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Biomedical subjects

E Fishbein

Publications and source records attributed to E Fishbein.

At least 19 recordsLinked to original sources
PubMed1997

Successful use of a chicken-based diet for the treatment of severely malnourished children with persistent diarrhea: a prospective, randomized study.

OBJECTIVE: To evaluate the efficacy of a chicken-based diet for the treatment of persistent diarrhea in severely malnourished children. STUDY DESIGN: Prospective, randomized, double-blind study that compared a chicken-based diet with elemental (Vivonex) and soy (Nursoy) diets. Hospitalized children with third-degree malnutrition and persistent diarrhea, aged 3 to 36 months, were included. Diets were isocaloric and given nasogastrically at 150 ml/kg per day in progressively increasing concentrations. RESULTS: Fifty-six children were included (18 received Vivonex, 19 Nursoy, 19 chicken). They had a mean age of 6.4 +/- 4.4 months, a mean weight of 3604 +/- 1232 gm, and a mean weight-for-age percentage of 51.4% +/- 7.2%. Sixty-four percent had associated conditions on admission to the hospital. Forty-one children (73.2%) were successfully treated (13 Vivonex, 13 Nursoy, 15 chicken). There were no differences in diarrheal outcomes, and all groups had significant weight gain. Failure was independent of the diet and was associated with the presence of infection on admission. There was a significantly higher nitrogen balance in the children from the chicken group (358.2 +/- 13 mg/kg per day) than in those receiving Vivonex (226.6 +/- 61) or Nursoy (291-4 +/- 111.6; p < 0.05) groups. CONCLUSIONS: The chicken-based diet was as effective as Vivonex or Nursoy. It is well tolerated, inexpensive, and widely available and thus represents an effective and inexpensive alternative to the treatment of severely malnourished children with persistent diarrhea.

Animals↗
PubMed1997

Decrease in birth weight in relation to maternal bone-lead burden.

OBJECTIVES: Birth weight predicts infant survival, growth, and development. Previous research suggests that low levels of fetal lead exposure, as estimated by umbilical cord blood-lead levels at birth, may have an adverse effect on birth weight. This report examines the relationship of lead levels in cord blood and maternal bone to birth weight. METHODS: Umbilical cord and maternal venous blood samples and anthropometric and sociodemographic data were obtained at delivery and 1-month postpartum. Blood-lead levels were analyzed by atomic absorption spectrophotometry. Maternal tibia and patella lead levels were determined at 1-month postpartum with use of a spot-source 109Cd K-X-ray fluorescence instrument. The relationship between birth weight and lead burden was evaluated by multiple regression with control of known determinants of size at birth. RESULTS: Data on all variables of interest were obtained for 272 mother-infant pairs. After adjustment for other determinants of birth weight, tibia lead was the only lead biomarker clearly related to birth weight. The decline in birth weight associated to increments in tibia lead was nonlinear and accelerated at the highest tibia lead quartile. In the upper quartile, neonates were on average, 156 grams lighter than those in the lowest quartile. Other significant birth weight predictors included maternal nutritional status, parity, education, gestational age, and smoking during pregnancy. CONCLUSIONS: Our results indicate that bone-lead burden is inversely related to birth weight. Taken together with other research indicating that lead can mobilize from bone into plasma without detectable changes in whole blood lead, these findings suggest that bone lead might be a better biomarker than blood lead. Because lead remains in bone for years to decades, mobilization of bone lead during pregnancy may pose a significant fetal exposure with health consequences, long after maternal external lead exposure has declined.

Birth Weight↗
PubMed1996

Dietary and environmental determinants of blood and bone lead levels in lactating postpartum women living in Mexico City.

