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Biomedical subjects

A Sundqvist

Publications and source records attributed to A Sundqvist.

17 recordsLinked to original sources
PubMed1995

Red cell folate levels in pregnant epileptic women.

Red cell folate concentrations were determined in 74 epileptic women in early pregnancy in a prospective study. All patients were treated continuously with antiepileptic drugs since before conception. The most frequently used drugs were carbamazepine (n = 39) and phenytoin (n = 26). Sixty-four patients (86%) were on monotherapy. Blood samples for red cell folate and antiepileptic drug concentrations were drawn before folate supplementation. Red cell folate levels in patients, 468 nmol.l-1, did not differ from those in non-epileptic, drug-free, pregnant women, 416 nmol.l-1 or from those in non-pregnant age-matched healthy controls, 412 nmol.l-1. No correlation was found between red cell folate concentrations and doses or plasma levels of phenytoin or carbamazepine.

Adult↗
PubMed1994

Linkage analysis of idiopathic generalised epilepsy in families of probands with Juvenile Myoclonic Epilepsy and marker loci in the region of EPM 1 on chromosome 21 q: Unverricht-Lundborg disease and JME are not allelic variants.

The locus for Unverricht-Lundborg disease, EPM 1, has recently been mapped to chromosome 21q22.3. A locus, EJM 1, predisposing to idiopathic generalised epilepsy in families of probands with juvenile myoclonic epilepsy has been localised to chromosome 6p by evidence of linkage to the HLA region. However, segregation analysis suggests a two-locus model for JME and evidence has been obtained for genetic heterogeneity within the JME/IGE phenotype. EPM 1 was therefore investigated as a candidate locus in the set of families segregating for IGE and JME which do not show linkage to markers on chromosome 6p. Linkage analysis was carried out in 25 families using three microsatellite DNA markers around the EPM 1 gene region using different models of inheritance. Multipoint linkage analysis provided definite exclusion for 20cM around PFKL, the closet linked marker to EPM 1, under three out of four models tested. These results strongly suggest that the EPM 1 gene is not linked to the phenotype expressed in these families, and therefore that Unverricht-Lundborg disease and juvenile myoclonic epilepsy are not allelic variants.

Adolescent↗
PubMed1994

[Nursing aspects in pain treatment].

Pain, the concept of pain and how pain is connected with culture are discussed in this article. The experience of pain in individual. It can not be questioned. The primary task of nursing is to help and support a patient to cope with pain in spite of the fact whether there is a cause for pain or not. Besides pharmacotherapy there are other possibilities to help a patient, e.g. by taking care of the surroundings, offering interesting subjects to think about, using imagination, relaxation, cognitive behavioral therapy, massage, therapeutic touch and thermat and cryotherapy.

Analgesia↗
PubMed1993

Linkage analysis of idiopathic generalized epilepsy (IGE) and marker loci on chromosome 6p in families of patients with juvenile myoclonic epilepsy: no evidence for an epilepsy locus in the HLA region.

Evidence for a locus (EJM1) in the HLA region of chromosome 6p predisposing to idiopathic generalized epilepsy (IGE) in the families of patients with juvenile myoclonic epilepsy (JME) has been obtained in two previous studies of separately ascertained groups of kindreds. Linkage analysis has been undertaken in a third set of 25 families including a patient with JME and at least one first-degree relative with IGE. Family members were typed for eight polymorphic loci on chromosome 6p: F13A, D6S89, D6S109, D6S105, D6S10, C4B, DQA1/A2, and TCTE1. Pairwise and multipoint linkage analysis was carried out assuming autosomal dominant and autosomal recessive inheritance and age-dependent high or low penetrance. No significant evidence in favor of linkage was obtained at any locus. Multipoint linkage analysis generated significant exclusion data (lod score < -2.0) at HLA and for a region 10-30 cM telomeric to HLA, the extent of which varied with the level of penetrance assumed. These observations indicate that genetic heterogeneity exists within this epilepsy phenotype.

Adolescent↗
PubMed1992

The haemagglutinin-neuraminidase glycoprotein of the porcine paramyxovirus LPMV: comparison with other paramyxoviruses revealed the closest relationship to simian virus 5 and mumps virus.

The complete nucleotide sequence of the haemagglutinin-neuraminidase (HN) gene of the porcine paramyxovirus LPMV, was determined from cDNA derived from viral genomic RNA. The gene was 1906 nucleotides long including a putative gene end and poly A signal. One long open reading frame was found encoding a protein of 576 amino acids with a calculated molecular weight of 63,324. The protein contains four potential N-glycosylation sites and a major hydrophobic region near the N-terminal, suggesting a membrane anchor domain. Comparison of the deduced amino acid sequence of the LPMV HN protein with that of other paramyxovirus HN proteins, revealed the highest amino acid identity to simian virus 5 of 43% and mumps virus of 41%.

