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Comparative outcomes between continuous ambulatory and automated peritoneal dialysis: a narrative review.
Bieber SD, Burkart J, Golper TA, Teitelbaum I, Mehrotra R
(2014) Am J Kidney Dis 63: 1027-37
MeSH Terms: Equipment Design, Humans, Kidney Failure, Chronic, Peritoneal Dialysis, Peritoneal Dialysis, Continuous Ambulatory, Peritonitis, Quality of Life, Telemedicine, Treatment Outcome
Show Abstract · Added March 19, 2014
Automated methods for delivering peritoneal dialysis (PD) to persons with end-stage renal disease continue to gain popularity worldwide, particularly in developed countries. However, the endeavor to automate the PD process has not been advanced on the strength of high-level evidence for superiority of automated over manual methods. This article summarizes available studies that have shed light on the evidence that compares the association of treatment with continuous ambulatory PD or automated PD (APD) with clinically meaningful outcomes. Published evidence, primarily from observational studies, has been unable to demonstrate a consistent difference in residual kidney function loss rate, peritonitis rate, maintenance of euvolemia, technique survival, mortality, or health-related quality of life in individuals undergoing continuous ambulatory PD versus APD. At the same time, the future of APD technology appears ripe for further improvement, such as the incorporation of voice commands and expanded use of telemedicine. Given these considerations, it appears that patient choice should drive the decision about PD modality.
Copyright © 2014 National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved.
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9 MeSH Terms
Tumour suppressor Fus1 provides a molecular link between inflammatory response and mitochondrial homeostasis.
Uzhachenko R, Issaeva N, Boyd K, Ivanov SV, Carbone DP, Ivanova AV
(2012) J Pathol 227: 456-69
MeSH Terms: Animals, Asbestos, Cytokines, Down-Regulation, Homeostasis, Inflammation, Ion Channels, Mice, Mice, Inbred C57BL, Mice, Knockout, Mitochondria, Mitochondrial Proteins, Models, Animal, Peritonitis, Reactive Oxygen Species, T-Lymphocyte Subsets, Tumor Suppressor Proteins, Uncoupling Protein 2
Show Abstract · Added March 20, 2014
Fus1, encoded by a 3p21.3 tumour suppressor gene, is down-regulated, mutated or lost in the majority of inflammatory thoracic malignancies. The mitochondrial localization of Fus1 stimulated us to investigate how Fus1 modulates inflammatory response and mitochondrial function in a mouse model of asbestos-induced peritoneal inflammation. Asbestos treatment resulted in a decreased Fus1 expression in wild-type (WT) peritoneal immune cells, suggesting that asbestos exposure may compromise the Fus1-mediated inflammatory response. Untreated Fus1(-/-) mice had an ~eight-fold higher proportion of peritoneal granulocytes than Fus1(+/+) mice, pointing at ongoing chronic inflammation. Fus1(-/-) mice exhibited a perturbed inflammatory response to asbestos, reflected in decreased immune organ weight and peritoneal fluid protein concentration, along with an increased proportion of peritoneal macrophages. Fus1(-/-) immune cells showed augmented asbestos-induced activation of key inflammatory, anti-oxidant and genotoxic stress response proteins ERK1/2, NFκB, SOD2, γH2AX, etc. Moreover, Fus1(-/-) mice demonstrated altered dynamics of pro- and anti-inflammatory cytokine expression, such as IFNγ, TNFα, IL-1A, IL-1B and IL-10. 'Late' response cytokine Ccl5 was persistently under-expressed in Fus1(-/-) immune cells at both basal and asbestos-activated states. We observed an asbestos-related difference in the size of CD3(+) CD4(-) CD8(-) DN T cell subset that was expanded four-fold in Fus1(-/-) mice. Finally, we demonstrated Fus1-dependent basal and asbestos-induced changes in major mitochondrial parameters (ROS production, mitochondrial potential and UCP2 expression) in Fus1(-/-) immune cells and in Fus1-depleted cancer cells, thus supporting our hypothesis that Fus1 establishes its immune- and tumour-suppressive activities via regulation of mitochondrial homeostasis.
