follow-up time of 3.3 years (2663 patient years), 37 patients suffered a CV death, 30 suffered a non-fatal myocardial infarction (MI) and 100 underwent a revascularization. Apolipoprotein (apo) A-I, high-density lipoprotein cholesterol and triglycerides were predictors of CV death or non-fatal MI in univariate analyses, but only apo A-I remained as an independent predictor in multivariate analyses. All lipid variables except low density lipoprotein cholesterol were related to the risk of revascularization in univariate analyses, but only apo A-I and apo B were independent predictors of such events. Triglycerides were weakly, but not independently, associated with prognosis. Verapamil and metoprolol had differential short-term effects on lipids, with a shift towards a more atherogenic profile in metoprolol treated patients. However, there was no significant impact of the treatment given, or of these treatment effects on the risk of CV events. Results of the present study suggest that apolipoprotein levels were better predictors of CV events than other lipid parameters in patients with stable angina pectoris.

Aged↗

Serum calcium: a new, independent, prospective risk factor for myocardial infarction in middle-aged men followed for 18 years.

BACKGROUND: Primary hyperparathyroidism (HPT) is a disease characterized by hypercalcemia, and associated with an increased mortality in cardiovascular diseases. However, serum calcium levels within the normal range have not been evaluated as a prospective cardiovascular risk factor. METHODS: A cohort of males aged 50 (n = 2183) were investigated in 1970-1973 for serum calcium and known cardiovascular risk factors. They were then followed up over the next 18 years. RESULTS: During the follow-up period, 180 subjects experienced a myocardial infarction (MI). The serum calcium levels were significantly elevated at the baseline (2.37 +/- 0.09 SD versus 2.35 +/- 0.09 mmol/l, p < 0.03) in the subjects who developed a MI when compared with the rest of the cohort. Also blood pressure, body mass index (BMI), fasting insulin, serum cholesterol, serum triglycerides, and the atherogenic index were significantly elevated in the MI group (p < 0.01), while HDL-cholesterol was lower at the baseline investigation (p < 0.01). Cox's proportional hazard analysis showed that only serum calcium (p < 0.01), BMI (p < 0.0003), diastolic blood pressure (p < 0.0009), and the atherogenic index (p < 0.002) were significantly independent risk factors for MI. The range of serum calcium levels from the mean value, -2 SDs to the mean value +2 SDs corresponds to a variation in estimated risk for MI ranging from 0.06 to 0.15. CONCLUSIONS: Serum calcium was found to be an independent, prospective risk factor for MI in middle-aged males suggesting a role for extracellular calcium levels in the atherosclerotic process.

Calcium↗

The alterations in insulin sensitivity during angiotensin converting enzyme inhibitor treatment are related to changes in the calcium/magnesium balance.

The present analysis was undertaken to investigate the relations between alterations in mineral factors, especially the balance between serum calcium and magnesium concentrations (S-Ca and S-Mg, respectively), and variables reflecting glucose and lipid metabolism during angiotensin converting enzyme (ACE) inhibitor treatment. A total of 96 patients with essential hypertension, participating in four double-blind studies with four different ACE inhibitors and similar protocols, were included. At the end of the initial placebo period and at the end of the period of active drug treatment, a hyperinsulinemic euglycemic clamp test was carried out, lipoprotein status was assessed, and the concentrations of serum electrolytes were measured. The serum ACE activity was determined in the group treated with fosinopril. Changes in insulin sensitivity index (M/I) were directly correlated to alterations in S-Mg (r = 0.24, P < .02), and inversely correlated to changes in S-Ca (r = -0.19, P = .07) and the ratio between serum calcium and magnesium concentrations (Ca/Mg) (r = -0.27, P < .008). The change in total serum triglycerides (S-Tg) was inversely correlated to the change in S-Mg (r = -0.35, P < .0005), and directly correlated to the change in Ca/Mg ratio (r = 0.36, P < .0004). The reduction in serum ACE activity correlated to a more pronounced increase in S-Mg r = -0.62, P < .002), and decrease in the Ca/Mg ratio (r = 0.73, P = .0002). We conclude that the changes in the studied metabolic variables and serum ACE activity during ACE inhibitor treatment are related to alterations in mineral status and the balance between calcium and magnesium concentrations in serum.

