• The Journal of Korean Medicine
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• v.42 no.1
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• pp.129-135
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• 2021

Objectives: The present study reports case of an elderly kwashiorkor patient who was treated with Korean Medicine. Methods: A 68-year-old female patient with weight loss, general weakness, chills, anorexia, and dizziness after over 100 episodes of diarrhea visited the hospital. Blood tests showed hypoalbuminemia and anemia, and ultrasonography revealed fatty liver disease. The patient was diagnosed with kwashiorkor, and her symptom differentiation was Yang deficiency followed by Both Qi-Blood deficiency. Sayeok-Tang, Soshiho-Tang, Insamyangyeong-Tang, and Gongjin-Dan, herbal drugs, were given to the patient during 40 days of hospitalization. Results: After 40 days of hospitalization, her symptoms were reduced, and the blood test results improved. Conclusion: This case presents the therapeutic potential of Korean medicine in the treatment of kwashiorkor.

• Korean Journal of Head & Neck Oncology
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• v.37 no.2
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• pp.67-69
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• 2021

Langerhans cell histiocytosis (LCH) is commonly characterized by abnormal function and differentiation or proliferation of monocytes. In LCH, granulomatous lesions, including langerine-positive histocytes and inflammatory infiltrates, can occur to all tissues, particularly well in the bones, skin, lungs, and pituitary gland. In case of external auditory canal LCH, conductive hearing loss may occur, and the most common symptom is otorrhea. Here we present a case that 49-year-old male with external auditory canal mass. Since no invasive findings were seen in radiologic study, endoscopic transcanal excision was performed and LCH was proven by pathologic report. We present this case of external auditory canal LCH with the review of literature.

• Molecules and Cells
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• v.45 no.6
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• pp.353-361
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• 2022

Chronic rhinosinusitis (CRS) is a multifactorial, heterogeneous disease characterized by persistent inflammation of the sinonasal mucosa and tissue remodeling, which can include basal/progenitor cell hyperplasia, goblet cell hyperplasia, squamous cell metaplasia, loss or dysfunction of ciliated cells, and increased matrix deposition. Repeated injuries can stimulate airway epithelial cells to produce inflammatory mediators that activate epithelial cells, immune cells, or the epithelial-mesenchymal trophic unit. This persistent inflammation can consequently induce aberrant tissue remodeling. However, the molecular mechanisms driving disease within the different molecular CRS subtypes remain inadequately characterized. Numerous secreted and cell surface proteins relevant to airway inflammation and remodeling are initially synthesized as inactive precursor proteins, including growth/differentiation factors and their associated receptors, enzymes, adhesion molecules, neuropeptides, and peptide hormones. Therefore, these precursor proteins require post-translational cleavage by proprotein convertases (PCs) to become fully functional. In this review, we summarize the roles of PCs in CRS-associated tissue remodeling and discuss the therapeutic potential of targeting PCs for CRS treatment.

• Clinical and Experimental Reproductive Medicine
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• v.25 no.2
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• pp.115-122
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• 1998

The maintenance of a viable pregnancy has long been viewed as an immunological paradox. The deveolping embryo and trophoblast are immunologically foreign to the maternal immune system due to their maternally inherited genes products and tissue-specific differentiation antigens (Hill & Anderson, 1988). Therefore, speculation has arisen that spontaneous abortion may be caused by impaired maternal immune tolerance to the semiallogenic conceptus (Hill, 1990). Loss of recall antigen has been reported in immunosuppressed transplant recipients and is associated with graft survival (Muluk et al., 1991; Schulik et al., 1994). Progesterone $(10^{-5}M)$ has immunosuppressive capabilities (Szekeres-Bartho et al., 1985). Previous study showed that fertile women, but not women with unexplained recurrent abortion (URA), lose their immune response to recall antigens when pregnant (Bermas & Hill, 1997). Therefore, we hypothesized that immunosuppressive doses of progesterone may affect proliferative response of lymphocytes to trophoblast antigen and alloantigen. Proliferative responses using $^3H$-thymidine ($^3H$-TdR) incorporation of peripheral blood mononuclear cells (PBMCs) to the irradiated allogeneic periperal blood mononuclear cells as alloantigen, trophoblast extract and Flu as recall antigen, and PHA as mitogen were serially checked in 9 women who had experienced unexplained recurrent miscarriage. Progesterone vaginal suppositories (100mg b.i.d; Utrogestan, Organon) beginning 3 days after ovulation were given to 9 women with unexplained RSA who had prior evidence of Th1 immunity to trophoblast. We checked proliferation responses to conception cycle before and after progesterone supplementation once a week through the first 7 weeks of pregnancy. All patients of alloantigen and PHA had a positive proliferation response that occmed in the baseline phase. But 4 out of 9 patients (44.4%) of trophoblast antigen and Flu antigen had a positive proliferative response. The suppression of proliferation response to each antigen were started after proliferative phase and during pregnancy cycles. Our data demonstrated that since in vivo progesterone treated PBMCs suppressed more T-lymphocyte activation and $^3H$-TdR incorporation compare to PBMCs, which are not influenced by progesterone. This data suggested that it might be influenced by immunosuppressive effect of progesterone. In conclusion, progesterone may play an important immunological role in regulating local immune response in the fetal-placental unit. Furthermore, in the 9 women given progesterone during a conception cycle, Only two (22%) repeat pregnancy losses occured in these 9 women despite loss of antigen responsiveness (one chemical pregnancy loss and one loss at 8 weeks of growth which was karyotyped as a Trisomy 4). These finding suggested that pregnancy loss due to fetal aneuploidy is not associated with immunological phenomena.

