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PubMed2005

Weak relationships between suppression of melatonin and suppression of sleepiness/fatigue in response to light exposure.

In this paper we examine the relationship between melatonin suppression and reduction of sleepiness through light by comparing three different data sets. In total 36 subjects participated in three studies and received 4 h of bright light either from midnight till 4:00 hours (experiments A and B) or from noon till 16:00 hours (experiment C). In experiment A (night-time light, partial illumination of the retina, pupil dilated) subjects were exposed to either 100 lx of ocular light on the temporal, 100 lx on the nasal part of the retina, or <10 lx of dim light on the whole retina. In experiments B (night-time light, whole retina, pupil not dilated) and C (daytime light, whole retina, pupil not dilated) subjects were exposed either to bright (5000 lx) or to dim light (<10 lx). Subjective sleepiness/fatigue and melatonin concentrations in saliva were assessed hourly in all three experiments. For experiment A, a significant suppression of melatonin due to nasal and temporal illumination of the retina was found, that was not accompanied by a detectable reduction of subjective sleepiness/fatigue. For experiment B we found a suppression of melatonin that was paralleled with a significant reduction in subjective sleepiness, but not in fatigue. During experiment C we found no melatonin suppression but a reduction of subjective sleepiness, but also no effect on fatigue. From these data we conclude that the effects of light on sleepiness/fatigue are not mediated by melatonin and that the influence of endogenous melatonin concentration on sleepiness/fatigue is restricted.

Adult↗

PubMed2004

Cyclooxygenase (COX)-2 inhibitor celecoxib abrogates activation of cigarette smoke-induced nuclear factor (NF)-kappaB by suppressing activation of IkappaBalpha kinase in human non-small cell lung carcinoma: correlation with suppression of cyclin D1, COX-2, and matrix metalloproteinase-9.

Cigarette smoke (CS) has been linked to cardiovascular, pulmonary, and malignant diseases. CS-associated malignancies including cancers of the larynx, oral cavity, and pharynx, esophagus, pancreas, kidney, bladder, and lung; all are known to overexpress the nuclear factor-kappaB (NF-kappaB)-regulated gene products cyclin D1, cyclooxygenase (COX)-2, and matrix metalloprotease-9. Whether the COX-2 inhibitor, celecoxib, approved for the treatment of colon carcinogenesis and rheumatoid arthritis, affects CS-induced NF-kappaB activation is not known, although the role of NF-kappaB in regulation of apoptosis, angiogenesis, carcinogenesis, and inflammation is established. In our study, in which we examined DNA binding of NF-kappaB in human lung adenocarcinoma H1299 cells, we found that cigarette smoke condensate (CSC)-induced NF-kappaB activation was persistent up to 24 h, and celecoxib suppressed CSC-induced NF-kappaB activation. Celecoxib was effective even when administered 12 h after CSC treatment. This effect, however, was not cell type-specific. The activation of inhibitory subunit of NF-kappaB kinase (IkappaB), as examined by immunocomplex kinase assay, IkappaB phosphorylation, and IkappaB degradation was also inhibited. Celecoxib also abrogated CSC-induced p65 phosphorylation and nuclear translocation and NF-kappaB-dependent reporter gene expression. CSC-induced NF-kappaB reporter activity induced by NF-kappaB inducing kinase and IkappaB alpha kinase but not that activated by p65 was also blocked by celecoxib. CSC induced the expression of NF-kappaB-regulated proteins, COX-2, cyclin D1, and matrix metalloproteinase-9, and celecoxib abolished the induction of all three. The COX-2 promoter that is regulated by NF-kappaB was activated by CSC, and celecoxib suppressed its activation. Overall, our results suggest that chemopreventive effects of celecoxib may in part be mediated through suppression of NF-kappaB and NF-kappaB-regulated gene expression, which may contribute to its ability to suppress inflammation, proliferation, and angiogenesis.

Carcinoma, Non-Small-Cell Lung↗

PubMed1985

Suppression of murine IgE responses with amino acid polymer/allergen conjugates. II. Suppressive activities in adjuvant-induced IgE responses.

Treatment with conjugates of polysarcosine and grass pollen allergen extracts efficiently suppressed the induction of IgE responses in mice. The suppressive activity was shown to be allergen-specific and required covalent linking of the polysarcosine. Inhibitory effects could be overcome by booster injections of native allergen when these were given 3-4 weeks after treatment with conjugates. Administration of conjugates had only marginal effects on established IgE responses. The variance of these results with those of other studies on IgE suppression and the suitability of murine models for investigating reaginic antibody suppression are discussed.

