2018 |
Diurut, R Autisme dan trikotilomania dalam remaja lelaki Artikel Jurnal Laporan Kes BMJ, 2018 , 2018, ISSN: 1757790X, (dipetik oleh 0). Abstrak | Pautan | BibTeX | Tag: Remaja, Alopecia, Keresahan, Artikel, Gangguan Defisit Perhatian, Gangguan Hiperaktifan Kekurangan Perhatian, Autisme, Gangguan Spektrum Autisme, Gangguan Tingkah Laku, Berat badan, Laporan kes, Perangsang Sistem Saraf Pusat, Senarai Semak Tingkah Laku Kanak-kanak, Artikel Klinikal, komorbiditi, Komplikasi, Diagnosis, Berbeza, Diagnosis pembezaan, Pentitratan Dos Ubat, Toleransi Dadah, DSM-5, Echolalia, Fluvoxamine, Susulan, Manusia, Hiperaktif, Kemerosotan Intelektual, Lelaki, Metilfenidat, Obesiti, Terapi pekerjaan, Indeks Penaakulan Persepsi, Jurnal Keutamaan, Indeks Kelajuan Pemprosesan, Skala Penarafan Status Psikiatri, Skala Penarafan Psikologi, Skala penilaian, Kegelisahan, Ganjaran, Perencat Serapan Serotonin, Perencat Serapan Serotonin, Pendidikan Khas, Kelewatan Pertuturan, Gangguan Pertuturan, Terapi ucapan, Trikotilomania, Indeks Kefahaman Lisan, Skala Kepintaran Wechsler, Indeks Memori Bekerja @artikel{Masiran2018b, tajuk = {Autisme dan trikotilomania dalam remaja lelaki}, pengarang = {R Diurut}, url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85053164449&doi = 10.1136% 2fbcr-2018-226270&rakan kongsi = 40&md5=7eed3f6af717df527dce73838feab571}, doi = {10.1136/bcr-2018-226270}, terbitan = {1757790X}, tahun = {2018}, tarikh = {2018-01-01}, jurnal = {Laporan Kes BMJ}, isi padu = {2018}, penerbit = {Kumpulan Penerbitan BMJ}, abstrak = {Remaja yang mengalami gangguan spektrum autisme dan gangguan hiperaktif kekurangan perhatian yang tidak dirawat dengan betul ditunjukkan dengan tarikan rambut berulang. Rawatan dengan perencat pengambilan semula serotonin terpilih dan perangsang memperbaiki keadaan ini. © © BMJ Publishing Group Limited 2018.}, nota = {dipetik oleh 0}, kata kunci = {Remaja, Alopecia, Keresahan, Artikel, Gangguan Defisit Perhatian, Gangguan Hiperaktifan Kekurangan Perhatian, Autisme, Gangguan Spektrum Autisme, Gangguan Tingkah Laku, Berat badan, Laporan kes, Perangsang Sistem Saraf Pusat, Senarai Semak Tingkah Laku Kanak-kanak, Artikel Klinikal, komorbiditi, Komplikasi, Diagnosis, Berbeza, Diagnosis pembezaan, Pentitratan Dos Ubat, Toleransi Dadah, DSM-5, Echolalia, Fluvoxamine, Susulan, Manusia, Hiperaktif, Kemerosotan Intelektual, Lelaki, Metilfenidat, Obesiti, Terapi pekerjaan, Indeks Penaakulan Persepsi, Jurnal Keutamaan, Indeks Kelajuan Pemprosesan, Skala Penarafan Status Psikiatri, Skala Penarafan Psikologi, Skala penilaian, Kegelisahan, Ganjaran, Perencat Serapan Serotonin, Perencat Serapan Serotonin, Pendidikan Khas, Kelewatan Pertuturan, Gangguan Pertuturan, Terapi ucapan, Trikotilomania, Indeks Kefahaman Lisan, Skala Kepintaran Wechsler, Indeks Memori Bekerja}, pubstate = {diterbitkan}, tppubtype = {artikel} } Remaja yang mengalami gangguan spektrum autisme dan gangguan hiperaktif kekurangan perhatian yang tidak dirawat dengan betul ditunjukkan dengan tarikan rambut berulang. Rawatan dengan perencat pengambilan semula serotonin terpilih dan perangsang memperbaiki keadaan ini. © © BMJ Publishing Group Limited 2018. |
2012 |
Cheah, P -S; Ramshaw, H S; Thomas, P; Toyo-Oka, K; Syiling, X; Martin, S; Coyle, P; Guthridge, M A; Stomski, F; Tetapi, Van Den M; Wynshaw-Boris, A; Lopez, A F; Schwarz, Q Neurodevelopmental and neuropsychiatric behaviour defects arise from 14-3-3ζ deficiency Artikel Jurnal Molecular Psychiatry, 17 (4), hlm. 451-466, 2012, ISSN: 13594184, (dipetik oleh 58). Abstrak | Pautan | BibTeX | Tag: 14-3-3 Proteins, Animal Experiment, Animal Model, Animal Tissue, Haiwan, Artikel, Autisme, Gangguan Tingkah Laku, Bipolar Disorder, Otak, Cell Movement, Sel, Cognitive Defect, Kajian Terkawal, Berbudaya, Disease Models, Disrupted in Schizophrenia 1 Protein, Embryo, Perempuan, Gen, Gene Deletion, Kecenderungan Genetik kepada Penyakit, Glutamic Acid, Hippocampal Mossy Fiber, Hippocampus, Manusia, Hiperaktif, Inbred C57BL, Isoprotein, Knockout, Belajar, Lelaki, Maze Learning, Memory, Tikus, Motor Activity, Tetikus, Neurogenesis, Neuronal Migration Disorder, Neurons, Neuropsychiatry, Bukan Manusia, Jurnal Keutamaan, Protein 14-3-3, Protein 14-3-3 Zeta, Protein Deficiency, Protein Interaction, Recognition, Faktor risiko, Skizofrenia, Sensory Gating, Synapse, Dadah yang tidak dikelaskan @artikel{Cheah2012451, tajuk = {Neurodevelopmental