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Pawel P Liberski - One of the best experts on this subject based on the ideXlab platform.
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Kuru the first human prion disease
Viruses, 2019Co-Authors: Pawel P Liberski, Beata Sikorska, Agata Gajos, Shirley LindenbaumAbstract:Kuru, the first human prion disease was transmitted to chimpanzees by D. Carleton Gajdusek (1923–2008). In this review, we summarize the history of this seminal discovery, its anthropological background, epidemiology, clinical picture, neuropathology, and molecular genetics. We provide descriptions of electron microscopy and confocal microscopy of Kuru amyloid plaques retrieved from a paraffin-embedded block of an old Kuru case, named Kupenota. The discovery of Kuru opened new vistas of human medicine and was pivotal in the subsequent transmission of Creutzfeldt–Jakob disease, as well as the relevance that bovine spongiform encephalopathy had for transmission to humans. The transmission of Kuru was one of the greatest contributions to biomedical sciences of the 20th century.
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Kuru the first prion disease
Advances in Experimental Medicine and Biology, 2012Co-Authors: Pawel P Liberski, Beata Sikorska, Paul BrownAbstract:Kuru disease is linked with the name of D. Carleton Gajdusek and he was the first to show that this human neurodegenerative disease can be transmitted to chimpanzees and subsequently classified as a transmissible spongiform encephalopathy (TSE), or slow unconventional virus disease. It was first reported to Western world in 1957 by Gajdusek and Vincent Zigas,1,2 and in 1975 a complete bibliography of Kuru was published by Alpers et al.3 “Kuru” in the Fore language in Papua New Guinea means to shiver from fever and cold. The disease has been found to spread through ritualistic cannibalism and is an invariably fatal cerebellar ataxia accompanied by tremor, choreiform and athetoid movements. Neuropathologically, Kuru is characterized by the presence of amyloid “Kuru” plaques.
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ultrastructural characteristics or evaluation of creutzfeldt jakob disease and other human transmissible spongiform encephalopathies or prion diseases
Ultrastructural Pathology, 2010Co-Authors: Pawel P Liberski, Beata Sikorska, Herbert Budka, J J Hauw, Nicolas Kopp, Nathalie Streichenberger, Pierrie Giraud, Jan Boellaard, Gabor G Kovacs, James W. IronsideAbstract:The authors report on a large series of human prion diseases to establish ultrastructural characteristics that may be useful for their diagnosis. For Creutzfeldt-Jakob disease (CJD and its variant, vCJD) and fatal familial insomnia (FFI) only vacuolation (spongiform change) and the presence of tubulovesicular structures are consistent findings. Other changes, such as the presence of myelinated vacuoles, branching cisternae, neuroaxonal dystrophy, and autophagic vacuoles, were present in different proportions in either CJD or FFI, but they are nonspecific ultrastructural findings that can also occur in other neurodegenerative conditions. The hallmark of Gerstmann-Straussler-Scheinker disease (GSS) and vCJD is the amyloid plaque, but plaques of GSS and Kuru are different than those of vCJD. Whereas the former are typical unicentric Kuru type or multicentric plaques, the latter are unicentric florid plaques. Also, Kuru plaques are nonneuritic, whereas GSS florid plaques are usually neuritic; however, a proportion of plaques from GSS was also found to have nonneuritic characteristics. Thus, the presence or absence of dystrophic neurites is not a discriminatory factor for GSS and vCJD. Furthermore, plaques from GSS with different mutations were also slightly different. In GSS with mutations P102L, 232T, and A117V plaques were stellate while in 1 case with 144 base-pair insertion and in GSS-A117V, round plaques were also observed, and typical primitive neuritic plaques, i.e., composed of dystrophic neurites with little or no amyloid, were found only in a P102L case from the original Austrian family. In 2 cases of sporadic CJD, the Kuru stellate plaque predominated.