Adolescent↗

Low-density lipoprotein metabolism and its association to plasma lipoprotein(a) in the nephrotic syndrome.

Patients with nephrotic syndrome have multiple abnormalities of lipoprotein metabolism, but the cause and exact nature of these abnormalities have not been established. In the present study we have determined the kinetics of plasma low-density lipoprotein (LDL) apoB in seven nephrotic patients demonstrating an elevated LDL apoB production rate (25.7 +/- 6.4 vs. 13.1 +/- 0.3 mgkg-1 day-1; P < 0.001) but a normal LDL apoB fractional catabolic rate (FCR) (0.31 +/- 0.04 vs. 0.33 +/- 0.008 pools day-1; NS) compared with 41 healthy control subjects. However, two out of the seven patients had a markedly low LDL apoB-FCR. Serum albumin was inversely correlated with the LDL apoB production rate (R = -0.82; P < 0.05). Plasma lipoprotein (a) [Lp(a)] levels were significantly (P < 0.001) increased in the nephrotic patients compared with control subjects. Significant correlations were observed between log Lp(a) and LDL apoB production rate (R = 0.90; P < 0.01), VLDL-cholesterol (R = 0.95; P < 0.001) and VLDL-triglycerides (R = 0.80; P < 0.05) respectively. In summary, the present study suggests that nephrotic hyperlipidaemia may be caused by at least two independent mechanisms. The elevated LDL apoB production rate is highly correlated with the prevailing levels of serum albumin, whereas some nephrotic patients seem to have a decreased LDL apoB clearance, suggesting impaired LDL receptor-mediated clearance. The present results also suggest that the elevated plasma Lp(a) levels in nephrosis are related to an increased hepatic synthesis rather than a decreased catabolism of lipoproteins.

Adolescent↗

The influence of age on low density lipoprotein metabolism: effects of cholestyramine treatment in young and old healthy male subjects.

OBJECTIVE: The plasma concentration of low density lipoproteins (LDL) increases with age, mainly as the result of a reduced clearance of LDL. Because the conversion of cholesterol to bile acids is reduced with age, we hypothesized that the response of plasma LDL to stimulation of bile acid production would be different in young and old subjects. DESIGN, SUBJECTS AND SETTING: Comparison of the response to cholestyramine treatment in two groups of normolipidaemic, normal weight males: seven young (23-34 years) and eight old (64-73 years). Outpatients at the metabolic ward of a university hospital given a standardized diet of natural type. INTERVENTION: Cholestyramine was given 8 g b.i.d. for 3 weeks and continued during the second LDL turnover study. MAIN OUTCOME MEASURES: Kinetics of autologous radiolabelled LDL before and during treatment. Mean values of lipoprotein lipid levels obtained during the two turnover studies. Changes in LDL particle composition and LDL receptor affinity between the two study periods. RESULTS: Both age groups responded with decreased levels of LDL cholesterol and apolipoprotein-B (apoB), the change being more pronounced in the old subjects. The LDL apoB fractional catabolic rate was increased by approximately 11% in both groups. In contrast, there was a reduced ability in the old subjects to sustain their production rates for LDL apoB with resin therapy, resulting in a 23% reduction in LDL input. No effect on the apparent LDL apoB synthesis rate was observed in the young subjects. LDL particles isolated from cholestyramine-treated subjects were triglyceride-enriched and cholesterol-depleted, and showed a lowered affinity for the LDL receptor in tissue culture studies. CONCLUSIONS: The results demonstrate that stimulation of bile acid production by cholestyramine treatment decreases LDL cholesterol levels in both young and old subjects. This therapy increases LDL apoB elimination in both age groups, but reduction of apparent LDL apoB production is only seen in old subjects.

Adult↗

Influence of variation at the apolipoprotein E locus on lipid and lipoprotein levels in CAPD patients.

