@artikel{Al-Hiyali201886,
tajuk = {Tinjauan dalam mengubah suai tingkah laku pengambilan makanan oleh rangsangan otak: Kes berat badan berlebihan},
pengarang = {M I Al-Hiyali dan A J Ishak dan H Harun dan S A Ahmad dan W A Wan Sulaiman},
url = {https://www.scopus.com/inward/record.uri?eid = 2-s2.0-85062843670&doi = 10.14704% 2fnq.2018.16.12.1894&rakan kongsi = 40&md5 = 235f66cef05a144be23472641f70bd1d},
doi = {10.14704/nq.2018.16.12.1894},
terbitan = {13035150},
tahun = {2018},
tarikh = {2018-01-01},
jurnal = {Kuantologi Neuro},
isi padu = {16},
nombor = {12},
halaman = {86-97},
penerbit = {Penerbit Anka},
abstrak = {Obesiti dan berat badan berlebihan sering ditetapkan untuk disfungsi dalam tingkah laku pengambilan makanan. Kerana banyaknya kegemukan pada tahun lalu, terdapat permintaan untuk lebih banyak kajian yang bertujuan untuk mengubah tingkah laku pengambilan makanan. Selama beberapa dekad yang lalu, banyak kajian telah dilakukan untuk mengubah pengambilan makanan melalui latihan otak atau rangsangan. Ulasan ini untuk kajian neurosains dalam mengubah tingkah laku pengambilan makanan, ia melibatkan tiga bahagian; Bahagian pertama menjelaskan peranan aktiviti otak dalam peraturan pengambilan makanan, idea umum mengenai alat bioperubatan dalam tingkah laku pengambilan makanan dibincangkan di bahagian kedua dan bahagian ketiga yang difokuskan pada sistem rangsangan otak. Akhirnya, makalah ini disimpulkan dengan perkara utama yang perlu diambil kira semasa merancang kajian eksperimental untuk mengubah tingkah laku pengambilan makanan oleh rangsangan otak mengikut cadangan dan cabaran kajian sebelumnya. © 2018, Penerbit Anka. Hak cipta terpelihara.},
nota = {dipetik oleh 2},
kata kunci = {Amygdala, Anoksia, Artikel, Autisme, Gangguan pesta minum-minum makan, Berat badan, Berat badan, Rangsangan Kedalaman Otak, Depolarisasi, Pengambilan diet, Keinginan Dadah, Gangguan Makan, Arus elektrik, Elektroencephalogram, Elektroensefalografi, Penggunaan tenaga, Penggunaan tenaga, Tingkah Laku Makan, Pengambilan makanan, Pengimejan Resonans Magnetik Berfungsi, Jantina, Status kesihatan, Homeostasis, Manusia, Kelaparan, Gaya hidup, Potensi Mantap Membran Sel Saraf, Keseronokan Saraf, Neurofeedback, Neuromodulasi, Penilaian Pemakanan, Penilaian Hasil, Soal selidik, Rangsangan Magnetik Transkranial Berulang, Pemprosesan isyarat, Latihan, Rangsangan Arus Langsung Transkranial, Rangsangan Magnetik Transkranial, Berat badan kurang},
pubstate = {diterbitkan},
tppubtype = {artikel}
}

@artikel{Tsuchida2018538,
tajuk = {GRIN2D variants in three cases of developmental and epileptic encephalopathy},
pengarang = {N Tsuchida and K Hamada and M Shiina and M Kato and Y Kobayashi and J Tohyama and K Kimura and K Hoshino and V Ganesan and K W Teik and M Nakashima and S Mitsuhashi and T Mizuguchi and A Takata and N Miyake and H Saitsu and K Ogata and S Miyatake and N Matsumoto},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85056487337&doi=10.1111%2fcge.13454&rakan kongsi = 40&md5=f0d32670db57261820bc244943cffd62},
doi = {10.1111/cge.13454},
terbitan = {00099163},
tahun = {2018},
tarikh = {2018-01-01},
jurnal = {Clinical Genetics},
isi padu = {94},
nombor = {6},
halaman = {538-547},
penerbit = {Blackwell Publishing Ltd},
abstrak = {N-methyl-d-aspartate (NMDA) receptors are glutamate-activated ion channels that are widely distributed in the central nervous system and essential for brain development and function. Dysfunction of NMDA receptors has been associated with various neurodevelopmental disorders. Baru-baru ini, a de novo recurrent GRIN2D missense variant was found in two unrelated patients with developmental and epileptic encephalopathy. Dalam kajian ini, we identified by whole exome sequencing novel heterozygous GRIN2D missense variants in three unrelated patients with severe developmental delay and