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Biomedical subjects

G Yu

Publications and source records attributed to G Yu.

At least 289 records · Page 16Linked to original sources
PubMed1988

Identification of the differentiation-associated p93 tyrosine protein kinase of HL-60 leukemia cells as the product of the human c-fes locus and its expression in myelomonocytic cells.

A differentiation-associated 93-kDa tyrosine kinase (p93) was purified previously from the human promyelocytic leukemia cell line HL-60. The present study conclusively identifies p93 as the c-fes proto-oncogene product and shows that expression of p93c-fes and its associated tyrosine kinase activity are marked in mature granulocytes, monocytes, and human myeloid leukemia cell lines. Antisera to peptides obtained by expression of c-fes cDNA fragments in Escherichia coli reacted strongly with p93 purified from HL-60 cells. Western blots using one of these antisera demonstrated high levels of p93c-fes protein in normal human granulocytes and monocytes, as well as the cell lines KG-1, THP-1, HEL, and U-937, all of which can be induced to differentiate along the myelomonocytic pathway. Conversely, in cell lines resistant to myeloid differentiation, p93c-fes expression was either very low or absent. Expression of immunoreactive p93c-fes in these cell lines showed a strong positive correlation with p93c-fes tyrosine kinase activity, which was measured in cell extracts using a nondenaturing gel assay. Finally, the expression of p93c-fes, its tyrosine kinase activity, and the binding of 125I-granulocyte-macrophage colony-stimulating factor (GM-CSF) were all coordinately increased in HL-60 cells treated with the granulocytic differentiation inducer dimethyl sulfoxide, while all three parameters were low in untreated or differentiation-resistant HL-60 cells. These results suggest that expression of p93c-fes tyrosine kinase activity may be an essential component of myeloid differentiation and responsiveness to granulocyte-macrophage colony-stimulating factor.

Blotting, Western↗
PubMed1988

Association of p93c-fes tyrosine protein kinase with granulocytic/monocytic differentiation and resistance to differentiating agents in HL-60 leukemia cells.

A 93-kDa tyrosine protein kinase (p93) identified previously as the gene product of the c-fes proto-oncogene, is highly expressed in HL-60 leukemia cells induced to differentiate to the granulocyte or monocyte phenotype. We have now studied the relationship of p93 to the differentiation process by using a dimethyl sulfoxide (DMSO)-resistant subline of HL-60 cells (HL-60/DMSO) or the parental cell line treated with peptide or protein substrates of p93. Treatment of HL-60/DMSO cells with DMSO induced neither differentiation nor the expression of p93; however, cotreatment with IFN-alpha and DMSO resulted in partial differentiation and the concomitant induction of p93 activity. Treatment of wild-type HL-60 cells by the coaddition of the p93 substrates poly(Glu,Tyr)1:1, poly(Glu,Tyr)4:1, poly(Glu,Ala,Tyr)6:3:1, angiotensin II or vasoactive intestinal peptide with DMSO or IFN-tau partially blocked differentiation and concurrently diminished the induction of p93 activity. The inhibitory concentrations of the p93 substrates were related to their Km values. These results indicate that there is an obligatory association between the expression of p93 and granulocyte/monocyte differentiation in this cell line.

Cell Differentiation↗
PubMed1987

Purification and characterization of p93fes- and p60src-related tyrosine protein kinase activities in differentiated HL-60 leukemia cells.

