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Biomedical subjects

K A Rickard

Publications and source records attributed to K A Rickard.

At least 91 records · Page 5Linked to original sources
PubMed1986

Stimulation of persisting colonies in agar cultures by sera from patients with CML and AML.

Cord plasma contains colony-stimulating activity (CSA) which stimulates the in vitro clonal growth of neutrophils, eosinophils, macrophages, erythrocytes, and persisting mast cells in semisolid cultures. Analysis of day 35 colonies in agar cultures was found to be a suitable means of demonstrating this activity and discriminating between it and granulocyte-macrophage colony-stimulating factor (GM-CSF). Serum (10%) from patients with acute and chronic myeloid leukemia (AML and CML) was added to normal human bone marrow cultures to search for similar activity in these patient's serum. Although the number of colonies on day 12 (predominantly neutrophils and macrophages) was not significantly different from the number of colonies in cultures containing normal serum, the number of colonies increased 500% in cultures containing CML serum on day 35. Serum from patients with AML during regeneration also stimulated an increased number of colonies on day 35. Although both eosinophil and mast cell colonies were still present on day 35, only mast cell colonies persisted for 150 days. On day 35, cultures containing 10% CML serum contained predominantly eosinophil colonies (84%), whereas cultures containing AML serum contained predominantly mast cell colonies (76%). Although serum contains various CSFs, the specific factor which stimulates persisting mast cell colonies may be the human equivalent of murine persisting (P) cell-stimulating factor (Multi-CSF).

Agar↗
PubMed1986

Specialized formulas and feedings for infants with malabsorption or formula intolerance.

The composition of specialized formulas for infants who experience malabsorption or formula intolerance is described in detail. The limited studies of efficacy, as well as a rationale for selecting an appropriate formula for infants with malabsorption or formula intolerance, are discussed. Infants with symptoms of diarrhea or emesis may have intolerance to milk lactose or milk protein. Soy formulas contain no lactose or cow's milk and should be the first choice of an alternative feeding because of cost and convenience. Some infants may be intolerant of soy as well as cow's milk protein. They benefit from formula containing neither cow's milk nor soy protein or from a specially processed milk-based formula containing hydrolyzed casein. A carbohydrate-free formula to which the desired type of carbohydrate is added may be helpful in the diagnosis and treatment of disaccharidase deficiencies and monosaccharide intolerances. Infants with extensive intestinal resections or intractable diarrhea may require specialized infant formulas with qualitative/quantitative modifications of fat, carbohydrate, and protein. Formulas with medium-chain triglycerides may be useful for infants with steatorrhea. "Preterm" formulas or milk from the infant's mother are preferred for preterm infants, since such feedings promote improved fat and carbohydrate absorption and better meet the infant's nutrient requirements.

Animals↗
PubMed1986

Human bone marrow progenitor cells stimulated by cord blood.

Agar cultures of human bone marrow cells stimulated by cord plasma or irradiated cord blood feeder layers demonstrated the presence of a multilineage hemopoietic growth factor in cord blood. When bone marrow cultures stimulated with giant cell tumor-conditioned medium (GCT-CM) were supplemented with this cord blood-derived growth factor, total colony numbers increased by more than 50% after day 23 and persisted in culture for approximately 40 days. Marrow cultures stimulated by the cord blood-derived growth factor formed colonies of neutrophils, monocyte-macrophages, eosinophils, mast cells, and a few colonies containing a mixed cell population. The results suggest that, while GCT-CM contains granulocyte-monocyte colony-stimulating factor (GM-CSF), cord blood contains a high concentration of a multilineage hemopoietic growth factor, which may be multi-CSF.

Bone Marrow Cells↗
PubMed1985

Short- and long-term effectiveness of enteral and parenteral nutrition in reversing or preventing protein-energy malnutrition in advanced neuroblastoma. A prospective randomized study.

