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Biomedical subjects

C L Anderson

Publications and source records attributed to C L Anderson.

At least 91 records · Page 5Linked to original sources
PubMed1992

Three genes for the human high affinity Fc receptor for IgG (Fc gamma RI) encode four distinct transcription products.

Three distinct but closely related classes of receptors that bind the Fc portion of immunoglobulin G (Fc gamma RI, -II, and -III) have been identified in humans. Only Fc gamma RI has high affinity for ligand and has a unique third extracellular domain (EC3). We have characterized three genes for human Fc gamma RI (A, B, and C). Each gene consists of six exons, spans 9.4 kilobase pairs, and localizes to chromosome 1. Although they are remarkably similar, genes B and C are notably different from A; in-frame stop codons are present in the EC3 domain of genes B and C, and deletions occur in a splice donor sequence of gene B. Four distinct Fc gamma RI transcripts were analyzed. One transcript, from gene A, would encode a transmembrane receptor with three external domains. A second transcript, an alternatively spliced product of gene B, would encode a two-external domain transmembrane receptor. Two transcripts, from genes B and C, have stop codons in EC3 and would be predicted to generate secreted receptors.

Amino Acid Sequence↗
PubMed1992

Effects of dexamethasone on the hypothalamic-pituitary-adrenal axis in preterm infants.

The effects of dexamethasone therapy on the hypothalamic-pituitary-adrenal axis were tested in 10 premature infants with bronchopulmonary dysplasia by means of the corticotropin-releasing hormone stimulation test before therapy and on the seventh day of therapy. Adrenocorticotropic hormone and cortisol levels were determined by radioimmunoassay. There was significant suppression of the hypothalamic-pituitary-adrenal axis after 7 days of a currently used dexamethasone treatment regimen. A site of suppression was located at the level of the pituitary gland.

Adrenocorticotropic Hormone↗
PubMed1992

Intact survival of a 280-g infant: an extreme case of growth retardation with normal cognitive development at two years of age.

The care of infants born weighing less then 500 g is not only controversial but is also associated with medical uncertainties. We report the management of a growth retarded infant who weighed 280 g at birth after 26.9 weeks' gestation. The child not only survived but appears developmentally normal at two years of age. Although the infant is the smallest survivor reported, the case demonstrates the importance of gestational assessment in deciding delivery room management.

Child Development↗
PubMed1992

The maximizing urinary functioning program: an innovative approach to managing incontinence in long term care.

Urinary incontinence is a common occurrence in long term care and, given the client population, continence is often an unrealistic expectation. However, it was recognized that nursing plays a pivotal role in the maintenance and enhancement of clients' abilities with respect to their urinary functioning. In our facility, it was found that a need existed not only to assist clients to maximize their urinary functioning, but also to encourage the independent decision-making of our professional staff. The MUF Program developed to meet these needs was based upon the use of a systematic method for decision-making in nursing. The Maximizing Urinary Functioning Program was implemented on a pilot unit and evaluated using a pre-test/post-test design. Based upon the results of this evaluation and projections for the benefit to new admissions, the program is now being implemented hospital-wide. This project has also served to raise several research questions of interest to those working in long term care and levelled practice: how will the management of new admissions with urinary incontinence change over several years with a program of systematic decision-making in place? will there be a decline in the number of incontinent clients at our facility over a two-year period? is there a relationship between independent decision-making and job satisfaction for professional nursing staff working in levelled practice? and what is the effect of enhancing the independent decision-making skills of professional nursing staff on the job satisfaction of the nonprofessional staff?

Humans↗
PubMed1992

Early endotoxin tolerance in suckling rats.

Early endotoxin tolerance has not been well investigated in the newborn. This study demonstrated that a sublethal dose of Salmonella enteritidis lipopolysaccharide (S. ent-LPS) or rough mutant Salmonella minnesota LPS (Re-LPS) induced early endotoxin tolerance in suckling rats, showing blunted hypoglycemia and decreased mortality. The mortality of endotoxic shock was lower in S. ent-LPS pretreated group than Re-LPS pretreated group. A sublethal dose of S. ent-LPS caused lactacidemia but Re-LPS did not. Therefore, early endotoxin tolerance appeared to be related to physiologic responses to the initial LPS exposure.

Animals↗
PubMed1991

Gene organization of the human high affinity receptor for IgG, Fc gamma RI (CD64). Characterization and evidence for a second gene.

