# ent

id: cord-032982-xri24v40
type: DISEASE
entity:
  oviduct esophagus heart small intestine duodenum jejunum ileum large intestine cecum colon rectum both kidneys larynx liver lung 4 lobes lymph nodes bronchial mandibular mediastinal mesenteric mammary glands nose


id: cord-009371-ub4p4ngr
type: GGP
entity:
  Intubitlon of mternahzatlon arylsulfatase 63 lmmunoglobulln 76 a 2 macroglobuhn 77 semlikl forest varus


id: cord-269358-dm3mdqhl
type: CELL_LINE
entity:
  human embryonic lung HEL human rhabdomyosarcoma RD rhesus monkey kidney LLC MKa primary rhesus monkey kidney


id: cord-327883-s9nbr5y8
type: DNA
entity:
  HindIII DNA fragments Jl 4 2 kbp 0 962 to 0 985 mu K 4 0 kbp 0 014 to 0 036 mu Pi 2 7 kbp 0 to 0 014 mu and P2 2 7 kbp 0 985 to 1 mu Nucleotide sequence


id: cord-327883-s9nbr5y8
type: DNA
entity:
  alpha and picornavirus superfamilies W ILG H MAIRHOFER C MARKERT and H WOLF Max v Pettenkofer Inst for Hygiene and Med Microbiology Univ D 8000 Munich


# bib

id: cord-004656-n4h295e5
title: Developmental Regulation of Angiotensinogen Gene Expression in Sheep
author: Olson, Ann Louise
date: 1990
txt: ./txt/cord-004656-n4h295e5.txt
cache: ./cache/cord-004656-n4h295e5.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7086511/
doi: 10.1203/00006450-199009000-00001
summary:
  In an effort to determine if this phenomenon is specific to the rat or applicable to other species, we compared the ontogenic changes in hepatic and renal angiotensinogen mRNA expression in fetal (60, 90, 118, and 138 d of gestation, term being 145 d), newborn (7 d postnatal), and adult sheep. Angiotensinogen mRNA sequences were detected in all fetal liver samples and appeared to increase 3-fold from 60 to 138 d gestation and then to decrease after birth. In an effort to determine if this phenomenon is specific to the rat or applicable to other species, we compared the ontogenic Received January 18, 1990 ; accepted April 16, 1990 changes in hepatic and renal angiotensinogen gene expression during the last trimester of gestation in fetal sheep. Northern blot analysis of liver and kidney RNA from fetal sheep (1 18 and 138 d gestational age) 1 and newborn lamb are shown in Figure 3 .

abstract:
  ABSTRACT: It has been suggested that the liver is not the main source of angiotensinogen during fetal life in rats, but that the kidney is an important site of fetal angiotensinogen synthesis. In an effort to determine if this phenomenon is specific to the rat or applicable to other species, we compared the ontogenic changes in hepatic and renal angiotensinogen mRNA expression in fetal (60, 90, 118, and 138 d of gestation, term being 145 d), newborn (7 d postnatal), and adult sheep. Total RNA was extracted, subjected to Northern blotting and hybridized using a full-length rat radiolabeled antisense RNA. Angiotensinogen mRNA sequences were detected in all fetal liver samples and appeared to increase 3-fold from 60 to 138 d gestation and then to decrease after birth. In contrast, angiotensiogen mRNA could not be detected in renal cortical tissue of 118 or 138 d fetuses, or newborn or adult sheep. We conclude that, unlike in the rat, liver angiotensinogen gene expression is detectable during the 2nd trimester of gestation in sheep and is developmentally regulated. Furthermore, in contrast to the fetal rat, angiotensinogen mRNA sequences were undetectable in fetal sheep kidney.


id: cord-004657-kmluql8h
author: Eibl, Martha M.
date: 1990
txt: ./txt/cord-004657-kmluql8h.txt
cache: ./cache/cord-004657-kmluql8h.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7086514/
doi: 10.1007/bf00918694
summary:
  title: Prophylaxis of necrotizing enterocolitis by oral IgA-IgG: Review of a clinical study in low birth weight infants and discussion of the pathogenic role of infection Necrotizing enterocolitis (NEC) is a severe gastrointestinal disease and an important cause of morbidity and mortality among premature, low birth weight infants (1) . There we described the effective prophylaxis of NEC by administration of an oral IgA-IgG preparation in low birth weight infants for whom breast milk from their mothers was not available. The purpose of the study was to investigate whether feeding of an oral IgA-IgG preparation to low birth weight infants for whom breast milk is not available can effectively prevent NEC. That the IgA-IgG feeding prevented NEC in our study has been further confirmed by the experience that, after termination of the study, the incidence of NEC among all low birth weight infants admitted to our hospital was again comparable to the incidence observed in the control group.

title:
  Prophylaxis of necrotizing enterocolitis by oral IgA-IgG: Review of a clinical study in low birth weight infants and discussion of the pathogenic role of infection

abstract:
  Necrotizing enterocolitis, a severe gastrointestinal disease in the neonatal period, affects primarily premature infants. Perinatal complications that predispose the neonate to systemic hypoxia are frequent in infants with necrotizing enterocolitis. Ischemia of the intestinal mucosa may facilitate the invasion of enteric microorganisms in stressed low birth weight infants. Geographical and temporal clustering of outbreaks of the disease and the termination of epidemics by standard infection control underline the importance of infectious agents in the development of this disease. Several studies have established the immunoprotective effect of orally administered antibodies against infection of the gastrointestinal mucosa in children and adults. Anecdotal evidence suggested that feeding of human immune globulin might have a positive effect on the incidence of necrotizing enterocolitis in premature infants. This paper reviews a prospective, randomized, controlled trial of the efficacy of an oral immune globulin preparation (published in detail in theNew England Journal of Medicine, Vol. 319, pp. 1–7, 1988) and discusses the pathogenic role of infection in necrotizing enterocolitis.