Amino Acid Sequence↗
PubMed1991

Identification of the porcine paramyxovirus LPMV matrix protein gene: comparative sequence analysis with other paramyxoviruses.

The complete nucleotide sequence of the gene encoding the matrix protein (M) of the porcine paramyxovirus LPMV has been determined. The gene is 1376 nucleotides long including 5' and 3' non-coding sequences with a protein-coding sequence of 1107 nucleotides. The deduced protein, containing 369 amino acids with a calculated Mr of 41,657, is hydrophobic overall with a net positive charge of +17.5. Comparative sequence analysis revealed high amino acid homology to other paramyxovirus M proteins, with the highest degree of identity (46%) with the human mumps virus. This is strong evidence that the porcine paramyxovirus LPMV is a genuine member of the paramyxovirus genus.

Amino Acid Sequence↗
PubMed1990

The structural proteins of a porcine paramyxovirus (LPMV).

The porcine paramyxovirus is a newly identified agent of a fatal disease in piglets, endemic in Mexico since 1980, where it was seen around the town of La Piedad, Michoacan, Mexico (hence LPM virus). At least six [35S]methionine-labelled proteins could be resolved by SDS-PAGE and five of them were clearly immunoprecipitated. Selective labelling of LPMV-infected cells with [3H]glucosamine revealed two bands with an Mr of about 66K and 59K, corresponding to the two viral glycoproteins, the haemagglutinin-neuraminidase protein and the fusion protein. Labelling of virus with [32P]orthophosphate disclosed one band with an Mr of 52K, corresponding to the phosphoprotein. Analysis of nucleocapsids obtained from purified virus or from a permanently infected cell line revealed one major band with an Mr of 68K, the nucleoprotein. Two other proteins were also identified, the large protein and the matrix protein, with apparent Mr of about 200K and 40K, respectively. The protein migration pattern of LPMV was compared, by SDS-PAGE, with that of Newcastle disease virus, bovine parainfluenza 3 virus and Sendai virus. Differences in the Mr of LPMV proteins and the proteins of these paramyxoviruses were observed. We propose that LPMV should be classified as a novel member of the genus Paramyxovirus.

Animals↗
PubMed1987

Acyclic guanosine analogs as inhibitors of human cytomegalovirus.

The acyclic guanosine analogs R- and S-enantiomers of 9-(3,4-dihydroxybutyl)guanine [(R)- and (S)-DHBG], 9-(4-hydroxybutyl)guanine (HBG), and 9-(2-hydroxyethoxymethyl)guanine (ACV) were examined for their effects on human cytomegalovirus (CMV) replication and on CMV DNA synthesis in cell culture as well as for their ability as triphosphates to interact with CMV DNA polymerase. Production of early CMV antigens was not affected. All analogs inhibited CMV DNA synthesis and late viral antigen synthesis. Primary CMV isolates were less susceptible to all tested analogs than was the laboratory strain CMV Ad.169. The triphosphate of ACV was the most potent inhibitor of CMV DNA polymerase, with an observed Ki of 0.0076 microM. The corresponding Ki values of the triphosphates of (R)-DHBG, (S)-DHBG, and HBG were 3.5, 13.0 and 0.23 microM, respectively. All triphosphates of the analogs given above inhibited CMV DNA polymerase in a competitive manner with respect to dGTP. The triphosphates of the analogs also inhibited reactions when the synthetic template poly(dC)oligo(dG)12-18 was used, whereas no inhibition was observed with poly(dA)oligo(dT)12-18. None of the triphosphate analogs supported DNA synthesis in the absence of dGTP, showing that no analog was an alternative substrate to dGTP.

Acyclovir↗
PubMed1986

Inhibition of herpes simplex virus-induced DNA polymerases and cellular DNA polymerase alpha by triphosphates of acyclic guanosine analogs.

