Search PubMed⌕ Search

Biomedical subjects

P Gregor

Publications and source records attributed to P Gregor.

At least 55 records · Page 3Linked to original sources
PubMed1993

mu opiate receptor: cDNA cloning and expression.

mu opiate receptors recognize morphine with high affinity. A 2.1-kb rat brain cDNA whose predicted translation product displays 63% identity with recently described delta and kappa opiate receptor sequences was identified through polymerase chain reaction and cDNA homology approaches. This cDNA recognizes a 10.5-kb mRNA that is expressed in thalamic neurons. COS-cell expression confers naloxonazine-, Na(+)-, and GTP-sensitive binding of mu but not delta or kappa opioid ligands. Expressing cells bind morphine, [D-Ala2,N-methyl-Phe4,glyol5]enkephalin (DAMGO), and [D-Ala2,D-Leu5]enkephalin (DADLE) with nanomolar or subnanomolar affinities, defining a mu opiate receptor that avidly recognizes analgesic and euphoric opiate drugs and opioid peptides.

Amino Acid Sequence↗
PubMed1993

Expression and novel subunit isoforms of glutamate receptor genes GluR5 and GluR6.

Molecular heterogeneity of kainate-selective glutamate receptor subunits GluR5 and GluR6 was revealed by identification of a human cDNA, GluR5-1d, and a murine cDNA, GluR6-2, that each encode subunits with novel carboxy-terminal sequences. Both GluR5-1d and GluR6-2 appear to be generated by alternative splicing at analogous sites 14 codons following the fourth putative transmembrane segment. The principal transcripts of GluR5 and GluR6 were detected by Northern analyses of several regions of mammalian brains as 4 and 6 kb bands, respectively. Potential roles for these receptors in development are indicated by detection of their mRNAs in mouse embryos of 11 days gestation. These findings add to the description of the remarkable diversity of glutamate receptor gene expression.

Amino Acid Sequence↗
PubMed1993

Chromosomal localization of glutamate receptor genes: relationship to familial amyotrophic lateral sclerosis and other neurological disorders of mice and humans.

Receptors for the major excitatory neurotransmitter glutamate may play key roles in neurodegeneration. The mouse Glur-5 gene maps to chromosome 16 between App and Sod-1. The homologous human GLUR5 gene maps to the corresponding region of human chromosome 21, which contains the locus for familial amyotrophic lateral sclerosis. This location, and other features, render GLUR5 a possible candidate gene for familial amyotrophic lateral sclerosis. In addition, dosage imbalance of GLUR5 may have a role in the trisomy 21 (Down syndrome). Further characterization of the murine glutamate receptor family includes mapping of Glur-1 to the same region as neurological mutants spasmodic, shaker-2, tipsy, and vibrator on chromosome 11; Glur-2 near spastic on chromosome 3; Glur-6 near waltzer and Jackson circler on chromosome 10; and Glur-7 near clasper on chromosome 4.

Amyotrophic Lateral Sclerosis↗
PubMed1993

Recent atrial fibrillation in acute myocardial infarction: a sign of pericarditis.

The association between recent atrial fibrillation during the course of acute myocardial infarction and pericarditis or pericardial effusion occurring during the hospital phase of myocardial infarction was studied by means of serial echocardiographic examinations in 192 patients presenting with their first myocardial infarction. Clinical pericarditis was found in 8%, echocardiographic effusion in 43%, and atrial fibrillation in 5% of all patients. Atrial fibrillation was present in only 2% of patients without pericardial effusion compared to 15% of patients with more than minimal effusion (p = 0.0094). Thus, pericarditis might play a role in the development of recent atrial fibrillation during the course of myocardial infarction. Recent atrial fibrillation may be a sign of pericardial effusion which may be otherwise silent.

Atrial Fibrillation↗
PubMed1993

The course of myocardial hypertrophy in hypertrophic cardiomyopathy. Results of a 10-year follow-up.

