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Ditemukan 308 dokumen yang sesuai dengan query
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Maria Widiastuti
Depok: Fakultas Matematika dan Ilmu Pengetahuan Alam Universitas Indonesia, 2009
S27824
UI - Skripsi Open  Universitas Indonesia Library
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Gustina Indriati
1999
T-pdf (Tesis sedang dalam proses digitalisasi)
UI - Tesis Membership  Universitas Indonesia Library
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Ahmad Ibrahim Badry
"Tesis ini adalah kajian filosofis atas pengembangan komputasi DNA yang menggunakan analisis Arkeologi dan Genealogi dari Michel Foucault. Dalam penelitian ini, ditemukan adanya kesejajaran antara tiga episteme yang telah diungkap Foucault dengan tiga teknologi komputasi yang telah dikembangkan (penerapan metode Arkeologi) dan suatu jenis exercise atas kekuasaanpengetahuan sebagaimana diurai Foucault dengan titik tekan pada normalisasi, pengembangan model Artificial Intelligent Creatures, dan kemungkinan model panopticon molekuler (penerapan metode Genealogi). Hasil penelitian ini juga mengandaikan bahwa problem yang muncul harus disikapi dengan rumusan etika baru. Sebab, etika yang sudah dikembangkan tidak dapat mengatasi persoalan yang sekiranya dapat terjadi dengan dikembangkannya komputasi DNA.

This thesis is a philosophical study about DNA computation development which uses Genealogical and Archaeological analytics from Michel Foucault. In this thesis had been found parallelism between three episteme which described by Foucault with the three technology of computation (Archaeological applied) and a kind of exercise of knowledge-power as identified by Foucault which focusing in normalization, developing Artificial Intelligent Creatures, and possibility of molecular panopticon (Genealogical applied). This thesis supposes to formulate a new ethical approach. It is because the ethics which were developed not have an adequacy to solve a problematical discourse which comes from DNA computation development.
"
Depok: Universitas Indonesia, 2011
T28641
UI - Tesis Open  Universitas Indonesia Library
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Meta W.Djojosubroto
"ABSTRAK
Analisis DNA mitokondria menggunakan enzim restriksi merupakan salah satu cara yang dapat digunakan untuk menunjukkan hubungan genetic antarpopulasi. Situs restriksi HaeIII pada pasangan basa (pb) 663 (HaeIII663), AluI pada pb 5176 (AluI5176), Ddel pada pb 10394 (Ddel10394), dan AluI pada pb 10397 (AluI10397) merupakan situs-situs restriksi tersebut, tertama presentase situs restriksi Ddel10394 dan AluI10397, pada populasi Minahasa, Kaili, Bugis, dan Makassar. Metode yang digunakan adalah amplifikasi DNA mitokondria dengan polymerase chain rection (PCR), elektroforesis pada gel agarosa atau gel poliakrilamida, dan digesti fragmen DNA mitokondria dengan enzim restriksi. Hasil pengamatan menunjukkan 6 situs restriksi, yaitu HaeIII663, AluI5176, AluI6022, AluI6891, Ddel10394, dan AluI10397. Berdasarkan terdapat atau tidaknya situs restriksi Ddel10394 dan AluI10397, hasil dikelompokkan menjadi 3 haplotipe, yaitu haplotype Ddel10394AluI10397 (+ +), Ddel10394AluI10397 (+ -), dan Ddel10394AluI10397 (- -). Haplotipe Ddel10394AluI10397 (+ +) merupakan yang paling banyak ditemukan pada masing-masing populasi yang diteliti yaitu pada 48,48% sampel Minahasa, 75% sampel Kaili, 53,85% sampel Bugis, dan 62,07% sampel Makassar. "
Depok: Fakultas Matematika dan Ilmu Pengetahuan Alam. Universitas Indonesia, 1999
S-Pdf
UI - Skripsi Membership  Universitas Indonesia Library
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Dwi Hilda Putri
"Pendahuluan: Infeksi dengue merupakan salah satu penyakit endemik di daerah tropis dan subtropis yang disebabkan oleh virus dengue (DENV). Hingga saat ini belum ada antiviral yang efektif untuk infeksi dengue. Penyebaran dan sirkulasi serotipe DENV berfariasi di setiap lokasi geografi, hal ini menyulitkan dalam melakukan evaluasi vaksin DENV. Oleh karena itu perlu dikembangkan kandidat vaksin DENV menggunakan strain Indonesia supaya dapat memberikan proteksi maksimal. Pada peneltian ini dikembangkan kandidat vaksin DNA tetravalen DENV berbasis gen prM-E DENV strain Indonesia.
