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Biomedical subjects

J A Pritchard

Publications and source records attributed to J A Pritchard.

At least 19 recordsLinked to original sources

Prophylactic transfusions of normal red blood cells during pregnancies complicated by sickle cell hemoglobinopathies.

Prophylactic transfusions of normal donor red cells were administered during 37 pregnancies to women with sickle cell anemia, sickle cell-hemoglobin C disease, or sickle cell-beta thalassemia disease. Once the diagnosis was confirmed, the transfusions were administered intermittently throughout the rest of the pregnancy in such amounts and at such frequencies that no more than 60% of the circulating red cells contained hemoglobin S and the hematocrit was above 25. The maternal mortality rate was zero and maternal morbidity as the consequence of the sickle cell hemoglobinopathy was minimal. The perinatal mortality rate was appreciably reduced when compared to that previously observed without prophylactic transfusions but perinatal morbidity was still excessive. Evidence that the intrauterine environment was compromised, in spite of the transfusions consisted of an increased frequency of growth-retarded fetuses, of meconium staining of amnionic fluid, and of ominous decelerations of fetal heart rate. Morbidity from the transfusions was troublesome. Nonetheless, it is concluded tentatively that both the mother with a sickle cell hemoglobinopathy and her fetus are likely to benefit from prophylactic transfusions of normal donor red cells administered during one pregnancy according to the protocol employed in this study.

Anemia, Sickle Cell

Cancer-specific density changes in lymphocytes after stimulation with phytohaemagglutinin.

A fluorescence polarisation technique ("S.C.M. test") for detecting responses to phytohaemagglutinin revealed that the responsive lymphocytes from patients with malignant disease had an abnormal distribution after centrifugation through lymphocyte separation medium. In a small blind series the technique accurately distinguished patients with histologically proven malignancies from those with nonmalignant disease and normal people.

Adenocarcinoma

Human fetal respiration. IV. Failure of severe distress to stimulate aspiration of amniotic fluid by the immature human fetus.

Reported herein are studies on fetal breathing, specifically the inhalation of labeled amniotic fluid, by immature human fetuses so severely distressed that they subsequently died in utero. Decreased rather than increased amounts of the amniotic fluid label were found in the lungs of the distressed fetuses compared to the amounts in fetuses of comparable weight that were not distressed. We conclude from this study of the immature human fetus that severe distress depresses rather than stimulates aspiration of amniotic fluid.

Abortion, Induced

The macrophage electrophoretic mobility (MEM) test--an investigation of its value as a routine laboratory test in the detection of malignant disease.

A previous study of the MOD-MEM test showed promising results. We have attempted to repeat the study using a blind coded series of 210 blood samples from normal subjects and patients with either benign or malignant disease. Using standard criteria the false negative rate for cancer patients averaged 43% and the false positive rate for non-cancer patients averaged 34%. The results indicate that the test at the present time, under routine laboratory conditions, is not reliably reproducible and does not have the ability to effectively discriminate between benign and malignant disease. It is suggested that blind coded studies be used more frequently in assessment of tests with cancer detection potential.

Antigens

Labor induction.

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Female

Fetal respiration. A review.

During recent years respiratory movements by the human fetus have been rediscovered. The types of movements have been defined, and their dependence on some physiologic conditions has been described. Pharmacologic agents influence not only the occurrence of the movements but also their rate and depth. A tidal flow of fluid between lung and amnionic sac has been established, which may play an important role in lung development. Demonstration of this route for exchange of water and soluble substances identifies the lung as an organ very likely involved in exchange between fetal compartments. Additionally, the deposition in the lung of the particulate matter contained in amnionic fluid may not be proof of pathologic aspiration as previously thought.

Adrenocorticotropic Hormone

The clinical assessment of cancer tests: a statistical approach to the prediction of "false positive" rates from controls.

As the sensitivity of the new in vitro cancer detection techniques increases, a larger number of "false positive" results can be expected from control populations apparently free from malignant disease at the time of the test. An attempt is made to predict the number of unexplained positives, together with the expected age and sex distribution, using published cancer registration statistics. The predicted numbers are compared with the observed numbers of unexplained positives in two clinical trials of the MEM test.

Adult

Fetal respiration: quantitative measurements of amnionic fluid inspired near term by human and rhesus fetuses.

Observations reported now on primate pregnancies, human and rhesus, combined with earlier studies from this laboratory, demonstrate that normally appreciable volumes of amnionic fluid are inhaled and presumably exhaled throughout much of pregnancy. Through use of isotope-labeled red cells and porcelain microspheres placed at varying times in the amnionic sac, as well as fetal squames already present, it has been shown conclusively that inhalation of amnionic fluid is not necessarily a pathologic event. The volumes of amnionic fluid inhaled per 24 hours by human and rhesus fetuses late in pregnancy were remarkably similar, amounting on the average to at least 200 ml per kilogram. These observations confirm the much earlier qualitative studies of some others that previously had generally been discounted by many fetal physiologists.

Amniotic Fluid

Coagulation changes in eclampsia: their frequency and pathogenesis.

The maternal coagulation mechanism has been investigated in an effort to identify its role, if any, in the pathogenesis of eclampsia. Thrombocytopenia was identified in 28 of 95 cases (29 per cent), a prolonged thrombin time in 19 of 38 (50 per cent), abnormally elevated serum fibrinogen-fibrin degradation products in two of 65 (3 per cent), and circulating fibrin monomer in one out of 20 (5 per cent). Overt hemolysis was rare (2 per cent). Thus the pattern as well as the degree of change in the maternal coagulation mechanism differed remarkably from that typical of severe abruptio placentae and of prolonged retention of a dead fetus, the classic obstetric models of fast and slow disseminated intravascular coagulation. It is concluded that the coagulation changes when present in eclampsia are effect rather than cause. Moreover, the changes may evolve primarily from platelet adherence at sites of vascular endothelial damage as the consequence of segmental vasospasm and vasodilatation rather than be triggered by the escape of thromboplastin from the placenta into the maternal circulation.

Abruptio Placentae

Clinical assessment of the MOD-MEM cancer test in controls with non-malignant diseases.

A control series of 105 patients in hospital with non-malignant diseases was used in a limited clinical assessment of the MOD-MEM test. Twenty-seven positive results could be explained on the basis of destruction of nervous parenchyma, tissue necrosis, tuberculosis, malignant disease, etc. The remaining 13 unexplained positives showed a sex and age distribution in agreement with that predicted from cancer registration statistics if the MOD-MEM test detects cancer about 16 years before the clinical appearance of the disease.

Evaluation Studies as Topic

Does coagulation have a causative role in eclampsia?

Alternations in the coagulation mechanism were looked for in a population of eclamptic women, most of when were young, nulliparous, and without evidence of chronic vascular disease, and all of whom survived. Thrombocytopenia was identified in 29% of these women. A prolonged plasma thrombin time was demonstrated in 51% yet elevated fibrinogen-fibrin degradation products in serum were uncommon, as was fibrin monomer in plasma. Overt microangiopathic hemolysis was rare. It is concluded that disseminated intravascular coagulation, when it does occur in eclampsia, is the consequence of the disease rather than the cause. Moreover, endothelial damage, rather contents, probably initiates the thrombocytopenia and other coagulation changes.

Adolescent