Two tyrosine protein kinase activities have been identified previously to be present in HL-60 leukemia cells during induction of granulocytic and monocytic differentiation with a variety of differentiating agents. We have copurified a membrane-associated tyrosine kinase (p93) and an activity associated with both the cytosol and membrane fractions (p60). Triton X-100 extracts from HL-60 cells treated with dimethyl sulfoxide were subjected to tyrosine-agarose chromatography, polypropyl aspartamide high performance liquid chromatography (HPLC), and HPLC using an antiphosphotyrosine IgG-derivatized column. Overall purification was 2700-fold for p93 and 1800-fold for p60. p60 and p93 are phosphorylated exclusively on tyrosine residues and can use poly(Glu,Tyr)4:1, histone H1 and vasoactive intestinal peptide as substrates. Poly(Glu,Tyr)1:1 and poly(Glu,Ala,Tyr)6:3:1 were less effective substrates for p60 and p93. The activity of p93 was dependent on Mg2+ or Mn2+, whereas p60 was dependent on Mg2+; however, the activity of p60 was stimulated in a synergistic manner by the presence of both Mg2+ and Mn2+, whereas the activity of p93 was not enhanced further by the combination of divalent ions. Both p60 and p93 were immunoprecipitated by an anti-v-src monoclonal antibody but only p93 was immunoprecipitated by an anti-v-fps/fes antibody. V8 protease digestion of p60 revealed one major proteolytic fragment containing phosphotyrosine, whereas V8 protease digestion of p93 produced two major peptides that were phosphorylated on tyrosine residues. These results suggest that, although p93 and p60 may possess some epitopic similarities, they have distinguishing phosphorylation sites. Moreover, p93, in contrast to p60, appears to be strictly associated with granulocytic/monocytic differentiation and related to the cellular fps/fes protooncogene.

Chromatography, Affinity↗
PubMed1987

Analysis of tyrosine kinase activity in cell extracts using nondenaturing polyacrylamide gel electrophoresis.

A general procedure for detecting tyrosine kinase activity in crude or purified preparations using nondenaturing gel electrophoresis is presented. Samples are resolved by electrophoresis in minigels which are then incubated in an assay mixture containing [gamma-32P]ATP, poly(glutamic acid, tyrosine)4:1, and cofactors. Subsequently, gels are fixed and washed in trichloroacetic acid-pyrophosphate, dried, and analyzed by autoradiography or liquid scintillation counting. The procedure is simple and fast and allows analysis of different molecular weight forms of tyrosine kinase under linear kinetics at 37 degrees C without interference from phosphatases and proteases.

Adenosine Triphosphate↗
PubMed1985

The superiority of maximum fiber elastance over maximum stress-volume ratio as an index of contractile state.

The end-systolic pressure-volume relationship has been used as a load-independent measure of ventricular pump performance. Since comparisons of load between ventricles of different size and thickness may be more accurately made with measurements of wall stress than with those of pressure, the end-systolic stress-volume relationship at one or more levels of end-systolic stress has been used to estimate contractile function in hypertrophied ventricles. Linear regression of end-systolic stress against end-systolic volume for differently loaded beats has a slope termed maximum fiber elastance (fiber Emax) and a volume intercept termed Vo; the maximum stress-volume ratio (MSVR) for a single beat is an approximation of fiber Emax but assumes Vo = 0. However, the influence of preload, afterload, and inotropic state on these indexes has not been examined. We therefore studied the stress-volume relationship in seven open-chest dogs instrumented with ultrasonic crystals and micromanometers. Postextrasystolic potentiation (PESP) increased both the MSVR (5.7 +/- 1.83 vs 4.85 +/- 1.43 at control, p less than .05) and fiber Emax (13.93 +/- 3.24 vs 9.24 +/- 2.15 at control; p less than .05). Augmentation of preload by infusion of dextran, with the use of nitroprusside to maintain afterload relatively constant, did not significantly influence either the MSVR or fiber Emax. Vo was not significantly influenced by PESP, but was shifted to higher values by augmentation of preload (17.5 +/- 14.8 vs 13.9 +/- 11.1 ml at control; p less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1982

Nonlymphomatous metastatic tumor to the testis.

A patient with pancreatic carcinoma presented with an initial left testicular mass that proved to be metastatic adenocarcinoma of the pancreas. Regional spread of the pancreatic carcinoma may have created venous and lymphatic obstruction with inferior passage of tumor emboli to the testis. A summary of nonlymphomatous secondary tumors of the testis also is presented.

Adenocarcinoma↗
PubMed1980

Electroacupuncture treatment of morphine-dependent mice reduces signs of withdrawal, without showing cross-tolerance.

Morphine pellets (75 mg morphine base per pellet) were implanted subcutaneously in mice (B6AF1/J) and were surgically removed after 3 or 8 days. During morphine abstinence (7 h after pellet removal), the mice were treated with electroacupuncture (EA). The results indicate that EA analgesia shows no cross-tolerance to morphine. Additionally, EA reduced withdrawal behaviour (jumping) in 50% of the mice during morphine abstinence.

