Adaptation of ICU ventilator to deliver isoflurane.
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Anesthetics, Inhalation↗
Biomedical subjects
K Robbins
Publications and source records attributed to K Robbins.
Anti-immunoglobulin E treatment decreases worm burden and egg production in Schistosoma mansoni-infected normal and interferon gamma knockout mice.
The immunoglobulin E (IgE) response is generally considered an essential component of the host defense against parasitic helminths such as Schistosoma mansoni. In contrast, work on antischistosome vaccines suggests that interferon gamma (IFN-gamma) is the critical immune mediator for vaccine-induced immunity to the parasite. In this study, the total IgE response to a primary S. mansoni infection was suppressed by anti-IgE treatment in both normal mice and in mice with defective IFN genes (gene knockout [GKO]). Reduction of the IgE response resulted in decreased worm burden and a decrease in the number of eggs produced per worm in both normal and GKO mice. Whereas anti-IgE treatment also resulted in reduced hepatosplenomegaly, granulomas around existing schistosome eggs showed normal cellularity. Serum interleukin 4 levels fell in response to the reduction in serum IgE as well. The data suggest that IgE plays a detrimental, rather than beneficial, role for the host in schistosomiasis. Furthermore, the absence of IFN-gamma was found to be of little consequence to the host-response to adults or eggs in a primary schistosome infection.
Animals↗
Reference accuracy in the dermatologic literature.
BACKGROUND: The reference list is an important part of a scientific article. To be useful it must be accurate. OBJECTIVE: The purpose of this study was to evaluate the accuracy of references in the dermatologic literature. METHODS: We randomly selected 240 references (60 per journal) from the Archives of Dermatology, the British Journal of Dermatology, this Journal, and the Journal of Investigative Dermatology and checked them against the original articles. RESULTS: The overall rate of citation error (the information identifying the source) was 41%, and the quotation error (inconsistency between the statement referenced and the original source) was 35%. Only 36% of references were free of error. CONCLUSION: This study shows that the rate of citation and quotation errors is unacceptably high in the dermatologic literature, which significantly diminishes the value of the reference list.
Bibliometrics↗
Immunological effects of insulin-like growth factor-I--enhancement of immunoglobulin synthesis.
In addition to its activity as a metabolic hormone and a regulator of somatic growth, insulin-like growth factor-I (IGF-I) has cytokine-like activities on lymphoid cells. A 14-day infusion of recombinant human (rh)IGF-I increased lymphocyte numbers in all the peripheral lymphoid organs examined. This increase was apparent for up to 3 weeks following cessation of hormone treatment. A second administration of rhIGF-I, given when the lymphocyte numbers in the rhIGF-I-treated mice had returned to control values, resulted in similar increases in the peripheral T and B cell populations. This increase in lymphocyte numbers had functional significance, since rhIGF-I-treated mice produced elevated antibody titres following primary or secondary antigen challenge compared with controls. In addition, when rhIGF-I-treated mice were immunized with a suboptimal dose of antigen they produced antibody titres which were equivalent to those generated by immunization with optimal doses of antigen. When examined in vitro, addition of rhIGF-I alone to cultures of splenocytes from antigen-primed mice stimulated immunoglobulin synthesis. These studies suggest that IGF-I produced locally by thymic and bone marrow stromal cells may be a natural component of B and T cell lymphopoiesis.
Animals↗
Administration of an anti-IgE antibody inhibits CD23 expression and IgE production in vivo.
High IgE responder BDF1 mice were immunized intraperitoneally (i.p.) with dinitrophenol4 (DNP4)-ovalbumin (OVA) in alum concomitant with intravenous (i.v.) administration of an anti-IgE monoclonal antibody (mAb). IgE levels were undetectable in mice treated with the anti-IgE antibody, whereas mice treated with isotype-matched irrelevant mAb had IgE levels comparable to that of untreated, immunized mice. Subsequent antigen challenges with DNP4-OVA, either at weekly or monthly intervals, failed to evoke an IgE response for greater than 2 months in mice treated with anti-IgE during the primary sensitization, even though the terminal half-life of the anti-IgE antibody was 7 days. This inhibition was specific for DNP4-OVA since the DNP4-OVA-suppressed mice were able to respond to keyhole limpet haemocyanin (KLH). To investigate the effects of antibody treatment at the cellular level, passive transfer experiments were performed. The primary DNP-specific IgE response of adoptive transfer recipient mice was the same whether the donor cells were from mice treated with IgG or anti-IgE. Transfer of enriched T- or B-cell populations indicated that T-cell help was not compromised by administration of the anti-IgE mAb. However, splenocytes from the anti-IgE-treated mice failed to synthesize IgE in vitro, and flow cytometric analysis of B cells from anti-IgE-treated mice showed a dose-dependent decrease in CD23+ cells following antibody treatment, which correlated with decreased serum IgE levels. Taken together, the results of these studies suggest that anti-IgE treatment suppresses IgE responses via effects on B cells rather than T cells, possibly through effects on CD23-dependent pathways.
