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Biomedical subjects

J F Martin

Publications and source records attributed to J F Martin.

At least 235 records · Page 13Linked to original sources
PubMed1985

Platelet volume subpopulations in acute myocardial infarction: an investigation of their homogeneity for smoking, infarct size and site.

Mean platelet volume and count were measured in three groups: patients with acute myocardial infarction, a control group with myocardial ischaemia but no infarction and an asymptomatic group of young males. Mean platelet volume was significantly larger in the myocardial infarction group compared with the ischaemic heart disease group or the asymptomatic group. Two subpopulations were present within the myocardial infarction group. One subgroup had a large mean platelet volume and low count. The other subpopulation was indistinguishable, with regard to platelet count and mean volume, from the ischaemic heart disease group. Over 60% of the myocardial infarction group lay in the area of high platelet volume and low count compared with 13% of the ischaemic heart disease control group and 38% of the asymptomatic group. Acute myocardial infarction is likely to be associated with a large mean platelet volume and low count compared with the ischaemic heart disease group. There is no statistical evidence that this condition is related to smoking or size and site of infarct. This evidence suggests that large mean platelet volume and low platelet count could be a major risk factor for myocardial infarction.

Blood Platelets↗
PubMed1985

High-frequency transformation of Brevibacterium lactofermentum protoplasts by plasmid DNA.

An efficient polyethylene glycol-assisted method for transformation of Brevibacterium lactofermentum protoplasts that uses plasmid vectors has been developed. Two small plasmids, pUL330 (5.2 kilobases) and pUL340 (5.8 kilobases), both containing the kanamycin resistance gene from transposon Tn5 and the replication origin of the natural plasmid pBL1 of B. lactofermentum, were selected as vectors. Supercoiled forms of the plasmids yielded a 100-fold higher transformation frequency than did linear forms. The optimal transformation frequency was achieved with 10 ng of DNA in 1 ml of transformation buffer. Higher concentrations of plasmid DNA resulted in a decrease in transformation frequency per microgram of DNA. Optimal transformation was obtained with 25 to 35% polyethylene glycol 6000. Under optimal conditions, 10(6) transformants per microgram of DNA were obtained.

Brevibacterium↗
PubMed1985

Implications of the introduction of the new killed poliomyelitis vaccine into the expanded programme of immunization (EPI).

Use of the oral live poliomyelitis vaccine in the Expanded Programme of Immunization (EPI) requires that the children to be vaccinated must be seen four times during the first ten months of life. In practice this requirement presents considerable problems for parents as is evident from the high drop-out rate. Introduction of the new inactivated poliomyelitis vaccine into vaccination programmes enables children to be effectivly protected against the six diseases of the EPI in only two visits. Vaccination coverage can thus be considerably increased. At the same time, by reducing the number of visits, both the recurrent costs and the investment costs can be reduced. However, the cost of the vaccines would be increased noticeably since production of the inactivated poliomyetlitis vaccine is much more expensive than the production of the live vaccine. An indication is provided of the likely price of the new concentrated and purified inactivated vaccine. The efficiency/cost ratio, measured by the cost of a completely vaccinated child, will, nevertheless, be considerably improved. Therefore, the new inactivated poliomyelitis vaccine allows the coverage of the EPI to be greatly increased under satisfactory conditions.

Child, Preschool↗
PubMed1984

Platelet production in myocardial infarction and sudden cardiac death.

Megakaryocyte cytoplasmic volumes were studied in 13 subjects 18 +/- 2 days after admittance to the coronary care unit. Seven had suffered a myocardial infarction (MI group) while six had chest pain but no recent infarction. Megakaryocytes were also studied in 10 subjects suffering coronary sudden unexpected death (CSD group) and 11 subjects suffering sudden unexpected un-natural death. There was no significant difference between the megakaryocyte cytoplasmic volume distributions of the MI and CSD groups, although they had a significantly greater mean (p less than 0.01) and range (p less than 0.001) than their respective control groups. There was no significant difference in platelet volumes observed within 24 hr of the infarct and 18 +/- 2 days later. Mean platelet volume was significantly correlated (r = 0.89, p less than 0.006) to mean megakaryocyte cytoplasmic volume in the MI group. A computer simulation of platelet production showed no significant difference between platelet volumes observed in the MI group and those estimated to be circulating before death in the CSD group.

Adult↗
PubMed1984

Diagnosis of deep-vein thrombosis: comparison of clinical evaluation, ultrasound, plethysmography, and venoscan with X-ray venogram.

