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Biomedical subjects

J L Finlay

Publications and source records attributed to J L Finlay.

At least 91 records · Page 5Linked to original sources
PubMed1987

Progress in the management of childhood brain tumors.

The authors have attempted to summarize the contributions that have been made towards improvements in the management of children with brain tumors by the development of sophisticated imaging tools for diagnosis, by the development of more sophisticated and versatile neurosurgical tools, by refinements in radiation therapy delivery equipment and techniques, and by the introduction of chemotherapy into therapy regimens. Overall, the interaction of all of these modalities is stressed, culminating in a comprehensive multidisciplinary approach to the management of children with brain tumors.

Biomarkers, Tumor↗
PubMed1986

A case report and literature review of "primary" pulmonary histiocytosis X of childhood.

"Primary" pulmonary histiocytosis X, a well-described entity in young adult males in which pulmonary disease is the overriding site of involvement, is exceedingly rare in children younger than 15 years old. We report a new case in a 2-year-old male and review other reported prepubertal cases. The diagnosis of pulmonary histiocytosis X is based on examination of lung tissue. Langerhans cells containing Birbeck granules, seen by electron microscopy, are virtually pathognomonic of histiocytosis X. These Langerhans cells also react with a monoclonal antibody (OKT6) as well as with antibody to S-100 protein. Based on the lack of consensus for the appropriate treatment of pulmonary histiocytosis X and on our patient's favorable response, we recommend initial therapy with corticosteroids alone, reserving more toxic agents for patients who fail to respond to this initial therapy.

Bone Diseases↗
PubMed1986

T-lymphoblasts with erythropoietic helper function in acute T-cell leukemia.

A patient with acute T-lymphoblastic leukemia was found to maintain a normal hemoglobin concentration both at presentation and preterminally several months later, despite a replaced bone marrow and over 80% circulating lymphoblasts on both occasions. Cell surface marker analysis demonstrated the T-lymphoblasts both at presentation and preterminally to belong to the T-helper subpopulation. In vitro culture studies demonstrated that the patient's T-lymphoblasts, as well as conditioned medium derived from these lymphoblasts, significantly stimulated normal bone marrow erythroid colony growth (CFU-E). These findings suggest that in this patient the preservation of erythropoiesis resulted from a helper effect exerted by his T-lymphoblasts.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1986

Oxidative metabolism of circulating neutrophils in infantile (Philadelphia chromosome-negative) chronic myelogenous leukemia.

Mature polymorphonuclear neutrophilic leukocytes (PMNL) from a 2.5-year-old female with infantile chronic myelogenous leukemia (CML) were stimulated with phorbol myristate acetate or opsonized zymosan. The resulting enzymatic NADPH oxidation and the cellular O2- release and luminol-enhanced chemiluminescence were measured. The patient's PMNL responded normally in all respects. Thus, mature infantile CML PMNL undergo a normal respiratory burst following either soluble or particulate stimulation. Our review of the literature emphasizes the importance of studying a well-defined population of PMNL in patients with myelodysplasia.

Child, Preschool↗
PubMed1986

Effects of recombinant human interferon gamma on hematopoietic progenitor cell growth.

Human bone marrow BFU-E, CFU-E, and CFU-GM were cultured in the presence of varying concentrations of recombinant human interferon gamma (rHuIFN-gamma). Concentration-dependent inhibition of both erythroid and myeloid precursors by rHuIFN-gamma was demonstrated. A more pronounced suppressive effect of rHuIFN-gamma was seen on the BFU-E than on the CFU-E, with CFU-GM most resistant. rHuIFN-gamma was also added at varying time points during the marrow cultures, demonstrating different time-dependent sensitivities to rHuIFN-gamma; CFU-E were no longer sensitive to rHuIFN-gamma by day 2 of culture, BFU-E by day 6, and CFU-GM by day 9, indicating a loss of sensitivity with maturation. Finally, exposure of marrow cells to rHuIFN-gamma for varying periods of time prior to initiation of hematopoietic cultures failed to inhibit erythroid colony growth in the absence of rHuIFN-gamma in the culture. These studies demonstrate a suppressive effect of rHuIFN-gamma on human erythroid and myeloid progenitor cell growth. This effect appears to be most pronounced on the more primitive stages of committed progenitor cell development.

Bone Marrow↗
PubMed1986

Transplantation of HLA-haploidentical T-cell-depleted marrow for leukemia: autologous marrow recovery with specific immune sensitization to donor antigens.