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ultrastructural study of florid plaques in variant creutzfeldt jakob disease a comparison with amyloid plaques in Kuru sporadic creutzfeldt jakob disease and gerstmann straussler scheinker disease
Neuropathology and Applied Neurobiology, 2009Co-Authors: Beata Sikorska, Pawel P Liberski, Herbert Budka, Tomasz Sobow, James W. IronsideAbstract:Background: Although the histological features of the amyloid plaques in variant Creutzfeldt–Jakob disease (vCJD) are distinct from those in other forms of prion disease [Kuru, sporadic Creutzfeldt–Jakob disease (sCJD) and Gerstmann–Straussler–Scheinker disease (GSS)], their ultrastructural features have only been described in a single case report. Aims: To study vCJD plaques systematically and compare them with plaques in Kuru, sCJD, GSS and Alzheimer disease (AD). Methods: Amyloid plaques were studied by transmission electron microscopy and image analysis in five cases of vCJD, three cases of GSS, two cases of sCJD, one case of Kuru and five cases of AD. Immunohistochemistry was performed on paraffin sections from one case of vCJD, two cases of GSS, one case of Kuru and two cases of sCJD. Results: The florid plaques in vCJD were either compact or more diffuse; in both forms, the radiating fibrils were organized into thick ‘tongues’, in contrast to Kuru plaques. Dystrophic neurites (DNs) containing lysosomal electron-dense bodies or vesicles surrounded florid plaques. Microglial cells were found within florid plaques; occasional amyloid fibrils were identified in membrane-bound pockets of microglial cells. In vCJD, there was significant tau immunoreactivity in DNs around florid plaques while, in sCJD, GSS and Kuru, minimal tau immunoreactivity was observed around plaques. Conclusions: The ultrastructure of the florid plaques and DNs in vCJD is more reminiscent of neuritic plaques in AD than Kuru or multicentric plaques. These findings may reflect differences both in the strains of the transmissible agents responsible for these disorders and in host factors.
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relationship of microglia and scrapie amyloid immunoreactive plaques in Kuru creutzfeldt jakob disease and gerstmann strausler syndrome
Acta Neuropathologica, 1994Co-Authors: Don C Guiroy, Pawel P Liberski, Ikuro Wakayama, Carleton D GajdusekAbstract:Kuru, Creutzfeldt-Jakob disease (CJD) and Gerstmann-Straussler syndrome (GSS) are transmissible dementias affecting humans characterized neuropathologically by intraneuronal vacuolation, spongiform change, astrocytic hypertrophy and hyperplasia and the variable presence of amyloid plaques. It has been suggested that microglia are amyloid-forming cells, which play an essential role in amyloid plaque formation. To study the relationship between microglia and amyloid plaques in Kuru, CJD and GSS, cerebellar tissues were examined by the double-immunostaining technique using anti-ferritin antibodies as the microglial marker and anti-scrapie amyloid antibody as plaque marker. Ferritin-immunoreactive microglia were observed interdigitating with and among unicentric, multicentric and diffuse types of scrapie amyloid-immunoreactive plaques and were found to a lesser extent in the neuropil. In Kuru and CJD, scrapie amyloid-immunoreactive plaques were predominantly unicentric and were observed in the granular layer. In Kuru, 53% of the amyloid plaques were associated with microglia, whereas only 30% of plaques in CJD were. In contrast, scrapie-amyloid-immunoreactive plaques in GSS were of the multicentric type, predominantly observed in the molecular layer, and 90% of these plaques were associated with microglia. Our data indicate that microglia are frequently associated with scrapie amyloid-immunoreactive plaques in GSS, less commonly in Kuru and to a much lesser extent in CJD, suggesting that microglia may play a variable but important role in the formation of plaques in the transmissible spongiform encephalopathies.
MP Alpers - One of the best experts on this subject based on the ideXlab platform.