In 50 patients with suspected deep-vein thrombosis the diagnostic accuracy of standardised clinical examination, doppler ultrasound, impedance plethysmography, and technetium-99m-labelled-fibrinogen scintigraphy (venoscan) was compared with that of X-ray venography. Physical examination was the least accurate method. Impedance plethysmography, venoscan, and ultrasound had accuracies of 65%, 80%, and 82%, respectively. The initial X-ray venogram report had an accuracy of 90% compared with the interpretation of two experienced radiologists. The venoscan was equivocal in 32% of patients, and in the remaining patients the accuracy was 97%. Objective methods of investigation are essential for diagnosing deep-vein thrombosis. Of those tested, the X-ray venogram was the only investigation suitable for definitive diagnosis. The venoscan may have a role as a screening procedure, to be followed by X-ray venography in patients with equivocal venoscan results.

Adolescent↗
PubMed1984

The origin of platelet count and volume.

Platelet count and volume were measured in man (n = 51) and rat (n = 9). Bone marrow megakaryocyte nuclear and megakaryocyte planimetric areas were measured in man (n = 11) and rat (n = 9). Megakaryocyte cytoplasmic volumes were computed from the planimetric areas. Rat had a significantly higher (p less than 0.001) mean megakaryocyte cytoplasmic volume than man and a significantly wider range (p less than 0.01). Rat mean platelet volume was significantly lower (p less than 0.001) than man while the rat platelet count was significantly higher (p less than 0.001) than man. A computer simulation of the random binary sequential division of megakaryocyte cytoplasm was used to explain these observations. Transmission electron microscopy shows that the site of this binary sequential division is probably the pulmonary circulation. The number of circulating megakaryocytes ml-1 of blood which would maintain the observed platelet counts was computed. The ellipses of constant density associated with the bivariate Gaussian distribution of platelet count and mean volume were computed. Platelet volume distributions of 13 men within two standard deviations of the composite mean of platelet count and mean volume were used to construct the platelet volume distribution signature in normal man. A similar platelet volume distribution signature for rat was constructed. The two distributions were significantly different. Neither rat nor man had a log Gaussian platelet volume distribution, however the measured volume distributions tended towards a log Gaussian curve.

Adult↗
PubMed1984

An analysis of the platelet and polyploid megakaryocyte response to acute thrombocytopenia and its biological implications.

Thrombocytopenia was induced in rabbit by a single injection of anti-platelet serum. The circulating platelet number and concomitant mean platelet volume were measured 6 h after the injection and daily thereafter. The megakaryocyte nuclear DNA content was measured in control rabbits and after 2 h and 24 h of thrombocytopenia respectively. The observed recovery of circulating platelet number is used to construct the variation of platelet destruction rate and platelet production rate with time during thrombocytopenia. The observed rebound thrombocytosis is explained by using a balance equation of these two rates. Platelet production is linked to the megakaryocyte by physical fragmentation theory and an explanation of the observed variation of mean platelet volume is used to obtain an estimated bleeding time and circulating platelet biomass during recovery from thrombocytopenia. An interpretation is given of the homeostatic control of megakaryocytopoiesis and thrombopoiesis.

Acute Disease↗
PubMed1984

Accrual of patients into a multihospital cancer clinical trial and its implications on planning future studies.

Little information exists on the population of cancer patients from which individual patients are selected for admission to a clinical trial. In fact, most reports of clinical trials of cancer chemotherapeutic agents begin by describing samples of treated patients but neglect to collect data and describe the population from which the samples were taken. In a multi-institutional VA Cooperative Study in which two different cancer treatments were compared, an attempt was made to screen all lung, colorectal, prostate, and head and neck patients seen at participating hospitals prior to randomization to a therapeutic regimen. Of a total of 2687 patients screened, 437 (16.3%) were randomized and 2250 (83.7%) were excluded for 2981 reasons. Protocol reasons were the basis for 68.6% of all exclusions, 21.3% were physician refusals, and 10.1% were patient refusals. The number of patients randomized did not correlate well with number of patients screened across participating centers. Patients admitted to the study tended to be younger and in better health than excluded patients. Overestimates of randomization rates projected initially from published information point to the need for improved screening data in the planning of future studies. Factors such as screening methods, physician acceptance of the experimental approach, number of competing protocols within each center, and cooperation among medical center departments and personnel all are important ingredients in any screening effort.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1983

The biological significance of platelet volume: its relationship to bleeding time, platelet thromboxane B2 production and megakaryocyte nuclear DNA concentration.

Bleeding time, platelet thromboxane B2 production and megakaryocyte nuclear DNA concentration were measured in rabbits recovering from thrombocytopenia caused by a single injection of anti-platelet serum. Similar measurements were made on rabbits in a steady state of normal platelet production. The effects of a sustained state of thrombocytopenia on megakaryocyte DNA concentration were investigated by repeated daily injections of anti-platelet serum. It is shown that bleeding time depends on both platelet count and mean platelet volume. Furthermore changes in mean platelet volume appear to play a more important role in haemostasis than changes in platelet count. The mean megakaryocyte nuclear DNA concentration is significantly increased after 24 hours of thrombocytopenia and continues to increase as thrombocytopenia is sustained. Thromboxane B2 production/unit volume of platelet is increased in platelets produced after 24 hours of thrombocytopenia compared with platelets produced in normal steady state function. As a consequence platelets produced in response to thrombocytopenia not only have a larger mean platelet volume but are also more reactive. Mean platelet volume, as well as platelet count, should be considered as an index of haemostasis and its dysfunction, thrombosis.