id: cord-004866-slqje8cq
title: The cytotoxin of Pseudomonas aeruginosa: Cytotoxicity requires proteolytic activation
author: Orlik-Eisel, Gabriele
date: 1990
txt: ./txt/cord-004866-slqje8cq.txt
cache: ./cache/cord-004866-slqje8cq.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7087514/
doi: 10.1007/bf00245265
summary:
  Like [(125)I] labeled material from Pseudomonas aeruginosa this polypeptide bound to membrane preparations from Ehrlich ascites cells, as evidenced by sedimentation through a sucrose gradient at neutral pH. Expression of the cytotoxin gene in Escherichia coli was inducible with IPTG (compare lanes 1 and 2 in Fig. 5 B) , again yielding material that migrated like the non-processed form of the cytotoxin in SDS-PAGE (compare with lane 4). We have established the sequence of a pore-forming cytotoxin from Pseudomonas aeruginosa by determining the amino-terminal amino acid sequence of the purified protein and sequencing of the structural gene, as identified by a pool of synthetic oligonucleotides. Within the N-terminal domain, a remarkable homology to a pentapeptide consensus sequence (TonB-box), commonly found in outer membrane receptor proteins of the Escherichia coli iron transport system, was detected. Pseudomonas aerugmosa cytotoxin: The nucleotide sequence of the gene and the mechanism of activation of the protein

abstract:
  The primary structure of a cytotoxin from Pseudomonas aeruginosa was determined by sequencing of the structural gene. The cytotoxin (31,700 Mr) lacks an N-terminal signal sequence for bacterial secretion but contains a pentapeptide consensus sequence commonly found in prokaryotic proteins which function in a TonB-dependent manner. The cytotoxin gene has a [G+C]-content of 53.8% which is considerably lower than generally observed for genes from Pseudomonas aeruginosa. The cytotoxin gene was exclusively detected in strain 158 but not in three other clinical isolates, as determined by Southern and Northern hybridization. The latter technique revealed that the toxin is translated from monocistronic mRNA. The promoter of the cytotoxin is inactive in Escherichia coli. Upon site-directed modification of the 5′-noncoding region by the polymerase chain reaction the gene was expressed under control of the trcpromoter. The gene product obtained in Escherichia coli was nontoxic. Toxicity was induced by subsequent treatment with trypsin. [(35)S]methionine-labeled cytotoxin with high specific radioactivity was obtained by in vitro transcription/translation. Like [(125)I] labeled material from Pseudomonas aeruginosa this polypeptide bound to membrane preparations from Ehrlich ascites cells, as evidenced by sedimentation through a sucrose gradient at neutral pH.


id: cord-006237-oxbquzeg
title: Bioluminescence, chemiluminescence
author: Dwenger, A.
date: 1990
txt: ./txt/cord-006237-oxbquzeg.txt
cache: ./cache/cord-006237-oxbquzeg.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7100654/
doi: 10.1007/bf00325727
abstract: nan
summary:
  The oxygen radical production was measured by luminol (0.4 mmol/1 test) and/or lucigenin (0.23 retool/1 test) enhanced chemiluminescence response (CL) (Biolumat LB 9505, Berthold) in absence or in presence of different stimuli, N-formyl-L-methionyl-L-leucyl-L-phenylalanine (FMLP, Sigma; 3.5 • 10-6 tool/1 test), zymosan A (Sigma; 3.5 mg/ml test), latex (Unisphere latex 22, 0.8 gin, Serva; 2 gl/ml test), lipopolysaccharide (LPS from E. The aim of the present study was to examine, if PGE 1 might 80 influence injury to EC, caused by LPS-primed neutrophils, and furthermore, if this effect could be explained by a diminished oxygen radical production, measured by chemiluminescence (CL). Addition of 0.1 gg of radical trap (MDTQ-DA) to each zymosan stimulated whole blood sample reduced CL response by 7 0 -90 p.c. Following induction of haemorrhagic-necrotising pancreatitis, high quantities of toxic oxygen metabolites are released from pancreatic tissue, contributing to the development of MOF.


id: cord-006393-jcj9nqfu
title: The use of immunoglobulin in bone marrow transplantation
author: Tutschka, Peter J.
date: 1990
txt: ./txt/cord-006393-jcj9nqfu.txt
cache: ./cache/cord-006393-jcj9nqfu.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7101739/
doi: 10.1007/bf00918696
summary:
  The role of bone marrow transplantation is to restore lymphohematopoietic function of a recipient whose marrow has been destroyed, either by disease or by the preparative therapy employed in an attempt to eradicate the patient''s lymphohematopoietic malignancy. There are several risk factors for the development of interstitial pneumonia such as TBI (if the lung dose exceeds 600 rads), acute GVHD, increased age of the patient, CMV seropositivity of the patient before the transplant, transfusion of blood products from CMV-positive donors, inability to generate an antiviral cytotoxicity (which is very common in the postengraftment phase), and inability to mount a humoral antibody response. Investigators from UCLA, Minnesota, and Sloan-Kettering all showed, in reasonably well-controlled studies, that the incidence of CMV interstitial pneumonia was reduced in patients given high-titered antibody preparations compared to that in the control group. The low incidence of CMV interstitial pneumonia in this group indicated that IVIG might be effective in the CMV-seronegative patient even when receiving a seropositive donor graft.