Metode: Konstruksi plasmid rekombinan kandidat vaksi dilakukan dengan cara menyisipkan gen prM-E setiap serotipe DENV ke dalam vektor pUMVC4a. Gen prM-E DENV merupakan strain Indonesia, yang diamplifikasi dari serum pasien yang terinfeksi dengan virus ini. Kemampuan plasmid rekombinan mengekspresikan protein prM-E DENV diuji di sel mamalia. Kemampuan kandidat vaksin menginduksi respon imun humoral dievaluasi secara monovalen dan tetravalen di mencit jenis ddY. Titer IgG anti dengue diperiksa menggunakan teknik ELISA, sedangkan titer antibodi netralisasi di tentukan dengan uji FRNT. Proteksi vaksin terhadap mencit yang diimunisasi dievaluasi dengan melakukan uji tantang menggunakan sel K562 yang diinfeksi DENV-2. Viremi virus di tentukan dengan menggunakan teknik foccus assay.
Hasil: Konstruksi plasmid rekombinan kandidat vaksin DENV-1 dan DENV-3 sudah berhasil dilakukan. Plasmid dapat mengekspresikan protein prM-E DENV di sel mamalia, namun karakteristik dan kinetik protein masih belum dapat diketahui dengan jelas. Keempat kandidat vaksin DNA yang sedang dikembangkan dapat menginduksi respon imun, baik secara monovalen maupun tetravalen. Imunisasi secara tetravalen dapat memberikan proteksi pada mencit yang diuji tantang dengan sel K562 yang diinfeksi dengan DENV-2.

Introduction: Dengue infections are caused by dengue viruses (DENV) and are endemic in tropical and subtropical regions. At present, there is no effective antiviral treatment for dengue infection. Distribution and circulation of DENV serotypes varies by geographic location, it is difficult to evaluate DENV vaccine. Therefore, it is necessary to develop a vaccine candidate DENV using Indonesian strains in order to provide maximum protection. However, in this study, we constructed a recombinant plasmid-based prM-E gene from the Indonesia strain as a DENV DNA vaccine candidate.
Methode: The recombinant plasmid was prepared by inserting the prM-E gene from each DENV serotypes into the plasmid backbone pUMVC4a. prM-E gene an Indonesia strain, which was amplified from patient sera infected with DENV. The ability of the recombinant plasmid expressing the prM-E DENV protein tested in mammalian cells. The ability of candidate vaccines induce humoral immune responses were evaluated monovalent and tetravalent in ddY mice. IgG titers of anti-dengue examined using ELISA technique, while neutralizing antibody titers determined with FRNT test. Vaccine protection against the immunized mice was evaluated by conducting challenge test using K562 cells infected by DENV-2. Viremia was determined by using the foccus assay.
Result: Construction of recombinant plasmid vaccine candidate DENV-1 and DENV-3 was successfully performed. Plasmids can express prM-E DENV proteins in mammalian cells, but the characteristics and kinetics of protein still can not clearly known. Fourth DNA vaccine candidate that is being developed to induce an immune response, either monovalent or tetravalent. Tetravalent immunization may provide protection in mice challenged tested with K562 cells infected with DENV-2.
"
Jakarta: Fakultas Kedokteran Universitas Indonesia, 2015
D-Pdf
UI - Disertasi Membership  Universitas Indonesia Library
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Agitha Nurul Komara Putri
"Pada penelitian ini dilakukan studi pembentukan DNA adduct 8-OHdG sebagai biomarker kerusakan DNA akibat oksidatif stress. Penelitian ini dilakukan dengan mereaksikan basa DNA 2?-deoksiguanosin 5?-monofosfat dengan senyawa-senyawa yang dapat berkontribusi menghasilkan radikal seperti Benzena, Naftalena, dan Ni(II). Profil pembentukan 8-OHdG dilakukan pada suhu 37°C dan 60°C, pH 7,4 dan pH 8,4 , dengan waktu inkubasi 5 jam serta dengan variasi penambahan hidrogen peroksida. Hasil adduct dianalisis menggunakan HPLC reversed phase dengan detektor UV pada panjang gelombang 254 nm. Eluen yang digunakan yaitu campuran Buffer fosfat pH 6,7 10 mM dan Metanol, dengan perbandingan 85:15. Waktu retensi dGMP standar yang diperoleh yaitu 7,3 menit dan 8-OHdG pada 9,0 menit. Hasil analisis yang diperoleh menunjukan bahwa 8-OHdG terbentuk akibat reaksi deoksiguanosin monofosfat dengan hidroksi radikal yang dihasilkan oleh benzena, naftalena, dan Ni(II). Pada penambahan hidrogen peroksida terlihat bahwa adduct terbentuk pada semua variasi kondisi, sedangkan tanpa penambahan hidrogen peroksida, adduct hanya terdeteksi pada suhu 60°C dengan pH 7,4 dan 8,4. Sementara itu pada suhu 37°C, adduct 8-OHdG tidak terdeteksi. Hasil penelitian menunjukan bahwa pembentukan adduct dipengaruhi oleh suhu. Pada kondisi suhu yang lebih tinggi, jumlah adduct yang dihasilkan lebih banyak.

