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At least 163 records · Page 9Linked to original sources
PubMed1989

A comparison between different models of the relation between recorded intradental nerve impulse activity and reported pain in man.

In this study three different models of the relation between intradental nerve impulse activity (INA) and pain report, expressed by finger-span (FS), in man were investigated. The techniques were (i) a previously described mathematical model, (ii) the relation between the Areas of INA and FS and (iii) the relation between the Peaks of INA and FS. Their usefulness in 533 clinical experiments on 15 subjects were evaluated by means of a statistical analysis of the variability and accuracy of the models. It was shown that the mathematical model was the most accurate and stable method of the three different methods investigated. This was indicated by, among other things, a significantly smaller variability for the mathematical model within experimental sessions than between sessions. The two other methods were found to be of less scientific value since they had an undesired high variability within sessions, and also showed contradicting results during control conditions.

Adult↗
PubMed1994

Identification of a mannose-acetate-specific 87-kDa receptor responsible for human NK and LAK activity.

Target cell recognition and cytotoxicity of human CD56+ NK and LAK cells is readily inhibited by acetylated mannose. Two respective NK cell receptor candidates were isolated from human leukocyte lysates by mannose acetate affinity chromatography. The 87-kDa receptor showed sequence homologies with lactoferrin and the 59-kDa receptor represented a complex of two Ca-binding proteins MRP-8 and MRP-14 reportedly expressed only by cells of myeloid origin. The 87-kDa receptor exhibited heterogeneity in isoelectric focusing and behaved entirely differently from lactoferrin. Preincubation of tumor target cells with the 87-kDa receptor inhibited competitively target cell recognition and cytotoxicity of human CD56+ NK and LAK cells.

Acetylation↗
PubMed1991

Priming action of inositol hexakisphosphate (InsP6) on the stimulated respiratory burst in human neutrophils.

After priming by a number of different host, bacterial and chemical agents, human neutrophils may be stimulated to produce a greater respiratory burst than would be elicited by the stimulus alone. Other neutrophil functions may be similarly enhanced by pre-exposure to a priming agent. We describe here a new extracellular role for inositol hexakisphosphate (InsP6) as a priming agent for a variety of human neutrophil functional responses. Preincubation of the cells with InsP6 alone (up to 250 microM) has no stimulatory effect upon the basal production of reactive oxygen intermediates but the response to a subsequent stimulus (FMLP, PMA or phagocytic particles) is substantially enhanced. Levels 100-200% higher than 'stimulus only' controls have been recorded. Peak enhancement of the FMLP-induced oxidative response occurs after 1-2 min preincubation with InsP6 and the effect is dose-dependent (maximum at approx. 100 microM InsP6). As others have shown FMLP stimulation of superoxide anion production has no external Ca2+ dependence but the presence of low levels of Ca2+ and Mg2+ (0.1 mM) during priming appears to be an essential requirement for full expression. Reports of intracellular concentrations of InsP6 in mammalian cells in the 30-100 microM range suggest that the local release of this inositol polyphosphate from damaged or effect cells could have a physiologically important modulatory role on neutrophil functions.

Calcium↗
PubMed2026

DAZL-targeted inducible kill switches enable efficient ablation of chicken primordial germ cells.

Competition from endogenous primordial germ cells (PGCs) in recipient embryos limits the generation of fully donor-derived offspring in avian surrogate-host systems. An inducible and germline-restricted ablation strategy is therefore needed to create sterile recipients without compromising somatic development. Using CRISPR/Cas9-mediated homology-directed repair, we inserted three inducible suicide-gene cassettes (iCaspase9, RapaCasp9, and CD) into the endogenous DAZL locus of chicken PGCs. All knock-in lines showed stable reporter expression and retained typical PGC morphology. Comparative functional analyses identified iCaspase9 activated by AP20187 as the most sensitive and specific ablation system, achieving near-complete killing at nanomolar concentrations without detectable toxicity in control cells. RapaCasp9 induced with rapamycin also ablated engineered PGCs efficiently, but rapamycin caused marked non-specific growth inhibition in control cells. Replacing rapamycin with the synthetic A/C heterodimerizer AP21967 largely eliminated this off-target toxicity while preserving rapid and robust killing. By contrast, yeast-derived CD variants did not substantially improve 5-fluorocytosine sensitivity in chicken PGCs. DAZL-restricted iCaspase9/AP20187 and the optimized RapaCasp9/AP21967 system provide efficient inducible kill switches for chicken PGCs in vitro. These platforms establish a practical genetic toolkit for generating sterile surrogate hosts to support avian genome editing, germline replacement, and Sire Dam Surrogate breeding.