abstract:
  The role of bone marrow transplantation is to restore lymphohematopoietic function of a recipient whose marrow has been destroyed, either by disease or by the preparative therapy employed in an attempt to eradicate the patient's lymphohematopoietic malignancy. The restoration of lymphohematopoietic function through the donor graft occurs in stages, requires several months, and is often not completed until 1 to 2 years after transplantation. These sequential steps of immuno-reconstitution are associated with a number of definable and predictable immune deficiencies and seem to be responsible for the pattern of complications that emerges after transplantation. Most of these complications are either the result of, or associated with, infections that also occur in an almost predictable pattern. In the various phases of immune deficiency following sequentially after transplantation, the humoral immune system is greatly affected, thus raising the possibility that passively administered antibodies in the form of immune globulin therapy might be beneficial in all phases of the marrow transplant procedure. This paper attempts to summarize the use of immune globulin preparations in clinical bone marrow transplantation, showing the rationale for and some of the results of therapeutic immune globulin administration.


id: cord-009371-ub4p4ngr
author: Mollenhauer, Hilton H.
date: 1990-05-07
txt: ./txt/cord-009371-ub4p4ngr.txt
cache: ./cache/cord-009371-ub4p4ngr.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7148783/
doi: 10.1016/0304-4157(90)90008-z
title:
  Alteration of intracellular traffic by monensin; mechanism, specificity and relationship to toxicity

abstract:
  Monensin, a monovalent ion-selective ionophore, facilitates the transmembrane exchange of principally sodium ions for protons. The outer surface of the ionophore-ion comples is composed largely of nonpolar hydrocarbon, which imparts a high solubility to the complexes in nonpolar solvents. In biological systems, these complexes are freely soluble in the lipid components of membranes and, presumably, diffuse or shuttle through the membranes from one aqueous membrane interface to the other. The net effect for monensin is a trans-membrane exchange of sodium ions for protons. However, the interaction of an ionophore with biological membranes, and its ionophoric expression, is highly dependent on the biochemical configuration of the membrane itself. One apparent consequence of this exchange is the neutralization of acidic intracellular compartments such as the trans Golgi apparatus cisternae and associated elements, lysosomes, and certain endosomes. This is accompanied by a disruption of trans Golgi apparatus cisternae and of lysosome and acidic endosome function. At the same time, Golgi apparatus cisternae appear to swell, presumably due to osmotic uptake of water resulting from the inward movement of ions. Monensin effects on Golgi apparatus are observed in cells from a wide range of plant and animal species. The action of monensin is most often exerted on the trans half of the stacked cisternae, often near the point of exit of secretory vesicles at the trans face of the stacked cisternae, or, especially at low monensin concentrations or short exposure times, near the middle of the stacked cisternae. The effects of monensin are quite rapid in both animal and plant cells; i.e., changes in Golgi apparatus may be observed after only 2–5 min of exposure. It is implicit in these observations that the uptake of osmotically active cations is accompanied by a concomitant efflux of H(+) and that a net influx of protons would be required to sustain the ionic exchange long enough to account for the swelling of cisternae observed in electron micrographs. In the Golgi apparatus, late processing events such as terminal glycosylation and proteolytic cleavages are most susceptible to inhibition by monensin. Yet, many incompletely processed molecules may still be secreted via yet poorly understood mechanisms that appear to bypass the Golgi apparatus. In endocytosis, monensin does not prevent internalization. However, intracellular degradation of internalized ligands may be prevented. It is becoming clear that endocytosis involves both acidic and non-acidic compartments and that monensin inhibits those processes that normally occur in acidic compartments. Thus, monensin, which is capable of collapsing Na(+) and H(+) gradients, has gained wide-spread acceptance as a tool for studying Golgi apparatus function and for localizing and identifying the molecular pathways of subcellular vesicular traffic involving acid compartments. Among its advantages are the low concentrations at which inhibitions are produced (0.01–1.0 μM), a minimum of troublesome side effects (e.g., little or no change of protein synthesis or ATP levels) and a reversible action. Because the affinity of monensin for Na(+) is ten times that for K(+), its nearest competitor, monensin mediates primarily a Na(+)-H(+) exchange. Monensin has little tendency to bind calcium. Not only is monensin of importance as an experimental tool, it is of great commercial value as a coccidiostat for poultry and to promote more efficient utilization of feed in cattle. The mechanisms by which monensin interact with coccidia and rumen microflora to achieved these benefits are reasonably well documented. However, the interactions between monensin and the tissues of the host animal are not well understood although the severe toxicological manifestations of monensin poisoning are well known. Equine species are particularly susceptible to monensin poisoning, and a common effect of monensin poisoning is vacuolization and/or swelling of mitochondria in striated muscle. Other pathological injuries to striated muscle, spleen, lung, liver and kidney also have been noted. A consistent observation is cardiac myocyte degeneration as well as vacuolization. Differences in cellular response resulting from exposure to monensin (i.e., Golgi apparatus swelling in cultured cells, isolated tissues, and plants vs.mitochondrial swelling in animals fed monensin) suggest that myocardial damage is due either to a monensin metabolite or is a secondary response to some other derivation. However, as pointed out by Bergen and Bates [26], the underlying mode of action of ionophores is on transmembrane ion fluxes which dissipate cation and proton gradients. Consequently, some or all of the observed monensin effects in vivo in animals could be secondary phenomena caused by disruption of normal membrane physiology resulting from altered ion fluxes.


