15 results on '"Schneider, M. T."'
Search Results
2. NOVEL MODEL OF ALCOHOL-INDUCED HEPATOCELLULAR CARCINOMA (HCC): 103
- Author
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Schmidt, C. M., Klein, P. J., Wentz, S. C., Hennig, M. E., Yip-Schneider, M. T., Matos-Bramblia, J. M., and Froehlich, J. C.
- Published
- 2007
Catalog
3. Comparison of skin closure techniques in patients undergoing open pancreaticoduodenectomy: A single center experience.
- Author
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Flick KF, Simpson RE, Soufi M, Fennerty ML, Yip-Schneider MT, Colgate CL, Ceppa EP, House MG, Zyromski NJ, Nakeeb A, and Schmidt CM
- Subjects
- Aged, Female, Follow-Up Studies, Humans, Incidence, Male, Middle Aged, Prognosis, Retrospective Studies, United States epidemiology, Pancreaticoduodenectomy methods, Postoperative Complications epidemiology, Wound Closure Techniques
- Abstract
Background: This study evaluated closure techniques and incisional surgical site complications (SSCs) and incisional surgical site infections (SSIs) after pancreaticoduodenectomy (PD)., Methods: Retrospective review of open PDs from 2015 to 2018 was performed. Outcomes were compared among closure techniques (subcuticular + topical skin adhesive (TSA); staples; subcuticular only). SSCs were defined as abscess, cellulitis, seroma, or fat necrosis. SSIs were defined according to the National Surgical Quality Improvement Program (NSQIP)., Results: Patients with subcuticular + TSA (n = 205) were less likely to develop an incisional SSC (9.8%) compared to staples (n = 139) (20.1%) and subcuticular (n = 74) (16.2%) on univariable analysis (P = 0.024). Multivariable analysis revealed no statistically significant difference in incisional SSC between subcuticular + TSA and subcuticular (P = 0.528); a significant difference remained between subcuticular + TSA and staples (P = 0.014). Unadjusted median length of stay (LOS) (days) was significantly longer for staples (9) vs. subcuticular (8) vs. subcuticular + TSA (7); P < 0.001. Incisional SSIs were evaluated separately according to the NSQIP definition. When comparing rates, the subcuticular + TSA group experienced lower incisional SSIs compared to the other two techniques (4.9% vs. 10.1%, 10.8%). However, this difference was not statistically significant by either univariable or multivariable analysis., Conclusions: Subcuticular suture + TSA reduces the risk of incisional SSCs when compared to staples alone after pancreaticoduodenectomy., Competing Interests: Declaration of competing interest None declared., (Copyright © 2020 Elsevier Inc. All rights reserved.) more...
- Published
- 2020
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4. Discussion on: Performance of candidate urinary biomarkers for pancreatic cancer - Correlation with pancreatic cyst malignant progression?
- Author
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Yip-Schneider MT, Soufi M, Carr RA, Flick KF, Wu H, and Schmidt CM
- Subjects
- Biomarkers, Humans, Pancreatic Cyst, Pancreatic Neoplasms
- Published
- 2020
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5. Early morphologic changes in trapeziometacarpal joint bones with osteoarthritis.