and neuropsychiatric behaviour defects arise from 14-3-3ζ deficiency}, pengarang = {P -S Cheah and H S Ramshaw and P Q Thomas and K Toyo-Oka and X Xu and S Martin and P Coyle and M A Guthridge and F Stomski and M Van Den Buuse and A Wynshaw-Boris and A F Lopez and Q P Schwarz}, url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-84859007028&doi=10.1038%2fmp.2011.158&rakan kongsi = 40&md5=7f507fef31a192a10b3cde7bf69b5442}, doi = {10.1038/mp.2011.158}, terbitan = {13594184}, tahun = {2012}, tarikh = {2012-01-01}, jurnal = {Molecular Psychiatry}, isi padu = {17}, nombor = {4}, halaman = {451-466}, abstrak = {Complex neuropsychiatric disorders are believed to arise from multiple synergistic deficiencies within connected biological networks controlling neuronal migration, axonal pathfinding and synapse formation. Di sini, we show that deletion of 14-3-3ζ causes neurodevelopmental anomalies similar to those seen in neuropsychiatric disorders such as schizophrenia, autism spectrum disorder and bipolar disorder. 14-3-3ζ-Deficient mice displayed striking behavioural and cognitive deficiencies including a reduced capacity to learn and remember, hyperactivity and disrupted sensorimotor gating. These deficits are accompanied by subtle developmental abnormalities of the hippocampus that are underpinned by aberrant neuronal migration. Significantly, 14-3-3ζ- deficient mice exhibited abnormal mossy fibre navigation and glutamatergic synapse formation. The molecular basis of these defects involves the schizophrenia risk factor, DISC1, which interacts isoform specifically with 14-3-3ζ. Our data provide the first evidence of a direct role for 14-3-3ζ deficiency in the aetiology of neurodevelopmental disorders and identifies 14-3-3ζ as a central risk factor in the schizophrenia protein interaction network. © 2012 Macmillan Publishers Limited All rights reserved.}, nota = {dipetik oleh 58}, kata kunci = {14-3-3 Proteins, Animal Experiment, Animal Model, Animal Tissue, Haiwan, Artikel, Autisme, Gangguan Tingkah Laku, Bipolar Disorder, Otak, Cell Movement, Sel, Cognitive Defect, Kajian Terkawal, Berbudaya, Disease Models, Disrupted in Schizophrenia 1 Protein, Embryo, Perempuan, Gen, Gene Deletion, Kecenderungan Genetik kepada Penyakit, Glutamic Acid, Hippocampal Mossy Fiber, Hippocampus, Manusia, Hiperaktif, Inbred C57BL, Isoprotein, Knockout, Belajar, Lelaki, Maze Learning, Memory, Tikus, Motor Activity, Tetikus, Neurogenesis, Neuronal Migration Disorder, Neurons, Neuropsychiatry, Bukan Manusia, Jurnal Keutamaan, Protein 14-3-3, Protein 14-3-3 Zeta, Protein Deficiency, Protein Interaction, Recognition, Faktor risiko, Skizofrenia, Sensory Gating, Synapse, Dadah yang tidak dikelaskan}, pubstate = {diterbitkan}, tppubtype = {artikel} } Complex neuropsychiatric disorders are believed to arise from multiple synergistic deficiencies within connected biological networks controlling neuronal migration, axonal pathfinding and synapse formation. Di sini, we show that deletion of 14-3-3ζ causes neurodevelopmental anomalies similar to those seen in neuropsychiatric disorders such as schizophrenia, autism spectrum disorder and bipolar disorder. 14-3-3ζ-Deficient mice displayed striking behavioural and cognitive deficiencies including a reduced capacity to learn and remember, hyperactivity and disrupted sensorimotor gating. These deficits are accompanied by subtle developmental abnormalities of the hippocampus that are underpinned by aberrant neuronal migration. Significantly, 14-3-3ζ- deficient mice exhibited abnormal mossy fibre navigation and glutamatergic synapse formation. The molecular basis of these defects involves the schizophrenia risk factor, DISC1, which interacts isoform specifically with 14-3-3ζ. Our data provide the first evidence of a direct role for 14-3-3ζ deficiency in the aetiology of neurodevelopmental disorders and identifies 14-3-3ζ as a central risk factor in the schizophrenia protein interaction network. © 2012 Macmillan Publishers Limited All rights reserved. |
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2018 |
Autisme dan trikotilomania dalam remaja lelaki Artikel Jurnal Laporan Kes BMJ, 2018 , 2018, ISSN: 1757790X, (dipetik oleh 0). |
2012 |
Neurodevelopmental and neuropsychiatric behaviour defects arise from 14-3-3ζ deficiency Artikel Jurnal Molecular Psychiatry, 17 (4), hlm. 451-466, 2012, ISSN: 13594184, (dipetik oleh 58). |