Babette Weksler - Academia.edu (original) (raw)

Papers by Babette Weksler

Research paper thumbnail of Expression of inflammatory genes induced by beta-amyloid peptides in human brain endothelial cells and in Alzheimer's brain is mediated by the JNK-AP1 signaling pathway

Neurobiology of Disease, Mar 18, 2009

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Research paper thumbnail of Abstract 8987: Prostacyclin Reduction Upregulates Tissue Factor and Predisposes COX-2 Knockout Mice to Thrombosis

Circulation, Nov 22, 2011

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Research paper thumbnail of Levels of Cyclooxygenase-2 Are Increased in the Oral Mucosa of Smokers: Evidence for the Role of Epidermal Growth Factor Receptor and Its Ligands

Cancer Research, Jan 15, 2005

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Research paper thumbnail of Acquired high-titer factor VIII inhibitor: fatal bleeding despite multimodal treatment including rituximab preceded by multiple plasmaphereses. Authors' reply

Blood, May 1, 2003

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Research paper thumbnail of Isolation and characterization of human bone marrow microvascular endothelial cells: hematopoietic progenitor cell adhesion

Blood, Jul 1, 1994

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Research paper thumbnail of Aging favors arteriosclerosis through dysregulation of growth factors for smooth muscle cell prolife

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Research paper thumbnail of Potentially Reduced Exposure Cigarettes Accelerate Atherosclerosis: Evidence for the Role of Nicotine

Cardiovasc Toxicol, 2007

The tobacco industry markets potentially reduced exposure products (PREPs) as less harmful or add... more The tobacco industry markets potentially reduced exposure products (PREPs) as less harmful or addictive alternatives to conventional cigarettes. This study compared the effects of mainstream smoke from Quest, Eclipse, and 2R4F reference cigarettes on the development of atherosclerosis in apolipoprotein E-deficient (apoE -/-) mice. Mice were exposed to smoke from four cigarette types for 12 weeks beginning at age of 12 weeks, and in a separate study for 8 weeks, beginning at age of 8 weeks. In both studies, mice exposed to smoke from high-nicotine, high-tar Quest 1, and 2R4F cigarettes developed greater areas of lipid-rich aortic lesions than did non-smoking controls. Exposure to smoke from the lower-nicotine products, Eclipse, and Quest 3, was associated with smaller lesion areas, but animals exposed to smoke from all of the tested types of cigarette had larger lesions than did control animals not exposed to smoke. Urinary levels of isoprostane F2 alpha VI, increased proportionally to cigarette nicotine yield, whereas induction of pulmonary cytochrome P4501A1 was proportional to tar yield. Lesion area was associated with both nicotine and tar yields, although in multiple regression analysis only nicotine was a significant predictor of lesion area. Smoke exposure did not alter systolic blood pressure (SBP), heart rate (HR), blood cholesterol, or leukocyte count. Taken together, these observations suggest that smoking may accelerate atherosclerosis by increasing oxidative stress mediated at least in part via the actions of nicotine.

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Research paper thumbnail of A rapid fluorometric DNA assay for the measurement of cell density and proliferation in vitro

In Vitro Cellular Developmental Biology Plant, Feb 29, 1988

Many research efforts require the accurate determination of cell density in vitro. However, physi... more Many research efforts require the accurate determination of cell density in vitro. However, physical cell counting is inaccurate, time-intensive and requires removal of the cells from their growth environment, thereby introducing a host of potential artifacts. The current studies document a very simple method of determining cell density in microtiter wells via DNA-enhanced fluorescence. Fixed cells are stained with the A-T intercalating DNA stains DAPI or Hoechst 33342 and then fluorescence is quantified in a plate fluorometer. Fluorescence is shown to be linearly related to cell density as determined by two physical counting methods. The validity of the method is established in determining serum-stimulated growth of smooth muscle cells and in mitogen-induced growth of endothelial cells. The fixed cells can be stored for prolonged periods, thus allowing time-course proliferation assays without interassay variations. The fixed cells are also suitable for determinations of antigens of interest by ELISA. This method is potentially valuable in many in vitro systems where the quantification of cell density and proliferation is necessary.

