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At least 145 records · Page 8Linked to original sources

PubMed1998

Recovery of growth hormone release from suppression by exogenous insulin-like growth factor I (IGF-I): evidence for a suppressive action of free rather than bound IGF-I.

To determine the time course of recovery of GH release from insulin-like growth factor I (IGF-I) suppression, 11 healthy adults (18-29 yr) received, in randomized order, 4-h i.v. infusions of recombinant human IGF-I (rhIGF-I; 3 microg/kg-h) or saline (control) from 25.5-29.5 h of a 47.5-h fast. Serum GH was maximally suppressed within 2 h and remained suppressed for 2 h after the rhIGF-I infusion; during this 4-h period, GH concentrations were approximately 25% of control day levels [median (interquartile range), 1.2 (0.4-4.0) vs. 4.8 (2.8-7.9) microg/L; P < 0.05]. A rebound increase in GH concentrations occurred 5-7 h after the end of rhIGF-I infusion [7.6 (4.6 -11.7) vs. 4.3 (2.5-6.0) microg/L; P < 0.05]. Thereafter, serum GH concentrations were similar on both days. Total IGF-I concentrations peaked at the end of the rhIGF-I infusion (432 +/- 43 vs. 263 +/- 44 microg/L; P < 0.0001) and remained elevated 18 h after the rhIGF-I infusion (360 +/- 36 vs. 202 +/- 23 microg/L; P = 0.001). Free IGF-I concentrations were approximately 140% above control day values at the end of the infusion (2.1 +/- 0.4 vs. 0.88 +/- 0.3 microg/L; P = 0.001), but declined to baseline within 2 h after the infusion. The close temporal association between the resolution of GH suppression and the fall of free IGF-I concentrations, and the lack of any association with total IGF-I concentrations suggest that unbound (free), not protein-bound, IGF-I is the major IGF-I component responsible for this suppression. The rebound increase in GH concentrations after the end of rhIGF-I infusion is consistent with cessation of an inhibitory effect of free IGF-I on GH release.

Adolescent↗

PubMed1985

Cyclic Cushing's syndrome combined with cortisol suppressible, dexamethasone non-suppressible ACTH secretion: a new variant of Cushing's syndrome.

A 55 year old woman with an unusual form of Cushing's disease was studied. During several periods (periods lasting up to 84 days) evidence of cortisol hypersecretion with cycles occurring every 6 days was found. Suppression of plasma cortisol through orally administered dexamethasone (up to 32 mg per day) could not be achieved either during periods of cyclic cortisol hypersecretion or during apparent remission with normal cortisol secretion. Marked suppression of plasma ACTH was measured in response to an iv infusion of 50 mg cortisol over a period of 55 min whereas a similar test with 2 mg dexamethasone (iv bolus) did not suppress ACTH secretion. Transsphenoidal exploration of the sella revealed a tumour surrounding the anterior pituitary. Examination of the pituitary showed a few tiny tumour structures embedded in normal tissue which could not be removed, when the tumour was resected selectively under preservation of normal appearing tissue. Post-operatively, clinical and chemical remission (normal response to 1 mg dexamethasone) was observed for about 4 months. Thereafter, cortisol hypersecretion occurred again necessitating bilateral adrenalectomy. Our results are compatible with the assumption that normal hypothalamic-pituitary-adrenal suppressibility with cortisol, but not with dexamethasone, was caused by the loss of feedback receptors for dexamethasone in the presence of cortisol receptors in the cells which secrete ACTH or CRF. The combination of cyclic hypercortisolism with dexamethasone non-suppressible Cushing's syndrome has not been reported before and thus represents a new variant of Cushing's syndrome.

Adrenocorticotropic Hormone↗

PubMed1968

Suppression of behavior by timeout punishment when suppression results in loss of positive reinforcement.