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A clinical study of Kuru patients with long incubation periods at the end of the epidemic in Papua New Guinea
PHILOSOPHICAL TRANSACTIONS OF THE ROYAL SOCIETY B-BIOLOGICAL SCIENCES, 2008Co-Authors: MP AlpersAbstract:Kuru is so far the principal human epidemic prion disease. While its incidence has steadily declined since the cessation of its route of transmission, endocannibalism, in Papua New Guinea in the 1950s, the arrival of variant Creutzfeldt-Jakob disease (vCJD), also thought to be transmitted by dietary prion exposure, has given Kuru a new global relevance. We investigated all suspected cases of Kuru from July 1996 to June 2004 and identified 11 Kuru patients. There were four females and seven males, with an age range of 46-63 years at the onset of disease, in marked contrast to the age and sex distribution when Kuru was first investigated 50 years ago. We obtained detailed histories of residence and exposure to mortuary feasts and performed serial neurological examination and genetic studies where possible. All patients were born a significant period before the mortuary practice of transumption ceased and their estimated incubation periods in some cases exceeded 50 years. The principal clinical features of Kuru in the studied patients showed the same progressive cerebellar syndrome that had been previously described. Two patients showed marked cognitive impairment well before preterminal stages, in contrast to earlier clinical descriptions. In these patients, the mean clinical duration of 17 months was longer than the overall average in Kuru but similar to that previously reported for the same age group, and this may relate to the effects of both patient age and PRNP codon 129 genotype. Importantly, no evidence for lymphoreticular colonization with prions, seen uniformly in vCJD, was observed in a patient with Kuru at tonsil biopsy.
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Kuru in the 21st century - an acquired human prion disease with very long incubation periods
LANCET, 2006Co-Authors: MP AlpersAbstract:Background Kuru provides the principal experience of epidemic human prion disease. Its incidence has steadily fallen after the abrupt cessation of its route of transmission (endocannibalism) in Papua New Guinea in the 1950s. The onset of variant Creutzfeldt-Jakob disease (vCJD), and the unknown prevalence of infection after the extensive dietary exposure to bovine spongiform encephalopathy (BSE) prions in the UK, has led to renewed interest in Kuru. We investigated possible incubation periods, pathogenesis, and genetic susceptibility factors in Kuru patients in Papua New Guinea.Methods We strengthened active Kuru surveillance in 1996 with an expanded field team to investigate all suspected patients. Detailed histories of residence and exposure to mortuary feasts were obtained together with serial neurological examination, if possible.Findings We identified 11 patients with Kuru from July, 1996, to June, 2004, all living in the South Fore. All patients were born before the cessation of cannibalism in the late 1950s. The minimum estimated incubation periods ranged from 34 to 41 years. However, likely incubation periods in men ranged from 39 to 56 years and could have been up to 7 years longer. PRNP analysis showed that most patients with Kuru were heterozygous at polymorphic codon 129, a genotype associated with extended incubation periods and resistance to prion disease.Interpretation Incubation periods of infection with human prions can exceed 50 years. In human infection with BSE prions, species-barrier effects, which are characteristic of cross-species transmission, would be expected to further increase the mean and range of incubation periods, compared with recycling of prions within species. These data should inform attempts to model variant CJD epidemiology.
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balancing selection at the prion protein gene consistent with prehistoric Kurulike epidemics
Science, 2003Co-Authors: Simon Mead, MP Alpers, Tracy Campbell, Michael P H Stumpf, Jerome Whitfield, Jonathan A Beck, M Poulter, James Uphill, David Goldstein, Elizabeth FisherAbstract:Kuru is an acquired prion disease largely restricted to the Fore linguistic group of the Papua New Guinea Highlands, which was transmitted during endocannibalistic feasts. Heterozygosity for a common polymorphism in the human prion protein gene (PRNP) confers relative resistance to prion diseases. Elderly survivors of the Kuru epidemic, who had multiple exposures at mortuary feasts, are, in marked contrast to younger unexposed Fore, predominantly PRNP 129 heterozygotes. Kuru imposed strong balancing selection on the Fore, essentially eliminating PRNP 129 homozygotes. Worldwide PRNP haplotype diversity and coding allele frequencies suggest that strong balancing selection at this locus occurred during the evolution of modern humans.
