Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Induction”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,657 records · Page 92Linked to original sources
PubMed1983

Induction of retrovirus gene expression by aflatoxin B1 and 2-acetylaminofluorene.

The abilities of 2-acetylaminofluorene (AAF) and aflatoxin B1 (AFB) to induce the expression of endogenous murine retrovirus in AKR mouse embryo fibroblasts were examined. AFB was able to induce virus expression at concentrations as low as 0.067 microM, although the induction efficiency was increased at higher doses. AAF gave somewhat more variable results. In some experiments induction was observed with as little as 0.1 microM while in other experiments induction was not observed at concentrations as high as 100 microM. Addition of an S9 metabolizing system enhanced the ability of AAF to induce virus expression but also increased the background induction frequency. These results are discussed in relation to the mechanism of virus induction and the potential usefulness of virus induction as an assay for carcinogenic potential.

2-Acetylaminofluorene↗
PubMed1991

Inhibition of protein synthesis results in super-induction of procyclin (PARP) RNA levels.

Procyclin is an abundant surface antigen found exclusively on the procyclic forms of African trypanosomes. We are interested in the induction of procyclin gene expression during differentiation from bloodstream forms. We find that increased levels of procyclin RNA are evident as early as 15 min after triggering differentiation. The increase in procyclin RNA levels requires the temperature shift from 37 degrees C to 27 degrees C and is aided by addition of the tricarboxylic acid cycle intermediate cis-aconitate. Maximal induction is observed with a combination of three triggers of differentiation: citrate, cis-aconitate and the temperature shift. Protein synthesis does not appear to be required for induction of procyclin RNA during differentiation. In fact, addition of protein synthesis inhibitors results in super-induction of procyclin RNA levels, even under conditions where no induction is normally observed (i.e., at 37 degrees C in the absence of citrate and cis-aconitate). This super-induction was observed with four different protein synthesis inhibitors that affect different stages of translation. Thus, the accumulation of procyclin transcripts may be under the control of a negative regulator whose effective levels are reduced during differentiation from bloodstream to procyclic forms.

Aconitic Acid↗
PubMed1990

Induction of fos and sis proto-oncogenes and genes of the extracellular matrix proteins during butyrate induced glioma differentiation.

Sodium butyrate has been shown to inhibit the growth and induce the differentiation of F-98 rat glioma cells. In agreement with the morphological changes, we have found that mRNAs for fibronectin and collagen in these cells could be reversibly induced by butyrate. While Ki-ras mRNA levels remained relatively unchanged, mRNAs for fos and sis increased significantly during the course of butyrate induced differentiation. c-fos induction can be detected 30 min after butyrate addition, a peak level (greater than 20 fold) was reached at 2 h, with a subsequent gradual decline. c-sis induction was detectable 24 h after butyrate exposure, at which time the cells have assumed morphological transition. Interestingly, the sis mRNA induction was not reversible upon butyrate withdrawal. The sis mRNA half-life increased from 40 min in the untreated cells to 100 min in the butyrate induced cells indicating that the increase in the stability of sis mRNA contributed, at least in part, to the elevated levels of sis expression. These findings demonstrate a coordinated induction of fibronectin and collagen genes in the butyrate-treated F-98 cells. In addition, fos and sis transcripts were differentially induced; a rapid and transient induction of fos followed by an irreversible induction of sis at a later stage of differentiation.

Animals↗
PubMed1993

The differential induction of alpha 1-acid glycoprotein and serum amyloid A genes by heavy metals.