The effectiveness of enteral and parenteral nutrition regimens in preventing or reversing protein-energy malnutrition (PEM) and in preventing treatment delays was evaluated in 32 children receiving treatment for newly diagnosed Stage III (3 patients) and IV (29 patients) neuroblastoma. Ten of 18 malnourished patients were randomized to central parenteral nutrition (CPN) and 8 to peripheral parenteral nutrition (PPN) plus enteral nutrition for 4 weeks and then received enteral nutrition (EN: intense nutrition counselling, oral foods and supplements) for weeks 5 through 10. Ten of 14 nourished patients received EN and 4 CPN for 4 weeks and EN thereafter. Dietary, anthropometric and biochemical measurements were determined for weeks 0, 1, 2, 3, 4, 7, and 10 for 24 patients who completed the protocols. In malnourished patients, both CPN (seven patients) and PPN (seven patients) were effective in reversing PEM in the first 4 weeks; thereafter, EN effectively maintained nutritional gains in both groups. In nourished patients, EN (seven patients) was not as effective as CPN (three patients) in preventing PEM during the first 4 weeks; afterwards, EN maintained gains in the CPN group but did not promote needed increases in weight nor fat reserves in the EN group. Patients supported by parenteral nutrition (PN, weeks 1-4) had fewer treatment delays (2/17, 12%) than EN patients (4/7, 57%, P less than 0.05). These data indicate that PN reverses or prevents PEM and prevents treatment delays during the first 4 weeks of intense oncologic treatment and provides nutritional benefits which can be maintained with EN thereafter.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1985

Multiple cerebral thrombosis in Fletcher factor (prekallikrein) deficiency: a case report.

Despite markedly prolonged activated partial thromboplastin times (APTT) patients with Fletcher factor (prekallikrein) deficiency do not clinically bleed. However, there is one reported case of myocardial infarction associated with prekallikrein deficiency. These clinical observations suggest that the contact mechanism has a minor role in normal in vivo hemostatic function. We report a further two cases of prekallikrein deficiency in Caucasian siblings. The propositus presented with multiple cerebral thrombosis. Cautious anticoagulation resulted in massive cerebral hemorrhage and death of this patient. The sibling was investigated in an attempt to establish a possible defective fibrinolytic pathway in vivo. New sensitive tests for fibrinolysis were used. These included radioimmunoassay of fibrin degradation product "D," B beta 15-42, and in vitro 125I-labelled fibrin lysis assays. The plasma half-life of prekallikrein in this patient was calculated to be 58 hr. Family studies of heterozygotes were also performed. Prekallikrein deficiency is found not to be important in normal in vivo fibrinolysis, which possibly operates via tissue or vessel wall fibrinolytic activator release.

Adolescent↗
PubMed1985

Lactoferrin in the myeloproliferative disorders: a search for granulopoietic regulator defects.

Evidence of a defect in the negative feedback control of granulopoiesis in the myeloproliferative disorders is presented. Neutrophil release of lactoferrin, plasma lactoferrin concentration, the number of lactoferrin receptor sites on mononuclear cells and granulocyte-monocyte colony stimulating factor (GM-CSF) release from peripheral blood cells were determined in patients with myeloproliferative disorders and compared with normal individuals. There was a significantly (P less than 0.001) decreased release of lactoferrin from the neutrophils of patients with myeloproliferative disorders which could be responsible for a reduced suppression of GM-CSF release from mononuclear cells which in turn may be responsible for the increased myeloid proliferative activity in patients with myeloproliferative disorders.

Colony-Stimulating Factors↗
PubMed1985

A factor IX gene probe: its use in carrier detection, antenatal diagnosis and characterisation of the molecular basis for hemophilia B.

Of hemophilia B carriers, 67% were shown to have informative restriction fragment length polymorphisms (Taq I or Xmn I) associated with the factor IX gene. Analysis of DNA for these polymorphisms can enable the detection of the hemophilia B carrier state in females and of hemophilia B in the male fetus in the first trimester. Extensive mapping of the factor IX gene in one hemophiliac who developed antibodies to factor IX failed to detect structural abnormalities in his gene. A non-deletional basis for hemophilia B is proposed in this instance.

Chromosome Mapping↗
PubMed1984

Abnormal T-cell subpopulations in hemophilic patients receiving factor VIII concentrates from voluntary donors.

Recently, Acquired Immune Deficiency Syndrome (AIDS) has been reported in hemophiliacs in the USA, Canada and Spain, and this has caused considerable concern amongst hemophiliacs regarding the use of factor VIII concentrates. The aim of this study was to determine whether hemophiliacs in Australia have T-lymphocyte subpopulation changes similar to those observed in patients with AIDS. Factor VIII produced in Australia is derived from a totally volunteer blood donor system and none of the hemophiliacs in this study had received commercial blood products. For the hemophiliacs, the T-helper cell to T-suppressor cell ratio was 1.1 +/- 0.6 (mean +/- SD) which was significantly less (p less than 0.001) than that of the normal age and sex-matched controls. There was a significant relative (p less than 0.001) and absolute (p less than 0.05) reduction of the helper cell subsets and a significant relative (p less than 0.001) and absolute (p less than 0.05) increase of the suppressor cell subsets, in the hemophiliacs compared to the normal controls. There appears to be no correlation between the amount of factor VIII therapy received during the last three years and the T-cell subset changes. All patients with Christmas disease had T-cell subsets within the normal range. All patients were negative for the hepatitis B virus antigen, but all were positive for the antibody, indicating that there had been exposure to the hepatitis virus in all cases. Cytomegalovirus titres were uniformly low and immunoglobulin levels were normal.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1984

An evaluation of serum erythropoietin estimation by a hemagglutination inhibition assay in the differential diagnosis of polycythemia.

