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Biomedical subjects

A Catto

Publications and source records attributed to A Catto.

At least 19 recordsLinked to original sources
PubMed1998

Methylene tetrahydrofolate reductase C677T genotype and stroke.

High levels of homocysteine are associated with atherosclerosis. A thermolabile form of the enzyme methylene tetrahydrofolate reductase (MTHFR) has been proposed as a major cause of a genetic predisposition to hyperhomocysteinaemia and a point mutation at nucleotide 677 of the MTHFR gene causing a thermolabile MTHFR has been described. We looked for this mutation in 271 patients with CT proven cerebrovascular accidents and 173 control subjects. No significant difference in the frequency of the mutant genotype was found between patients with strokes and the control group. Separate analysis of those under 65 and subdividing stroke patients by anatomical location also revealed no significant difference. We conclude, therefore, that in this population the mutation evaluated is not a major contributor to the aetiology of cerebrovascular disease.

Adult↗
PubMed1996

The influence of Helicobacter pylori status on circulating levels of the coagulation factors fibrinogen, von Willebrand factor, factor VII, and factor VIII.

BACKGROUND: Helicobacter pylori (H. pylori) infection has been associated with an increased risk of developing ischemic heart disease (IHD). It has been suggested that a persisting low-grade acute phase response results from the chronic inflammation caused by H. pylori infection, which may give rise to increased circulating levels of certain coagulation factors. MATERIALS AND METHODS: One hundred three (53 male) nonconsecutive, randomly selected white subjects with symptoms of dyspepsia were recruited for study from an outpatient endoscopy clinic at Leeds General Infirmary. The presence of H. pylori was determined by histological and microbiological investigation, a rapid urease test, and a 13carbon urea breath test (13C-UBT). Fibrinogen was measured by the Clauss method, factor VIII:C (FVIII:C) and factor VII:C (FVII:C) were measured by clotting rate assays, and the von Willebrand factor (vWF) was determined by an enzyme-linked immunosorbent assay. RESULTS: No difference was found in levels of coagulation factors according to H. pylori status. Multiple regression models were used to account for the effect of covariates and H. pylori status on levels of FVII:C, FVIII:C, vWF, and fibrinogen, and again H. pylori status was not a significant determinant of levels of any of these coagulation factors. No difference occurred in full blood count, platelet count, white cell count, or plasma viscosity in individuals who were H. pylori-positive compared with those who were negative. CONCLUSIONS: H. pylori infection is not associated with increased circulating levels of fibrinogen, FVII:C, vWF.Ag, or FVIII:C or hemorrheology in this patient group.

Adult↗
PubMed1996

The angiotensin-I converting enzyme (ACE) gene I/D polymorphism and ACE levels in Pima Indians.

An insertion/deletion (I/D) polymorphism of the angiotensin converting enzyme (ACE) gene is associated with plasma ACE levels in white populations. The occurrence of the I/D polymorphism and relationship to ACE levels was examined in a Pima Indian group (n = 305). The frequency of the D allele was lower in Pimas than whites (0.29 v 0.52 respectively). ACE levels were significantly associated with genotype in both groups (p = 0.0001), which accounted for 6.5% of the variation in ACE levels in Pimas and 18% in whites. The association of the I/D polymorphism with ACE levels confirms the relationship across ethnic groups. The low frequency of the D allele in Pima Indians shows that ethnic differences should be accounted for when studying the ACE gene.

Adult↗
PubMed1996

Angiotensin-converting enzyme insertion/deletion polymorphism and cerebrovascular disease.

BACKGROUND AND PURPOSE: There is evidence that an allelic variation in the angiotensin-converting enzyme (ACE) gene may confer an increased risk of vascular disease. The roles of the ACE insertion/deletion polymorphism and circulating ACE levels are unknown in cerebrovascular disease. METHODS: We studied an insertion/deletion polymorphism within intron 16 of the ACE gene by polymerase chain reaction and plasma ACE activity in 467 cases of stroke, the pathological type of which was established by cranial CT, and 231 control subjects. ACE genotype and activity were related to stroke type and mortality at 4 weeks and 3 months. RESULTS: No difference in genotype frequency was observed between all subjects with stroke and control subjects or between control subjects and subjects with cerebral infarction or cerebral hemorrhage. Plasma ACE activity was significantly lower in stroke patients at presentation (64.1 IU/L) than in control subjects (79.6 IU/L; P<.0001). Twenty-one patients (4.5%) with cerebral infarction died within 4 weeks and 56 patients (12%) within 3 months. These patients had significantly lower plasma ACE activity than patients who survived. There was some evidence that risk of death within 4 weeks increased with the number of D alleles (P=.02). Among survivors, plasma ACE activity showed a mean increase of 6.9 IU/L (95% confidence interval, 3.0 to 10.8) between levels at presentation and at 3 months (73.6 IU/L), the latter being similar to ACE activity in control subjects. CONCLUSIONS: Low ACE activity at sroke presentation and possession of the D allele may be associated with increased risk of early death from acute cerebral infarction.

