Professor, Medicine, University of Louisville School of Medicine
Nephrology
Dr. Kenneth McLeish, MD
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Kenneth McLeish is an expert in the field of Nephrology. He went to Indiana University School of Medicine. Indiana University School of Medicine has a rank of 45 in research and a 47 in primary care Kenneth McLeish has written publications. He has 101 publications published with PubMed. The lastest publication is: 'Bacterial phagocytosis activates extracellular signal-regulated kinase and p38 mitogen-activated protein kinase cascades in human neutrophils.' Kenneth McLeish is registered with Medicare and accepts Medicare payments.
Publications
- TAT-SNAP-23 treatment inhibits the priming of neutrophil functions contributing to shock and/or sepsis-induced extra-pulmonary Acute lung injury.
- The Pore-Forming Toxin Listeriolysin O Is Degraded by Neutrophil Metalloproteinase-8 and Fails To Mediate Listeria monocytogenes Intracellular Survival in Neutrophils.
- Technical note: proteomic approaches to fundamental questions about neutrophil biology.
- Inhibition of neutrophil exocytosis ameliorates Acute lung injury in rats.
- Failure of plasma exchange and immunosuppression to improve renal function in Goodpasture''s syndrome.
- Regulation of G-protein-mediated signal transfer by ions.
- Massive post-transplant proteinuria With minimal histological changes.
- Variable susceptibility to immune complex Glomerulonephritis among mice sharing the same major histocompatibility complex.
- Mechanism by which methylprednisolone inhibits Acute immune complex-induced changes in vascular permeability.
- Prostaglandin E1 therapy of murine Chronic serum sickness.
- Alteration in immune complex Glomerulonephritis by arachidonic acid.
- Regulation of oxygen radical release from murine peritoneal macrophages by pharmacologic doses of PGE2.
- Serial changes in humoral and cellular immunity induced by prostaglandin E2 treatment of murine immune complex Glomerulonephritis.
- Rapidly progressive Glomerulonephritis in adults: clinical and histologic correlations.
- Treatment of murine immune complex Glomerulonephritis with prostaglandin E2: dose--response of immune complex deposition, antibody synthesis, and glomerular damage.
- Rapid degradation of NAD by retinoic acid-differentiated HL-60 granulocyte membranes prevents ADP ribosylation.
- Chronic serum sickness in the mouse. Relationship of antigen dose to glomerular pathology.
- Effect of cyclosporine on glomerular prostaglandin production.
- Evidence that activation of a common G-protein by receptors for leukotriene B4 and N-formylmethionyl-leucyl-phenylalanine in HL-60 cells occurs by different mechanisms.
- Body fat and the activity of the autonomic nervous system.
- Differential cholera-toxin- and pertussis-toxin-catalysed ADP-ribosylation of G-proteins coupled to formyl-peptide and leukotriene B4 receptors.
- Hypertrophic cardiomyopathy: an acquired disorder of end-stage Renal disease.
- Potential mechanisms of cytosolic Calcium modulation in interferon-gamma treated U937 cells.
- Suppression of antibody synthesis by prostaglandin E as a mechanism for preventing murine immune complex Glomerulonephritis.
- A simultaneous flow cytometric measurement of neutrophil phagocytosis and oxidative burst in whole blood.
- Desensitization uncouples the formyl peptide receptor-guanine nucleotide-binding protein interaction in HL60 cells.
- Mechanism of prostaglandin E2 inhibition of Acute changes in vascular permeability.
- Biochemical basis of HLA-DR and CR3 modulation on human peripheral blood monocytes by lipopolysaccharide.
- Alterations in select immunologic parameters following total artificial Heart implantation.
- Use of OKT3 monoclonal antibody in the treatment of Acute cardiac allograft rejection.
- Quantitative and qualitative differences in guanine nucleotide binding protein activation by formyl peptide and leukotriene B4 receptors.
- Role of intracellular Calcium in priming of human peripheral blood monocytes by bacterial lipopolysaccharide.
- Differential uncoupling of chemoattractant receptors from G proteins in retinoic acid-differentiated HL-60 granulocytes.
- Polymorphonuclear leukocyte function during hemodialysis: relationship to complement activation.
