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Biomedical subjects

K Berg

Publications and source records attributed to K Berg.

At least 145 records · Page 8Linked to original sources
PubMed1997

A DNA polymorphism at the angiotensin II type 1 receptor (AT1R) locus and myocardial infarction.

Two hundred and thirty-five survivors of myocardial infarction (MI) were compared to 384 controls with respect to distribution of genotypes and gene frequencies in the A1166C polymorphism at the angiotensin II type 1 receptor (AT1R) locus. No differences in allele frequencies or genotype distribution were observed when all patients were compared with all controls. When comparing CC homozygotes with the combined group of CA heterozygotes and AA homozygotes (CA/AA), a difference in borderline significance between the MI group and controls was observed (p=0.05). In males alone, this difference was much more pronounced because of the larger proportion of males with the CC genotype in MI cases than in male controls (p=0.01). No significant differences were observed between female cases and controls. No interaction between the insertion/deletion (I/D) polymorphism at the angiotensin I-converting enzyme (ACE) locus and the polymorphism at the AT1R locus was detected. When subdividing the subjects into a "low-risk" and a "high-risk" group, based on levels of apolipoprotein B (apoB) and body mass index (BMI), and whether or not the person used lipid-lowering drugs, the frequency of CC homozygotes in male cases of the "low-risk" group differed significantly compared to the frequency in male controls of the "low-risk" group (p<0.001). No differences were observed in females, but the number of "low-risk" group female cases was low (n=3). Thus, CC homozygosity appears to be associated with MI in Norwegian males, especially among those with a "low-risk" phenotype.

Apolipoproteins B↗
PubMed1997

Analyses of mutations in the human renal kallikrein (hKLK1) gene and their possible relevance to blood pressure regulation and risk of myocardial infarction.

The kallikrein-kinin system is involved in the maintenance of blood pressure (BP), and studies have shown an inverse correlation between BP and urinary kallikrein levels. These and other effects, make the human tissue kallikrein (hKLK1) gene a candidate gene with respect to BP regulation as well as risk of myocardial infarction (MI). By analysis for single-stranded conformation polymorphisms (SSCPs), patterns consistent with four different variants of the gene were detected and further characterized by DNA sequencing. Three of the variants have not been described before. Two of the polymorphisms changed the codon for an amino acid. Methods based on the polymerase chain reaction (PCR) were developed to analyze these polymorphisms at the hKLK1 locus. We found no evidence of association between any genotype in the polymorphisms and normal BP level in two series of healthy, unrelated individuals. In a third series, diastolic BP exhibited a weak association with genotypes in three of the four polymorphisms. Since no such association was detected in the other two series, we conclude that no effect on normal BP level is exerted by variants in the hKLK1 as expressed in these polymorphisms. In two series of monozygotic (MZ) twin pairs, there were no differences between genotypes in within-pair difference in systolic BP or diastolic BP. Finally, no differences in allele frequencies or genotype frequencies in the four polymorphisms at the hKLK1 locus were found between a series of young MI survivors and a series of controls. Thus, genes in the four polymorphisms at the hKLK1 locus detected by SSCP and DNA sequencing did not exhibit associations with MI, and had neither "level gene" nor "variability gene" effects on normal blood pressure.

Adult↗
PubMed1997

Discordance between malignant hyperthermia susceptibility and RYR1 mutation C1840T in two Scandinavian MH families exhibiting this mutation.

The ryanodine receptor 1 (RYR1) mutation C1840T has been reported to segregate with malignant hyperthermia (MH) susceptibility in several families. We have investigated several Scandinavian MH families with respect to five different RYR1 mutations reported to cause predisposition to MH, and we here report on two of the families in which the C1840T mutation was detected. In these two families there was recombination between MH susceptibility and this mutation in one and three individuals, respectively. These findings may suggest that it is necessary to reconsider the specificity of the IVCT and the role of C1840T as a cause of MH susceptibility in some families exhibiting this mutation.

Anesthesia↗
PubMed1997

Cardiovascular risk factors in people with different genotypes in the insertion/deletion (I/D) polymorphism at the locus for angiotensin I-converting enzyme (ACE).

