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유방암의 두경부 전이 관련 연하장애로 오인한 피부근염: 증례보고
Lee Ryeojin,Lee Chae Hyeon,Yun Yeo Joon,Seo Han Gil,Park Sung-Hye,Oh Byung-Mo 대한연하장애학회 2024 대한연하장애학회지 Vol.14 No.1
Dysphagia often occurs in cancer patients. The primary causes of dysphagia in cancer patients include new local dissemination of cancer cells or metastatic brain lesions, which needs to be accurately differentiated. Dermatomyositis is often associated with cancer and may manifest before or after the cancer diagnosis. Although early diagnosis and immunotherapy can improve dermatomyositis, its identification may be delayed in cancer patients due to complex comorbidities. We report a case of a 33-year-old woman with metastatic breast cancer who presented with dysphagia. The primary consideration was metastatic lesions. However, subsequent diagnosis revealed dermatomyositis. Symptoms, including facial swelling, dysarthria, and dysphagia, emerged 26 months after the cancer diagnosis. No new metastatic lesion was identified through imaging studies. A videofluoroscopic study (VFSS) revealed velopharyngeal insufficiency, reduced pharyngeal contraction, and excessive pharyngeal residue with silent aspiration. After a combination of further clinical, laboratory, and muscle biopsy findings, dermatomyositis was identified as the actual cause of dysphagia. The patient was treated with immunosuppressive and rehabilitative swallowing therapies, which improved her symptoms. This case underscores the critical importance of accurately identifying and promptly treating dysphagia in cancer patients. It particularly emphasizes the need to recognize dermatomyositis as a potential differential diagnosis in cancer patients presenting with dysphagia.
Pim1 promotes IFN-β production by interacting with IRF3
Ko Ryeojin,Seo Jeongin,Park Hana,Lee Nawon,Lee Soo Young 생화학분자생물학회 2022 Experimental and molecular medicine Vol.54 No.-
The Pim (proviral integration site for Moloney murine leukemia virus) proteins compose a serine threonine kinase family whose members regulate cell proliferation, migration and cell survival. However, whether Pim kinases participate in innate immune responses is unclear. Here, we show for the first time that Pim1 plays an essential role in the production of interferon (IFN)-β by macrophages after their Toll-like receptor (TLR) pathway is activated by pathogen-associated molecular patterns (PAMPs). Specifically, Pim1 was quickly upregulated in an NF-κB-dependent manner after TLR stimulation with PAMPs. Pim1 deficiency reduced TLR3- or TLR4-stimulated IFN-β and IFN-stimulated gene (ISG) expression but not proinflammatory cytokine expression in macrophages. Mechanistically, Pim1 specifically upregulates IRF3 phosphorylation and nuclear translocation. However, this role is not dependent on Pim1 kinase activity. Rather, Pim1 appears to promote IRF3 phosphorylation by enhancing the formation of IFN-β signaling complexes composed of TRIF, TRAF3, TBK1, and IRF3. Poly (I:C)-treated Pim1−/− mice produced less serum IFN-β and were less likely to survive than wild-type mice. These findings show for the first time that Pim1 participates in TLR-mediated IFN-β production, thus revealing a novel target for controlling antiviral innate immune responses.
재가 중증 뇌병변 장애인의 기능상태 및 케어요구 목록 평가
고려진,유원섭,이꽃메,이소나,김교현,오희영 대한간호행정학회 2008 간호행정학회지 Vol.14 No.4
Purpose: Using comprehensive and valid instrument, MDS-HC 2.0, this study aimed to analyze the functional status and to evaluate the care needs of the community-dwelling disabled with cerebral impairment. Method: With a convenient sample of 88 disabled with cerebral impairment, the data were collected at a community health center located in rural area in Choongchung providence in August 2005. Subject's functional status and care needs were evaluated using Minimum Data Set-Home Care version 2.0. Result: Significant proportion of subjects were totally dependent for locomotion-outdoor (26.1%), personal hygiene (24.1%), bathing (24.1%). For IADLs, over 40% of subjects were totally dependent for ordinary house work, managing finances, or shopping. Top five ranked care needs were preventive health care measures (100%), communication disorders (71.6%), visual function (55.7%), health promotion (52.3%), and pressure ulcers (48.9%). The proportion of triggered clinical assessment protocols were significantly higher in disability level I group for the risk of institutionalization (p=<.001), communication disorders (p=.004), cognitive problems (p=.001), pressure ulcers (p=<.001), skin and foot conditions (p=.010), and urinary incontinence and indwelling catheters (p=<.001). Conclusions: It is necessary to provide community based rehabilitation services that are individualized for their service needs thus enhance optimal level of functioning.