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Research paper thumbnail of Effects of Transforming Growth Factor-β1 on Human Vocal Fold Fibroblasts

The Annals of Otology Rhinology Laryngology, 2009

Objectives: We studied the effect of transforming growth factor (TGF)-β on immortalized human voc... more Objectives: We studied the effect of transforming growth factor (TGF)-β on immortalized human vocal fold fibroblasts. Methods: Normal human vocal fold fibroblasts were subjected to sequential lentiviral transduction with genes for human telomerase (hTERT) and SV40 large T ...

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Research paper thumbnail of PD.163 Induction of COX-2 in the oral cavity ofsmokers. Evidence for crosstalk between COX-2 and EGFR

Oral Oncology Supplement, 2005

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Research paper thumbnail of Transcription of cyclooxygenase-2 is enhanced in transformed mammary epithelial cells

Cancer Research, Jan 10, 1996

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Research paper thumbnail of Enzymatic conversion of prostaglandin endoperoxide H2 and arachidonic acid to prostacyclin by cultured human endothelial cells

Journal of Biological Chemistry, Oct 25, 1978

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Research paper thumbnail of Collagen and glomerular membrane effects on platelets

Transactions - American Society for Artificial Internal Organs

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Research paper thumbnail of Antiplatelet agents in stroke prevention: Combination therapy: Present and future

Cerebrovascular Diseases

Platelets contribute to arterial thrombosis by multiple mechanisms that promote blood clotting, f... more Platelets contribute to arterial thrombosis by multiple mechanisms that promote blood clotting, favor vasoconstriction, activate the procoagulant capacity of endothelium, and stimulate inflammation. These activities are augmented by turbulent blood flow. Classic antiplatelet therapy with aspirin to prevent occlusive stroke offers significant clinical benefit (20-25% risk reduction), yet is less effective than in prevention of coronary artery occlusion (up to 50% risk reduction of myocardial infarction in unstable angina). Since aspirin's antiplatelet effects are limited to blocking a single metabolic pathway - namely inhibition of thromboxane A(2) formation -, and aspirin fails to alter platelet adhesion, other antiplatelet agents that target ADP receptors, platelet surface glycoproteins (such as the GPIIb/IIIa complex), or platelet-dependent thrombin generation offer additional clinical benefits by blocking additional separate pathways or the final common pathway of platelet activation. Combinations of antiplatelet agents, such as aspirin/dipyridamole, aspirin/clopidogrel, or aspirin/GPIIb/IIIa inhibitors, have recently been tested for improved efficacy in clinical trials. Soluble recombinant CD39, an ecto-ADPase, protects against stroke in animal models by metabolizing released ADP/ATP to antiplatelet derivatives. In general, combinations of antiplatelet agents promise greater efficacy than single drugs in preventing stroke, since interactions among different antiplatelet mechanisms can be synergistic. However, such combinations may also increase the risk of bleeding, so that precise understanding of risk/benefit ratios that address the possibility of intracranial as well as gastrointestinal bleeding will require careful monitoring in large clinical trials of patients at risk of stroke, with particular attention to the elderly.

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Research paper thumbnail of 2 Macroglobulin/Transforming Growth Factor?1 Interactions.: Modulation by Heparin-like Molecules and Effects on Vascular Smooth Muscle Cells a

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Research paper thumbnail of Alpha 2-macroglobulin/transforming growth factor-beta 1 interactions. Modulation by heparin-like molecules and effects on vascular smooth muscle cells

Annals of the New York Academy of Sciences

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Research paper thumbnail of Production of prostaglandin E2 induced by cigarette smoke modulates tissue factor expression and activity in endothelial cells

FASEB journal : official publication of the Federation of American Societies for Experimental Biology, Jan 11, 2015

Cigarette smoke (CS) increases the incidence of atherothrombosis, the release of prostaglandin (P... more Cigarette smoke (CS) increases the incidence of atherothrombosis, the release of prostaglandin (PG) E2, and the amount of tissue factor (TF). The link between PGE2 and TF, and the impact of this interaction on CS-induced thrombosis, is unknown. Plasma from active smokers (AS) showed higher concentration of PGE2, TF total antigen and microparticle-associated TF (MP-TF) activity compared with never smokers (NS). Similar results were obtained in mice and in endothelial cells (MCEC) after treatment with aqueous CS extracts (CSEs) plus IL-1β [CSE (6.4 puffs/L)/IL-1β (2 μg/L)]. A significant correlation between PGE2 and TF total antigen or MP-TF activity were observed in both human and mouse plasma or tissue. Inhibition of PGE synthase (PGES) reduced TF in vivo and in vitro and prevented the arterial thrombosis induced by CSE/IL-1β. Only PG E receptor (EP) 1 receptor antagonists (SC51089:IC50 ∼ 1 μM, AH6809:IC50 ∼ 7.5 μM) restored the normal TF and sirtuin 1 (SIRT1) levels in MCEC before ...