This research was carried out to study DNA adduct 8-OHdG formation as biomarkers of DNA damage due to oxidative stress. This research was conducted by reacting the nucleotide 2?deoxyguanosine-5'-monophosphate with compounds that can contribute to generate radicals such as Benzene, Naphthalene, and Ni(II). Formation of 8-OHdG was performed at 37°C and 60°C, pH 7,4 and pH 8,4 for 5 hour incubation time and variation of the addition of hydrogen peroxide. The adduct obtained from these reactions were analyzed using reversed phase HPLC with UV detector at a wavelength of 254 nm. Eluent was used in this study was a mixture of phosphate buffer pH 6,7 10 mM and methanol at ratio 85:15 The retention time of dGMP and 8-OHdG obtanied at 7,3 minute and at 9,0 minute respectively. The HPLC analysis showed that 8-OHdG was successfully formed by reaction of deoxyguanosine monophosphate with hydroxy radical generated by benzene, naphthalene, and Ni (II). In the presence of hydrogen peroxide, 8-OHdG was formed in all variation conditions, whereas in absence of hydrogen peroxide, the adduct was detected only in the condition at temperature of 60°C with a pH of 7,4 and 8,4 . While at 37°C, 8-OHdG was undetected. This study shows that adduct formation was affected by temperature. The higher the temperatures, the greater the number of adducts would be obtained."
Depok: Universitas Indonesia, 2016
S62592
UI - Skripsi Membership  Universitas Indonesia Library
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Dyah Haryuningtyas Sawitri
"ABSTRAK
Pendahuluan :Trypanosoma evansi adalah protozoa berflagella yang bersirkulasi
di dalam darah secara ekstraseluler sebagai agen penyakit Surra serta menyerang
seluruh hewan vertebrata, serta berpotensi sebagai zoonosis. Informasi virulensi
isolat T. evansi sangat dibutuhkan untuk penentuan strategi pengobatan Surra di
daerah wabah dan endemis. Penelitian ini bertujuan untuk mengetahui variasi
virulensi isolat T. evansi yang dikoleksi dari berbagai wilayah di Indonesia
termasuk memperoleh marka genetik serta mengetahui profil sitokin pada mencit.
Disamping itu, dilakukan juga uji serologis pada peternak di daerah wabah Surra
Metode : Sebanyak 32 isolat lokal T. evansi dikonfimasi dengan PCR multiplex
(ITS-1; Te Ro Tat 1,2 VSG dan ESAG6/7), selanjutnya diuji virulensinya dengan
menginfeksikan104 parasit pada mencit galur DDY. Studi genotyping populasi
T. evansi dievaluasi dengan 8 marka mikrosatelit Tbb-1, Tbb-5, Tbb-9, Tbb-10,
MORF2-CA, M6C8-CA, MEST-19AT, MT3033-AT. Dua isolat yang berbeda
virulensi (tinggi-Bang87 dan rendah-Pml 287) dipilih untuk uji imunopatogenitas
sedangkan serum peternak diuji dengan metode FELISA dan CATT T. evansi.
Hasil : Dari 32 isolat tersebut terbagi menjadi 17 isolat bervirulensi tinggi, 11
isolat bervirulensi moderat dan 4 isolat bervirulensi rendah dengan 8 pola tingkat
parasitemia. Analisis Neigbour Joining (NJ) terhadap 8 lokus berdasarkan Multi
Lokus Genotipe (MLG) mikrosatelit terbagi menjadi 4 populasi, yaitu MLG A,
MLG B, MLG C dan MLG D. Analisis terhadap struktur populasi juga
memberikan hasil yang sama dengan terbentuknya 4 klaster. Hasil ini juga
membuktikan bahwa marka yang digunakan bersifat spesifik lokasi. Sebanyak
tiga marka mengindikasikan adanya asosiasi antara virulensi dan MLG (Tbb-1,
M6C8-CA dan MEST-19). Kadar IFN-γ meningkat secara tajam pada mencit
yang diinfeksi isolat Bang 87 pada 4hpi berkorelasi negatif yang signifikan
(p<0,05) dengan kadar IL-10, sedangkan pada mencit yang diinfeksi isolat Pml
287, peningkatan kadar IFNγ berkorelasi positif dengan kadar IL-10. Kematian
dini pada mencit yang diinfeksi isolat Bang 87 disebabkan oleh sindrom respon
inflamasi sitemik. Hasil uji serologis menunjukkan bahwa 4 dari 24 serum
peternak (16,67%) didaerah wabah positif dan seluruh serum negatif untuk
daerah non wabah.
Kesimpulan : Variasi virulensi T. evansi isolat Indonesia memiliki karakter
molekular yang berbeda serta menginduksi pola mediator sitokin pro dan
antiinflamasi yang berhubungan dengan pola manifestasi patologi yang berbeda.
Marka mikrosatelit pada studi ini mampu mengidentifikasi asal usul sumber
infeksi, dan tingkat virulensi isolat yang sedang bersirkulasi. Surra berpotensi
sebagai emerging zoonosis, terutama bagi peternak didaerah wabah dan endemis.