Sixty-nine patients with hypertrophic cardiomyopathy were followed up for a minimum period of 10 years, with detailed quantitation of myocardial hypertrophy using two-dimensional echocardiography at a two-year interval. The parameters determined included maximum myocardial wall thickness, mean myocardial wall thickness (defined as the arithmetic mean of myocardial wall thickness values measured in ten areas of approximately the same size the LV and septal myocardium had been divided into), and the extent of hypertrophy (percentage of the myocardium affected by hypertrophy). Other echocardiographic parameters as well as clinical, ECG and Holter data were also assessed. Seven patients (10%) showed a gradual increase in mean myocardial wall thickness (associated with an increase in maximum myocardial wall thickness and in the extent of hypertrophy in two). By contrast, a progressive decrease in hypertrophy was observed in six patients (9%). In either case, the observed changes tended to involve areas in segments outside the zone of maximum wall thickness. Generally, the changes in hypertrophy were not related to the development of clinical or Holter manifestations, and were unaffected by verapamil or beta-blocker therapy. There was no death among these patients unlike the five deaths in a group with stationary hypertrophy. Based on their results, the authors conclude that changes in myocardial hypertrophy (regardless of whether there is progression or regression) probably make part of natural variations in the course of the disease, and have no clinical or prognostic implications for the majority of patients.

Adult↗
PubMed1993

[The optimal diagnostic approach in myocardial infarct].

In the submitted review the authors discuss rational criteria for the diagnosis of myocardial infarction, indications for thrombolysis, coronarography and possibly PTCA, the method of indirect (non-invasive) assessment of an occluded coronary artery and the most frequent mistakes in the diagnosis of infarction. Essential examinations in the acute stage of myocardial infarction are: case-history, ECG, CK-MB (possibly echocardiography). For indication of thrombolysis of acute PTCA case-history and ECG (or echocardiography) are sufficient. Indications of early coronarography before discharge from hospital: postinfarction angina pectoris, malignant arrhythmia (except on the first day), haemodynamic instability, evidence of myocardial ischaemia (restricted symptoms) during a maximal load before discharge.

Humans↗
PubMed1992

Cloning of an apparent splice variant of the rat N-methyl-D-aspartate receptor NMDAR1 with altered sensitivity to polyamines and activators of protein kinase C.

Molecular cloning identified complementary DNA species, from a rat ventral midbrain library, encoding apparent splice variants of the N-methyl-D-aspartate (NMDA) receptor NMDAR1 (which we now term NR1a). Sequencing revealed that one variant, NR1b, differs from NR1a by the presence of a 21-amino acid insert near the amino end of the N-terminal domain and by an alternate C-terminal domain in which the last 75 amino acids are replaced by an unrelated sequence of 22 amino acids. NR1b is virtually identical to NR1a in the remainder of the N- and C-terminal domains, at the 5' and 3' noncoding ends, and within the predicted transmembrane domains and extracellular and cytoplasmic loops. These findings suggest that the two forms of the receptor arise by differential splicing of a transcript from the same gene. Sequencing of other clones indicates the existence of a third variant, NR1c, identical to NR1b in its C terminus but lacking the N-terminal insert. NR1b RNA injected into Xenopus oocytes generated functional homomeric NMDA channels with electrophysiological properties distinct from those of NR1a homomeric channels. NR1b channels exhibited a lower apparent affinity for NMDA and for glutamate. NR1b channels exhibited a lower affinity for D-2-amino-5-phosphonovaleric acid and a higher affinity for Zn2+. The two receptor variants showed nearly identical affinities for glycine, Mg2+, and phencyclidine. Spermine potentiation of NMDA responses, prominent in oocytes injected with rat forebrain message, was also prominent for NR1a receptors, but was greatly reduced or absent for NR1b receptors. Treatment with the protein kinase C activator phorbol 12-myristate 13-acetate potentiated NMDA responses in NR1b-injected oocytes by about 20-fold; potentiation of NMDA responses in NR1a-injected oocytes was much less, about 4-fold. These findings support a role for alternate splicing in generating NMDA channels with different functional properties.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1992

Organization and expression of the gene encoding chick kainate binding protein, a member of the glutamate receptor family.