CRISPR/Cas9↗
PubMed1995

Comparison of coronary lesions obtained by directional coronary atherectomy in unstable angina, stable angina, and restenosis after either atherectomy or angioplasty.

The present study investigated the incidence of the histopathologic lesions and of growth factor expression in a consecutive series of directional coronary atherectomy (DCA) samples from 40 unstable angina pectoris patients without prior acute myocardial infarction and compared the findings with those obtained in DCA samples from 18 patients with stable angina without previous infarction and 18 patients with restenosis. We investigated coronary thrombosis, neointimal hyperplasia, and inflammation. For unstable angina, we correlated the angiographic Ambrose plaque subtypes with the histopathologic findings. The immunophenotype of plaque cells and the growth factor expression were assessed with specific antibodies for cell characterization and for the expression of basic fibroblast and platelet-derived AA and AB growth factors and receptors. The incidence of coronary thrombosis was 35% in patients with unstable angina, 17% in those with stable angina, and 11% in patients with restenosis. Neointimal hyperplasia was found in 38% of unstable angina cases, in 17% of stable angina cases, and in 83% of restenosis cases. Inflammation without thrombus or accelerated progression occurred in 20% of unstable angina and 6% of stable angina samples. In 52% of unstable angina cases, inflammation coexisted with thrombosis and/or neointimal hyperplasia. In the unstable angina group, 71% of the plaques with thrombus had a corresponding angiographic pattern of complicated lesions. The growth factor expression, reported as percentage of cells immunostaining with different growth factor antibodies, was highest in restenosis, followed by unstable angina and stable angina lesions.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Isolation of a cDNA clone encoding a biologically active thyroid hormone receptor.

We have isolated a c-erbA cDNA clone from a GH3 cell library. The clone, denoted erb62, is 4.5 kilobases long and encodes a 461-amino acid beta-type c-erbA protein. This c-erbA protein binds 3,5,3'-triiodothyronine (T3) and T3 analogs with affinities similar to those of the authentic T3 receptor. By RNA gel blot analysis, erb62 hybridizes to a 6-kilobase RNA found in organs that express T3 receptors--e.g., heart, kidney, and brain. A COS-cell transient cotransfection system was used to show that erb62 encodes a biologically active T3 receptor. An oligonucleotide, corresponding to a portion of the rat growth hormone gene 5'-flanking region that contains a T3 response element, was inserted on the 5' side of the herpes simplex virus thymidine kinase promoter in a chloramphenicol acetyltransferase-expressing plasmid. Reporter gene expression directed by this hybrid promoter was T3 inducible only if this plasmid was cotransfected with an erb62-expressing plasmid.

Amino Acid Sequence↗
PubMed1989

Monoclonal antibodies to human lymphocyte homing receptors define a novel class of adhesion molecules on diverse cell types.

A 90-kD lymphocyte surface glycoprotein, defined by monoclonal antibodies of the Hermes series, is involved in lymphocyte recognition of high endothelial venules (HEV). Lymphocyte gp90Hermes binds in a saturable, reversible fashion to the mucosal vascular addressin (MAd), a tissue-specific endothelial cell adhesion molecule for lymphocytes. We and others have recently shown that the Hermes antigen is identical to or includes CD44 (In[Lu]-related p80), human Pgp-1, and extracellular matrix receptor III-molecules reportedly expressed on diverse cell types. Here, we examine the relationship between lymphoid and nonlymphoid Hermes antigens using serologic, biochemical, and, most importantly, functional assays. Consistent with studies using mAbs to CD44 or Pgp-1, mAbs against five different epitopes on lymphocyte gp90Hermes reacted with a wide variety of nonhematolymphoid cells in diverse normal human tissues, including many types of epithelium, mesenchymal elements such as fibroblasts and smooth muscle, and a subset of glia in the central nervous system. To ask whether these non-lymphoid molecules might also be functionally homologous to lymphocyte homing receptors, we assessed their ability to interact with purified MAd using fluorescence energy transfer techniques. The Hermes antigen isolated from both glial cells and fibroblasts--which express a predominant 90-kD form similar in relative molecular mass, isoelectric point, and protease sensitivity to lymphocyte gp90Hermes--was able to bind purified MAd. In contrast, a 140-160-kD form of the Hermes antigen isolated from squamous epithelial cells lacked this capability. Like lymphocyte binding to mucosal HEV, the interaction between glial gp90Hermes and MAd is inhibited by mAb Hermes-3, but not Hermes-1, suggesting that similar molecular domains are involved in the two binding events. The observation that the Hermes/CD44 molecules derived from several nonlymphoid cell types display binding domains homologous to those of lymphocyte homing receptors suggests that these glycoproteins represent a novel type of cell adhesion/recognition molecule (H-CAM) potentially mediating cell-cell or cell-matrix interactions in multiple tissues.