ABSTRACT
Introduction: Trypanosoma evansi is an extracellular homoflagellate of
protozoan blood causing Surra. The disease attacks all vertebrates and potentially
as zoonosis. Virulence analysis of T. evansi is a fundamental knowledge to
determine treatment strategies of Surra in both outbreak and endemic areas. The
aims of this study was to determine virulence variation of T. evansi isolates
collected from various regions in Indonesia and to obtained genetic markers as
well as cytokine profile in mice. In addition, serological test was also carried out
to farmers living in a Surra outbreak area
Methods: Total of 32 isolates of T. evansi corfirmed with multiplex PCR (ITS-1;
Te Ro Tat 1.2 VSG and ESAG6 / 7), were further tested with inoculation 104
parasite in DDY mice strain. The population genotype study of T. evansi was
evaluated with 8 microsatellite markers (Tbb-1, Tbb-5, Tbb-9, Tbb-10-CA
MORF2, M6C8-CA, MEST-19AT, MT3033-AT). Two different virulence
isolates, high-Bang87 and low-PML287 was selected to cytokine profile analysis
using ELISA, while farmers sera were tested using CATT and FELISA kits
Results: A total of 32 local isolates of T. evansi tested were divided into three
different virulences, i.e. 17 high virulence isolates, 11 moderate virulence and 4
low virulence isolates forming 8 pattern parasitemia levels. Based on Neigbour
Joining (NJ) on 8 Microsatellite Multilocus Genotype (MLGs) was grouped into
4 populations (MLG A, MLG B, MLG C and MLG D). Stucture population
analysis also provided the similar result generating 4 clusters. These results
indicated that the markers used in this study had a specific location property.
Three markers (TBB-1, and MEST M6C8-CA-19) showed an association
between virulence and MLG. IFN-γ levels increased significantly in mice
infected with Bang 87 isolate on 4th day post infection (dpi) having a significant
negative correlation (p <0.05) with increased IL-10 levels, whereas in mice
infected by PML 287 isolate, IFN-γ levels were positively correlated with IL- 10
levels. Early death in mice infected with Bang87 isolates was caused by systemic
inflammatory response syndrome (SIRS). Result of serological test showed that 4 out
of 24 farmers sera (16.67%) from outbreak areas are positive and all sample from
free area are negative.
Conclusion: Virulence variation of T. evansi isolates from Indonesia has
different molecular character and induces cytokine pattern of pro and antiinflammatory
mediators associated with distinct patterns of pathological
manifestations. The microsatellite markers found in this study are able to identify
origin of infection sources dan determine virulence of isolates that circulate on the
outbreak area. Surra is potential new emerging disease, particularly for farmers or
immunosurpressed individuals who living in both endemic and outbreak areas;Introduction: Trypanosoma evansi is an extracellular homoflagellate of
protozoan blood causing Surra. The disease attacks all vertebrates and potentially
as zoonosis. Virulence analysis of T. evansi is a fundamental knowledge to
determine treatment strategies of Surra in both outbreak and endemic areas. The
aims of this study was to determine virulence variation of T. evansi isolates
collected from various regions in Indonesia and to obtained genetic markers as
well as cytokine profile in mice. In addition, serological test was also carried out
to farmers living in a Surra outbreak area
Methods: Total of 32 isolates of T. evansi corfirmed with multiplex PCR (ITS-1;
Te Ro Tat 1.2 VSG and ESAG6 / 7), were further tested with inoculation 104
parasite in DDY mice strain. The population genotype study of T. evansi was
evaluated with 8 microsatellite markers (Tbb-1, Tbb-5, Tbb-9, Tbb-10-CA
MORF2, M6C8-CA, MEST-19AT, MT3033-AT). Two different virulence
isolates, high-Bang87 and low-PML287 was selected to cytokine profile analysis
using ELISA, while farmers sera were tested using CATT and FELISA kits
Results: A total of 32 local isolates of T. evansi tested were divided into three
different virulences, i.e. 17 high virulence isolates, 11 moderate virulence and 4
low virulence isolates forming 8 pattern parasitemia levels. Based on Neigbour
Joining (NJ) on 8 Microsatellite Multilocus Genotype (MLGs) was grouped into
4 populations (MLG A, MLG B, MLG C and MLG D). Stucture population
analysis also provided the similar result generating 4 clusters. These results
indicated that the markers used in this study had a specific location property.
Three markers (TBB-1, and MEST M6C8-CA-19) showed an association
between virulence and MLG. IFN-γ levels increased significantly in mice
infected with Bang 87 isolate on 4th day post infection (dpi) having a significant
negative correlation (p <0.05) with increased IL-10 levels, whereas in mice
infected by PML 287 isolate, IFN-γ levels were positively correlated with IL- 10
levels. Early death in mice infected with Bang87 isolates was caused by systemic
inflammatory response syndrome (SIRS). Result of serological test showed that 4 out
of 24 farmers sera (16.67%) from outbreak areas are positive and all sample from
free area are negative.