The deletion (D) allele of an insertion/deletion (I/D) polymorphism at the locus for angiotensin I-converting enzyme (ACE) has been reported to be an independent risk factor for myocardial infarction (MI), particularly in people lacking traditional risk factors. Furthermore, a borderline association between Lp(a) lipoprotein level and the I/D polymorphism at the ACE locus was reported in one study. We have searched for possible "level gene" or "variability gene" effects of ACE genes on Lp(a) lipoprotein, total cholesterol (TC), high density lipoprotein (HDL) cholesterol (HDLC), low density lipoprotein (LDL) cholesterol (LDLC), triglycerides (TG), apolipoprotein B (apoB), apolipoprotein A-I (apoA-I), and body mass index (BMI). None of these variables differed significantly between genotypes in the I/D polymorphism in any of three population samples. A single population sample created by combining the three series, exhibited an insignificant trend towards individuals carrying the D-allele having a higher level of Lp(a) lipoprotein than those lacking it, and DD homozygotes had a significantly higher Lp(a) lipoprotein level than the combined group of ID/II individuals (p = 0.03). These results may indicate that the D-allele of the I/D polymorphism at the ACE locus could influence the level of Lp(a) lipoprotein.

Adult↗
PubMed1997

Lp(a) lipoprotein level predicts survival and major coronary events in the Scandinavian Simvastatin Survival Study.

The Scandinavian Simvastatin Survival Study (4S) was a double-blind, randomized placebo-controlled multi-centre clinical trial of long-term Simvastatin therapy in patients with coronary heart disease who had total cholesterol levels between 5.5 and 8.0 mmol/l, comprising 4444 patients, equally distributed to a Simvastatin and a placebo group. Patients achieved a significant 30% relative reduction in overall mortality with Simvastatin therapy through a 42% relative reduction in coronary heart disease mortality. Lp(a) lipoprotein levels in Scandinavian coronary heart disease patients were strikingly higher than in healthy controls. Numbers of deaths in the Simvastatin group differed significantly between quartiles of Lp(a) lipoprotein levels, the reduction in deaths being most pronounced in the second (next to lowest) quartile. Subjects with major coronary events had significantly higher Lp(a) lipoprotein levels than subjects without such events, in all groups. The relationship between Lp(a) lipoprotein level and total mortality as well as between Lp(a) lipoprotein level and major coronary events was significantly different from zero, in logistic regression analyses. The findings show that Lp(a) lipoprotein predicts major coronary events as well as death in secondary prevention with Simvastatin. This prospective study provides independent confirmation that a high Lp(a) lipoprotein level is a significant coronary heart disease risk factor.

Adult↗
PubMed1997

High-degree sequence conservation in LPA kringle IV-type 2 exons and introns.

In the search for factors contributing to the regulation of the Lp(a) lipoprotein concentration, we have sequenced the kringle IV-type 2 encoding exons 1 and 2 together with the flanking intron sequences of the LPA gene in individuals with different serum concentrations of Lp(a) lipoprotein. The high degree of sequence identity between the kringle IV-type 2 repeats made it possible to analyse all the 3-42 kringles simultaneously by polymerase chain reaction and direct DNA sequencing. The strategy used allowed us to determine approximately 700 bp from each kringle IV-type 2 repeat, resulting in a rapid screen of on average 28,000 bp of the LPA gene from each individual. Comparing these bipartite kringle IV-type 2 repeat sequences from 12 individuals with high and 11 individuals with low Lp(a) lipoprotein level revealed that: 1. no sequence polymorphism could be detected in the exons examined; 2. no sequence polymorphism could be detected in the consensus GT/AG splicing signals of exon/intron junctions; and 3. the proximal intron sequences seemed almost completely conserved in the 76-135 bp analysed. Only one position in the intron sequences exhibited the pattern of a G/A polymorphism. We observed no differences between the group with high and the group with low Lp(a) lipoprotein level. The very high conservation of intron sequences could support the hypothesis that the LPA gene evolved relatively recently. The contradictory finding of a corresponding sequence conservation between the human LPA and the plasminogen gene suggests that an evolutionary pressure has preserved these intron sequences over the last 40-90 million years.

Conserved Sequence↗
PubMed1997

Studies on effects of Lp(a) lipoprotein on gene expression in endothelial cells in vitro.