Despite the recent declines in environmental lead exposure in the United States and Mexico, the potential for delayed toxicity from bone lead stores remains a significant public health concern. Some evidence indicates that mobilization of lead from bone may be markedly enhanced during the increased bone turnover of pregnancy and lactation, resulting in lead exposure to the fetus and the breast-fed infant. We conducted a cross-sectional investigation of the interrelationships between environmental, dietary, and lifestyle histories, blood lead levels, and bone lead levels among 98 recently postpartum women living in Mexico City. Lead levels in the patella (representing trabecular bone) and tibia (representing cortical bone) were measured by K X-ray fluorescence (KXRF). Multivariate linear regression models showed that significant predictors of higher blood lead included a history of preparing or storing food in lead-glazed ceramic ware, lower milk consumption, and higher levels of lead in patella bone. A 34 micrograms/g increase in patella lead (from the medians of the lowest to the highest quartiles) was associated with an increase in blood lead of 2.4 micrograms/dl. Given the measurement error associated with KXRF and the extrapolation of lead burden from a single bone site, this contribution probably represents an underestimate of the influence of trabecular bone on blood lead. Significant predictors of bone lead in multivariate models included years living in Mexico City, lower consumption of high calcium content foods, and nonuse of calcium supplements for the patella and years living in Mexico City, older age, and lower calcium intake for tibia bone. Low consumption of milk and cheese, as compared to the highest consumption category (every day), was associated with an increase in tibia bone lead of 9.7 micrograms Pb/g bone mineral. The findings of this cross-sectional study suggest that patella bone is a significant contributor to blood lead during lactation and that consumption of high calcium content foods may protect against the accumulation of lead in bone.

Adolescent↗
PubMed1983

Effect of pregnancy on functions of circulating T cells from patients with systemic lupus erythematosus: correction of T-cell suppression and autologous mixed-lymphocyte responses.

Pregnant systemic lupus erythematosus (SLE) patients with inactive disease were found to have normal spontaneously generated suppressor-cell function and slightly higher concanavalin A-induced suppressor function as compared to matched normal pregnant and nonpregnant females. In six SLE patients studied sequentially throughout pregnancy and postpartum, suppressor functions were found to fall sharply within the first week after delivery. One of these patients had been studied before she became pregnant and found to have a decreased suppressor function. Nonpregnant SLE patients had both suppressor functions diminished despite their disease being similarly inactive. This group was also the only one to have decreased responses in autologous mixed-lymphocyte cultures. Both pregnant and nonpregnant SLE patients had decreased absolute numbers of total lymphocytes, T cells, and their subpopulations, but the proportions of these cells were similar in all four groups. Despite this apparent normalcy of immune regulation, pregnant SLE patients had higher levels of Clq-binding immune complexes than did nonpregnant ones. Functional T-cell abnormalities found in SLE patients tend to be corrected by pregnancy. This may explain in part the disease remissions that occur in them during the second half of pregnancy.

Concanavalin A↗
PubMed1983

Cellular bases of the production of and response to interleukin-2 in man: role of autologous rosette-forming T-cell subsets defined with monoclonal antibodies.

In this paper we present experiments that indicate that, in man, most T-cell subpopulations produce interleukin-2 (IL-2), but that the main cell subpopulation which produces it, both upon activation with phytohaemagglutinin or in autologous mixed lymphocyte cultures, is that of autologous rosette-forming (Tar) T4+ T cells. Conversely, the main IL-2-responding T-cell subpopulation is that composed of T cells depleted of Tar (T-Tar) that are T8+. IL-2 was also found to be more effectively produced by Tar cells that do not bind peanut agglutinin (PNA) than by those that do. The PNA-T4+Tar cells were also found to respond best to interleukin-1 (IL-1).

Antibodies, Monoclonal↗
PubMed1982

Abnormalities in the content of nucleic acids of peripheral blood mononuclear cells from patients with systemic lupus erythematosus.