We have isolated, characterized, and sequenced the gene coding for the 72-kDa human high affinity IgG FcR, hFc gamma RI. It consists of six exons and spans 9.4 kilobase pairs. The leader sequence is encoded by two exons, the second of which is 21 base pairs long and contains the predicted site of peptidase cleavage. The third, fourth, and fifth exons each encode homologous Ig-like extracellular domains. The hydrophobic transmembrane region and a highly charged cytoplasmic tail are encoded by a single final exon. The sequence of the 5'-flanking region was determined. Two major transcription initiation sites were identified by RNase protection. The first, more downstream site was confirmed by primer extension studies; canonical CAAT and TATA boxes are located in appropriate positions upstream from this site. The second transcription initiation site was utilized only in RNA from cells incubated with gamma-interferon. This site initiates transcription upstream from the first major site. These data are consistent with the finding of two species of mRNA for hFc gamma RI in myeloid cells that are upregulated when cultured with gamma-interferon. Southern analysis of genomic DNA confirms the restriction map generated from the cloned DNA. One additional HindIII fragment was observed in genomic DNA from 13 randomly selected individuals that was not present in the phage clone used to characterize the gene. This observation suggests the existence of a second hFc gamma RI gene which lacks one of the two internal HindIII sites rather than a restriction fragment length polymorphism.

Amino Acid Sequence↗
PubMed1991

Anti-GPIIb/IIIa (CD41) monoclonal antibody-induced platelet activation requires Fc receptor-dependent cell-cell interaction.

We studied platelet activation by UR1, a murine IgG1 anti-CD41 mAb. Like thrombin and crosslinked anti-Fc gamma RII mAb IV3, UR1 initiates prompt aggregation and Ca2+ mobilization. UR1 F(ab')2 fragments failed to activate, yet inhibited UR1 IgG-mediated activation. UR1-induced activation was blocked by anti-Fc gamma RII mAb. High viscosity (15% dextran or Ficoll), which impedes cell-cell interaction, inhibited activation by UR1. Cell-cell interaction was confirmed by cell-mixing studies. UR1 binding to platelets of one pool was blocked with UR1 F(ab')2 allowing UR1 binding only to Fc gamma RII. IV3 Fab fragments blocked ligand binding to Fc gamma RII on platelets of a second pool; thus, UR1 could bind only its epitope. UR1 initiated an immediate [Ca2+]i increase in the intermixed pools at low ionic strength. These studies indicate that UR1 IgG binds CD41 on one platelet to form immune complexes which then crosslink and stimulate Fc gamma RII on nearby platelets. Two other anti-CD41 mAb, 6C9 and C17, and two anti-CD9 mAb, AG1 and mAb7, activated platelets in a UR1-like manner. We propose that platelet Fc gamma RII crosslinking that follows the interaction of IgG-opsonized platelets may be a common mechanism by which anti-platelet antibodies activate platelets.

Antibodies, Monoclonal↗
PubMed1991

Identification and structural characterization of Fc gamma-receptors on pulmonary alveolar macrophages.

Little is known about the structure of the cell surface receptors for the Fc portion of immunoglobulin G (Fc gamma R) on tissue macrophages. Studies on leukocytes indicate the existence of three classes of Fc gamma R, denoted I, II, and III. The purpose of this study was to structurally characterize Fc gamma R on alveolar macrophages obtained by bronchoalveolar lavage, comparing them with Fc gamma R of monocytes, neutrophils, and U937 cells. Flow-cytometric evaluation, utilizing anti-Fc gamma R class-specific monoclonal antibodies, showed that alveolar macrophages expressed three Fc gamma R classes. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis analysis of the immunopurified Fc gamma R molecules revealed the following apparent molecular mass for each Fc gamma R class: Fc gamma RI, 70 kDa; Fc gamma RII, 44 kDa; and Fc gamma RIII, 57-65 kDa. RNA blot analysis demonstrated a 1.7-kb transcript for Fc gamma RI, 2.5 and 1.6 kb transcripts for Fc gamma RII, and a 2.2 kb mRNA for Fc gamma RIII. Fc gamma RII displayed the high-responder/low-responder polymorphism. Fc gamma RIII did not express the neutrophil antigen-type specific structural polymorphism of the deglycosylated Fc gamma R molecule and appeared to be a transmembrane molecule.

Antibodies, Monoclonal↗
PubMed1991

Emerging developmental sequelae in the 'normal' extremely low birth weight infant.