Copyright © 2012 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
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18 MeSH Terms
Prostaglandin E2 restrains macrophage maturation via E prostanoid receptor 2/protein kinase A signaling.
Zaslona Z, Serezani CH, Okunishi K, Aronoff DM, Peters-Golden M
(2012) Blood 119: 2358-67
MeSH Terms: Animals, Antigens, Differentiation, CD11b Antigen, Cell Line, Tumor, Cells, Cultured, Cyclic AMP-Dependent Protein Kinases, Dinoprostone, Female, Flow Cytometry, Gene Expression, Macrophage Colony-Stimulating Factor, Macrophages, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Misoprostol, Peritonitis, Prostaglandin Antagonists, Receptor, Macrophage Colony-Stimulating Factor, Receptors, Prostaglandin E, EP2 Subtype, Reverse Transcriptase Polymerase Chain Reaction, Signal Transduction, Thioglycolates, Xanthones
Show Abstract · Added May 4, 2017
Prostaglandin E(2) (PGE(2)) is a lipid mediator that acts by ligating 4 distinct G protein-coupled receptors, E prostanoid (EP) 1 to 4. Previous studies identified the importance of PGE(2) in regulating macrophage functions, but little is known about its effect on macrophage maturation. Macrophage maturation was studied in vitro in bone marrow cell cultures, and in vivo in a model of peritonitis. EP2 was the most abundant PGE(2) receptor expressed by bone marrow cells, and its expression further increased during macrophage maturation. EP2-deficient (EP2(-/-)) macrophages exhibited enhanced in vitro maturation compared with wild-type cells, as evidenced by higher F4/80 expression. An EP2 antagonist also increased maturation. In the peritonitis model, EP2(-/-) mice exhibited a higher percentage of F4/80(high)/CD11b(high) cells and greater expression of macrophage colony-stimulating factor receptor (M-CSFR) in both the blood and the peritoneal cavity. Subcutaneous injection of the PGE(2) analog misoprostol decreased M-CSFR expression in bone marrow cells and reduced the number of peritoneal macrophages in wild-type mice but not EP2(-/-) mice. The suppressive effect of EP2 ligation on in vitro macrophage maturation was mimicked by a selective protein kinase A agonist. Our findings reveal a novel role for PGE(2)/EP2/protein kinase A signaling in the suppression of macrophage maturation.
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25 MeSH Terms
Activated factor XI inhibits chemotaxis of polymorphonuclear leukocytes.
Itakura A, Verbout NG, Phillips KG, Insall RH, Gailani D, Tucker EI, Gruber A, McCarty OJ
(2011) J Leukoc Biol 90: 923-7
MeSH Terms: Blood Coagulation, Cell Movement, Cells, Cultured, Chemotaxis, Leukocyte, Factor XIa, Humans, Inflammation, Interleukin-8, N-Formylmethionine Leucyl-Phenylalanine, Neutrophils, Peritonitis, Protein Binding
Show Abstract · Added May 19, 2014
PMN leukocytes are the most abundant leukocytes in the circulation and play an important role in host defense. PMN leukocyte recruitment and inflammatory responses at sites of infection are critical components in innate immunity. Although inflammation and coagulation are known to have bidirectional relationships, little is known about the interaction between PMN leukocytes and coagulation factors. Coagulation FXI participates in the intrinsic coagulation pathway upon its activation, contributing to hemostasis and thrombosis. We have shown previously that FXI-deficient mice have an increased survival and less leukocyte accumulation into the peritoneum in severe polymicrobial peritonitis. This result suggests a role for FXI in leukocyte trafficking and/or function. In this study, we characterized the functional consequences of FXIa binding to PMN leukocytes. FXIa reduced PMN leukocyte chemotaxis triggered by the chemokine, IL-8, or the bacterial-derived peptide, fMLP, perhaps as a result of the loss of directed migration. In summary, our data suggest that FXIa modulates the inflammatory response of PMN leukocytes by altering migration. These studies highlight the interplay between inflammation and coagulation and suggest that FXIa may play a role in innate immunity.