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the incubation period of Kuru
Epidemiology, 2002Co-Authors: Jerome Huillard N Daignaux, MP Alpers, Simon Cousens, Jean Maccario, Dominique Costagliola, P G R Smith, Annick AlperovitchAbstract:Background. Kuru is a transmissible spongiform encephalopathy that was identified in Papua New Guinea in the late 1950s. Several thousand cases of the disease occurred during a period of several decades. Epidemiologic investigations implicated ritual endocannibalistic funeral feasts as the likely ro
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increased susceptibility to Kuru of carriers of the prnp 129 methionine methionine genotype
The Journal of Infectious Diseases, 2001Co-Authors: Heesuk Lee, MP Alpers, Paul Brown, Larisa Cervenakova, Ralph M Garruto, Carleton D Gajdusek, Lev G GoldfarbAbstract:Kuru reached epidemic proportions by the mid-twentieth century among the Fore people of New Guinea and disappeared after the abolition of cannibalistic rituals. To determine susceptibility to Kuru and its role in the spread and elimination of the epidemic, we analyzed the PRNP gene coding sequences in 5 Kuru patients; no germline mutations were found. Analysis of the PRNP 129 methionine (M)/valine (V) polymorphism in 80 patients and 95 unaffected controls demonstrated that the Kuru epidemic preferentially affected individuals with the M/M genotype. A higher representation of M/M carriers was observed among the affected young Fore males entering the age of risk, whereas a lower frequency of M/M homozygotes was found among the survivors. M/V and V/V genotypes predisposed to a lower risk of disease development and longer incubation times. These findings are relevant to the current outbreak of variant Creutzfeldt-Jakob disease (vCJD) in the United Kingdom, because all vCJD patients tested thus far have been M/M carriers.
Carleton D Gajdusek - One of the best experts on this subject based on the ideXlab platform.
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Increased Susceptibility to Kuru of Carriers of the PRNP 129 Methionine/
2016Co-Authors: Methionine Genotype, Ralph M Garruto, Carleton D Gajdusek, Michael P. Alpers, Lev G GoldfarbAbstract:Kuru reached epidemic proportions by the mid-twentieth century among the Fore people of New Guinea and disappeared after the abolition of cannibalistic rituals. To determine susceptibility to Kuru and its role in the spread and elimination of the epidemic, we analyzed the PRNP gene coding sequences in 5 Kuru patients; no germline mutations were found. Analysis of the PRNP 129 methionine (M)/valine (V) polymorphism in 80 patients and 95 unaffected controls demonstrated that the Kuru epidemic preferentially affected individuals with the M/M genotype. A higher representation of M/M carriers was observed among the affected young Fore males entering the age of risk, whereas a lower frequency of M/M ho-mozygotes was found among the survivors. M/V and V/V genotypes predisposed to a lower risk of disease development and longer incubation times. These ®ndings are relevant to the current outbreak of variant Creutzfeldt-Jakob disease (vCJD) in the United Kingdom, because all vCJD patients tested thus far have been M/M carriers. Kuru, the prototype human transmissible spongiform en-cephalopathy (TSE), was until recently the only example of oral transmission occurring in humans. The latest TSE member
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oral transmission of Kuru creutzfeldt jakob disease and scrapie to nonhuman primates commentary
The Journal of Infectious Diseases, 2004Co-Authors: Clarence J Gibbs, Colin L Masters, Carleton D Gajdusek, H L Amyx, Alfred Bacole, Kenneth L TylerAbstract:Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were exposed to the infectious agents only by their nonforced consumption of known infectious tissues. The asymptomatic incubation period in the one monkey exposed to the virus of Kuru was 36 months; that in the two monkeys exposed to the virus of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively. Careful physical examination of the buccal cavities of all of the monkeys failed to reveal signs of oral lesions. One additional monkey similarly exposed to Kuru has remained asymptomatic during the 39 months that it has been under observation.
