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Biomedical subjects

L J Bernstein

Publications and source records attributed to L J Bernstein.

26 records · Page 2Linked to original sources
PubMed1986

Circulating thymulin and thymosin-alpha 1 activity in pediatric acquired immune deficiency syndrome: in vivo and in vitro studies.

Twenty-five children with acquired immune deficiency syndrome (AIDS) or AIDS-related complex had a characteristic pattern of T cell deficiency. Abnormally low plasma thymulin levels preceded the development of peripheral blood T cell abnormalities. In contrast to patients with congenital T cell deficiencies, our patients had elevated serum levels of thymosin-alpha 1. Treatment with thymosin fraction 5 in three children with AIDS resulted in only transient clinical and immunologic improvement.

Acquired Immunodeficiency Syndrome↗
PubMed1985

Defective humoral immunity in pediatric acquired immune deficiency syndrome.

Specific antibody production was assessed in six young children with the acquired immune deficiency syndrome (AIDS). All patients were immunized with bacteriophage phi X 174, a T cell-dependent neoantigen. In addition, antibody responses to pneumococcal vaccine and tetanus toxoid, lymphocyte responses to mitogens, and serum immunoglobulin levels were determined. Polyclonal hypergammaglobulinemia was documented in three patients. Responses to bacteriophage phi X 174 were abnormal in all patients: primary responses were blunted, secondary responses were markedly decreased, and the class switch (IgM-IgG) was absent in five of six patients. Antibody formation to pneumococcal vaccine and tetanus toxoid was also diminished. Lymphocyte mitogenic responses to phytohemagglutinin, concanavalin A, pokeweed mitogen, and staphylococcal Cowan A were generally decreased. These findings confirm that pediatric patients with AIDS have significant abnormalities in humoral immunity. Dysfunction of both T cells and B cells plays a role in the resultant poor specific antibody production.

Acquired Immunodeficiency Syndrome↗
PubMedDate not supplied

Corticosteroid treatment for pulmonary lymphoid hyperplasia in children with the acquired immune deficiency syndrome.

Five children with positive serology for human immunodeficiency virus (HIV) infection by enzyme-linked immunosorbent assay and Western blot were followed for chronic pulmonary disease. Lung biopsies were performed in all patients, and confirmed the diagnosis of pulmonary lymphoid hyperplasia. All children demonstrated progressive hypoxia and increasing alveolar capillary oxygen gradients over at least 1 year of follow-up. All children were on periodic intravenous gamma globulin treatment for a B-cell defect prior to the initiation of corticosteroid therapy. Prednisone was initially given at a dose of 2 mg/kg daily and was subsequently tapered to an alternate day regimen. All children showed improvement in oxygenation. No deterioration in immune function was noted, and there was no increase in bacterial infection. This study indicates that corticosteroids can successfully reverse the severe hypoxia that may result from pulmonary lymphoid hyperplasia in pediatric AIDS patients.

Acquired Immunodeficiency Syndrome↗
PubMedDate not supplied

Bacterial infection in the acquired immunodeficiency syndrome of children.

We have followed 46 children with acquired immunodeficiency syndrome and acquired immunodeficiency syndrome-related complex. Twenty-six patients had at least one episode of serious bacterial infection. Twenty-seven episodes of sepsis were documented in 21 patients. Soft tissue infection was common in both the presence and the absence of documented bacteremia. Urinary tract infection commonly presented as worsening diarrhea in the absence of sepsis. Organisms commonly isolated included Streptococcus pneumoniae, Haemophilus influenzae and Salmonella sp. Staphylococcal infection accompanied episodes of cellulitis/abscess. Escherichia coli commonly caused urinary tract infection in the absence of sepsis. Enteric and nosocomial sepsis was limited to hospitalized, instrumented patients or to individuals who had received prior antibiotic therapy as outpatients. We conclude that bacterial infection causes serious morbidity in acquired immunodeficiency syndrome and acquired immunodeficiency syndrome-related complex and may be further evidence for altered humoral immunity in the disorder.

Acquired Immunodeficiency Syndrome↗
PubMedDate not supplied

Guanidinobenzoatase and UPA in high-grade human astrocytomas and after xenografting cell suspensions into the rat cerebral cortex: proteases for metastasis and disease progression.

BACKGROUND: Invasion and metastasis is aided by the secretion of guanidinobenzoatase, that cleaves the link peptide to fibronectin, and urokinase plasminogen activator (uPA), which initiates a molecular cascade to activate plasmin and collagenases. This process permits malignant cell migration through the extracellular matrix. MATERIALS: Original human astrocytomas were examined for guanidinobenzoatase and uPA. Suspensions of high-grade human astrocytomas were xenografted into pockets in host cerebral cortex for 1-7 days. RESULTS: A class of guanidinobenzoatase positive cells was observed in the original human astrocytomas and in tumor masses formed in the implantation pocket and around blood vessels. Secondary foci containing guanidinobenzoatase positive cells formed around blood vessels and individual positive astrocytoma cells migrated on the glia limitans along parallel and intersecting nerve fiber fascicles and the corpus callosum. uPA and GFAP were colocalized with guanidinobenzoatase. CONCLUSION: The high-grade astrocytomas reestablish themselves and maintain their characteristics as a tissue although grafted as individual cells.

Animals↗