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Biomedical subjects

J S Fine

Publications and source records attributed to J S Fine.

At least 19 recordsLinked to original sources
PubMed1995

Interleukin 4 retards dissemination of a human B-cell lymphoma in severe combined immunodeficient mice.

We have examined the antitumor activity of murine interleukin 4 (IL-4) on development of a human B-cell lymphoma (Daudi) in severe combined immunodeficient (SCID) mice. The progression of Daudi cells in SCID mice was followed by histological staining and by flow cytometric analysis of CD20+ cells in spleen, liver, bone marrow, and kidneys. By day 35, CD20+ Daudi cells populate the majority of space in the bone marrow and kidney in vehicle-treated mice. Mice receiving i.p. injections of IL-4, commencing 7 or 14 days after tumor inoculation, exhibit a reduction in tumor burden as well as a decrease in CD20+ cells in both compartments. The antitumor activity of IL-4 does not appear to be due to an antiproliferative effect, since the cytokine does not alter the growth of Daudi cells in vitro, nor does it correlate with any marked cellular infiltrate in tumor-bearing tissues. In 51Cr-release assays, we observed that splenocytes from IL-4-treated mice were capable of lysing YAC-1 but not Daudi cell targets. Our findings demonstrate that: (a) systemic administration of IL-4 retards dissemination of a human B-cell lymphoma in SCID mice; and (b) antitumor activity elicited by IL-4 may not involve a direct effect on proliferation of Daudi cells or on the induction of cytolytic activity.

Animals↗
PubMed1995

D-phenylalanyl-L-prolyl-L-arginine chloromethyl ketone (PPACK): alternative anticoagulant to heparin salts for blood gas and electrolyte specimens.

D-Phenylalanyl-L-prolyl-L-arginine chloromethyl ketone (PPACK), a selective thrombin inhibitor, was evaluated as an alternative anticoagulant to lithium heparin (LiHep) for blood gas and whole-blood electrolyte analyses. Initial studies in serum revealed a negative proportional bias for ionized calcium (iCa) concentration measured in the range of increasing concentrations of LiHep (-0.02 mmol/L iCa per 33 kIU/L), whereas no bias in iCa concentration was detected with increasing concentrations of PPACK. No anticoagulant-dependent changes in serum sodium, potassium, chloride, glucose, lactate, ionized magnesium, or pH were detected with either PPACK or LiHep. Similarly, no bias was observed in the measurement of whole-blood PO2, PCO2, pH, or sodium or potassium concentrations with either anticoagulant. Whole blood anticoagulated with LiHep (33 kIU/L) demonstrated a consistent -0.06 +/- 0.01 mmol/L bias for iCa compared with a nonanticoagulated whole-blood control. In comparison, no iCa bias was observed with PPACK-anticoagulated whole blood. We conclude that PPACK has ideal bias-free properties as an anticoagulant in analyses for blood gases, electrolytes, and iCa.

Amino Acid Chloromethyl Ketones↗
PubMed1995

BibleCard: network-based virtual database for laboratory information.

The clinical laboratory's use of computers has evolved beyond the single minicomputer stand-alone system. Our laboratory information system is now part of an institutional network. The laboratory also uses smaller systems and workstations for a wide variety of functions, often with much data duplication among systems. We have been developing a network-based virtual database for laboratory test information. This system uses World Wide Web standards for hypertext and multimedia displays, which allows for the display of information retrieved from various department computer sources without the necessity of data duplication, modification of existing systems, or centralization of data. The medical technologists can continue to write testing procedures on their word processors. Maintenance of reference values, specimen requirements, etc., can continue as a laboratory information system function. Yet information from all of these disparate sources can be viewed in a consolidated format that has platform independence.

Chemistry, Clinical↗
PubMed1994

Interleukin-10 enhances gamma delta T cell development in the murine fetal thymus.

We have investigated the ability of interleukin-10 (IL-10) to modulate murine intrathymic T cell differentiation using a fetal thymic organ culture (FTOC) model. Addition of as little as 11 ng of recombinant murine IL-10 (mIL-10) per day produced a significant increase in the proportion and number of gamma delta-TCR+ cells in 4-day cultures derived from Gestational Day 14 mice, compared to vehicle-treated cultures. This effect occurred in the absence of any changes in other parameters of intrathymic T cell development. The increase in the gamma delta-TCR population included an enlargement of the V gamma 2+, V gamma 3+, and V delta 4+ populations. The enhancement of gamma delta cell development was not observed in 2- or 7-day cultures, indicating the time dependence of this response. Overall, these results reveal that IL-10 treatment of FTOC can affect murine gamma delta T cell development and suggest that this cytokine may mediate specific events in the generation of the gamma delta T cell repertoire.

