• Biomolecules & Therapeutics
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• v.18 no.3
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• pp.246-256
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• 2010

Atopic dermatitis is a common skin disease affecting up to 10% of children and approximately 2% of adults. Atopic dermatitis exhibits four major symptoms, including intense itching, dry skin, redness and exudation. The "itch-scratch-itch" cycle is one of the major features in atopic dermatitis. The pathophysiology and neurobiology of pruritus is unclear. Currently there are no single and universally effective pharmacological antipruritic drugs for treatment of atopic dermatitis. Thus, controlling of itch is a very important unmet need in patients suffering from atopic dermatitis. This article will update progress during the past 10 years of research in the field of pruritus of atopic dermatitis, focusing on aspects of pruritogens (including inflammatory lipids, histamine, serotonin, proteinases, proteinase-activating receptors, neurotransmitters, neuropeptides, and opioid peptides), antipruritic therapies, and emerging new targets. Based on recent progress, researchers expect to identify exciting possibilities for improved treatments and to develop new antipruritic drugs acting through novel targets, such as histamine H4 receptor, gastrin-releasing peptide receptor, MrgprA3, thromboxane A2 receptor and the putative SPC receptor.

• Journal of Korean Neurosurgical Society
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• v.61 no.3
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• pp.319-332
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• 2018

Germline mutations in cancer causing genes result in high risk of developing cancer throughout life. These cancer predisposition syndromes (CPS) are especially prevalent in childhood brain tumors and impact both the patient's and other family members' survival. Knowledge of specific CPS may alter the management of the cancer, offer novel targeted therapies which may improve survival for these patients, and enables early detection of other malignancies. This review focuses on the role of CPS in pediatric high grade gliomas (PHGG), the deadliest group of childhood brain tumors. Genetic aspects and clinical features are depicted, allowing clinicians to identify and diagnose these syndromes. Challenges in the management of PHGG in the context of each CPS and the promise of innovative options of treatment and surveillance guidelines are discussed with the hope of improving outcome for individuals with these devastating syndromes.

• Annals of Clinical Neurophysiology
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• v.17 no.1
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• pp.1-16
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• 2015

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease that is characterized by progressive death of motor neurons in the cortex, brainstem, and spinal cord. Until now, many treatment strategies have been tested in ALS, but so far only Riluzole has shown efficacy of slightly slowing disease progression. The pathophysiological mechanisms underlying ALS are multifactorial, with a complex interaction between genetic factors and molecular pathways. Other motor neuron disease such as spinal muscular atrophy (SMA) and spinobulbar muscular atrophy (SBMA) are also progressive neurodegenerative disease with loss of motor neuron as ALS. This common thread of motor neuron loss has provided a target for the development of therapies for these motor neuron diseases. A better understanding of these pathogenic mechanisms and the potential pathological relationship between the various cellular processes have suggested novel therapeutic approaches, including stem cell and genetics-based strategies, providing hope for feasible treatment of ALS.

• Journal of Integrative Natural Science
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• v.6 no.3
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• pp.138-142
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• 2013

The HIV-1 envelope glycoprotein gp120 plays a vital role in the entry of the virus into the host cells. The crucial role of the glycoprotein suggests gp120 as potential drug target for the future antiviral therapies. Identification of the binding mode of small drug like compounds has been an important goal in drug design. In the current study we attempt to propose binding mode of indole derivatives in the binding pocket of gp120. These derivatives are reported to inhibit HIV-1 by acting as attachment inhibitors that bind to gp120 and prevent the gp120-CD4 interaction and thus inhibit the infectivity of HIV-1. To elucidate the molecular basis of the small molecules interactions to inhibit the glycoprotein function we employed the molecular docking simulation approach. This study provides insights to elucidate the binding pattern of indole-based gp120 inhibitors and may help in the rational design of novel HIV-1 inhibitors with improved potency.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.7
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• pp.3079-3081
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• 2015

Cancer-testis antigens (CTAs) are a group of tumor associated antigens with a restricted expression pattern in normal gametogenic tissues but expression in a broad range of malignancies. Their expression pattern has made them potential targets for immunotherapy. However, expression of some of these antigens has been demonstrated in normal stem cells as well as cancer stem cells (CSCs). As CSCs have been shown to be sources of metastasis and tumor recurrence, novel therapies are being focused on their eradication. On the other hand, CTA expression in normal stem cells raises the possibility that CTA based immunotherapies cause side effects in normal tissues.