Conclusion: Virulence variation of T. evansi isolates from Indonesia has
different molecular character and induces cytokine pattern of pro and antiinflammatory
mediators associated with distinct patterns of pathological
manifestations. The microsatellite markers found in this study are able to identify
origin of infection sources dan determine virulence of isolates that circulate on the
outbreak area. Surra is potential new emerging disease, particularly for farmers or
immunosurpressed individuals who living in both endemic and outbreak areas;Introduction: Trypanosoma evansi is an extracellular homoflagellate of
protozoan blood causing Surra. The disease attacks all vertebrates and potentially
as zoonosis. Virulence analysis of T. evansi is a fundamental knowledge to
determine treatment strategies of Surra in both outbreak and endemic areas. The
aims of this study was to determine virulence variation of T. evansi isolates
collected from various regions in Indonesia and to obtained genetic markers as
well as cytokine profile in mice. In addition, serological test was also carried out
to farmers living in a Surra outbreak area
Methods: Total of 32 isolates of T. evansi corfirmed with multiplex PCR (ITS-1;
Te Ro Tat 1.2 VSG and ESAG6 / 7), were further tested with inoculation 104
parasite in DDY mice strain. The population genotype study of T. evansi was
evaluated with 8 microsatellite markers (Tbb-1, Tbb-5, Tbb-9, Tbb-10-CA
MORF2, M6C8-CA, MEST-19AT, MT3033-AT). Two different virulence
isolates, high-Bang87 and low-PML287 was selected to cytokine profile analysis
using ELISA, while farmers sera were tested using CATT and FELISA kits
Results: A total of 32 local isolates of T. evansi tested were divided into three
different virulences, i.e. 17 high virulence isolates, 11 moderate virulence and 4
low virulence isolates forming 8 pattern parasitemia levels. Based on Neigbour
Joining (NJ) on 8 Microsatellite Multilocus Genotype (MLGs) was grouped into
4 populations (MLG A, MLG B, MLG C and MLG D). Stucture population
analysis also provided the similar result generating 4 clusters. These results
indicated that the markers used in this study had a specific location property.
Three markers (TBB-1, and MEST M6C8-CA-19) showed an association
between virulence and MLG. IFN-γ levels increased significantly in mice
infected with Bang 87 isolate on 4th day post infection (dpi) having a significant
negative correlation (p <0.05) with increased IL-10 levels, whereas in mice
infected by PML 287 isolate, IFN-γ levels were positively correlated with IL- 10
levels. Early death in mice infected with Bang87 isolates was caused by systemic
inflammatory response syndrome (SIRS). Result of serological test showed that 4 out
of 24 farmers sera (16.67%) from outbreak areas are positive and all sample from
free area are negative.
Conclusion: Virulence variation of T. evansi isolates from Indonesia has
different molecular character and induces cytokine pattern of pro and antiinflammatory
mediators associated with distinct patterns of pathological
manifestations. The microsatellite markers found in this study are able to identify
origin of infection sources dan determine virulence of isolates that circulate on the
outbreak area. Surra is potential new emerging disease, particularly for farmers or
immunosurpressed individuals who living in both endemic and outbreak areas;Introduction: Trypanosoma evansi is an extracellular homoflagellate of
protozoan blood causing Surra. The disease attacks all vertebrates and potentially
as zoonosis. Virulence analysis of T. evansi is a fundamental knowledge to
determine treatment strategies of Surra in both outbreak and endemic areas. The
aims of this study was to determine virulence variation of T. evansi isolates
collected from various regions in Indonesia and to obtained genetic markers as
well as cytokine profile in mice. In addition, serological test was also carried out
to farmers living in a Surra outbreak area
Methods: Total of 32 isolates of T. evansi corfirmed with multiplex PCR (ITS-1;
Te Ro Tat 1.2 VSG and ESAG6 / 7), were further tested with inoculation 104
parasite in DDY mice strain. The population genotype study of T. evansi was
evaluated with 8 microsatellite markers (Tbb-1, Tbb-5, Tbb-9, Tbb-10-CA
MORF2, M6C8-CA, MEST-19AT, MT3033-AT). Two different virulence
isolates, high-Bang87 and low-PML287 was selected to cytokine profile analysis
using ELISA, while farmers sera were tested using CATT and FELISA kits
Results: A total of 32 local isolates of T. evansi tested were divided into three
different virulences, i.e. 17 high virulence isolates, 11 moderate virulence and 4
low virulence isolates forming 8 pattern parasitemia levels. Based on Neigbour
Joining (NJ) on 8 Microsatellite Multilocus Genotype (MLGs) was grouped into
4 populations (MLG A, MLG B, MLG C and MLG D). Stucture population
analysis also provided the similar result generating 4 clusters. These results
indicated that the markers used in this study had a specific location property.
