The Experts below are selected from a list of 4527 Experts worldwide ranked by ideXlab platform
A C Ludolph - One of the best experts on this subject based on the ideXlab platform.
-
Slow toxins, biologic markers, and long-latency neurodegenerative disease in the western Pacific region.
Neurology, 1991Co-Authors: P S Spencer, G E Kisby, A C LudolphAbstract:The western Pacific parkinsonism-dementia and amyotrophic lateral sclerosis complex is a prototypical neurodegenerative disorder found among inhabitants of Guam, New Guinea (Irian Jaya, Indonesia) and Japan (Kii Peninsula, Honshu). Nonviral environmental factors peculiar to the affected populations seem to play a prominent etiologic role. Although cause-effect relationships cannot be established by epidemiologic studies alone, we have shown in all three affected population groups that individuals develop the amyotrophic lateral sclerosis variant of this disorder after heavy exposure to the raw or incompletely detoxified seed of neurotoxic Cycad plants. Since long periods may elapse between Cycad exposure and the appearance of neurological disease in humans, Cycads may harbor a "slow toxin" that causes the postmitotic neuron to undergo slow irreversible degeneration. Two Cycad neurotoxins are recognized, one of which (cycasin) is known to have long-latency effects (tumorigenesis) on mitotic neurons and replicating cells in other tissues. This paper explores the possible relationship between tumorigenesis and long-latency neurotoxicity, and discusses possible biologic markers of Cycad exposure and subclinical neurodegenerative disease.
-
Long-latency neurodegenerative disease in the western Pacific.
Geriatrics, 1991Co-Authors: P S Spencer, G E Kisby, A C LudolphAbstract:The western Pacific parkinsonism-dementia and amyotrophic lateral sclerosis complex is a prototypical neurodegenerative disorder found among inhabitants of Guam, New Guinea (Irian Jaya, Indonesia) and Japan (Kii Peninsula, Honshu). Nonviral environmental factors peculiar to the affected populations seem to play a prominent etiologic role. Although cause-effect relationships cannot be established by epidemiologic studies alone, we have shown in all three affected population groups that individuals develop the amyotrophic lateral sclerosis variant of this disorder after heavy exposure to the raw or incompletely detoxified seed of neurotoxic Cycad plants. Since long periods may elapse between Cycad exposure and the appearance of neurological disease in humans, Cycads may harbor a "slow toxin" that causes the postmitotic neuron to undergo slow irreversible degeneration. Two Cycad neurotoxins are recognized, one of which (cycasin) is known to have long-latency effects (tumorigenesis) on mitotic neurons and replicating cells in other tissues. This paper explores the possible relationship between tumorigenesis and long-latency neurotoxicity, and discusses possible biologic markers of Cycad exposure and subclinical neurodegenerative disease.
-
Slow toxins, biologic markers, and long‐latency neurodegenerative disease in the western Pacific region
Neurology, 1991Co-Authors: Peter S. Spencer, Glen E Kisby, A C LudolphAbstract:The western Pacific parkinsonism-dementia and amyotrophic lateral sclerosis complex is a prototypical neurodegenerative disorder found among inhabitants of Guam, New Guinea (Irian Jaya, Indonesia) and Japan (Kii Peninsula, Honshu). Nonviral environmental factors peculiar to the affected populations seem to play a prominent etiologic role. Although cause-effect relationships cannot be established by epidemiologic studies alone, we have shown in all three affected population groups that individuals develop the amyotrophic lateral sclerosis variant of this disorder after heavy exposure to the raw or incompletely detoxified seed of neurotoxic Cycad plants. Since long periods may elapse between Cycad exposure and the appearance of neurological disease in humans, Cycads may harbor a "slow toxin" that causes the postmitotic neuron to undergo slow irreversible degeneration. Two Cycad neurotoxins are recognized, one of which (cycasin) is known to have long-latency effects (tumorigenesis) on mitotic neurons and replicating cells in other tissues. This paper explores the possible relationship between tumorigenesis and long-latency neurotoxicity, and discusses possible biologic markers of Cycad exposure and subclinical neurodegenerative disease.
Thomas E. Marler - One of the best experts on this subject based on the ideXlab platform.