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Research paper thumbnail of Regulatory Mechanisms in Prostacyclin-Blood Vessel Interactions

Prostaglandins, Leukotrienes, and Lipoxins, 1985

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Research paper thumbnail of Synthesis of Prostacyclin by Cultured Endothelial Cells

Pathobiology of the Endothelial Cell, 1982

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Research paper thumbnail of CD40-ligand stimulates myelopoiesis by regulating flt3-ligand and thrombopoietin production in bone marrow stromal cells

Blood, Jan 15, 2000

CD40 ligand (CD40L)/CD40 interactions play a central role in T-cell-dependent B-cell activation a... more CD40 ligand (CD40L)/CD40 interactions play a central role in T-cell-dependent B-cell activation as previously shown by in vitro studies, the phenotype of CD40L knockout mice and the defective expression of CD40L in patients who have X-linked immunodeficiency with hyper-IgM. The distribution of CD40 in cells other than of myeloid and lymphoid lineages has suggested additional functions for this receptor/ligand couple. Here we show that CD40L stimulates myelopoiesis with a noticeable effect on megakaryocytopoiesis in cocultures of hematopoietic progenitor cells and bone marrow stromal cells. These results suggest a mechanism by which T-cell or platelet-associated or soluble CD40L may regulate myelopoiesis. (Blood. 2000;95:3758-3764)

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Research paper thumbnail of Expression of inflammatory genes induced by beta-amyloid peptides in human brain endothelial cells and in Alzheimer's brain is mediated by the JNK-AP1 signaling pathway

Neurobiology of Disease, Mar 18, 2009

Bookmarks Related papers MentionsView impact

Research paper thumbnail of Abstract 8987: Prostacyclin Reduction Upregulates Tissue Factor and Predisposes COX-2 Knockout Mice to Thrombosis

Circulation, Nov 22, 2011

Bookmarks Related papers MentionsView impact

Research paper thumbnail of Levels of Cyclooxygenase-2 Are Increased in the Oral Mucosa of Smokers: Evidence for the Role of Epidermal Growth Factor Receptor and Its Ligands

Cancer Research, Jan 15, 2005

Bookmarks Related papers MentionsView impact

Research paper thumbnail of Acquired high-titer factor VIII inhibitor: fatal bleeding despite multimodal treatment including rituximab preceded by multiple plasmaphereses. Authors' reply

Blood, May 1, 2003

Bookmarks Related papers MentionsView impact

Research paper thumbnail of Isolation and characterization of human bone marrow microvascular endothelial cells: hematopoietic progenitor cell adhesion

Blood, Jul 1, 1994

Bookmarks Related papers MentionsView impact

Research paper thumbnail of Aging favors arteriosclerosis through dysregulation of growth factors for smooth muscle cell prolife

Bookmarks Related papers MentionsView impact

Research paper thumbnail of Potentially Reduced Exposure Cigarettes Accelerate Atherosclerosis: Evidence for the Role of Nicotine

Cardiovasc Toxicol, 2007

The tobacco industry markets potentially reduced exposure products (PREPs) as less harmful or add... more The tobacco industry markets potentially reduced exposure products (PREPs) as less harmful or addictive alternatives to conventional cigarettes. This study compared the effects of mainstream smoke from Quest, Eclipse, and 2R4F reference cigarettes on the development of atherosclerosis in apolipoprotein E-deficient (apoE -/-) mice. Mice were exposed to smoke from four cigarette types for 12 weeks beginning at age of 12 weeks, and in a separate study for 8 weeks, beginning at age of 8 weeks. In both studies, mice exposed to smoke from high-nicotine, high-tar Quest 1, and 2R4F cigarettes developed greater areas of lipid-rich aortic lesions than did non-smoking controls. Exposure to smoke from the lower-nicotine products, Eclipse, and Quest 3, was associated with smaller lesion areas, but animals exposed to smoke from all of the tested types of cigarette had larger lesions than did control animals not exposed to smoke. Urinary levels of isoprostane F2 alpha VI, increased proportionally to cigarette nicotine yield, whereas induction of pulmonary cytochrome P4501A1 was proportional to tar yield. Lesion area was associated with both nicotine and tar yields, although in multiple regression analysis only nicotine was a significant predictor of lesion area. Smoke exposure did not alter systolic blood pressure (SBP), heart rate (HR), blood cholesterol, or leukocyte count. Taken together, these observations suggest that smoking may accelerate atherosclerosis by increasing oxidative stress mediated at least in part via the actions of nicotine.