Autologous marrow recovery without engraftment of donor marrow was observed after bone marrow transplantation (BMT) for two patients with acute lymphoblastic leukemia. Each had received marrow from a haploidentical mixed lymphocyte culture (MLC) reactive donor after pretransplant conditioning with total body irradiation and high-dose cyclophosphamide. To minimize graft-vs-host disease, the marrow was depleted of T cells in vitro by treatment with a monoclonal anti-T-cell antibody and complement. Two weeks after each transplant, reactive lymphocytes were noted transiently in the blood of each patient. Analysis of karyotype, HLA type, and in vitro MLC responsiveness proved the lymphocytes to be of host, not donor, origin. MLC studies showed rapid proliferative responses specifically to stimulating cells from the BMT donor, indicating in vivo sensitization to donor antigens. Return of hematopoietic function was markedly delayed, but it eventually normalized after several months, without evidence of chimerism. These studies confirm that some immune and hematopoietic stem cells of host origin survive the high-dose chemoradiotherapy used as transplant conditioning. Because these immune cells are specifically reactive to donor alloantigens, more potent suppression of host immunity may be needed to prevent nonengraftment of T-cell-depleted, HLA-mismatched bone marrow.

Adult↗
PubMed1986

In vitro analysis of donor bone marrow following monoclonal antibody treatment for the prevention of acute graft versus host disease.

Graft-versus-host disease (GVHD) remains a major cause of morbidity and mortality following bone marrow transplantation. The in vitro removal of the GVHD-causing T-lymphocytes from donor marrow is one approach which could control this complication. Treatment of the donor bone marrow with lectins and erythrocyte-forming rosette depletion, anti-T-cell antisera or monoclonal antibodies are methods currently being tested to accomplish this. CT-2 is an immunoglobulin monoclonal antibody specific for the T-cell erythrocyte-forming rosette receptor. Bone marrow from 23 consecutive donors was treated in vitro with CT-2 and complement, prior to infusion, as a potential means of controlling GVHD. Surface marker analysis using erythrocyte-forming rosetting, and OKT-3 and OKT-11 monoclonal antibodies on paired samples of treated and untreated marrow demonstrated a mean depletion to 1% of the original number of T-cells. Proliferative responses to alloantigens and mitogens as well as cytotoxic and natural killer cell function were tested and found to be markedly reduced. Despite these effects on T-lymphocytes, viable hematopoietic stem cell colonies were retained. Clinical results following the in vitro T-lymphocyte depletion of donor bone marrow for the 8 histocompatible and 15 nonhistocompatible bone marrow transplantation are reported. Prompt engraftment with minimal GVHD, despite no posttransplant GVHD prophylaxis, was seen in seven of the matched patients. In the nonhistocompatible bone marrow transplantation, failure of engraftment occurred in 11 patients. Grades III-IV GVHD were seen in two of the four patients that engrafted despite good T-lymphocyte depletion. No predictive correlation could be found between the in vitro analysis of marrow following CT-2 treatment and clinical outcome.

Acute Disease↗
PubMed1985

Clinical trial depleting T lymphocytes from donor marrow for matched and mismatched allogeneic bone marrow transplants.

Nine patients received T-lymphocyte-depleted histocompatible bone marrow and 28 patients received T-lymphocyte-depleted histoincompatible bone marrow. Eight of nine patients receiving matched bone marrow quickly engrafted without severe graft-versus-host disease (GvHD). None of the eight patients received anti-GvHD prophylaxis medications. Two of these eight patients are currently alive. Nonengraftment and severe GvHD were problems seen in some of the patients given the histoincompatible bone marrow. Additional cytarabine pretransplant permitted engraftment in those patients undergoing histoincompatible transplants for treatment of malignancy, and prednisone and cyclosporine posttransplant reduced the incidence of acute GvHD in those given T-lymphocyte-depleted grafts. Seven of these 28 patients are currently alive. T-lymphocyte-depleted marrow can reduce the occurrence or prevent severe acute GvHD, especially when combined with additional prednisone and cyclosporine; however, the impact on relapse patterns and survival remains to be determined. The occurrence of nonengraftment and treatment-related lymphomas are formidable problems to overcome.

Adolescent↗
PubMed1985

Mismatched bone marrow transplantation in children with hematologic malignancy using T lymphocyte depleted bone marrow.

Twenty children with hematologic malignancies were treated with bone marrow transplantation using histoincompatible donor marrow depleted of T lymphocytes. CT-2 and complement were used to deplete the T lymphocytes. Engraftment was not a major problem in those receiving increased pre- and posttransplant immunosuppression. Five of the 20 children are currently alive and disease-free. Complications in the other children included engraftment problems, cyclosporin toxicity, infections, and bleeding. However, for most children, durable engraftment was seen. Thus, the nonavailability of histocompatible donors is no longer a contraindication to allogeneic bone marrow transplantation for those at high risk of relapse.

Adolescent↗
PubMed1984

Depletion of T cells from human bone marrow with monoclonal antibody CT-2 and complement.