-
Does Phytogeography Change with Shifts in Geopolitics? The Curious Case of Cycads in the United States
Diversity, 2020Co-Authors: Benjamin E. Deloso, Ulysses F. Ferreras, Thomas E. MarlerAbstract:The United States is currently home to five native Cycad species. We provide a discussion on these five Cycad species to illuminate how evolutionary and geopolitical processes influence phytogeography and published checklists of threatened plants. The number of threatened species in need of protection within any given country is a product of speciation that is contingent with evolutionary processes. However, this number may change instantaneously along with shifting of geopolitical boundaries brought about by armed conflict between rival states and multilateral negotiations. There are five contemporary Cycad species within the United States, and the various historical bilateral and multilateral agreements that have generated this list are reviewed. Three of these five Cycad species are threatened and in need of urgent protection. A discussion on the history of United States Cycads as a microcosm of worldwide conservation issues is presented, with a focus on how federal conservation endeavors of individual nations may influence the world’s biodiversity crisis.
-
Does Cycad aulacaspis scale (Aulacaspis yasumatsui, Hemiptera: Diaspididae) play a direct role in causing soil phytotoxicity?
Communicative & integrative biology, 2014Co-Authors: Gillian W. Watson, Thomas E. MarlerAbstract:Cycad aulacaspis scale (CAS, Aulacaspis yasumatsui, Hemiptera: Diaspididae) was accidentally introduced to Guam in 2003, and has caused acute mortality of the dominant, endemic forest tree Cycas micronesica. A phytotoxic legacy in the soils beneath Cycad trees killed by CAS over a period of about three years has been demonstrated. The origin of the toxicity may be large quantities of CAS-encrusted Cycad leaf litter. We explore the possibility that a major contribution to this toxic legacy may come from the scale insects, not just from the plant material.
-
Evolutionary developmental biology in Cycad phenology
Communicative & integrative biology, 2012Co-Authors: Root Gorelick, Thomas E. MarlerAbstract:We recently described lack of phenotypic plasticity in reproductive organ development and substantial plasticity in vegetative organ development for the Cycad Cycas micronesica. Is there an evo-devo explanation for the disparity in phenotypic plasticity of vegetative vs. reproductive organs? Despite modularity, might evolution of Cycad phenology be controlled more by drift than selection?
-
Novel tools for an old lineage: Population genomics for Cycads.
Communicative & integrative biology, 2011Co-Authors: Angélica Cibrián-jaramillo, Thomas E. MarlerAbstract:With a ca. 300 million year-old evolutionary history, Cycads are often perceived as ‘living fossils’, relicts of their previously widespread dominance. Patterns of genetic variation for a member of the most basal Cycad genus, Cycas micronesica, support the notion that Cycads are a dynamic group with ongoing diversification. Herein we hypothesize that Cycad’s hefty genomes enable rapid adaptive change and facilitate specific beneficial interactions with varying assemblages of symbionts. Characterizing population-level genomic patterns of Cycads and their symbionts, pollinators in particular, will enlighten our understanding of these mechanisms and of adaptive variation that underlies Cycad evolution. In the light of rapid climate and landscape change, Cycads are a beacon for understanding the ecological processes that ultimately enable species long-term survival.
-
Rethinking Cycad metabolite research
Communicative & integrative biology, 2011Co-Authors: Laura R. Snyder, Thomas E. MarlerAbstract:Cycads are among the most ancient of extant Spermatophytes, and are known for their numerous pharmacologically active compounds. One compound in particular, β-methylamino-L-alanine (BMAA), has been implicated as the cause of amyotrophic lateral sclerosis/parkinson dementia complex (ALS/PDC) on Guam. Previous studies allege that BMAA is produced exclusively by cyanobacteria, and is transferred to Cycads through the symbiotic relationship between these cyanobacteria and the roots of Cycads. We recently published data showing that Cycas micronesica seedlings grown without endophytic cyanobacteria do in fact increase in BMAA, invalidating the foundation of the BMAA hypothesis. We use this example to suggest that the frenzy centered on BMAA and other single putative toxins has hindered progress. The long list of Cycad-specific compounds may have important roles in signaling or communication, but these possibilities have been neglected during decades of attempts to force single metabolites into a supposed anti-...
Jason T.c. Tzen - One of the best experts on this subject based on the ideXlab platform.
-
Stable oil bodies sheltered by a unique caleosin in Cycad megagametophytes.