Animals↗
PubMed1994

Influence of IL-10 on murine CFU-pre-B formation.

We have examined the ability of interleukin-10 (IL-10) to influence murine B cell development in vitro and in vivo. In vitro treatment of young adult mouse bone marrow cells with 0.5 to 10 ng/ml human IL-10 (hIL-10) produced a significant enhancement of IL-7-mediated colony-forming unit-pre-B (CFU-pre-B) formation, while IL-10 concentrations > 10 ng/ml had no net effect. IL-10 by itself was unable to stimulate pre-B cell colony formation, even at optimal concentrations. The increase in CFU-pre-B produced by IL-10 was specifically blocked by anti-hIL-10 antibody, but not by anti-stem cell factor (SCF) antibody, and was observed with both unfractionated and purified B220+ surface immunoglobulin (sIg-) bone marrow cells. CFU-pre-B from the IL-10 treatment group contained a higher percentage of CD43+B220+ blast-like cells than colonies exposed to IL-7 only. In vivo administration of 0.1 microgram hIL-10 per day to mice treated with a single sublethal dose of cyclophosphamide (CY) resulted in a dramatic and accelerated recovery of CFU-pre-B numbers as compared to vehicle-administered mice. This enhancement was seen as early as day 11 post-CY, and the number of CFU-pre-B was comparable to normal age-matched control mice by day 16. In contrast, the number of CFU-pre-B in vehicle-treated mice remained significantly lower than age-matched and IL-10-treated animals as long as day 22 post-CY. No differences in the number of pre-B and mature B cells in bone marrow or in the number of mature B cells in peripheral lymphoid organs were detected in IL-10-treated mice. Myeloid cell recovery, assessed by the CFU-granulocyte/macrophage (CFU-GM) assay and the number of marrow Mac-1+ cells, was unaffected by IL-10 treatment of CY-dosed animals. These results indicate that IL-10 enhanced IL-7-stimulated murine pre-B cell colony formation and imply a role for IL-10 in normal B lymphopoiesis.

Animals↗
PubMed1993

Effects of media, atmosphere, and incubation time on colonial morphology of Arcanobacterium haemolyticum.

Arcanobacterium haemolyticum causes pharyngitis as well as skin and other wound infections. Although it is a beta-hemolytic organism, the hemolysis is less well defined than that of beta-hemolytic streptococci and may be overlooked in cultures with heavy growth of commensal throat flora. To determine whether routine throat culture conditions are sufficient to produce recognizable colonies of A. haemolyticum, the morphology of six distinct strains was studied after various combinations of incubation time, medium, and atmosphere. The agar media, containing 5% sheep blood, were Trypticase soy agar, Columbia agar, and heart infusion agar. Cultures were incubated in ambient air, 6 to 8% CO2, or an anaerobic atmosphere. Cultures were compared after 24, 48, and 72 h of incubation for colony size, clarity and size of hemolytic zone, and macroscopic evidence of agar pitting. A minimum of 48 h was needed for expression of beta-hemolysis and pitting. Trypticase soy agar was the superior medium and CO2 was the superior atmosphere for beta-hemolysis. Agar pitting was not significantly affected by variations in medium or atmosphere. Strains differed in their expression of hemolysis and production of pits at 48 h. After 72 h of incubation, beta-hemolysis and pitting were visible in over 96% of culture observations.

Atmosphere↗
PubMed1993

The Avianca plane crash: an emergency medical system's response to pediatric survivors of the disaster.