We have investigated the differential regulation of the mouse (Balb/c) acute phase reactants, alpha 1-acid glycoprotein and serum amyloid A by heavy metals (Hg, Cd, Pb, Cu, Ni and Zn). Mice have two distinct alpha 1-acid glycoprotein mRNAs encoded by alpha 1-acid glycoprotein gene-1, (AGP-1) and alpha 1-acid glycoprotein gene-2 (AGP-2) and 3 distinct serum amyloid A mRNAs encoded by serum amyloid A gene-1, (SAA-1), serum amyloid A gene-2 (SAA-2) and serum amyloid A gene-3 (SAA-3). Using specific oligonucleotides as probes we have demonstrated that the AGP-1 and AGP-2 genes, and the SAA-1 and SAA-2 genes are differentially induced by heavy metals in the liver. At the peak of induction, AGP-2 mRNA is 80-100-fold higher than the AGP-1 mRNA level; the SAA-1 mRNA level is approx. 40-fold higher than SAA-2, and SAA-3 mRNA is not detected. A similar differential pattern of expression is observed in bacterial lipopolysaccharide mediated inductions. However, low levels of SAA-3 are also seen in this treatment. Adrenalectomy has no effect on the inductions by heavy metals of AGP-2 and the SAAs, indicating that the glucocorticoid receptor pathway may not function in this regulation. However, AGP-1 induction is significantly delayed, indicating that glucocorticoid may be essential for a rapid response to Hg. The liver is the major site of heavy metal induction of AGP and SAA genes; Hg induces AGP-1 and 2, and SAA-1 and 2 only in the liver. Our studies clearly show that the AGP and SAA genes belong to a subgroup of acute-phase reactants that respond to heavy metals. CRP is another member of this family. Furthermore, our data suggest that the mechanism is not directly mediated by glucocorticoid or cytokine induction pathways.

Adrenalectomy↗
PubMed1987

Steroids and tuftsin fail to prevent the induction of altered plasma proteinase homeostasis in mice bearing the B16 melanoma or treated with C. parvum.

The effects of tuftsin and steroids (methyl prednisolone) on the induction of disrupted plasma proteinase regulation in mice bearing the B16 melanoma or treated with Corynebacterium parvum was investigated. Tuftsin treatment inhibited tumor progression only if treatment was started at the time of tumor transplantation. However, tuftsin inhibited the development of splenomegaly in mice with established tumors. In contrast, tuftsin did not influence either the induction of elevated plasma proteinase activity or the activity in plasma from animals with established tumors. Treatment of mice with high, anti-inflammatory, doses of steroid (20 mg/kg/day) partially inhibited tumor progression, inhibited the induction of splenomegaly, but did not inhibit the induction of disrupted plasma proteinase regulation. Likewise, steroid treatment did not suppress the induction of elevated plasma proteinase activity following treatment of mice with C. parvum. Thus the induction of elevated plasma proteinase activity, previously demonstrated to be a host regulated phenomenon, is resistant to regulation by this anti-inflammatory drug and likely not a component of the anti-tumor response. These findings raise the possibility that this phenomenon results from the interaction of activated RES elements with components of the plasma proteinase cascades.

Animals↗
PubMed1991

Unexpected up-regulation of gene expression by cyclosporin A and FK-506 in a T-cell lymphoma: both immunosuppressants augment Ly-6E antigen induction by interferon-gamma in the presence of ionomycin.

Cyclosporin A (CsA) and FK-506 inhibit lymphokine gene activation in T-cells. In the present study, we investigated the effects of these immunosuppressants on the regulation of a non-lymphokine molecule, the Ly-6E surface antigen, in the YAC-1 T-cell lymphoma. These cells do not normally express Ly-6E mRNA or Ly-6E surface molecules but are induced to do so upon treatment with IFN-gamma. At submicromolar concentrations, CsA or FK-506 did not alter this induction. However, at higher concentrations (1-12 microM), they both increased the induction of Ly-6E mRNA expression. Cyclosporin A or FK-506 also markedly affected Ly-6E induction when the cultures were co-treated with the calcium ionophore, ionomycin. In the absence of CsA or FK-506, ionomycin suppressed Ly-6E induction by IFN-gamma. Both immunosuppressants reversed this inhibitory effect and increased Ly-6E mRNA and Ly-6E surface expression to levels that were 2- to 3-fold higher than in cells induced with IFN-gamma alone. In this system, the two immunosuppressants were active at pharmacologically relevant concentrations, similar to those inhibiting normal T-cell activation, with FK-506 being 30- to 50-fold more potent than CsA. The ability of CsA analogs to enhance Ly-6E induction in the presence of ionomycin also correlated with their immunosuppressive activity. Therefore, through mechanisms apparently related to those involved in their immunosuppressive action, both CsA and FK-506 convert the negative effect of ionomycin on IFN-gamma-mediated Ly-6E induction into an overall positive effect. The YAC-1 cell model, described here, provides a unique example of upregulation of gene expression by these two immunosuppressants.