id: cord-010036-6czkzek0
title: Treatment of idiopathic spasmodic torticollis with botulinum‐A toxin: a pilot study of 19 patients
author: Lorentz, I T
date: 1990-05-01
txt: ./txt/cord-010036-6czkzek0.txt
cache: ./cache/cord-010036-6czkzek0.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7168378/
doi: 10.5694/j.1326-5377.1990.tb125354.x
summary:
  title: Treatment of idiopathic spasmodic torticollis with botulinum‐A toxin: a pilot study of 19 patients Nineteen patients with spasmodic torticollis, unresponsive to standard therapy, were administered local injections of botulinum‐A toxin into the affected muscles. Botulinum toxin is a very effective and safe method of treatment for spasmodic torticollis, (Med J Aust 1990; 152: 528-530) T he term "dystonia" was coined by Oppenheim in 1911 1 in describing six patients with alterations in muscle tone, sustained posturing and involuntary movements. A 48-year-old male mechanic suffering from haemochromatosis, which was treated with weekly venesections, developed spasmodic torticollis 18 months before he was referred for botulinum toxin treatment. In up to 15% of patients with ST the symptoms may remit in the first five years of the illness, so some cases of improvement may be examples of a natural remission hastened by botulinum toxin injections. Controlled trial of botulinum toxin injections in the treatment of spasmodic torticollis

abstract:
  Nineteen patients with spasmodic torticollis, unresponsive to standard therapy, were administered local injections of botulinum‐A toxin into the affected muscles. During an average follow‐up period of 11.5 months, a more than 25% improvement was noted in 14 of 19 patients. All those with purely focal dystonia and 9 of 10 patients with a disease history of less than three years benefited from treatment. Side effects were insignificant and transient. Botulinum toxin is a very effective and safe method of treatment for spasmodic torticollis.


id: cord-032982-xri24v40
author: MEDINSKY, M. A.
date: 1990-08-17
txt: ./txt/cord-032982-xri24v40.txt
cache: ./cache/cord-032982-xri24v40.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7529062/
doi: 10.1093/toxsci/15.2.308
summary:
  The objective of the studies reported here was to describe the toxic effects in rats and mice of inhalation exposure for 2 or 13 weeks to airborne concentrations of ADA as high as 200 mg/m 3 . In the 2-week study, serum (approximately 0.5 ml) was obtained from five male and five female rats and mice 3 days prior to the first day of exposure, and was analyzed for antibody titers to specific bacteria and viruses (Mycoplasma pulmonis, M. At the end of the 13-week study, serum from 5 male and 5 female rats from all exposure groups and controls (40 rats total) were analyzed for titers to Sendai virus, PVM, RCV/SDA, and Mycoplasma. There were no significant differences in methemoglobin levels or acetylcholinesterase activities in whole blood of male and female rats or mice exposed to any concentration of ADA, when compared to controls.

title:
  Effect of Inhaled Azodicarbonamide on F344/N Rats and B6C3F(1) Mice with 2-Week and 13-Week Inhalation Exposures

abstract:
  Effect of Inhaled Azodicarbonamide on F344/N Rats and B6C3F, Mice with 2-Week and 13-Week Inhalation Exposures. MEDINSKY, M. A., BECHTOLD, W. E., BIRNBAUM, L. S., BOND, J. A., BURT, D. G., CHENG, Y. S., GILLFTT, N. A., GULATI, D. K., HOBBS, C. H., AND PICK-RELL, J. A. (1990). Fundam. Appl. Toxicol 15, 308/319. Azodicarbonamide (ADA), a compound used in the baking and plastics industries, has been reported to cause pulmonary sensiti-zation and dermatitis in people. Two-week repeated and 13-week subchronic inhalation exposures of F344/N rats and B6C3F, mice to ADA were conducted to determine the toxicity of inhaled ADA. The mean air concentrations of ADA in the 2-week studies were 207, 102, 52, 9.4, or 2.0 mg/m3. No exposure-related mortality nor abnormal clinical signs were observed in rats or mice during or after exposure. The terminal body weights were slightly depressed in the highest exposure group. Liver weights were lower in male rats exposed to 200 mg ADA/m3. No significant lesions were noted on either gross or histologic evaluation of rats or mice. In the 13-week subchronic study, the mean air concentrations of ADA were 204, 100, or 50 mg/m3. No mortality or clinical signs related to exposure were observed. The terminal body weights of exposed rats were not significantly different from those of control rats but were significantly depressed in mice exposed to 100 or 200 mg ADA/m3. No histopathological lesions were noted in mice. Lung weights were increased and enlarged mediastinal and/or tracheobronchial lymph nodes were noted in rats exposed to 50 mg ADA/m3. No exposure-related lesions were observed microscopically in rats exposed to 100 or 200 mg ADA/m3. All rats in the 50 mg ADA/m3 exposure group only had lung lesions that consisted of perivascular cuffing with lymphocytes and a multifocal type II cell hyperplasia, suggesting a possible immune reaction to an antigen in the lung. Viral titers for rats exposed to 50 mg ADA/m3 were negative for Sendai virus and pneumonia virus of mice, which produce similar lesions. The possibility of an unknown viral antigen causing this lesion cannot be eliminated. Lung tissue from male rats was analyzed for ADA and biurea, the major metabolite of ADA. No ADA was detected. The amount of biurea in the lungs increased nonlinearly with increasing exposure concentration, suggesting that clearance was somewhat impaired with repeated exposures. However, even at the highest exposure concentration, this amount of biurea was less than 1 % of the estimated total ADA deposited over the exposure period. In summary, ADA is rapidly cleared from the lungs, even when inhaled at concentrations up to 200 mg/m3. Exposure to ADA for up to 13 weeks did not appear to be toxic to rodents