GSK3β Inhibitor Peptide Protects Mice from LPS-induced Endotoxin Shock
Ko, Ryeojin,Jang, Hyun Duk,Lee, Soo Young The Korean Association of Immunobiologists 2010 Immune Network Vol.10 No.3
Background: Glycogen synthase kinase $3{\beta}$ ($GSK3{\beta}$) is a ubiquitous serine/threonine kinase that is regulated by serine phosphorylation at 9. Recent studies have reported the beneficial effects of a number of the pharmacological $GSK3{\beta}$ inhibitors in rodent models of septic shock. Since most of the $GSK3{\beta}$ inhibitors are targeted at the ATP-binding site, which is highly conserved among diverse protein kinases, the development of novel non-ATP competitive $GSK3{\beta}$ inhibitors is needed. Methods: Based on the unique phosphorylation motif of $GSK3{\beta}$, we designed and generated a novel class of $GSK3{\beta}$ inhibitor (GSK3i) peptides. In addition, we investigated the effects of a GSK3i peptide on lipopolysaccharide (LPS)-stimulated cytokine production and septic shock. Mice were intraperitoneally injected with GSK3i peptide and monitored over a 7-day period for survival. Results: We first demonstrate its effects on LPS-stimulated pro-inflammatory cytokine production including interleukin (IL)-6 and IL-12p40. LPS-induced IL-6 and IL-12p40 production in macrophages was suppressed when macrophages were treated with the GSKi peptide. Administration of the GSK3i peptide potently suppressed LPS-mediated endotoxin shock. Conclusion: Collectively, we present a rational strategy for the development of a therapeutic GSK3i peptide. This peptide may serve as a novel template for the design of non-ATP competitive GSK3 inhibitors.
Glycogen synthase kinase 3β in Toll-like receptor signaling
Ko, Ryeojin,Lee, Soo Young Korean Society for Biochemistry and Molecular Biol 2016 BMB Reports Vol.49 No.6
Toll-like receptors (TLRs) play a critical role in the innate immune response against pathogens. Each TLR recognizes specific pathogen-associated molecular patterns, after which they activate the adaptor protein MyD88 or TRIF-assembled signaling complex to produce immune mediators, including inflammatory cytokines and type I IFNs. Although the activation of TLR is important for host defense, its uncontrolled activation can damage the host. During the past decade, numerous studies have demonstrated that GSK3β is a key regulator of inflammatory cytokine production in MyD88-mediated TLR signaling via TLR2 and TLR4. Recently, GSK3β has also been implicated in the TRIF-dependent signaling pathway via TLR3. In this review, we describe current advances on the regulatory role of GSK3β in immune responses associated with various TLRs. A better understanding of the role of GSK3β in TLR signaling might lead to more effective anti-inflammatory interventions.
Hong Sunmok,Park Seoyeong,Lee Yeji,Lee Ryeojin,Hyun Sung Eun 대한근전도전기진단의학회 2023 대한근전도 전기진단의학회지 Vol.25 No.1
Patients diagnosed with Japanese encephalitis (JE) may present with flaccid paralysis. JE has also been reported to be accompanied by anterior horn cell disease or motor axonal polyneuropathy. We report a case of a patient with JE with prolonged limb and respiratory muscle weakness who underwent electrodiagnostic studies, including a phrenic nerve conduction study, 10 months after the onset of paralysis. During that 10-month period, severe weakness of the upper and lower extremities showed no recovery, and the patient required long-term ventilator support through a tracheostomy. Nerve conduction studies and electromyography revealed chronic anterior horn cell disease with abundant denervation potentials involving the craniobulbar, cervical, thoracic, and lumbosacral segments. In addition to the nerves in the upper and lower extremities, the phrenic motor nerves showed abnormalities indicative of diaphragmatic weakness. Therefore, in patients with JE with chronic limb weakness and respiratory difficulty, thorough electrodiagnostic studies should be performed to diagnose the combination of anterior horn cell disease with encephalitis and to evaluate the condition’s severity and prognosis.