• KOL
    • Photodynamic Therapy
    • David H Kessel
    • David H Kessel: Influence Statistics

      David H Kessel

      David H Kessel

      Show email address

      Department of Pharmacology, Wayne State University School of Medicine, Detroit, MI 48201, USA. | Department of Pharmacology, Wayne State University School of Medicine, Detroit ...

      Is this your profile? manage_accounts Claim your profile content_copy Copy URL code Embed Link to your profile

      David H Kessel:Expert Impact

      Concepts for whichDavid H Kesselhas direct influence:Photodynamic therapy,Apoptotic response,Lysosomal photodamage,L1210 cells,Plasma lipoproteins,Ursodeoxycholic acid,Mitochondrial photodamage,Leukemia l1210.

      David H Kessel:KOL impact

      Concepts related to the work of other authors for whichfor which David H Kessel has influence:Photodynamic therapy,Cell death,Singlet oxygen,Autophagic flux,Oxidative stress,Breast cancer,Photosensitizing agents.

      KOL Resume for David H Kessel

      Year
      2022

      Department of Pharmacology, Wayne State University School of Medicine, Detroit, MI 48201, USA.

      2021

      Department of Pharmacology, Wayne State University School of Medicine, Detroit, MI 48201, USA

      2020

      Wayne State Univ. School of Medicine (United States)

      Department of Pharmacology, School of Medicine.

      2019

      Department of Pharmacology, Wayne State University School of Medicine, Detroit, MI 48201, USA.

      2018

      Wayne State University School of Medicine Detroit MI

      2017

      Department of Pharmacology Wayne State University School of Medicine Detroit MI

      2016

      Wayne State University Department of Pharmacology Detroit MI

      2015

      Department of Pharmacology, Wayne State University School of Medicine, 48201, Detroit, MI, USA

      2013

      Cancer Biology program Wayne State University School of Medicine Detroit MI

      2012

      Department of Pharmacology, Wayne State University School of Medicine, Detroit, MI 48201 (USA) phone: +001 313 577 1787

      Wayne State Univ. (USA)

      2011

      Department of Pharmacology, Wayne State University School of Medicine, 540 East Canfield Street, Detroit, MI 48201.

      2010

      Wayne State University School of Medicine, Cancer Biology Program and Department of Pharmacology, Detroit, Michigan, 48201

      2009

      Departments of Pharmacology and Medicine, Wayne State University School of Medicine, Detroit, MI

      2007

      Department of Pharmacology and Medicine, Wayne State University, School of Medicine, Detroit, MI

      David Kessel

      2006

      Departments of Pharmacology and Medicine, Wayne State University, Detroit, MI 48201, USA

      Department of Pharmacology, WSU School of Medicine, 540, E. Canfield St., Detroit MI 48201.

      2005

      Department of Pharmacology, Wayne State University School of Medicine, 540 E Canfield St, Detroit, MI 48201, USA

      2004

      Department of Pharmacology, Wayne State University School of Medicine, 540 E Canfield Street, Detroit, MI 48201, USA

      2003

      Wayne State Univ. School of Medicine (USA)

      2002

      Department of Pharmacology, Wayne State University School of Medicine, Detroit MI 48201, USA.

      2001

      WSU School of Medicine, Detroit, MI, USA

      2000

      Wayne State University Pharmacology Department, Detroit, Michigan, USA

      1999

      Department of Pharmacology, Wayne State University School of Medicine, 48201, Detroit, Michigan, USA

      1998

      Department of Pharmacology, Wayne State University, School of Medicine, Detroit, Ml, USA

      1997

      Department of Pharmacology, Wayne State University, Detroit, MI 48201, USA

      1996

      Department of Pharmacology, Wayne State University School of Medicine, 540 E. Canfield Street, Detroit, Michigan, 48201

      Wayne State University, School of Medicine, Detroit, MI, USA

      1995

      Department of Pharmacology, Wayne State University School of Medicine, 48201, Detroit, Michigan

      1994

      Department of Pharmacology, Wayne State University School of Medicine, Detroit, MI 48201

      1993

      Departments of Pharmacology and Medicine, Wayne State University School of Medicine, Detroit, MI 48201 USA

      1992

      b Michigan Cancer Foundation and Department of Pharmacology , Division of Hematology/Oncology, Wayne State University School of Medicine , P.O. Box 02188, Detroit , MI , 48202 , U.S.A.

