• The Journal of Internal Korean Medicine
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• v.42 no.1
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• pp.53-66
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• 2021

Objective: The purpose of this study was to collect and evaluate evidence of herbal medicine treatments for the residual effects of COVID-19. Methods: Nine electronic databases, namely PubMed, Science Direct, CINAHL, CNKI, Wanfang, J-STAGE, CiNii, OASIS, and Science ON, were searched with the following keywords: 'COVID-19'; 'sequelae'; 'Convalescence' for 'P (Population)' and 'Medicine, Chinese Traditional'; 'Korean medicine'; 'Herbal medicine' for 'I (Intervention)'. For the selected studies, various clinical data were extracted including patient symptoms, pattern identification, herbal medicines prescribed, and treatment results. Results: A total of nine clinical studies were identified (two case control trials; one case series; and six case reports). Various residual symptoms had been detected in the recovery stage of COVID-19 with the most commonly used pattern identifications being deficiency in both lung and spleen and in both qi and yin. Any herbal medicine prescriptions were written using these patterns. We found several reports of the positive effect of herbal medicines in that it improved symptoms, lung function, and lung inflammation. No adverse events were reported. Conclusions: The results indicate that treatment with herbal medicines has a possible therapeutic effect on the residual symptoms of COVID-19. Large-scale studies are necessary to confirm the effectiveness of these approaches.

• The Journal of Korean Medicine Ophthalmology and Otolaryngology and Dermatology
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• v.34 no.3
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• pp.55-69
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• 2021

Objectives : The purpose of this study is to review the latest discussions on the mechanism of Itching. Methods : Articles that reviewed the mechanism of itching were searched from Pubmed (January 2016 to June 2021). In addition, review articles discussing the gastrointestinal tract and the mechanisms of pruritus were searched seperately. Results : The articles are classified into three categories. These categories are the classification according to the passage of time (acute, chronic), the immune factors involved (inflammatory, non-inflammatory), and the neurophysiological mechanism (pruritoceptive itching, neuropathic itching, neurogenic itching, psychogenic itching). In each category, the articles over the past five years are summarized and reviewed. Also, how the status of the gastrointestinal tract is reflected in itching was discussed in terms of leaky gut syndrome, neuro/gastrointestinal peptides, and gut microbiota. Conclusions : This review introduces the recently discussed mechanism of itching, and in particular, examines how the gastrointestinal tract is related to skin itching. Based on these considerations, it is expected that more diverse therapeutic approaches can be explored in the future.

• Journal of Ginseng Research
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• v.45 no.2
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• pp.273-286
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• 2021

Background: Prostate carcinoma is the second most common cancer among men worldwide. Developing new therapeutic approaches and diagnostic biomarkers for prostate cancer (PC) is a significant need. The Chinese herbal medicine Panax quinquefolius saponins (PQS) have been reported to show anti-tumor effects. We hypothesized that PQS exhibits anti-cancer activity in human PC cells and we aimed to search for novel biomarkers allowing early diagnosis of PC. Methods: We used the human PC cell line DU145 and the prostate epithelial cell line PNT2 to perform cell viability assays, flow cytometric analysis of the cell cycle, and FACS-based apoptosis assays. Microarray-based gene expression analysis was used to display specific gene expression patterns and to search for novel biomarkers. Western blot and quantitative real-time PCR were performed to demonstrate the expression levels of multiple cancer-related genes. Results: Our data showed that PQS inhibited the viability of DU145 cells and induced cell cycle arrest at the G1 phase. A significant decrease in DU145 cell invasion and migration were observed after 24 h treatment by PQS. PQS up-regulated the expression levels of p21, p53, TMEM79, ACOXL, ETV5, and SPINT1 while it down-regulated the expression levels of bcl2, STAT3, FANCD2, DRD2, and TMPRSS2. Conclusion: PQS promoted cells apoptosis and inhibited the proliferation of DU145 cells, which suggests that PQS may be effective for treating PC. TMEM79 and ACOXL were expressed significantly higher in PNT2 than in DU145 cells and could be novel biomarker candidates for PC diagnosis.

• Biomolecules & Therapeutics
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• v.30 no.3
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• pp.213-220
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• 2022

Although there have been advances in cancer therapy and surgical improvement, lung cancer has the lowest survival rate (19%) at all stages. This is because most patients are diagnosed with concurrent metastasis, which occurs due to numerous related reasons. Especially, lung cancer is one of the most common and malignant cancers in the world. Although there are advanced therapeutic strategies, lung cancer remains one of the main causes of cancer death. Recent work has proposed that epithelial-mesenchymal transition (EMT) is the main cause of metastasis in most cases of human cancers including lung cancer. EMT involves the conversion of epithelial cells, wherein the cells lose their epithelial abilities and become mesenchymal cells involved in embryonic development, such as gastrulation and neural crest formation. In addition, recent research has indicated that EMT contributes to altering the cancer cells into cancer stem cells (CSCs). Although EMT is important in the developmental stages, this process also activates lung cancer progression, including complicated and diverse signaling pathways. Despite the numerous investigations on signaling pathways involved in the progression of lung cancer, this malignancy is considered critical for treatment. EMT in lung cancer involves many transcription factors and inducers, for example, Snail, TWIST, and ZEB are the master regulators of EMT. EMT-related factors and signaling pathways are involved in the progression of lung cancer, proposing new approaches to lung cancer therapy. In the current review, we highlight the signaling pathways implicated in lung cancer and elucidate the correlation of these pathways, indicating new insights to treat lung cancer and other malignancies.