Antibodies, Monoclonal↗
PubMed1995

Decreased expression of glutathione S-transferases and increased fatty change in peroxisomal enzyme-negative foci induced by clofibrate in rat livers.

Alteration in glutathione S-transferase (GST) isoenzymes was compared with that of a peroxisomal enzyme, enoyl-CoA hydratase (ECH), during hepatocarcinogenesis caused by clofibrate (CF) administration in male Sprague-Dawley rats. The amount of alpha class GST forms, determined by single radial immunodiffusion using anti-GST 1-2 antibody, was inversely correlated with that of ECH and was decreased at week 2 of CF administration to approximately 50% of the value prior to treatment and then slightly increased to 70% of the control value by week 15, without change thereafter up to 93 weeks. Resolution of GST subunits by high performance liquid chromatography revealed an approximately 60% decrease in the amounts of subunits 1 and 3 at week 93 and a 25% decrease in the amounts of subunits 2 and 4. Immunohistochemical staining of rat livers revealed hepatic foci and minifoci negative for ECH at week 60 and thereafter. Almost all ECH-negative foci (95.1-97.9%) were clear cell in character, along with a somewhat lower proportion (68.0-73.8%) of ECH-negative minifoci. Numerous fat-positive granules were detected in 78.3% of those lesions exhibiting a clear cell change. Although the amounts of GST and ECH exhibited contrasting patterns of alteration in whole livers following CF administration, the expression of both alpha and mu class GST forms was decreased in the majority of ECH-negative foci at week 93, but were not altered in minifoci. The repression of GST forms appeared to be a later event than the loss of ECH or the clear cell change in CF-associated hepatic lesions and was in clear contrast to the enhanced expression reported for preneoplastic lesions induced by mutagenic carcinogens.

Animals↗
PubMed1995

Dissecting a locus control region: facilitation of enhancer function by extended enhancer-flanking sequences.

Using transgenic mice, we have defined novel gene regulatory elements, termed "facilitators." These elements bilaterally flank, by up to 1 kb, a 200-bp T-cell-specific enhancer domain in the human adenosine deaminase (ADA) gene. Facilitators were essential for gene copy-proportional and integration site-independent reporter expression in transgenic thymocytes, but they had no effect on the enhancer in transfected T cells. Both segments were required. Individual segments had no activity. A lack of facilitator function caused positional susceptibility and prevented DNase I-hypersensitive site formation at the enhancer. The segments were required to be at opposed ends of the enhancer, and they could not be grouped together. Reversing the orientation of a facilitator segment caused a partial loss of function, suggesting involvement of a stereospecific chromatin structure. trans-acting factor access to enhancer elements was modeled by exposing nuclei to a restriction endonuclease. The enhancer domain was accessible to the 4-cutter DpnII in a tissue- and cell-type-specific fashion. However, unlike DNase I hypersensitivity and gene expression, accessibility to the endonuclease could occur without the facilitator segments, suggesting that an accessible chromatin domain is an intermediate state in the activational pathway. These results suggest that facilitators (i) are distinct from yet positionally constrained to the enhancer, (ii) participate in a chromatin structure transition that is necessary for the DNase I hypersensitivity and the transcriptional activating function of the enhancer, and (iii) act after cell-type-specific accessibility to the enhancer sequences is established by factors that do not require the facilitators to be present.