CT-2 mouse monoclonal antibody to the E-rosette receptor was used with complement to deplete bone marrow of E-rosette-positive cells (T cells). Depletion of E-rosette-positive cells was complete and nontoxic to hematopoietic progenitor cells. Depletion of E-rosette-positive cells with CT-2 may decrease the severity of graft-versus-host disease following bone marrow transplantation and extend the application of bone marrow transplantation to those without HLA-identical donors.

Antibodies, Monoclonal↗
PubMed1983

Fusarium brain abscess. Case report.

The common soil fungus, Fusarium, is rarely pathogenic in man but occasionally causes serious disease, particularly in immunocompromised hosts. A case is reported of Fusarium brain abscess and meningitis occurring in a patient with chronic infectious mononucleosis syndrome and immunodeficiency. The patient died despite aspiration of the abscess and treatment with amphotericin B. This case demonstrates the importance of identifying the offending pathological organism through abscess aspiration in immunocompromised patients.

Adolescent↗
PubMed1983

Pediatric bone marrow transplantation: current progress and future prospects.

Ongoing clinical and laboratory research is being directed at the many problems and complications associated with clinical bone marrow transplantation. The most important goals are to increase the long-term survival of patients receiving bone marrow transplants, decrease the morbidity associated with the process, and extend this therapeutic modality to patients in need of a transplant, but without an HLA identical sibling. In addition, as these problems are resolved, and the toxicity of BMT is controlled, this form of therapy may become the treatment of choice for a number of inherited and acquired hematologic, immunologic, and metabolic disorders that are chronically progressive but ultimately fatal, yet are not now routinely treated with BMT due to the acute morbidity and mortality associated with this major procedure.

Bone Marrow Transplantation↗
PubMed1982

Clear cell sarcoma and selective IgM deficiency: a case report.

A case of clear cell sarcoma of tendons and aponeuroses and a co-existent IgM deficiency is reported. The tumor arose in the Achilles tendon with metastases to the skin, bone, and lymph nodes. The tumor, examined by light and electron microscopy, consisted of glycogen-containing clear cells with melanotic and amelanotic features. There was no detectable serum IgM. The IgA levels were normal and IgG levels were elevated. Peripheral blood lymphocytes contained a normal amount (4.5%) of IgM-bearing cells. Cultured mononuclear cells from the patient suppressed production of IgM by normal lymphocytes, suggesting a role of suppressor cells in the IgM deficiency. The co-existence of soft tissue sarcomas and immunoglobulin deficiency states is reviewed.

Achilles Tendon↗
PubMed1982

Lymphocyte dysfunction in congenital hypoplastic anemia.

Congenital hypoplastic anemia (Diamond-Blackfan syndrome) is thought to involve the erythropoietic cell line alone. In this study, the evaluation of lymphocyte function in five patients with this syndrome revealed a number of abnormalities. Peripheral blood T lymphocyte percentages as assessed by monoclonal antibodies were decreased in three patients. T-helper/T-suppressor cell (OKT4:OKT8) ratios were almost unity in four of the five patients. We usually find a ratio of 2:1 in normal populations. Studies of lymphocyte-mediated suppression of lymphoproliferation demonstrated an inability to generate concanavalin A-induced suppressor cells in the same four patients and impaired prostaglandin-mediated suppression in two patients. Co-culture studies revealed a T lymphocyte-mediated suppression of erythropoiesis in a single patient, who also showed suppression of the mixed lymphocyte reaction. The four remaining patients showed no excessive suppressor effects either upon erythropoiesis or lymphoproliferation. These studies demonstrate that in congenital hypoplastic anemia, the cellular defect is not restricted to the erythroid progenitor cells, but extends to the lymphocytes.

Adolescent↗
PubMed1980

Bone-marrow microenvironment defect in congenital hypoplastic anemia.

An abnormal bone-marrow microenvironment has been thought to have an important role in the pathogenesis of aplastic and hypoplastic anemia in some patients, but direct evidence of such a defect has not been found. We have investigated the pathogenesis of chronic anemia in a young woman. Her bone-marrow cells, obtained by means of aspiration, showed exuberant erythroid growth in methylcellulose despite marked erythroid hypoplasia. The erythroid nature of the colony growth was further confirmed through measurement of heme synthesis and messenger RNA-globin accumulation in a liquid-culture system. In contrast, when whole bone fragments were similarly cultured, no appreciable hemoglobin synthesis was observed. The experimental evidence suggests that, in this patient, hypoplastic anemia resulted from an unfavorable microenvironment.

Adult↗
PubMed1980

Immunologic mechanisms in aplastic anemia.

The existence of abnormalities of the immune system in patients with aplastic anemia is controversial. Review of the evidence for immune deficiency as a component of the aplastic process in these patients reveals generally intact lymphocyte function, but a variable degree of monocyte impairment. Evidence is presented that excessive T-lymphocyte activity may be implicated in the pathogenesis of aplastic anemia, but this complicated by the possible induction of such suppressor cells in response to blood transfusions.

Adolescent↗