Three markers (TBB-1, and MEST M6C8-CA-19) showed an association
between virulence and MLG. IFN-γ levels increased significantly in mice
infected with Bang 87 isolate on 4th day post infection (dpi) having a significant
negative correlation (p <0.05) with increased IL-10 levels, whereas in mice
infected by PML 287 isolate, IFN-γ levels were positively correlated with IL- 10
levels. Early death in mice infected with Bang87 isolates was caused by systemic
inflammatory response syndrome (SIRS). Result of serological test showed that 4 out
of 24 farmers sera (16.67%) from outbreak areas are positive and all sample from
free area are negative.
Conclusion: Virulence variation of T. evansi isolates from Indonesia has
different molecular character and induces cytokine pattern of pro and antiinflammatory
mediators associated with distinct patterns of pathological
manifestations. The microsatellite markers found in this study are able to identify
origin of infection sources dan determine virulence of isolates that circulate on the
outbreak area. Surra is potential new emerging disease, particularly for farmers or
immunosurpressed individuals who living in both endemic and outbreak areas;Introduction: Trypanosoma evansi is an extracellular homoflagellate of
protozoan blood causing Surra. The disease attacks all vertebrates and potentially
as zoonosis. Virulence analysis of T. evansi is a fundamental knowledge to
determine treatment strategies of Surra in both outbreak and endemic areas. The
aims of this study was to determine virulence variation of T. evansi isolates
collected from various regions in Indonesia and to obtained genetic markers as
well as cytokine profile in mice. In addition, serological test was also carried out
to farmers living in a Surra outbreak area
Methods: Total of 32 isolates of T. evansi corfirmed with multiplex PCR (ITS-1;
Te Ro Tat 1.2 VSG and ESAG6 / 7), were further tested with inoculation 104
parasite in DDY mice strain. The population genotype study of T. evansi was
evaluated with 8 microsatellite markers (Tbb-1, Tbb-5, Tbb-9, Tbb-10-CA
MORF2, M6C8-CA, MEST-19AT, MT3033-AT). Two different virulence
isolates, high-Bang87 and low-PML287 was selected to cytokine profile analysis
using ELISA, while farmers sera were tested using CATT and FELISA kits
Results: A total of 32 local isolates of T. evansi tested were divided into three
different virulences, i.e. 17 high virulence isolates, 11 moderate virulence and 4
low virulence isolates forming 8 pattern parasitemia levels. Based on Neigbour
Joining (NJ) on 8 Microsatellite Multilocus Genotype (MLGs) was grouped into
4 populations (MLG A, MLG B, MLG C and MLG D). Stucture population
analysis also provided the similar result generating 4 clusters. These results
indicated that the markers used in this study had a specific location property.
Three markers (TBB-1, and MEST M6C8-CA-19) showed an association
between virulence and MLG. IFN-γ levels increased significantly in mice
infected with Bang 87 isolate on 4th day post infection (dpi) having a significant
negative correlation (p <0.05) with increased IL-10 levels, whereas in mice
infected by PML 287 isolate, IFN-γ levels were positively correlated with IL- 10
levels. Early death in mice infected with Bang87 isolates was caused by systemic
inflammatory response syndrome (SIRS). Result of serological test showed that 4 out
of 24 farmers sera (16.67%) from outbreak areas are positive and all sample from
free area are negative.
Conclusion: Virulence variation of T. evansi isolates from Indonesia has
different molecular character and induces cytokine pattern of pro and antiinflammatory
mediators associated with distinct patterns of pathological
manifestations. The microsatellite markers found in this study are able to identify
origin of infection sources dan determine virulence of isolates that circulate on the
outbreak area. Surra is potential new emerging disease, particularly for farmers or
immunosurpressed individuals who living in both endemic and outbreak areas;Introduction: Trypanosoma evansi is an extracellular homoflagellate of
protozoan blood causing Surra. The disease attacks all vertebrates and potentially
as zoonosis. Virulence analysis of T. evansi is a fundamental knowledge to
determine treatment strategies of Surra in both outbreak and endemic areas. The
aims of this study was to determine virulence variation of T. evansi isolates
collected from various regions in Indonesia and to obtained genetic markers as
well as cytokine profile in mice. In addition, serological test was also carried out
to farmers living in a Surra outbreak area
Methods: Total of 32 isolates of T. evansi corfirmed with multiplex PCR (ITS-1;
Te Ro Tat 1.2 VSG and ESAG6 / 7), were further tested with inoculation 104
parasite in DDY mice strain. The population genotype study of T. evansi was
evaluated with 8 microsatellite markers (Tbb-1, Tbb-5, Tbb-9, Tbb-10-CA
MORF2, M6C8-CA, MEST-19AT, MT3033-AT). Two different virulence
isolates, high-Bang87 and low-PML287 was selected to cytokine profile analysis
using ELISA, while farmers sera were tested using CATT and FELISA kits
Results: A total of 32 local isolates of T. evansi tested were divided into three
different virulences, i.e. 17 high virulence isolates, 11 moderate virulence and 4
low virulence isolates forming 8 pattern parasitemia levels. Based on Neigbour
Joining (NJ) on 8 Microsatellite Multilocus Genotype (MLGs) was grouped into
4 populations (MLG A, MLG B, MLG C and MLG D). Stucture population
analysis also provided the similar result generating 4 clusters. These results
indicated that the markers used in this study had a specific location property.