• Physical Therapy Rehabilitation Science
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• v.11 no.1
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• pp.8-15
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• 2022

Objective: Post stroke motor recovery is facilitated by the brain reorganization or the neuroplastic changes. The therapeutic approach mentioned in the current case is one of the approaches for enhancing motor recovery by stimulating the damaged neural networks directing the motor behaviour of a person. The aim of the present study was to establish the changes in the balance and gait pattern of an individual through multi target stimulation of areas of cerebral cortex by utilising multichannel trans cranial direct current stimulation (M-tDCS) in a sub-acute stroke survivor. Design: A Case Report Methods: The present patient was the participant of the trial (CTRI/2021/02/031044).The patient was intervened with M-tDCS (anodes over left primary motor cortex that is C3 point and left dorsolateral prefrontal cortex i.e., F3 point and cathodes over supraorbital areas, Intensity - 1.2mA) for the duration of 20 minutes along with turbo med extern - an AFO to facilitate ankle dorsi flexion and conventional physiotherapy rehabilitation. The Fugl-Meyer assessment lower extremity (FMA-LE), Berg Balance Scale (BBS), Wisconsin Gait Scale (WGS) and the Stroke Specific Quality of Life (SSQOL) measures were used for outcome assessment. Baseline assessment was done on day 0 followed by assessment on 10 and 20 post intervention. Results: Improvement was seen in all the tools i.e. (FMA -LE), BBS, SSQOL and WGS over the time period of 20 days. Conclusions: M-tDCS resulted in improvement in gait parameters, balance and motor functions of lower extremity of the patient.

• BMB Reports
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• v.54 no.12
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• pp.608-613
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• 2021

Melanoma, the most serious type of skin cancer, exhibits a high risk of metastasis. Although chemotherapeutic treatment for metastatic melanoma improves disease outcome and patient survival, some patients exhibit resistance or toxicity to the drug treatment regime. OTUB1 is a deubiquitinating enzyme overexpressed in several cancers. In this study, we investigated the effects of inhibiting OTUB1 expression on melanoma-cell proliferation and viability and identified the underlying molecular mechanism of action of OTUB1. We did endogenous OTUB1 knockdown in melanoma cells using short interfering RNA, and assessed the resulting phenotypes via MTT assays, Western blotting, and cell-cycle analysis. We identified differentially expressed genes between OTUB1-knockdown cells and control cells using RNA sequencing and confirmed them via Western blotting and reverse transcription polymerase chain reaction. Furthermore, we investigated the involvement of apoptotic and cell survival signaling pathways upon OTUB1 depletion. OTUB1 depletion in melanoma cells decreased cell viability and caused simultaneous accumulation of cells in the sub-G1 phase, indicating an increase in the apoptotic-cell population. RNA sequencing of OTUB1-knockdown cells revealed an increase in the levels of the apoptosis-inducing protein TRAIL. Additionally, OTUB1-knockdown cells exhibited increased sensitivity to PLX4032, a BRAF inhibitor, implying that OTUB1 and BRAF act collectively in regulating apoptosis. Taken together, our findings show that OTUB1 induces apoptosis of melanoma cells in vitro, likely by upregulating TRAIL, and suggest that approaches targeting OTUB1 can be developed to provide novel therapeutic strategies for treating melanoma.

• Journal of Ginseng Research
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• v.46 no.4
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• pp.592-600
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• 2022

Background: Di-(2-ethylhexyl) phthalate (DEHP) is the most common endocrine disrupting chemical used as a plasticizer. DEHP is associated with the development of endometrium-related diseases through the induction of inflammation. The major therapeutic approaches against endometrial cancer and endometriosis involve the suppression of inflammatory response. Korean Red Ginseng (KRG) is a natural product with anti-inflammatory and anti-carcinogenic properties. Thus, the purpose of this study is to investigate the effects of KRG on DEHP-induced inflammatory response in endometrial cancer Ishikawa cells and a mouse model of endometriosis. Methods: RNA-sequencing was performed and analyzed on DEHP-treated Ishikawa cells in the presence and absence of KRG. The effects of KRG on DEHP-induced cyclooxygenase-2 (COX-2) mRNA levels in Ishikawa cells were determined by RT-qPCR. Furthermore, the effects of KRG on the extracellular signal-regulated kinases (ERKs) pathway, COX-2, and nuclear factor-kappa B (NF-kB) p65 after DEHP treatment of Ishikawa cells were evaluated by western blotting. In the mouse model, the severity of endometriosis induced by DEHP and changes in immunohistochemistry were used to assess the protective effect of KRG. Results: According to the RNA-sequencing data, DEHP-induced inflammatory response-related gene expression was downregulated by KRG. Moreover, KRG significantly inhibited DEHP-induced ERK1/2/NF-κB/COX-2 levels in Ishikawa cells. In the mouse model, KRG administration significantly inhibited ectopic endometriosis growth after DEHP-induced endometriosis. Conclusions: Overall, these results suggest that KRG may be a promising lead for the treatment of endometrial cancer and endometriosis via suppression of the inflammatory response.