id: cord-104223-ht3ry9i0
title: Sorting within the regulated secretory pathway occurs in the trans- Golgi network
author: nan
date: 1990-01-01
txt: ./txt/cord-104223-ht3ry9i0.txt
cache: ./cache/cord-104223-ht3ry9i0.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2115992/
doi: nan
summary:
  Bioactive peptides cleaved from the egg-laying hormone precursor in the bag cell neurons of Aplysia are sorted into distinct dense core vesicle classes (DCVs). All other changes were minor in comparison, and in the compartments important in these studies-small and large immature vesicles, clear vesicles, and Golgi apparatus-the results between calculations at three HD values differ by no more than 5 % in any experiment. Both amino and carboxy terminal-associated radioactivity are transported through the Golgi stacks and enter small immature DCVs (defined by membrane extensions, connection to tubules, or nonspherical morphology) and clear vesicles after a 30-min pulse and 30-min chase (Fig. 4 B, Fig. 5 , and Table I ). After the initial cleavage event, the ELH-containing carboxy-terminal intermediate condenses in one region of the TGN (small immature vesicles) and the amino-terminal bag cell peptide-containing intermediate condenses in another region of the TGN (large immature vesicles).

abstract:
  Bioactive peptides cleaved from the egg-laying hormone precursor in the bag cell neurons of Aplysia are sorted into distinct dense core vesicle classes (DCVs). Bag cell prohormone processing can be divided into two stages, an initial cleavage occurring in a late Golgi compartment, which is not blocked by monensin, and later cleavages that occur within DCVs and are blocked by monensin. Prohormone intermediates are sorted in the trans-Golgi network. The large soma-specific DCVs turn over, while the small DCVs are transported to processes for regulated release. Thus, protein trafficking differentially regulates the levels and localization of multiple biologically active peptides derived from a common prohormone.


id: cord-260109-vgbrwegt
author: Charley, B.
date: 1990-02-28
txt: ./txt/cord-260109-vgbrwegt.txt
cache: ./cache/cord-260109-vgbrwegt.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pubmed/2167506/
doi: 10.1016/0923-2494(90)90133-j
summary:
  Furthermore, addition of anti-MHC (class II) mAb during PBMC incubation with virus-infected cells reduced IFN yields, suggesting that masking of these surface antigens alters PBMC responsiveness to IFN induction. Moreover, experiments in which IFN0c production was inhibited by monoclonal antibodies (mAb) directed at some epitopes of the TGEV glycoprotein E1 suggested that a defined domain of this transmembrane viral protein played a key role in the IFN0t induction process (Charley and Laurie, 1988) . In the present report, we analysed the nature of lymphocyte subpopulation(s) responsive to IFNa induction by TGEV-infected cell monolayers by using cell-depletion experiments with mAb plus complement. In addition, IFN induction-blocking experiments conducted with anti-MHC (SLA, swine leukocyte antigens) class II mAb without complement suggest a functional role for these membrane molecules in the IFN induction process. However, two preparations of anti-SLA class II mAb (TH22A5 and MSA3) could directly block IFN induction when added during co-incubation of PBMC with i''GEV-infected fixed monolayers or TGE alone (5 independent experiments).

title:
  Characterization of blood mononuclear cells producing IFNα following induction by coronavirus-infected cells (porcine transmissible gastroenteritis virus)

abstract:
  Abstract Porcine blood mononuclear cells (PBMC) were shown to produce interferon-α (IFNα) following incubation with cells infected by a coronavirus, transmissible gastroenteritis virus. Monoclonal antibodies (mAb) with specificities for leukocyte subsets and major histocompatibility complex (MHC) antigens were used to characterize IFNα producer cells. The production of IFNα was found to be a function of non-phagocytic, non-adherent, non-T, non-B, CD4+ (and to a lesser extent CD8+) MHC-class-II-positive cells. Furthermore, addition of anti-MHC (class II) mAb during PBMC incubation with virus-infected cells reduced IFN yields, suggesting that masking of these surface antigens alters PBMC responsiveness to IFN induction.


id: cord-263025-mmdeyph3
author: Paton, D. J.
date: 1990
txt: ./txt/cord-263025-mmdeyph3.txt
cache: ./cache/cord-263025-mmdeyph3.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pubmed/2168106/
doi: 10.1007/bf00350714
summary:
  title: Sows infected in pregnancy with porcine respiratory coronavirus show no evidence of protecting their sucking piglets against transmissible gastroenteritis On the basis of weight gain, clinical signs and survival, no differences in response to challenge was detected when piglets suckled by PRCV inoculated sows were compared with those suckled by uninoculated sows. On the basis of weight gain, clinical signs and survival, no differences in response to challenge was detected when piglets suckled by PRCV inoculated sows were compared with those suckled by uninoculated sows. Such a difference was evident when the litters of sows successfully pm-immunized with TGEV were compared with those of uninoculated or PRCV-inoculated sows. A lyophilized stock of the virus which had been passaged three times in primary pig kidney monolayers (PPKM) was passaged once more, either in PPKM or in a five-day-old colostrum-deprived piglet, to provide the virus for inoculation of the pregnant sows.