Adenosine Deaminase↗
PubMed1995

Vasoactive intestinal peptide: an important trophic factor and developmental regulator?

It has been proposed that vasoactive intestinal peptide (VIP) or a very closely related peptide has important actions very early in embryonic development. Recent data supporting this hypothesis are that subnanomolar concentrations of VIP significantly increased the growth rate of cultured embryonic day-9.5 (E9.5) mouse embryos, and that embryos at this and later stages exhibit a high degree of VIP binding in the brain stem and spinal cord. It is not known whether VIP is derived from the fetus, placenta, or mother at these early stages, or whether VIP acts in this culture system in place of a related peptide. The earliest reported expression of VIP in rat embryos is at E13.5, when the peptide and mRNA are expressed transiently in a high percentage of cells in the rat stellate ganglia. The time course of events mapped in other sympathetic ganglia at this stage suggest that transient expression of VIP in the ganglia might function to regulate neuroblast and/or glial cell proliferation, maturation or survival. Tissue culture studies indicate that VIP can support many of these trophic functions at concentrations that are the same or lower than that necessary to increase cAMP levels by way of classical VIP receptors. For example, VIP at 10(-10) M stimulates the release of neurotrophic factors from glial cells and maximally stimulates the proliferation of astrocytes. Two VIP receptors encoded on different genes have now been cloned. Both are members of the seven transmembrane G-protein-coupled receptor family and, when expressed in mammalian cells, mediate an increase in cAMP.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Localization of transforming growth factor alpha and its receptor in gastric mucosal cells. Implications for a regulatory role in acid secretion and mucosal renewal.

Transforming growth factor alpha (TGF alpha) shares with epidermal growth factor (EGF) structural homology (35%), a common cell-surface membrane receptor (TGF alpha/EGF receptor), and a nearly identical spectrum of biological activity, including inhibition of gastric acid secretion. Herein, we report expression of TGF alpha mRNA in normal gastric mucosa of the adult guinea pig, rat, and dog. TGF alpha mRNA was also detected in matched surgically resected gastric mucosa and adjacent gastric carcinoma from 10 patients, and in gastric mucosa adjacent to a benign ulcer from an additional patient. TGF alpha protein was quantitated by radioimmunoassay and was present in tumor and adjacent mucosa. TGF alpha/EGF receptor mRNA was also detected in gastric mucosa from all species studied. Localization of TGF alpha and TGF alpha/EGF receptor mRNA expression was examined in samples of unfractionated guinea pig gastric mucosa and from chief cell-enriched and parietal cell-enriched fractions. All samples exhibited TGF alpha and TGF alpha/EGF receptor expression. The TGF alpha signal was greatest in the parietal cell fraction (5.8-fold increase), but was also enhanced in the chief cell fraction (1.9-fold increase) relative to the unfractionated gastric mucosa. Like TGF alpha expression, TGF alpha/EGF receptor mRNA expression was most intense in the parietal cell-enriched fraction (7.8-fold increase), but was also increased in the chief cell-enriched fraction (2.7-fold increase) relative to the unfractionated guinea pig gastric mucosa. We conclude that TGF alpha and TGF alpha/EGF receptor genes are expressed in normal adult mammalian gastric mucosa. These findings, when interpreted in light of described actions of TGF alpha and EGF, provide evidence that local production of TGF alpha could play an important role in the regulation of acid secretion and mucosal renewal in the stomach.

Adult↗
PubMed1992

Hormone withdrawal triggers a premature and sustained gene activation from delayed secondary glucocorticoid response elements.

