@artikel{Eow2020,
tajuk = {Faktor-faktor yang berkaitan dengan keparahan autisme di kalangan kanak-kanak Malaysia dengan Autism Spectrum Disorder},
pengarang = {S Y Eow dan W Y Gan dan P Y Lim dan H Awang dan Z Mohd Shariff},
url = {https://www.scopus.com/inward/record.uri?eid = 2-s2.0-85081212440&doi = 10.1016% 2fj.ridd.2020.103632&rakan kongsi = 40&md5 = a2814a66b9d649278ea7f764ed7e4125},
doi = {10.1016/j.ridd.2020.103632},
terbitan = {08914222},
tahun = {2020},
tarikh = {2020-01-01},
jurnal = {Penyelidikan Ketidakupayaan Pembangunan},
isi padu = {100},
penerbit = {Elsevier Inc.},
abstrak = {Latar belakang: Kanak-kanak dengan Gangguan Spektrum Autisme (ASD) tahap keparahan gejala yang berlainan boleh menunjukkan pelbagai tingkah laku dan ciri. Terdapat kajian berkaitan pemakanan terhad pada kanak-kanak dengan ASD dengan tahap keparahan yang berbeza di Malaysia. Matlamat: Kajian keratan rentas ini bertujuan untuk mengetahui perkaitan antara faktor sosiodemografi, faktor ibu bapa, dan faktor gaya hidup dengan keparahan autisme pada kanak-kanak dengan ASD. Kaedah dan prosedur: Sejumlah 224 kanak-kanak dengan ASD dimasukkan dalam kajian ini. Ibu mereka melengkapkan borang soal selidik mengenai ciri sosiodemografi, keterukan autisme, gaya keibubapaan, amalan memberi makan ibu bapa, tekanan keibubapaan, tabiat tidur anak dan tingkah laku makan. Hasil dan hasil: Setinggi 78.1 % kanak-kanak dengan ASD menunjukkan tahap keparahan autisme yang tinggi. Regresi linear berganda menunjukkan bahawa status pekerjaan bapa (B = 6.970, 95 % CI = 3.172, 10.768, hlm < 0.001) and perceived child weight (B = 3.338, 95 % CI = 1.350, 5.327},
nota = {dipetik oleh 0},
kata kunci = {Artikel, Autisme, Berat badan, Anak-anak, Kajian Lintas Bahagian, Demografi, Persatuan Penyakit, Keterukan Penyakit, Pekerjaan, Perempuan, Manusia, Gaya hidup, Kajian Klinikal Utama, Malaysia, Orang Malaysia, Lelaki, Ibu bapa, Kanak-kanak Prasekolah, Budak sekolah, Status sosial},
pubstate = {diterbitkan},
tppubtype = {artikel}
}

@artikel{Paudel2018145,
tajuk = {Peranan keradangan dalam epilepsi dan komorbiditi neurobehavioral: Implikasi untuk terapi},
pengarang = {Y N Paudel dan MF Shaikh dan S Shah dan Y Kumari dan I Othman},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85053082063&doi = 10.1016% 2fj.ejphar.2018.08.020&rakan kongsi = 40&md5=27ff0199bae72f156425637a7ad02228},
doi = {10.1016/j.ejphar.2018.08.020},
terbitan = {00142999},
tahun = {2018},
tarikh = {2018-01-01},
jurnal = {Jurnal Farmakologi Eropah},
isi padu = {837},
halaman = {145-155},
penerbit = {Elsevier B.V.},
abstrak = {Epilepsi adalah keadaan yang dahsyat yang menjejaskan sekeliling 70 juta orang di seluruh dunia. Lebih-lebih lagi, kualiti hidup penghidap epilepsi (PWE) diburukkan oleh beberapa siri komorbiditi. Komorbiditi neurobehavioral yang dibincangkan di sini berkongsi hubungan timbal balik dan kompleks dengan epilepsi, yang akhirnya merumitkan proses rawatan di PWE. Memahami laluan mekanistik yang mana komorbiditi ini dikaitkan dengan epilepsi mungkin memainkan peranan penting dalam membangunkan campur tangan terapeutik. Isyarat sitokin radang dalam otak mengawal fungsi otak yang penting termasuk metabolisme neurotransmitter, fungsi neuroendokrin, keplastikan sinaptik, penghantaran dopaminergik, laluan kynurenine, dan menjejaskan neurogenesis serta litar saraf mood. Dalam ulasan ini, kami