• Tuberculosis and Respiratory Diseases
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• v.76 no.1
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• pp.1-7
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• 2014

Maintenance therapy has emerged as a novel therapeutic paradigm for advanced non-small-cell lung cancer (NSCLC). Maintenance therapy that aims to sustain a clinically favorable state after first-line chemotherapy has two strategies. Switch maintenance therapy entails switching to a new and non-cross-resistant agent in an alternating or sequential manner, on completion of first-line chemotherapy. Continuous maintenance therapy keeps ongoing administration of a component of the current regimen after four to six cycles of chemotherapy, if there is a stable disease, or better response. Both maintenance therapies can be continued, until disease progression. The potential evidence regarding maintenance therapy includes providing the opportunity to receive additional treatment, through sustaining tumor shrinkage, and delayed emergence of tumor-related symptom. Thus far, debates over the parameters used to predict the effectiveness of maintenance therapy, financial burden, and uncertainty of improving the quality of life exist. Despite many debates, maintenance therapy, which is currently recommended, has been disclosed to be beneficial.

• International journal of advanced smart convergence
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• v.9 no.1
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• pp.90-97
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• 2020

Oncolytic viruses are characterized by their ability to selectively kill cancer cells, and thus they have potential for application as novel anticancer agents. Despite an increase in the number of studies on methodologies involving oncolytic viruses, bioinformatic studies generating useful data are lacking. We constructed a database for oncolytic virus research (the oncolytic virus database, OVDB) by integrating scattered genetic information on oncolytic viruses and proposed a systematic means of using the biological data in the database. Our database provides data on 14 oncolytic viral strains and other types of viruses for comparative analysis. We constructed the OVDB using the basic local alignment search tool, and therefore can provides genetic information on highly homologous oncolytic viruses. This study contributes to facilitate systematic bioinformatics research, providing valuable data for development of oncolytic virus-based anticancer therapies.

• Journal of Integrative Natural Science
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• v.8 no.2
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• pp.81-88
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• 2015

c-Jun N-terminal kinase-3 (JNK3) is a member of the mitogen-activated protein kinase family (MAPK), and plays an important role in neurological disorders. Therefore, identification of selective JNK3 inhibitor may contribute towards neuroprotection therapies. In this work, we performed hologram quantitative structure-activity relationship (HQSAR) on a series of thiophene trisubstituted derivatives. The best predictions were obtained for HQSAR model with $q^2=0.628$ and $r^2=0.986$. Statistical parameters from the generated QSAR models indicated the data is well fitted and have high predictive ability. HQSAR result showed that atom, bond and chirality descriptors play an important role in JNK3 activity and also shows that electronegative groups is highly favourble to enhance the biological activity. Our results could be useful to design novel and selective JNK3 inhibitors.

• BMB Reports
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• v.49 no.9
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• pp.459-473
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• 2016

Neurodegenerative diseases (NDs) often involve the formation of abnormal and toxic protein aggregates, which are thought to be the primary factor in ND occurrence and progression. Aged neurons exhibit marked increases in aggregated protein levels, which can lead to increased cell death in specific brain regions. As no specific drugs/therapies for treating the symptoms or/and progression of NDs are available, obtaining a complete understanding of the mechanism underlying the formation of protein aggregates is needed for designing a novel and efficient removal strategy. Intracellular proteolysis generally involves either the lysosomal or ubiquitin-proteasome system. In this review, we focus on the structure and assembly of the proteasome, proteasome-mediated protein degradation, and the multiple dynamic regulatory mechanisms governing proteasome activity. We also discuss the plausibility of the correlation between changes in proteasome activity and the occurrence of NDs.

• Clinical and Experimental Pediatrics
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• v.58 no.7
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• pp.239-244
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• 2015

The complement system is part of the innate immune response and as such defends against invading pathogens, removes immune complexes and damaged self-cells, aids organ regeneration, confers neuroprotection, and engages with the adaptive immune response via T and B cells. Complement activation can either benefit or harm the host organism; thus, the complement system must maintain a balance between activation on foreign or modified self surfaces and inhibition on intact host cells. Complement regulators are essential for maintaining this balance and are classified as soluble regulators, such as factor H, and membrane-bound regulators. Defective complement regulators can damage the host cell and result in the accumulation of immunological debris. Moreover, defective regulators are associated with several autoimmune diseases such as atypical hemolytic uremic syndrome, dense deposit disease, age-related macular degeneration, and systemic lupus erythematosus. Therefore, understanding the molecular mechanisms by which the complement system is regulated is important for the development of novel therapies for complement-associated diseases.