Animals↗
PubMed1983

Changes in volume and density of platelets in myocardial infarction.

The distributions of platelet volume and density were measured in 15 men suffering myocardial infarction and in 22 healthy controls. The method used separated 93% of the total platelet population from whole blood. Mean platelet volume of the study group compared with that of controls was increased by a mean of 0.98 fl (p less than 0.001) in the first 12 hours after myocardial infarction, and by 1.24 fl six weeks later (p less than 0.001). Distribution of platelet volume remained log normal after myocardial infarction. Modal platelet density was increased by a mean of 25 g/l (p less than 0.05) after myocardial infarction. Platelet volume is probably chronically large in men suffering myocardial infarction and may be related to changes in megakaryocytes. It is suggested that the increase in platelet volume occurs before infarction.

Adult↗
PubMed1983

Platelet production: a computer based biological interpretation.

The platelet volume distribution was measured in rat and rabbit in normal steady state platelet production. The animals were then sacrificed and the planimetric megakaryocyte and nuclear areas in each animal were measured using histological techniques. These areas were used to obtain an estimate of the megakaryocyte, megakaryocyte cytoplasm and nuclear volume distributions. The production, by physical fragmentation, of the platelet population from the measured megakaryocyte cytoplasm volume distribution was simulated on a computer. The platelet volume distribution predicted by physical fragmentation was then compared with the measured circulating platelet volume distribution from each animal. The physical fragmentation theory gave an accurate quantitative prediction of the observed platelet volume distribution over the whole volume range. Furthermore fragmentation theory predicted the mean platelet volume, the mode, the maximum frequency of the platelet volume distribution and the range of this distribution. Autopsy studies of megakaryocytes volume distributions in healthy man were fragmented to obtain predicted normal platelet volume distributions from the computer simulation. These distributions were compared with measured circulating platelet volume distributions from apparently healthy men who had a similar mean platelet volume. The platelet volume distribution predicted by physical fragmentation was again in quantitative agreement with the measured distribution over the whole volume range. This study provides further evidence that platelet production from megakaryocyte cytoplasm is by physical fragmentation. Furthermore the computer simulation suggests that the mode of production has a specific form. It also explains why different mammals have different mean platelet volumes.

Animals↗
PubMed1983

The megakaryocyte in thrombocytopenia: a microscopic study which supports the theory that platelets are produced in the pulmonary circulation.

Thrombocytopenia can increase platelet production and thereby facilitate investigations into the mechanism. Megakaryocytes in the bone marrow, lung, spleen and liver have been studied by light and transmission electron microscopy after 6 days of experimentally induced thrombocytopenia in the rabbit. The findings support the theory that platelets are produced in the pulmonary circulation by the physical fragmentation of megakaryocyte cytoplasm.

Animals↗
PubMed1983

Platelets, coagulation and fibrinolysis in patients with diabetic retinopathy.

Twenty control subjects, 12 insulin treated and 10 non-insulin treated diabetics were studied. All diabetics had retinopathy documented by fluorescein angiography and fluorophotometry. Factor VIIIR:Ag and plasma fibrinogen concentrations were elevated in both diabetic groups, but more so in the insulin treated patients. Within this latter group the plasma fibrinogen was also correlated with the degree of retinopathy. Platelets separated on linear isosmolar Percoll gradients showed an increase in intraplatelet beta TG content and concentration and a slight increase in volume of the lightest platelets in the insulin treated diabetics. Plasma platelet factor 4 and antithrombin III concentrations were normal and plasma beta TG levels were elevated only in those patients with renal insufficiency. Platelet aggregometry was performed in 18 diabetic subjects and found to be normal. It is concluded that abnormalities of coagulation and platelets in diabetes are determined by metabolic factors rather than the severity of microvascular disease per se.

Adult↗
PubMed1983

The relationship between the age and density of circulating 51-Cr labelled platelets in the sub-human primate.

Change in the density of circulating platelets in monkeys was studied by using a method that removed greater than 90% of the platelet population from whole blood. These were labelled with 51-Cr and reinjected, having been protected by prostacyclin while in vitro. Platelets were separated into density subpopulations the following day by continuous linear gradients of polyvinyl pyrrolidone coated silica (Percoll) under conditions that approximated well to equilibrium centrifugation. The 51-Cr labelled platelets were then found to be distributed equally throughout all density subpopulations. When the same procedure was repeated at 5 days after re-injection an average of 5% of the density range increase in platelet density had occurred in the reinjected platelets compared to the circulating population (p less than 0.001). Lighter platelets may have a slightly shorter survival time than dense ones. Monkey platelet volume is log normally distributed.

Animals↗