- Author
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Schneider MTY, Zhang J, Walker CG, Crisco JJ, Weiss AC, Ladd AL, Nielsen PMF, and Besier T
- Subjects
- Carpometacarpal Joints physiopathology, Disease Progression, Female, Follow-Up Studies, Humans, Male, Middle Aged, Osteoarthritis physiopathology, Thumb diagnostic imaging, Time Factors, Carpometacarpal Joints diagnostic imaging, Osteoarthritis diagnosis, Range of Motion, Articular physiology, Thumb physiopathology, Tomography, X-Ray Computed methods
- Abstract
Objective: Characterising the morphological differences between healthy and early osteoarthritic (EOA) trapeziometacarpal (TMC) joints is important for understanding osteoarthritis onset, and early detection is important for treatment and disease management. This study has two aims: first, to characterise morphological differences between healthy and EOA TMC bones. The second aim was to determine the efficacy of using a statistical shape model (SSM) to detect early signs of osteoarthritis (OA)., Methods: CT image data of TMC bones from 22 asymptomatic volunteers and 47 patients with EOA were obtained from an ongoing study and used to generate a SSM. A linear discriminant analysis (LDA) classifier was trained on the principal component (PC) weights to characterise features of each group. Multivariable statistical analysis was performed on the PC to investigate morphologic differences. Leave-one-out classification was performed to evaluate the classifiers performance., Results: We found that TMC bones of EOA subjects exhibited a lower aspect ratio (P = 0.042) compared with healthy subjects. The LDA classifier predicted that protrusions (up to 1.5 mm) at the volar beak of the first metacarpal were characteristic of EOA subjects. This was accompanied with widening of the articular surface, deepening of the articular surface, and protruding bone growths along the concave margin. These characteristics resulted in a leave-one-out classification accuracy of 73.9% (95% CI [61.9%, 83.8%]), sensitivity of 89.4%, specificity of 40.9%, and precision of 75.9%., Conclusion: Our findings indicate that morphological degeneration is well underway in the EOA TMC joint, and shows promise for a clinical tool that can detect these features automatically., (Copyright © 2018 Osteoarthritis Research Society International. Published by Elsevier Ltd. All rights reserved.) more...
- Published
- 2018
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6. Men and women have similarly shaped carpometacarpal joint bones.
- Author
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Schneider MT, Zhang J, Crisco JJ, Weiss AP, Ladd AL, Nielsen P, and Besier T
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- Adult, Carpometacarpal Joints anatomy & histology, Carpometacarpal Joints diagnostic imaging, Female, Humans, Male, Middle Aged, Radiography, Sex Characteristics, Thumb anatomy & histology, Thumb diagnostic imaging, Trapezium Bone diagnostic imaging, Young Adult, Trapezium Bone anatomy & histology
- Abstract
Characterizing the morphology of the carpometacarpal (CMC) joint bones and how they vary across the population is important for understanding the functional anatomy and pathology of the thumb. The purpose of this paper was to develop a statistical shape model of the trapezium and first metacarpal bones to characterize the size and shape of the whole bones across a cohort of 50. We used this shape model to investigate the effects of sex and age on the size and shape of the CMC joint bones and the articulating surface area of the CMC joint. We hypothesized that women have similar shape trapezium and first metacarpal bones compared to men, following scaling for overall size. We also hypothesized that age would be a significant predictor variable for CMC joint bone changes. CT image data and segmented point clouds of 50 CMC bones from healthy adult men and women were obtained from an ongoing study and used to generate two statistical shape models. Statistical analysis of the principal component weights of both models was performed to investigate morphological sex and age differences. We observed sex differences, but were unable to detect any age differences. Between men and women the only difference in morphology of the trapezia and first metacarpal bones was size. These findings confirm our first hypothesis, and suggest that the women have similarly shaped trapezium and first metacarpal bones compared to men. Furthermore, our results reject our second hypothesis, indicating that age is a poor predictor of CMC joint morphology., (Copyright © 2015 Elsevier Ltd. All rights reserved.) more...
- Published
- 2015
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7. Cell cycle effects of nonsteroidal anti-inflammatory drugs and enhanced growth inhibition in combination with gemcitabine in pancreatic carcinoma cells.