Thirty-six extremely low birth weight (less than 1000 g birth weight) children received neurodevelopmental testing in infancy (mean age = 19.1 months), and again in early childhood (mean age = 46.5 months). Children were categorized into a high-risk group (n = 20) if bronchopulmonary dysplasia and/or Grades III or IV intracranial hemorrhage were present or a low-risk group (n = 16) if neither were present. Using standardized testing and neuromotor examination, 24 (67%) of 36 children showed normal infant development. Only 11 (31%) of 36 children (P less than .005) had normal development upon reassessment in early childhood. A decline in developmental status occurred in both groups. This indicates that for the extremely low birth weight population, normal infant development is poorly predictive of continued normal development. With or without major complications, extremely low birth weight places children at substantial risk for ongoing and emerging developmental problems with age.

Child Development↗
PubMed1991

Expression of IgG Fc receptor antigens in placenta and on endothelial cells in humans. An immunohistochemical study.

Expression of leukocyte IgG Fc receptor (Fc gamma R) antigens by placenta, endothelial cells (EC) of normal tissues, and ECs of kidney and skin from subjects with immune complex diseases was studied immunohistochemically using anti-Fc gamma R monoclonal antibodies (MAb). Monoclonal antibodies against all three leukocyte Fc gamma R classes stained placental villous macrophages. Placental villous trophoblasts were stained intensely by anti-Fc gamma RIII MAb 3G8, while both anti-Fc gamma RI (MAb 32) and anti-Fc gamma RII MAbs IV3, KU79, CIKM5, 2E1, KB61, and 41H16) antibodies did not react with these cells. Anti-Fc gamma RII MAbs IV3, KU79, CIKM5, 2E1, KB61, and 41H16 immunostained placental villous capillary EC, in contrast to anti-Fc gamma RI MAb 32 and anti-Fc gamma RIII MAb 3G8, CLB-Granl, and B73.1, which did not bind. Anti-Fc gamma RI MAb 32, anti-Fc gamma RII MAb IV3 and CIKM5, and anti-Fc gamma RIII MAb 3G8 did not react with the ECs of tonsil, liver, kidney, spleen, intestine, lung, or uterus. Similarly no EC staining was seen with these four MAbs in 14 skin and 14 kidney biopsies from subjects with immune-complex diseases. Fc gamma R antigens are expressed constitutively only by placental villous ECs and are not induced on nonplacental ECs by immune-complex-mediated diseases.

Antibodies, Monoclonal↗
PubMed1990

Signal transduction by the platelet Fc receptor.

We have evaluated the mechanism by which crosslinking human platelet Fc receptor (FcR) for IgG triggers platelet aggregation and the platelet release reaction. Platelet FcR was crosslinked by incubating purified human platelets with anti-FcRII monoclonal antibody and F(ab')2 anti-mouse Ig. The resultant [Ca2+]i increase, monitored by Fura-2 and measured in the absence of extracellular Ca2+, reached a peak of 750 +/- 50 nmol/L. The effects of cyclooxygenase inhibitors, aspirin and indomethacin, and a phospholipase A2 inhibitor, dibromoacetophenone, were examined. Regardless of the inhibitor, at least 25% of the [Ca2+]i increase remained. Thrombin (0.2 U/mL) stimulated an immediate [Ca2+]i increase that reached 1.95 +/- 0.8 mumol/L. The [Ca2+]i increase generated by thrombin was only slightly reduced by these inhibitors. Crosslinking the FcRII of platelets resulted in a fivefold increase in the production of [3H]inositol phosphates, (IP) which, in the absence of extracellular Ca2+ was insensitive to aspirin. The activation of a [Ca2+]i increase along with the measured increases in IP indicate that FcRII crosslinking leads to the activation of phospholipase C (PLC). In contrast to thrombin, platelet activation via FcRII depends to a large extent on arachidonic acid metabolites. However, neither cyclooxygenase nor phospholipase A2 inhibitors completely blocked FcRII-stimulated [Ca2+]i increase. These observations led us to propose that crosslinking of platelet FcRII initially activates PLC.

Acetophenones↗
PubMed1990

Alveolar and peritoneal macrophages bear three distinct classes of Fc receptors for IgG.