membuat hipotesis bahawa hubungan kompleks antara epilepsi dan komorbiditi yang berkaitan (kecacatan kognitif, kemurungan, kegelisahan, autisme, dan skizofrenia) boleh dirungkai melalui mekanisme keradangan yang memainkan peranan penting dalam semua keadaan individu ini. Sebilangan besar bukti tersedia melaporkan peranan keradangan dalam epilepsi dan semua keadaan komorbid individu tetapi hubungan kompleks mereka dengan epilepsi masih belum diterokai melalui prospek laluan keradangan.. Kajian kami menunjukkan bahawa epilepsi dan komorbiditi neurobehavioralnya dikaitkan dengan peningkatan tahap beberapa penanda keradangan utama. Kajian ini juga memberi penerangan tentang persatuan mekanistik antara epilepsi dan komorbiditi neurobehavioralnya. Lebih-lebih lagi, kami menganalisis beberapa terapi anti-radang yang tersedia untuk epilepsi dan komorbiditi neurobehavioralnya. Kami mencadangkan, terapi anti-radang ini mungkin merupakan campur tangan yang mungkin dan boleh menjadi strategi yang menjanjikan untuk mencegah epileptogenesis dan komorbiditi neurobehavioral yang berkaitan.. © 2018 Elsevier B.V.},
nota = {dipetik oleh 14},
kata kunci = {3 Dioksigenase, Asid Acetylsalicylic, Adalimumab, Anakinra, Haiwan, Agen Anti-Radang, Keresahan, Autacoid, Autisme, Gangguan Spektrum Autisme, Gangguan Tingkah Laku, Belnacasan, Celecoxib, Kognisi, komorbiditi, Komplikasi, Cyclooxygenase 2, Cyclooxygenase 2 Perencat, Sitokin, Sitokin, Kemurungan, Dexmedetomidine, Persatuan Penyakit, Penghantaran Dopaminergik, Elektroencephalogram, Elektroensefalografi, Epilepsi, Epileptogenesis, Esculetin, Protein Kumpulan B1 Mobiliti Tinggi, Manusia, Ibuprofen, Icariin, IImmunoglobulin Enhancer Mengikat Protein, Imunologi, Indoleamine 2, Keradangan, Pengantara Inflamasi, Infliximab, Interleukin 1beta, Interleukin 6, Minocycline, Keplastikan Sel Saraf, Pembangunan Sistem Saraf, Keradangan Sistem Saraf, Peraturan Neuroendokrin, Pelepasan Neurotransmitter, Bukan Manusia, Palmidrol, Paracetamol, Fisiologi, Jurnal Keutamaan, Prostaglandin E2, Psikologi, Kaji semula, SC 51089, Skizofrenia, Reseptor Seperti Tol 4, Mengubah Faktor Pertumbuhan Beta, Tryptophan Hydroxylase, Faktor Nekrosis Tumor, Dadah yang tidak dikelaskan},
pubstate = {diterbitkan},
tppubtype = {artikel}
}

@artikel{Nor201463,
tajuk = {Does Bisphenol A contribute to autism spectrum disorder?},
pengarang = {Z M Nor and S N Yusof and H F Ghazi and Z M Isa},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-84939185210&rakan kongsi = 40&md5=57e7aabc3aa2ec1ab51747608ab6a9b2},
terbitan = {09728228},
tahun = {2014},
tarikh = {2014-01-01},
jurnal = {Current Topics in Toxicology},
isi padu = {10},
halaman = {63-70},
penerbit = {Research Trends},
abstrak = {Gangguan Spektrum Autisme (ASD) includes a range of conditions classified as neurodevelopmental disorders that have an onset from infancy. Multiple factors have been identified as causes for the autism spectrum disorder; namun begitu, the cascade of the disease is still not clearly defined. An increasing number of cases have been reported globally, for instance in US, UK, Canada and Australia. Environmental factors were suspected to be one of the causes. Bisphenol A (BPA) is an Endocrine Disruptor Compound (EDC) and used primarily as a monomer for the production of polycarbonate and epoxy resins, especially in feeding bottles for infants. Ongoing discussions