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PubMed1991

[Non-neoplastic central hearing loss--a review].

Acquired central auditory disorders not due to a tumour are unusual. The well-known conditions such as hypoxic encephalopathy, erythroblastosis, bacterial meningitis and trauma are reviewed. Recent experimental and clinical studies contribute to progress in the understanding of the pathogenesis and etiology of these conditions. The pattern of presbyacusis and cortical deafness is discussed also. AIDS must be considered as a new cause of acquired central auditory dysfunction.

AIDS Dementia Complex↗
PubMed1991

erg, an ets-related gene, codes for sequence-specific transcriptional activators.

E26 is a replication-defective avian acute leukemia virus which causes erythroblastosis and myeloblastosis in chickens. It carries two distinct oncogenes, v-myb and v-ets, both of which contribute to its transforming properties. Several genes related to the ets oncogene (c-ets-1, ets-2, erg, elk-1, elk-2, PU.1/Spi-1, E74 and Fli-1) have been described. Previously we have shown that the erg gene (ets-related gene) codes for at least two proteins (erg-1 and erg-2) because of alternative splicing and alternative usage of the initiation codon. We have expressed erg-1 and erg-2 proteins in Escherichia coli and have used these recombinant proteins to show that they bind to DNA in a sequence-specific manner. erg proteins exhibited different sequence specificity and affinity for the oligonucleotides recognized by c-ets-1, ets-2, some of PU.1/Spi-1 and elk-1, suggesting that the DNA-binding specificities of erg and other members may overlap but are not necessarily identical. The erg gene was found to transactivate a reporter gene that was linked to erg target sequences. These results suggest that erg-1 and erg-2 are sequence-specific transcriptional activators like the other members of the ets oncogene superfamily which represent a distinct class of transcriptional activators.

Animals↗
PubMed1975

Cytopathogenic XC assay for bone marrow from mice infected with murine leukemia viruses.

Virus production "in vitro" by bone marrow cells of murine leukemia virus-infected BALB/c mice was determined with a modified reverse XC cell assay. Bone marrow of mice infected by either Rauscher leukemia virus or Soulé myeloid leukemia virus was cocultivated with XC cells and quantification was done by counting syncytia. During the development of both erythroblastosis and myeloid leukemia, the number of syncytia induced by cocultivation increased. High numbers of syncytia were especially obtained with myeloid leukemia cells; the phenomenon was evident as early as one month following inoculation with virus and before the onset of conspicuous clinical signs of disease.

Animals↗
PubMed1991

[Parasitologic, clinical, hematologic and serologic findings in puppies after lactogenic infection with Ancylostoma caninum ERCOLANI 1859 (Ancylostomidae)].

The correlation between intensity of Ancylostoma caninum infections in bitches and the intensity of lactogenic infections and clinical signs of their puppies was investigated. On average, 825, 1,867 or 2,125 specimens were observed in litters of two bitches inoculated with 5,000, 10,000 or 20,000 third stage larvae (LIII) respectively, at the day of conception. Adverse effects of the infection on the growth and behaviour of the puppies were observed after onset of their second week of life: 11/27 puppies died during the fourth week. The body weight of puppies surviving 28 days was up to 750 g less than that of uninfected controls. Eosinophilia, erythroblastosis and microcytic, hypochromic anemia developed in all puppies during their first four weeks. The IFA test (LIII antigen) was positive for only 5/18 heavily infected puppies after uptake of colostrum.

Ancylostoma↗
PubMed1991

[Immunoglobulins in prevention and therapy].

Injected immunoglobulins (= Ig) substitute for a patient's failing active antibody production = passive immunization. They provide immediate protection (time factor!). Commercially available human Ig-concentrates contain mainly IgG. Poly- and mono-specific preparations are available. Five indications are listed. Only the first, prophylactic use, is treated extensively, because it must be familiar to every physician. Correct application enables to avoid many viral diseases (e.g. measles), toxin-mediated diseases (e.g. tetanus), and erythroblastosis fetalis.

Antibody Formation↗
PubMed1991

[Pregnancy and fetal complications after bone marrow transplantation].