Animals↗
PubMed1992

Induction of DNA breaks in SV40 by heavy ions.

Simian virus (SV40) DNA was used to study the induction of DNA strandbreaks by heavy ions varying in LET. DNA was exposed to X-rays and to accelerated particles either in dilute solution or in the presence of different radical scavengers. Relative proportions of the intact supercoiled DNA, nicked form arising from single strand breaks (SSB) and linear molecules produced by double strandbreaks (DSB) were quantified on the base of their electrophoretic mobility in agarose gels. Cross sections for the induction of SSBs and DSBs were calculated from the slope of dose effect curves. Mercaptoethanol was found to protect more efficiently against DNA strand breakage than Tris. When the biological efficiency, i.e. the number of strand breaks per unit dose and molecule weight was evaluated as a function of LET, curves for SSB induction always showed a continuous decrease. For DSB induction, an increase in the yield of DSBs with a maximum around 500 keV/micrometer was observed in the presence of radical scavenger. This peak of biological efficiency gradually disappeared when the radiosensitivity of the system was increased, and was no longer apparent in the dilute buffer system, where DNA showed a high susceptibility to strand breakage. When the relative biological efficiency was plotted versus LET, the curve for DSB induction observed in a low radical scavenging environment paralleled the curve obtained for SSB induction.

DNA Damage↗
PubMedDate not supplied

Stressor-specific induction of heat shock proteins in rat hepatoma cells.

In order to determine whether induction of specific stress proteins is dependent on a given stressor and whether induction of these proteins is linked to survival, Reuber H35 rat hepatoma cells were exposed to five different environmental stressors (heat shock, arsenite, cadmium, dinitrophenol and ethanol). The effect of these stressors was studied on cell survival as well as on inhibition and recovery of protein synthesis and on induction of heat shock proteins (hsps). In this article, we present evidence that several well-known hsp-inducers fail to stimulate specific hsps in a degree that is comparable to the induction of these hsps by heat shock. Most evidently, hsp60 is not induced by cadmium-treatment, whereas hsp100 is hardly induced by sodium arsenite. Treatment with DNP only slightly induces hsp68 and hsp84, whereas no detectable induction of hsps is observed after treatment with ethanol. In contrast, treatment with cadmium raises the amount of hsp28 to a higher level as compared to heat shock. A comparison of the stressor-specific induction of major hsps was also made under conditions of similar impact on cellular physiology: (a) stressor conditions up to the critical point that cell death starts to occur, and (b) conditions of iso-survival (50%). We conclude that hsps cannot be simply used as a general risk-assessment tool, and that the validation of stressor-specific risk-assessment warrants further research with larger groups of proteins.

Animals↗
PubMed1983

Inhibition of 12-O-tetradecanoylphorbol-13-acetate-induced induction in Epstein-Barr virus early antigen in Raji cells.

Retinol, 5 flavonoids, 3 steroids and 7 sweetening agents were studied for their effects on 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced early antigen (EA) of Epstein-Barr virus (EBV) in Raji cells. Concomitant treatment of Raji cells with TPA and retinol showed inhibition of EA induction. Among flavonoids, quercetin resulted in effective inhibition of EA induction by TPA and alpha-naphthoflavone showed the weakly inhibitory effect. None of the other flavonoids such as rutin, catechin and beta-naphthoflavone affected the induction of EBV-EA by TPA. beta-Estradiol obviously inhibited EBV-EA induction by TPA, but hydrocortisone did not show any inhibitory effect on it. Glycyrrhetinic acid, steviol, phyllodulcin and perrillartine also showed the remarkable inhibition of EBV-EA induction. On the other hand, glycyrrhizin and stevioside, glycosides of glycyrrhetinic acid and steviol, did not inhibit the induction of EBV-EA by TPA. Some of the inhibitors reported here may be effective on the inhibition of the in vivo tumor promotion by TPA.

Antigens, Viral↗
PubMed1988

Effects of 3-aminobenzamide on the induction of gamma-glutamyl-transpeptidase-positive foci by various chemicals in rat liver.