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Yip-Schneider MT, Sweeney CJ, Jung SH, Crowell PL, and Marshall MS
- Subjects
- Apoptosis drug effects, Blotting, Western, Cell Cycle Proteins biosynthesis, Cell Division drug effects, Cyclooxygenase 2, Cyclooxygenase 2 Inhibitors, Cyclooxygenase Inhibitors pharmacology, Deoxycytidine analogs & derivatives, Humans, Isoenzymes biosynthesis, Isoenzymes drug effects, Male, Membrane Proteins, Pancreatic Neoplasms metabolism, Prostaglandin-Endoperoxide Synthases biosynthesis, Prostaglandin-Endoperoxide Synthases drug effects, Sulindac pharmacology, Tumor Cells, Cultured, Gemcitabine, Anti-Inflammatory Agents, Non-Steroidal pharmacology, Cell Cycle drug effects, Deoxycytidine pharmacology, Enzyme Inhibitors pharmacology, Pancreatic Neoplasms pathology
- Abstract
Increased cyclooxygenase-2 (COX-2) expression in human pancreatic adenocarcinomas, as well as the growth-inhibitory effect of nonsteroidal anti-inflammatory drugs (NSAIDs) in vitro, suggests that NSAIDs may be an effective treatment for pancreatic cancer. Gemcitabine is currently the most effective chemotherapeutic drug available for patients with pancreatic cancer, but is only minimally effective against this aggressive disease. Clearly, other treatment options must be identified. To design successful therapeutic strategies involving compounds either alone or in combination with others, it is necessary to understand their mechanism of action. In the present study, we evaluated the effects of three NSAIDs (sulindac, indomethacin, and NS-398) or gemcitabine in two human pancreatic carcinoma cell lines, BxPC-3 (COX-2-positive) and PaCa-2 (COX-2-negative), previously shown to be growth-inhibited by these NSAIDs. Effects on cell cycle and apoptosis were investigated by flow cytometry or Western blotting. Treatment with NSAIDs or gemcitabine altered the cell cycle phase distribution as well as the expression of multiple cell cycle regulatory proteins in both cell lines, but did not induce substantial levels of apoptosis. Furthermore, we demonstrated that the combination of the NSAID sulindac or NS-398 with gemcitabine inhibited cell growth to a greater degree than either compound alone. These results indicate that the antiproliferative effects of NSAIDs and gemcitabine in pancreatic tumor cells are primarily due to inhibition of cell cycle progression rather than direct induction of apoptotic cell death, regardless of COX-2 expression. In addition, NSAIDs in combination with gemcitabine may hold promise in the clinic for the treatment of pancreatic cancer. more...
- Published
- 2001
8. Pancreatic tumor cells with mutant K-ras suppress ERK activity by MEK-dependent induction of MAP kinase phosphatase-2.
- Author
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Yip-Schneider MT, Lin A, and Marshall MS
- Subjects
- Animals, Blotting, Western, Carcinoma enzymology, Cell Line, Down-Regulation, Dual-Specificity Phosphatases, Enzyme Inhibitors pharmacology, Humans, Kinetics, Mitogen-Activated Protein Kinase Phosphatases, Pancreatic Neoplasms enzymology, Phosphorylation drug effects, Protein Phosphatase 2, Rats, Signal Transduction, Time Factors, Tumor Cells, Cultured, Up-Regulation, Vanadates pharmacology, Carcinoma genetics, Gene Expression Regulation, Enzymologic, Genes, ras genetics, Mitogen-Activated Protein Kinase Kinases metabolism, Mitogen-Activated Protein Kinases metabolism, Mutation, Pancreatic Neoplasms genetics, Protein Tyrosine Phosphatases metabolism
- Abstract
Activating mutations within the K-ras gene occur in a high percentage of human pancreatic carcinomas. We reported previously that the presence of oncogenic, activated K-ras in human pancreatic carcinoma cell lines did not result in constitutive activation of the extracellular signal-regulated kinases (ERK1 and ERK2). In the present study, we further characterized the ERK signaling pathway in pancreatic tumor cell lines in order to determine whether the ERK pathway is subject to a compensatory downregulation. We found that the attenuation of serum-induced ERK activation was not due to a delay in the kinetics of ERK phosphorylation. Treatment with the tyrosine phosphatase inhibitor orthovanadate increased the level of ERK phosphorylation, implicating a vanadate-sensitive tyrosine phosphatase in the negative regulation of ERK. Furthermore, expression of a dual specificity phosphatase capable of inactivating ERK known as mitogen-activated protein (MAP) kinase phosphatase-2 (MKP-2) was elevated in most of the pancreatic tumor cell lines and correlated with the presence of active MAP kinase kinase (MEK). Taken together, these results suggest that pancreatic tumor cells expressing oncogenic K-ras compensate, in part, by upregulating the expression of MKP-2 to repress the ERK signaling pathway., (Copyright 2001 Academic Press.) more...
- Published
- 2001
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9. Regulation of the Raf-1 kinase domain by phosphorylation and 14-3-3 association.