Animals↗
Human IgE receptor alpha-chain IgG chimera blocks passive cutaneous anaphylaxis reaction in vivo.
Cross-linking of the high affinity IgE receptor (Fc epsilon RI) expressed on mast cells and basophils is essential for triggering anaphylaxis in vivo. Previously, other investigators have tried to produce competitive inhibitors using IgE peptide analogues and anti-IgE antibodies with limited success. To create a novel specific inhibitor of IgE that can block binding of IgE to Fc epsilon RI without the capacity to stimulate degranulation, we made an Fc epsilon RI-IgG immunoadhesin. The Fc epsilon RI-IgG was constructed by gene fusion of the extracellular portion of the human alpha-chain of Fc epsilon RI, which contains the high affinity binding site for IgE, with a truncated human IgG1 H chain C region. The Fc epsilon RI-IgG recognizes both human and murine IgE. Coincubation of Fc epsilon RI-IgG with murine IgE prevented sensitization of RBL-2H3 cells and the subsequent histamine release in response to anti-IgE. Similarly, when the Fc epsilon RI-IgG was preincubated with equimolar concentrations of either hyperimmune mouse sera or purified mouse IgE, it completely blocked the passive cutaneous anaphylaxis reaction in rats. Furthermore, i.v. administration of Fc epsilon RI-IgG following intracutaneous injection of serum from DNP-immunized mice was able to block the passive cutaneous anaphylaxis reaction in a time-dependent fashion. These results demonstrate that Fc epsilon RI-IgG is a potent inhibitor of IgE binding to intracutaneous mast cells in vivo and may prove clinically useful for the treatment of IgE-mediated disease.
Amino Acid Sequence↗
Activin induces cell death in hepatocytes in vivo and in vitro.
While studying endocrine responses to activin in female rats, we discovered that activin caused a marked reduction in liver mass. The regressed livers exhibited no gross signs of necrosis or infarction, but histopathological evaluation revealed extensive cell death in the centrilobular regions. The dying cells appeared to fragment into structures resembling apoptotic bodies. Liver mass and histological appearance were restored after cessation of activin infusion, indicating that on an organ level, this effect was reversible. To determine whether the effects observed in vivo were caused by direct actions on the liver, we then tested activin on isolated hepatocytes in serum-free medium. Under these conditions, activin caused many hepatocytes to undergo fragmentation, which was accompanied by a loss of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT)-reducing activity, an index of viability. We compared the effects of activin with those of transforming growth factor-beta because activin is structurally related to transforming growth factor-beta and because transforming growth factor-beta has been shown previously to induce cell death in hepatocytes. Both proteins caused cell death of comparable magnitude, as defined by the extent of loss of MTT-reducing activity, but transforming growth factor-beta was active at one tenth of the effective activin concentrations. A neutralizing monoclonal antibody to transforming growth factor-beta blocked the response to transforming growth factor-beta but had no effect on the response to activin. Conversely, follistatin, an activin-binding protein, blocked the response to activin but not to transforming growth factor-beta. Inhibin, which antagonizes the effects of activin in many systems, had little effect on the response to activin. Activin and transforming growth factor-beta differed in their onset of action; exposure to transforming growth factor-beta for only 1 hr induced a maximal response, whereas maximal response to activin required its continuous presence for 24 hr. These results show a novel effect of activin on cell death in hepatocytes in vivo and in vitro, suggesting that activin may have a previously unrecognized role in regulating hepatic function.
Activins↗
Insulin-like growth factor-1 stimulation of lymphopoiesis.