• BMB Reports
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• v.50 no.2
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• pp.103-108
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• 2017

Heme oxygenase (HO-1) catalyzes heme to carbon monoxide (CO), biliverdin/bilirubin, and iron and is known to prevent the pathogenesis of several human diseases. We assessed the beneficial effect of heme degradation products on osteoclastogenesis induced by receptor activator of NF-${\kappa}B$ ligand (RANKL). Treatment of RAW264.7 cells with CORM-2 (a CO donor) and bilirubin, but not with iron, decreased RANKL-induced osteoclastogenesis, with CORM-2 having a more potent anti-osteogenic effect. CORM-2 also inhibited RANKL-induced osteoclastogenesis and osteoclastic resorption activity in marrow-derived macrophages. Treatment with hemin, a HO-1 inducer, strongly inhibited RANKL-induced osteoclastogenesis in wild-type macrophages, but was ineffective in $HO-1^{+/-}$ cells. CORM-2 reduced RANKL-induced NFATc1 expression by inhibiting IKK-dependent NF-${\kappa}B$ activation and reactive oxygen species production. These results suggest that CO potently inhibits RANKL-induced osteoclastogenesis by inhibiting redox-sensitive NF-${\kappa}B$-mediated NFATc1 expression. Our findings indicate that HO-1/CO can act as an anti-resorption agent and reduce bone loss by blocking osteoclast differentiation.

• Journal of Physiology & Pathology in Korean Medicine
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• v.27 no.2
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• pp.153-166
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• 2013

Yang deficiency pattern is a representative syndrome differentiation. This article is a study on to which categories of modern diseases yang deficiency is assigned by reference to modern clinical papers and the meaning of yang deficiency interpreted with a perspective of Korean Medicine and a modern perspective. Yang deficiency, yang qi deficiency, lack of yang qi and yang qi debilitation are the words found in "Nei Ching" and yang qi can be interpreted as something to warm, drive and arouse. Zhangzhongjing considered recovery or loss of Yang as the key to life in "Shanghanlun". Danxi proposed "Yang being liable to hyperactivity, Yin being insufficient" and emphasized pathological ministerial fire of Yang exuberance rather than physiological ministerial fire of Yang deficiency. Zhangjingyue proposed "Yang not being in excess, Yin being often deficient" and understood growth and decline of yin qi are all led by yang qi and put emphasis on true yin in addition to yang qi. Diseases of yang deficiency pattern are related with decline of metabolic level, hypofunction of internal secretion, disorder of immune function, disorder of automatic nerve system, sympathetic nerve inhibition, metabolic disorder of microelements, increase of cGMP, change of microcirculation, low speed of blood stream, kidney malfunction. Diseases related with kidney are sterility, polycystic ovary syndrome, spinal stenosis, edema, renal failure, IgA nephropathy, erectile dysfunction, nephritis, prostatitis, benign prostatic hyperplasia, decrease of adrenal cortical hormone by nephrotic syndrome, myelodysplastic syndrome. Disease related with heart are heart failure, arrhythmia, cardiomyopathy, atherosclerosis heart disease, hypertension, hyperlipidemia, pulmonary heart disease. Diseases related with spleen are irritable bowel syndrome, ulcerative colitis. Diseases related with liver are hypothyroidism, liver cirrhosis ascites, hepatitis B, chronic hepatitis, hepatic diabetes. Diseases related with lung are allergic rhinitis, cough variant asthma, bronchial asthma, pulmonary emphysema. And diabetes mellitus, metabolic syndrome, aplastic anemia, headache, encephalatrophy, Alzheimer's disease are also related with yang deficiency.