intractable epilepsy. All altered residues were highly conserved across vertebrates and among the four GluN2 subunits. Structural consideration indicated that all three variants are probably to impair GluN2D function, either by affecting intersubunit interaction or altering channel gating activity. We assessed the clinical features of our three cases and compared them to those of the two previously reported GRIN2D variant cases, and found that they all show similar clinical features. This study provides further evidence of GRIN2D variants being causal for epilepsy. Genetic diagnosis for GluN2-related disorders may be clinically useful when considering drug therapy targeting NMDA receptors. © 2018 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd},
nota = {dipetik oleh 4},
kata kunci = {Remaja, Allele, Amino Acid Sequence, Amino Acid Substitution, Amino Terminal Sequence, Anemia, Antibiotic Agent, Antibiotic Therapy, Artikel, Atonic Seizure, Gangguan Defisit Perhatian, Autisme, Binding Affinity, Otak, Brain Atrophy, Carbamazepine, Laporan kes, Channel Gating, Kimia, Anak-anak, Artikel Klinikal, Clinical Feature, Clobazam, Clonazepam, Conformational Transition, Continuous Infusion, Contracture, Crystal Structure, Cysteine Ethyl Ester Tc 99m, Kelewatan Perkembangan, Gangguan Perkembangan, Elektroencephalogram, Elektroensefalografi, Epilepsi, Epileptic Discharge, Ethosuximide, Eye Tracking, Febrile Convulsion, Perempuan, Frontal Lobe Epilepsy, Gen, Gene Frequency, Genetic Variation, Genetik, Genotype, GRIN2D Protein, Heterozygosity, Home Oxygen Therapy, Manusia, Sel Manusia, Hydrogen Bond, Kemerosotan Intelektual, Intelligence Quotient, Intractable Epilepsy, Ketamine, Lacosamide, Lamotrigine, Lennox Gastaut Syndrome, Levetiracetam, Magnetoencephalography, Lelaki, Maternal Hypertension, Melatonin, Migraine, Missense Mutation, Molecular Dynamics, Molecular Dynamics Simulation, Mutation, Myoclonus Seizure, N Methyl Dextro Aspartic Acid Receptor, N Methyl Dextro Aspartic Acid Receptor 2D, N-Methyl-D-Aspartate, Neonatal Pneumonia, Neonatal Respiratory Distress Syndrome, Neuroimaging, Nuclear Magnetic Resonance Imaging, Phenobarbital, Premature Labor, Prasekolah, Kanak-kanak Prasekolah, Jurnal Keutamaan, Protein Conformation, Proximal Interphalangeal Joint, Pyridoxine, Receptors, Respiratory Arrest, Sanger Sequencing, Budak sekolah, Single Photon Emission Computed Tomography, Sleep Disordered Breathing, Static Electricity, Stridor, Structure-Activity Relationship, Subglottic Stenosis, Superior Temporal Gyrus, Supramarginal Gyrus, Thiopental, Tonic Seizure, Valproic Acid, Wakefulness, Wechsler Intelligence Scale for Children, Whole Exome Sequencing},
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{Khosrowabadi2015335,
tajuk = {Dynamic screening of autistic children in various mental states using pattern of connectivity between brain regions},
pengarang = {R Khosrowabadi and C Quek and K K Ang and A Wahab and S -H Annabel Chen},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-84927922520&doi=10.1016%2fj.asoc.2015.03.030&rakan kongsi = 40&md5=5973f80db5649e5c61e344907819a18b},
doi = {10.1016/j.asoc.2015.03.030},
terbitan = {15684946},
tahun = {2015},
tarikh = {2015-01-01},
jurnal = {Applied Soft Computing Journal},
isi padu = {32},
halaman = {335-346},
penerbit = {Elsevier Ltd.},