Adult↗
PubMed1995

Factor V Leiden gene mutation and thrombin generation in relation to the development of acute stroke.

To determine the prevalence of the factor V Leiden gene mutation in relation to the phenotypes of cerebral infarction and cerebral hemorrhage, we studied 386 randomly selected cases of acute stroke and 247 control subjects. Factor V genotype was determined by amplification of a 267-bp sequence of exon/intron 10 of the factor V gene. Levels of prothrombin fragment F(1 + 2), a marker of thrombin generation, were determined in both acute and convalescent stroke and related to factor V genotype. Prothrombin fragment F(1 + 2) was assessed by using an enzyme-linked immunosorbent assay. Sixteen stroke cases (4.1%) were identified as having the mutation compared with 14 (5.6%) control subjects. Prothrombin fragment F(1 + 2) levels were estimated in 191 cases and found to be elevated both acutely and after 3 months, but they were not related to factor V genotype. Prothrombin fragment F(1 + 2) is elevated in acute stroke and requires further evaluation in relation to cerebrovascular disease. These results suggest that the factor V Leiden gene mutation is not a risk factor for arterial thrombosis causing stroke.

Base Sequence↗
PubMed1995

The effect of insulin-induced hypoglycaemia on factor VIII:C concentrations and thrombin activity in subjects with type 1 (insulin-dependent) diabetes.

The effect of insulin-induced hypoglycaemia on plasma coagulant activity was studied in 11 subjects with well-controlled, uncomplicated type 1 diabetes. Thrombin generation was determined in plasma by a computer ex-vivo assisted chromogenic method and by the activated partial thromboplastin time (APTT). In addition, factor VIII:C, thrombin-antithrombin III (TAT) complex and fibrinopeptide A (FPA) levels were measured. Hypoglycaemia induced a rise in mean (SD) factor VIII:C concentrations from a baseline level of 1.13 (0.32) IU/ml to a peak 15 min after onset of symptoms and they remained increased at 90 min [1.54 (0.57) and 1.5 (0.54) IU/ml, p < 0.001 respectively]. A corresponding reduction in time to generate 50% maximal thrombin activity occurred from a pre-insulin value of 56 (6) s to a minimum reading of 46 (7) s at 15 min (p < 0.001) and remained low at 90 min [48 (6) s, p < 0.001]. APTT shortened from 43.3 (4.8) s to 40.1 (4.6) s at 30 min (p < 0.001) but did not fall below the normal range (37.6-42.7 s) and no significant changes in TAT or FPA levels were noted. Factor VIII:C correlated inversely with time to generate 50% maximal thrombin activity and APTT (r = -0.580, p < 0.001; r = -0.673, p < 0.001, n = 66, respectively). The results show that the rise in plasma factor VIII:C levels induced by hypoglycaemia is accompanied by accelerated rates of generation of thrombin in contact-activated plasma, though concentrations of FPA and TAT remain unchanged, although TAT complexes are not a sensitive marker of in vivo thrombin generation.

Acute Disease↗
PubMed1993

Action of povidone-iodine against methicillin-sensitive and -resistant cultures of Staphylococcus aureus.

Forty clinical isolates of methicillin-resistant and methicillin-sensitive Staphylococcus aureus were studied for their susceptibility to povidone-iodine (available iodine 11%) under a variety of conditions. The cultures varied in properties, notably in their sensitivity to other therapeutic agents. No differences were observed between the resistant and sensitive cultures in destruction by povidone-iodine. When bactericidal activity occurred, > 99% of the bacterial cells were lethally damaged within 10 seconds of exposure to povidone-iodine. The bacterial cells that had been washed and resuspended thrice in distilled water were most susceptible, with as little as 1 x 10(-16) G (2.36 x 10(5) atoms) of iodine being required to destroy one bacterial cell. Attempts were made to select variants resistant to iodine from the surviving minority population in such experiments. These experiments failed to select resistance, and it is concluded that any apparent variation in vulnerability to povidone-iodine results from aggregation of the bacteria and differences in penetration of povidone-iodine. Substances were studied for their ability to inactivate povidone-iodine. The most potent agents were the free sulphur-containing amino acids, cysteine and methionine. These are present in high concentrations in nutrient broth and most other culture media. This explains the reports of 'pseudo-resistance' to povidone-iodine in certain laboratory experiments. Suggestions are made for the optimum use and formulation of povidone-iodine.