Adjuvants, Immunologic↗

PubMed2003

Comparing the bispectral index and suppression ratio with burst suppression of the electroencephalogram during pentobarbital infusions in adult intensive care patients.

OBJECTIVE: The bispectral index (BIS), a processed variable derived from the raw electroencephalogram (EEG) used to guide sedation in the intensive care unit (ICU), has not been tested during barbiturate therapy for elevated intracranial pressure. We determined the BIS and suppression ratio (SR) values during traditional burst monitoring of the raw EEG during pentobarbital infusions. DESIGN: Prospective, observational cohort study. SETTING: A 42-bed multidisciplinary ICU in a tertiary care medical center. PATIENTS: Twelve consecutive patients with elevated intracranial pressure treated with pentobarbital infusions. INTERVENTION: All patients were monitored continuously with the Aspect Medical Systems A-1050 bedside EEG monitor using a bilateral referential montage. Pentobarbital doses were titrated based on the raw EEG to attain a burst-suppression pattern with a goal of 3-5 bursts/minute. Drug dosage, intracranial pressure, cerebral perfusion pressure values, EEG bursts/minute, BIS version 3.2, and SR were recorded daily. MEASUREMENTS AND MAIN RESULTS: The 12 patients were monitored for 62 patient-days. Mean +/- SD age was 32 +/- 15 years, seven (58%) patients were male, mean Acute Physiology and Chronic Heath Evaluation II score was 17.0 +/- 5.0, and hospital mortality was 42%. The mean pentobarbital infusion rate was 124 +/- 49 mg/hour or 2.3 +/- 1.3 mg/kg/hour, and mean pentobarbital serum concentration was 29.7 +/- 13 microg/ml. The mean BIS value was 18 +/- 14, mean SR 56% +/- 36%; BIS correlated well with SR (r=-0.99, p<0.001). For patient-days with a burst-suppression pattern, BIS 3.2 (r=0.90, p<0.001) and SR (r=-0.89, p<0.001) strongly correlated with the number of bursts/minute. The mean BIS value corresponding to 3-5 bursts/minute was 15 (95% confidence interval [CI] 10-20); SR value was 71 (95% CI 61-80). CONCLUSION: The Aspect A-1050 applied to patients and monitored by nurses and physicians works well as a bedside EEG monitor, providing a raw EEG signal to titrate barbiturate therapy. The continuous data trend and real-time digital output for the BIS and SR quantify the degree of EEG suppression well and may prove helpful in facilitating titration of barbiturate infusions.

Adult↗

PubMed1976

The suppressive effect of immunization on the proliferative responses of rat T cells in vitro. II. Abrogation of antigen-induced suppression by selective cytotoxic agents.

Rats given large i.v. doses of ovalbumin or sheep erythrocytes manifest suppressed spleen cell responses (3H-thymidine incorporation) to PHA within hours. Removal of glass wool-adherent cells totally restores responsiveness to that of normal nonadherent spleen cell cultures. Carrageenan, selectively toxic for macrophages, partially restores responses of antigen-suppressed spleen cells in culture, suggesting a supportive role for macrophages in the suppression phenomenon. Treatment of donors with low doses of cyclophosphamide (20 to 50 mg/kg) at the time of antigen injection abrogates the ability of their spleen cells to suppress the responses of normal cells to PHA. The low dose of cyclophosphamide required indicates a target other than the B cell or macrophage and suggests the possibility that cyclophosphamide eliminates the suppressor T cell component of the macrophage-T cell complex.

Animals↗

PubMed1986

Baclofen suppresses hippocampal epileptiform activity at low concentrations without suppressing synaptic transmission.

Baclofen is used clinically to treat spasticity, but has received little attention as a potential antiepileptic agent. To explore the antiepileptic potential of baclofen further, we tested its effect on stimulus train-induced bursting, an in vitro model of hippocampal epileptiform activity. In hippocampal slices prepared from male rats, extracellular field potentials were recorded in stratum pyramidale of CA3, and electrical stimuli were delivered to s. radiatum of CA3. After stable responses to single stimuli were established, stimulus trains were delivered every 5 min until stable triggered and spontaneous population bursting were elicited. (+/-)-Baclofen was bath-applied to the slices at varying concentrations to study its ability to suppress synaptic transmission and epileptiform activity. EC50 values for suppression of orthodromic population spike amplitude, of triggered burst duration and of spontaneous burst frequency were 2300, 355 and 26.9 nM, respectively; all statistically significantly different. These findings suggest that baclofen suppresses epileptiform electrical activity in the hippocampus at concentrations well below those which suppress normal synaptic transmission, and support renewed consideration of baclofen as an antiepileptic agent.