abstrak = {Dalam kajian ini, a dynamic screening strategy is proposed to discriminate subjects with autistic spectrum disorder (ASD) from healthy controls. The ASD is defined as a neurodevelopmental disorder that disrupts normal patterns of connectivity between the brain regions. Oleh itu, the potential use of such abnormality for autism screening is investigated. The connectivity patterns are estimated from electroencephalogram (LIHAT) data collected from 8 brain regions under various mental states. The EEG data of 12 healthy controls and 6 kanak-kanak autistik (age matched in 7-10) were collected during eyes-open and eyes-close resting states as well as when subjects were exposed to affective faces (happy, sad and calm). Subsequently, the subjects were classified as autistic or healthy groups based on their brain connectivity patterns using pattern recognition techniques. Performance of the proposed system in each mental state is separately evaluated. The results present higher recognition rates using functional connectivity features when compared against other existing feature extraction methods. © 2015 Published by Elsevier B.V.},
nota = {dipetik oleh 6},
kata kunci = {Gangguan Spektrum Autisme, Pemprosesan Isyarat Bioperubatan, Otak, Connectivity Feature, Connectivity Pattern, Penyakit, Elektroensefalografi, Face Perceptions, Pengekstrakan Ciri, Functional Connectivity, Pengecaman Corak, Pattern Recognition Techniques},
pubstate = {diterbitkan},
tppubtype = {artikel}
}

@artikel{Bhat2014851,
tajuk = {Automated diagnosis of autism: In search of a mathematical marker},
pengarang = {S Bhat and U R Acharya and H Adeli and G M Bairy and A Adeli},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-84925286949&doi=10.1515%2frevneuro-2014-0036&rakan kongsi = 40&md5=04858a5c9860e9027e3113835ca2e11f},
doi = {10.1515/revneuro-2014-0036},
terbitan = {03341763},
tahun = {2014},
tarikh = {2014-01-01},
jurnal = {Reviews in the Neurosciences},
isi padu = {25},
nombor = {6},
halaman = {851-861},
penerbit = {Walter de Gruyter GmbH},
abstrak = {Autism is a type of neurodevelopmental disorder affecting the memory, behavior, emotion, learning ability, and communication of an individual. An early detection of the abnormality, due to irregular processing in the brain, can be achieved using electroencephalograms (LIHAT). The variations in the EEG signals cannot be deciphered by mere visual inspection. Computer-aided diagnostic tools can be used to recognize the subtle and invisible information present in the irregular EEG pattern and diagnose autism. This paper presents a state-of-theart review of automated EEG-based diagnosis of autism. Various time domain, frequency domain, time-frequency domain, and nonlinear dynamics for the analysis of autistic EEG signals are described briefly. A focus of the review is the use of nonlinear dynamics and chaos theory to discover the mathematical biomarkers for the diagnosis of the autism analogous to biological markers. A combination of the time-frequency and nonlinear dynamic analysis is the most effective approach to characterize the nonstationary and chaotic physiological signals for the automated EEGbased diagnosis of autism spectrum disorder (ASD). The features extracted using these nonlinear methods can be used as mathematical markers to detect the early stage of autism and aid the clinicians in their diagnosis. This will expedite the administration of appropriate therapies to treat the disorder. © 2014 Walter de Gruyter GmbH.},
nota = {dipetik oleh 34},
kata kunci = {Algoritma, Artikel, Autisme, Gangguan Spektrum Autisme, Automasi, Biological Model, Otak, Chaos Theory, Correlation Analysis, Detrended Fluctuation Analysis, Disease Marker, Electrode, Elektroencephalogram, Elektroensefalografi, Entropy, Fourier Transformation, Fractal Analysis, Frequency Domain Analysis, Manusia, Mathematical Analysis, Mathematical Marker, Mathematical Parameters, Models, Neurologic Disease, Neurological, Nonlinear Dynamics, Nonlinear System, Patofisiologi, Jurnal Keutamaan, Prosedur, Pemprosesan isyarat, Model Statistik, Masa, Time Frequency Analysis, Wavelet Analysis},
pubstate = {diterbitkan},
tppubtype = {artikel}
}

@artikel{Modugumudi2013321,
tajuk = {Efficacy of collaborative virtual environment intervention programs in emotion expression of children with autism},