BACKGROUND: Variation at the apolipoprotein E (apo E) locus influence lipid and lipoprotein levels in the normal population, and is associated with premature coronary artery disease. Patients with end-stage kidney disease or undergoing dialysis treatment are particularly prone to develop accelerated atherosclerosis. METHODS: To evaluate the influence of genetic variation at the apo E locus, apo E genotypes and serum lipid and lipoprotein levels were measured in 51 subjects undergoing continuous ambulatory peritoneal dialysis (CAPD). RESULTS: The distribution of apo E phenotypes and apo E allelic frequency among the CAPD subjects (epsilon 2 0.049; epsilon 3 0.745: epsilon 4 0.206) corresponded to the healthy Swedish population. In the CAPD subjects, total serum and LDL cholesterol levels were high (6.7 +/- 1.5 mmol/l and 4.2 +/- 1.3 mmol/l respectively) and HDL cholesterol levels were low (1.2 +/- 0.5 mmol/l). When directly comparing the two major apo E groups. E 3/3 subjects (n = 30) and E4/3 and 4/4 subjects, epsilon 4-carriers, (n = 16), LDL cholesterol levels were significantly higher among epsilon 4-carriers (4.8 +/- 1.1 vs 4.0 +/- 1.2 mmol/l, P < 0.03), but total serum cholesterol levels was not higher among the epsilon 4-carriers (7.3 +/- 1.3 vs 6.5 +/- 1.5 mmol/l, P < 0.08). Serum triglycerides or HDL cholesterol levels did not differ significantly between epsilon 3-homozygotes and epsilon 4-carriers. CONCLUSIONS: The results demonstrate a strong effect of variation of the apo E locus on LDL cholesterol levels in CAPD subjects, suggesting that epsilon 4-carriers may be more susceptible to accelerated development of atherosclerosis in this condition.

Adult↗

Detection of Francisella tularensis in ulcers of patients with tularemia by PCR.

The diagnosis of human cases of tularemia is usually confirmed by the demonstration of an antibody response to Francisella tularensis, which occurs about 2 weeks after the onset of disease. Due to a high risk of infection in the laboratory, cultivation of the causative agent tends to be avoided. During an outbreak in Sweden, the use of PCR for diagnosing the ulceroglandular form of tularemia was evaluated. Extraction and preparation of F. tularensis DNA from swab samples from the wounds of patients with tularemia involved the use of the nuclease inhibitor guanidine thiocyanate. The DNA was detected by multiplex PCR targeting the 16S rRNA gene and a 17-kDa lipoprotein gene of F. tularensis. In 29 of 40 (73%) patients with serologically confirmed tularemia, F. tularensis DNA was successfully amplified. Considering the limitations of current diagnostic procedures, PCR may become useful for the early diagnosis of tularemia.

Adolescent↗

Antibodies against cardiolipin and oxidatively modified LDL in 50-year-old men predict myocardial infarction.

Autoantibodies against oxidatively modified low-density lipoproteins (oxLDL) and cardiolipin occur in patients with vascular diseases, including atherosclerosis. The ability of such antibodies to predict myocardial infarction (MI) was investigated in a prospective nested case-control study in which healthy 50-year-old men were followed up for 20 years. Raised levels of antibodies against oxLDL and cardiolipin at 50 years of age correlated positively with the incidence of MI and mortality related to MI 10 to 20 years later. IgG and IgA antibodies against cardiolipin were associated with MI between 50 to 60 years of age and IgG and IgA antibodies against oxLDL with MI at 60 to 70 years of age. Moreover, higher antibody levels were noted in those who died from acute MI in comparison to those who survived. The predictive power of IgA and IgG antibodies was strong and largely independent of that of other strong risk factors. In conclusion, raised levels of antibodies against oxLDL and cardiolipin may predict MI and MI-related death.

Aged↗

Association of apo E polymorphism with plasma lipid levels in a multiethnic elderly population.