The triphosphates of the antiherpes acyclic guanosine analogs (R)- and (S)-enantiomers of 9-(3,4-dihydroxybutyl)guanine [BCVTP and (S)-DHBGTP], 9-(4-hydroxybutyl)guanine (HBGTP), and 9-(2-hydroxyethoxymethyl)guanine (ACVTP) were investigated for their effects on partially purified DNA polymerases of herpes simplex virus type 1 and type 2 (HSV-1 and HSV-2) as well as cellular DNA polymerase alpha of calf thymus and Vero cells. The triphosphates of the four analogs were all competitive inhibitors when dGTP was the variable substrate with both the viral and the cellular DNA polymerases with activated calf thymus DNA or poly(dC)oligo(dG)12-18 as template. No inhibition was observed with deoxythymidine 5'-triphosphate as substrate and poly(dA)oligo(dT)12-18 as template. All analogs were preferential inhibitors of the viral DNA polymerases. Ordering the compounds according to their decreasing binding affinities, as reflected by their increasing inhibition constants for the viral DNA polymerases, gave ACVTP greater than HBGTP greater than BCVTP greater than (S)-DHBGTP. The DNA polymerase from the HSV-1 mutant, CI(101)P2C5, resistant to ACV, showed a stronger decrease in sensitivity for ACVTP and HBGTP than for BCVTP compared to the effects on DNA polymerase from the wild-type strain CI(101). The analogs were not able to support DNA synthesis in the absence of the competing substrate dGTP. A decrease in the ability of calf thymus DNA to serve as primer template for HSV-2 DNA polymerase was observed after preincubation with the triphosphates of the acyclic guanosine analogs. The analogs showed a progressive inhibition of the HSV-2 DNA polymerase activity with incubation time, and the inhibition could be reversed by high concentrations of dGTP both with and without addition of fresh enzyme or fresh template. However, no reversion was obtained when fresh enzyme or template was added if dGTP was omitted. The data indicate that these analogs inhibited the DNA polymerases by a similar mechanism and that the inhibition was reversible.

Acyclovir↗
PubMedDate not supplied

Vertebral arch nonfusion and juvenile myoclonic epilepsy.

Neural tube defects (NTD) are known to occur at a higher rate in pregnancies of women with epilepsy. Antiepileptic drugs (AEDs), notably valproate (VPA) and carbamazepine (CBZ), have been identified as risk factors, but a familial aggregation of this condition also occurs in the absence of pharmacologic teratogens. Spina bifida occulta, defined as a nonsymptomatic nonfusion of vertebral arches, has been suggested to be genetically determined, with an increased prevalence in patients with primary generalized epilepsy, and that the presence of this trait in fetal development can be enhanced pharmacologically to produce NTD such as meningomyelocele. In this study, plain abdominal radiographs were obtained from 56 patients with juvenile myoclonic epilepsy (JME) and 56 age- and sex-matched controls. The radiographs were presented in a random order to an unbiased radiologist. No difference in prevalence of vertebral arch nonfusion (VAN) was noted between the two groups. Even if it has no increased frequency in patients with epilepsy, however, VAN is a common radiologic finding, and its relation to symptomatic neural tube defects should be clarified in future studies.

Adolescent↗
PubMedDate not supplied

Epilepsy and pregnancy: a prospective study of seizure control in relation to free and total plasma concentrations of carbamazepine and phenytoin.

Seizure control and plasma concentrations of antiepileptic drugs (AEDs) were determined in a prospective, population-based study of 93 pregnancies (cases) of 70 patients with epilepsy. Seventy-seven cases were treated with monotherapy, which in 70 cases consisted of carbamazepine (CBZ) or phenytoin (PHT). Dosage was kept constant unless poor seizure control prompted an increase. Plasma concentrations were determined at monthly intervals throughout pregnancy and compared with baseline levels obtained at least 10 weeks postpartum. Both free and total CBZ and PHT concentrations were analyzed. Seizure frequency during pregnancy for the group as a whole was not different as compared with the 9 pregestational months and was unaltered or improved in 85% of cases. Total CBZ concentration was slightly lower during the third trimester as compared with baseline, whereas free concentration was unchanged. In contrast, PHT levels decreased steadily as pregnancy progressed. Total plasma concentration was 39% of baseline during the third trimester, whereas free PHT concentration decreased far less, being 82% of baseline level during the third trimester. No clear-cut relation could be demonstrated between seizure control and plasma concentrations, which may be explained by the limited changes in free AED concentrations and the small number of cases with an increased seizure frequency. Our results indicate that total plasma concentrations may be misleading and that monitoring of free concentrations, in particular of PHT concentrations, may be advantageous during pregnancy.

Adult↗
PubMedDate not supplied

Disposition of carbamazepine and phenytoin in pregnancy.

Free and total plasma concentrations of phenytoin (PHT) and carbamazepine (CBZ) and its active metabolite carbamazepine-10, 11-epoxide (CBZ-E) were determined in a prospective study of 86 pregnant epileptic women. The pharmacokinetics of PHT and CBZ during the three trimesters were compared with kinetics at least 10 weeks postpartum. Plasma clearance and unbound CBZ clearance were slightly decreased during the last trimester. Total and free plasma CBZ-E concentrations did not change significantly during pregnancy. Plasma PHT clearance, on the other hand, increased from the first trimester. A less pronounced increase was observed for clearance of unbound PHT; the increase was statistically significant only during the third trimester.

Adult↗