The effects of 3-aminobenzamide (ABA), a representative inhibitor of poly(ADP-ribose)polymerase, on the induction of gamma-glutamyl-transpeptidase (GGT)-positive foci, an early lesion occurring during hepatocarcinogenesis, in rat liver by various chemicals were studied in Fischer 344 and Wistar rats. ABA exhibited an enhancing effect on the induction of GGT-positive foci by benzo[a]pyrene, but no effects on induction by a methylating agent, N-methyl-N-nitrosourea, in both rat strains. In contrast, the induction of GGT-positive foci by another methylating agent, 1,2-dimethylhydrazine, was enhanced by ABA in Wistar rats, but not affected in Fischer rats. There were no effects of ABA on the induction of GGT-positive foci by N-bis(2-hydroxypropyl) nitrosamine in Wistar rats. These results indicate a differential effect of ABA on the induction of GGT-positive foci by different chemicals in different rat strains.

1,2-Dimethylhydrazine↗
PubMed1993

Muscarinic receptor-mediated induction of Fos protein in rat brain.

Recent studies have shown that the centrally active muscarinic agonist pilocarpine induces c-fos mRNA in rat cortex. Here we describe the localization of muscarinic receptor-induced FOS protein, within the rat central nervous system (CNS), following administration of pilocarpine (25 mg/kg). High levels of FOS induction were apparent in many forebrain structures including the primary olfactory (piriform) cortex, nucleus accumbens, amygdala, hippocampus, neocortex and supra-optic nucleus of the hypothalamus. Within the neocortex FOS induction followed a laminar distribution being highest in layers 4 and 6 with lower induction seen in layers 2 and 5. Other areas showing FOS induction included the striatum, septum, inferior colliculus, thalamus, hypothalamus and several brainstem nuclei. Both atropine (10 mg/kg) and pirenzepine (100 mg/kg) reduced FOS induction suggesting that a pirenzepine-sensitive muscarinic receptor was involved. The possible significance of muscarinic-mediated FOS induction, to cholinergic kindling and the cholinergic hypothesis of learning and memory, is discussed.

Animals↗
PubMed1993

Comparison of number of extrastimuli versus change in basic cycle length for induction of ventricular tachycardia by programmed ventricular stimulation.

OBJECTIVES: The purpose of this study was to examine the effects of varying basic cycle lengths in a programmed stimulation protocol if up to seven extrastimuli were available at each basic cycle length. BACKGROUND: There is no uniformly accepted protocol for induction of ventricular tachycardia. Most protocols limit the number of extrastimuli to two or three but use several basic cycle lengths. METHODS: Twenty-eight patients with coronary artery disease and documented spontaneous sustained ventricular tachycardia or ventricular fibrillation were studied. In the absence of antiarrhythmic drugs, each patient underwent three inductions of ventricular tachycardia/ventricular fibrillation using sinus rhythm or right ventricular pacing at 600 or 400 ms as the basic cycle length. Up to seven extrastimuli were allowed at each basic cycle length. RESULTS: The maximal yield of clinical tachycardia (96%) was identical for each basic cycle length and was achieved using a maximum of seven, five and four extrastimuli for sinus rhythm and 600 and 400 ms, respectively. A basic cycle length of 400 ms required fewer extrastimuli (2.4 +/- 0.7) to induce ventricular tachycardia/ventricular fibrillation than did 600 ms (2.7 +/- 1.1, p = 0.014) or sinus rhythm (3.4 +/- 1.2, p < 0.001). There was no significant difference in the cycle lengths of the induced ventricular tachycardia, incidence of induced ventricular fibrillation or requirement for direct current countershock. CONCLUSIONS: The use of an adequate number of extrastimuli obviates the need for multiple basic cycle lengths for induction of ventricular tachycardia and does not increase induction of unwanted ventricular fibrillation. If only one basic cycle length is used, the ease of inducibility can be quantified in terms of the number of extrastimuli required. Fewer extrastimuli were required for induction of ventricular tachycardia if a basic cycle length of 400 ms was used. These data favor the use of ventricular pacing at a basic cycle length of 400 ms with up to at least four extrastimuli as the standard stimulation protocol for induction of ventricular tachycardia.

Adult↗
PubMed1987

Anesthetic induction with fentanyl and intravenous lidocaine for coronary artery surgery.