OBJECTIVE: On January 25, 1990, a jetliner crashed on Long Island, New York. Twenty-two children survived the crash. The purpose of this study was to evaluate the emergency medical system's response to these pediatric survivors. METHODS: A questionnaire was sent to all local, acute care hospitals to determine their specific pediatric capabilities and to rank them as level I, II, or III pediatric centers; level I centers are tertiary care facilities. A second questionnaire was sent to all hospitals that received pediatric survivors to collect specific clinical information for each patient. Based on this clinical information a Pediatric Trauma Score (PTS) was assigned to each patient. Children with a PTS < or = 8 are considered to be at increased risk of trauma-related mortality. The assigned PTS was compared to the level of the pediatric center to which each patient was transported. RESULTS: Of 25 children on board the plane, 22 (88%) survived the crash; of 135 adults on board, 70 (52%) survived (chi 2 = 9.9, P = .002). Seven children had a PTs < or = 8; only 1 of these high-risk patients was transported directly to a level I pediatric center, and only 2 of the 5 high-risk children initially transported to level III facilities were transferred to higher level pediatric centers. CONCLUSIONS: Pediatric survivors were neither adequately triaged nor transported to appropriate facilities which could optimize their care. Possible explanations for this include: (1) unique features of the rescue operation, (2) limited pediatric training of prehospital personnel, and (3) deficiencies of the regional disaster plan. Emergency medical services systems and disaster plans can be made more responsive to children's needs by: (1) acknowledging that children have special needs requiring referral, (2) improving the training of prehospital personnel in pediatric emergency care, (3) classifying ill and injured children according to appropriate triage criteria, (4) recognizing existing tertiary care pediatric centers as the optimal location for the treatment of critically ill and injured children, and (5) designating these centers as the appropriate transport destination for critically ill and injured children.

Accidents, Aviation↗
PubMed1992

Update in medical toxicology.

This article examines some current issues in toxicologic care. First there is a review of the scope of pediatric poisonings and some aspects of initial management. Then there is a discussion of the decision-making process required to properly use gastric decontamination in the management of poisonings. Each of the common methods available--emesis, gastric lavage, activated charcoal, catharsis, and whole bowel irrigation--is discussed. Finally, several new and old antidotes are reviewed, namely naloxone, glucagon, bicarbonate, dimercaptosuccinic acid, digoxin-specific fab fragments, and flumazenil.

Antidotes↗
PubMed1992

Changes in the methylation pattern of the TCR zeta-chain gene correlate with its expression in T cells and developing thymocytes.

The tight regulation of T-cell gene expression during thymic ontogeny is essential to the development of a normal immune system. One set of developmentally regulated genes encodes the multicomponent T-cell antigen receptor (TCR). The zeta chain, a component of the TCR, has been shown to play important roles in signal transduction from antigen binding to T-cell activation and in transport of the TCR complex to the cell surface. In this study, we examine the regulation of zeta gene expression in murine T-cell hybridomas. In these cells, zeta expression is correlated with complex, but predictable, changes in the pattern of cytosine methylation of its gene. Some of these structural changes are identical to those observed in murine fetal thymocytes and correlate with the rapid alteration of zeta message seen in the thymus between days 15 and 18 of gestation.

Animals↗
PubMed1991

The role of LFA-1/ICAM-1 interactions during murine T lymphocyte development.

We have examined the expression and function of the cell adhesion molecules LFA-1 (CD11a/CD18), ICAM-1 (CD54), and ICAM-2 in murine fetal thymic ontogeny and in the adult thymus. On fetal days 14 and 15, 40 to 50% of thymocytes coexpress high levels of LFA-1 and ICAM-1, as determined by flow cytometry. By day 16, more than 90% of fetal thymocytes are LFA-1+ ICAM-1hi, and all IL-2R+ cells are located in this population. Although LFA-1 expression remains unchanged thereafter, ICAM-1 expression appears to be differentially regulated in different thymocyte subpopulations, with CD4+8+ cells being ICAM-1lo and CD4-8- thymocytes remaining ICAM-1hi. ICAM-2 surface expression is dull on both fetal and adult thymocytes. Surprisingly, the expression of ICAM-1 is differentially up-regulated on T cells having a mature phenotype in thymus and in peripheral lymphoid organs, with CD8+ T cells bearing the highest amount of surface ICAM-1. Addition of anti-ICAM-1 or anti-LFA-1 antibodies to fetal thymic organ cultures results in the impaired generation of CD4+8+ cells. These results indicate that LFA-1/ICAM-1 interactions facilitate murine thymic development and suggest that cell adhesion molecules mediate important events in T cell differentiation.