A commercially available hemagglutination inhibition assay kit for the measurement of erythropoietin (EPO) was evaluated for its usefulness in the differential diagnosis of the polycythemic states. Serum samples were obtained from patients with polycythemia rubra vera (active and controlled), secondary and relative polycythemia and from normal controls. Firstly, we found that the mean EPO level (+/- SD) of our normal controls (81 +/- 69 miu/ml) was higher than the manufacturer's quoted normal range (15-59 miu/ml) and that there was a significant spread of values (7-233 miu/ml). Secondly, within each patient subgroup studied, the spread of data points was so wide that interpretation of individual data points would be impossible. We conclude that this assay kit is of little value for serum EPO estimation and in the differential diagnosis of polycythemia.

Diagnosis, Differential↗
PubMed1983

Measurement of factor VIII CAg by immunoradiometric assay in human tissue extracts.

Samples of normal tissues taken from three patients within 24 hours of death were physically disrupted, washed and extracted. Centrifuged supernatants were tested for factor VIII coagulant antigen (VIII CAg) and factor VIII related antigen (VIII RAg) by radioimmunoassays using homologous and heterologous antisera respectively. VIII RAg was readily washed out by isotonic saline whereas VIII CAg required 1.5 M sodium chloride for optimal extraction from tissue homogenates. Highest levels of VIII CAg were detected in some lymph nodes followed by lung, liver and spleen. There was rapid loss of VIII CAg from most tissues in the absence of proteolytic inhibitors.

Antigens↗
PubMed1983

Effect of nutrition staging on treatment delays and outcome in Stage IV neuroblastoma.

The effect of the state of nutrition of 18 children with Stage IV neuroblastoma at diagnosis and during initial therapy, was evaluated with respect to treatment delays, drug dosage alterations, tumor response, days to first event (relapse or death), and survival. All patients received similar therapy (CCSG protocol CCG 371). Based on nutrition staging at diagnosis, nine were classified as malnourished; four were randomized to receive total parenteral nutrition (TPN) and four peripheral parenteral nutrition plus enteral nutrition for 28 days (through 2 chemotherapy courses), and one died before randomization. Nine were nourished at diagnosis; seven received a comprehensive enteral nutrition program and two received TPN. By life-table analysis, the duration of remission was significantly greater in the nourished than the malnourished (P less than 0.01) and a trend towards improved survival was evident at one year (P = 0.08). The median length of survival for children nourished at diagnosis was approximately 12 months, whereas those malnourished had a median survival of only 5 months. Nine children remained nourished or were becoming renourished during the first 21 days of therapy, and one of these had treatment delays and decreased drug dosages. Seven were becoming malnourished or remained malnourished during this period and six had treatment delays (P less than 0.01). These data support the idea that nutrition staging at diagnosis and during initial treatment should be an integral part of protocol design and initial evaluation of children with Stage IV neuroblastoma.

Abdominal Neoplasms↗
PubMed1983

The use of peripheral blood feeder layers as a source of GM-CSF for human bone marrow cultures.

The use of peripheral blood feeder layers as a source of stimulus for colony formation by human granulocytic progenitor cells in semi-solid agar cell cultures was examined. Comparison with various conditioned media demonstrated that cultures stimulated by peripheral blood feeder layers produced the greatest number and largest colonies. The cell concentration in the feeder layers was more important than the total cell number. Feeder layer plates containing 2 X 10(5) cells at a concentration of 1 X 10(6) cells/ml proved to be just potent as the conventional feeder layer plates containing 1 x 10(6) cells/ml in 1 ml. Thus feeder layer plates can be more economical in terms of cell numbers than has previously been reported. By using a known panel of donors for the leukocytes, the number of sub-optimal batches of feeder layers was reduced. Addition of 1 microM adenosine 3':5'-cyclic-monophosphate or 10 micrograms/ml Li2CO3 to poor feeder layers enhanced their colony-stimulating ability.

Bone Marrow Cells↗