- Author
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Yip-Schneider MT, Miao W, Lin A, Barnard DS, Tzivion G, and Marshall MS
- Subjects
- 14-3-3 Proteins, Animals, Binding, Competitive, COS Cells, Catalytic Domain, Enzyme Activation drug effects, Mutation genetics, Oncogene Protein pp60(v-src) genetics, Oncogene Protein pp60(v-src) metabolism, Peptide Fragments chemistry, Peptide Fragments metabolism, Phosphorylation, Phosphoserine metabolism, Protein Binding, Protein Structure, Tertiary, Proto-Oncogene Proteins c-raf genetics, Tetradecanoylphorbol Acetate pharmacology, Tyrosine 3-Monooxygenase genetics, Proto-Oncogene Proteins c-raf chemistry, Proto-Oncogene Proteins c-raf metabolism, Tyrosine 3-Monooxygenase metabolism
- Abstract
The Raf-1 kinase domain is kept in an inactive state by the N-terminal regulatory domain. Activation of the kinase domain occurs following release from the N-terminal repression and possible catalytic upregulation. To distinguish the regulatory mechanisms that directly influence the catalytic activity of the enzyme from those which act through the inhibitory domain, the catalytic domain of Raf-1 (CR3) was expressed in COS-7 cells. The role of phosphorylation in the direct regulation of this domain was determined by substituting non-phosphorylatable amino acids for known serine and tyrosine phosphorylation sites. The intrinsic activity of each mutant protein was determined as well as stimulation by v-Src and phorbol esters. Both v-Src and phorbol esters were potent activators of CR3, requiring the serine 338/339 (p21-activated protein kinase, Pak) and tyrosine 340/341 (Src) phosphorylation sites for full stimulation of CR3. In contrast, loss of the serine 497/499 protein kinase C phosphorylation sites had little effect on CR3 activation by either v-Src or phorbol esters. Loss of serine 621, a 14-3-3 adaptor-protein-binding site, prevented activation of CR3 by v-Src or phorbol esters and partially decreased the high basal activity of the kinase fragment. When co-expressed in COS-7 cells, 14-3-3 associated strongly with full-length Raf-1, weakly with wild-type CR3 and not at all with the A621 and D621 CR3 mutants. The role of 14-3-3 in maintaining the activity of the catalytic domain of Raf-1 was investigated further by performing peptide-competition studies with wild-type CR3, wild-type CR3 and v-Src or constitutively active CR3 (CR3[YY340/341DD]). In each case, incubation of the proteins with a phosphoserine-621 Raf-1 peptide, which we show displaced Raf-1 and CR3[YY340/341DD] from 14-3-3, was found to substantially reduce catalytic activity. Taken together, our results support a model of Raf regulation in which the activity of the Raf-1 catalytic domain is directly upregulated by phosphorylation, following relief of inhibition by the N-terminal regulatory domain upon Ras-GTP binding. Moreover, the presence of serine 621 in the free catalytic fragment is required for full CR3 activation by stimulatory factors, and the continuous presence of 14-3-3 at this site is necessary for retaining activity once the kinase is activated. more...
- Published
- 2000
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10. Cyclooxygenase-2 expression in human pancreatic adenocarcinomas.
