Search PubMed⌕ Search

Biomedical subjects

H B Levy

Publications and source records attributed to H B Levy.

At least 91 records · Page 5Linked to original sources
PubMed1977

Specific restoration of delayed hypersensitivity by lymphoid tissue extracts.

Mice lose demonstrable delayed hypersensitivity (DH) to DNFB, picryl chloride, or sheep red blood cells. Reconstitution of immune responsiveness can be accomplished by administration of cell-free lysates of spleens from mice with active DH to structurally related, but not to unrelated antigens. Peritoneal exudate cell lysates from mice with active DNFB-DH also restore DH to this antigen. Sera from sensitized mice, and sera and lymphoid tissue extracts from unsensitized mice are without activity. The restorative property of splenic lysates from DNFB-sensitized mice is unstable at 56 degrees C, not sedimented at 90,000 X G and inactivated by trypsin or magnesium ions. The presence of unexpressed, restorable DH may provide a biologic basis for the so called "transfer factor" phenomenon.

Animals↗
PubMed1976

Modification of chronic hepatitis-B virus infection in chimpanzees by administration of an interferon inducer.

Chimpanzees chronically infected with hepatitis-B virus showed transient changes in several markers of infection when treated with the interferon inducer polyriboinosinic-polyribocytidylic acid-poly-l-lysine carboxymethyl cellulose. Serum Dane-particle-associated D.N.A. polymerase, e antigen and hepatitis-B surface antigen, and intrahepatic hepatitis-B surface and core antigens diminished during treatment. Defective (D.N.A.-polymerase-negative) Dane particles increased in titre transiently during treatment; these may play a role in the modulation of hepatitis-B virus infection. Humoral immune responses in chronic hepatitis-B carrier chimps were unaffected. Interferon inducers (or exogenous interferon) may be useful for the treatment of chronic hepatitis-B virus infection.

Animals↗
PubMed1976

Prophylactic control of simian hemorrhagic fever in monkeys by an interferon inducer, polyriboinosinic-polyribocytidylic acid-poly-L-lysine.

A nuclease-resistant complex of polyriboinosinic-polyribocytidylic acid containing poly-L-lysine and carboxymethylcellulose was used as prophylactic treatment of simian hemorrhagic fever in rhesus monkeys. This infection has proven uniformly fatal to more than 50 monkeys. Treatment 8 hr before infection and repeatedly thereafter completely prevented the development of viremia and death. Untreated animals died before development of antibodies to the virus. None of the treated animals developed antibody to the virus, a fact which suggested that viral growth was essentially completely blocked by the compound.

Animals↗
PubMed1976

A phase I-II trial of multiple-dose polyriboinosic-polyribocytidylic acid in patieonts with leukemia or solid tumors.

Polyriboinosinic-polyribocytidylic acid (poly I - poly C), an interferon inducer, was administered in multiple doses of 0.3-75 mg/m2 to 26 patients with a variety of solid tumors, 9 with acute leukemia, and 2 with chronic myelogenous leukemia in blast crisis. Forty-four separate drug trials were comprised of various schedules and routes of administration. Toxic reactions included fever (in 66% of the trials), transient elevation of serum glutamic-oxaloacetic transaminase and serum glutamic-pyruvic transaminase (25%), minimal laboratory evidence of coagulation abnormalities (59%), and hypersensitivity (5%). These toxic manifestations did not relate to dose level or magnitude of interferon induction. Poly I - poly C administered iv induced low serum concentrations of interferon in 24/38 trials (63%), but the correlation between drug dose and peak interferon titer was not linear. Poly I - poly C administered iv or im was not effective as an inducer of interferon in the cerebrospinal fluid. Similarly, poly I - poly C administered im or by inhalation did not produce detectable serum levels of interferon. No patients experienced an objective tumor response to the administration of poly I - poly C, and most (76%) had progression of their disease while receiving the drug.

Acute Disease↗
PubMed1976

Minimal brain dysfunction/specific learning disability: a clinical approach for the primary physician.

Minimal brain dysfunction is a neurodevelopmental disorder which can be found in nearly 20% of school children. It is characterized by evidences of immaturity involving control of activity, emotions, and behavior, and by specific learning disabilities involving the communicating skills needed in reading, writing, and mathematics. The prime deficits in the classroom are an inability to maintain attention and concentration and an inability to skillfully blend the auditory and visual functions essential in language performance. Medical evaluation will reveal many of the "soft signs" of neurologic involvement, and educational appraisal will indicate a wide scatter in testing scores with a marked discrepancy between evaluated potential and actual classroom achievement. Remedial efforts directed at early detection, relief from pressure and unjust punishment or ridicule from parents and teachers, and adjustment of the educational environment with consideration of the child's individual talents, combined with the judicious use of medications to prolong attention span and improve neurodevelopmental maturity, hold promise of improving the lot of most involved children. There are valid indications that expansion of such programs can do much to prevent these youngsters from developing severe personality maladjustment and delinquent behavior, as well as emotional illness in later life.