- P2 purinoceptor stimulation attenuates PTH inhibition of phosphate uptake by a G protein-dependent mechanism.
- Interferon-gamma enhances superoxide production by HL-60 cells stimulated With multiple agonists.
- Bacterial lipopolysaccharide enhances polymorphonuclear leukocyte function independent of changes in intracellular Calcium.
- IFN-gamma enhances expression of formyl peptide receptors and guanine nucleotide-binding proteins by HL-60 granulocytes.
- Role of carboxylmethylation in chemoattractant receptor-stimulated G protein activation and functional responses.
- TNF-alpha stimulates increased plasma membrane guanine nucleotide binding protein activity in polymorphonuclear leukocytes.
- Modulation of transmembrane signalling in HL-60 granulocytes by tumour necrosis factor-alpha.
- Deficient homologous desensitization of formyl peptide receptors stably expressed in undifferentiated HL-60 cells.
- Chemoattractant receptor-specific differences in G protein activation rates regulate effector enzyme and functional responses.
- The Calcium-sensing receptor stimulates JNK in MDCK cells.
- The Calcium-sensing receptor regulates Calcium absorption in MDCK cells by inhibition of PMCA.
- Role of isoprenoid Metabolism in chemotactic peptide receptor-mediated G protein activation.
- Priming of the HL-60 cell respiratory burst response by tumor necrosis factor-alpha.
- Desensitization by protein kinase C activation differentially uncouples formyl peptide receptors from effector enzymes in HL-60 granulocytes.
- TNF translationally modulates the expression of G1 protein alpha(i2) subunits in human polymorphonuclear leukocytes.
- Effect of prenylcysteine analogues on chemoattractant receptor-mediated G protein activation.
- Dopamine regulates phosphate uptake by opossum Kidney cells through multiple counter-regulatory receptors.
- Polymorphonuclear leukocyte oxidative burst is enhanced in patients with Chronic renal insufficiency.
- Influence of suspension on the oxidative burst by rat neutrophils.
- Interferon-gamma induces phosphorylation of multiple small-molecular-weight proteins in U937 cells.
- Effect of gamma subunit carboxyl methylation on the interaction of G protein alpha subunits With beta gamma subunits of defined composition.
- Role of extracellular signal-regulated kinase and phosphatidylinositol-3 kinase in chemoattractant and LPS delay of constitutive neutrophil apoptosis.
- Transplantation, not dialysis, corrects azotemia-dependent priming of the neutrophil oxidative burst.
- Bacterial phagocytosis activates extracellular signal-regulated kinase and p38 mitogen-activated protein kinase cascades in human neutrophils.
- Activation of mitogen-activated protein kinase cascades during priming of human neutrophils by TNF-alpha and GM-CSF.
- Activation of mitogen-activated protein kinases by formyl peptide receptors is regulated by the cytoplasmic tail.
- Role of intracellular Calcium concentration and protein kinase C activation in IFN-gamma stimulation of U937 cells.
- Soluble TNF alpha receptors are increased in Chronic renal insufficiency and hemodialysis and inhibit neutrophil priming by TNF alpha.
- Azotemia, TNF alpha, and LPS prime the human neutrophil oxidative burst by distinct mechanisms.
- p38 Kinase-dependent MAPKAPK-2 activation functions as 3-phosphoinositide-dependent kinase-2 for Akt in human neutrophils.
- Priming of the neutrophil respiratory burst involves p38 mitogen-activated protein kinase-dependent exocytosis of flavocytochrome b558-containing granules.
- Differential mitogen-activated protein kinase stimulation by Fc gamma receptor IIa and Fc gamma receptor IIIb determines the activation phenotype of human neutrophils.
- Granulocyte-macrophage colony-stimulating factor delays neutrophil constitutive apoptosis through phosphoinositide 3-kinase and extracellular signal-regulated kinase p...
- Parathyroid hormone stimulates extracellular signal-regulated kinase (ERK) activity through two independent signal transduction pathways: role of ERK in sodium-phospha...
- Formyl peptide receptors are coupled to multiple mitogen-activated protein kinase cascades by distinct signal transduction pathways: role in activation of reduced nico...