Three markers (TBB-1, and MEST M6C8-CA-19) showed an association
between virulence and MLG. IFN-γ levels increased significantly in mice
infected with Bang 87 isolate on 4th day post infection (dpi) having a significant
negative correlation (p <0.05) with increased IL-10 levels, whereas in mice
infected by PML 287 isolate, IFN-γ levels were positively correlated with IL- 10
levels. Early death in mice infected with Bang87 isolates was caused by systemic
inflammatory response syndrome (SIRS). Result of serological test showed that 4 out
of 24 farmers sera (16.67%) from outbreak areas are positive and all sample from
free area are negative.
Conclusion: Virulence variation of T. evansi isolates from Indonesia has
different molecular character and induces cytokine pattern of pro and antiinflammatory
mediators associated with distinct patterns of pathological
manifestations. The microsatellite markers found in this study are able to identify
origin of infection sources dan determine virulence of isolates that circulate on the
outbreak area. Surra is potential new emerging disease, particularly for farmers or
immunosurpressed individuals who living in both endemic and outbreak areas;Introduction: Trypanosoma evansi is an extracellular homoflagellate of
protozoan blood causing Surra. The disease attacks all vertebrates and potentially
as zoonosis. Virulence analysis of T. evansi is a fundamental knowledge to
determine treatment strategies of Surra in both outbreak and endemic areas. The
aims of this study was to determine virulence variation of T. evansi isolates
collected from various regions in Indonesia and to obtained genetic markers as
well as cytokine profile in mice. In addition, serological test was also carried out
to farmers living in a Surra outbreak area
Methods: Total of 32 isolates of T. evansi corfirmed with multiplex PCR (ITS-1;
Te Ro Tat 1.2 VSG and ESAG6 / 7), were further tested with inoculation 104
parasite in DDY mice strain. The population genotype study of T. evansi was
evaluated with 8 microsatellite markers (Tbb-1, Tbb-5, Tbb-9, Tbb-10-CA
MORF2, M6C8-CA, MEST-19AT, MT3033-AT). Two different virulence
isolates, high-Bang87 and low-PML287 was selected to cytokine profile analysis
using ELISA, while farmers sera were tested using CATT and FELISA kits
Results: A total of 32 local isolates of T. evansi tested were divided into three
different virulences, i.e. 17 high virulence isolates, 11 moderate virulence and 4
low virulence isolates forming 8 pattern parasitemia levels. Based on Neigbour
Joining (NJ) on 8 Microsatellite Multilocus Genotype (MLGs) was grouped into
4 populations (MLG A, MLG B, MLG C and MLG D). Stucture population
analysis also provided the similar result generating 4 clusters. These results
indicated that the markers used in this study had a specific location property.
Three markers (TBB-1, and MEST M6C8-CA-19) showed an association
between virulence and MLG. IFN-γ levels increased significantly in mice
infected with Bang 87 isolate on 4th day post infection (dpi) having a significant
negative correlation (p <0.05) with increased IL-10 levels, whereas in mice
infected by PML 287 isolate, IFN-γ levels were positively correlated with IL- 10
levels. Early death in mice infected with Bang87 isolates was caused by systemic
inflammatory response syndrome (SIRS). Result of serological test showed that 4 out
of 24 farmers sera (16.67%) from outbreak areas are positive and all sample from
free area are negative.
Conclusion: Virulence variation of T. evansi isolates from Indonesia has
different molecular character and induces cytokine pattern of pro and antiinflammatory
mediators associated with distinct patterns of pathological
manifestations. The microsatellite markers found in this study are able to identify
origin of infection sources dan determine virulence of isolates that circulate on the
outbreak area. Surra is potential new emerging disease, particularly for farmers or
immunosurpressed individuals who living in both endemic and outbreak areas;Introduction: Trypanosoma evansi is an extracellular homoflagellate of
protozoan blood causing Surra. The disease attacks all vertebrates and potentially
as zoonosis. Virulence analysis of T. evansi is a fundamental knowledge to
determine treatment strategies of Surra in both outbreak and endemic areas. The
aims of this study was to determine virulence variation of T. evansi isolates
collected from various regions in Indonesia and to obtained genetic markers as
well as cytokine profile in mice. In addition, serological test was also carried out
to farmers living in a Surra outbreak area
Methods: Total of 32 isolates of T. evansi corfirmed with multiplex PCR (ITS-1;
Te Ro Tat 1.2 VSG and ESAG6 / 7), were further tested with inoculation 104
parasite in DDY mice strain. The population genotype study of T. evansi was
evaluated with 8 microsatellite markers (Tbb-1, Tbb-5, Tbb-9, Tbb-10-CA
MORF2, M6C8-CA, MEST-19AT, MT3033-AT). Two different virulence
isolates, high-Bang87 and low-PML287 was selected to cytokine profile analysis
using ELISA, while farmers sera were tested using CATT and FELISA kits
Results: A total of 32 local isolates of T. evansi tested were divided into three
different virulences, i.e. 17 high virulence isolates, 11 moderate virulence and 4
low virulence isolates forming 8 pattern parasitemia levels. Based on Neigbour
Joining (NJ) on 8 Microsatellite Multilocus Genotype (MLGs) was grouped into
4 populations (MLG A, MLG B, MLG C and MLG D). Stucture population
analysis also provided the similar result generating 4 clusters. These results
indicated that the markers used in this study had a specific location property.