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increased susceptibility to Kuru of carriers of the prnp 129 methionine methionine genotype
The Journal of Infectious Diseases, 2001Co-Authors: Heesuk Lee, MP Alpers, Paul Brown, Larisa Cervenakova, Ralph M Garruto, Carleton D Gajdusek, Lev G GoldfarbAbstract:Kuru reached epidemic proportions by the mid-twentieth century among the Fore people of New Guinea and disappeared after the abolition of cannibalistic rituals. To determine susceptibility to Kuru and its role in the spread and elimination of the epidemic, we analyzed the PRNP gene coding sequences in 5 Kuru patients; no germline mutations were found. Analysis of the PRNP 129 methionine (M)/valine (V) polymorphism in 80 patients and 95 unaffected controls demonstrated that the Kuru epidemic preferentially affected individuals with the M/M genotype. A higher representation of M/M carriers was observed among the affected young Fore males entering the age of risk, whereas a lower frequency of M/M homozygotes was found among the survivors. M/V and V/V genotypes predisposed to a lower risk of disease development and longer incubation times. These findings are relevant to the current outbreak of variant Creutzfeldt-Jakob disease (vCJD) in the United Kingdom, because all vCJD patients tested thus far have been M/M carriers.
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relationship of microglia and scrapie amyloid immunoreactive plaques in Kuru creutzfeldt jakob disease and gerstmann strausler syndrome
Acta Neuropathologica, 1994Co-Authors: Don C Guiroy, Pawel P Liberski, Ikuro Wakayama, Carleton D GajdusekAbstract:Kuru, Creutzfeldt-Jakob disease (CJD) and Gerstmann-Straussler syndrome (GSS) are transmissible dementias affecting humans characterized neuropathologically by intraneuronal vacuolation, spongiform change, astrocytic hypertrophy and hyperplasia and the variable presence of amyloid plaques. It has been suggested that microglia are amyloid-forming cells, which play an essential role in amyloid plaque formation. To study the relationship between microglia and amyloid plaques in Kuru, CJD and GSS, cerebellar tissues were examined by the double-immunostaining technique using anti-ferritin antibodies as the microglial marker and anti-scrapie amyloid antibody as plaque marker. Ferritin-immunoreactive microglia were observed interdigitating with and among unicentric, multicentric and diffuse types of scrapie amyloid-immunoreactive plaques and were found to a lesser extent in the neuropil. In Kuru and CJD, scrapie amyloid-immunoreactive plaques were predominantly unicentric and were observed in the granular layer. In Kuru, 53% of the amyloid plaques were associated with microglia, whereas only 30% of plaques in CJD were. In contrast, scrapie-amyloid-immunoreactive plaques in GSS were of the multicentric type, predominantly observed in the molecular layer, and 90% of these plaques were associated with microglia. Our data indicate that microglia are frequently associated with scrapie amyloid-immunoreactive plaques in GSS, less commonly in Kuru and to a much lesser extent in CJD, suggesting that microglia may play a variable but important role in the formation of plaques in the transmissible spongiform encephalopathies.
Beata Sikorska - One of the best experts on this subject based on the ideXlab platform.
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Kuru the first human prion disease
Viruses, 2019Co-Authors: Pawel P Liberski, Beata Sikorska, Agata Gajos, Shirley LindenbaumAbstract:Kuru, the first human prion disease was transmitted to chimpanzees by D. Carleton Gajdusek (1923–2008). In this review, we summarize the history of this seminal discovery, its anthropological background, epidemiology, clinical picture, neuropathology, and molecular genetics. We provide descriptions of electron microscopy and confocal microscopy of Kuru amyloid plaques retrieved from a paraffin-embedded block of an old Kuru case, named Kupenota. The discovery of Kuru opened new vistas of human medicine and was pivotal in the subsequent transmission of Creutzfeldt–Jakob disease, as well as the relevance that bovine spongiform encephalopathy had for transmission to humans. The transmission of Kuru was one of the greatest contributions to biomedical sciences of the 20th century.