pengarang = {Y R Modugumudi and J Santhosh and S Anand},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-84881262807&doi=10.1166%2fjmihi.2013.1167&rakan kongsi = 40&md5=c8e767c8eba2bbbec5ff36a43eb59af6},
doi = {10.1166/jmihi.2013.1167},
terbitan = {21567018},
tahun = {2013},
tarikh = {2013-01-01},
jurnal = {Journal of Medical Imaging and Health Informatics},
isi padu = {3},
nombor = {2},
halaman = {321-325},
abstrak = {Exploratory empirical studies on Collaborative Virtual Environments (CVEs) were conducted to determine if children with autism could make basic emotional recognition effectively, with the use of CVEs as assistive technology. In this paper we report the results of electro-physiological study of two groups of autistic children after an intervention program with and without using Collaborative Virtual Environment. The group trained with CVE showed better results compared to the group trained without Collaborative virtual Environment. There is an emphasized early emotion expression positivity component at around 120 ms latency for CVE trained group which clearly distinguishes the CVE untrained group. Also there are differences observed in Event Related Potential component at about 170 ms latency after the stimulus. Results indicate that the Collaborative Virtual Environments are effective in training Autistic children. © 2013 American Scientific Publishers.},
nota = {dipetik oleh 4},
kata kunci = {Remaja, Dewasa, Artikel, Autisme, Anak-anak, Artikel Klinikal, Collaborative Virtual Environment, Kajian Terkawal, DSM-IV, Elektroencephalogram, Elektroensefalografi, Electrooculogram, Emosi, Ketua Penolong Pengarah, Event Related Potential, Ekspresi wajah, Perempuan, Manusia, Latent Period, Lelaki, Recognition, Budak sekolah},
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}
}

@artikel{Tan2012123,
tajuk = {Generalized epilepsy with febrile seizure plus (GEFS+) spectrum: Novel de novo mutation of SCN1A detected in a Malaysian patient},
pengarang = {E H Tan and A A M Yusoff and J M Abdullah and S A Razak},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-84870194979&doi=10.4103%2f1817-1745.102575&rakan kongsi = 40&md5=b73f0bdb583e84404e0fff232faf30cb},
doi = {10.4103/1817-1745.102575},
terbitan = {18171745},
tahun = {2012},
tarikh = {2012-01-01},
jurnal = {Journal of Pediatric Neurosciences},
isi padu = {7},
nombor = {2},
halaman = {123-125},
abstrak = {Dalam laporan ini, we describe a 15-year-old Malaysian male patient with a de novo SCN1A mutation who experienced prolonged febrile seizures after his first seizure at 6 months of age. This boy had generalized tonic clonic seizure (GTCS) which occurred with and without fever. Sequencing analysis of voltage-gated sodium channel a1-subunit gene, SCN1A, confirmed a homozygous A to G change at nucleotide 5197 (c.5197A > G) in exon 26 resulting in amino acid substitution of asparagines to aspartate at codon 1733 of sodium channel. The mutation identified in this patient is located in the pore-forming loop of SCN1A and this case report suggests missense mutation in pore-forming loop causes generalized epilepsy with febrile seizure plus (GEFS+) with clinically more severe neurologic phenotype including intellectual disabilities (mental retardation and autism features) and neuropsychiatric disease (anxiety disorder).},
nota = {dipetik oleh 3},
kata kunci = {Remaja, Anxiety Disorder, Artikel, Autisme, Carbamazepine, Laporan kes, Computer Assisted Tomography, Elektroencephalogram, Elektroensefalografi, Febrile Convulsion, Gen, Generalized Epilepsy, Generalized Epilepsy with Febrile Seizure Plus, Manusia, Karyotype, Malaysia, Lelaki, Medical History, Mental Deficiency, Missense Mutation, Nuclear Magnetic Resonance Imaging, Fenotip, SCN1A Gene, Tonic Clonic Seizure, Topiramate, Valproic Acid},
pubstate = {diterbitkan},
tppubtype = {artikel}
}