We have completed 59 cytofluorographic studies of DNA/RNA content in acridine orange-stained peripheral blood mononuclear cells from 44 patients with systemic lupus erythematosus, most of whom received no medications. Most such cells were in resting phases of the cell cycle, particularly those from patients with inactive disease. Nine patients with systemic lupus erythematosus had increased percentages of these cells in the synthesis and postsynthesis phases of the cell cycle; the B lymphocyte had a greatest proportions of activated cells. In 11 patients, we found that cells, particularly T lymphocytes, had increased RNA content without a proportional increase in DNA. This DNA block occurred primarily in patients with serum antibodies to DNA and it could be reproduced in normal mitogen-stimulated mononuclear cells incubated in heat-inactivated sera from patients with systemic lupus erythematosus whose own cells showed abnormalities of DNA/RNA content or in purified native DNA antibody. The DNA blocking potential of the DNA antibody was dependent on its Fc portion and on the presence of Fc receptors on T cells. Thus, saturation of Fc receptors by pretreatment with aggregated IgG or incubation with the whole antibody in the cold prevented the DNA block, indicating that it was an active process.

Antibodies↗
PubMed1980

A method for high yield isolation and purification of anti-native DNA antibodies present in lupus sera.

Antibodies to nucleic acids may serve as biochemical tools or as probes of cellular function. Particularly important, but also particularly difficult to obtain, is antibody which reacts exclusively with double stranded DNA. We describe here a method for the separation of antibodies to double stranded DNA from SLE serum, using hydroxyapatite to which DNA is adsorbed at a low molarity of phosphate buffer. Having applied the serum to the column we passed it through a continuous gradient of phosphate buffer ranging from 0.005 to 0.5 M. Deoxyribonuclease and magnesium ions were added when the gradient had reached the molarity at which single stranded DNA had already been desorbed and double stranded DNA began to be eluted. The antibody to native DNA that we obtained reacted in complement fixation, counterimmunoelectrophoresis and Farr's assay with native DNA and did not react with single stranded DNA, single and double stranded RNA or with a panel of 24 protein-coupled nucleosides, nucleotides and dinucleotides.

Antibodies↗
PubMed1979

Antibody penetration into living cells. I. Intranuclear immunoglobulin in peripheral blood mononuclear cells in mixed connective tissue disease and systemic lupus erythematosus.

We have shown recently (Alarcón-Segovia, Ruíz-Argüelles & Fishbein, 1978) that an IgG anti-RNP antibody obtained from a patient with mixed connective tissue disease (MCTD) can penetrate viable mononuclear cells (MNC) from normal donors via their Fc receptors. Live MNC from twelve MCTD patients incubated with goat anti-Ig antibody had intranuclear antibody with a speckled pattern in a mean of 5.5% of all MNC and 57.3% of all Fc receptor-bearing MNC. We found intranuclear immunoglobulins in all twelve patients with MCTD which were present only in cells with Fc receptors. Only three out of twenty-one patients with systemic lupus erythematosus (SLE) were found to have intranuclear antibody in a mean of 17.2% of their Fc receptor-bearing cells. Further experiments with MNC from SLE patients revealed a partial blocking of penetration of antibody via Fc receptors. MNC from ten scleroderma, ten rheumatoid arthritis patients and eleven normal controls did not have intranuclear immunoglobulin. In vivo penetration of autoantibodies into Fc receptor-bearing cells in MCTD, and probably in SLE as well, may represent an important pathogenetic mechanism.

Arthritis, Rheumatoid↗
PubMed1979

Antibodies to histones in systemic lupus erythematosus.

Antibodies to histones were investigated in the serum of forty-five patients with spontaneously occurring systemic lupus erythematosus (SLE) who were not receiving any form of treatment. Twenty-three had active and twenty-two had inactive disease. Thos with active disease were also studied after the initiation of corticosteroid treatment to determine the effect of treatment on anti-histone antibodies. Both a complement fixation method and indirect immunofluorescence of acid-eluted histone-reconstituted tissue sections were used, with excellent correlation between these two methods. Eleven of the forty-five SLE patients, but none of forty-five normal controls had antibodies to histone. Untreated patients with active and inactive disease had a similar incidence of antibodies to histone. They disappeared, however, soon after the initiation of treatment in the patients with active disease. Patients with antibodies to histones had a higher prevalence of cutaneous vasculitis, anaemia, lupus nephropathy and Raynaud's phenomenon, but a lower prevalence of lupus brain involvement than those without such antibodies. Only the latter, however, reached statistical significance.