Apolipoprotein E polymorphisms are important determinants of blood lipid levels and have been associated with longevity and atherosclerosis. However, information is limited on the effects of apo E variation on the lipids of nonwhite and elderly individuals. We tested the hypothesis that apo E polymorphisms are associated with plasma lipid levels in an elderly, multiethnic population. Cross-sectional data from 1068 noninstitutionalized individuals from northern Manhattan over the age of 64 who were not on a lipid-lowering diet or drug were analyzed. The ethnic distribution was 34% African-Americans, 47% Hispanics, and 19% non-Hispanic Caucasians. In the entire group, the most prevalent apo E allele was epsilon 3 (76%), followed by epsilon 4 (16%) and epsilon 2 (8%); epsilon 4 was more prevalent in African-Americans (21%) than in non-Hispanic Caucasians (12%) or Hispanics (14%). The apo epsilon 2 allele was the most important correlate of plasma lipids, but association varied across ethnoracial groups. After being adjusted for age, sex, obesity, diabetes mellitus, and alcohol intake, LDL cholesterol levels declined with each apo epsilon 2 allele by 8.8 mg/dL in Hispanics and by 25.6 and 18.1 mg/dL in non-Hispanic Caucasians and African-Americans, respectively (P < .001). No significant independent effect was noted for any apo E genotype on HDL cholesterol. Overall, there was a reduction in the total/HDL cholesterol ratio, per apo epsilon 2 allele, of 0.82 in non-Hispanic Caucasians and 0.43 and 0.48 in African-American and Hispanic individuals, respectively (P < .05). In a multivariate model, apo epsilon 4 did not significantly affect plasma lipid levels. Plasma triglyceride levels were inversely correlated with the number of apo epsilon 4 alleles (175, 159, and 143 mg/dL with 0, 1, and 2 alleles, respectively; P =.002), and this effect increased with age. Thus, in an elderly, multiethnic population, apolipoprotein E polymorphisms were important determinants of blood lipids, with differing effects depending on ethnicity. The presence of apo epsilon 2 was associated with lower LDL cholesterol levels and total/HDL cholesterol ratio, although apo epsilon genotype did not influence HDL cholesterol levels. Prospective studies are needed to test whether apo epsilon 2 protects against incident cardiovascular disease in the elderly.

Age Factors↗

Hormonal regulation of lipoprotein(a) levels: effects of estrogen replacement therapy on lipoprotein(a) and acute phase reactants in postmenopausal women.

Estrogen lowers lipoprotein(a) [Lp(a)] levels, but the mechanisms involved have not been clarified. To address the relationship between estrogenic effects on Lp(a) and serum lipids, and on other plasma proteins of hepatic origin, 15 healthy postmenopausal women participated in a randomized, double-blinded, placebo-controlled, crossover study with 4 weeks of oral conjugated estrogens (0.625 mg/d) and placebo, separated by a 6-week period. Lp(a) levels decreased during estrogen treatment in 14 of the 15 subjects (mean decrease, 23%; P < .001). In response to estrogen, apolipoprotein A-I (apoA-I), HDL cholesterol, and triglyceride levels increased by 12% (P = .001), 11% (P < .001), and 10% (P = .02), respectively. Apolipoprotein B (apoB) and LDL cholesterol levels decreased by 7% (P = .01) and 12% (P = .03), respectively, ApoB, LDL cholesterol, and Lp(a) levels fell within 1 week of treatment, whereas apoA-I and HDL cholesterol levels rose more slowly. Levels of acid alpha 1-glycoprotein (AAG) and haptoglobin (HPT), two hepatically derived acute phase proteins, also decreased during estrogen treatment by 18% (P < .001) and 25% (P = .002), respectively. Although the changes in AAG and HPT in response to estrogen were highly correlated (r = .67, P = .009), we were unable to detect a correlation between change in either acute phase protein and change in Lp(a) (r = -.14 and -.24, P = .64 and .41). The lack of correlation between the changes in two acute phase reactants and Lp(a) suggests different underlying mechanisms for the effects of estrogen on these liver-derived proteins.

Acute-Phase Proteins↗

Race-ethnicity and determinants of carotid atherosclerosis in a multiethnic population. The Northern Manhattan Stroke Study.

