Identifikasi Patogen Penyebab Penyakit Tanaman Sawit (Elaeis Guineensis Jacq. ) di Desa Bertam Kecamatan Jambi Luar Kota

The research is about identification of pathogenic fungi in oil palm plant (Elaeis guineensis Jacq.) In Bertam Kecamatan Jambi Luar Kota and Agriculture Quarantine Laboartory Jambi has done for six months. The aim of this research is to identificated disease in oil palm plants (Elaeis guineensis Jacq.) that caused by fungi in Bertam Kecamatan Jambi Luar Kota. The research was conducted by observing the disease which in palm oil plants area, and identificated pathogenic fungi in laboratory in moist chamber and using microscop and also fungi identifications book.The result of this research is showed that the four pathogenic fungi which attack oil palm plants in Bertam Kecamatan Jambi Luar Kota namely: 1) Fusarium sp fungi rown Disease, 2) Curvularia fungi caused Leaf Disease, 3) Phytopthora sp fungi caused Leaf Rot disease and 4) Drechslera sp fungi which the cause of Drechslera leaft Disease

Identifikasi Jamur Patogen Penyebab Penyakit Tanaman Karet (Havea Brasiliensis) Di Sukajaya Kecamatan Bayung Lincir Kabupaten Musi Banyuasin Sumatera Selatan

The research about identification of pathogenic fungi in rubber plant (Havea Brasiliensis) In Sukajaya Kecamatan Bayung Lincir Kabupaten Musi Banyuasin and Agriculture Quarantine Laboartory Jambi has been done for six months. The aim of research is to identificated disease in rubber plants (Havea Brasiliensis) that caused by fungi in Sukajaya Kecamatan Bayung Lincir Kabupaten Musi Banyuasin. The research maked to see disease sign in rice plants area and to identificated pathogenic fungi in laboratory by microscop and fungi identifications book.The result of this research indicated that find four pathogenic fungi to attack rice plants in Lubuk Ruso Kabupaten Batanghari that is: 1) Rigidoporus lignosus fungi caused White root fungus disease, 2) Fusarium sp fungi caused Rubber bark necrosis disease, 3) Colletotrichum gloeosporiosides fungi caused Colletotrichum Leaf disease and 4) Phytopthora botryosa fungi caused Phytopthora Leaf disease

Restoration of p16INK4A protein induces myogenic differentiation in RD rhabdomyosarcoma cells

p16INK4A (p16) tumour suppressor induces growth arrest by inhibiting function of cyclin-dependent kinase (CDK)4 and CDK6. Homozygous p16 gene deletion is frequent in primary rhabdomyosarcoma (RMS) cells as well as derived cell lines. To confirm the significance of p16 gene deletion in tumour biology of RMS, a temperature-sensitive p16 mutant (E119G) gene was retrovirally transfected into the human RMS cell line RD, which has homozygous gene deletion of p16 gene. Decrease from 40°C (restrictive) to 34°C (permissive) culture temperature reduced CDK6-associated kinase activity and induced G1 growth arrest. Moreover, RD-p16 cells cultured under permissive condition demonstrated differentiated morphology coupled with expressions of myogenin and myosin light chain. These suggest that deletion of p16 gene may not only facilitate growth but also inhibit the myogenic differentiation of RD RMS cells. © 1999 Cancer Research Campaig

Epidermal Growth Factor Receptor Activation in Glioblastoma through Novel Missense Mutations in the Extracellular Domain

BACKGROUND: Protein tyrosine kinases are important regulators of cellular homeostasis with tightly controlled catalytic activity. Mutations in kinase-encoding genes can relieve the autoinhibitory constraints on kinase activity, can promote malignant transformation, and appear to be a major determinant of response to kinase inhibitor therapy. Missense mutations in the EGFR kinase domain, for example, have recently been identified in patients who showed clinical responses to EGFR kinase inhibitor therapy. METHODS AND FINDINGS: Encouraged by the promising clinical activity of epidermal growth factor receptor (EGFR) kinase inhibitors in treating glioblastoma in humans, we have sequenced the complete EGFR coding sequence in glioma tumor samples and cell lines. We identified novel missense mutations in the extracellular domain of EGFR in 13.6% (18/132) of glioblastomas and 12.5% (1/8) of glioblastoma cell lines. These EGFR mutations were associated with increased EGFR gene dosage and conferred anchorage-independent growth and tumorigenicity to NIH-3T3 cells. Cells transformed by expression of these EGFR mutants were sensitive to small-molecule EGFR kinase inhibitors. CONCLUSIONS: Our results suggest extracellular missense mutations as a novel mechanism for oncogenic EGFR activation and may help identify patients who can benefit from EGFR kinase inhibitors for treatment of glioblastoma