are currently in progress on the reported low-dose effects of BPA, particularly its neurodevelopmental and behavioural effects. Many countries have banned the usage of BPA due to its harmful effects on children. This review aims at presenting an overview of the association between exposure to BPA and the neurobehavioural changes it triggers in children. Articles were obtained from the Science Direct and ProQuest search engines. The keywords used in the search were 'BPA' or 'bisphenol A' and áutism'. Fourty-seven articles were shortlisted, of which only five that fulfilled the requisite criteria were selected for review. All of them were cohort studies. Secara keseluruhan, an association has been established between prenatal and childhood exposure to BPA and neurobehavioural changes. The exposure during pregnancy was observed to have a greater impact on children. Earlier exposure during the prenatal period resulted in stronger associations. Walau bagaimanapun, no association was found between BPA concentration of the child and neurobehavioural outcomes.},
nota = {dipetik oleh 1},
kata kunci = {4' Isopropylidenediphenol, Artikel, Autisme, Behaviour Change, Persatuan Penyakit, Faktor Persekitaran, First Pass Effect, Manusia, Population, Pregnancy, Prenatal Period},
pubstate = {diterbitkan},
tppubtype = {artikel}
}

@artikel{Karim20141213,
tajuk = {The role of viruses in neurodegenerative and neurobehavioral diseases},
pengarang = {S Karim and Z Mirza and M A Kamal and A M Abuzenadah and E I Azhar and M H Al-Qahtani and G A Damanhouri and F Ahmad and S H Gan and S S Sohrab},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-84911396470&doi=10.2174%2f187152731307141015122638&rakan kongsi = 40&md5=7564c64b2fe5d0737f83e65e1fdff60a},
doi = {10.2174/187152731307141015122638},
terbitan = {18715273},
tahun = {2014},
tarikh = {2014-01-01},
jurnal = {CNS and Neurological Disorders - Drug Targets},
isi padu = {13},
nombor = {7},
halaman = {1213-1223},
penerbit = {Bentham Science Publishers B.V.},
abstrak = {Neurodegenerative and neurobehavioral diseases may be caused by chronic and neuropathic viral infections and may result in a loss of neurons and axons in the central nervous system that increases with age. Sehingga kini, there is evidence of systemic viral infections that occur with some neurodegenerative conditions such as Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, multiple sclerosis, autism spectrum disorders, and HIV-associated neurocognitive disorders. With increasing lifespan, the incidence of neurodegenerative diseases increases consistently. Neurodegenerative diseases affect approximately 37 million people worldwide and are an important cause of mortality. In addition to established non-viral-induced reasons for neurodegenerative diseases, neuropathic infections and viruses associated with neurodegenerative diseases have been proposed. Neuronal degeneration can be either directly or indirectly affected by viral infection. Viruses that attack the human immune system can also affect the nervous system and interfere with classical pathways of neurodegenerative diseases. Viruses can enter the central nervous system, but the exact mechanism cannot be understood well. Various studies have supported viral- and non-viral-mediated neurodegeneration at the cellular, molecular, genomic and proteomic levels. The main focus of this review is to illustrate the association between viral infections and both neurodegenerative and neurobehavioral diseases, so that the possible mechanism and pathway of neurodegenerative diseases can be better explained. This information will strengthen new concepts and ideas for neurodegenerative and neurobehavioral disease treatment. © 2014 Bentham Science Publishers.},
