• Korean Journal of Clinical Pharmacy
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• v.27 no.3
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• pp.136-142
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• 2017

Background: Dementia is one of important social and economic healthcare issues in the aging age. Therefore, it signifies to analyze the relationship between chronic disease or cardiovascular drug use and the incidence of dementia to establish a basis for increasing or preventing the risk of dementia. The purpose of this study was to investigate the correlation between the prevalence of chronic diseases and the use of cardiovascular drugs in patients diagnosed with dementia. Methods: In this study, we used data from sample of elderly patients from the Health Insurance Review and Assessment Service. We analyzed by logistic regression analysis with age, gender, and medication as covariates. KCD-7 was used to diagnosis of the disease, and drugs were analyzed using ATC codes and Korean standardized drug classification codes. Results: A total of 1,276,331 patients were analyzed in the sample of the elderly population, of which 532,075 (41.7%) were male and 744,256 (58.3%) were female. The patients have the higher risk of dementia in the older, women, and lower socioeconomically status. Cerebral infarction and ischemic heart disease increases risk of dementia. Patients taking statins, angiotensin converting enzyme inhibitor (ACEI) or angiotensin II receptor antagonists (ARB) showed low incidence of dementia. Conclusion: This study has been shown that ACEI, ARB, and statin drugs may associate with lower incidence of Alzheimer's and other dementia except vascular dementia.

• The Korean Journal of Cytopathology
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• v.6 no.1
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• pp.1-9
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• 1995

This study was carried out to determine the usefulness of imprint cytology for detecting p53 protein in breast carcinoma. NCL-DO7 (Novocastra, U.K.) was used to detect p53 protein immunocytochemically. A total of 33 cases was studied, Immunostaining of imprint cytology with NCL-DO7 was positive in 64% (21/33) and showed relatively high coincident rate (80%) with immunostaining of formalin-fixed, paraffin-embedded specimen p53 protein was related to negative estrogen receptor status, but not to the nuclear grade, lymph node metastasis, or tumor size. The fact that p53 protein expression was not related to nuclear grade might be due to predominance of nuclear grade 3. It was easier to determine the nuclear grade is one of the most important prognostic factors, in imprint cytology than in tissue specimen. p53 protein tended to be stained more strongly in imprint cytology than in tissue. It is concluded that the application of imprint cytology in p53 protein detection can be performed easily, and that it may contribute to the evaluation of prognostic factors in breast carcinoma.

• Journal of Yeungnam Medical Science
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• v.30 no.1
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• pp.4-9
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• 2013

Leptin, a 16-kDa cytokine, is secreted by adipose tissue in response to the surplus of fat store. Thereby, the brain is informed about the body's energy status. In the hypothalamus, leptin triggers specific neuronal subpopulations (e.g., POMC and NPY neurons) and activates several intracellular signaling events, including the JAK/STAT, MAPK, PI3K, and mTOR pathway, which eventually translates into decreased food intake and increased energy expenditure. Leptin signal is inhibited by a feedback inhibitory pathway mediated by SOCS3. PTP1B involves another inhibitory pathway of leptin. Leptin potently promotes fat mass loss and body weight reduction in lean subjects. However, it is not widely used in the clinical field because of leptin resistance, which is a common feature of obesity characterized by hyperleptinemia and the failure of exogenous leptin administration to provide therapeutic benefit in rodents and humans. The potential mechanisms of leptin resistance include the following: 1) increases in circulating leptin-binding proteins, 2) reduced transport of leptin across the blood-brain barrier, 3) decreased leptin receptor-B (LRB), and/or 4) the provocation of processes that diminish cellular leptin signaling (inflammation, endoplasmic reticulum stress, feedback inhibition, etc.). Thus, interference of the cellular mechanisms that attenuate leptin signaling improves leptin action in cells and animal models, suggesting the potential utility of these processes as points of therapeutic intervention. Various experimental trials and compounds that improve leptin resistance are introduced in this paper.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.9
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• pp.5193-5198
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• 2013

The glycemic index (GI) and glycemic load (GL) have been considered risk factors for breast cancer, but association studies of breast cancer risk using simple GI and GL might be affected by confounding effects of the overall diet. A total of 357 cases and 357 age-matched controls were enrolled, and dietary intake was assessed using a validated food frequency questionnaire (FFQ) with 103 food items. GI and GL dietary patterns were derived by reduced rank regression (RRR) method. The GI and GL pattern scores were positively associated with breast cancer risk among postmenopausal women [OR (95%CI): 3.31 (1.06-10.39), p for trend=0.031; 9.24 (2.93-29.14), p for trend<0.001, respectively], while the GI pattern showed no statistically significant effects on breast cancer risk, and the GL pattern was only marginally significant, among premenopausal women (p for trend=0.043). The GI and GL pattern scores were positively associated with the risk of breast cancer in subgroups defined by hormone receptor status in postmenopausal women. The GI and GL patterns based on all food items consumed were positively associated with breast cancer.

• Journal of the Korean Society of Food Science and Nutrition
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• v.28 no.3
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• pp.685-690
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• 1999

The insulin like growth factors(IGFs) are bound to several binding proteins(IGFBPs) that appear to regulate IGF transfort, receptor binding, and its action. The concentrations of these peptides are regulated by quantity and nutritional quality of dietary proteins. The aim of this study was to compare the effects of two diets, which differed in their protein source, Carassius carassius(CC), Carassius carassius hot water extract(CCHE), for 4 weeks. Body weight was significantly increased in the CC group(74.14$\pm$12.00 to 266.31$\pm$36.62g; p<0.01). