Other search tools

About this data

The publication data currently available has been vetted by Vanderbilt faculty, staff, administrators and trainees. The data itself is retrieved directly from NCBI's PubMed and is automatically updated on a weekly basis to ensure accuracy and completeness.

If you have any questions or comments, please contact us.

Results: 51 to 60 of 68

Publication Record

Connections

Neocytolysis on descent from altitude: a newly recognized mechanism for the control of red cell mass.
Rice L, Ruiz W, Driscoll T, Whitley CE, Tapia R, Hachey DL, Gonzales GF, Alfrey CP
(2001) Ann Intern Med 134: 652-6
MeSH Terms: Adaptation, Physiological, Adult, Altitude, Cell Count, Erythrocytes, Erythropoietin, Ferritins, Hematocrit, Hemoglobins, Hemolysis, Humans, Male, Middle Aged, Polycythemia, Prospective Studies, Reticulocytes
Show Abstract · Added March 20, 2014
BACKGROUND - Studies of space-flight anemia have uncovered a physiologic process, neocytolysis, by which young red blood cells are selectively hemolyzed, allowing rapid adaptation when red cell mass is excessive for a new environment.
OBJECTIVES - 1) To confirm that neocytolysis occurs in another situation of acute plethora-when high-altitude dwellers with polycythemia descend to sea level; and 2) to clarify the role of erythropoietin suppression.
DESIGN - Prospective observational and interventional study.
SETTING - Cerro de Pasco (4380 m) and Lima (sea level), Peru.
PARTICIPANTS - Nine volunteers with polycythemia.
INTERVENTIONS - Volunteers were transported to sea level; three received low-dose erythropoietin.
MEASUREMENTS - Changes in red cell mass, hematocrit, hemoglobin concentration, reticulocyte count, ferritin level, serum erythropoietin, and enrichment of administered(13)C in heme.
RESULTS - In six participants, red cell mass decreased by 7% to 10% within a few days of descent; this decrease was mirrored by a rapid increase in serum ferritin level. Reticulocyte production did not decrease, a finding that establishes a hemolytic mechanism.(13)C changes in circulating heme were consistent with hemolysis of young cells. Erythropoietin was suppressed, and administration of exogenous erythropoietin prevented the changes in red cell mass, serum ferritin level, and(13)C-heme.
CONCLUSIONS - Neocytolysis and the role of erythropoietin are confirmed in persons with polycythemia who descend from high altitude. This may have implications that extend beyond space and altitude medicine to renal disease and other situations of erythropoietin suppression, hemolysis, and polycythemia.
0 Communities
1 Members
0 Resources
16 MeSH Terms
Vascular tumors in livers with targeted inactivation of the von Hippel-Lindau tumor suppressor.
Haase VH, Glickman JN, Socolovsky M, Jaenisch R
(2001) Proc Natl Acad Sci U S A 98: 1583-8
MeSH Terms: Albumins, Alleles, Animals, Erythropoietin, Genes, Tumor Suppressor, Hemangioma, Heterozygote, Ligases, Liver Neoplasms, Mice, Mice, Inbred BALB C, Mice, Knockout, Mice, Mutant Strains, Phenotype, Polycythemia, Proteins, Tumor Suppressor Proteins, Ubiquitin-Protein Ligases, Vascular Neoplasms, Von Hippel-Lindau Tumor Suppressor Protein
Show Abstract · Added August 19, 2013
von Hippel-Lindau (VHL) disease is a pleomorphic familial tumor syndrome that is characterized by the development of highly vascularized tumors. Homozygous disruption of the VHL gene in mice results in embryonic lethality. To investigate VHL function in the adult we have generated a conditional VHL null allele (2-lox allele) and null allele (1-lox allele) by Cre-mediated recombination in embryonic stem cells. We show here that mice heterozygous for the 1-lox allele develop cavernous hemangiomas of the liver, a rare manifestation of the human disease. Histologically these tumors were associated with hepatocellular steatosis and focal proliferations of small vessels. To study the cellular origin of these lesions we inactivated VHL tissue-specifically in hepatocytes. Deletion of VHL in the liver resulted in severe steatosis, many blood-filled vascular cavities, and foci of increased vascularization within the hepatic parenchyma. These histopathological changes were similar to those seen in livers from mice heterozygous for the 1-lox allele. Hypoxia-inducible mRNAs encoding vascular endothelial growth factor, glucose transporter 1, and erythropoietin were up-regulated. We thus provide evidence that targeted inactivation of mouse VHL can model clinical features of the human disease and underline the importance of the VHL gene product in the regulation of hypoxia-responsive genes in vivo.
0 Communities
1 Members
0 Resources
20 MeSH Terms
Impaired biological activity of erythropoietin by cyanate carbamylation.
Mun KC, Golper TA
(2000) Blood Purif 18: 13-7
MeSH Terms: Animals, Body Weight, Carbamates, Cyanates, Erythrocyte Count, Erythropoietin, Hematocrit, Hemoglobins, Male, Rats, Rats, Sprague-Dawley, Sodium Chloride, Time Factors
Show Abstract · Added August 7, 2015
AIMS - During advanced renal failure, particularly in patients with end-stage renal disease (ESRD), proteins are carbamylated as a result of a reaction with cyanate. Some or all of the cyanate is derived from urea. If the carbamylation of proteins adversely alters their biologic activities, then urea must be viewed as an uremic toxin, rather than a surrogate. Therefore, we studied the effect of cyanate carbamylation on the erythropoietic activity of erythropoietin (EPO) in a rodent model.
METHODS - EPO was carbamylated by incubation with cyanate at 37 degrees C. The extent of carbamylation was monitored using trinitrobenzenesulfonic acid. In Sprague-Dawley rats the erythrocyte count, hemoglobin concentration, and hematocrit were measured after the twice-weekly subcutaneous injection of either EPO or carbamylated EPO for 3 weeks. Two additional control groups received physiologic saline or 0.2 ml of 1 M cyanate.
RESULTS - The level of carbamylated EPO was increased as the time of exposure to cyanate increased from 1 to 6 h, and as the cyanate concentration increased from 8 to 2,000 mM. EPO injections caused significantly large increases in all erythropoietic measures. Physiologic saline or 1 M cyanate-injected controls and the carbamylated EPO-injected animals demonstrated no change from baseline in erythropoietic parameters.
CONCLUSION - These results support that EPO exposed to high levels of cyanate in vitro demonstrates diminished biologic activity in healthy Sprague-Dawley rats. This effect may be manifested by the carbamylation of EPO by the cyanate. Should this occur in ESRD patients, it may contribute to the suboptimal erythropoietic response to EPO therapy associated with high urea levels, especially related to inadequate dialysis. Targeting dialysis doses specifically to urea concentrations may be more important than previously considered.
Copyright 2000 S. Karger AG, Basel
0 Communities
1 Members
0 Resources
13 MeSH Terms
Neocytolysis contributes to the anemia of renal disease.
Rice L, Alfrey CP, Driscoll T, Whitley CE, Hachey DL, Suki W
(1999) Am J Kidney Dis 33: 59-62
MeSH Terms: Adult, Aged, Anemia, Cell Survival, Erythrocytes, Erythropoietin, Hemolysis, Humans, Kidney Failure, Chronic, Middle Aged, Recombinant Proteins, Terminology as Topic, Time Factors
Show Abstract · Added March 20, 2014
Neocytolysis is a recently described physiological process affecting the selective hemolysis of young red blood cells in circumstances of plethora. Erythropoietin (EPO) depression appears to initiate the process, providing the rationale to investigate its contributions to the anemia of renal disease. When EPO therapy was withheld, four of five stable hemodialysis patients showed chromium 51 (51Cr)-red cell survival patterns indicative of neocytolysis; red cell survival was short in the first 9 days, then normalized. Two of these four patients received oral 13C-glycine and 15N-glycine, and there was a suggestion of pathological isotope enrichment of stool porphyrins when EPO therapy was held, again supporting selective hemolysis of newly released red cells that take up the isotope (one patient had chronic hemolysis indicated by isotope studies of blood and stool). Thus, neocytolysis can contribute to the anemia of renal disease and explain some unresolved issues about such anemia. One implication is the prediction that intravenous bolus EPO therapy is metabolically and economically inefficient compared with lower doses administered more frequently subcutaneously.
0 Communities
1 Members
0 Resources
13 MeSH Terms
Endogenous p53 regulation and function in early stage Friend virus-induced tumor progression differs from that following DNA damage.
Kelley LL, Hicks GG, Hsieh FF, Prasher JM, Green WF, Miller MD, Eide EJ, Ruley HE
(1998) Oncogene 17: 1119-30
MeSH Terms: Animals, Antibiotics, Antineoplastic, Apoptosis, Cell Differentiation, Cell Division, Cell Survival, Cyclin-Dependent Kinase Inhibitor p21, Cyclins, DNA Damage, Dactinomycin, Disease Progression, Erythroblasts, Erythropoietin, Female, Friend murine leukemia virus, G1 Phase, Gene Expression, Genes, p53, Leukemia, Erythroblastic, Acute, Male, Mice, Mice, Inbred C57BL, Mice, Inbred Strains, Mutation, Transcriptional Activation, Tumor Cells, Cultured, Tumor Suppressor Protein p53
Show Abstract · Added May 29, 2014
Erythroleukemia induced by the anemia strain of Friend virus occurs in two stages. The first stage results in rapid expansion of pre-leukemic proerythroblasts (FVA cells) dependent on erythropoietin (Epo) for differentiation and survival in vitro. The second stage is characterized by emergence of erythroleukemic clones (MEL cells) which typically bear activation of the ets-oncogene, PU.1/spi.1, and loss of functional p53. We developed a Friend virus-sensitive, p53-deficient mouse model to investigate the biological advantage conferred by p53-loss during tumor progression. Here we report p53 was not required for cell survival or growth arrest during differentiation of FVA cells, nor was p53 required for induction of apoptosis upon Epo withdrawal. However, we detected induction of the p21Cip1 cyclin-dependent kinase inhibitor gene during differentiation, which was markedly enhanced in the presence of p53. p53-dependent expression of p21Cip1 occurred in the absence of an increase in p53 mRNA and protein levels and was specific for p21Cip1, since expression of gadd45, mdm-2, cyclin G and bax were unaffected by p53. In contrast, treatment of FVA cells with DNA damaging agents led to rapid accumulation of p53 protein resulting in transcription of multiple p53-regulated genes, leading to either apoptosis or growth arrest, depending on the agent used. These data demonstrate that p53-dependent activities during differentiation of preleukemic erythroblasts are distinct from those observed in response to genotoxic agents. We propose that enhancement of p53-dependent gene expression during differentiation may represent a tumor suppressor function which is necessary to monitor differentiation of preleukemic cells and which is selected against during tumor progression.
0 Communities
1 Members
0 Resources
27 MeSH Terms
Erythropoietin-induced hypertension.
Ismail N, Ikizler TA
(1997) J Med Liban 45: 25-30
MeSH Terms: Anemia, Blood Pressure, Clinical Trials as Topic, Erythropoietin, Hemodynamics, Humans, Hypertension, Kidney Failure, Chronic, Male, Monitoring, Physiologic, Multicenter Studies as Topic, Recombinant Proteins, Renal Dialysis, Risk Factors, Vascular Resistance
Added September 29, 2014
0 Communities
1 Members
0 Resources
15 MeSH Terms
Chronic administration of transforming growth factor-beta suppresses erythropoietin-dependent erythropoiesis and induces tumour necrosis factor in vivo.
Chuncharunee S, Carter CD, Studtmann KE, Caro J, Coffey RJ, Dessypris EN
(1993) Br J Haematol 84: 374-80
MeSH Terms: Animals, Blood Cell Count, Erythropoiesis, Erythropoietin, Hematopoietic Stem Cells, Mice, Mice, Inbred BALB C, Recombinant Proteins, Spleen, Transforming Growth Factor beta, Tumor Necrosis Factor-alpha
Show Abstract · Added March 27, 2014
Transforming growth factor beta is a known inhibitor of the proliferation and differentiation of early haematopoietic progenitors but has no effect on mature erythroid cells in vitro. Mice injected with rhTGF beta 1 exhibited severe and progressive suppression of erythropoiesis manifested by a decline of reticulocyte count, marrow erythroblasts and marrow and spleen CFU-E, which could be prevented by administration of erythropoietin. This suppression of erythropoiesis was associated with the appearance of tumour necrosis factor in the blood, development of pronounced cachexia and depression of serum erythropoietin levels. TGF beta induces TNF in vivo that leads to cachexia, decrease of serum erythropoietin levels and suppression of erythropoietin dependent erythropoiesis.
1 Communities
1 Members
0 Resources
11 MeSH Terms
Apoptosis in erythroid progenitors deprived of erythropoietin occurs during the G1 and S phases of the cell cycle without growth arrest or stabilization of wild-type p53.
Kelley LL, Green WF, Hicks GG, Bondurant MC, Koury MJ, Ruley HE
(1994) Mol Cell Biol 14: 4183-92
MeSH Terms: Animals, Apoptosis, Cell Cycle, Cell Division, Cell Line, Cells, Cultured, DNA, DNA Damage, Erythropoietin, Flow Cytometry, Friend murine leukemia virus, G1 Phase, Genes, p53, Hematopoietic Stem Cells, Kinetics, Mice, Mice, Inbred Strains, Protein Conformation, S Phase, Thymidine, Time Factors, Tumor Suppressor Protein p53
Show Abstract · Added May 29, 2014