The gene encoding chick cerebellar Bergmann glia-specific kainate binding protein (chKBP), has been isolated, characterized and expressed in heterologous systems. The structural gene spans 11.2 kb and contains 11 exons and 10 introns. Several of the exons encode specific receptor domains, including each of the predicted transmembrane regions. Exon/intron boundaries flanking the second, putative channel-forming transmembrane domain are conserved between chKBP and other glutamate/kainate receptor subunits. The putative promoter region 5' to the first exon displays high GC content and TATA, CAAT and AP1 consensus sequences. Transcription of the chKBP gene is evident prior to full cerebellar cortical maturation. Transcripts are abundant in cells consistent with Bergmann glia, as revealed by in situ hybridization. Transfection of 293 kidney cell cultures with chKBP cDNA or chKBP gene expression constructs confers CNQX-sensitive kainate binding with the pharmacological specificity displayed by both chKBP and kainate receptors. However, expression of the same constructs in Xenopus oocytes fails to yield detectable agonist-activated currents.

Amino Acid Sequence↗
PubMed1992

A genetic study in hypertrophic cardiomyopathies (Czech population).

In order to verify the type of heredity and to identify other genealogical characteristics in the Czech population, the authors examined 105 families with incidence of hypertrophic cardiomyopathy (HCM). The probands' siblings presented a 24-percent empiric risk of the disease; in male probands the risk for brothers was four times that for sisters, in female probands it was three times higher for sisters than brothers. Sex ratio of affected siblings was 20:4 in male and 3:14 in female probands. Disease risk for children was substantially higher in younger probands (under 30 yrs. of age: 40%, above 51 yrs.: 6.7%). Reproduction fitness was decreased in the whole group more so in women. Gene penetration was estimated using the "safe carriers" method, as 50 p.c. Anticipation and more severe course were recorded in all families with HCM incidence in more than two generations. The HCM heredity does not resemble that of the autosomal dominant type. The heterogeneity, phenocopy and sexual modulation could not be excluded. Genetic counselling and, possibly, DNA diagnostics would be necessary to elucidate the hereditary nature of hypertrophic cardiomyopathy.

Adolescent↗
PubMed1992

[Immunogenetic study in hypertrophic cardiomyopathy].

Results of assessment of HLA antigens in hypertrophic cardiomyopathies in the world literature are very controversial. Work dealing with this problem in sufficiently large groups of patients is lacking, i.e. work which takes into account different functional and morphological forms of the disease. The authors made therefore a detailed investigation of 60 class 1 and 2 antigens in 117 patients with this disease. Values of the relative risk and chi 2 test revealed a number of possible associations. After correction for the number of examined antigens a significantly higher prevalence was proved only in HLA-B21 in patients with the obstructive form and in patients with advanced myocardial hypertrophy (thickness of more than 30 mm). Examination of HLA antigens can have in the mentioned cases a certain importance during comprehensive examinations of not quite typical forms of the disease. Carriership of antigen B21 is associated with an increased risk of serious cardiological disease, manifested already in young age.

Adolescent↗
PubMed1992

[Genealogic study of hypertrophic cardiomyopathy in the Czech population].

In order to test the type of heredity and to assess further genealogical characteristics in our population the authors examined 105 families with hypertrophic cardiomyopathy. The families were subjected to clinical, electrocardiographic and echocardiographic examination of relatives (72% grade 1 relatives) as well as to a genealogical and psychological examination. For the proband's siblings the empirical risk of disease was 24%, in male probands it wts four times higher for brothers than sisters, in female probands it was three times higher in sisters. The sex ratio of six siblings in men was 20:4, in women 3:14. For children the risk was substantially higher in youner probands (under 30 years risk 40%, above 51 years 6.7%). The proband's parents were affected in 28%, fathers almost twice as frequently in male probands, and equally frequently in female probands. Fitness (reproduction fitness, f) was substantially reduced in the entire group, in isolated and familial cases and in different age groups, more in women than in men. The gene penetrance (assuming monofactorial heredity) was estimated by the method of definite carriers as 50%. Earlier manifestations (anticipation) and a more severe course of the disease was observed practically in all families with occurrence of the disease in more than 2 generations (influence of selection--sampling error). In our group the heredity in hypertrophic cardiomyopathies was not simple autosomal dominance, it was not possible to rule out heterogeny, phenocopy, sexual influence. On the other hand, the group was too small to make possible unequivocal conclusions and the data were not quite consistent with data in the literature. Genetic counselling, possibly DNA diagnosis, would be needed to elucidate heredity of this disease.