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12 MeSH Terms
Survival advantage of coagulation factor XI-deficient mice during peritoneal sepsis.
Tucker EI, Gailani D, Hurst S, Cheng Q, Hanson SR, Gruber A
(2008) J Infect Dis 198: 271-4
MeSH Terms: Animals, Blood Coagulation, Cecum, Factor XI, Factor XI Deficiency, Inflammation, Mice, Mice, Inbred C57BL, Mice, Knockout, Peritoneal Diseases, Peritonitis, Punctures, Reference Values, Sepsis, Survivors
Show Abstract · Added May 19, 2014
Anticoagulation is a rational approach to the treatment of sepsis-associated consumptive coagulopathy, but its application is limited because of the risk of excessive bleeding. Factor XI (FXI) contributes substantially to pathological blood coagulation (thrombosis), whereas it contributes only modestly to normal hemostasis. We found that FXI-deficient mice have reduced coagulopathy and increased survival relative to FXI-expressing wild-type mice during cecal ligation and puncture-induced acute peritonitis/sepsis. This finding suggests that FXI contributes to coagulopathy and/or inflammation during sepsis and that pharmacologic inhibition of FXI activity may alter the course and outcome of some infections.
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15 MeSH Terms
Differential effect of imipenem treatment on wild-type and NK cell-deficient CD8 knockout mice during acute intra-abdominal injury.
Enoh VT, Fairchild CD, Lin CY, Varma TK, Sherwood ER
(2006) Am J Physiol Regul Integr Comp Physiol 290: R685-93
MeSH Terms: Abdominal Injuries, Animals, Anti-Bacterial Agents, Bacterial Infections, CD8 Antigens, CD8-Positive T-Lymphocytes, Cecum, Cytokines, Female, Imipenem, Killer Cells, Natural, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Peritonitis, Treatment Outcome
Show Abstract · Added October 18, 2015
CD8 knockout mice depleted of natural killer (NK) cells by treatment with anti-asialoGM1 (CD8KO/alphaAsGM1 mice) are resistant to injury caused by cecal ligation and puncture (CLP). However, CLP-induced injury is complex. Potential sources of injury include bacterial dissemination, cecal ischemia, and translocation of bacterial toxins. We treated wild-type and CD8KO/alphaAsGM1 mice with imipenem after CLP to decrease bacterial dissemination. Additional mice were subjected to cecal ligation without puncture of the cecal wall or cecal ligation and removal of cecal contents. Imipenem treatment decreased bacterial counts by at least two orders of magnitude. However, all wild-type mice, whether treated with saline or imipenem, died by 42 h after CLP and exhibited significant hypothermia, metabolic acidosis, and high plasma cytokine concentrations. Wild-type mice subjected to cecal ligation without puncture also died, despite very low bacterial counts in blood, but wild-type mice subjected to cecal ligation and washout of cecal contents survived. In CD8KO/alphaAsGM1 mice subjected to CLP, imipenem treatment increased survival from 50% to 100%. After cecal ligation without puncture, long-term survival was 80-90% in CD8KO/alphaAsGM1 mice. Hypothermia, metabolic acidosis, and cytokine production were attenuated in CD8KO/alphaAsGM1 mice compared with wild-type controls. These results indicate that bacterial dissemination is not a major source of injury in wild-type mice after CLP, but the presence of gut flora in the cecal lumen is required for induction of systemic inflammation after cecal injury. CD8KO/alphaAsGM1 mice are resistant to the systemic manifestations of cecal injury.
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17 MeSH Terms
Hemodynamic and cardiac contractile function during sepsis caused by cecal ligation and puncture in mice.