4 patients (3 female, 1 male) bone marrow transplanted for severe aplastic anemia (3 allogeneic, 1 syngeneic) became pregnant or parented children 19, 37, 81, and 34, 52 months, respectively, after BMT. Conditioning regimen consisted of 200 mg/kg Cyclophosphamide. Donor buffy coat cells were used for rejection prophylaxis, and methotrexate was used as GVHD prophylaxis. 1 female patient developed a mild chronic graft versus host disease with vaginal sclerosis which made a cesarean section necessary. 3 out of 5 pregnancies were uneventful. 1 patient had mumps in the 14th week, another patient had a late abortion in the 25th week of unknown cause. A high incidence of offspring complications was noticed including 1) persistence of fetal circulation syndrome, 2) erythroblastosis fetalis, and 3) prolonged newborn-icterus. These observations confirm previous reports on resumed fertility after BMT for SAA. A relation between the unexpected high incidence of pre-, peri-, and postpartal complications and the BMT procedure can neither be proved nor excluded.

Adolescent↗
PubMed1990

[Complete remission in erythroleukemia: induced with low dose Ara-C, consolidated with high dose Ara-C].

A 20-year-old man was admitted because of general fatigue. Peripheral blood examination revealed pancytopenia (WBC 1,700/microliters, RBC 210 x 10(4)/microliters, Plt 3.2 x 10(4)/microliters) with remarkable erythroblastosis. Bone marrow examination revealed erythroid hyperplasia and an increase of abnormal myeloblasts with Auer bodies (37% of non erythroid cells). A diagnosis of erythroleukemia (AML M6) was made. He received two courses of combination chemotherapy (BHAC-DMP and VAMA (VP-16, Ara-C, 6-MP, and doxorubicin (ADR)) but complete remission (CR) could not be achieved. Consequently, he was treated with LDAC. After two courses of LDAC. CR was obtained. Subsequently, he received two courses of HDAC as consolidation, and therapy has been off thereafter. He remains in CR state for more than 12 months.

Adult↗
PubMed1990

Maturation and externalization of EGF-receptor: a cell-surface located oncoprotein.

The EGF-receptor is a proto-oncogene encoded membrane protein related to the verb-B oncogene product of avian erythroblastosis virus. Here we report studies on expression and maturation characteristics of this receptor. The expression of intact 170 kDa EGF-receptor as well as a 100 kDa homologue that contains only the external domain is enhanced by the ligand EGF. EGF acts at transcriptional and post-transcriptional levels. To dissociate these pre-translational effects and the effects of EGF on receptor polypeptide synthesis from those on receptor export, pulse-chase experiments were conducted. These studies indicate that EGF stimulates post-translational transport and processing of the receptor, and this stimulation can occur in the absence of new protein synthesis. Other studies show that EGF accelerates at least two slow events in receptor maturation--the deoxynojirimycin-sensitive processing in endoplasmic reticulum (ER) and the swainsonine-sensitive processing in golgi, suggesting that EGF may influence one or more of the rate determining steps that control receptor export from ER. Overall the results demonstrate that EGF controls EGF-receptor expression at multiple levels, viz. at transcriptional, pre-translational and post-translational pathways of receptor biosynthesis.

Blotting, Northern↗
PubMed1990

Transformation of early erythroid precursor cells (BFU-E) by a recombinant murine retrovirus containing v-erb-B.

Avian erythroblastosis virus (AEV) is a replication-defective retrovirus that transforms erythroid and fibroblast cells in vitro and in vivo. The transforming ability of AEV is due primarily to the oncogene v-erb-B. A recombinant murine retrovirus has been constructed by inserting a chimeric gag-v-erb-B gene into a Moloney murine leukemia virus based vector. This retrovirus was used to examine v-erb-B-induced transformation of murine hematopoietic cells. Infection of murine primary fetal liver, adult bone marrow or adult spleen cells with the recombinant virus generated large hemoglobinized erythroid colonies in the absence of exogenous growth factors. Generation of such colonies usually requires the presence of erythropoietin (Epo) and interleukin-3 (IL-3). These growth-factor independent colonies were shown to be derived from early (BFU-E) and not late (CFU-E) erythroid progenitor cells, and the effect was not attributable to growth factors elicited by the virus-producing cell lines. In order to confirm that the recombinant virus was responsible for this transformation of BFU-E to growth factor independence, bone marrow cells from post 5-fluorouracil treated mice were infected and used to repopulate lethally-irradiated mice. Growth factor-independent BFU-E were obtained in up to 30% of day-13 spleen colonies and it was shown by DNA analysis that cells from these colonies contained integrated provirus. Our results indicate that v-erb-B transforms early erythroid progenitors to growth factor independent growth and subsequent differentiation to erythrocytes -a process that normally requires Epo plus either IL-3 or granulocyte-macrophage colony stimulating factor (GM-CSF).

Alpharetrovirus↗
PubMed1990

Does hyperbilirubinemia damage the brain of healthy full-term infants?