The reason(s) for the atherogenic properties of Lp(a) lipoprotein is still unclear, and several mechanisms have been studied. Alterations in gene expression in endothelial cells (ECs) could be important with respect to risk for coronary heart disease (CHD). We have tested the effects of Lp(a) lipoprotein or the apolipoprotein of Lp(a) lipoprotein (apo(a)) on cultured human umbilical vein endothelial cells (HUVECs) with respect to: (1) the level of endothelin-1 (ET-1) mRNA; (2) release of ET-1 into the culture medium; (3) plasminogen activator inhibitor-1 (PAI-1) secretion into the culture medium and; (4) total gene expression in HUVECs, examined by a polymerase chain reaction (PCR)-based technique, differential display-reverse transcription-PCR (DD-RT-PCR). Lp(a) lipoprotein reduced the level of ET-1 mRNA as well as the release of ET-1. The reduction of ET-1 in the medium was even more pronounced when HUVECs were incubated with apo(a), but we found no effect of apo(a) on ET-1 mRNA level. Neither Lp(a) lipoprotein nor apo(a) had a significant influence on PAI-1 secretion. DD-RT-PCR revealed 11 fragments that could represent differences between cells exposed or not exposed to Lp(a) lipoprotein. Following subcloning and sequencing, 18 sequences that differed between exposed and unexposed cultures were obtained. Four of the subcloned fragments have up to now been used as a probe for northern blot analyses, and one fragment was confirmed to be regulated by Lp(a) lipoprotein. In conclusion, Lp(a) lipoprotein is shown to control ET-1 mRNA levels and the function of at least one more gene, the nature of which is unknown.

Apolipoproteins A↗
PubMed1997

Plasma concentrations of Lp(a) lipoprotein and TGF-beta1 are altered in preeclampsia.

This study was performed to investigate the possible association between preeclampsia and the plasma concentrations of Lp(a) lipoprotein and TGF-beta1 in a large series of patients. Additionally, correlation between the concentrations of these molecules and the severity of preeclampsia or fetal growth retardation was evaluated. Following clinical examination and biochemical analyses, both electroimmunoassay and RIA technique were used for quantitative determinations of plasma Lp(a) lipoprotein. ELISA technique was used to measure the active form of TGF-beta1 in plasma of pregnant normotensive and preeclamptic women. We examined 154 women with preeclampsia (preeclampsia group) and 76 healthy, pregnant normotensive women (control group). The preeclampsia group was further divided into the following subgroups: mild preeclampsia, severe preeclampsia and preeclampsia with fetal growth retardation. Plasma levels of Lp(a) lipoprotein were lower in the total preeclampsia group as well as in all preeclampsia subgroups (5.45+/-7.41, 5.58+/-8.02, 5.08+/-5.38, and 4.32+/-5.28 mg/dl in the total preeclampsia group, and in subgroups with mild preeclampsia, severe preeclampsia, and preeclampsia with fetal growth retardation, respectively) than in the control group (7.84+/-9.26 mg/dl) as determined by quantitative electroimmunoassay. Corresponding results were obtained with a radioimmunoassay (166.03+/-200.2 U/l in the total preeclampsia group vs. 229.18+/-257.7 U/l in controls). There was good correlation between the two methods used for Lp(a) lipoprotein measurement. The differences between controls and the total preeclampsia group as well as each preeclampsia subgroup were statistically significant by a non-parametric test (one-way Kruskal-Wallis test). Plasma concentrations of the active form of TGF-beta1 were increased in all preeclampsia subgroups as well as in the total group (5.63+/-1.68 ng/ml) compared to controls (4.67+/-1.33 ng/ml). This increase in TGF-beta1 was statistically highly significant. Plasma concentrations of Lp(a) lipoprotein and the active form of TGF-beta1 did not differ significantly between the preeclampsia subgroups. The outcome of this study may suggest involvement of both parameters in the pathophysiology of preeclampsia and may substantiate the notion of a multifactorial etiology of the disease.

Adult↗
PubMed1997

Increased levels of intercellular adhesion molecules and vascular cell adhesion molecules in pre-eclampsia.