Tao W, Deyo DJ, Traber DL, Johnston WE, Sherwood ER
(2004) Shock 21: 31-7
MeSH Terms: Animals, Blood Pressure, Body Temperature, Cardiovascular Physiological Phenomena, Cecum, Disease Models, Animal, Female, Hot Temperature, Ligation, Mice, Mice, Inbred C57BL, Myocardial Contraction, Myocardium, Peritonitis, Pressure, Punctures, Sepsis, Time Factors, Ventricular Function, Left
Show Abstract · Added October 18, 2015
Sepsis is among the leading causes of death in the critically ill, yet the pathophysiology of sepsis is incompletely understood. Genetically engineered mice offer a unique opportunity to explore the cellular and molecular pathogenesis of sepsis. However, the hemodynamic responses of mice during sepsis are not completely understood because of the difficulty in performing cardiovascular measurements in mice. We used a 1.4-F pressure and conductance catheter to measure hemodynamics in wild-type C57BL/6J mice during sepsis caused by cecal ligation and puncture. Septic mice exhibited significant hypothermia compared with the sham group. In addition, there was a progressive decrease in mean arterial blood pressure and systemic vascular resistance in septic mice as well as an increase in stroke volume and cardiac output. Sepsis also caused a significant time-dependent impairment of left ventricular function as indicated by decreased dp/dtmax and dp/dtmin. The slope of end systolic pressure volume relationship also decreased over time, as did the time varying maximum elastance and preload-recruitable stroke work of the left ventricle. In conclusion, septic mice exhibit hemodynamic alterations during sepsis that are similar to those observed in humans. The miniaturized conductance catheter allows for effective measurements of hemodynamic function in septic mice and provides measurements that cannot be obtained using other cardiovascular monitoring techniques.
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19 MeSH Terms
Beta 2 microglobulin knockout mice are resistant to lethal intraabdominal sepsis.
Sherwood ER, Lin CY, Tao W, Hartmann CA, Dujon JE, French AJ, Varma TK
(2003) Am J Respir Crit Care Med 167: 1641-9
MeSH Terms: Adoptive Transfer, Animals, CD8-Positive T-Lymphocytes, Cecum, Disease Models, Animal, Female, G(M1) Ganglioside, Immunity, Innate, Inflammation, Killer Cells, Natural, Ligation, Lymphopenia, Mice, Mice, Inbred C57BL, Mice, Knockout, Peritonitis, Sepsis, Survival Analysis, beta 2-Microglobulin
Show Abstract · Added October 18, 2015
beta 2 microglobulin knockout (beta2M-/-) mice lack CD8+ T and natural killer T cells. We hypothesized that beta 2M-/- mice are resistant to lethal intraabdominal sepsis. To test this hypothesis, mortality, cytokine production, and physiologic function were assessed in beta 2M-/- mice during sepsis caused by cecal ligation and puncture (CLP). beta 2M-/- mice survived significantly longer than wild-type mice after CLP but ultimately exhibited 100% mortality. Treatment of beta 2M-/- mice with anti-asialoGM1 to deplete natural killer cells conferred greater than 70% long-term survival. Compared with wild-type mice, beta 2M-/- mice treated with anti-asialoGM1 produced decreased amounts of proinflammatory cytokines and did not exhibit hypothermia or metabolic acidosis after CLP. Adoptive transfer of CD8+ T and natural killer cells into beta 2M-/- mice treated with anti-asialoGM1 re-established CLP-induced mortality. CD8 knockout mice treated with anti-asialoGM1, which are specifically deficient in CD8+ T and natural killer cells, exhibited 40% long-term survival after CLP. Furthermore, treatment of wild-type mice with antibodies to CD8 and asialoGM1 conferred a significant survival benefit compared with wild-type mice treated with nonspecific IgG. These findings demonstrate that beta 2M-/- mice treated with anti-asialoGM1 are resistant to CLP-induced mortality and that depletion of CD8+ T and natural killer cells largely accounts for the survival benefit observed in these mice.