- Hemodialysis With cellulose membranes primes the neutrophil oxidative burst.
- Writing a first grant proposal.
- Granule Exocytosis Contributes to Priming and Activation of the Human Neutrophil Respiratory Burst.
- Identification of phosphoproteins associated With human neutrophil granules following chemotactic peptide stimulation.
- Application of proteomics to neutrophil biology.
- Counterregulation of clathrin-mediated endocytosis by the actin and microtubular cytoskeleton in human neutrophils.
- Anti-proteinase 3 antibodies both stimulate and prime human neutrophils.
- Comparison of proteins expressed on secretory vesicle membranes and plasma membranes of human neutrophils.
- Proteomic analysis defines altered cellular redox pathways and advanced glycation end-product Metabolism in glomeruli of db/db diabetic mice.
- Proteomic identification and immunolocalization of increased Renal calbindin-D28k expression in OVE26 diabetic mice.
- Heat shock protein 27 regulates neutrophil chemotaxis and exocytosis through two independent mechanisms.
- The actin cytoskeleton regulates exocytosis of all neutrophil granule subsets.
- Proteomic analysis of human neutrophils.
- A proteomic screen identified stress-induced chaperone proteins as targets of Akt phosphorylation in mesangial cells.
- Proteomic analysis of human neutrophil granules.
- Myeloid-related protein-14 is a p38 MAPK substrate in human neutrophils.
- Gamma-amino butyric acid type B receptors stimulate neutrophil chemotaxis during ischemia-reperfusion.
- p38 MAPK/HSP25 signaling mediates cadmium-induced contraction of mesangial cells and Renal glomeruli.
- Parathyroid hormone-mediated regulation of Na+-K+-ATPase requires ERK-dependent translocation of protein kinase Calpha.
- Defining mitogen-activated protein kinase pathways With mass spectrometry-based approaches.
- Methylglyoxal: a stimulus to neutrophil oxygen radical production in chronic renal Failure?
- Alterations in the Renal elastin-elastase system in type 1 diabetic nephropathy identified by proteomic analysis.
- Urinary proteomics and biomarker discovery for glomerular Diseases.
- Proteomic approach to identification of novel kinase substrates in mesangial cells.
- Proteomics and diabetic Nephropathy.
- MAPK-activated protein kinase-2 participates in p38 MAPK-dependent and ERK-dependent functions in human neutrophils.
- Proteomic identification of 14-3-3zeta as a mitogen-activated protein kinase-activated protein kinase 2 substrate: role in dimer formation and ligand binding.
- Identification of the p16-Arc subunit of the Arp 2/3 complex as a substrate of MAPK-activated protein kinase 2 by proteomic analysis.
- Heat shock protein 27 controls apoptosis by regulating Akt activation.
- Akt phosphorylates p47phox and mediates respiratory burst activity in human neutrophils.
- Oxidant stress in hemodialysis patients: what are the determining factors?
Schools
Indiana University School Of Medicine
Indiana University Medical Center
Procedures Preformed
- Hemodialysis
- Peritoneal Dialysis
Conditions Treated
- Acidosis
- Acute Kidney Failure
- Calcium Metabolism Disorders
- Chronic Glomerulonephritis
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Doctors Specialties
- Nephrology
Accepted Insurances
Education
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Indiana University School of Medicine -
Brigham and Women's Hospital
Hospital
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Jewish Hospital -
Norton Hospital -
University of Louisville Hospital
Drug Facts
| NPI NUMBER | 1023099066 | |
| NPPES Provider LastName | MCLEISH | |
| NPPES Provider FirstName | KENNETH | |
| NPPES Provider ZIPCode | 402021715 | |
| NPPES Provider State | KY | |
| Specialty Description | Nephrology | |
| Total Claim Count | 184.0 | |
| Distinct Opioid Count | 0.0 | |
| Opioid Claim Count | 0.0 | |
| Percent Opioid Claims | 0.0 |
Helpful Reviews
Medicare Facts
| National Provider Identifier [NPI] | 1023099066 |
| Last Name Of The Provider | MCLEISH |
| First Name Of The Provider | KENNETH |
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