Bookmarks Related papers MentionsView impact

Research paper thumbnail of A rapid fluorometric DNA assay for the measurement of cell density and proliferation in vitro

In Vitro Cellular Developmental Biology Plant, Feb 29, 1988

Many research efforts require the accurate determination of cell density in vitro. However, physi... more Many research efforts require the accurate determination of cell density in vitro. However, physical cell counting is inaccurate, time-intensive and requires removal of the cells from their growth environment, thereby introducing a host of potential artifacts. The current studies document a very simple method of determining cell density in microtiter wells via DNA-enhanced fluorescence. Fixed cells are stained with the A-T intercalating DNA stains DAPI or Hoechst 33342 and then fluorescence is quantified in a plate fluorometer. Fluorescence is shown to be linearly related to cell density as determined by two physical counting methods. The validity of the method is established in determining serum-stimulated growth of smooth muscle cells and in mitogen-induced growth of endothelial cells. The fixed cells can be stored for prolonged periods, thus allowing time-course proliferation assays without interassay variations. The fixed cells are also suitable for determinations of antigens of interest by ELISA. This method is potentially valuable in many in vitro systems where the quantification of cell density and proliferation is necessary.

Bookmarks Related papers MentionsView impact

Research paper thumbnail of Effects of Transforming Growth Factor-β1 on Human Vocal Fold Fibroblasts

The Annals of Otology Rhinology Laryngology, 2009

Objectives: We studied the effect of transforming growth factor (TGF)-β on immortalized human voc... more Objectives: We studied the effect of transforming growth factor (TGF)-β on immortalized human vocal fold fibroblasts. Methods: Normal human vocal fold fibroblasts were subjected to sequential lentiviral transduction with genes for human telomerase (hTERT) and SV40 large T ...

Bookmarks Related papers MentionsView impact

Research paper thumbnail of PD.163 Induction of COX-2 in the oral cavity ofsmokers. Evidence for crosstalk between COX-2 and EGFR

Oral Oncology Supplement, 2005

Bookmarks Related papers MentionsView impact

Research paper thumbnail of Transcription of cyclooxygenase-2 is enhanced in transformed mammary epithelial cells

Cancer Research, Jan 10, 1996

Bookmarks Related papers MentionsView impact

Research paper thumbnail of Enzymatic conversion of prostaglandin endoperoxide H2 and arachidonic acid to prostacyclin by cultured human endothelial cells

Journal of Biological Chemistry, Oct 25, 1978

Bookmarks Related papers MentionsView impact

Research paper thumbnail of Collagen and glomerular membrane effects on platelets

Transactions - American Society for Artificial Internal Organs

Bookmarks Related papers MentionsView impact

Research paper thumbnail of Antiplatelet agents in stroke prevention: Combination therapy: Present and future

Cerebrovascular Diseases

Platelets contribute to arterial thrombosis by multiple mechanisms that promote blood clotting, f... more Platelets contribute to arterial thrombosis by multiple mechanisms that promote blood clotting, favor vasoconstriction, activate the procoagulant capacity of endothelium, and stimulate inflammation. These activities are augmented by turbulent blood flow. Classic antiplatelet therapy with aspirin to prevent occlusive stroke offers significant clinical benefit (20-25% risk reduction), yet is less effective than in prevention of coronary artery occlusion (up to 50% risk reduction of myocardial infarction in unstable angina). Since aspirin's antiplatelet effects are limited to blocking a single metabolic pathway - namely inhibition of thromboxane A(2) formation -, and aspirin fails to alter platelet adhesion, other antiplatelet agents that target ADP receptors, platelet surface glycoproteins (such as the GPIIb/IIIa complex), or platelet-dependent thrombin generation offer additional clinical benefits by blocking additional separate pathways or the final common pathway of platelet activation. Combinations of antiplatelet agents, such as aspirin/dipyridamole, aspirin/clopidogrel, or aspirin/GPIIb/IIIa inhibitors, have recently been tested for improved efficacy in clinical trials. Soluble recombinant CD39, an ecto-ADPase, protects against stroke in animal models by metabolizing released ADP/ATP to antiplatelet derivatives. In general, combinations of antiplatelet agents promise greater efficacy than single drugs in preventing stroke, since interactions among different antiplatelet mechanisms can be synergistic. However, such combinations may also increase the risk of bleeding, so that precise understanding of risk/benefit ratios that address the possibility of intracranial as well as gastrointestinal bleeding will require careful monitoring in large clinical trials of patients at risk of stroke, with particular attention to the elderly.