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19 MeSH Terms
Impact of chronic fructose infusion on hepatic metabolism during TPN administration.
Donmoyer CM, Lacy DB, Zhang Y, Chen SS, McGuinness OP
(2002) Am J Physiol Endocrinol Metab 283: E1151-8
MeSH Terms: Alanine, Animals, Blood Glucose, Catheterization, Dogs, Escherichia coli Infections, Fatty Acids, Nonesterified, Fructose, Glucagon, Glucose, Hemodynamics, Hepatic Artery, Hormones, Infusions, Intravenous, Insulin, Lactic Acid, Liver, Parenteral Nutrition, Total, Peritonitis, Portal Vein, Time, Vena Cava, Inferior
Show Abstract · Added December 10, 2013
During chronic total parenteral nutrition (TPN), net hepatic glucose uptake (NHGU) is markedly elevated. However, NHGU is reduced by the presence of an infection. We recently demonstrated that a small, acute (3-h) intraportal fructose infusion can correct the infection-induced impairment in NHGU. The aim of this study was to determine whether the addition of fructose to the TPN persistently enhances NHGU in the presence of an infection. TPN was infused continuously into the inferior vena cava of chronically catheterized dogs for 5 days. On day 3, a bacterial clot was implanted in the peritoneal cavity, and either saline (CON, n = 5) or fructose (+FRUC, 1.0 mg. kg(-1). min(-1), n = 6) infusion was included with the TPN. Forty-two hours after the infection was induced, hepatic glucose metabolism was assessed in conscious dogs with arteriovenous and tracer methods. Arterial plasma glucose concentration was lower with chronic fructose infusion (120 +/- 4 vs. 131 +/- 3 mg/dl, +FRUC vs. CON, P < 0.05); however, NHGU was not enhanced (2.2 +/- 0.5 vs. 2.8 +/- 0.4 mg. kg(-1). min(-1)). Acute removal of the fructose infusion dramatically decreased NHGU (2.2 +/- 0.5 to -0.2 +/- 0.5 mg. kg(-1). min(-1)), and net hepatic lactate release also fell (1.6 +/- 0.3 to 0.5 +/- 0.3 mg. kg(-1). min(-1)). This led to an increase in the arterial plasma glucose (Delta13 +/- 3 mg/dl, P < 0.05) and insulin (Delta5 +/- 2 micro U/ml) concentrations and to a decrease in glucagon (Delta-11 +/- 3 pg/ml) concentration. In conclusion, the addition of chronic fructose infusion to TPN during infection does not lead to a persistent augmentation of NHGU.
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22 MeSH Terms
Indications for vancomycin in dialysis patients.
Golper TA, Schulman G, D'Agata EM
(2000) Semin Dial 13: 389-92
MeSH Terms: Anti-Bacterial Agents, Bacteremia, Humans, Peritoneal Dialysis, Peritonitis, Prosthesis-Related Infections, Renal Dialysis, Vancomycin
Show Abstract · Added August 7, 2015
Resistance to vancomycin has emerged among Staphylococcus aureus, coagulase-negative staphylococci (CNS), and enterococci, and this emergence has particular prevalence in dialysis units. It has therefore become imperative that physicians use vancomycin judiciously. General recommendations regarding the appropriate use of vancomycin have been developed. Although in theory implementation of these guidelines should not be difficult, the medical community may be unable or unwilling to make the necessary adjustments in practice. The onslaught of cost constraints and bureaucratic encumbrance has occurred simultaneously with the increase in vancomycin resistance among pathogens commonly isolated among the dialysis population. When a patient responds to empiric antibiotic therapy and susceptibility data indicate that an antibiotic other than vancomycin would be appropriate, the clinician far too often does not make the change to this alternative. Previously there was no biological imperative to change the antibiotic. That complacency has infected an entire generation of physicians, and especially nephrologists. Furthermore, there is an active movement against change, driven by concerns such as malpractice accusations and frank errors in the interpretation of medical facts.
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8 MeSH Terms