      Wayne State University, Detroit, MI, USA

      1991

      Department of Pharmacology, Wayne State University, Detroit, Michigan 48201.

      1990

      Department of Pharmacology, Wayne State University School of Medicine, 48201, Detroit, Mi, USA

      1989

      Department of Pharmacology, Wayne State University School of Medicine, Detroit, MI 48201.

      Wayne State University (United States)

      1988

      Harper Hospital Detroit, MI 48201 USA

      Wayne State University, School of Medicine, Detroit, MI 48201 U.S.A.

      1987

      Departments of Medicine and Pharmacology, Wayne State University School of Medicine, Detroit, MI 48201, USA

      Wayne State University School of Medicine and Harper Hospital (United States)

      Sign-in to see all concepts, it's free!
      Sample of concepts for which David H Kessel is among the top experts in the world.
      Concept World rank
      cells porphycene concentrations #1
      interferometry characterization #1
      photosensitizing agents distribution #1
      nonpeptidic bcl2 ligand #1
      cell fragmentation cells #1
      e6 product #1
      ethanol delivery systems #1
      form herbicide analog #1
      monomeric hpd components #1
      experimental approaches elucidation #1
      lysyl analogs #1
      snet2h2 #1
      3p aminophenyl fluorescein #1
      porphyrin preparation #1
      sequential protocol photofrin #1
      chloro enamines ynamines #1
      iron complex presence #1
      cremophor concentrations cmc #1
      subsequent division cells #1
      parpcleavage assay #1
      shutdown tumor vasculature #1
      contrast dadpo #1
      murine leukemia cells #1
      bcl2 photodamage target #1
      experimental adr #1
      vivo effectiveness compounds #1
      apoptosis subcellular sites #1
      purpurins nt2 #1
      spectrometry hpd #1
      cpo rapid activation #1
      camptothecin formation #1
      cremophor drug formulation #1
      oligomeric hematoporphyrin #1
      autophagy lethal consequences #1
      vinblastine daunorubicin accumulation #1
      effects photodynamic therapy #1
      insertion polarizers #1
      extensive lysosomal photodamage #1
      paraptosis efficacy #1
      dimer oligomer fraction #1
      photodamaged lysosomes #1
      hematoporphyrin‐derived #1
      detroit inhibitor #1
      cmc p388 #1
      wavelength pathway #1
      hematoporphyrin residues #1
      agent cell types #1
      mitochondria lysosomes initiates #1
      apoptotic effects photodamage #1
      cell lysis presence #1
      Sign-in to see all concepts, it's free!

      Prominent publications by David H Kessel

      KOL-Index: 10402

      Photodynamic therapy (PDT) protocols employing lysosomal sensitizers induce apoptosis via a mechanism that causes cytochrome c release prior to loss of mitochondrial membrane potential (ΔΨm). The current study was designed to determine how lysosomal photodamage initiates mitochondrial-mediated apoptosis in murine hepatoma 1c1c7 cells. Fluorescence microscopy demonstrated that the photosensitizer N-aspartyl chlorin e6 (NPe6) localized to the lysosomes. Irradiation of cultures preloaded ...

      Known for Bid Cleavage | Release Cytochrome | Lysosomal Photodamage | 8 Caspase | Fluorescence Microscopy
      KOL-Index: 10203

      Research in autophagy continues to accelerate,(1) and as a result many new scientists are entering the field. Accordingly, it is important to establish a standard set of criteria for monitoring macroautophagy in different organisms. Recent reviews have described the range of assays that have been used for this purpose.(2,3) There are many useful and convenient methods that can be used to monitor macroautophagy in yeast, but relatively few in other model systems, and there is much ...