Attention Deficit Disorder with Hyperactivity↗
PubMed1976

Modified polyriboinosinic-polyribocytidylic acid, an immunological adjuvant.

Stabilization of polyriboinosinic-polyribocytidylic acid against enzymatic hydrolysis by addition of poly-1-lysine and carboxymethylcellulose (PICLC) resulted in a compound with marked adjuvanticity. The primary antibody response of rhesus monkeys to formalin-inactivated Venezuelan equine encephalomyelitis virus vaccine was significantly potentiated if the vaccine was combined with PICLC prior to vaccination. The antibody response was maintained at a significantly higher level than controls for 2.5 months postvaccination and paralleled immunological responses reported for live, attenuated (TC-83) vaccine.

Adjuvants, Immunologic↗
PubMed1976

Kinetics of the rapid action of interferon.

The present study was undertaken to examine some factors which lead to early-appearing resistance in human cells treated with interferon. It was previously shown that two conditions required for rapid development of resistance were continuous maintenance of cultures at 37 degrees and use of more than 10 units/ml of interferon. The decay kinetics of the established resistance appear to be approximately the same whether the resistance was induced under conditions favoring rapid or slow development. With the use of actinomycin D it was shown that the mRNA for the antiviral protein is produced between 30 and 45 min after the first contact with interferon. Ruled out were the possibilities that a priming action of interferon and a newly synthesized intermediary protein were necessary for rapid development of resistance.

Cycloheximide↗
PubMed1975

A modified polyriboinosinic-polyribocytidylic acid complex that induces interferon in primates.

A comlex of polyriboinosinic-polyribocytidylic acid (poly I-poly C) with poly-L-lysine and carboxymethylcellulose has been prepared. This complex is five to 10 times as resistant to hydrolysis by primate serum as the parent poly I-poly C. It has a thermal denaturation temperature about 40 C higher than that of poly I-poly C. The complex induces significant levels of serum interferon in monkeys and chimpanzees under conditions in which poly I-poly C itself induces no interferon.

Animals↗
PubMed1974

Post-exposure prophylaxis of murine rabies with polyinosinic-polycytidylic acid and chlorite-oxidized amylose.

Chlorite-oxidized amylose (COAM), polyinosinic-polycytidylic acid [poly(I:C)], and combinations of the two drugs were evaluated for their interferon-inducing properties and their ability to protect mice against rabies infection. Post-exposure administration of one or two doses (100 mug each) of poly(I:C) significantly protected mice against rabies infection. Pretreatment of mice with COAM 3 h before poly(I:C) stimulation resulted in an enhancement of the interferon response. However, the increased interferon titers were not reflected by increased protection against rabies infection over that achieved with poly(I:C) therapy alone. Therapy with COAM alone did not protect mice against rabies but, rather, was associated with enhanced mortality.

Amylose↗
PubMed1973

Effect of interferon treatment on cellular messenger RNA.

Cell monolayers wre treated with interferon, and then were labeled with RNA precursors. Messenger ribonucleoprotein and transfer RNA were liberated from isolated polysomes, and analyzed by electrophoresis on polyacrylamide gels. The messenger ribonucleoproteins and transfer RNA from interferon-treated cells migrated slightly slower than did the corresponding components from control cells. It was shown that the differences in migration speeds was attributable to the fact that the messenger RNAs and transfer RNA that were polysomebound (i.e., being translated) were slightly larger than control-cell RNAs. This phenomenon was seen in mouse L cells, primary mouse-embryo cells, and rabbit-kidney cells. Ribosomal 28S and 18S RNA was not altered, nor was nuclear RNA. Several types of evidence indicate that the biochemical changes are attributable to the interferon in the preparations, and not to impurities. These data may bear on the mechanism by which interferon-treated cells recognize and translate viral RNA poorly. It is tentatively suggested that interferon treatment of cells leads to a change in cellular messenger RNA such that the cell can distinguish it from the subsequently infecting viral RNA.

Amino Acids↗
PubMed1973

Chlorite-oxidized amylose as an adjuvant for interferon production.

Chlorite-oxidized amylose (COAM), when given intraperitoneally to mice and to cats, increased the titer of serum interferon subsequently induced by polyinosinic.polycytidylic acid (In.Cn). Increases ranged from 6- to 100-fold. Maximal effect was observed when COAM was given 3 h prior to In.Cn. COAM given intravenously prior to Newcastle disease virus also significantly increased serum interferon titers.

Adjuvants, Immunologic↗