The Experts below are selected from a list of 138 Experts worldwide ranked by ideXlab platform

Om Kumar - One of the best experts on this subject based on the ideXlab platform.

  • The Fas/Fas Ligand Apoptotic Pathway Is Involved in Abrin-Induced Apoptosis
    Toxicological sciences : an official journal of the Society of Toxicology, 2013
    Co-Authors: Nandita Saxena, Preeti Yadav, Om Kumar
    Abstract:

    Abrin is a plant glycoprotein Toxin from the seeds of Abrus precatorius, sharing similarity in structure and properties with ricin. Abrin is highly toxic, with an estimated human fatal dose of 0.1-1 µg/kg, causing death after accidental or intentional poisoning. It is a potent Biological Toxin warfare agent. There is no chemical antidote available against the abrin. The elucidation of molecular mechanism of abrin-induced cell death is important for development of therapy. Intrinsic pathway-mediated apoptosis has been well established in abrin-induced cell death. However, the detailed mechanism especially extrinsic receptor-mediated pathway remains uncharacterized. To assess whether some of the apoptosis known to occur after abrin exposure might be mediated by Fas/Fas ligand (Fas L) interactions, we analyzed effect of abrin on Fas pathway in Jurkat cells. Here, we report that activation of the Fas pathway is involved in abrin-induced apoptosis. Following treatment of abrin, Fas L was induced, which stimulated the Fas pathway by cross-linking Fas receptor (Fas R). Apoptosis was mediated by cleavage of the Fas R proximal caspase-8 and the downstream caspase-3, resulting in activation of the prototype caspase substrate poly-(ADP-ribose) polymerase and caspase-activated DNase. Blocking Fas L/Fas R interaction by using Fas inhibitor reduced abrin-induced apoptosis, further confirms involvement of Fas pathway. Activation of components of Fas pathway and caspases upon abrin treatment was also found in splenocytes in mice. Our findings offer new perspective for understanding the fundamental mechanism in abrin-induced apoptotic mechanism and may have implication in developing novel therapeutic strategies in the management for abrin-induced complications.

  • the fas fas ligand apoptotic pathway is involved in abrin induced apoptosis
    Toxicological Sciences, 2013
    Co-Authors: Nandita Saxena, Preeti Yadav, Om Kumar
    Abstract:

    Abrin is a plant glycoprotein Toxin from the seeds of Abrus precatorius, sharing similarity in structure and properties with ricin. Abrin is highly toxic, with an estimated human fatal dose of 0.1-1 µg/kg, causing death after accidental or intentional poisoning. It is a potent Biological Toxin warfare agent. There is no chemical antidote available against the abrin. The elucidation of molecular mechanism of abrin-induced cell death is important for development of therapy. Intrinsic pathway-mediated apoptosis has been well established in abrin-induced cell death. However, the detailed mechanism especially extrinsic receptor-mediated pathway remains uncharacterized. To assess whether some of the apoptosis known to occur after abrin exposure might be mediated by Fas/Fas ligand (Fas L) interactions, we analyzed effect of abrin on Fas pathway in Jurkat cells. Here, we report that activation of the Fas pathway is involved in abrin-induced apoptosis. Following treatment of abrin, Fas L was induced, which stimulated the Fas pathway by cross-linking Fas receptor (Fas R). Apoptosis was mediated by cleavage of the Fas R proximal caspase-8 and the downstream caspase-3, resulting in activation of the prototype caspase substrate poly-(ADP-ribose) polymerase and caspase-activated DNase. Blocking Fas L/Fas R interaction by using Fas inhibitor reduced abrin-induced apoptosis, further confirms involvement of Fas pathway. Activation of components of Fas pathway and caspases upon abrin treatment was also found in splenocytes in mice. Our findings offer new perspective for understanding the fundamental mechanism in abrin-induced apoptotic mechanism and may have implication in developing novel therapeutic strategies in the management for abrin-induced complications.