Glucocorticoid regulatory elements, denoted GREs and delayed secondary GREs (sGREs), bind the purified glucocorticoid receptors via distinctive sequence motifs and confer a primary and delayed secondary hormone inducibility, respectively, upon a linked reporter construct in stably transfected mammalian cells. The delayed secondary responses, but not the primary responses, are preceded by a time lag of several hours and blocked by protein synthesis inhibitors. In this report, we further characterized and distinguished these hormonal inductions. A 206-base pair DNA fragment from the hepatic rat alpha 2u-globulin (RUG) gene, containing at least two delayed sGREs, was specifically activated by glucocorticoids in a dose-dependent manner via a process which is sensitive to receptor antagonist RU486. Delayed sGRE-stimulated production of correctly initiated transcripts was preceded by a time lag of 2 h, a time when the GRE-mediated induction had reached maximal levels. A pulse of glucocorticoids sustained maximal activation of the delayed secondary response but not the primary response. In fact, hormone withdrawal triggered a premature induction of this delayed secondary response, suggesting that delayed sGREs are under both negative and positive control of the hormone receptor. Two separable elements of the 206-base pair fragment, including the 29-base pair sequence of a single receptor binding site, activated the reporter expression as effectively with transient, pulsatile exposure to hormone as with continuous exposure. Our results suggest that the information content of a hormonal pulse is retained, or "memorized," more persistently by a receptor binding site of delayed sGREs than those of the prototypical GREs.

Alpha-Globulins↗
PubMed1992

Molecular cloning of cDNAs for the human granulocyte colony-stimulating factor receptor from HL-60 and mapping of the gene to chromosome region 1p32-34.

Early studies examining the effects of purified or recombinant granulocyte colony-stimulating factor (G-CSF) on human leukemia cell lines demonstrated that some cell lines, such as HL-60, could be induced to differentiate in response to G-CSF. In two recent studies reporting the cloning of the human G-CSF receptor (hGCSFR), four classes of receptor cDNA were identified and, surprisingly, the message for this receptor was reportedly expressed by HL-60 at either very low levels or not at all. Using a mouse G-CSF receptor probe, we cloned and sequenced a cDNA for hGCSFR from an HL-60 cDNA library in plasmid and used it to identify 31 additional clones from an HL-60 cDNA library in phage. Polymerase chain reaction analysis of the 31 phage clones established that 29 were derived from class I hGCSFR mRNA, one was derived from class III mRNA, and one was derived from class IV mRNA. In addition, the hGCSFR gene was chromosomally localized by Southern blot analysis of its segregation pattern in a panel of rodent-human hybrid DNAs using the radiolabeled cDNA probe. The hGCSFR locus was present in hybrids retaining the distal short arm of human chromosome 1 and absent in hybrids that did not retain this region. Chromosomal in situ hybridization refined the localization of the hGCSFR gene to region 1p32-p34. The combination of hybrid DNA analysis and in situ hybridization places the hGCSFR gene telomeric to the CSF1, JUN, and TCL-5 loci.

Base Sequence↗
PubMed1992

The difference in p53 antioncogene transcription in human monocytes and lymphocytes.

The p53 gene is associated with malignant transformation as well as 'antioncogene' activity. In this report expression of p53 in resting and activated human blood monocytes and lymphocytes was studied. It is shown that human monocytes freshly isolated by continuous Percoll-gradient centrifugation contain detectable levels of p53 mRNA. Stimulation of monocytes by the potent activation inducer Staphylococcus aureus Cowan I (SAC) for 3-5 h caused the disappearance of p53 mRNA. In contrast, induction of a high level of tumor necrosis factor alpha mRNA was detected. The addition of cycloheximide did not increase the p53 mRNA content in stimulated monocytes, and decreased the mRNA level in resting cells. p53 mRNA was absent in freshly isolated lymphocytes and in resting cells cultured for 20 h. Activation of lymphocytes by phytohemagglutinin caused accumulation of p53 mRNA. We suggest that p53 gene regulation and functions might be different in human monocytes and lymphocytes.

Blotting, Northern↗
PubMed1991

The receptor for yolk lipoprotein deposition in the chicken oocyte.