In the 1950s, exchange transfusion to keep the total serum bilirubin below 20 mg/dl was shown to be an effective way of preventing kernicterus in babies with erythroblastosis fetalis. For the last 15 to 20 years this level has also been used to determine the need for intervention in healthy full-term infants who do not have hemolytic disease. A critical review of all the available data including six studies from the collaborative perinatal project (more than 30,000 infants) and several smaller studies of term infants without hemolysis reveals essentially no evidence of adverse effects of bilirubin on IQ, neurologic examination, or hearing. The investigation and treatment of normal infants with jaundice is expensive and potentially harmful. We need to reassess our approach to hyperbilirubinemia in healthy full-term infants.

Bilirubin↗
PubMed1990

[Automated exchange transfusion in premature and newborn infants with hyperbilirubinemia using a peripheral arteriovenous vascular access device].

The technique of exchange transfusion using a plastic catheter in the umbilical vein developed by Diamond and modified by Allen was instrumental in decreasing the mortality and morbidity in newborn infants with jaundice. Allen et al. demonstrated that the development of kernicterus in infants with erythroblastosis with indirect hyperbilirubinemia could be prevented by this method. Since that time numerous modifications of this "single site, push pull technique" have been described to further reduce the risk of morbidity and mortality. On the basis of the successful use of percutaneous radial artery catheters for arterial blood gas monitoring, we developed a technique for exchange transfusion using a peripheral arterial catheter inserted in the radial artery for blood withdrawal and a peripheral venous catheter for replacement of heparinized compatible donor blood. For simultaneous withdrawal and replacement we used two volumetric infusion pumps, one aspirating patients' arterial blood, the other replacing equal volumes of donor blood at exactly the same time. We evaluated our new procedure in 19 newborn infants (group 1) with hyperbilirubinemia who required exchange transfusion. Retrospectively we analysed the data in 18 newborn infants (group 2) treated over a previous period by means of the conventional "one site, push pull" technique using the umbilical vein, and compared the data. Mean birth weights, gestational ages and Apgar scores were similar in both groups, as were volumes of blood used for exchange transfusions. The results were superior in group 1 infants, as reflected by the significantly greater percentage decreases in serum bilirubin concentration and fewer complications. No baby died.(ABSTRACT TRUNCATED AT 250 WORDS)

Arm↗
PubMed1990

Regulation of stability and synthesis of EGF-receptor mRNAs encoding for intact and truncated receptor forms.

The EGF-receptor is a proto-oncogene encoded membrane protein related to the v-erb-B oncogene product of avian erythroblastosis virus. Here we have studied the expression and stability characteristics of two forms of receptor mRNA--a 5.6 kb form that encodes for the intact transmembrane 170 kDa receptor and a 3' deleted 2.6 kb form that encodes for a 100 kDa secreted EGF-receptor. In previous studies we showed that EGF increased the synthesis of its own receptor in human cytotrophoblasts and A431 cells. Now we show that EGF stimulates the transcription of the receptor gene and blocks the degradation of transcripts, and thus elevates the level of receptor mRNA in these cells. To test the role of prior protein synthesis in these phenomena, we examined the effect of cycloheximide, and found that this reagent, either alone or in combination with EGF, leads to an increase in the level of EGF-receptor mRNA. Increases were seen in both size classes of receptor mRNA. Further analysis showed that cycloheximide enhances both synthesis and stability of receptor mRNA. While the intrinsic stability of the 3'-truncated 2.6 kb mRNA is approximately 2-fold higher than that of the 5.6 kb species, it is enhanced by more than 10-fold in the presence of cycloheximide and EGF acting in a synergistic manner. The extent of stabilization was less for the larger mRNA form. The results suggest the involvement of ligand as well as labile proteins in the control of synthesis and stability of EGF-receptor mRNA, and imply the involvement of 3' located structural features in the control of receptor mRNA stability.

Blotting, Northern↗
PubMed1989

Expression of ets genes in mouse thymocyte subsets and T cells.