Bookmarks Related papers MentionsView impact

Research paper thumbnail of 2 Macroglobulin/Transforming Growth Factor?1 Interactions.: Modulation by Heparin-like Molecules and Effects on Vascular Smooth Muscle Cells a

Bookmarks Related papers MentionsView impact

Research paper thumbnail of Alpha 2-macroglobulin/transforming growth factor-beta 1 interactions. Modulation by heparin-like molecules and effects on vascular smooth muscle cells

Annals of the New York Academy of Sciences

Bookmarks Related papers MentionsView impact

Research paper thumbnail of Production of prostaglandin E2 induced by cigarette smoke modulates tissue factor expression and activity in endothelial cells

FASEB journal : official publication of the Federation of American Societies for Experimental Biology, Jan 11, 2015

Cigarette smoke (CS) increases the incidence of atherothrombosis, the release of prostaglandin (P... more Cigarette smoke (CS) increases the incidence of atherothrombosis, the release of prostaglandin (PG) E2, and the amount of tissue factor (TF). The link between PGE2 and TF, and the impact of this interaction on CS-induced thrombosis, is unknown. Plasma from active smokers (AS) showed higher concentration of PGE2, TF total antigen and microparticle-associated TF (MP-TF) activity compared with never smokers (NS). Similar results were obtained in mice and in endothelial cells (MCEC) after treatment with aqueous CS extracts (CSEs) plus IL-1β [CSE (6.4 puffs/L)/IL-1β (2 μg/L)]. A significant correlation between PGE2 and TF total antigen or MP-TF activity were observed in both human and mouse plasma or tissue. Inhibition of PGE synthase (PGES) reduced TF in vivo and in vitro and prevented the arterial thrombosis induced by CSE/IL-1β. Only PG E receptor (EP) 1 receptor antagonists (SC51089:IC50 ∼ 1 μM, AH6809:IC50 ∼ 7.5 μM) restored the normal TF and sirtuin 1 (SIRT1) levels in MCEC before ...

Bookmarks Related papers MentionsView impact

Research paper thumbnail of Regulatory Mechanisms in Prostacyclin-Blood Vessel Interactions

Prostaglandins, Leukotrienes, and Lipoxins, 1985

Bookmarks Related papers MentionsView impact

Research paper thumbnail of Synthesis of Prostacyclin by Cultured Endothelial Cells

Pathobiology of the Endothelial Cell, 1982

Bookmarks Related papers MentionsView impact

Research paper thumbnail of CD40-ligand stimulates myelopoiesis by regulating flt3-ligand and thrombopoietin production in bone marrow stromal cells

Blood, Jan 15, 2000

CD40 ligand (CD40L)/CD40 interactions play a central role in T-cell-dependent B-cell activation a... more CD40 ligand (CD40L)/CD40 interactions play a central role in T-cell-dependent B-cell activation as previously shown by in vitro studies, the phenotype of CD40L knockout mice and the defective expression of CD40L in patients who have X-linked immunodeficiency with hyper-IgM. The distribution of CD40 in cells other than of myeloid and lymphoid lineages has suggested additional functions for this receptor/ligand couple. Here we show that CD40L stimulates myelopoiesis with a noticeable effect on megakaryocytopoiesis in cocultures of hematopoietic progenitor cells and bone marrow stromal cells. These results suggest a mechanism by which T-cell or platelet-associated or soluble CD40L may regulate myelopoiesis. (Blood. 2000;95:3758-3764)

Bookmarks Related papers MentionsView impact