Animals↗

PubMed1985

Human C3a-mediated suppression of the immune response. I. Suppression of murine in vitro antibody responses occurs through the generation of nonspecific Lyt-2+ suppressor T cell.

C3a derived from the third component of human complement was found to suppress in vitro murine anti-SRBC responses. C3a-mediated suppression occurs through the generation of nonspecific Lyt-2+ suppressor T cells. The generation of suppressor cells occurs at an early phase in the response because incubation of naive T cells with C3a for as little as 30 min results in suppression of the anti-SRBC response. The generation of suppressor T cells requires the interaction of T cells, C3a, and a Sephadex G-10-adherent cell, presumably a macrophage. Although the mechanism of action of these suppressor cells has not been elucidated, several possibilities have been eliminated. C3a-suppressor T cells do not apparently release inhibitory lymphokines, nor is helper cell activity inhibited by a 2-day co-culture with these suppressor cells. The observation that interleukin 2 (IL 2)-containing lymphokine preparations could overcome C3a-induced suppression led us to investigate the interaction of the suppressors with IL 2 producer cells. However, neither C3a nor C3a-generated suppressor T cells can block the synthesis of IL 2.

Animals↗

PubMed1980

Determinant specific suppression of antigen-induced T cell proliferation in the guinea pig. I. Quantitation of suppressed antigen-specific T cell responses as a consequence of prior exposure to antigen in incomplete Freund's adjuvant.

We have asked whether a correlation exists between T cell proliferation and the in vivo suppression of delayed type hypersensitivity observed after administration of antigen in incomplete Freund's adjuvant before exposure to antigen in complete Freund's adjuvant. We find that in vivo suppression is indeed paralleled by diminished in vitro responsiveness to the immunogen. Suppression of T cell proliferation is antigen-specific, dependent upon prior immunization of antigen in IFA, and can be transferred adaptively into unprimed but not primed animals by lymphoid cells from actively suppressed syngeneic donors.

Animals↗

PubMed1982

Gamma interferon (IFN gamma) and IFN alpha/beta suppress murine myeloid colony formation (CFU-C)N: magnitude of suppression is dependent upon level of colony-stimulating factor (CSF).

The effect of different types of interferon (IFN) on macrophage and granulocyte colony formation (CFU-C) in vitro was studied using bone marrow cells from C57BL/6 mice. CFU-C formation was measured at 7 days using a standard methylcellulose culture system with L-cell conditioned medium (LCCM) as a source of colony-stimulating factor activity (CSF), IFN gamma was obtained from staphylococcal enterotoxin A- (SEA) stimulated mouse spleen cells and was partially purified (50-fold) using affinity chromatography. IFN alpha/beta was obtained from Newcastle disease virus-infected mouse L-cells and was partially purified (286-fold) using an AcA 202 column. IFN gamma inhibited CFU-C formation in a dose-dependent manner and was 100 times more inhibitory than IFN alpha/beta. IFN gamma completely suppressed CFU-C formation with as little as 15 units of antiviral activity. In contrast, 1000 to 2000 units of antiviral activity of IFN alpha/beta was required for complete suppression of CFU-C formation. The ability of IFN gamma to inhibit CFU-C formation was completely abolished after pH 2 treatment (24 hr), heat treatment (60 degrees C, 2 hr), or treatment with a specific antiserum against IFN gamma, which indicated that IFN gamma was the mediator of CFU-C inhibition. When IFN gamma and IFN alpha/beta were mixed together and added to bone marrow cells, they had a synergistic effect on the suppression of CFU-C formation. The level of inhibition mediated by both IFN gamma and IFN alpha/beta was totally dependent upon the amount of CSF present in the culture system; increasing the level of CSF could completely overcome the IFN suppressive effect. These results suggest that IFN gamma and IFN alpha/beta may have regulatory roles in hematopoiesis.

Animals↗

PubMed1983

Suppressive B-cell factor (SBF) produced by FcR-bearing B cells; suppression of B, but not non-B-cell proliferation.