The cellular ets genes (ets-1, ets-2, and erg) have been identified by their sequence similarity with the v-ets oncogene of the avian erythroblastosis virus, E26. Products of the ets-2 gene have been detected in a wide range of normal mouse tissues and their expression appears to be associated with cell proliferation in regenerating liver. In contrast, the ets-1 gene was previously shown to be more highly expressed in the mouse thymus than in other tissues. Because the thymic tissue contains various subsets of cells in different stages of proliferation and maturation, we have examined ets gene expression in fetal thymocytes from different stages of development, in isolated subsets of adult thymocytes, and in peripheral T lymphocytes. Expression of the ets-1 gene was first detected at day 18 in fetal thymocytes, corresponding to the first appearance of CD4+ (CD4+, CD8-) thymocytes, and reaches maximal/plateau levels of expression in the thymus at 1 to 2 days after birth. The ets-2 gene expression is detected at least 1 day earlier, coinciding with the presence of both double-positive (CD4+, CD8+) and double-negative (CD4-, CD8-) blast thymocytes and reaches maximal/plateau levels 1 day before birth. In the adult thymus, ets-1 and ets-2 mRNA expression is 10- to 8-fold higher respectively in the CD4+ subset than in the other subsets examined. Higher levels of p55 ets-1 protein were also shown to exist in the CD4+ subset. Because the CD4+ thymic subset is the pool from which the CD4+ peripheral, helper/inducer T cells are derived, the ets gene expression was examined in lymph node T cells. Both the CD4+ and the CD8+ T cells subsets had lower ets RNA levels than the CD4+ thymocytes. These results suggest that ets-2 and more particularly ets-1 gene products play an important role in T cell development and differentiation and are not simply associated with proliferating cells, which are observed at a higher frequency in fetal thymocytes, or dull Ly-1 (low CD5+), and double-negative (CD4-, CD8-) adult thymocytes. Selectively enhanced expression of ets-1 gene may be observed in thymic CD4+ thymocytes because these cells have uniquely encountered MHC class II or other Ag in the thymic environment. These cells may have been subsequently stimulated to activate the ets genes in conjunction with their differentiation of helper/inducer function(s) and expression of mature TCR.(ABSTRACT TRUNCATED AT 400 WORDS)

Aging↗
PubMed1989

The c-erbA alpha-encoded thyroid hormone receptor is phosphorylated in its amino terminal domain by casein kinase II.

The c-erbA alpha progenitor of the v-erbA oncogene of avian erythroblastosis virus (AEV) encodes a nuclear receptor for the thyroid hormone triiodothyronine (T3) which acts as a ligand-dependent transcription factor. As previously reported (Goldberg et al., EMBO J., 7, 2425-2433), the 46 kd chicken c-erbA alpha-encoded T3 receptor (ck-ErbA alpha) is phosphorylated at two major sites. Only one of these sites (Ser28/Ser29) is retained in the v-erbA-encoded P75gag-v-erbA protein. We report here the identification of the second phosphorylation site of ck-ErbA alpha as a single serine residue localized at position 12. We propose that casein kinase II, a protein kinase distributed in the cytosolic and nuclear compartments of a number of different tissues, is responsible for serine 12 phosphorylation on the following grounds. First, serine 12 is part of a sequence containing multiple acidic amino-acids, a feature common to all sites phosphorylated by casein kinase II in physiological substrates. Second, ck-ErbA alpha was found to be phosphorylated by purified casein kinase II in vitro at the same site, as defined by two-dimensional mapping experiments, as that observed in vivo. Third, conversion of serine 12 into an unphosphorylatable alanine residue by site directed mutagenesis abolishes the phosphorylation of ck-ErbA alpha by casein kinase II in vitro. Phosphorylation of serine 12 is likely to play a role in the modulation of ErbA alpha function since both serine 12 and the casein kinase II phosphorylation sequence motif are phylogenetically conserved in all known members of the c-erbA alpha gene family encoding T3 binding proteins. The codon specifying serine 12 in ck-ErbA alpha being precisely the point where recombination between gag and ck-c-erbA alpha occurred to generate v-erbA, our results furthermore suggest that deletion of serine 12 could contribute to the oncogenic activation of v-erbA.

Amino Acid Sequence↗
PubMed1989

Fetal diagnosis and fetal surgery.