BACKGROUND AND PURPOSE: Risk factors for carotid atherosclerosis have been studied in white populations but infrequently in multiethnic cohorts. The aim of this study was to determine the importance of race-ethnicity and other factors associated with carotid atherosclerosis in a mixed population of Hispanics, blacks, and whites. METHODS: As part of the Northern Manhattan Stroke Study, 526 stroke-free community residents (aged > or = 40 years; 41% men, 59% women; 46% Hispanic, 31% black, 23% white) were recruited through random-digit dialing and had vascular risk factor evaluations. Maximum internal carotid artery plaque thickness (MICPT) was measured with B-mode ultrasound. The frequency distribution of MICPT was examined in the three race-ethnic groups, and multivariate regression was performed to identify factors that were independently associated with MICPT. RESULTS: Mean MICPT in the entire sample was 1.5 +/- 1.4 mm, increased directly with age, and was greater in whites and blacks than Hispanics. Other independent determinants of MICPT included smoking, glucose, LDL cholesterol, and hypertension. After we controlled for these covariates, Hispanic (versus non-Hispanic) race-ethnicity was still an independent determinant of less carotid plaque. There was a significant interaction between race-ethnicity and LDL cholesterol, with a greater effect of increasing LDL cholesterol among Hispanics. CONCLUSIONS: Atherosclerotic risk factors were predictive of MICPT in this mixed-ethnic cohort. Hispanics had significantly less carotid plaque after adjustment for other known risk factors, but they also had a greater impact of increasing LDL cholesterol.

Adult↗

Size at birth and hypertension in longitudinally followed 50-70-year-old men.

We investigated the relationship between weight at birth and the prevalence of hypertension (defined as treatment and/or systolic blood pressure > 160 mmHg) at ages 50, 60 and 70 years in a cohort of Swedish men followed longitudinally, in which we had previously found a strong inverse association of birthweight with blood pressure at age 50. In men of above median adult height (> 176 cm), a 1000 g decrease in birthweight was associated with an odds ratio for hypertension of 2.53 (95% CI 1.10, 5.85) at age 50, 1.63 (95% CI 0.97, 2.72) at 60 and 1.72 (95% CI 1.10, 2.69) at 70. As the overall prevalence of hypertension increased steeply with age, the absolute difference in the risk of hypertension between those of low and high birthweight increased with age. In men of below median height, birthweight was not significantly associated with blood pressure at any age. Small size at birth is associated with hypertension at 50, 60 and 70 years in men of a high growth potential. The strength of the relationship between birthweight and hypertension does not increase from 50 to 70 years, although the risk of hypertension attributable to low birthweight does increase with age.

Age Factors↗

The serum cholesterol ester fatty acid composition but not the serum concentration of alpha tocopherol predicts the development of myocardial infarction in 50-year-old men: 19 years follow-up.

A low serum tocopherol concentration and a low proportion of linoleic acid in plasma cholesterol esters have been reported to be associated with coronary heart disease. This study was undertaken to evaluate the predictive importance of the serum cholesterol ester fatty acid composition and serum tocopherol concentration in addition to established risk factors for myocardial infarction. The study comprised 2322 fifty-year-old men who participated in a health survey in 1970-1973 regarding risk factors for coronary heart disease. The proportions of myristic, palmitic, palmitoleic, and dihomogammalinolenic acid were significantly higher in 1970-1973 in subjects who suffered myocardial infarction during the following 19 years, while the proportion of linoleic acid was lower, than in those who remained healthy. Serum tocopherol did not differ significantly between the groups. LDL/HDL ratio, systolic blood pressure, and arachidonic acid/dihomogammalinolenic acid ratio were significant independent discriminators between cases and controls in a stepwise logistic regression analysis. This study suggests that middle-aged men who later develop a myocardial infarction are characterized not only by conventional risk factors but also by an altered fatty acid composition of serum cholesterol esters, with a low arachidonic to dihomogammalinolenic acid ratio, indicating reduced delta 5 desaturase activity. This may imply that changes in the quality of dietary fat intake, or an altered capacity to metabolize fatty acids in the body, could precede the development of coronary heart disease.

Biomarkers↗

Structural characterization of bovine CD36 from the milk fat globule membrane.

Bovine CD36 from milk fat globule membranes was characterized and a full-length CD36 cDNA of 2772 nucleotides was isolated from a bovine mammary gland cDNA library. The deduced protein sequence contains 472 amino acid residues with 82-84% identity to the amino acid sequences of CD36 from other species. Peptides corresponding to 43% of the protein were sequenced. All eight potential N-glycosylation sites were glycosylated and the carbohydrate compositions of the individual sites were determined.

Amino Acid Sequence↗