B cells that have receptors for the Fc portion of IgG (FcR gamma + B cell) elaborate an immunoregulatory lymphokine termed suppressive B-cell factor (SBF) after binding immune complexes, such as sheep erythrocytes sensitized with IgG anti-sheep erythrocyte antibody (EA). For producing SBF, de novo protein is required, but not DNA or DNA-dependent RNA synthesis. This mediator is released into the culture supernatant of FcR gamma + B cells during 6 to 48 hr after stimulation by EA. SBF suppresses the proliferation of B, but not non-B cells. Thus, it suppressed (i) plaque-forming cell responses in the induction phase in an antigen-non-specific manner, (ii) DNA synthesis of lipopolysaccharide-activated B cells, but neither concanavalin A nor phytohaemagglutinin-activated T cells, and (iii) the proliferation of B but not non-B tumour-cell lines by acting at the G1-S junction in the cell cycle. Concordance of H-2 haplotype between SBF-producing mice and target B cells is necessary for the suppression. Thus, the action of SBF is B-cell specific and antigen-non-specific. Immune complex-mediated negative feedback regulation seems to be operated by lymphokines such as SBF which may be also involved in the surveillance for B-cell tumours.

Animals↗

PubMed1993

Mortality following ventricular arrhythmia suppression by encainide, flecainide, and moricizine after myocardial infarction. The original design concept of the Cardiac Arrhythmia Suppression Trial (CAST).

OBJECTIVE: To test the hypothesis that in survivors of myocardial infarction, the suppression of ventricular premature depolarizations improves survival free of cardiac arrest and arrhythmic death. DESIGN: International, prospective, multicenter, randomized, placebo-controlled trial. SETTING: University and community hospitals. PATIENTS: A total of 3549 patients with myocardial infarction and left ventricular dysfunction. INTERVENTION: Administration of encainide, flecainide, moricizine, or placebo to suppress ventricular premature depolarizations. MAIN OUTCOME MEASURES: Overall survival and survival free of cardiac arrest or arrhythmic death were compared in patients randomized to long-term, active antiarrhythmic drug therapy vs corresponding placebo, using the stratified log rank statistic. RESULTS: At 1 year from the time of randomization to blinded therapy, 95% of placebo-treated patients vs 90% of active drug-treated patients remained alive (P = .0006). Similarly, at 1 year, 96% of placebo-treated patients vs 93% of active drug-treated patients remained free of cardiac arrest or arrhythmic death (P = .003). CONCLUSIONS: The suppression of asymptomatic or mildly symptomatic ventricular arrhythmias after myocardial infarction does not improve survival and can increase mortality. Treatment strategies designed solely to suppress these arrhythmias should no longer be followed.

Aged↗

PubMed1977

Antibody-mediated suppression of tumor growth. I. Suppression by murine IgG1 isolated from alloantiserum.

The tumor suppressive activity of murine IgG1 antibody was studied in vivo. IgG1 was isolated from hyperimmune alloantisera against a murine lymphoma, 6C3HED, by absorption with heat-killed, formalinized Staphylococcus aureus. Cowan strain I, followed by DEAE ion exchange chromatography and Sephadex G-200 gel filtration chromatography. The isolated IgG1, which had no detectable IgM, IgA, IgG2a, IgG2b or IgG3, could suppress the growth of the tumor. In addition, DEAE and Sephadex G-200 column profiles of the in vivo tumor suppressive activity showed good correlation with the profiles of total IgG1 immunoglobulin and anti-tumor antibody assayed for IgG1 heavy chains and kappa light chains. The IgG1 tumor suppressive activity was not diminished after heating at 56 degrees C for 30 min.

Animals↗

PubMed1998

Suppression of immune responses by CD8 cells. II. Qa-1 on activated B cells stimulates CD8 cell suppression of T helper 2 responses.

We have investigated the role of MHC class I products and CD8 T cells in regulating Ab responses using beta2-microglobulin deficient (beta2m-/-) mice. Beta2m-/- mice produced stronger IgM and IgG responses than did control beta2m+/+ mice to both cellular and viral Ags. These Ab responses could be suppressed by infusion of activated B cells from beta2m+/+ mice. Further investigation showed that the beta2m-associated molecule on activated B cells that induced CD8 suppression was Qa-1 and that the Th2 component of CD4 cells was most affected by CD8-suppressive activity. Our findings suggest a novel pathway of Th inhibition in which B cell presentation of Qa-1-associated peptides stimulates CD8 suppressive activity.

Animals↗

PubMed1980

Suppression of asporogeny in Bacillus subtilis. Allele-specific suppression of a mutation in the spoIIA locus.

From a strain carrying spoIIA69, a mutation giving rise to asporogeny, a revertant was isolated which sporulated at about 10(-2) of the wild-type frequency but in which the time-course of sporulation was much protracted. Genetic analysis of this revertant showed that it retained spoIIA69 but had acquired a secondary mutation sas. sas failed to suppress mutations in spoIID, spoIIE or spoIIG; it also failed to suppress another mutation in the spoIIA locus. sas is extremely closely linked (recombination frequency less than or equal to 1%) with the mutation spoIIA69 that it specifically suppresses. Strains carrying sas alone sporulated at a frequency at least two orders of magnitude below that in the spoIIA69 sas double mutant. It is suggested that spoIIA60 and sas lead to compensating amino acid changes in the protein specified by the spoIIA locus.