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Kuru the first prion disease
Advances in Experimental Medicine and Biology, 2012Co-Authors: Pawel P Liberski, Beata Sikorska, Paul BrownAbstract:Kuru disease is linked with the name of D. Carleton Gajdusek and he was the first to show that this human neurodegenerative disease can be transmitted to chimpanzees and subsequently classified as a transmissible spongiform encephalopathy (TSE), or slow unconventional virus disease. It was first reported to Western world in 1957 by Gajdusek and Vincent Zigas,1,2 and in 1975 a complete bibliography of Kuru was published by Alpers et al.3 “Kuru” in the Fore language in Papua New Guinea means to shiver from fever and cold. The disease has been found to spread through ritualistic cannibalism and is an invariably fatal cerebellar ataxia accompanied by tremor, choreiform and athetoid movements. Neuropathologically, Kuru is characterized by the presence of amyloid “Kuru” plaques.
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ultrastructural characteristics or evaluation of creutzfeldt jakob disease and other human transmissible spongiform encephalopathies or prion diseases
Ultrastructural Pathology, 2010Co-Authors: Pawel P Liberski, Beata Sikorska, Herbert Budka, J J Hauw, Nicolas Kopp, Nathalie Streichenberger, Pierrie Giraud, Jan Boellaard, Gabor G Kovacs, James W. IronsideAbstract:The authors report on a large series of human prion diseases to establish ultrastructural characteristics that may be useful for their diagnosis. For Creutzfeldt-Jakob disease (CJD and its variant, vCJD) and fatal familial insomnia (FFI) only vacuolation (spongiform change) and the presence of tubulovesicular structures are consistent findings. Other changes, such as the presence of myelinated vacuoles, branching cisternae, neuroaxonal dystrophy, and autophagic vacuoles, were present in different proportions in either CJD or FFI, but they are nonspecific ultrastructural findings that can also occur in other neurodegenerative conditions. The hallmark of Gerstmann-Straussler-Scheinker disease (GSS) and vCJD is the amyloid plaque, but plaques of GSS and Kuru are different than those of vCJD. Whereas the former are typical unicentric Kuru type or multicentric plaques, the latter are unicentric florid plaques. Also, Kuru plaques are nonneuritic, whereas GSS florid plaques are usually neuritic; however, a proportion of plaques from GSS was also found to have nonneuritic characteristics. Thus, the presence or absence of dystrophic neurites is not a discriminatory factor for GSS and vCJD. Furthermore, plaques from GSS with different mutations were also slightly different. In GSS with mutations P102L, 232T, and A117V plaques were stellate while in 1 case with 144 base-pair insertion and in GSS-A117V, round plaques were also observed, and typical primitive neuritic plaques, i.e., composed of dystrophic neurites with little or no amyloid, were found only in a P102L case from the original Austrian family. In 2 cases of sporadic CJD, the Kuru stellate plaque predominated.