- Author
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Yip-Schneider MT, Barnard DS, Billings SD, Cheng L, Heilman DK, Lin A, Marshall SJ, Crowell PL, Marshall MS, and Sweeney CJ
- Subjects
- Adenocarcinoma genetics, Animals, Cell Line, Transformed, Codon genetics, Cricetinae, Cyclooxygenase 2, Cyclooxygenase 2 Inhibitors, Cyclooxygenase Inhibitors pharmacology, Dinoprostone biosynthesis, Dinoprostone genetics, Enzyme Induction, Humans, Indomethacin pharmacology, Isoenzymes genetics, Membrane Proteins, Mesocricetus, Neoplasm Proteins genetics, Nitrobenzenes pharmacology, Pancreas enzymology, Pancreatic Neoplasms genetics, Prostaglandin-Endoperoxide Synthases genetics, Signal Transduction, Sulfonamides pharmacology, Sulindac pharmacology, Adenocarcinoma enzymology, Gene Expression Regulation, Neoplastic, Genes, ras, Isoenzymes biosynthesis, Neoplasm Proteins biosynthesis, Pancreatic Neoplasms enzymology, Point Mutation, Prostaglandin-Endoperoxide Synthases biosynthesis
- Abstract
Cyclooxygenase-2 (COX-2) expression is up-regulated in several types of human cancers and has also been directly linked to carcinogenesis. To investigate the role of COX-2 in pancreatic cancer, we evaluated COX-2 protein expression in primary human pancreatic adenocarcinomas (n = 23) and matched normal adjacent tissue (n = 11) by immunoblot analysis. COX-2 expression was found to be significantly elevated in the pancreatic tumor specimens compared with normal pancreatic tissue. To examine whether the elevated levels of COX-2 protein observed in pancreatic tumors correlated with the presence of oncogenic K-ras, we determined the K-ras mutation status in a subset of the tumors and corresponding normal tissues. The presence of oncogenic K-ras did not correlate with the level of COX-2 protein expressed in the pancreatic adenocarcinomas analyzed. These observations were also confirmed in a panel of human pancreatic tumor cell lines. Furthermore, in the pancreatic tumor cell line expressing the highest level of COX-2 (BxPC-3), COX-2 expression was demonstrated to be independent of Erk1/2 activation. The lack of correlation between COX-2 and oncogenic K-ras expression suggests that Ras activation may not be sufficient to induce COX-2 expression in pancreatic tumor cells and that the aberrant activation of signaling pathways other than Ras may be required for up-regulating COX-2 expression. We also report that the COX inhibitors sulindac, indomethacin and NS-398 inhibit cell growth in both COX-2-positive (BxPC-3) and COX-2-negative (PaCa-2) pancreatic tumor cell lines. However, suppression of cell growth by indomethacin and NS-398 was significantly greater in the BxPC-3 cell line compared with the PaCa-2 cell line (P = 0.004 and P < 0.001, respectively). In addition, the three COX inhibitors reduce prostaglandin E(2) levels in the BxPC-3 cell line. Taken together, our data suggest that COX-2 may play an important role in pancreatic tumorigenesis and therefore be a promising chemotherapeutic target for the treatment of pancreatic cancer. more...
- Published
- 2000
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11. Lack of elevated MAP kinase (Erk) activity in pancreatic carcinomas despite oncogenic K-ras expression.
- Author
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Yip-Schneider MT, Lin A, Barnard D, Sweeney CJ, and Marshall MS
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- Cell Line, Enzyme Activation, Fibroblasts metabolism, Humans, Mitogen-Activated Protein Kinase 3, Pancreatic Neoplasms genetics, Reference Values, Tumor Cells, Cultured, Calcium-Calmodulin-Dependent Protein Kinases metabolism, Gene Expression Regulation, Neoplastic physiology, Genes, ras, Mitogen-Activated Protein Kinase 1 metabolism, Mitogen-Activated Protein Kinases, Pancreatic Neoplasms enzymology
- Abstract
Activating mutations within the K-ras gene have been found in up to 90% of pancreatic carcinomas. Although multiple Ras effector pathways have been identified, the Raf protein kinases which are upstream regulators of the mitogen-activated protein kinases (MAPK/Erk) are believed to be the primary mitogenic effectors. Constitutive upregulation of this pathway by oncogenic ras is thought to promote cellular transformation. To explore the biological effects of mutated K-ras, we analyzed the Ras signaling pathway in a panel of cell lines derived from human pancreatic carcinomas. We found that despite high levels of Ras-GTP in each cell line expressing mutant K-ras, elevated levels of active Erk1 and Erk2 were not detectable under conditions of exponential growth or serum-starvation. Depending upon the cell line, the block in Erk signaling was observed to occur at either the level of Raf or Erk. Increased levels of active Erk1 and Erk2 were detected in only 2 out of 10 normal tissue-matched primary pancreatic tumors with mutated K-ras. Our results suggest that Erk signaling is not aberrantly upregulated in pancreatic cancers containing oncogenic K-ras mutations. The lack of Erk activation observed in both cell lines and primary tumor tissue suggests that constitutive Erk activation may not be required for tumor maintenance or progression in K-ras transformed pancreatic cells. We hypothesize that other Ras-dependent signaling pathways or an unidentified Raf/Mek-dependent pathway may be important for carcinogenesis in the pancreas. These findings may have important implications for drug treatment strategies which currently target the MAP kinase branch of the Ras signaling pathway. more...