Accurate fetal diagnosis became possible by the steadily increasingly complex techniques of amniocentesis, ultrasound, and ultrasound-guided fetal blood sampling and chorion villous sampling. A high degree of diagnostic accuracy for a wide variety of structural and metabolic anomalies is required. The field of fetal diagnosis has been extended to the point that a journal dedicated to this subject alone is a viable proposition. It is becoming apparent, however, that lesions that were well known and well understood when recognized in neonatal life appear in general to have a worse prognosis if the lesion is diagnosed in utero. Fetal surgery began with attempts to perform in utero transfusions for babies with erythroblastosis fetalis. For a while, there was competition between open surgical procedures and the percutaneous placement of blood through catheters introduced into the fetal peritoneal cavity from outside the mother's abdomen. For fetal transfusion, closed techniques proved far safer and just as efficacious. There has been a worldwide interest in shunting of hydrocephalus and obstructive uropathy. The results of shunting hydrocephalus have been disappointing, with most of the patients surviving, but most of the survivors being severely handicapped. The results of shunting obstructive uropathy were that only about 50 per cent of the babies survived, but it appeared that those that did survive did well. Other lesions that have been shunted have been hydrothoraces or fetal ascites. A limited number of open procedures have been carried out in the last few years in San Francisco, and it may well be that diaphragmatic hernia (in appropriately selected patients) will be a lesion that can be corrected by in utero surgery. The future of this field is exciting, but before this form of treatment becomes routine, the ethical implications of the possibility of fetal surgery must be defined much more clearly than is currently the case.

Female↗
PubMed1989

Granulocytic fragments in sepsis.

We report here three patients with sepsis and one with acute pancreatitis and possible sepsis who developed granulocytic fragments on blood smears obtained prior to death. In case 1, these fragments were identified cytochemically. In case 3, granulocytic cytoplasmic projections and fragments were identified by electron microscopy of the buffy coat. All patients had leukerythroblastosis. The average corrected white blood count (WBC) was 46 X 10(9)/liter with 34 nucleated red blood cells (nRBC)/100 WBC. Patient 1 had thrombocytosis whereas patients 2, 3, and 4 were thrombocytopenic. Terminal complement levels were decreased in patients 3 and 4 as previously noted in sepsis (Sprung CL, Shultz DR, Marcial E, et al.: Complement activation in septic shock patients. Crit Care Med 14:525, 1986). A general correlation between nRBC and granulocytic fragments/100 hpf (high power field) was observed in patients 3 and 4. Granulocytic fragments were not identified on the blood smears of several patients with leukemoid reactions without erythroblastosis. Although the precise etiology of these fragments is unclear, we believe their recognition is important because all patients died within 32 hours after granulocytic fragments were identified. Furthermore, these fragments can falsely elevate the platelet count. Although myeloid fragments have previously been noted in leukemia and lymphoma, this is the first report of their association with conditions unrelated to hematologic neoplasms. These fragments can easily be recognized by careful examination of the blood smear and represent a newly recognized aspect of the septic shock syndrome.

Anemia, Myelophthisic↗
PubMedDate not supplied

[The effect of 3'-azido-2',3'-dideoxythymidine on experimental viral infections].

3'-Azido-2',3'-dideoxythymidine (az-T) inhibited effectively the reproduction of some retroviruses; among these viruses were the four serological subgroups of sarcoma Raus virus in chicken embryo, avian myeloblastosis virus and erythroblastosis virus in chicken. This inhibition was specific towards retroviruses and practically was not observed in the case of infections DNA- and RNA-genome model viruses of vaccinia and influenza, at whose reproduction reverse transcriptase is not involved. Three other 3'-modified nucleosides did not block the above-listed retroviruses. For chickens, az-T showed low toxicity. The molecular mechanisms of the action of az-T are discussed.

Acquired Immunodeficiency Syndrome↗
PubMed1988

Abnormal glycosylation of the env-sea oncogene product inhibits its proteolytic cleavage and blocks its transforming ability.

Cells transformed by the avian erythroblastosis virus S13 contain three proteins derived from the v-sea oncogene, gp155, gp70 (a cleavage product of gp155), and p38. It is not clear whether only one or all three of these proteins are required for transformation by S13. S13 transformed erythroblasts and fibroblasts revert to a normal morphology in the presence of the alpha glucosidase-1 inhibitor castanospermine, whereas cells transformed by the v-src or v-erbB oncogenes are unaffected by this drug. Treatment with castanospermine does not alter the tyrosine kinase autophosphorylation activity of any of the v-sea products, and the synthesis and processing of p38 is unaffected. Castanospermine modifies the structure of the carbohydrate chains of gp155 such that the glucose residues are retained, thereby inhibiting complex chain formation. Analysis of revertant S13 transformed cells shows that the proteolytic cleavage of the modified form of gp155 is inhibited, resulting in a very low yield of a modified form of gp70. There is no detectable effect of castanospermine on the transport of v-sea gene products to the cell surface. However, due to the inhibition of proteolytic cleavage, the modified form of gp155 is now the major v-sea encoded protein expressed on the cell surface. Thus it appears that the cell surface expression of a v-sea encoded protein with tyrosine kinase autophosphorylating activity is insufficient for cell transformation.

Alkaloids↗