Adult↗
PubMed1992

Aortoenteric fistula 24 years after aortic endarterectomy.

Aortoenteric fistula is a well-recognized and potentially catastrophic complication of aortic surgery. It usually follows aortic graft placement and removal of the prosthesis. Extra-anatomic bypass is the treatment generally recommended. The authors report the case of a 74-year-old woman who presented with an aortoenteric fistula 24 years after aortic endarterectomy. The fistula was managed with an anatomically placed Dacron graft. The radiologic findings and approach to management of this uncommon problem are discussed.

Aged↗
PubMed1991

Cloning and expression of a cocaine-sensitive dopamine transporter complementary DNA.

A rat dopamine (DA) transporter complementary DNA has been isolated with combined complementary DNA homology and expression approaches. The DA transporter is a 619-amino acid protein with 12 hydrophobic putative membrane-spanning domains and homology to the norepinephrine and gamma-aminobutyric acid transporters. The expressed complementary DNA confers transport of [3H]DA in Xenopus oocytes and in COS cells. Binding of the cocaine analog [3H]CFT ([3H]2 beta-carbomethoxy-3 beta-(4-fluorophenyl)tropane) to transfected COS cell membranes yields a pharmacological profile similar to that in striatal membranes.

Amino Acid Sequence↗
PubMed1991

Prolonged hemorrhagic shock does not impair regeneration of plasma coagulant masses in the rabbit.

BACKGROUND AND METHODS: Twelve adult male albino rabbits were assigned alternately to normotensive and hypotensive groups to assess the effect of hypovolemic shock on spontaneous correction of dilutional coagulopathy. All animals underwent dilutional exchange transfusion with 200 mL of rabbit RBCs and 5% human albumin. Half the animals were then acutely hemorrhaged and subsequent aliquots of blood removed as needed to maintain the mean arterial pressure at 40 mm Hg. RESULTS: By 6 hr after production of dilutional coagulopathy, masses and plasma concentrations of fibrinogen and Factor II had increased modestly but significantly, and Factor VII mass and concentration and in vitro coagulation had returned almost to normal; plasma volume was unchanged in the normotensive animals. In the hypovolemic shock animals, where coagulant mass regeneration was as rapid as in the normotensive animals, a doubling of total plasma volume (p less than .01) prevented the concentrations of fibrinogen and Factor II, and hence the coagulation times, from improving. CONCLUSIONS: Dilutional coagulopathy corrects spontaneously within hours. Normovolemic shock prolongs dilutional coagulopathy not by impairment of factor regeneration but because of further (internal) dilution due to plasma expansion. Rapid correction of dilutional coagulopathy is likely to necessitate cryoprecipitate administration.

Animals↗
PubMed1991

An immunogenetic study in hypertrophic cardiomyopathy.

Research of the relevant international literature on HLA studies in patients with hypertrophic cardiomyopathy yielded controversial results. There are no studies, conducted in sufficiently large groups of patients, that would consider the different functional and morphological forms of the disease. Therefore, the authors carried out detailed typing of 60 Class I and II antigens in 117 patients known to suffer from hypertrophic cardiomyopathy. Values of the relative risk and chi-square test showed a number of possible associations. However, after correction for the number of antigens tested, only HLA-B21 was shown to have a significantly high frequency (in patients with the obstructive form and in those with advanced myocardial hypertrophy, defined as a wall thickness greater than 30 mm). An association with this antigen has previously been demonstrated in a number of cases of ischaemic heart disease, myocardial infarction of young people, and in hypertensive subjects. HLA typing may be helpful in recognizing forms which are not fully typical. In Czechoslovakia, HLA-B21 carriers are at increased risk of developing a serious heart disease manifesting already in young age.

Adolescent↗