This investigation, using rats as subjects and punishment by timeout for responses maintained on a ratio schedule, sought to determine whether behavior would be suppressed by timeout punishment when such suppression also reduced reinforcement density or frequency. A series of experiments indicated that timeout punishment suppressed responding, with the degree of suppression increasing as a function of the duration of the timeout period. Suppressive effects were found to decrease as a function of increases in deprivation (body weight) and were eliminated when the punished response also was reinforced. It was concluded that timeout can produce aversive effects even when loss of reinforcement results. An alternative interpretation of the findings, based on the effects of extinction periods and delay of reinforcement on chained behavior, was discussed.

Animals↗

PubMed1983

Suppression of the immune response in tumor-bearing mice. III. Induction of functionally suppressive antigen-driven macrophages.

A functionally suppressive antigen-driven subpopulation of macrophages has been demonstrated in mice-bearing tumors produced by MSV-transformed BALB/3T3 cells. The suppressor macrophages depressed markedly both allogeneic and syngeneic mixed leukocyte culture responses and functioned even when assayed at low concentrations, suggesting that high concentrations of normal macrophages were not responsible for the suppression. Studies also showed that suppressor macrophages acted to suppress the proliferation of hyperreactive Lyt 1+,2- cells found in the splenic cell suspensions of tumor-bearing mice after the removal of the adherent suppressor cells. Finally, the suppressive activity of macrophages induced in tumorous mice could be augmented by KiMSV or MMSV but not by MuLV antigen. These results suggest that suppression might be a direct response to transformation-associated determinants expressed on the tumor cells as well as on the MSV virions or the result of cellular interactions between suppressor macrophages and other antigen-specific spleen cell populations.

Animals↗

PubMed1976

Splenic suppressing factor: purification and characterization of a factor suppressing thymidine incorporation into activated lymphocytes.

Suppressing activity upon the mitogen-activated lymphocytes was found in the supernatant (SUP) from the culture of mouse spleen, high-density subpopulation of thymocytes, and peritoneal exudate cells. Suppressing factor was obtained from the non-stimulated lymphocytes cultured for 24 to 36 hr with or without serum. Suppressing activity in the SUP was observed in the incorporation of 3H-thymidine, 3H-uridine, and 3H-leucine into Con A-activated lymphocytes or in the proliferation of L cells. Suppressing factor partially purified by Sephadex G-25 column chromatography was a heat-stable and dialyzable substance(s). Further purification and isolation of this factor by two-dimensional thin layer chromatography revealed that this was thymidine and thymidine monophosphate. The suppression in 3H-thymidine incorporation was attributed to the dilution effect of cold thymidine released from cultured lymphocytes.

Animals↗

PubMed1975

Studies in congenital generalized lipodystrophy. VI. Suppressible and non-suppressible insulin-like activities of plasma.

1. Suppressible and non-suppressible insulin-like activities (ILA) of plasma from 3 patients with congenital generalized lipodystrophy have been studied, employing isolated fat cells from rat epididymal adipose tissue. 2. In all 3 patients the fasting ILA was markedly increased compared with the normal controls. In one of the patients (I.T.) total ILA rose to about 800 muU per ml during an iv glucose tolerance test. 3. The observed total ILA was in all cases (controls included) equal to or slightly higher than the previously determined immunoreactive plasma insulin (IRI). The exact determination of ILA was, however, hampered by a dilution effect, which was present even at high plasma dilutions. 4. In 2 of the patients addition of insulin antiserum inhibited plasma ILA by about 50%. In the third patient (I.T.), who exhibited the highest insulin level, at least 85% of the activity was suppressed by insulin antibodies. The levels of non-suppressible ILA were higher than in the controls in terms of muU per ml, but lower than in the controls when related to total ILA. 5. These findings strongly support our previous conclusion that the elevated plasma insulin seen in congenital generalized lipodystrophy is mainly due to true pancreatic insulin. 6. Since the effect of plasma insulin on isolated fat cells were freely expressed, i.e. suppressible ILA was equal to or slightly lower than IRI, the presence of a circulating insulin antagonist in this disease may be excluded.

Adipose Tissue↗

PubMedDate not supplied

Recovery from allotype suppression in rabbits and release from this suppression in specific immune response.