In a randomized, double-blind trial, 59 patients undergoing coronary artery surgery received fentanyl 10, 15, or 25 microg/kg infused over 5 minutes for anesthetic induction. Half of the patients received intravenous lidocaine, 1.5 mg/kg, 1 minute before laryngoscopy. Efficacy of induction as judged by loss of consciousness was evaluated, and hemodynamic values during induction, laryngoscopy, and tracheal intubation were recorded each minute for 10 minutes. Plasma fentanyl concentrations were determined after termination of the fentanyl infusion. Opioid induction with fentanyl was successful in 90% (18 of 20) of patients receiving 25 microg/kg, 89% (17 of 19) of patients receiving 15 microg/kg, but only 55% (11 of 20) of patients receiving 10 microg/kg (P < .01). While plasma fentanyl concentrations were proportional to the dose infused (25 ng/mL, 18 ng/mL, and 14 ng/mL in the 25, 15. and 10 microg/kg fentanyl groups, respectively), there was no relationship between plasma fentanyl concentration and hemodynamic response to laryngoscopy or intubation. Opioid induction caused a gradual decrease in blood pressure that was restored with intubation. Lidocaine partially blocked this restoration (systolic blood pressure 122 +/- 5 v 138 +/- 5 mmHg, lidocaine v placebo, 1 minute after laryngoscopy, P < .05). Fentanyl, 15 or 25 microg/kg, intravenously, is an effective induction agent for patients with coronary artery disease. Supplementation with intravenous lidocaine, 1.5 mg/kg, will obtund the increase in blood pressure that occurs with laryngoscopy and intubation and help prevent infrequent hypertensive responses seen with this opioid technique.

Adjuvants, Anesthesia↗
PubMed1992

Protein kinase C initially inhibits the induction of meiotic cell division in Xenopus oocytes.

We have used one activator and two inhibitors of protein kinase C (PKC) to examine the role of this enzyme in the induction of meiotic cell division. At 1 U/ml, phosphatidylcholine-specific phospholipase C increases DAG, alters intracellular pH and inhibits the induction of meiosis by insulin or progesterone. However, when added about 1.6 h after progesterone, the enzyme speeds the induction of cell division. Microinjection of inhibitor peptide (19-36) of PKC has little effect on progesterone action but stimulates the induction of meiosis by insulin. When the inhibitor peptide is injected about 2h after insulin addition, the peptide inhibits. A second PKC inhibitor, staurosporine, decreases PKC-dependent intracellular pH and in vitro oocyte PKC activity. At similar concentrations, staurosporine stimulates insulin or progesterone action, but, when added after about 2 h, the drug inhibits induction by insulin. We conclude that PKC is initially inhibitory to the induction of meiotic cell division but then may become synergistic.

Alkaloids↗
PubMedDate not supplied

Gastroesophageal reflux during anesthetic induction with thiopental and succinylcholine.

The effects of patient physiology and the prior administration of a nondepolarizing muscle relaxant on the frequency of gastroesophageal reflux during induction with thiopental sodium and succinylcholine were investigated. Forty patients underwent anesthetic induction during continuous esophageal pH monitoring. Twenty patients had preoperative symptoms of gastroesophageal reflux, and 20 asymptomatic patients served as controls. Half the patients in each group received a small dose of nondepolarizing muscle relaxant prior to induction. Five patients (25%) with gastroesophageal reflux and none of the control patients showed significant decreases in esophageal pH during induction. Two of these patients received prior administration of a nondepolarizing drug. In all five patients, reflux occurred during laryngoscopy and intubation, suggesting the possibility that succinylcholine did not play a role in the generation of reflux. Preoperative gastroesophageal reflux symptomatology is associated with an increased frequency of reflux during induction, and the vulnerable period seems to occur after the achievement of neuromuscular blockade during laryngoscopy. Preinduction administration of a non-depolarizing muscle relaxant prior to succinylcholine use had no demonstrable effect on the frequency of reflux during induction, although the numbers studied were too small to be conclusive.

Adult↗
PubMed1995

Efficient inspired concentration of sevoflurane for vital capacity rapid inhalation induction (VCRII) technique.