title:
  Sows infected in pregnancy with porcine respiratory coronavirus show no evidence of protecting their sucking piglets against transmissible gastroenteritis

abstract:
  Eighteen litters of sucking piglets were challenged with one of two strains of transmissible gastroenteritis virus (TGEV). During pregnancy, their seronegative dams had been either inoculated intranasally with porcine respiratory coronavirus (PRCV), inoculated orally with TGEV or left untreated. On the basis of weight gain, clinical signs and survival, no differences in response to challenge was detected when piglets suckled by PRCV inoculated sows were compared with those suckled by uninoculated sows. Such a difference was evident when the litters of sows successfully pre-immunized with TGEV were compared with those of unicoculated or PRCV-inoculated sows. The possibility of transplacental transmission of PRCV was investigated in two litters born to sows that had been inoculated with this virus in late pregnancy. All sixteen live-born piglets were seronegative for the virus at birth and PRCV was not isolated from tissues taken from two stillborn piglets.


id: cord-269358-dm3mdqhl
title: Inactivation and stability of viral diagnostic reagents treated by gamma radiation
author: White, L. A.
date: 1990-10-31
txt: ./txt/cord-269358-dm3mdqhl.txt
cache: ./cache/cord-269358-dm3mdqhl.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pubmed/2126734/
doi: 10.1016/1045-1056(90)90029-y
summary:
  Influenza antigens inactivated with 1·7 Mrad displayed comparable potency, sensitivity, specificity and stability to those inactivated by standard procedures with beta-propiolactone (BPL). Gamma radiation is safer than chemical inactivation procedures and is a reliable and effective replacement for BPL in preparing diagnostic reagents. Because of the potential carcinogenic hazard to the laboratorian associated with the use of BPL1'' and the deleterious effects of BPL on some hemagglutinating (HA) antigens, our laboratory investigated inactivation ofviral reagents by gamma radiation from a cobalt-60 source. i5 The CDC Inventoryil of reference antigens and antisera were used as test controls and for evaluating the sensitivity and specificity of all radiation-inactivated reagents. Preliminary experiments were conducted to determine the amount of gamma radiation required to inactivate the infectivity of 13 influenza virus strains. These viruses were inactivated by gamma radiation of 0.42 to 3.70 Mrad without adverse effect on the potency, sensitivity or specificity of the antigen.

abstract:
  Abstract The objective of this study was to apply the pertinent findings from gamma inactivation of virus infectivity to the production of high quality diagnostic reagents. A Gammacell 220 (Atomic Energy of Canada, Ltd., Ottawa, Canada § § Use of trade names is for identification only and does not imply endorsement by the Public Health Service or by the U.S. Department of Health and Human Services. ) was used to subject 38 viruses grown in either susceptible tissue cultures or embryonated chicken eggs to various doses of gamma radiation from a cobalt-60 source. The radiation required to reduce viral infectivity was 0·42 to 3·7 megarads (Mrad). The effect of gamma treatment on the antigenic reactivity of reagents for the complement fixation (CF), hemagglutination (HA) and neuraminadase assays was determined. Influenza antigens inactivated with 1·7 Mrad displayed comparable potency, sensitivity, specificity and stability to those inactivated by standard procedures with beta-propiolactone (BPL). Significant inactivation of influenza N1 and B neuraminidase occurred with >2·4 Mrad radiation at temperatures above 4°C. All 38 viruses were inactivated, and CF or HA antigens were prepared successfully. Antigenic potency remained stable with all antigens for 3 years and with 83% after 5 years storage. Influenza HA antigens evaluated after 9 years of storage demonstrated 86% stability. Gamma radiation is safer than chemical inactivation procedures and is a reliable and effective replacement for BPL in preparing diagnostic reagents.


id: cord-300796-rmjv56ia
author: nan
date: 1990-09-01
txt: ./txt/cord-300796-rmjv56ia.txt
cache: ./cache/cord-300796-rmjv56ia.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pubmed/2391367/
doi: nan
summary:
  In this work we show that the p62 protein of Semliki Forest virus contains an uncleaved signal sequence at its NH2-terminus and that this becomes glycosylated early during synthesis and translocation of the p62 polypeptide. As the glycosylation of the signal sequence most likely occurs after its release from the ER membrane our results suggest that this region has no role in completing the transfer process. Furthermore, the p62-reporter hybrid should be translocated across microsomal membranes and possibly glycosylated at Asn~3 of the p62 sequence if the 40 residues long NH2-terminal p62 peptide carries a signal sequence. This must involve Asn~3 of the p62 peptide as it is part of the only potential glycosylation site on the hybrid polypeptides (Garoff et al., 1980 ; references on dhfr sequence in legend to Fig. 1) , Finally, we can also conclude that the p62 signal sequence does not provide a stable membrane anchor to the translocated chain.