      Known for Higher Eukaryotes | Interpretation Assays | Monitoring Autophagy | Model Systems | Key Point
      KOL-Index: 8947

      Singlet oxygen (1O2) is the primary oxidant generated in photodynamic therapy (PDT) protocols involving sensitizers resulting in type II reactions. 1O2 can give rise to additional reactive oxygen species (ROS) such as the hydroxyl radical (*OH). The current study was designed to assess 3'-p-(aminophenyl) fluorescein (APF) and 3'-p-(hydroxyphenyl) fluorescein (HPF) as probes for the detection of 1O2 and *OH under conditions relevant to PDT. Cell-free studies indicated that both APF and ...

      Known for Hydroxyl Radical | Singlet Oxygen | Photodynamic Therapy | Formation Ros | Fluorescent Probes
      KOL-Index: 8303

      Photodynamic therapy (PDT) involves photosensitizing agents that, in the presence of oxygen and light, initiate formation of cytotoxic reactive oxygen species (ROS). PDT commonly induces both apoptosis and autophagy. Previous studies with murine hepatoma 1c1c7 cells indicated that loss of autophagy-related protein 7 (ATG7) inhibited autophagy and enhanced the cytotoxicity of photosensitizers that mediate photodamage to mitochondria or the endoplasmic reticulum. In this study, we examined ...

      Known for Cell Death | Lysosomal Photodamage | Photosensitizing Agents | Pdt Apoptosis | Autophagy Protein
      KOL-Index: 8111

      Irradiation of murine hepatoma 1c1c7 cultures presensitized with N-aspartyl chlorin e6 (NPe6) caused lysosomal disruption and apoptosis. Tao cells, a variant of the 1c1c7 line having lower aryl hydrocarbon receptor (AhR) contents, were resistant to the pro-apoptotic effects of NPe6 in the same photodynamic therapy protocol. Colony-forming assays were used to establish light dose-dependent and NPe6 concentration-dependent cytotoxicity curves. Lysosomal breakage and cell survival ...

      Known for Aryl Hydrocarbon | Murine Hepatoma | Tao Cells | Lysosomal Photosensitizer | Cell Lines
      KOL-Index: 8022

      BACKGROUND AND OBJECTIVES: This study was designed to examine modes of cell death after photodynamic therapy (PDT).

      STUDY DESIGN: Murine leukemia L1210 cells and human prostate Bax-deficient DU145 cells were examined after PDT-induced photodamage to the endoplasmic reticulum (ER). Phase contrast, fluorescence and electron microscopy were used to identify changes in cellular morphology, chromatin condensation, loss of mitochondrial membrane potential, and formation of phagolysosomes. ...

      Known for Photodynamic Therapy | Pdt Apoptosis | Electron Microscopy | Autophagy Blotting | Cell Death
      KOL-Index: 7911

      Photodynamic therapy (PDT) can cause lethal photodamage by both direct and indirect mechanisms. Direct modes of cell death relate to nonspecific necrosis and the initiation of signaling pathways that elicit apoptosis, autophagy or both. In this report, effects of low-dose and high-dose PDT are explored, comparing sensitizers that localize in the endoplasmic reticulum (the porphycene termed CPO) or mitochondria (mesochlorin). To explore the role of autophagy, two cell lines were ...

      Known for Endoplasmic Reticulum | Pdt Dose | Apoptosis Autophagy | Cell Lines | Bcl2 Protein
      KOL-Index: 7718

      OBJECTIVE: A relatively low level of lysosomal photodamage has been shown capable of promoting the efficacy of photodamage simultaneously or subsequently directed to mitochondrial/ER sites. The procedure has hitherto involved the use of two photosensitizing agents that require irradiation at two different wavelengths and different formulation techniques. This, together with different pharmacokinetic profiles of the photosensitizers, adds a layer of complexity to a protocol that we have ...