The recovery of allotypic expression in allotype suppressed rabbits was followed up in specific antibodies and in bulk immunoglobulins. The primary antigenic stimulation with BSA and/or MS2 phage was given at 4 weeks of age. In the early recovery group, where the recovery from suppression began at 11-13 weeks of age, specific antibodies bearing the suppressed allotype were found to be synthesized by the primary stimulation or with successive allotype was scarely expressed in specific antibodies despite its recovered expression in bulk immunoglobulins. The X-ray irradiation followed by the immunization procedures promoted the recovery of the suppressed allotype expression in anti-BSA antibody and in bulk immunoglobulins but not in anti-MS2 phage antibody. The results are discussed in terms of regulatory mecahnisms of immune response in allotype suppressed animals.

Animals↗

PubMed1989

Suppression of in vitro immunoglobulin synthesis by CD16(Leu11a)+ CD56 (NKH1,Leu19)+non-T lineage NK cells; lack of suppression of cells from immunodeficient patients.

We examined the effect of both CD3-CD16(Leul la)+CD56(NKH1,Leu19)+ non-T lineage natural killer (NK) cells and CD3+CD8+CD16-CD56+ T lineage NK cells on B cell proliferation and differentiation. Fluorescence-activated cell sorter (FACS) purified CD16+CD56+ cells suppressed pokeweed mitogen (PWM) induced immunoglobulin synthesis. However, the T lineage NK cells tended to suppress immunoglobulin synthesis only when CD8+ cells were eliminated from the culture, and even then CD16+ NK cells suppressed antibody production more efficiently than did CD3+CD8+ NK cells. CD16+ NK cells did not suppress B cell proliferative responses to several mitogens. CD16+ NK cells from patients with Wiskott-Aldrich syndrome, who showed the high percentage of CD16+ NK cells, did not inhibit immunoglobulin synthesis. We concluded that non-T NK cells are the major immunoregulatory NK cells for immunoglobulin synthesis in normal immune systems, and that they suppress immunoglobulin synthesis through their action on B cell differentiation.

Adult↗

PubMed1989

In vivo hematopoietic effects of recombinant interleukin-1 alpha in mice: stimulation of granulocytic, monocytic, megakaryocytic, and early erythroid progenitors, suppression of late-stage erythropoiesis, and reversal of erythroid suppression with erythropoietin.

Interleukin-1 alpha (IL-1 alpha) is a macrophage-derived, multifunctional cytokine that broadly potentiates myelopoiesis and induces the synthesis of hematopoietic colony-stimulating factors (CSF) in vitro and in vivo. To evaluate the possibility for use of IL-1 alpha in ameliorating in vivo bone marrow suppression induced by drugs or radiation, we examined the in vivo effects of the cytokine on erythropoietic and other hematopoietic progenitor cells. Normal mice were treated with a single intraperitoneal (IP) injection of recombinant human IL-1 alpha at varying doses and were assayed at various times post-treatment. By six hours postinjection, a significant suppression of mature erythroid progenitors (CFU-E) was observed in animals treated with IL-1 alpha (0.5 micrograms/mouse), with maximum suppression of CFU-E and peripheral blood reticulocyte counts occurring at 24 hours. Decreases in peripheral blood hematocrit did not occur after a single IL-1 alpha injection but were observed after multiple injections of the cytokine. The suppressive effects of IL-1 alpha on late-stage erythropoiesis were abrogated by simultaneous administration of erythropoietin (EPO). At 48 hours post-treatment, a marked stimulation was observed in the numbers of spleen and marrow immature erythroid (BFU-E), macrophage (CFU-M), granulocyte (CFU-G), granulocyte-macrophage (CFU-GM), and megakaryocyte (CFU-meg) progenitor cells. These results demonstrate the potential use of IL-1 alpha as a generalized stimulator of hematopoiesis and show that the cytokine-induced suppression of late-stage erythropoiesis can be prevented by EPO.

Animals↗

PubMed1985

Suppression and abrogation of suppression of induced nonspecific cytotoxicity against tumor cells.