• Journal of Radiopharmaceuticals and Molecular Probes
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• v.9 no.1
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• pp.23-33
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• 2023

Prostate cancer ranks as the world's second most frequently diagnosed cancer among men, and is responsible for the fifth highest number of cancer-related deaths in this population. The development of effective diagnostic and therapeutic approaches for prostate cancer remains a major challenge in the field of oncology. Over the past few years, the prostate-specific membrane antigen (PSMA) has raised as a hopeful tracer for the diagnosis and treatment of prostate cancer.Various radioisotopes, such as ¹³¹I, ^99mTc, ⁶⁸Ga, and ¹⁷⁷Lu, have been used to label PSMA analogues, with varying degrees of success. Among these, ⁶⁸Ga-PSMA-11 and ¹⁷⁷Lu-PSMA-617 have emerged as the most promising radioligands for clinical use. Recently, researchers have been exploring the use of other radioisotopes, such as ²¹¹At, ⁸⁹Zr, ^64/67Cu, and ^203/212Pb, for the labeling of PSMA-targeted radioligands. These radioisotopes have unique properties that may offer advantages over existing radioligands, such as longer half-lives, higher specific activities, and different emission profiles. Efforts are currently underway to develop these radiopharmaceuticals and make them more widely available for clinical use. These exciting developments highlight the potential of PSMA-targeted radioligands for the diagnosis and treatment of prostate cancer, and provided significant implications for the management of this disease in the future. The current study aims to provide a comprehensive summary of the latest research and clinical applications of radiolabeled PSMA inhibitors for diagnoses and therapy of prostate cancer, emphasizing the exciting developments in the field and their potential impact on clinical practice.

• Physical Therapy Korea
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• v.29 no.2
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• pp.147-155
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• 2022

Background: Although various conventional approaches have been employed to reduce spasticity in neurological rehabilitation, only a few studies have shown scientific evidence for its effectiveness. Thus, we introduced a different concept (Ueda method) of rehabilitation therapy that can complement the limitations of conventional therapy. Objects: This study aimed to investigate the immediate effects of the application of the Ueda method on patients with spasticity after stroke via an electrophysiological study. Methods: We conducted a randomized double-blind pilot study in two rehabilitation hospitals involving 30 stroke patients who were randomly allocated to the Ueda (n = 15) and convention (n = 15) groups. Electromyographic data of six examined muscles in both upper extremities of all patients were recorded. The A-ApA index and activation ratios of upper extremity muscles were evaluated and compared between the groups to confirm post-intervention changes in upper-extremity flexor spasticity and flexion synergies. Repeated-measures analysis of variance was conducted to confirm the therapeutic effect (2 × 2) as a function of group (Ueda vs. convention) and time (pre-/post-intervention) on all outcome measures (p < 0.05). Results: In the Ueda group, the mean A-ApA index values differed significantly before and after the intervention (p = 0.041), indicating a weak evidence level; however, the effect size was medium (d = -0.503). The interaction effects of the A-ApA index between the Ueda and convention groups and between pre-intervention and post-intervention stages were significant (p = 0.012). The effect size was large (n_p² = 0.220). In the Ueda group, the activation ratios of the anterior deltoid fiber significantly decreased after the intervention in all reaching tasks. Conclusion: The Ueda method reduces upper-extremity flexor spasticity and changes its synergy in stroke patients and should be considered a rehabilitation therapy for spastic stroke patients.

• IMMUNE NETWORK
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• v.22 no.1
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• pp.8.1-8.20
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• 2022

Rheumatoid arthritis (RA) is a representative autoimmune disease that is primarily characterized by persistent inflammation and progressive destruction of synovial joints. RA has a complex and heterogeneous pathophysiology, involving interactions among various immune and joint stromal cells and a diverse network of cytokines and intracellular signaling pathways. With improved understanding of RA, over the past decades, therapeutic strategies have become considerably advanced and now included targeted molecular therapies, such as tumor necrosis factor inhibitors, IL-6 blockers, B-cell depletion agents, as well as inhibitors of T-cell co-stimulation and Janus kinases. However, a considerable proportion of RA patients experience refractory disease and interrupted treatment owing to the associated risk of developing serious infections and cancers. In contrast, although IL-1β, IL-17A, and p38α play significant roles in RA pathogenesis, several drugs targeting these factors have not been approved because of their low efficacy and severe adverse effects. In this review, we provide an overview of the working mechanism, advantages, and limitations of the currently available targeted drugs for RA. Additionally, we suggest potential mechanistic causes for clinically approved and failed drugs. Thus, this review provides perspectives on approaches for basic and translational studies that hold promise for identifying future next-generation therapeutics for RA.