The final rapid growth phase of the chicken oocyte is characterized by massive uptake of hepatically synthesized yolk precursor proteins from the plasma. The two major yolk-forming components, very low density lipoprotein (VLDL) and vitellogenin (VTG), have been shown to interact with a 95-kDa protein present in detergent extracts of ovarian membranes; this protein is absent in hens of a mutant nonlaying chicken strain (Nimpf, J., Radosavljevic, M., and Schneider, W. J. (1989) J. Biol. Chem. 264, 1393-1398). Here, we have purified the 95-kDa protein by ligand and immunoaffinity chromatography and demonstrated its role in receptor-mediated endocytosis by ultrastructural immunolocalization, structural, and functional studies. The receptor was visualized exclusively in the oocyte proper and was absent from somatic cells, in agreement with the previously reported expression of two different lipoprotein receptors in somatic cells and oocytes, respectively, of laying hens (Hayashi, K., Nimpf, J., and Schneider, W. J. (1989) J. Biol. Chem. 264, 3131-3139). Amino acid sequences of tryptic fragments of the oocyte receptor were obtained, and its kinship to somatic low density lipoprotein receptors was confirmed through the demonstration of sequence conservation in three characteristic domains. In particular, the chicken receptor's internalization sequence, Phe-Asp-Asn-Pro-Val-Tyr, is identical with that in low density lipoprotein receptors from mammals as well as Xenopus laevis. The ligand-binding properties, specificity, and kinetic parameters of the oocyte receptor were characterized in filtration assays employing pure ligands and receptor. In conjunction with ligand-blotting experiments following limited protease digestion of the receptor, the binding assay data suggest that VTG recognizes a substructure of the VLDL-binding site. These studies establish that a cell-specific receptor mediates the endocytosis of VTG and VLDL into growing chicken oocytes and thus possibly plays a key role in control of oocyte growth.

Amino Acid Sequence↗
PubMed1991

Restricted Ig H chain V gene usage in the human antibody response to Haemophilus influenzae type b capsular polysaccharide.

The mechanisms that govern the content of the human antibody repertoire are poorly understood. To investigate the antibody response to a clinically relevant Ag, we have produced heterohybridomas secreting human antibodies directed against the capsular polysaccharide of Haemophilus influenzae type b (Hib PS). Immune lymphocytes were harvested 7 days after immunization with either of two vaccine formulations, a plain polysaccharide vaccine (Hib PS) or a polysaccharide-protein conjugate of Hib PS and diphtheria toxoid (Hib PS-D). H chain V region gene nucleic acid sequences were determined for five stable hybridomas. All use members of the VHIII gene family and are 83% to 98% homologous to two candidate germ-line sequences. A variety of D and JH segments are used. Thus the Ig H chain repertoire appears to be restricted to a limited group of VHIII family members. The previously reported expression of homologous sequences in the human fetal repertoire suggests that the inability of young children to respond to this Ag is not caused by deficiencies of these important elements early in development. The restricted use of VHIII gene segments suggests that this gene family plays a pivotal role in the immune response to this important childhood pathogen.

Amino Acid Sequence↗
PubMed1991

[Pearson's syndrome. Pancytopenia with exocrine pancreatic insufficiency: new mitochondrial disease in the first childhood].

Pearson's syndrome is a lethal disorder of a still unknown cause, responsible for pancytopenia and exocrine pancreatic dysfunction in the first months of life. Permanent hyperlactacidemia and increased mitochondrial and cytoplasmic oxidoreduction ratios were observed in 6 unrelated children presenting with this disease. This led to study the oxidative phosphorylation in lymphocytes and thus to relate Pearson's syndrome to an enzymatic disease of the respiratory chain (NADH oxidase activity deficiency). The study of the mitochondrial genome allowed identifying major changes in mitochondrial DNA in all patients and all studied tissues. Thus, Pearson's syndrome is the first mitochondriopathy with a non neuromuscular expression reported to date.

DNA, Mitochondrial↗
PubMed1987

Configuration of the immunoglobulin and T cell receptor gene regions in hairy cell leukemia and B-chronic lymphocytic leukemia.

The configuration of the immunoglobulin heavy and light chain genes and of the T cell receptor (TCR) beta region was examined in a series of patients with hairy cell leukemia (HCL) and compared with the findings in B cell chronic lymphocytic leukemia (B-CLL). In all cases of HCL and B-CLL studied a rearrangement of the immunoglobulin heavy chain loci coupled to a reorganization of the light chain genes was documented. However, in all HCL and all but one B-CLL the TCR beta gene region was in a germ-line configuration. These findings confirm that HCL is characterized by the expansion of relatively mature B cell elements with a molecular configuration similar to that of B-CLL and indicate that the reported expression of T cell related markers, particularly in B-CLL, is not coupled to a rearrangement of the TCR beta-chain gene. Analyses of the immunoglobulin gene regions in HCL represent an important diagnostic tool as well as a possible aid toward monitoring the response to treatment.

B-Lymphocytes↗