We show that treatment of adult mice with recombinant human insulin-like growth factor 1 (rhIGF-1) induces striking modifications in lymphocyte number and function. 9-mo-old male mice received rhIGF-1 (4 mg/kg per d) or its excipient by subcutaneous infusion from osmotic minipumps for 7 or 14 d. Mice were weighed daily and bled at sacrifice; the spleen and thymus were harvested and single cell suspensions were made for analysis of cell phenotype and cell number. The responses of splenocytes to mitogens (concanavalin A, lipopolysaccharide, and pokeweed mitogen), alloantigens and dinitrophenyl ovalbumin were measured. After either 7 or 14 d of treatment, rhIGF-1 had an overall whole-body anabolic effect, resulting in increased body and organ weights with prominent increases in the weight of the spleen and thymus. Furthermore, the rhIGF-1 treated mice were normoglycemic but had reduced blood urea nitrogens, again reflecting the anabolic activity of rhIGF-1. The increased spleen and thymus weights were associated with a large increase in the number of lymphocytes in both organs. In addition to an increase in T cells, specifically CD4+ T cells, a dramatic increase in splenic B cells was also observed. This increase was accompanied by an enhanced responsiveness to dinitrophenyl ovalbumin resulting in increased immunoglobulin production. However, despite the increases in cellularity, there was a decrease in the in vitro responses of spleen cells to mitogens after 7 d of rhIGF-1 treatment. In contrast, treatment with rhIGF-1 for 14 d increased both the cell number and mitogenic responses of splenocytes suggesting that some time is required for the cells populating the peripheral organs to gain mitogenic responsiveness. It is clear from these data that rhIGF-1, at doses that have whole-body anabolic activity, can expand cell number in lymphoid tissue in a normal adult mouse. These dual effects of rhIGF-1, of increasing lymphocyte number and activity, indicate that, in a normal adult animal, rhIGF-1 can cause major changes in lymphoid tissues that are of potential benefit to the functioning of the immune system.
Animals↗
Use of MEDLINE by health sciences faculty at the University of Minnesota.
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Academic Medical Centers↗
Side effects of methylphenidate in children with attention deficit hyperactivity disorder: a systemic, placebo-controlled evaluation.
The frequency and severity of 17 side effects presumably associated with stimulant medication were assessed during a rigorous, triple-blind, placebo-controlled, crossover evaluation of methylphenidate, 0.3 and 0.5 mg/kg twice a day, in 83 children with attention deficit hyperactivity disorder. Side effects were rated by parents and teachers at the end of each weekly drug condition. Three children (3.6%) had side effects that were sufficiently serious to warrant immediate discontinuation of medication. Parent ratings indicated that only the side effects of decreased appetite, insomnia, stomachaches, and headaches increased significantly in frequency and severity during the two active medication doses as compared with the placebo condition. Fewer than half of the children experienced these side effects and among those who did, ratings of mean severity remained in the mild range. Teacher ratings showed little change over drug conditions, except on ratings of staring, sadness, and anxiety, which declined with increasing dose of medication. Parent ratings indicated that only the side effects of decreased appetite, insomnia, stomachaches, and headaches increased significantly in frequency and severity during the two active medication doses as compared with the placebo condition. Fewer than half of the children experienced these side effects and among those who did, ratings of mean severity remained in the mild range. Teacher ratings showed little change over drug conditions, except on ratings of staring, sadness, and anxiety, which declined with increasing dose of medication. Surprisingly, a high frequency of these behavior side effects were reported during the placebo condition. Stimulant medication within this therapeutic range, therefore, results in few, generally mild side effects.(ABSTRACT TRUNCATED AT 250 WORDS)
Adolescent↗
Hospital library evaluation using focus group interviews.
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Evaluation Studies as Topic↗
The response of aggressive and nonaggressive ADHD children to two doses of methylphenidate.
Differences between 37 aggressive and 37 nonaggressive children with attention deficit hyperactivity disorder (ADHD) were evaluated as was their response to two doses of methylphenidate (0.3 and 0.5 mg/kg) using a multimethod battery of behavior ratings, laboratory tests, and direct observations. Aggressive ADHD children differed little from nonaggressive ADHD children except that nonaggressives displayed more problems with inattentiveness at school than aggressives while mothers of aggressives reported more symptoms of psychopathology in themselves than mothers of nonaggressives. In their drug responding, aggressives and nonaggressives were quite similar. The few exceptions were on measures of conduct, on which the aggressives were initially rated as more extreme and subsequently showed the greater degree of improvement from medication than nonaggressives. Results replicated those of a previous study and further indicate that aggressive and nonaggressive ADHD children share a common disorder of ADHD but aggressives have more impaired family situations.