Age Factors↗
PubMed1990

Impairment of prothymocyte activity by 2,3,7,8-tetrachlorodibenzo-p-dioxin.

Exposure of experimental animals to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) results in severe thymic atrophy and suppression of cell-mediated and humoral immune functions. However, despite much effort the mechanism by which TCDD produces these responses, particularly thymic atrophy, remains unclear. In this report, we have examined the effect of acute TCDD exposure on lymphocyte stem cells in young adult BALB/c mice to determine whether alterations to events early in T lymphopoiesis contribute to TCDD-induced thymic atrophy. TCDD produced a dose-dependent reduction in thymic weight and cellularity following a single dose of 5 to 120 micrograms TCDD/kg. This thymic atrophy correlated with a dose-dependent suppression of the biosynthesis and mRNA levels of the lymphocyte stem cell-specific DNA polymerase terminal deoxynucleotidyl transferase in bone marrow and thymus. However, the reduction in thymic terminal deoxynucleotidyl nucleotidyl transferase synthesis, on a per cell basis, was less than that observed in bone marrow. Intrathymic CD4/CD8 and IL-2R expression demonstrated only mild alterations after exposure to 30 micrograms TCDD/kg. These data suggest that thymocytes are more refractory to TCDD than are pre-T cells. To assess this possibility directly, bone marrow prothymocytes from TCDD-treated donor mice were examined for their capacity to reconstitute the thymuses of adoptive, irradiated recipients. Our results indicate that prothymocyte activity was severely impaired by TCDD exposure and that this effect occurred at low tissue levels of TCDD. In contrast, we observed no reduction in the number of colony-forming unit-granulocyte macrophage and a moderate decrease in colony-forming unit-spleen. These data suggest that TCDD-induced thymic atrophy is the result, at least in part, of impaired thymic seeding by prothymocytes.

Animals↗
PubMed1990

Prothymocyte activity is reduced by perinatal 2,3,7,8-tetrachlorodibenzo-p-dioxin exposure.

The mechanism by which exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) produces thymic atrophy and cell-mediated immune suppression in experimental animals is poorly understood. A previous study from our laboratory found that terminal deoxynucleotidyl transferase-synthesizing lymphocyte stem cell populations in fetal liver and neonatal bone marrow, but not thymus, were profoundly altered after perinatal TCDD exposure, implying that a defect in the prothymocyte population in liver and marrow may play a role in the etiology of thymic atrophy in TCDD-exposed animals. In this report, we present results of experiments designed to directly assess the prothymocyte compartment in mice exposed to TCDD perinatally by examining the ability of these stem cells to reconstitute an irradiated thymus. Maternal TCDD exposure (15 micrograms/kg) caused a significant impairment of both fetal liver and neonatal bone marrow prothymocyte activity. These alterations occurred at tissue concentrations less than 200 fg of TCDD per mg. TCDD treatment also resulted in a mild reduction in colony-forming unit-spleen in these organs and a decrease in colony-forming unit-granulocyte-macrophage in fetal and neonatal liver, but not bone marrow. Overall, these data provide evidence that alterations to early stages of T-lymphopoiesis, at the level of the prothymocyte, may be involved in the development of TCDD-induced thymic atrophy and cell-mediated immunosuppression.

Animals↗
PubMed1989

Lymphocyte stem cell alterations following perinatal exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin.

Perinatal exposure of experimental animals to the environmental contaminant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) leads to thymic atrophy and a suppression of cell-mediated immunity that is more severe and persistent than that caused by adult exposure, suggesting that events involved in the maturation of the immune system are particularly sensitive to TCDD. We report here that perinatal TCDD exposure produces an alteration in the lymphocyte stem cell population in the fetus and neonate, as evidenced by a significant reduction in the lymphocyte stem cell-specific enzyme terminal deoxynucleotidyl transferase (TdT). After maternal treatment with a single dose of TCDD (10 micrograms/kg of body weight) on gestational day (gd) 14, TdT biosynthesis and TdT-specific mRNA were reduced more than 50% in fetal liver lymphoid cells on gd 18. An even more extensive reduction was seen in neonatal bone marrow through postnatal day 18. In contrast, thymic TdT synthesis appeared to be relatively unaffected on a per cell basis by perinatal TCDD exposure, although the actual number of TdT-synthesizing thymocytes was diminished due to extensive thymic atrophy. These effects occurred at concentrations of 1-31 fg of TCDD/mg of thymus. Flow cytometric analysis of thymocyte surface marker expression revealed a slight decrease in the percentage of Lyt-2+L3T4+ thymocytes on gd 18 and postnatal day 4. This alteration was no longer apparent by postnatal day 11, when marrow TdT biosynthesis was most suppressed. These results suggest that TCDD-induced thymic atrophy during the perinatal period may be due, in part, to an effect on the prothymocyte.