      Known for Photodynamic Therapy | Liposomal Formulation | Lysosomes Mitochondria | Photosensitizing Agents | Lysosomal Photodamage
      KOL-Index: 7710

      The phenoxypropionic acid derivative 2-{4-[(7-chloro-2-quinoxalinyl)oxy]phenoxy}propionic acid (XK469) and an analogue termed 2-{4-[(7-bromo-2-quinalinyl)oxy]phenoxy}propionic acid (SH80) can eradicate malignant cell types resistant to many common antitumor agents. Colony formation assays indicated that a 24 h exposure of L1210 cells to XK469 or SH80 inhibited clonogenic growth with CI(90) values of 10 and 13 micromol/L, respectively. This effect was associated with G(2)-M arrest and the ...

      Known for Cells Xk469 | Apoptosis Autophagy | Cell Cycle | Acid Sh80 | Antineoplastic Agents
      KOL-Index: 7433

      The photosensitizer 9-capronyloxytetrakis (methoxyethyl) porphycene localizes predominantly in the endoplasmic reticulum (ER) and, to a lesser extent, in mitochondria of murine leukemia L1210 cells. Subsequent irradiation results in the loss of ER > mitochondrial Bcl-2 and an apoptotic response. Although an increase in cytosolic Ca2+ was observed after irradiation, apoptosis was not inhibited by either the presence of the calcium chelator BAPTA or by the mitochondrial uniporter inhibitor ...

      Known for Endoplasmic Reticulum | Reactive Oxygen | Mitochondrial Ca2 | Photodynamic Therapy | Loss Bcl2
      KOL-Index: 7086

      Photodynamic therapy (PDT) of neoplastic cell lines is sometimes associated with the rapid initiation of apoptosis, a mode of cell death that results in a distinct pattern of cellular and DNA fragmentation. The apoptotic response appears to be a function of both the sensitizer and the cell line. In this study, we examined photodynamic effects of several photosensitizers on murine leukemia P388 cells. Two drugs, a porphycene dimer (PcD) and tin etiopurpurin (SnET2), which localized at ...

      Known for Photodynamic Therapy | Rapid Initiation | Pdt Doses | Apoptosis Dna | Cell Death
      KOL-Index: 6875

      Apoptosis is a cellular death process involving the sequential activation of a series of caspases, endonucleases, and other enzymes. The initiation of apoptosis can be inhibited by overexpression of bcl-2 and certain other members of a related family of proteins. We examined the effects of bcl-2 overexpression on the apoptotic response to photodynamic therapy (PDT), using aluminum phthalocyanine as the photosensitizing agent. In this study, we compared the immortalized human breast ...

      Known for Apoptotic Response | Photodynamic Therapy | Bax Pdt | Proteins Bcl2 | Photosensitizing Agent

      Key People For Photodynamic Therapy

      Top KOLs in the world
      #1
      Thomas J Dougherty
      photodynamic therapy hematoporphyrin derivative malignant tumors
      #2
      Johan Emilian Moan
      photodynamic therapy topical application aminolevulinic acid
      #3
      Michael Richard Hamblin
      photodynamic therapy wound healing blue light
      #4
      David H Kessel
      photodynamic therapy apoptotic response lysosomal photodamage
      #5
      Barbara W Henderson
      photodynamic therapy fluence rate light dose
      #6
      Tayyaba Hasan
      photodynamic therapy pancreatic cancer singlet oxygen

      Department of Pharmacology, Wayne State University School of Medicine, Detroit, MI 48201, USA. | Department of Pharmacology, Wayne State University School of Medicine, Detroit MI 48201, USA. Electronic address: dhkessel@med.wayne.edu. | Department of

    Download on the App StoreGet it on Google Play

    Copyright © 2023 Key Opinion Leaders, LLC.