Adolescent↗
The effect of method of biopsy and timing of mastectomy on the development of postmastectomy nosocomial wound infection.
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Biopsy↗
Gonococcal pilin variants in experimental gonorrhea.
When pilus+ Gc were introduced into a male subject's urethra, they gave rise to pilus+ variants whose pilin mRNAs differed from that of input Gc. The differences stemmed from the Gc genome's single complete pilin gene having undergone gene conversion by different partial pilin genes' sequences and by different length stretches of a single partial pilin gene. In some instances, the variant's pilin mRNA appeared to reflect two independent gene-conversion events that used sequences from two different partial pilin genes. The resulting variants' pilins exhibited antigenic differences compared with the pilin polypeptide of input Gc; these differences were discernible by immunoblotting with mAbs. Amino acid and antigenic changes occurred in a segment of the variants' pilin polypeptides that previously was thought to be conserved or constant in sequence.
Amino Acid Sequence↗
Gene conversion variations generate structurally distinct pilin polypeptides in Neisseria gonorrhoeae.
Pilus+ to pilus- phenotype change occurs in Neisseria gonorrhoeae through gene conversion of the gonococcus' complete, expressed pilin gene by nucleotides homologous to the pilS1 copy 5 partial pilin gene; assembly missense pilin is synthesized but pili are not. Reversion to pilus+ occurs by a subsequent recombinational event that replaces the complete pilin gene's pilS1 copy 5-like sequence with nucleotides from a different partial gene to effect expression of an orthodox (i.e., pilus producing) pilin. Sibling pilus+ revertants of common parentage can carry different sequences in their expressed pilin genes because they have undergone nonidentical gene conversion events such as recombinations with sequences from different partial genes, or recombinations with different length nucleotide stretches of the same partial gene; either can yield structurally and antigenically variant pilin polypeptides.
Amino Acid Sequence↗
Effects of recA mutations on pilus antigenic variation and phase transitions in Neisseria gonorrhoeae.
Intragenic recombination between the single complete pilin gene (expression locus) and multiple, distinct, partial pilin gene copies (silent, storage loci) is thought to account for the generation of pilus antigenic diversity and piliation phase (on-off) changes exhibited by Neisseria gonorrhoeae. The mechanisms operating in the genomic rearrangements associated with these forms of pilus variation were investigated through the study of isogenic strains of gonococci bearing either wild-type or altered recA alleles. Examination of the rates of pilus phase variation and the genetic basis for changes in piliation status displayed by these strains show that recA mediated homologous recombination is required for these high frequency events and confirm that the nonpiliated state results from mutations in the expressed pilin gene. In a strain that is deficient in recA mediated homologous recombination, pilus phase variation occurs at a 100-1000-fold reduced rate and results predominantly from one class of spontaneous frameshift mutations within the pilin structural gene.
Alleles↗
Gene conversion involving the pilin structural gene correlates with pilus+ in equilibrium with pilus- changes in Neisseria gonorrhoeae.
Gonococci (Gc) exhibit pilus+----pilus- "phase transitions" at high frequency, but only some of the pilus- Gc can revert to pilus+ phenotype. We examined reversible phase transitions between pilus+ Gc and a particular pilus- variant (P-rp+ phenotype) whose pilin mRNA carries a unique block of nucleotides encoding an "assembly missense" pilin polypeptide. The results show that Gc pilus+ in equilibrium with P-rp+ transitions can result from intragenic recombination in which there is nonreciprocal exchange of partially homologous DNA sequences from a partial pilin gene (in silent, storage form) into the expression locus' complete pilin gene. Hence Gc pilus phase variation, like pilus antigenic variation, can occur by gene conversion of the pilin structural gene expression locus.
Bacterial Adhesion↗
Piliation control mechanisms in Neisseria gonorrhoeae.
Gonococci (Gc) undergo pilus+ to pilus- "phase transitions" readily in vitro. In the present study we sequenced pilin mRNA from reverting, pilus- Gc by oligonucleotide primer extension and compared these pilin mRNA sequences with those expressed by their pilus+ predecessors and pilus+ revertants. The results suggest that genetic rearrangement within the pilin structural gene can generate defective pilin gene products, resulting in a pilus- phenotype. These pilus- Gc give rise to pilus+ revertants upon reconstitution of their modified pilin gene.
Bacterial Outer Membrane Proteins↗