nota = {dipetik oleh 12},
kata kunci = {Alzheimer Disease, Amyotrophic Lateral Sclerosis, Haiwan, Artikel, Autisme, Beta Interferon, Borna Disease Virus, Cytomegalovirus, Degenerative Disease, Persatuan Penyakit, Enterovirus, Epstein Barr virus, Hepatitis Virus, Herpes Simplex Virus, HIV Associated Dementia, Manusia, Sistem Imun, Keradangan, Influenza Virus, Influenza Virus A H5N1, Mental Disease, Gangguan Mental, Multiple Sclerosis, Nerve Cell Degeneration, Neurodegenerative Diseases, Bukan Manusia, Parkinson Disease, Patofisiologi, Picornavirus, Roseolovirus, Varicella Zoster Virus, Virology, Virus Infection, Virus Pathogenesis, Virus Transmission, West Nile Flavivirus},
pubstate = {diterbitkan},
tppubtype = {artikel}
}

@artikel{Tan2012210,
tajuk = {De-novo mutations and genetic variation in the SCN1A gene in Malaysian patients with generalized epilepsy with febrile seizures plus (GEFS+)},
pengarang = {E H Tan and S A Razak and J M Abdullah and A A Mohamed Yusoff},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-84870296042&doi=10.1016%2fj.eplepsyres.2012.08.004&rakan kongsi = 40&md5=25cc4eeb07db2492a7c04c6b3b3b2167},
doi = {10.1016/j.eplepsyres.2012.08.004},
terbitan = {09201211},
tahun = {2012},
tarikh = {2012-01-01},
jurnal = {Epilepsy Research},
isi padu = {102},
nombor = {3},
halaman = {210-215},
abstrak = {Generalized epilepsy with febrile seizures plus (GEFS+) comprises a group of clinically and genetically heterogeneous epilepsy syndrome. Di sini, we provide the first report of clinical presentation and mutational analysis of SCN1A gene in 36 Malaysian GEFS+ patients. Mutational analysis of SCN1A gene revealed twenty seven sequence variants (missense mutation and silent polymorphism also intronic polymorphism), as well as 2 novel de-novo mutations were found in our patients at coding regions, c.5197A>G (N1733D) and c.4748A>G (H1583R). Our findings provide potential genetic insights into the pathogenesis of GEFS+ in Malaysian populations concerning the SCN1A gene mutations. © 2012 Elsevier B.V.},
nota = {dipetik oleh 2},
kata kunci = {Alanine, Amino Acid Substitution, Arginine, Artikel, Asparagine, Aspartic Acid, Anak-anak, Artikel Klinikal, Clinical Feature, Kajian Terkawal, Persatuan Penyakit, DNA Mutational Analysis, DNA Sequence, Elektroensefalografi, Epilepsi, Febrile, Febrile Convulsion, Perempuan, Gen, Gene Frequency, Pengenalan Gen, Generalized, Generalized Epilepsy, Persatuan Genetik, Kecenderungan Genetik, Genetic Screening, Genetic Variability, Glycine, Histidine, Manusia, Bayi, Malaysia, Lelaki, Missense Mutation, Molecular Pathology, Mutation, Mutational Analysis, Mutator Gene, Nav1.1 Voltage-Gated Sodium Channel, Onset Age, Patient Assessment, Polimorfisme, Kanak-kanak Prasekolah, Jurnal Keutamaan, Promoter Region, Budak sekolah, Seizure, Sequence Analysis, Nukleotida Tunggal, Polimorfisme Nukleotida Tunggal, Sodium Channel Nav1.1, Voltage Gated Sodium Channel Alpha1 Subunit Gene},
pubstate = {diterbitkan},
tppubtype = {artikel}
}