- Published
- 1999
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12. Transcriptional induction of pim-1 protein kinase gene expression by interferon gamma and posttranscriptional effects on costimulation with steel factor.
- Author
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Yip-Schneider MT, Horie M, and Broxmeyer HE
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- Base Sequence, Binding Sites genetics, Drug Synergism, Gene Expression drug effects, Humans, Leukemia metabolism, Molecular Sequence Data, Promoter Regions, Genetic genetics, Protein Serine-Threonine Kinases biosynthesis, Protein Serine-Threonine Kinases genetics, Proto-Oncogene Proteins genetics, Proto-Oncogene Proteins c-pim-1, RNA, Messenger biosynthesis, Recombinant Proteins, Stem Cell Factor, Transcription, Genetic drug effects, Tumor Cells, Cultured, Hematopoietic Cell Growth Factors pharmacology, Interferon-gamma pharmacology, Proto-Oncogene Proteins biosynthesis
- Abstract
Steel factor (SLF) synergizes with interferon gamma (IFN gamma) to stimulate proliferation of the human factor-dependent cell line MO7e. We examined the effects of IFN gamma and SLF treatment, alone or in combination, on the expression of a 33-kD cytoplasmic protein serine/threonine kinase designated pim-1 whose expression has been closely associated with proliferation induced by related myeloid cytokines. IFN gamma alone, but not SLF, stimulated expression of pim-1 RNA and protein in MO7e cells; compared with IFN gamma alone, costimulation with IFN gamma and SLF resulted in a twofold to threefold increase in pim-1 message and protein expression, correlating with synergistic effects on cell proliferation. Both IFN gamma and IFN gamma/SLF induced pim-1 mRNA in the absence of de novo protein synthesis. Nuclear run-on assays showed that, although IFN gamma alone increased the rate of pim-1 gene transcription, costimulation with IFN gamma and SLF did not further potentiate this effect; however, the stability of pim-1 message was significantly enhanced in the presence of both cytokines. An IFN gamma-responsive element within the 5' flanking region of the pim-1 gene that could confer IFN gamma responsiveness on a heterologous promoter was identified. This sequence, designated PMGAS, formed a specific complex with Stat (signal transducers and activators of transcription) 1 alpha (the p91 subunit of the transcription factor ISGF3 [interferon-stimulated gene factor 3]) in IFN gamma-treated cell extracts, suggesting that the transcriptional effects of IFN gamma on pim-1 expression may be mediated by Stat 1 alpha. more...
- Published
- 1995
13. Characterization of interleukin-7-induced changes in tyrosine phosphorylation and c-myc gene expression in normal human T cells.
- Author
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Yip-Schneider MT, Horie M, and Broxmeyer HE
- Subjects
- 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine, Blotting, Northern, Cell Division, Humans, Immunoblotting, Isoquinolines pharmacology, Molecular Weight, Phosphorylation, Phosphotyrosine, Piperazines pharmacology, Protein Kinase Inhibitors, Protein Kinases metabolism, Signal Transduction, T-Lymphocytes cytology, Tetradecanoylphorbol Acetate pharmacology, Transcription, Genetic, Tyrosine metabolism, Gene Expression drug effects, Genes, myc, Interleukin-7 pharmacology, Phosphoproteins metabolism, T-Lymphocytes metabolism, Tyrosine analogs & derivatives
- Abstract
Interleukin-7 (IL-7) is a growth factor involved in regulating lymphopoiesis. We have chosen to study the signal transduction pathway of IL-7 in normal human peripheral blood T lymphocytes. Two early events that occur as a consequence of specific ligand-receptor interaction were examined: activation of protein tyrosine kinases and induction of primary response gene expression. Following treatment of human peripheral blood T cells with IL-7, four cellular proteins with relative molecular weights of 95- (doublet), 105-, and 130-kd were rapidly tyrosine phosphorylated as detected by immunoblotting with an antiphosphotyrosine monoclonal antibody (MAB). The 105-kd tyrosine-phosphorylated protein was membrane-associated after IL-7 stimulation. Treatment of human peripheral blood T cells with IL-7 enhanced expression of the primary response gene c-myc approximately three-fold, as detected by Northern blotting, in the presence or absence of protein synthesis. The rate of c-myc gene transcription increased in the presence of IL-7 and could account for the observed elevation of c-myc RNA levels. In addition, IL-7 treatment induced a slight increase in c-myc message stability. Experiments performed with the protein tyrosine kinase inhibitor genistein and the serine-threonine kinase inhibitor 1-(5-isoquinolinylsulfonyl)-2-methyl-piperazine (H-7) demonstrated that these kinases were required for IL-7 enhancement of c-myc expression. Treatment with tetradecanoyl phorbol acetate (TPA), a potent activator of protein kinase C (PKC), in combination with IL-7 induced a level of c-myc expression greater than that elicited by either factor alone, suggesting that TPA and IL-7 utilize cooperative signaling pathways to increase c-myc gene expression. more...