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ultrastructural study of florid plaques in variant creutzfeldt jakob disease a comparison with amyloid plaques in Kuru sporadic creutzfeldt jakob disease and gerstmann straussler scheinker disease
Neuropathology and Applied Neurobiology, 2009Co-Authors: Beata Sikorska, Pawel P Liberski, Herbert Budka, Tomasz Sobow, James W. IronsideAbstract:Background: Although the histological features of the amyloid plaques in variant Creutzfeldt–Jakob disease (vCJD) are distinct from those in other forms of prion disease [Kuru, sporadic Creutzfeldt–Jakob disease (sCJD) and Gerstmann–Straussler–Scheinker disease (GSS)], their ultrastructural features have only been described in a single case report. Aims: To study vCJD plaques systematically and compare them with plaques in Kuru, sCJD, GSS and Alzheimer disease (AD). Methods: Amyloid plaques were studied by transmission electron microscopy and image analysis in five cases of vCJD, three cases of GSS, two cases of sCJD, one case of Kuru and five cases of AD. Immunohistochemistry was performed on paraffin sections from one case of vCJD, two cases of GSS, one case of Kuru and two cases of sCJD. Results: The florid plaques in vCJD were either compact or more diffuse; in both forms, the radiating fibrils were organized into thick ‘tongues’, in contrast to Kuru plaques. Dystrophic neurites (DNs) containing lysosomal electron-dense bodies or vesicles surrounded florid plaques. Microglial cells were found within florid plaques; occasional amyloid fibrils were identified in membrane-bound pockets of microglial cells. In vCJD, there was significant tau immunoreactivity in DNs around florid plaques while, in sCJD, GSS and Kuru, minimal tau immunoreactivity was observed around plaques. Conclusions: The ultrastructure of the florid plaques and DNs in vCJD is more reminiscent of neuritic plaques in AD than Kuru or multicentric plaques. These findings may reflect differences both in the strains of the transmissible agents responsible for these disorders and in host factors.
Tarigan Hendri - One of the best experts on this subject based on the ideXlab platform.
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PENYEBARAN KURA-KURA BERDASARKAN HABITAT SUNGAI DAN RAWA DI HUTAN SUAKA ALAM PASAR NGALAM, AIR PERIUKAN, KABUPATEN SELUMA
2007Co-Authors: Fitri Yunia, Ruyani Aceng, Tarigan HendriAbstract:Telah dilakukan penelitian tentang penyebaran kura-kura berdasarkan habitat sungai dan rawa di sekitar Hutan Suaka Alam (HSA) Pasar Ngalam, Air Periukan, Kabupaten Seluma. Penelitian ini dimulai dari bulan Desember 2006 hingga Maret 2007. Metode yang digunakan adalah metode survai. Adapun tujuan dari penelitian ini yaitu mengetahui jenis kura–kura yang terdapat di sekitar Hutan Suaka Alam Pasar Ngalam, Air Periukan, Kabupaten Seluma dan untuk mengetahui penyebaran kura–kura berdasarkan habitat sungai dan rawa. Hasil pengukuran faktor-faktor abiotik pada habitat sungai yaitu berupa suhu dengan kisaran 27-32 0 C, pH dengan kisaran 6-7, kecepatan arus dengan kisaran 0,12-0,46m/d dan kekeruhan dengan kisaran 29-73 cm, sedangkan pada rawa suhunya berkisar 29-33 0 C, dan pH dengan kisaran 4-6. Berdasarkan hasil penelitian yang dilakukan selama + 2 bulan ditemukan kura-kura sebanyak 58 ekor, dimana pada habitat rawa ditemukan kura-kura Cuora amboinensis sebanyak 35 ekor (60,34%) dan Cyclemys oldhamii ditemukan sebanyak 21 ekor (36,21%), sedangkan pada habitat sungai hanya ditemukan satu jenis kurakura yaitu Cyclemys oldhamii yang berjumlah 2 ekor (3,45%). Kura-kura Cuora amboinensis merupakan kura-kura yang paling banyak ditemukan. Adapun penyebaran kura-kura di Desa Pasar Ngalam ini meliputi seluruh kawasan Desa Pasar Ngalam, Air Periukan, Kabupaten Seluma sedangkan pada kawasan Hutan Suaka Alam sendiri sudah jarang ditemukan kura-kura