Nandita Saxena - One of the best experts on this subject based on the ideXlab platform.

  • The Fas/Fas Ligand Apoptotic Pathway Is Involved in Abrin-Induced Apoptosis
    Toxicological sciences : an official journal of the Society of Toxicology, 2013
    Co-Authors: Nandita Saxena, Preeti Yadav, Om Kumar
    Abstract:

    Abrin is a plant glycoprotein Toxin from the seeds of Abrus precatorius, sharing similarity in structure and properties with ricin. Abrin is highly toxic, with an estimated human fatal dose of 0.1-1 µg/kg, causing death after accidental or intentional poisoning. It is a potent Biological Toxin warfare agent. There is no chemical antidote available against the abrin. The elucidation of molecular mechanism of abrin-induced cell death is important for development of therapy. Intrinsic pathway-mediated apoptosis has been well established in abrin-induced cell death. However, the detailed mechanism especially extrinsic receptor-mediated pathway remains uncharacterized. To assess whether some of the apoptosis known to occur after abrin exposure might be mediated by Fas/Fas ligand (Fas L) interactions, we analyzed effect of abrin on Fas pathway in Jurkat cells. Here, we report that activation of the Fas pathway is involved in abrin-induced apoptosis. Following treatment of abrin, Fas L was induced, which stimulated the Fas pathway by cross-linking Fas receptor (Fas R). Apoptosis was mediated by cleavage of the Fas R proximal caspase-8 and the downstream caspase-3, resulting in activation of the prototype caspase substrate poly-(ADP-ribose) polymerase and caspase-activated DNase. Blocking Fas L/Fas R interaction by using Fas inhibitor reduced abrin-induced apoptosis, further confirms involvement of Fas pathway. Activation of components of Fas pathway and caspases upon abrin treatment was also found in splenocytes in mice. Our findings offer new perspective for understanding the fundamental mechanism in abrin-induced apoptotic mechanism and may have implication in developing novel therapeutic strategies in the management for abrin-induced complications.

  • the fas fas ligand apoptotic pathway is involved in abrin induced apoptosis
    Toxicological Sciences, 2013
    Co-Authors: Nandita Saxena, Preeti Yadav, Om Kumar
    Abstract:

    Abrin is a plant glycoprotein Toxin from the seeds of Abrus precatorius, sharing similarity in structure and properties with ricin. Abrin is highly toxic, with an estimated human fatal dose of 0.1-1 µg/kg, causing death after accidental or intentional poisoning. It is a potent Biological Toxin warfare agent. There is no chemical antidote available against the abrin. The elucidation of molecular mechanism of abrin-induced cell death is important for development of therapy. Intrinsic pathway-mediated apoptosis has been well established in abrin-induced cell death. However, the detailed mechanism especially extrinsic receptor-mediated pathway remains uncharacterized. To assess whether some of the apoptosis known to occur after abrin exposure might be mediated by Fas/Fas ligand (Fas L) interactions, we analyzed effect of abrin on Fas pathway in Jurkat cells. Here, we report that activation of the Fas pathway is involved in abrin-induced apoptosis. Following treatment of abrin, Fas L was induced, which stimulated the Fas pathway by cross-linking Fas receptor (Fas R). Apoptosis was mediated by cleavage of the Fas R proximal caspase-8 and the downstream caspase-3, resulting in activation of the prototype caspase substrate poly-(ADP-ribose) polymerase and caspase-activated DNase. Blocking Fas L/Fas R interaction by using Fas inhibitor reduced abrin-induced apoptosis, further confirms involvement of Fas pathway. Activation of components of Fas pathway and caspases upon abrin treatment was also found in splenocytes in mice. Our findings offer new perspective for understanding the fundamental mechanism in abrin-induced apoptotic mechanism and may have implication in developing novel therapeutic strategies in the management for abrin-induced complications.

Preeti Yadav - One of the best experts on this subject based on the ideXlab platform.