Alleles↗

PubMed1986

The suppression of endogenous protein degradation by fractions of foetal calf serum: dialysed serum is less able to suppress degradation in aged cells.

We have studied the effect of various fractions of foetal bovine serum upon the endogenous degradation of long labelled proteins in cultured MRC5 cells, and upon other cellular functions. Only heat-inactivated serum was capable of suppressing protein degradation to a similar extent to complete serum. Acid-treated and delipidized sera were moderately effective. Albumin on its own was able to replace 40 per cent of the effect of serum, indicating the exogenous protein might compete with endogenous protein for degradation in lysosomes. Albumin was not capable of supporting DNA synthesis. Dialysed serum showed an age-related effect suppressing protein degradation to a lesser extent and being less effective in supporting DNA synthesis or cellular proliferation in aged cells. All the effects noted were related to lysosomal protein degradation. Serum diffusate did not suppress protein degradation.

Blood↗

PubMed1981

Compensation for idiotype suppression. I. Acquirement of ability to compensate for TEPC-15 idiotype suppression in mice during the early neonatal period.

Neonatal injection of BALB/c mice with antibodies specific for the idiotype of TEPC-15 myeloma protein (T15id), which is serologically identical to the major idiotype of anti-phosphorylcholine (PC) antibody, renders the recipients completely unresponsive to PC. C57BL/6, (BALB/c X C57BL/6)F1 and C.B20 mice, similarly treated with anti-T15id antibody, also displayed tolerance to PC although they were relatively more resistant (8-13%) than BALB/c mice (less than 2% control response). When anti-T15id antibody was injected into 15-day-old neonates, the resistance to the tolerance in C57BL/6 and C.B20 mice was much more apparent (up to 80% of the control response) in contrast to that in BALB/c mice, which was not significant. Adoptive transfer of spleen cells from idiotypically suppressed BALB/c mice into 20-day-old, normal C. B20 mice resulted in suppression of T15id but not in tolerance to PC, due to increased production of non-T15id-bearing anti-PC antibody. These results suggest that the ability of clonal compensation for T15id suppression is acquired during early life (2-10 days), under the influence of gene(s) associated or linked with the Igh.

Animals↗

PubMed1994

Increased actin cable organization after single chromosome introduction: association with suppression of in vitro cell growth rather than tumorigenic suppression.

We previously showed that introduction of a single human chromosome 1, 6, or 9 derived from normal fibroblasts into HHUA endometrial carcinoma cells resulted in suppression of tumorigenicity. The tumorigenic suppression was accompanied by remarkable morphological changes in the microcell hybrids containing an extra copy of chromosome 1. The study presented here was undertaken to search for target cytoskeletal components affected by chromosome 1 transfer into endometrial carcinoma cells. We found that the microcell hybrids containing an extra copy of chromosome 1 were characterized by intracellular actin bundle formation and an excessive accumulation of actin and vinculin. The latter was a result of increased stabilization of the proteins. Additionally, chromosome 3 introduction into RCC23 human renal carcinoma cells resulted in prolongation of cell division and in senescence of a significant proportion of the microcell hybrids. In these microcell hybrids, the intracellular actin network was also reorganized, but the amounts of actin and vinculin protein were not increased. These findings suggest that the increased actin organization, which appeared not to cause tumorigenic suppression in the microcell hybrids, is associated with complementation of tumor suppressor genes and senescence by multiple mechanisms.

Actin Cytoskeleton↗

PubMedDate not supplied

T2-weighted magnetic resonance imaging of the liver: comparison of fat-suppressed GRASE with conventional spin echo, fat-suppressed turbo spin echo, and gradient echo at 1.0 T.

BACKGROUND: Fat-suppressed T2-weighted gradient and spin echo (GRASE) magnetic resonance imaging in the liver was compared with three other sequences: conventional spin echo (SE), fat-suppressed and respiratory-triggered turbo SE (TSE), and fast field echo (FFE). METHODS: All sequences were applied in 48 prospective patients. Quantitative and qualitative analyses were performed. Biopsy or clinical follow-up established the final diagnosis of the lesions. RESULTS: GRASE showed the second best contrast-to-noise ratio, the second best artifact level, the same lesion detectability as TSE, and very short acquisition time. GRASE and TSE had the highest sensitivity, specificity, and accuracy. CONCLUSION: Fat-suppressed GRASE offers a fast and accurate method for imaging the liver.

Adult↗