OBJECTIVE: To investigate the correlation between soluble forms of the intercellular adhesion molecule (sICAM-1) and vascular cell adhesion molecule (sVCAM-1) and the severity of pre-eclampsia or its possible consequences for fetal growth. DESIGN: Prospective observational study. SETTING: Institute of Medical Genetics, University of Oslo, Department of Medical Genetics and Haematological Research Laboratory, Ullevål University Hospital; and the Department of Obstetrics and Gynaecology, The National Hospital, Oslo, Norway. PARTICIPANTS: Seventy-six women with normotensive pregnancies and 157 women with pre-eclampsia divided into three subgroups: mild, severe and pre-eclampsia with fetal growth retardation. METHODS: ELISA-measurements of plasma sICAM-1 and sVCAM-1 were performed in a group of healthy pregnant normotensive women and three groups of women with varying degrees of pre-eclampsia. RESULTS: sICAM-1 concentrations were higher in the pre-eclampsia group compared with the control group, but this difference was not statistically significant. Plasma concentrations of sVCAM-1 were significantly greater (P < 0.0001) in all pre-eclampsia subgroups (835.34, 855.25 and 964.05 ng/mL) compared with the control group (667.62 ng/mL). Within the pre-eclampsia group, plasma concentration of sVCAM-1 was significantly higher in the subgroup exhibiting fetal growth retardation (P = 0.03) compared with mild pre-eclampsia. CONCLUSION: The observed increases in plasma concentrations of sVCAM-1 suggest that measurements of this adhesion molecule may be useful in monitoring pregnancies with respect to the development of pre-eclampsia or fetal growth retardation.

Adult↗
PubMed1997

Ankle injuries and ankle strength, flexibility, and proprioception in college basketball players.

OBJECTIVE: To determine if ankle muscular strength, flexibility and proprioception can predict ankle injury in college basketball players and to compare ankle injury rates in female and male players. DESIGN AND SETTING: In this prospective, correlational study, subjects were tested at the start of the competitive season for ankle joint muscle strength, flexibility, and proprioception. The first ankle injury for each subject was recorded on an injury report form, and the data were analyzed to determine if any of these preseason measurements predicted future injury. The setting was a competitive 9-week season for four women's and four men's college basketball teams. SUBJECTS: A convenience sample of 31 female and 11 male college basketball players. MEASUREMENTS: Subjects were tested for ankle dorsiflexion range of motion, various measures of ankle proprioception, and isokinetic peak torque of ankle dorsiflexion-plantar flexion and eversion-inversion at 30 degrees /sec and 180 degrees /sec before the start of the conference basketball seasons. Data were analyzed using a series of multiple regression equations to determine the variance in ankle injury attributed to each variable. RESULTS: Various measures of proprioception predicted left ankle injury in all subjects (p < .05), while ankle strength and flexibility measures failed to account for additional variance. There was no statistically significant difference in ankle injury rate between women and men. CONCLUSIONS: Ankle joint proprioceptive deficits can be used to predict ankle injury, but further research is needed to identify other sources of variance. In our study, ankle injury rate was similar in female and male college basketball players.

Journal Article↗
PubMed1997

Heterozygosity for apolipoprotein A-I(R160L)Oslo is associated with low levels of high density lipoprotein cholesterol and HDL-subclass LpA-I/A-II but normal levels of HDL-subclass LpA-I.

We studied a Norwegian patient and his family, who presented with low HDL-cholesterol. DNA sequence analysis of the apoA-I gene revealed heterozygosity for a mutation in the apoA-I gene that causes a leucine for arginine replacement at residue 160. Compared to unaffected family members, heterozygous carriers of apoA-1 (R160L)Oslo had 60-70% lower mean levels of HDL-cholesterol, 50-60% lower mean levels of apoA-I and 70-80% lower levels of apoA-II. Moreover, the serum concentration of the apoA-II-containing HDL-subclass LpA-I/A-II was decreased by 70% whereas the concentration of the apoA-II-free HDL-subclass LpA-I did not differ from that in unaffected family members. The decrease of LpA-I/A-II was associated with the lack of large LpA-I/A-II. ApoA-I(R160L)Oslo was present at increased concentrations relative to normal apoA-I in plasma, HDL3, and LpA-I. However, only trace amounts of the variant isoform were detectable in immunopurified LpA-I/A-II. Pre beta1-LpA-I contained normal and variant apoA-I isoforms. We conclude that the failure of apoA-I(R160L)Oslo to form LpA-I/A-II causes low HDL-cholesterol in heterozygous carriers of this apoA-I variant.

Adult↗
PubMed1997

Prenatal diagnosis in Norway.

Prenatal diagnosis (PND) of genetic disorders is provided without costs to the woman or family, in Norway. However, the volume of examinations is significantly smaller than in most other Western European countries. Prenatal diagnosis because of relatively high maternal age is accepted only if the woman will be 38 years or older at the time of delivery. Adequate technologies and know-how are available. The limitations on the amount of work done in this field are a result of political decisions which may have been strongly influenced by fundamentalist groups. PND in Norway has reduced the number of infants born with anomalies of the autosomal chromosomes. The impact on births of infants with other disorders is very small.