Animals↗
PubMed1988

Regional creatine kinase, adenylate kinase, and lactate dehydrogenase in normal canine brain.

Following acute stroke, creatine kinase and other enzymes are released into the cerebrospinal fluid and blood from injured brain tissue. To determine whether regional differences in brain enzyme activity might exist and therefore affect the amount of enzyme released, we quantified the levels of creatine kinase, adenylate kinase, and lactate dehydrogenase in 12 regions of normal canine brain (n = 4). Adenylate kinase activity varied the least among regions (49 +/- 7 units/g), followed by lactate dehydrogenase activity (122 +/- 28 units/g). The pattern for both adenylate kinase and lactate dehydrogenase was higher activity in predominantly gray matter areas, lower activity in white matter, and intermediate activity in mixed regions. The distribution of creatine kinase brain isoenzyme and mitochondrial creatine kinase in canine brain was less predictable, showing wider variations among regions (isoenzyme, 462 +/- 116 units/g; mitochondrial, 42 +/- 20 units/g). Even cerebral gray matter demonstrated substantial regional variations in creatine kinase brain isoenzyme, ranging from 606 units/g in the parietal cortex to 329 units/g in the temporal cortex. We conclude that the content of creatine kinase brain isoenzyme varies more than twofold among areas of brain. This regional variation may be important in the interpretation of creatine kinase brain isoenzyme measurements in cerebrospinal fluid and serum used to assess neurologic injury following stroke.

Adenylate Kinase↗
PubMed1988

Survey of alpha-amylase activity and isoamylases in autopsy tissue.

We quantified total amylase and its isoenzymes in 22 different human tissues obtained at autopsy. Isoenzymes were separated by use of wheat-germ inhibition (WI) and electrophoresis on cellulose acetate (CA) and agarose (AG). Mean (+/- SD) total activity was highest in salivary glands (parotid 1710 +/- 897 U/g, submandibular 605 +/- 354 U/g), and pancreas (258 +/- 137 U/g). All other tissues contained 100- to 1000-fold less amylase. As assessed with WI, pancreas, jejunum, liver, placenta, testis, skeletal muscle, and spleen contained more than 90% pancreatic isoamylase. Salivary glands and thyroid contained more than 90% salivary isoamylase. All other tissues contained a mixture of the two isoenzymes. CA and AG often produced different results. For both CA and AG the most common pancreatic isoforms were P2 and S1. Salivary gland homogenates demonstrated a band migrating in the P3 position on CA. We conclude that both types of amylase isoenzymes can be found in tissues other than salivary gland and pancreas, but that their low total amylase concentrations diminish their clinical importance.

Electrophoresis, Polyacrylamide Gel↗
PubMed1988

Effect of creatine kinase-MM subtype composition on a CK-MB immunoinhibition assay.

Immunoinhibition (INH) by use of polyclonal anti-human CK-M antibody may be used to measure CK-MB in serum. Previous studies have shown that inhibiting antibodies prepared against purified muscle extracts may inhibit CK-MM by greater than 99%. Using patients' sera and muscle homogenates incubated with human serum, we studied the effect of CK-MM subtype composition on an INH assay. We found that with increasing time from the CK-releasing event, e.g., myocardial infarction, or with longer in vitro incubation, the proportion of CK-MM1 increased and the proportion of uninhibited CK-MM increased from 0.2% to 0.7-0.8%. As a consequence, CK-MB activity may be overestimated by as much as 1.6% of total CK when uncorrected INH results are used. Inhibition was maximal in samples containing 100% CK-MM3, the tissue subtype. Because of the time-dependent change in CK-MM subtypes, published results for INH from studies in which CK-MM purified from muscle was used may not be directly applicable to clinical specimens.

Creatine Kinase↗