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Biomedical subjects

K Miloszewski

Publications and source records attributed to K Miloszewski.

18 recordsLinked to original sources
PubMed2002

Evaluation of the impact of pharmacist-led therapeutic tutorials on third-year medical students' knowledge and understanding of drugs used in clinical practice.

Three cohorts of third-year medical students on clinical placements were compared (n = 48). One cohort (study group, n = 18) attended a series of therapeutic tutorials led by the pharmacist. The other two cohorts (control group A and control group B) did not. The tutorials focused on using problem-based cases to review the therapeutic management of common medical conditions. The performance of the three cohorts was assessed using a written therapeutics test consisting of multiple-choice questions and problem-based cases. The study group also completed a questionnaire, which sought to obtain their opinions on the tutorials. The study group performed significantly better than control group A and control group B in both the multiple-choice questions and problem-based cases (p < 0.05, Student's t-test). The responses to the questionnaires indicated that all students welcomed the opportunity for structured teaching of therapeutics during their clinical placements. The students identified the need for more teaching of therapeutics in the undergraduate medical curriculum. All the students agreed that the pharmacist was an appropriate person to lead the tutorials.

Cohort Studies↗
PubMed1995

Mutations causing coagulation factor XIII subunit A deficiency: characterization of the mutant proteins after expression in yeast.

We identified the mutations causing factor XIII A subunit deficiency in two families. Two distinct mutations were identified in the S family: the nonsense mutation Tyr 441-->stop in exon 11, inherited through the paternal line, and the missense mutation Asn 60-->Lys in exon 3, inherited through the maternal line. Two members of the J family were heterozygous for the previously described type 3 A subunit. The substitution giving rise to the type 3 variant was found to be Gly 501-->Arg in exon 12. The Asn 60-->Lys and Gly 501-->Arg mutations were constructed in cDNA clones and expressed in yeast (Saccharomyces cerevisiae AH22). Although mRNA could be detected, protein containing the Asn 60-->Lys substitution could not be detected, suggesting extreme instability or susceptibility to proteolysis. A subunits containing the Gly 501-->Arg substitution were expressed and found to be enzymatically active in fresh yeast lysates. This variant has thermal instability and lost activity during storage or purification. Gel filtration studies suggested that the type 3 variant assembled as a dimer, as do normal A subunits. The data suggest that the Gly 501-->Arg (Type 3 variant) would cause severe factor XIII deficiency if inherited in the homozygous form or as a compound heterozygote with another deleterious mutation.

Adult↗
PubMed1995

Pharmacokinetics and tolerability of factor XIII concentrates prepared from human placenta or plasma: a crossover randomised study.

The pharmacokinetics and tolerability of factor XIII (FXIII) from plasma were compared with those of FXIII from placenta in a randomised, double-blind, crossover study involving 13 patients with congenital FXIII deficiency. Both FXIII activity and FXIII antigen were monitored. No difference was seen in the mean half-lives of the two preparations (9.3 days and 9.1 days for plasma and placenta FXIII activity, respectively). Response was similar for both preparations, but was slightly greater for FXIII from plasma (1.6 ormula: see text] vs 1.5 [formula: see text]). Similar results were found for recovery (65% vs 60%). The area under the data completed by extrapolation was significantly higher for FXIII from plasma. No differences between preparations in terms of efficacy or tolerability were observed. It can be concluded that treatment with FXIII concentrate from plasma is as efficient as with FXIII concentrate from placenta in terms of recovery and half-life. Both preparations were equivalent in terms of safety during the observation period. With the administration of monthly injections of approximately 30 U/kg serious bleeding events were prevented and no other serious adverse events occurred.

Adolescent↗
PubMed1992

Identification of a point mutation in factor XIII A subunit deficiency.

Oligonucleotide primers have been designed for the amplification of all 15 exons of the human coagulation factor XIII A subunit gene. Each exon and its intron flanking regions has been amplified and sequenced from a patient with severe A subunit deficiency. A single G to A transition in the last base of exon 14 has been identified in the homozygous proband and in his heterozygous parents. The mutation would result in the substitution 681 Arg to His in the mature protein product. However, because the mutation is at a splice junction, the deficiency may result from a defect in pre-messenger RNA splicing.

Adolescent↗
PubMed1976

Plasma factor XIII and platelet factor XIII in hyperlipaemia.

Plasma factor XIII activity measured by a quantitative assay was found to be significantly higher in hypertriglyceridaemic patients (type IV and combined hyperlipoproteinaemia), as compared to normolipaemic controls. No such elevation in plasma factor XIII activity was found in patients with type Ha hyperlipaemia. Plasma pseudocholinesterase was found to parallel the elevated factor XIII activity in hypertriglyceridaemic subjects. In contrast, platelet factor XIII activity was not raised in hyperlipaemic subjects, and plasma factor XIII was found to be normal in a normolipaemic subjects with thrombocythaemia. It was concluded that there is no significant contribution from platelets to plasma factor XIII activity, and that the observed increase in plasma factor XIII in hypertriglyceridaemia results from enhanced hepatic synthesis of the enzyme.

Adult↗
PubMed1976

Diagnosis of Mallory-Weiss lesions. A common cause of upper gastrointestinal bleeding.

Mallory-Weiss lesions were considered to be the source of bleeding 21 (13.4%) of 157 unselected patients admitted to a general medical unit because of suspected upper gastrointestinal haemorrhage over a period of 30 months. They represented 16.7% of the 126 patients in whom there was ultimately good evidence of upper gastrointestinal blood-loss. In the total series of 200 suspected bleeding episodes the incidence was 11.5%. It is suggested that endoscopy of the upper gastrointestinal tract, peformed as early as possible after resuscitation, enables the diagnosis of the Mallory-Weiss lesion to be made, shows that it is a relatively common source of haemorrhage, and establishes whether bleeding has stopped, thereby helping to identify patients who can be managed without transfusion and those who are likely to require surgery.

Adult↗
PubMed1975

Increase in urinary indican excretion in pancreatic steatorrhoea following replacement therapy.

Urinary indican excretion was studied in 5 patients with steatorrhoea of pancreatic origin, 4 patients with steatorrhoea due to other causes, and 5 normal subjects. Treatment with pancreatic extract resulted in an immediate increase in indican excretion to above the normal range in patients with steatorrhoea due to pancreatic insufficiency. Administration of pancreatic extract did not result in a rise in the patients with steatorrhoea not due to pancreatic insufficiency, or in the normal subjects. In one patient with pancreatic insufficiency maintained on a low protein diet, the rise in indican excretion on replacement therapy was much slower and did not reach as high a level as in the patients on a normal protein diet. The possible mechanisms underlying these observations are discussed. It is suggested that the finding of a low indican excretion in the presence of steatorrhoea and its rise to above normal on pancreatic enzyme therapy is strongly suggestive of exocrine pancreatic insufficiency.

Adult↗