title:
  The signal sequence of the p62 protein of Semliki Forest virus is involved in initiation but not in completing chain translocation

abstract:
  So far it has been demonstrated that the signal sequence of proteins which are made at the ER functions both at the level of protein targeting to the ER and in initiation of chain translocation across the ER membrane. However, its possible role in completing the process of chain transfer (see Singer, S. J., P. A. Maher, and M. P. Yaffe. Proc. Natl. Acad. Sci. USA. 1987. 84:1015-1019) has remained elusive. In this work we show that the p62 protein of Semliki Forest virus contains an uncleaved signal sequence at its NH2-terminus and that this becomes glycosylated early during synthesis and translocation of the p62 polypeptide. As the glycosylation of the signal sequence most likely occurs after its release from the ER membrane our results suggest that this region has no role in completing the transfer process.


id: cord-303662-ro9879dl
title: Demyelination induced by murine hepatitis virus JHM strain (MHV-4) is immunologically mediated
author: Wang, Fun-In
date: 1990-11-30
txt: ./txt/cord-303662-ro9879dl.txt
cache: ./cache/cord-303662-ro9879dl.txt
extension: .txt
mime: text/plain
url: https://www.sciencedirect.com/science/article/pii/016557289090050W
doi: 10.1016/0165-5728(90)90050-w
summary:
  Un-In view of the finding that whole body irradiairradiated mice demonstrated intense disease at tion at day 6 p.i. prevents JHMV-induced paraday 9 p.i. By contrast, mice given 850 rad at day 6 lytic-demyelinating disease, differential irradiation p.i. had few histological changes at day 9 p.i. In studies were conducted to determine whether critiaddition, a second mouse strain, BALB/cJ mice cal radiosensitive targets reside in the systemic or a Immune donor mice were 6-week-old C57BL/6J males given 106 PFU of JHMV 2.2-V-1 i.p. 6 days prior to transfer. These they resemble the original JHMV isolates, which experiments indicate that populations of murine in early passages primarily caused a nonfatal paradonor spleen cells, which are enriched for T lytic disease (Bailey et al., 1949; Cheever et al., lymphocytes and appear to be MHC-restricted, 1949) ; only after many i.c. passages did the virus restore demyelination to infected, irradiated re-acquire marked neurovirulence.

abstract:
  Abstract The neurotropic mouse hepatitis viruses (MHV), in particular strain JHM (JHMV or MHV-4), cause experimental central nervous system demyelination that pathologically resembles multiple sclerosis, an important human demyelinating disease. The mechanism of JHMV-induced demyelination remains unclear, though its tropism for oligodendrocytes had led to the belief that JHMV causes demyelination by direct lysis of these myelin-producing cells. However, several studies have also implicated the involvement of immune responses in the demyelinating process. In this communication, we present evidence that generalized immunosuppression with gamma irradiation prevents JHMV-induced demyelination, a finding that was not limited to a particular strain of JHMV or to one strain of mouse. In addition, significant paralytic-demyelinating disease was restored to infected, irradiated mice after the adoptive transfer of nylon wool nonadherent splenic cells and appeared to be restricted by the major histocompatibility complex (MHC). These observations indicate that the principal mechanisms of JHMV-induced demyelination are most likely immunopathological.


id: cord-321868-xk4yuibj
author: Belcourt, Michael F.
date: 1990-07-27
txt: ./txt/cord-321868-xk4yuibj.txt
cache: ./cache/cord-321868-xk4yuibj.txt
extension: .txt
mime: text/plain
url: https://api.elsevier.com/content/article/pii/009286749090371K
doi: 10.1016/0092-8674(90)90371-k
summary:
  Our tRNA overproduction data suggest that a leucyl-tRNA, probably tRNALeu UAG, an unusual leucine isoacceptor that recognizes all six leucine codons, slips from CUU-Leu onto UUA-Leu (in the +1 reading frame) during a translational pause at the AGG-Arg codon induced by the low availability of tRNAArg CCU, encoded by a single-copy essential gene. In these systems, a simultaneous slippage of tRNAs in the A and P sites of the translating ribosome on the homopolymeric sequence results in a frameshift to the pro orpol reading frame and suppression of the gag frame termination codon. The 14 nucleotide frameshift site has a Gln residue (rather than His) following Gly. The amino acid sequence through the 14 nucleotide site confirms the Gln residue after Gly (data not shown), supporting the notion that translation shifts to the +l reading frame by peptidyl-tRNA slippage on the CUU-Leu codon.

title:
  Ribosomal frameshifting in the yeast retrotransposon Ty: tRNAs induce slippage on a 7 nucleotide minimal site

abstract:
  Abstract Ribosomal frameshifting regulates expression of the TYB gene of yeast Ty retrotransposons. We previously demonstrated that a 14 nucleotide sequence conserved between two families of Ty elements was necessary and sufficient to support ribosomal frameshifting. This work demonstrates that only 7 of these 14 nucleotides are needed for normal levels of frameshifting. Any change to the sequence CUU-AGG-C drastically reduces frameshifting; this suggests that two specific tRNAs, tRNALeu UAG and tRNAArg CCU, are involved in the event. Our tRNA overproduction data suggest that a leucyl-tRNA, probably tRNALeu UAG, an unusual leucine isoacceptor that recognizes all six leucine codons, slips from CUU-Leu onto UUA-Leu (in the +1 reading frame) during a translational pause at the AGG-Arg codon induced by the low availability of tRNAArg CCU, encoded by a single-copy essential gene. Frameshifting is also directional and reading frame specific. Interestingly, frameshifting is inhibited when the “slip” CUU codon is located three codons downstream, but not four or more codons downstream, of the translational initiation codon.