Culture Media↗
PubMed1989

Synthesis and anticonvulsant evaluation of 1,2-diphenylethane derivatives, potential metabolites of denzimol.

A number of new 1,2-diphenylethane derivatives were synthesized and tested for anticonvulsant activity. Their structure was designed on the basis of the potential metabolic degradation of the imidazole ring present in denzimol ( ( +/- )-N-[2-[4-(beta-phenylethyl)phenyl]-2-hydroxethyl]imidazole), a potent anticonvulsant. The compounds which inhibited the electroshock-induced seizures (MES) in mice, namely N-[4-(beta-phenylethyl)phenacyl]formamide (VII) and N-[2-[4-(beta-phenylethyl)phenyl]-2-hydroxyethyl]formamide (IX), proved active also as inhibitors of the pentylenetetrazole-induced tonic seizures. The results of the pharmacological screening were evaluated in relation to the lipophilicity of the compounds.

Animals↗
PubMed1987

1-(2-pyridinyl)piperazine derivatives with antianaphylactic, antibronchospastic, and mast cell stabilizing activities.

New 1-(2-pyridinyl)piperazine derivatives were synthesized and tested as inhibitors of the reaginic passive cutaneous anaphylaxis in the rat (PCA), of the histamine-induced bronchospasm in the guinea pig, and of the rat mesenteric mast cell degranulation induced by compound 48/80. On the basis of test results, a series of N-(substituted phenyl)-omega-[4-(2-pyridinyl)-1-piperazinyl]alkanamides was prepared. The nature of substituents at the anilide ring strongly influenced mast cell stabilizing activity, whereas it was less determining in the case of the other two tests. No clear correlation between the most common physicochemical parameters (pi, sigma, Vw volume) of substituents and activity could be detected. With regard to the position of substituents at the anilide ring, the rank order of potency, in the PCA and bronchoconstriction tests, was para greater than meta greater than ortho. Introduction of substituents in the 1-(2-pyridinyl)piperazinyl moiety of the N-(substituted phenyl)propanamide derivatives hardly affected activity, or the effect was deleterious. Some of the new compounds exhibited a simultaneous remarkable activity in all the three assays employed.

Animals↗
PubMed1985

[New 2,4-dibromo-6-(N-cyclohexyl-N-methyl)-aminomethylanilides of derivatives of cysteine and cystine with expectorant activity].

New 2,4-dibromo-6-(N-cyclohexyl-N-methyl)aminomethylanilides of N-acetylcysteine and N-acetyl-S-carboxymethylcisteine derivatives, N-benzyloxycarbonylcysteine and N,N'-bisbenzyloxycarbonylcystine were synthesized. The compounds were tested for the expectorant activity in rabbit and mouse. N,N'-Bisbenzyloxycarbonylcystin-bis [2,4-dibromo-6-(N-cyclohexyl-N-methyl)aminomethyl]anilide (XIX) was selected for further investigations.

Anilides↗
PubMed1981

New alpha-aryl-beta,N-imidzolylethyl benzyl and naphthylmethyl ethers with antimycotic and antibacterial activity.

A new series of alpha-aryl-beta,N-imidazolylethyl benzyl and naphthylmethyl ethers was synthesized and tested for antimycotic and antimicrobial activity. All compounds showed antifungal activity; most of them were also active against gram-positive bacteria, whereas no activity was detected against gram-negative bacteria. Structure-activity relationships are discussed. The alpha-(2,4-dichlorophenyl)-beta,N-imidazolylethyl 4-phenylthiobenzyl ether nitrate (8), which showed good skin tolerability and in vivo antimycotic activity comparable with or better than 1-[2,4-dichloro-beta-(2,4-dichlorobenzyloxy)phenethyl]imidazole (miconazole) and 1-(alpha-(o-chlorophenyl)benzhydryl]imidazole (clotrimazole), was selected for further researches.

Animals↗
PubMedDate not supplied

The thrombomodulin gene mutation G(127)-->A (Ala25Thr) and cerebrovascular disease.

BACKGROUND AND PURPOSE: Thrombomodulin is an integral part of the protein C anticoagulation pathway, and polymorphisms of its gene have been implicated in thrombosis. The point mutation G(127)-->A has recently been found to be associated with myocardial infarction. METHODS: We investigated this mutation in 465 patients with acute stroke and 353 control subjects. Genomic DNA containing the region of interest was amplified by PCR, and differing genotypes were identified by RFLP. RESULTS: The A allele frequency was not statistically significantly different in the two groups, being 0.5% in the stroke group and 0.7% in the control group. CONCLUSIONS: The point mutation G(127)-->A is an uncommon finding and, in this population, is unlikely to be a major risk factor for cerebrovascular disease.

Aged↗