Fresh spleen cells obtained from normal mice of various strains including athymic mice and NK-less beige mice were found to suppress in a H-2-nonrestricted manner nonspecific cytotoxic activity of in vitro-cultured normal mouse spleen cells or that of nonadherent peritoneal exudate cells from mice treated with Propionibacterium acnes. Natural killer-insensitive MM2 ascites tumor cells were used as the target of assay of the cytotoxicity. The suppressive activity of fresh spleen cells was not affected by elimination of glass-adherent cells and of Thy-1.2-positive cells but partly decreased after removal of Sephadex G-10- or nylon wool-adherent cells. The suppressive activity of the cells seemed to be mediated, at less partly, by a soluble factor (or factors) which was released by fresh spleen cells into medium during short term culturing. The suppressive factor was a heat-resistant, dialyzable material which was stable at wide range of pH. Cells did not produce the factor at low temperature and its production was insensitive to indomethacin. Long term culture supernatant of spleen cells contained the suppressive factor and a relatively unstable high molecular weight substance which abrogated its activity. The characteristics of the cells which produced such desuppressive factor seemed to be identical to those of the induced cytotoxic effector cells. Kinetical analyses indicated that these two factors influenced, directly or indirectly, cytolytic activity of the effector cells without changing binding affinity between the effector and the target.

Adjuvants, Immunologic↗

PubMed1985

Suppression of natural cytotoxicity in tumor-bearing mice and inhibition of the suppression by D-mannose.

Natural cytotoxic activity of spleen cells from normal and tumor-bearing BALB/c and C57BL/6 mice was assayed using Meth A, MH136 and MM2 ascites tumor cells as the target by 51Cr-release during 18 h incubation. The cytolytic activity of the cells from tumor-bearers, especially in the early stage of tumor progression, was considerably lower than that of cells from normal controls. When Meth A and MH134 target cells were used, it was found that such change was not due to decrease of effectors but was caused by increase of activity of cells suppressive to the lytic reaction. The suppressive cells were recovered in nylon wool-adherent fraction of the spleen cells. The suppression was mediated, at least partly, by a very stable soluble factor. The suppression by the cell and that by the factor were both inhibited by addition of D-mannose. When MM2 was used as the target, such inhibition of the suppressive activity by D-mannose was not observed.

Animals↗

PubMed1982

Tumor cell-triggered macrophage-mediated suppression of the T-cell cytotoxic response to tumor-associated antigens. I. Characterization of the cell components for induction of suppression.

A tumor cell-triggered macrophage-mediated suppressor mechanism was demonstrated. It suppressed the induction of specific tumor immunity in the syngeneic, primary mixed lymphocyte tumor cell culture reactions. Preexposure of splenic adherent cells (SAC) to syngeneic FBL-3 tumor cells induced complete suppression of the generation of cytotoxic T-cells. The SAC responsible for inducing suppression were consistent with being macrophages. They were resistant to the treatment of anti-Thy-1.2 antibody plus complement and were relatively radioresistant (at least less than or equal to 750 R X-radiation). Adherent cells obtained from lymph nodes or thymuses acted in the same way as SAC. However, preexposure of peritoneal adherent cells to tumor cells failed to induce suppression. In contrast, the simultaneous presence of peritoneal adherent cells with SAC upon exposure to tumor cells prevented the induction of suppression. These peritoneal cells were also consistent with being macrophages. These results confirmed our previous observations obtained with experiments performed in the allogeneic system. An immunoregulatory circuit existed between two subsets of macrophages that were derived from the population of cells in the peritoneal cavity and from spleen, lymph nodes, or thymus. In the presence of tumor cells, these macrophages produced both positive regulation and negative regulation of the T-cell-mediated cytotoxic response against syngeneic tumor cells. The tumor cells may have utilized the host's own immune network to activate the suppressor mechanisms, thus successfully evading the host's immune surveillance.

Animals↗

PubMed1980

Mechanism of neonatal idiotype suppression. I. State of the suppressed B cells.