  • The Fas/Fas Ligand Apoptotic Pathway Is Involved in Abrin-Induced Apoptosis
    Toxicological sciences : an official journal of the Society of Toxicology, 2013
    Co-Authors: Nandita Saxena, Preeti Yadav, Om Kumar
    Abstract:

    Abrin is a plant glycoprotein Toxin from the seeds of Abrus precatorius, sharing similarity in structure and properties with ricin. Abrin is highly toxic, with an estimated human fatal dose of 0.1-1 µg/kg, causing death after accidental or intentional poisoning. It is a potent Biological Toxin warfare agent. There is no chemical antidote available against the abrin. The elucidation of molecular mechanism of abrin-induced cell death is important for development of therapy. Intrinsic pathway-mediated apoptosis has been well established in abrin-induced cell death. However, the detailed mechanism especially extrinsic receptor-mediated pathway remains uncharacterized. To assess whether some of the apoptosis known to occur after abrin exposure might be mediated by Fas/Fas ligand (Fas L) interactions, we analyzed effect of abrin on Fas pathway in Jurkat cells. Here, we report that activation of the Fas pathway is involved in abrin-induced apoptosis. Following treatment of abrin, Fas L was induced, which stimulated the Fas pathway by cross-linking Fas receptor (Fas R). Apoptosis was mediated by cleavage of the Fas R proximal caspase-8 and the downstream caspase-3, resulting in activation of the prototype caspase substrate poly-(ADP-ribose) polymerase and caspase-activated DNase. Blocking Fas L/Fas R interaction by using Fas inhibitor reduced abrin-induced apoptosis, further confirms involvement of Fas pathway. Activation of components of Fas pathway and caspases upon abrin treatment was also found in splenocytes in mice. Our findings offer new perspective for understanding the fundamental mechanism in abrin-induced apoptotic mechanism and may have implication in developing novel therapeutic strategies in the management for abrin-induced complications.

  • the fas fas ligand apoptotic pathway is involved in abrin induced apoptosis
    Toxicological Sciences, 2013
    Co-Authors: Nandita Saxena, Preeti Yadav, Om Kumar
    Abstract:

    Abrin is a plant glycoprotein Toxin from the seeds of Abrus precatorius, sharing similarity in structure and properties with ricin. Abrin is highly toxic, with an estimated human fatal dose of 0.1-1 µg/kg, causing death after accidental or intentional poisoning. It is a potent Biological Toxin warfare agent. There is no chemical antidote available against the abrin. The elucidation of molecular mechanism of abrin-induced cell death is important for development of therapy. Intrinsic pathway-mediated apoptosis has been well established in abrin-induced cell death. However, the detailed mechanism especially extrinsic receptor-mediated pathway remains uncharacterized. To assess whether some of the apoptosis known to occur after abrin exposure might be mediated by Fas/Fas ligand (Fas L) interactions, we analyzed effect of abrin on Fas pathway in Jurkat cells. Here, we report that activation of the Fas pathway is involved in abrin-induced apoptosis. Following treatment of abrin, Fas L was induced, which stimulated the Fas pathway by cross-linking Fas receptor (Fas R). Apoptosis was mediated by cleavage of the Fas R proximal caspase-8 and the downstream caspase-3, resulting in activation of the prototype caspase substrate poly-(ADP-ribose) polymerase and caspase-activated DNase. Blocking Fas L/Fas R interaction by using Fas inhibitor reduced abrin-induced apoptosis, further confirms involvement of Fas pathway. Activation of components of Fas pathway and caspases upon abrin treatment was also found in splenocytes in mice. Our findings offer new perspective for understanding the fundamental mechanism in abrin-induced apoptotic mechanism and may have implication in developing novel therapeutic strategies in the management for abrin-induced complications.

Yoshihiro Nishida - One of the best experts on this subject based on the ideXlab platform.