Acupuncture Therapy↗
PubMed1978

Relationship between diazepam dose, plasma level, age, and central nervous system depression.

Patients undergoing elective cardioversion for treatment of arrhythmias were premedicated with diazepam. The dose was individualized to achieve a degree of central nervous system CNS) depression characterized by response to painful but not vocal stimulation. Promptly following each cardioversion, blood was drawn and the plasma diazepam concentration was measured by gas chromatography. The plasma levels varied as widely as the diazepam doses so that there was no fixed plasma level of diazepam associated with the degree of CNS depression produced in these patients. However, both the dose of diazepam and the resulting plasma level were inversely correlated to age, indicating that age is a critical factor in the use of diazepam for cardioversion premedication; elderly are more sensitive to the depressant effects of this drug than the young.

Adult↗
PubMed1977

Sensitization to cocaine stimulation in mice.

Repeated administration of cocaine to B6AF1/J mice increased their running response to 20 mg/kg cocaine as much as four-fold over the response to the first injection. After four daily injections, the extent of the increase was proportional to the dose of cocaine that was used for pretreatment. Sensitization persisted for as long as 2 months after the last injection of cocaine. Cocaine-pretreated mice did not show an increased running response to either morphine or d-amphetamine. The response to cocaine was increased two-fold by treatment with morphine and three-fold by pretreatment with d-amphetamine. Pretreatment with either imipramine or reserpine did not produce sensitization to cocaine. There was no correlation between cocaine sensitization and whole-brain catecholamine levels. There were marked differences in both the running response to cocaine and the extent of cocaine sensitization betwee the parental strains, C57B1/6J and A/J. Experiments with recombinant-inbred lines, derived from C57B1/6By and BALB/cBy mice, suggest that the initial response to cocaine and the development of sensitization are controlled by different genetic determinants.

Animals↗
PubMed1975

A genetic analysis of the response to morphine in mice: analgesia and running.

Two progenitor strains, BALB/cBy and C57BL/6By, their reciprocal F1 hybrids, and seven of their recombinant-inbred derived lines were used to examine the genetic basis of the response to thermal pain, and morphine analgesia at doses of 2.5, 5.0 and 10.0mg/kg. Both the latency of response to thermal pain and the analgesic response differed significantly among the various strains tested. Strong genetic determinants appear to control their responses. Analyses of the data did not permit clarification regarding the linkage of these determinants. Photoelectric activity cages were used to test the running response of the same strains to 12.5, 25 and 40 mg/kg morphine sulfate. The genetic determinants for running activity were different from those for analgesia. There is clear evidence for two or more loci controlling the behavior at 60 and 75 min after injection, but not enough information to define the loci involved.

Analgesia↗
PubMed1975

Perinatal narcotic addiction in mice: sensitization to morphine stimulation.

The injection of morphine sulfate into baby mice twice daily for 5 days increased their running reaponse to morphine when they were tested as adults. If treatment was completed before the mice were )5 days old there was no effect. Sensitization to morphine running was longer-lasting than either analgesic tolerance or tolerance to morphine running may be a form of denervation hypersensitivity that has several features in common with noise-induced sensitization to audiogenic seizures.

Age Factors↗
PubMed1975

Increased running response to morphine in morphine-pretreated mice.

The running response of B6AF1/J mice to 25 mg/kg of morphine sulfate was increased up to 3-fold when this dose was administered either twice daily for 5 days or once a week for 2 or 3 weeks. The effect of weekly pretreatment was proportional to the dose of morphine and lasted as long as 1 month after pretreatment was stopped. There was no sensitization when the mice were less than 15 days old at the time of pretreatment. Of the parental strains, untreated C57Bl/6J mice showed a good running response to morphine, while A/J mice showed little response. Pretreatment of either of these strains produced only slight sensitization. Pretreatment of the hybrids with levorphanol increased the response to morphine. Dextrorphan and naloxone were ineffective. Sensitization by morphine was blocked by naloxone. Increased morphine running was not associated with analgesic tolerance as measured by the tail-flick assay. Morphine pretreatment produced some increase in the running response to amphetamine and to cocaine. Pretreatment with amphetamine or cocaine did not increase the response to morphine.

Aging↗