Neonatal BALB/c mice, given small amounts of an anti-idiotype serum directed against the TEPC-15 idiotype, are chronically unresponsive to immunization with PC antigens. These mice recover from suppression slowly over a period of 10 mo, and their response is not of TEPC-15 idiotype. However, the PC-specific precursors, as analyzed by the splenic fragment culture technique, in 8-mo-old suppressed mice are normal with respect to their frequency and idiotype dominance. Furthermore, the PC-precursors in neonatally suppressed BALB/c are sensitive to tolerance induction, as are precursors from neonatal liver and spleen cells. When chronic suppressed mice are immunized with a novel TI-1 antigen, PC-LPS, shown to stimulate immature PC-specific precursors, their response to PC is 80% of TEPC-15 idiotype, whereas their response to a TI-2 PC antigen and to a TD PC antigen is not TEPC-15 dominant. These results indicate that the TEPC-15 positive B cells in neonatally idiotype suppressed mice are in a state of immaturity that resembles the developmental characteristics of normal neonatal BALB/c mice.

Animals↗

PubMed1993

Cancer-associated SCM-recognition, immunedefense suppression, and serine protease protection peptide. Part II. Immunedefense suppressive effects of the CRISPPs peptide.

The cancer SCM-recognition, immunedefense suppression, and serine protease protection (CRISPP) peptide, a product of a hereditary or acquired heritable alpha 1-PI gene DNA mutation in cancer cells, is a potent suppressor of the natural killer (NK) and lymphokine activated killer (LAK) cytotoxicity against cancer cells. The "NK suppression epitope" encompasses amino acid residues 8 to 29 of the 29 amino acid sequence of the CRISPPs peptide. The NK suppression is peptide dose and incubation time dependent. The formation of conjugates between effector and target cells is not affected by the peptide, but the release of interleukin-2 (IL-2) and of tumor necrosis factor-alpha (TNF alpha) from lymphocytes is significantly decreased after treatment of lymphocytes with the CRISPPs peptide. The suppression of NK and LAK activity of lymphocytes by the CRISPPs peptide cannot be removed by washing, nor can it be reversed by subsequent treatment with recombinant interleukin-2 (rIL-2). However, autologous cell-free blood plasma, especially plasma ultrafiltrates of molecular weights higher than 100 kDa, can restore up to 83% of the NK activity. Scavenging of the CRISPPs peptide with anti-CRISPPs antibodies prevents the suppression of NK cytotoxicity. The relevance of CRISPP peptides for adoptive immunotherapy is discussed.

Cytotoxicity, Immunologic↗

PubMed1994

[Fat suppression failure artifacts at the susceptibility interface on frequency selective fat suppression MR imaging in the head and neck].

Fat suppression MR imaging is a valuable technique mainly used for the orbit, head and neck, and spine, where the high signal from fat can often obscure adjacent pathology. Fat suppression failure artifact manifested as a high signal area without geographic distortion. The purpose of this study was to investigate the frequency and common location of these artifacts in clinical MR imaging and to caution against their misinterpretation. Fat suppression MR imaging of the head and neck was performed in 30 consecutive patients. The artifact was found in the orbital floor (57%), the skull base (10%), and subcutaneous fat (10%), where the air-fat interface is parallel to the static magnetic field direction. The fat signal in the air-fat interface perpendicular to the static magnetic field was well suppressed. This artifact was independent of the duration of TE, frequency/phase encoding direction, and the strength of gradient amplitude, and appeared to be related to the amount of surrounding air. This may simulate pathology if fat suppression is only performed following Gd-DTPA administration. The radiologist should be aware of the presence of artifact by considering the geographic relation to the static magnetic field.

Adipose Tissue↗

PubMed1996

Strategies for the suppression of peroxidase gene expression in tobacco. II. In vivo suppression of peroxidase activity in transgenic tobacco using ribozyme and antisense constructs.