The FcR for IgG on the plasma membrane of cells of the mononuclear phagocyte system mediate a number of different biologic responses such as phagocytosis, pinocytosis, superoxide generation, and antibody-dependent cytotoxicity. In the interest of understanding the pathophysiology of these processes we have begun to characterize the FcR for IgG on two readily available sources of macrophages--the lung and the peritoneum--using antireceptor mAb. We find that all three of the distinct classes of FcR for IgG which have been described in man are present on both pulmonary and peritoneal macrophages. Most monocytes, we suggest, bear low numbers of Fc gamma RIII whereas a small subpopulation of monocytes expresses substantial numbers of Fc gamma RIII. Furthermore, we find that two different forms of Fc gamma RIII differ in their capacity to bind anti-Fc gamma RIII mab 3G8 in the presence of human IgG. Human IgG does not block the binding of mAb 3G8 to neutrophils, but it does block 3G8 binding to macrophages and large granular lymphocytes; this finding correlates with the expression of the two Fc gamma RIII genes, I and II, in man. Studies aimed at illuminating the molecular mechanisms of Fc gamma R-mediated processes in macrophages will require consideration of the receptors of all three classes.

Antibodies, Monoclonal↗
PubMed1990

Phagocytosis mediated by three distinct Fc gamma receptor classes on human leukocytes.

We have evaluated the capacity of the three major classes of human Fc gamma R to mediate phagocytosis by measuring the ability of adherent phagocytes to internalize erythrocytes coated with anti-Fc gamma R mAb. Five different cell types were studied, freshly purified monocytes, cultured monocytes, alveolar macrophages, freshly purified polymorphonuclear neutrophilic leukocytes, and PMNs cultured in IFN-gamma. Fc gamma RI and Fc gamma RII on whichever cells they were expressed were capable of phagocytosing anti-Fc gamma R mAb-coated erythrocytes. Furthermore, Fc gamma RIII on mononuclear phagocytes, which appears to be a conventional integral membrane protein that spans the lipid bilayer, was capable of phagocytosing anti-Fc gamma RIII-coated erythrocytes. However, Fc gamma RIII on neutrophils, a molecule linked to the membrane by a phosphatidylinositol-glycan moiety, although binding anti-Fc gamma RIII-coated erythrocytes vigorously was incapable of mounting a phagocytic response. This deficiency correlates with the limited capacity of Fc gamma RIII on neutrophils to mediate superoxide generation and antibody-dependent cell-mediated cytotoxicity and it may be related to the unique structural features of Fc gamma RIII.

Antibodies↗
PubMed1990

The monoclonal antibody 41H16 detects the Leu 4 responder form of human Fc gamma RII.

Human FcR for IgG can be divided into three classes (Fc gamma RI, II, and III) based on their structure and reactivity with mAb. Fc gamma RII can be further subdivided into two categories based on functional and biochemical assays. These two Fc gamma RII subtypes were initially recognized by the failure of T cells from 40% of individuals to proliferate in response to mAb Leu 4 (mouse IgG1, anti-CD3), a response that requires the binding of the Fc region of the Leu 4 mAb to Fc gamma RII on monocyte accessory cells. Inas-much as mouse IgG1, does not bind efficiently to the nonresponder form of Fc gamma RII, mAb Leu 4 is unable to induce proliferation in these individuals. IEF data on Fc gamma RII from Leu 4 responder and nonresponder individuals suggested that the structural gene for Fc gamma RII consisted of two allelic forms R (responder) and N (nonresponder) producing the phenotypes RR, RN, and NN. Thus, exclusive expression of the nonresponder allele in monocytes of "nonresponder" individuals, appeared to be responsible for the lack of proliferation observed. In cooperation with the IVth International Conference on Human Leukocyte Differentiation Antigens, we analyzed CDw32 mAb to determine if they could distinguish the responder and nonresponder forms of Fc gamma RII. We report that mAb 41H16 binds preferentially to the responder allotypic form of Fc gamma RII expressed on human monocytes. When quantitative flow cytometry is used to measure the binding of both mAb 41H16 (responder Fc gamma RII) and mAb IV.3 (all myeloid cell Fc gamma RII), we are able to subdivide the responder population into homozygous and heterozygous responders. In addition, mAb 41H16 blocks the binding of mAb IV.3 to monocytes and inhibits proliferation when added to cells before addition of mAb Leu 4. We also show that polymorphonuclear leukocytes and platelets have the same allotypic differences in the binding of 41H16 as do monocytes. However, a subset of lymphocytes (previously shown to be B cells) expresses the 41H16 epitope with no evidence for donor to donor variability.

Alleles↗