Three markers (TBB-1, and MEST M6C8-CA-19) showed an association
between virulence and MLG. IFN-γ levels increased significantly in mice
infected with Bang 87 isolate on 4th day post infection (dpi) having a significant
negative correlation (p <0.05) with increased IL-10 levels, whereas in mice
infected by PML 287 isolate, IFN-γ levels were positively correlated with IL- 10
levels. Early death in mice infected with Bang87 isolates was caused by systemic
inflammatory response syndrome (SIRS). Result of serological test showed that 4 out
of 24 farmers sera (16.67%) from outbreak areas are positive and all sample from
free area are negative.
Conclusion: Virulence variation of T. evansi isolates from Indonesia has
different molecular character and induces cytokine pattern of pro and antiinflammatory
mediators associated with distinct patterns of pathological
manifestations. The microsatellite markers found in this study are able to identify
origin of infection sources dan determine virulence of isolates that circulate on the
outbreak area. Surra is potential new emerging disease, particularly for farmers or
immunosurpressed individuals who living in both endemic and outbreak areas;Introduction: Trypanosoma evansi is an extracellular homoflagellate of
protozoan blood causing Surra. The disease attacks all vertebrates and potentially
as zoonosis. Virulence analysis of T. evansi is a fundamental knowledge to
determine treatment strategies of Surra in both outbreak and endemic areas. The
aims of this study was to determine virulence variation of T. evansi isolates
collected from various regions in Indonesia and to obtained genetic markers as
well as cytokine profile in mice. In addition, serological test was also carried out
to farmers living in a Surra outbreak area
Methods: Total of 32 isolates of T. evansi corfirmed with multiplex PCR (ITS-1;
Te Ro Tat 1.2 VSG and ESAG6 / 7), were further tested with inoculation 104
parasite in DDY mice strain. The population genotype study of T. evansi was
evaluated with 8 microsatellite markers (Tbb-1, Tbb-5, Tbb-9, Tbb-10-CA
MORF2, M6C8-CA, MEST-19AT, MT3033-AT). Two different virulence
isolates, high-Bang87 and low-PML287 was selected to cytokine profile analysis
using ELISA, while farmers sera were tested using CATT and FELISA kits
Results: A total of 32 local isolates of T. evansi tested were divided into three
different virulences, i.e. 17 high virulence isolates, 11 moderate virulence and 4
low virulence isolates forming 8 pattern parasitemia levels. Based on Neigbour
Joining (NJ) on 8 Microsatellite Multilocus Genotype (MLGs) was grouped into
4 populations (MLG A, MLG B, MLG C and MLG D). Stucture population
analysis also provided the similar result generating 4 clusters. These results
indicated that the markers used in this study had a specific location property.
Three markers (TBB-1, and MEST M6C8-CA-19) showed an association
between virulence and MLG. IFN-γ levels increased significantly in mice
infected with Bang 87 isolate on 4th day post infection (dpi) having a significant
negative correlation (p <0.05) with increased IL-10 levels, whereas in mice
infected by PML 287 isolate, IFN-γ levels were positively correlated with IL- 10
levels. Early death in mice infected with Bang87 isolates was caused by systemic
inflammatory response syndrome (SIRS). Result of serological test showed that 4 out
of 24 farmers sera (16.67%) from outbreak areas are positive and all sample from
free area are negative.
Conclusion: Virulence variation of T. evansi isolates from Indonesia has
different molecular character and induces cytokine pattern of pro and antiinflammatory
mediators associated with distinct patterns of pathological
manifestations. The microsatellite markers found in this study are able to identify
origin of infection sources dan determine virulence of isolates that circulate on the
outbreak area. Surra is potential new emerging disease, particularly for farmers or
immunosurpressed individuals who living in both endemic and outbreak areas"
2016
D-Pdf
UI - Disertasi Membership  Universitas Indonesia Library
cover
McClintock, J. Thomas
Boca Raton: CRC Press, Taylor & Francis Group, 2008
614.1 MCC f
Buku Teks SO  Universitas Indonesia Library
cover
Sykes, Bryan
"How science uncovered the true identity of the Yeti, Bigfoot, Almasty and other mysterious creatures."
London: Hodder & Stoughton Ltd., 2014
591.35 SYK n
Buku Teks SO  Universitas Indonesia Library
cover
Butler, John M.
Amsterdam: Elseiver Academic Press, 2005
572.86 BUT f
Buku Teks SO  Universitas Indonesia Library
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