id: cord-325740-ak7bf0gq
title: Bovine coronavirus antigen in the host cell plasmalemma
author: Payne, H. R.
date: 1990-10-31
txt: ./txt/cord-325740-ak7bf0gq.txt
cache: ./cache/cord-325740-ak7bf0gq.txt
extension: .txt
mime: text/plain
url: https://api.elsevier.com/content/article/pii/001448009090039G
doi: 10.1016/0014-4800(90)90039-g
summary:
  Abstract Expression of bovine coronavirus (BCV) antigen in the plasmalemma of epithelioid human rectal tumor (HRT-18) and fibroblastic bovine fetal spleen (BFS) cell lines was traced by immunofluorescence and immunoelectron microscopy facilitated by colloidal gold. Analysis of the labeling characteristics established that the goldmarked-sites represented de novo expression of BCV antigen in the plasma membrane of infected cells. Bovine fetal spleen (BFS) cells are highly susceptible to BCV-induced cell fusion if trypsin is added to the medium of infected cultures. Viral antigen did not increase in the plasma membrane after the onset of cell fusion in infected BFS cell cultures. The differences among infected BFS and HRT-18 cells in the surface expression of viral antigen and fusion might result from the kinetics and mechanisms of protein expression and the differences in the composition of the two plasma membranes.

abstract:
  Abstract Expression of bovine coronavirus (BCV) antigen in the plasmalemma of epithelioid human rectal tumor (HRT-18) and fibroblastic bovine fetal spleen (BFS) cell lines was traced by immunofluorescence and immunoelectron microscopy facilitated by colloidal gold. Cytoplasmic fluorescence was first observed at 12 hr postinfection (h.p.i) in infected HRT-18 cultures. This fluorescence coincided with the appearance of cell surface antigen reacting with colloidal gold-labeled antibodies to BCV antigens. At 24 h.p.i the amount of viral antigens at the surface of HRT-18 had increased, although cytoplasmic fluorescence remained constant. Infected BFS cells but not HRT-18 cells formed polykaryons when incubated in the presence of trypsin. One viral antigen in the plasma membrane of BFS cells was thus identified as the S glycoprotein with a fusion domain. In contrast to HRT-18 cells, the overall amount of BCV antigens at the surface of BFS cells remained constant after the onset of fusion. Analysis of the labeling characteristics established that the goldmarked-sites represented de novo expression of BCV antigen in the plasma membrane of infected cells.


id: cord-327883-s9nbr5y8
title: Section Virology
author: nan
date: 1990-03-31
txt: ./txt/cord-327883-s9nbr5y8.txt
cache: ./cache/cord-327883-s9nbr5y8.txt
extension: .txt
mime: text/plain
url: https://www.sciencedirect.com/science/article/pii/S0934884011800393
doi: 10.1016/s0934-8840(11)80039-3
abstract: nan
summary:
  By improving the enzyme-linked immunosorbent assay (ELISA) for HSV-2-antibodies and additional testing of sera by Western blot, we were able to specifically identify HSV-l-and HSV-2-antibodies in serum samples. To get some insight into the molecular basis of processes controlling the viral expression we studied the sequence-specific DNA-protein interactions within the genomic regulatory regions. for Med. Microbiology, Univ., D-5300 Bonn Semiquantitative detection of Hepatitis B Virus (HBV) DNA in sera of infected individuals has become an important means of modern serological hepatitis diagnostics. THOMSSEN 1 In the course of acute Epstein-Barr virus (EBV) infection IgM antibodies always occur against two cellular antigens that were characterized as proteins with a molecular weight of 26 kD (p26) and 29 kD (p29), respectively. The frequency and specificity of antibodies to P-gene encoded proteins of human hepatitis B virus was tested in sera of acute and chronically infected patients with and without hepatocellular carcinoma (HCC).


id: cord-347246-0vofftmj
title: Infectious diseases of the upper respiratory tract: implications for toxicology studies.
author: Everitt, J I
date: 1990-04-17
txt: ./txt/cord-347246-0vofftmj.txt
cache: ./cache/cord-347246-0vofftmj.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pubmed/2200664/
doi: nan
summary:
  This paper reviews several important infectious diseases of the upper airway of rats and mice and discusses the potential influence of these conditions on the results of toxicology studies. All three agents cause significant rodent respiratory disease, with lesions in the upper airways, including the nasal passages. Although there are many excellent descriptive studies ofthe histogenesis of Sendai virus-induced lesions within the lower respiratory tract, few pathology reports include a description of lesions in the nasal cavity and upper airway. Although numerous bacteria can infect the upper airway of the rat and mouse, they are not generally prevalent in well-conducted toxicology studies begun with animals free of adventitious murine pathogens and maintained with modern methods of laboratory animal husbandry. A variety of important microbial pathogens including viruses, mycoplasmas, bacteria, and fungi infect the upper respiratory tract of the mouse and rat and result in significant pathologic alterations.

abstract:
  The consequences of adventitious infectious agents upon the interpretation of toxicology studies performed in rats and mice are incompletely understood. Several prevalent murine pathogens cause alterations of the respiratory system that can confuse the assessment of chemically induced airway injury. In some instances the pathogenesis of infection with these agents has been relatively well studied in the lower respiratory tract. However, there are few well-controlled studies that have examined the upper respiratory region, which result in interpretive problems for toxicologic pathologists. The conduct and interpretation of both short-term and chronic rodent bioassays can be compromised by both the clinical and subclinical manifestations of infectious diseases. This paper reviews several important infectious diseases of the upper airway of rats and mice and discusses the potential influence of these conditions on the results of toxicology studies.