Erythropoietin (Epo) inhibits apoptosis in murine proerythroblasts infected with the anemia-inducing strain of Friend virus (FVA cells). We have shown that the apoptotic process in FVA cell populations deprived of Epo is asynchronous as a result of a heterogeneity in Epo dependence among individual cells. Here we investigated whether apoptosis in FVA cells correlated with cell cycle phase or stabilization of p53 tumor suppressor protein. DNA analysis in nonapoptotic FVA cell subpopulations cultured without Epo demonstrated little change in the percentages of cells in G1,S, and G2/M phases over time. Analysis of the apoptotic subpopulation revealed high percentages of cells in G1 and S, with few cells in G2/M at any time. When cells were sorted from G1 and S phases prior to culture without Epo, apoptotic cells appeared at the same rate in both populations, indicating that no prior commitment step had occurred in either G1 or S phase. Steady-state wild-type p53 protein levels were very low in FVA cells compared with control cell lines and did not accumulate in Epo-deprived cultures; however, p53 protein did accumulate when FVA cells were treated with the DNA-damaging agent actinomycin D. These data indicate that erythroblast apoptosis caused by Epo deprivation (i) occurs throughout G1 and S phases and does not require cell cycle arrest, (ii) does not have a commitment event related to cell cycle phase, and (iii) is not associated with conformational changes or stabilization of wild-type p53 protein.
0 Communities
1 Members
0 Resources
22 MeSH Terms
Infrequent dosing of subcutaneous erythropoietin for the treatment of anemia in patients on CAPD.
Bunke M, Bartlett DK, Brier ME, Golper TA
(1993) Adv Perit Dial 9: 331-5
MeSH Terms: Adult, Anemia, Drug Administration Schedule, Erythropoietin, Female, Hematocrit, Hemoglobins, Humans, Injections, Subcutaneous, Kidney Failure, Chronic, Male, Middle Aged, Peritoneal Dialysis, Continuous Ambulatory
Show Abstract · Added August 7, 2015
Erythropoietin (EPO) given subcutaneously (SC) once per week has been successful in the treatment of anemia in continuous ambulatory peritoneal dialysis (CAPD) patients. We have identified a population of CAPD patients that requires EPO administration once per week or less often. To determine if specific variables could be identified that would predict which CAPD patients would require infrequent EPO dosing, we reviewed the charts of all our CAPD patients who were receiving EPO as of 1 June 1992. Patients had to have been on CAPD for 3 months and EPO for 3 months to be considered for analysis. We identified 12 patients who required EPO once per week or less frequently (infrequent EPO) and 9 patients who required EPO more than once per week (frequent EPO). Parameters that were analyzed included age, gender, race, time on CAPD, history of gastrointestinal bleeding, exit-site infection or peritonitis in the last 60 days, diabetes, amount of dialysate instilled per day, and the number of exchanges per day. Laboratory data that were analyzed included hemoglobin, hematocrit, serum iron, total iron-binding capacity, ferritin, blood urea nitrogen (BUN), creatinine, BUN/creatinine ratio, albumin, total protein, parathyroid hormone, and aluminum. Categorical data were analyzed via chi-square, and numerical data were analyzed via the t-test. The infrequent EPO group required only 35% as much EPO as the frequent group to maintain hemoglobin and hematocrit, which were significantly greater. The only parameter that was different between the two groups was age (infrequent EPO 42 +/- 13.2 vs frequent EPO 55.8 +/- 11.9 years, p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
0 Communities
1 Members
0 Resources
13 MeSH Terms
The sympathetic nervous system and the physiologic consequences of spaceflight: a hypothesis.
Robertson D, Convertino VA, Vernikos J
(1994) Am J Med Sci 308: 126-32
MeSH Terms: Anemia, Blood Volume, Catecholamines, Erythropoietin, Heart Rate, Humans, Hypotension, Orthostatic, Kidney, Posture, Receptors, Adrenergic, Space Flight, Sympathetic Nervous System, Weightlessness
Show Abstract · Added December 10, 2013
Many of the physiologic consequences of weightlessness and the cardiovascular abnormalities on return from space could be due, at least in part, to alterations in the regulation of the autonomic nervous system. In this article, the authors review the rationale and evidence for an autonomic mediation of diverse changes that occur with spaceflight, including the anemia and hypovolemia of weightlessness and the tachycardia and orthostatic intolerance on return from space. This hypothesis is supported by studies of two groups of persons known to have low catecholamine levels: persons subjected to prolonged bedrest and persons with syndromes characterized by low circulating catecholamines (Bradbury-Eggleston syndrome and dopamine beta-hydroxylase deficiency). Both groups exhibit the symptoms mentioned. The increasing evidence that autonomic mechanisms underlie many of the physiologic consequences of weightlessness suggests that new pharmacologic approaches (such as administration of beta-blockers and/or sympathomimetic amines) based on these findings may attenuate these unwanted effects.
0 Communities
1 Members
0 Resources
13 MeSH Terms