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SEBARAN KURA-KURA AIR TAWAR DAN KURA-KURA TERRESTRIAL DI KABUPATEN KEPAHIANG BENGKULU
2007Co-Authors: Puspitasari Rita, Ruyani Aceng, Tarigan HendriAbstract:Penelitian ini bertujuan untuk mengetahui jenis serta sebaran kura-kura habitat air tawar dan terrestrial di Kabupaten Kepahiang Bengkulu. Pengambilan data dilakukan selama bulan Juni sampai Agustus 2007. Data diambil melalui penyebaran kuesioner dan wawancara dengan kolektor dan penangkap kura-kura. Kemudian dilakukan pengkoleksian kura-kura dan verifikasi lapangan untuk penangkapan kurakura secara langsung dan pengukuran faktor-faktor abiotik. Kura-kura yang telah terkumpul didentifikasi dengan mencocokkan spesimen dengan gambar pada buku identifikasi Iskandar (2000) dan Ernst dan Barbour (1989). Berdasarkan hasil wawancara dan penyebaran kuesioner kepada sepuluh responden sebaran kura-kura di Kabupaten Kepahiang ada di delapan kecamatan yaitu Kecamatan Kepahiang, Ujan Mas, Bermani Ilir, Tebat Karai, Kabawetan, Merigi, Muara Kemumu dan Seberang Musi. Hasil pengkoleksian didapatkan 17 ekor kura-kura dari empat jenis kura-kura yaitu Cyclemys oldhamii, Siebenrockiella crassicollis, Dogania subplana dan Amyda cartilaginea. Jenis Dogania subplana merupakan jenis kura-kura yang paling banyak ditemukan, yaitu berjumlah 8 ekor. Sebaran dari empat jenis kura-kura yang berhasil ditemukan meliputi kecamatan Kepahiang dan kecamatan Seberang Musi
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DEPARTEMEN PENDIDIKAN NASIONAL SEBARAN KURA-KURA AIR TAWAR DAN KURA-KURA TERESTERIAL DI KABUPATEN BENGKULU UTARA
2007Co-Authors: Novieta Yuyun, Ruyani Aceng, Tarigan HendriAbstract:Penelitian ini bertujuan untuk mengetahui jenis-jenis sebaran kura-kura air tawar dan teresterial yang ada di Kabupaten Bengkulu Utara. Pengambilan data dilakukan dari bulan Juni-Agustus 2007 di Kabupaten Bengkulu Utara. Data diperoleh dari hasil wawancara serta jawaban dari kuesioner yang di isi oleh pengumpul kura-kura yang berperan sebagai responden yang ada di Kabupaten Bengkulu Utara. Berdasarkan hasil wawancara dan pengisisan kuesioner daerah sebaran kura-kura di Bengkulu Utara ada di Enam kecamatan yaitu kecamatan Kerkap, Lais, Ketahun, Argamakmur, Batik Nau dan Padang Jaya. Kemudian dilakukan pengkoleksian dan verifikasi lapangan. Setelah dilakukan pengkoleksisan kura-kura yang kemudian di identifikasi dengan mencocokkan spesimen pada pustaka acuan yaitu buku Ernst dan Barbour (1989) “ Turtle of the word” dan Iskandar (2000)” Kura-kura dan Buaya Indonesia dan Papuanugini”. Selama melakukan penelitian, dari pengumpul peneliti menemukan 16 ekor kura-kura yang kemudian diukur panjang karapaks lebar karapaks dan berat badan karapaks, sedikitnya jumlah kura-kura yang ditemukan di karenakan kurangnya minat pengumpul dan pedagang kura-kura untuk mengumpulkan kura-kura dikarenakan turunnya harga jual kura-kura. Pada saat survey lapangan Peneliti juga melakukan pengukuran faktor abiotik, hasil pengukuran faktor abiotik diperoleh suhu berkisar pada 26- 32 o C, pH berkisar 5- 6, Kecepatan arus berkisar 0,29-0,41, Kekeruhan berkisar 33-52,5 dan kelembaban udara 51-91%. Dari hasil penelitian kura-kura yang ditemukan di kabupaten Bengkulu Utara ada 4 jenis yaitu: Notochelys platynota, Cyclemys oldhamii, Cuora amboinensis dan Dogania subplan