Several strategies involving the use of antisense and ribozyme constructs in different expression vectors were investigated as methods of suppressing gene expression in planta. We had previously identified an efficiently cleaving ribozyme (Rz), with two catalytic units and 60 nucleotide (nt) of complementary sequence, to the lignin-forming peroxidase of tobacco (TPX). This Rz was cloned behind the 35S CaMV (35S) and nopaline synthase (NOS) promoters, and into a vector utilising the tobacco tyrosine tRNA for expression. For comparison with more traditional antisense strategies, full-length TPX antisense (AS) constructs were also constructed behind the NOS and 35S promoters. Populations of transgenic tobacco containing these constructs were produced and compared to control plants transformed with the vector only. Significant suppression of peroxidase expression in the range of 40-80% was seen in the T0 and T1 populations carrying 35S-AS, 35S-Rz and tRNA-Rz constructs. Co-segregation of the suppressed peroxidase phenotype and the tRNA-Rz transgenes was demonstrated. Northern blot analysis indicated that levels of TPX mRNA were lower in the Rz plants. No evidence of mRNA cleavage was observed and thus it was unclear if the Rz constructs were acting as Rzs in vivo. Transgenic plants containing the tRNA-Rz construct had significantly lower levels of peroxidase than the other transgenic plants. There was no significant difference in levels of suppression of TPX between the short Rz in the 35S vector and the full-length AS constructs. Although peroxidase levels were significantly reduced in transgenic plants carrying 35S-AS, 35S-Rz and tRNA-Rz constructs, no significant difference in lignin levels was observed.

Agrobacterium tumefaciens↗

PubMed1996

The transcription of human alpha 1(I) procollagen gene (COL1A1) is suppressed by tumour necrosis factor-alpha through proximal short promoter elements: evidence for suppression mechanisms mediated by two nuclear-factorbinding sites.

Recent studies have demonstrated that tumour necrosis factor-alpha (TNF-alpha) decreases alpha 1(I) procollagen gene (COL1A1) expression in cultured human dermal fibroblasts. The purpose of this study was to analyse the transcriptional control of COL1A1 by TNF-alpha. Cultured human dermal fibroblasts were transiently transfected with plasmids containing 5' flanking sequences of COL1A1 fused to the chloramphenicol acetyltransferase (CAT) gene, and were incubated for 48 h in medium with or without TNF-alpha. TNF-alpha inhibited the CAT activity of fibroblasts transfected with plasmids containing 2.3 kb of 5' flanking sequences of COL1A1, whereas the activity of control plasmids containing the herpes simplex thymidine kinase promoter gene (pBLCAT) was unaltered. A series of deletion constructs of various small substitution mutations of the COL1A1 5' flanking region fused to the CAT gene were also transfected, and CAT activity was measured after incubation with TNF-alpha. TNF-alpha suppressed COL1A1 promoter activity through proximal short promoter elements containing only 107 bp. Short substitution mutations between -101 and -97 bp or between -46 and -38 bp abolished TNF-alpha suppression of COL1A1 promoter activity. DNA-protein complex formation was observed involving both sites in gel retardation assays. These results suggest that TNF-alpha suppressed COL1A1 promoter activity through elements located between -101 and -97 bp and between -46 and -38 bp of the COL1A1 promoter, and that the suppression involved DNA-protein interactions.

Base Sequence↗

PubMed1981

Allotype suppression in the chicken. II. Suppression in homozygous chickens with antiallotype antibody and allotype-disparate B cells.

Injection of heterozygous (M-1a/M-1b, G1g/G-1i) B 14-line chickens with antisera directed against either IgM-1a or IgM-1b induced suppression of the relevant IgM-1 and genetically linked IgG-1 allotypes, whereas a mixture of anti-M-1a and anti-M-1b antibodies failed to produce allotype suppression. Injection of anti-M-1 antiserum into M-1 homozygous chickens induced only a transient delay of a few days in the appearance and rise of serum IgM-1 levels. However, suppression of host allotypes was induced by injecting M-1, G-1 homozygous neonatal or embryonal recipients with anti-M-1 antisera together with B locus- histocompatible allotype-disparate spleen, bone marrow or bursal cells. The active cell type were donor B cells, which established chimerism in the injected host, whereas peripheral blood T lymphocytes from agammaglobulinemic donors were ineffective. Allotype suppression was attributed to a homeostatic control mechanism which is exerted by normal B cells (but not T cells) over B cell recruitment in anti-M-1 antibody-treated, immature hosts.

Animals↗