- Published
- 1993
14. [Inservice training and evaluation in a thoracic surgical intensive care service].
- Author
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Seltzer D, Schneider MT, and Unger S
- Subjects
- Humans, Nursing Staff, Hospital standards, Critical Care, Education, Nursing, Continuing organization & administration, Nursing Staff, Hospital education, Thoracic Surgery
- Published
- 1992
15. Fine structural characteristics and synaptic connections of trigeminocerebellar projection neurons in rat trigeminal nucleus oralis.
- Author
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Falls WM, Moore BJ, and Schneider MT
- Subjects
- Animals, Male, Microscopy, Electron, Rats, Rats, Inbred Strains, Cerebellum ultrastructure, Neurons, Afferent ultrastructure, Trigeminal Nerve ultrastructure
- Abstract
In order to classify the presynaptic terminals contacting trigeminocerebellar projection neurons (TCPNs) in rat trigeminal nucleus oralis (Vo), electron-microscopic examination of sequential thin sections made from TCPNs located in the border zone (BZ) of Vo, labeled by the retrograde transport of horseradish peroxidase, was undertaken. The use of BZ TCPNs, labeled in Golgi-like fashion so that many of their dendrites and axons were visible, allowed for the determination of the distribution of each bouton type along the soma and dendrites, as well as for the characterization of the morphology and synaptic relations of the labeled axon and its terminals. Three types of axon terminals contacting labeled BZ TCPNs have been recognized, depending upon whether they contain primarily spherical-shaped, agranular synaptic vesicles (S endings); predominantly flattened, agranular synaptic vesicles (F endings); or a population of pleomorphic-shaped, agranular synaptic vesicles (P endings). The S endings represent the majority of axon terminals contacting labeled BZ TCPNs and establish asymmetrical axosomatic and axodendritic synaptic contacts. Many S endings are situated in one of two types of synaptic glomeruli. One type of glomerulus has a large S ending at its core, whereas the other contains a small S ending. Large-S-ending glomeruli include only labeled distal dendrites of BZ TCPNs; small-S-ending glomeruli contain either a labeled soma, proximal dendrite, or distal dendritic shaft. The remaining S endings are extraglomerular, synapsing on distal dendrites. P endings are less frequently encountered and establish intermediate axosomatic and axodendritic synapses. These endings exhibit a generalized distribution along the entire somatodendritic tree. F endings make symmetrical axodendritic synapses with distal dendrites, are only found in glomeruli containing small S endings, and are the least frequently observed ending contacting labeled BZ TCPNs. The majority of axonal endings synapsing on labeled BZ TCPNs are located along distal dendrites, with only a relatively few synapsing terminals situated on proximal dendrites and somata. The axons of labeled BZ TCPNs arise from the cell body and generally give rise to a single short collateral near their points of origin. This collateral remains unbranched and generates several boutons within BZ, while the parent axon acquires a myelin sheath and, without branching further, travels dorsolaterally toward the inferior cerebellar peduncle. The collateral boutons resemble extraglomerular S endings. They contain agranular, spherical-shaped synaptic vesicles and make asymmetrical axodendritic synapses with small-diameter unlabeled dendritic shafts in the BZ neuropil. more...
- Published
- 1990
- Full Text
- View/download PDF
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