  • Bis(β-lactosyl)-[60]fullerene as novel class of glycolipids useful for the detection and the decontamination of Biological Toxins of the Ricinus communis family.
    Beilstein journal of organic chemistry, 2014
    Co-Authors: Hirofumi Dohi, Hirotaka Uzawa, Yasuo Seto, Keita Sato, Takeru Kanazawa, Akihiro Saito, Yoshihiro Nishida
    Abstract:

    Glycosyl-[60]fullerenes were first used as decontaminants against ricin, a lactose recognition proteoToxin in the Ricinus communis family. A fullerene glycoconjugate carrying two lactose units was synthesized by a [3 + 2] cycloaddition reaction between C60 and the azide group in 6-azidohexyl β-lactoside per-O-acetate. A colloidal aqueous solution with brown color was prepared from deprotected bis(lactosyl)-C60 and was found stable for more than 6 months keeping its red color. Upon mixing with an aqueous solution of Ricinus communis agglutinin (RCA120), the colloidal solution soon caused precipitations, while becoming colorless and transparent. In contrast, a solution of concanavalin A (Con A) caused no apparent change, indicating that the precipitation was caused specifically by carbohydrate–protein interactions. This notable phenomenon was quantified by means of sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE), and the results were discussed in terms of detection and decontamination of the deadly Biological Toxin in the Ricinus communis family.

  • Glycotechnology for Decontamination of Biological Agents: A Model Study Using Ricin and Biotin-Tagged Synthetic Glycopolymers
    ACS applied materials & interfaces, 2012
    Co-Authors: Takehiro Nagatsuka, Hirotaka Uzawa, Isaac Ohsawa, Yasuo Seto, Keita Sato, Yoshihiro Nishida
    Abstract:

    Two types of biotin-tagged glycopolymers carrying lactose or glucose in clusters along the polyacrylamide backbone were prepared and subjected to decontamination analyses with the plant Toxin ricin. A buffer solution containing the Toxin was treated with one glycopolymer followed by streptavidin-magnetic particles. Supernatant solutions were analyzed with surface plasmon resonance and capillary electrophoresis, and revealed that the lactose glycopolymer “captured” this Toxin more effectively than the glucose polymer. Free Toxin was not detectable in the supernatant after treatment with the glycopolymer and magnetic particles; >99% decontamination was achieved for this potentially fatal Biological Toxin.

  • Use of lactose against the deadly Biological Toxin ricin.
    ACS applied materials & interfaces, 2010
    Co-Authors: Takehiro Nagatsuka, Hirotaka Uzawa, Isaac Ohsawa, Yasuo Seto, Yoshihiro Nishida
    Abstract:

    Developing a technology for detecting and decontaminating Biological Toxins is needed. Ricin from Ricinus communis is a highly poisonous Toxin; it was formerly used for an assassination in London and in postal attacks in the United States. Ricin is readily available from castor beans and could be used as a Biological agent. We propose using glycotechnology against the illegal use of ricin. Lactose (a natural ligand of this Toxin) was incorporated into polyacrylamide-based glycopolymers at variable sugar densities (18−100%) and evaluated with surface plasmon resonance (SPR) spectroscopy and the real agent, ricin. Glycopolymers (18−65% lactose densities) effectively interfered with the Toxin-lactoside adhesion event (>99% efficiency within 20 min). This supported the notion of using the mammary sugar lactose against a deadly Biological Toxin.

Andrzej Kryszewski - One of the best experts on this subject based on the ideXlab platform.

  • Side effects of botulinum Toxin injection for benign anal disorders.
    European journal of gastroenterology & hepatology, 2002
    Co-Authors: Mariusz H Madaliński, Jarosław Sławek, Wojciech Duzyński, Blazej Zbytek, Krzysztof Jagiełło, Adrich Z, Andrzej Kryszewski
    Abstract:

    Background Botulinum Toxin A (BT-A) is a powerful Biological Toxin. Nevertheless, it has proved to be a remarkable therapeutic agent for the treatment of benign anal disorders. Higher doses of BT-A could change the outcome of treatment. It is not known whether doses of BT-A higher than 20 units of B