Plant Physiology and Biochemistry, 2009Co-Authors: Pei-luen Jiang, Jeff C.f. Chen, Shau-ting Chiu, Jason T.c. TzenAbstract:Stable oil bodies of smaller sizes and higher thermostability were isolated from mature Cycad (Cycas revoluta) megagametophytes compared with those isolated from sesame seeds. Immunological cross-recognition revealed that Cycad oil bodies contained a major protein of 27 kDa, tentatively identified as caleosin, while oleosin, the well-known structural protein, was apparently absent. Mass spectrometric analysis showed that the putative Cycad caleosin possessed a tryptic fragment of 15 residues matching to that of a theoretical moss caleosin. A complete cDNA fragment encoding this putative caleosin was obtained by PCR cloning using a primer designed according to the tryptic peptide and another one designed according to a highly conservative region among diverse caleosins. The identification of this clone was subsequently confirmed by immunodetection and MALDI-MS analyses of its recombinant fusion protein over-expressed in Escherichia coli and the native form from Cycad oil bodies. Stable artificial oil bodies were successfully constituted with triacylglycerol, phospholipid and the recombinant fusion protein containing the Cycad caleosin. These results suggest that stable oil bodies in Cycad megagametophytes are mainly sheltered by a unique structural protein caleosin.
Peter S. Spencer - One of the best experts on this subject based on the ideXlab platform.
-
Is Neurodegenerative Disease a Long-Latency Response to Early-Life Genotoxin Exposure?
International Journal of Environmental Research and Public Health, 2011Co-Authors: Glen E Kisby, Peter S. SpencerAbstract:Western Pacific amyotrophic lateral sclerosis and parkinsonism-dementia complex, a disappearing neurodegenerative disease linked to use of the neurotoxic Cycad plant for food and/or medicine, is intensively studied because the neuropathology (tauopathy) is similar to that of Alzheimer’s disease. Cycads contain neurotoxic and genotoxic principles, notably cycasin and methylazoxymethanol, the latter sharing chemical relations with nitrosamines, which are derived from nitrates and nitrites in preserved meats and fertilizers, and also used in the rubber and leather industries. This review includes new data that influence understanding of the neurobiological actions of Cycad and related genotoxins and the putative mechanisms by which they might trigger neurodegenerative disease.
-
Slow toxins, biologic markers, and long‐latency neurodegenerative disease in the western Pacific region
Neurology, 1991Co-Authors: Peter S. Spencer, Glen E Kisby, A C LudolphAbstract:The western Pacific parkinsonism-dementia and amyotrophic lateral sclerosis complex is a prototypical neurodegenerative disorder found among inhabitants of Guam, New Guinea (Irian Jaya, Indonesia) and Japan (Kii Peninsula, Honshu). Nonviral environmental factors peculiar to the affected populations seem to play a prominent etiologic role. Although cause-effect relationships cannot be established by epidemiologic studies alone, we have shown in all three affected population groups that individuals develop the amyotrophic lateral sclerosis variant of this disorder after heavy exposure to the raw or incompletely detoxified seed of neurotoxic Cycad plants. Since long periods may elapse between Cycad exposure and the appearance of neurological disease in humans, Cycads may harbor a "slow toxin" that causes the postmitotic neuron to undergo slow irreversible degeneration. Two Cycad neurotoxins are recognized, one of which (cycasin) is known to have long-latency effects (tumorigenesis) on mitotic neurons and replicating cells in other tissues. This paper explores the possible relationship between tumorigenesis and long-latency neurotoxicity, and discusses possible biologic markers of Cycad exposure and subclinical neurodegenerative disease.
Pei-luen Jiang - One of the best experts on this subject based on the ideXlab platform.
-
Stable oil bodies sheltered by a unique caleosin in Cycad megagametophytes.
Plant Physiology and Biochemistry, 2009Co-Authors: Pei-luen Jiang, Jeff C.f. Chen, Shau-ting Chiu, Jason T.c. TzenAbstract:Stable oil bodies of smaller sizes and higher thermostability were isolated from mature Cycad (Cycas revoluta) megagametophytes compared with those isolated from sesame seeds. Immunological cross-recognition revealed that Cycad oil bodies contained a major protein of 27 kDa, tentatively identified as caleosin, while oleosin, the well-known structural protein, was apparently absent. Mass spectrometric analysis showed that the putative Cycad caleosin possessed a tryptic fragment of 15 residues matching to that of a theoretical moss caleosin. A complete cDNA fragment encoding this putative caleosin was obtained by PCR cloning using a primer designed according to the tryptic peptide and another one designed according to a highly conservative region among diverse caleosins. The identification of this clone was subsequently confirmed by immunodetection and MALDI-MS analyses of its recombinant fusion protein over-expressed in Escherichia coli and the native form from Cycad oil bodies. Stable artificial oil bodies were successfully constituted with triacylglycerol, phospholipid and the recombinant fusion protein containing the Cycad caleosin. These results suggest that stable oil bodies in Cycad megagametophytes are mainly sheltered by a unique structural protein caleosin.