Chromosome Aberrations↗
PubMed1997

[Laparoscopic cholecystectomy--effect of position changes and CO2 pneumoperitoneum on hemodynamic, respiratory and endocrinologic parameters].

UNLABELLED: The effect of laparoscopic cholecystectomy on cardiopulmonary and endocrinological parameters results from various factors such as increased intraabdominal pressure (IAP), CO2, and the positioning. However, positioning has not yet been regarded. Reliable examination of the individual influencing factors requires standardized anesthesiological procedure and constant IAP. Presently, the effect of positioning is observed separately from those effects caused by the pneumoperitoneum with CO2 (PP) under standardized conditions. METHODS: 40 patients with no history of cardiopulmonary disease were analyzed. Preoperative medication, induction and management of general anesthesia, positioning of the patient and IAP (12 mmHg) were standardized. Hemodynamic, respiratory and endocrinological parameters were determined with the patient in a supine position and in the position typical for the procedure (15 degrees head-down and 10 degrees slant to the left), each with and without PP. Heart rate (ECG), endexpiratory pCO2 (peECO2), invasive blood pressure (radial art.), central venous pressure, partial arterial O2 saturation (psaO2), and ventilation pressures (peak, plateau) were monitored throughout anesthesia. The parameters pH, pCO2, BE, HCO3-, COHb, vasopressin, lactate, and ammonia were analysed in arterial and venous blood samples at predetermined set points: base line, 10 min after CO2 insufflation, 10 min after desufflation, and 1 h after extubation (cf. table 1). Statistical analysis was performed using the Wilcoxon-test with p < or = 0.05 considered statistically significant. RESULTS: Insufflation of CO2 lead to a 12% increase of heart rate in supine position and to even 18% in the position required for surgery. Same significant changes were observed for arterial blood pressure (21 or respectively 28%). Central venous pressure increased by more than 200% after CO2 insufflation. Endexpiratory pCO2 increased by 2.4 mmHg after CO2 insufflation in the supine position and by 5 mmHg in the surgical position. Ventilation pressures increased significantly by 16%. Analysis of the effect of PP on blood gases showed that pH decreased from 7.47 to 7.43, and arterial pCO2 increased by 5.1 mmHg to 38.7 mmHg and increased further after desufflation to values of up to 43.9 mmHg. Arterial pO2 decreased steadily (18% after insufflation). Vasopressin plasma levels increased exponentially from 3.03 to maximal values of 104.45 pg/ml. Ammonia and lactate showed the expected, nearly identical course. Lactate increased within the clinically and methodically irrelevative range, from 1.12 to 1.159 mmol/l. Ammonia decreased by 29%. CONCLUSIONS: The observed changes, i.e. heart rate, central venous pressure, and arterial blood pressure are caused and altered by CO2 insufflation and the various positioning of patients. The increased vasopressin concentration more than likely contributes to these changes. The query whether the position of the patient also causes a change in respiratory parameters and blood gas analysis cannot be differentiated except for the end-tidal pCO2. Inspite of the observed changes no cardiopulmonary complications occurred in this patient group. Therefore, it seems possible to omit invasive monitoring in cardiopulmonary healthy patients. In patients with concomitant history of cardiopulmonary disease, however, deteriorations due to laparoscopy should be thoroughly taken into consideration and studied further.

Acid-Base Equilibrium↗
PubMed1996

Enhanced antitumour effect of photodynamic therapy by microtubule inhibitors.

The combination of photodynamic therapy (PDT) and the microtubule (MT) inhibitor, vincristine (VCR) or taxol, was studied in the CaD2 mammary tumour model in mice. Meso-tetra(di-adjacent-sulphonatophenyl) porphine (TPPS2a) was used as a photosensitizer. An enhanced antitumour effect was found when VCR, at an almost non-toxic dose (1 mg/kg1, was injected i.p. into the mice 6 h before PDT, while no such enhanced effect was observed when the same dose of VCR was given either 12 or 24 h before PDT or immediately before PDT. Furthermore, it was found that the number of mitotic cells increased 4-5-fold 6 h after the injection of VCR into the mice. VCR did not enhance the sensitivity of normal skin to PDT. Combination of PDT and taxol was also studied. The antitumour activity of PDT could be increased by taxol when the drug (35 mg/kg) was administered i.p. either 6 h prior to PDT or immediately after or before PDT. No significant enhancement in PDT efficiency was found when PDT with photofrin was combined with VCR.

Animals↗