Adrenal Cortex Hormones↗
PubMed1978

Free serum ribonucleoprotein in mixed connective tissue disease and other connective tissue diseases.

Free ribonucleoprotein (RNP) was found by means of a hemagglutination inhibition assay in 21 sera from 11 of 25 patients with mixed connective tissue disease (MCTD) who had 299 sera studied. Free RNP tended to appear when anti-RNP antibody titers fell or when prednisone was initiated or increased. Five of 72 SLE patients (211 sera) had free RNP in at least one serum. Three of them had anti-RNP antibodies in other sera. Free serum RNP was found in one of 20 patients with scleroderma and in two of seven patients with connective tissue disease "overlap" syndromes without anti-RNP.

Antibodies, Antinuclear↗
PubMed1976

Immunochemical characterization of the anti-RNA antibodies found in scleroderma and systemic lupus erythematosus. II. Reactivity with hsa-coupled, uridine-containing, monophosphoric ribodinucleotides.

Sera from patients with scleroderma have been found to have anti-RNA antibodies which react with human serum albumin (HSA)-coupled uridine and uridine monophosphate (UMP) and are inhibited by uracil, uridine and UMP. Scleroderma sera react uniformly with 5'-polyuridylic acid (poly(U)) and fail to react with polyadenylic, polyuridylic acid poly(A) - poly(U)) which is also indicative of their uracil specificity. Anti-RNA antibodies found in systemic lupus erythematosus (SLE) are immunochemically different from those found in scleroderma in that, instead of being uniformly specific to uracil, they are markedly heterogeneous and may react with uracil, uridine and/or UMP. SLE sera frequently react with poly(A) - poly(U), indicating also their ability to recognize the double helical structure of double-stranded RNA. Thirty-seven scleroderma and thirty-four SLE sera from as many patients with either of these conditions were tested against HSA-coupled, uridine-containing monophosphoric dinucleotides in an attempt to characterize further their anti-RNA antibodies. Scleroderma sera were found to react primarily with dinucleotides in which uridine was the base proximal to the carrier protein and, except for sera that also contained antibodies to adenosine which reacted with UpA, they failed to react with dinucleotides in which uridine was in a terminal position only. Reaction with dinucleotides in which uridine was proximal to the carrier protein could be inhibited by uracil but not by the corresponding terminal base. Some lupus sera were found to react with both dinucleotides that contain the same bases in opposite sequence, e.g. ApU and UpA, while others were found to react with only one of the sequences. They were also found to react more frequently with dinucleotides in which HSA was coupled to a base other than uridine, suggesting that the reaction is primarily due to anti-DNA antibodies. Because immunization with dinucleotides coupled to protein prepared by the same method we have used, yields higher specificity to the base attached to the carrier protein, our findings suggest that, in scleroderma, a single event, akin to that of immunization with a purified antigen, gives rise to the anti-RNA antibodies, whereas in systemic lupus erythematosus there is a considerably wider immunological aberration.

Adenosine↗
PubMed1975

Uracil-specific anti-R.N.A. antibodies in scleroderma.

Antibodies to single-stranded R.N.A. were found by counter immunoelectrophoresis in all of 40 sera from patients with scleroderma. These antibodies were specific to the uracil bases of R.N.A. Antibodies to R.N.A. were also found in 20 of 40 sera from patients with systemic lupus erythematosus (S.L.E.), but in none of forty controls. Antibodies to R.N.A. found in S.L.E. sera could be differentiated immunochemically from those found in scleroderma in that they were more heterogeneous and could react selectively with either uridine or uridine monophosphate. Antibodies ot D.N.A. were more frequent in S.L.E. than in scleroderma. That antibodies to D.N.A. are actually present in scleroderma and precipitin lines are not the result of cross reactivity with anti-R.N.A. antibodies is indicated by the finding that 10 of the 18 scleroderma sera which reacted with D.N.A. also reacted with thymidine, a base present in D.N.A. but not in R.N.A.

Adenosine↗
PubMed1975

Patterns of antinuclear antibodies and lupus-activating drugs.

