Ujian - National Autism Resource Centre (NARC)

2018

Paudel, Y N; Syeikh, M F; Shah, S; Kumari, Y; Othman, Saya

Peranan keradangan dalam epilepsi dan komorbiditi neurobehavioral: Implikasi untuk terapi Artikel Jurnal

Jurnal Farmakologi Eropah, 837 , hlm. 145-155, 2018, ISSN: 00142999, (dipetik oleh 14).

Abstrak | Pautan | BibTeX | Tag: 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

@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}
}

Tutup

Gudang, Dengan Y; Lal, S K

The human gut microbiome - A potential controller of wellness and disease Artikel Jurnal

Frontiers in Microbiology, 9 (AUG), 2018, ISSN: 1664302X, (dipetik oleh 80).

Abstrak | Pautan | BibTeX | Tag: Acetylcholine, Autisme, Blood Clotting Factor 13, CD14 Antigen, Celiac Disease, Clostridium Difficile Infection, Colorectal Cancer, Cyanocobalamin, Dysbiosis, Enterotoxin, G Protein Coupled Bile Acid Receptor 1, G Protein Coupled Receptor 41, Gamma Interferon, Manusia, Hydrocortisone, Immunity, Immunoglobulin A, Penyakit Usus Keradangan, Interleukin 10, Interleukin 12, Interleukin 15, Interleukin 17, Interleukin 1beta, Interleukin 22, Interleukin 6, Interleukin 8, Flora usus, Leptin, Protein Membran, Metabolisme, Metabolite, Nervous System, Bukan Manusia, Obesiti, Pantothenic Acid, Pathogenesis, Protein Bcl-2, Ekspresi Protein, Protein ZO1, Kaji semula, RNA 16S, Reseptor Seperti Tol 4, Transcription Factor FOXP3, Faktor Nekrosis Tumor, Dadah yang tidak dikelaskan, Unindexed Drug, Uvomorulin, Vasculotropin

@artikel{Kho2018,
tajuk = {The human gut microbiome - A potential controller of wellness and disease},
pengarang = {Z Y Kho and S K Lal},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85051459505&doi=10.3389%2ffmicb.2018.01835&rakan kongsi = 40&md5=d89097ac9c0963d8ef7666aa99cff46f},
doi = {10.3389/fmicb.2018.01835},
terbitan = {1664302X},
tahun = {2018},
tarikh = {2018-01-01},
jurnal = {Frontiers in Microbiology},
isi padu = {9},
nombor = {AUG},
penerbit = {Frontiers Media S.A.},
abstrak = {Interest toward the human microbiome, particularly gut microbiome has flourished in recent decades owing to the rapidly advancing sequence-based screening and humanized gnotobiotic model in interrogating the dynamic operations of commensal microbiota. Although this field is still at a very preliminary stage, whereby the functional properties of the complex gut microbiome remain less understood, several promising findings have been documented and exhibit great potential toward revolutionizing disease etiology and medical treatments. Dalam ulasan ini, the interactions between gut microbiota and the host have been focused on, to provide an overview of the role of gut microbiota and their unique metabolites in conferring host protection against invading pathogen, regulation of diverse host physiological functions including metabolism, development and homeostasis of immunity and the nervous system. We elaborate on how gut microbial imbalance (dysbiosis) may lead to dysfunction of host machineries, thereby contributing to pathogenesis and/or progression toward a broad spectrum of diseases. Some of the most notable diseases namely Clostridium difficile infection (infectious disease), inflammatory bowel disease (intestinal immune-mediated disease), celiac disease (multisystemic autoimmune disorder), obesity (metabolic disease), colorectal cancer, and autism spectrum disorder (neuropsychiatric disorder) have been discussed and delineated along with recent findings. Novel therapies derived from microbiome studies such as fecal microbiota transplantation, probiotic and prebiotics to target associated diseases have been reviewed to introduce the idea of how certain disease symptoms can be ameliorated through dysbiosis correction, thus revealing a new scientific approach toward disease treatment. Toward the end of this review, several research gaps and limitations have been described along with suggested future studies to overcome the current research lacunae. Despite the ongoing debate on whether gut microbiome plays a role in the above-mentioned diseases, we have in this review, gathered evidence showing a potentially far more complex link beyond the unidirectional cause-and-effect relationship between them. © 2018 Kho and Lal.},
nota = {dipetik oleh 80},
kata kunci = {Acetylcholine, Autisme, Blood Clotting Factor 13, CD14 Antigen, Celiac Disease, Clostridium Difficile Infection, Colorectal Cancer, Cyanocobalamin, Dysbiosis, Enterotoxin, G Protein Coupled Bile Acid Receptor 1, G Protein Coupled Receptor 41, Gamma Interferon, Manusia, Hydrocortisone, Immunity, Immunoglobulin A, Penyakit Usus Keradangan, Interleukin 10, Interleukin 12, Interleukin 15, Interleukin 17, Interleukin 1beta, Interleukin 22, Interleukin 6, Interleukin 8, Flora usus, Leptin, Protein Membran, Metabolisme, Metabolite, Nervous System, Bukan Manusia, Obesiti, Pantothenic Acid, Pathogenesis, Protein Bcl-2, Ekspresi Protein, Protein ZO1, Kaji semula, RNA 16S, Reseptor Seperti Tol 4, Transcription Factor FOXP3, Faktor Nekrosis Tumor, Dadah yang tidak dikelaskan, Unindexed Drug, Uvomorulin, Vasculotropin},
pubstate = {diterbitkan},
tppubtype = {artikel}
}

Tutup

Interest toward the human microbiome, particularly gut microbiome has flourished in recent decades owing to the rapidly advancing sequence-based screening and humanized gnotobiotic model in interrogating the dynamic operations of commensal microbiota. Although this field is still at a very preliminary stage, whereby the functional properties of the complex gut microbiome remain less understood, several promising findings have been documented and exhibit great potential toward revolutionizing disease etiology and medical treatments. Dalam ulasan ini, the interactions between gut microbiota and the host have been focused on, to provide an overview of the role of gut microbiota and their unique metabolites in conferring host protection against invading pathogen, regulation of diverse host physiological functions including metabolism, development and homeostasis of immunity and the nervous system. We elaborate on how gut microbial imbalance (dysbiosis) may lead to dysfunction of host machineries, thereby contributing to pathogenesis and/or progression toward a broad spectrum of diseases. Some of the most notable diseases namely Clostridium difficile infection (infectious disease), inflammatory bowel disease (intestinal immune-mediated disease), celiac disease (multisystemic autoimmune disorder), obesity (metabolic disease), colorectal cancer, and autism spectrum disorder (neuropsychiatric disorder) have been discussed and delineated along with recent findings. Novel therapies derived from microbiome studies such as fecal microbiota transplantation, probiotic and prebiotics to target associated diseases have been reviewed to introduce the idea of how certain disease symptoms can be ameliorated through dysbiosis correction, thus revealing a new scientific approach toward disease treatment. Toward the end of this review, several research gaps and limitations have been described along with suggested future studies to overcome the current research lacunae. Despite the ongoing debate on whether gut microbiome plays a role in the above-mentioned diseases, we have in this review, gathered evidence showing a potentially far more complex link beyond the unidirectional cause-and-effect relationship between them. © 2018 Kho and Lal.

Tutup