• BMB Reports
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• v.48 no.11
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• pp.595-596
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• 2015

Skeletal muscle exhibits a loss of muscle mass and function with age. Decreased regenerative potential of muscle stem/progenitor cells is a major underlying cause of sarcopenia. We analyzed microRNAs (miRNA) that are differentially expressed in young and old myoblasts, to identify novel intrinsic factors that play a degenerative role in aged skeletal muscle. miR-431, one of decreasing miRNAs in old myoblasts, improved the myogenic differentiation when overexpressed in old myoblast, but suppressed their myogenic capability in knockdowned young myoblasts. We found that miR-431 directly binds to 3` untranslated regions (UTR) of Smad4 mRNA, and decreases its expression. Given that SMAD4 is one of the downstream effectors of TGF-β, a well-known degenerative signaling pathway in myogenesis, the decreased miR-431 in old myoblast causes SMAD4 elevation, thus resulting in defective myogenesis. Exogenous expression of miR-431 greatly improved the muscle regeneration in the cardiotoxin-injured hindlimb muscle of old mice by reducing SMAD4 levels. Since the miR-431 seed sequence is conserved in human SMAD4 3'UTR, miR-431 regulates the myogenic capacity of human skeletal myoblasts in the same manner. Our results suggest that age-associated miR-431 is required for the maintenance of the myogenic capability in myoblasts, thus underscoring its potential as a therapeutic target to slow down muscle aging.

• Biomedical Science Letters
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• v.7 no.4
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• pp.167-172
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• 2001

Nebulin is an approximately 700 kDa filamentous protein in vertebrate skeletal muscle. It binds to the Z line and also binds side-by-side to the entire thin actin filament in a sarcomere. The correlation of nebulin size with thin filament length have led to the suggestion that nebulin acts as a molecular ruler for the length of thin filaments. The C-terminal part of human nebulin is anchored in the sarcomeric Z-disk and contains an SH3 domain. SH3 domains have been identified in an ever-increasing number of proteins important for a wide range of cellular processes, from signal transduction to cytoskeleton assembly and membrane localization. However, the exact physiological role of SH3 domains remains, in many cases, unclear. To explore the role of nebulin SH3 in the cytoskeletal rearrangement that accompanies myoblast differentiation, we transfected sense and antisense nebulin SH3 domain fused to enhanced green fluorescent protein in myoblast. Cells expressing nebulin SH3 fragment showed decrease of cell-cell adhesion, and cells transfected with antisense nebulin SH3 gene showed a rounded cell morphology and loss of cell-matrix adhesion. No alteration in cell shape and differentiation were observed in control cells expressing enhanced green fluorescent protein. Perturbation of nebulin altered the cell shape and disrupted cell adhesion in myoblast, demonstrating that nebulin can affect cytoskeleton rearrangement.

• Journal of Periodontal and Implant Science
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• v.40 no.4
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• pp.172-179
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• 2010

Purpose: Accurate and exact measurement is an important factor for generating meaningful results in any properly designed study. If all the participating examiners are able to yield similar results, it will be possible to evaluate the objective results of the study more easily and quickly. The purpose of this study was to evaluate the intra- and inter-examiner reproducibility of histometric measurements in the intrabony periodontal defect model. Methods: One wall intrabony defects were surgically created at the distal aspect of the second and the medial aspect of the fourth mandibular premolars in the right and left jaw quadrants in twenty beagle dogs and the defect sites received the following ${\beta}$-tri calcium phosphate, growth differentiation factor-0, growth differentiation factor-100 and sham surgery. Histometric analysis was performed after 8 weeks. Histometric parameters were recorded and repeated at three months interval by three examiners. Intra- and inter-examiner reproducibility was assessed. Results: Most parameters of all the groups showed high intra- and inter-examiner reproducibility. Parameters including defect height, bone regeneration height, cementum regeneration height, and formation of junctional epithelium yielded interexaminer correlation ${\geq}0.9$. The intra-examiner reproducibility showed a high result, over 0.9. Conclusions: Histometric evaluation of the one-wall intra-alveolar periodontal defect model showed high reproducibility not only for a single given examiner but also among the three examiners.

• Molecules and Cells
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• v.39 no.4
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• pp.330-336
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• 2016

Long non-coding RNAs (lncRNAs) are involved in multiple cellular events, as well as in tumorigenesis. Colon cance-rassociated transcript-1 (CCAT1) gene encodes an lncRNA whose over-activation was observed in an expanding list of primary human solid tumors and tumor cell lines, however its biological roles in acute myeloid leukaemia (AML) has not been reported yet at present. In this study, the aberrant upregulation of CCAT1 was detected in French-American-British M4 and M5 subtypes of adult AML patients. By gain- and loss-of-function analysis, we determined that CCAT1 repressed monocytic differentiation and promoted cell growth of HL-60 by sequestering tumor suppressive miR-155. Accordingly, a significant decrease in miR-155 level was detected in AML patients. Reintroduction of miR-155 into HL-60 cells restored monocytic maturation and repressed cell proliferation. Furthermore, CCAT1 could up-regulated c-Myc via its competing endogenous RNA (ceRNA) activity on miR-155. In conclusion, these results revealed new mechanism of lncRNA CCAT1 in AML development, and suggested that the manipulation of CCAT1 expression could serve as a potential strategy in AML therapy.