STUDY OBJECTIVES: To evaluate the efficient inspired concentration of sevoflurane for a vital capacity rapid inhalation induction (VCRII) technique with respect to induction time, characteristics, and acceptability. DESIGN: Prospective study. SETTING: Medical college hospital. PATIENTS: 68 unpremedicated healthy adult volunteers were assigned to one of four groups in order of sequential entry of informed consent. INTERVENTIONS: 3%, 4.5%, 6%, or 7.5% concentrations of sevoflurane were administered for 5 minutes (3% and 4.5%) or 3 minutes (6% and 7.5%) using a single breath technique. MEASUREMENTS AND MAIN RESULTS: The mean induction time required with 3%, 4.5%, 6%, or 7.5% sevoflurane was 120 +/- 26 sec, 79 +/- 18 sec, 52 +/- 15 sec, or 47 +/- 17 seconds, respectively. Each induction time was significantly different from the others (p < 0.05) except for that between 6% and 7.5%. There appeared to be a direct inverse relationship between the mean induction time and the logarithm of inspired concentration of sevoflurane, but this relationship did not extend beyond concentrations above 6%. Blood pressure decreased by approximately 18% from baseline at the end of inhalation of the drug, and heart rate remained constant in all groups. Except of one subject in the 7.5% group, no coughing was observed and laryngospasm, breath-holding, and secretions were not seen in any subjects. Slight limb movement was observed in a few subjects in each group. All subjects except one in the 3% group would accept undergoing a similar procedure again. CONCLUSION: Sevoflurane 6% can be recommended for VCRII, but increasing the concentration higher than this does not markedly shorten the induction time and thus seems to add little benefit.

Adult↗
PubMed1996

Parental presence plus oral midazolam decreases frequency of 5% halothane inductions in children.

STUDY OBJECTIVE: To determine the frequency of 5% halothane induction and behavioral distress during inhalation induction with both oral midazolam and parental presence compared with parental presence alone. DESIGN: Randomized, controlled, double blind study. SETTING: Same day anesthesia at a university department of anesthesiology. PATIENTS: 72 ASA status I and II children, 3 to 10 years of age, scheduled for first time anesthesia. INTERVENTIONS: Children were assigned to one of two groups to receive midazolam 0.5 mg/kg orally or placebo. A parent was present during induction. Children were videotaped at baseline, after treatment, and during induction. Tapes were scored for behavioral distress using the revised Observational Scale of Behavioral Distress. MEASUREMENTS AND MAIN RESULTS: Children who received midazolam in the setting of parental presence had significantly fewer 5% halothane inductions than those who received placebo (p < 0.02). They also had less behavioral distress (p < 0.01). CONCLUSIONS: The combination of parental presence plus oral midazolam reduces the likelihood of needing a 5% rapid halothane induction when compared with parental presence without premedication.

Adjuvants, Anesthesia↗
PubMed1992

Induction of HLA class I mRNA by cytokines in human fibroblasts: comparison of TNF, IL-1 and IFN-beta.

Expression of HLA class I antigens is known to be regulated by various cytokines at both the mRNA and protein levels. We have examined the induction of HLA-B7 by tumor necrosis factor alpha (TNF), interleukin 1 alpha (IL-1) and interferon beta (IFN-beta) in normal human diploid FS-4 fibroblasts. Optimal induction of HLA-B7 by TNF at 24 h was shown to require a continuous presence of TNF. Since TNF also induces IFN-beta in these cells and the latter cytokine itself has the capacity to upregulate HLA class I expression, we investigated the role of autocrine IFN-beta in the induction of HLA-B7 by TNF. Experiments with neutralizing polyclonal antibodies to recombinant IFN-beta showed that the induction of HLA-B7 mRNA by TNF was partially dependent on autocrine IFN-beta. However, TNF and IFN-beta induced HLA-B7 mRNA with similar kinetics and treatment with saturating concentrations of both TNF and IFN-beta resulted in an additive or possibly synergistic response. The latter findings support the idea that induction of HLA class I by TNF is not mediated solely by autocrine IFN-beta produced in response to TNF. In addition, experiments with the protein synthesis inhibitor cycloheximide suggested that the induction of mRNAs for both the heavy and light (beta 2-microglobulin) chains of the HLA class I antigen by TNF did not require de novo protein synthesis. IL-1 was also shown to increase steady-state mRNA levels of HLA-B7 with kinetics similar to those of TNF and IFN-beta in FS-4 cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Cell Line↗