Patterns of antinuclear antibodies (ANA) occurring in individuals consuming lupus-activating drugs who have not developed systemic lupus erythematosus (SLE), may give insight into their mode of action as SLE triggering agents. We have studied the antigenic specificity of ANA induced by isoniazid (INH), anticonvulsants and chlorpromazine. ANA found in INH treated subjects are primarily directed at soluble nucleoprotein (sNP), an antigen which is physicochemically altered in vivo by INH. Antibodies to INH altered sNP were found in 78 per cent of 214 subjects receiving INH, while none had anti-DNA antibodies. Different anticonvulsants give rise to different patterns of ANA. Antibodies to Sm antigen were found only in patients receiving hydantoins. Antibodies to native and denatured DNA were found in 14 per cent and 22 per cent respectively, of 170 patients receiving anticonvulsants. Antibodies to denatured DNA were most frequently found in patients receiving chlorpromazine, which correlated with the known reactivity of this drug to denatured DNA.

Antibodies, Antinuclear↗
PubMed1975

Immunochemical characterization of the anti-RNA antibodies found in scleroderma and systemic lupus erythematosus. I. Differences in reactivity with Poly (U) and Poly-(A) Poly (U).

In a previous study, all 40 sera from patients with scleroderma, 20 of 40 sera from SLE patients, but none of 40 sera from normal controls, were found to have antibodies to ssRNA. All scleroderma sera were also found to react with HSA-coupled uridine and UMP and their reaction with HSA-coupled uridine and UMP and their reaction with ssRNA could be inhibited by uracil, uridine, and UMP. To characterize further these uracil-specific anti-RNA antibodies found in scleroderma and compare them with the anti-RNA antibodies found in SLE, we tested their reactivity with Poly (U) and with Poly (A)-Poly (U) and all but one failed to react with Poly (A)-Poly (U). This same serum was the only one in which the reaction with Poly (U) could not be inhibited with uracil. Reactivity of SLE sera was strikingly different from that found in scleroderma sera. Seventeen of 34 SLE sera studied reacted with ssRNA but only four of these reacted with Poly (U). Conversely, two SLE sera that reacted with Poly (U) did not react with ssRNA. Fifteen reacted with Poly (A)-Poly (U) and only two of these failed to react with ssRNA. Five SLE sera which were reactive with ssRNA did not precipitate with Poly (A)-Poly (U). All SLE sera which reacted with Poly (U) could be inhibited with uracil, although less effectively than in scleroderma. Reactivity with Poly (A)-Poly )U) was not inhibited with uracil nor with adenosine. These findings confirm that antibodies to RNA that are found in scleroderma are directed to uracil and thus specific to ssRNA, whereas RNA antibodies found in SLE sera are heterogeneous and directed to either the base, to the site of union of the base and sugar moiety to the ribose backbone, or to the helical structure of double stranded RNA. These differences and the respective antigenic specificities of these anti-RNA antibodies found in scleroderma and SLE may be theoretically important.

Adenine↗
PubMed1975

The heterogeneity of anti-DNA antibodies in systemic lupus erythematosus and other diseases.

The antigenic specificities of antinucleic acid antibodies occurring in systemic lupus erythematosus (SLE), chronic active liver disease, and progressive systemic sclerosis (PSS) have been studied by means of haptenic nucleosides and nucleotides coupled to human serum albumin. SLE sera were also tested with dinucleotides. SLE and chronic active liver disease sera showed marked heterogeneity, producing precipitin lines with nucleosides or nucleotides, or both. The reaction might occur with a nucleoside and not with the corresponding nucleotide, or vice versa. The SLE sera reacted to dinucleotides with marked specificity, being able to recognize base sequences or to react with a dinucleotide despite the absence of a reaction with the individual bases. All sera from patients with PSS showed precipitins with RNA, uridine and UMP. PSS sera which reacted with a nucleoside also reacted with the corresponding nucleotide. Antibodies to DNA were found in a smaller proportion of PSS sera than in sera from SLE or chronic active liver disease. Their presence was confirmed by reactivity with thymidine and TMP.

Antibodies, Anti-Idiotypic↗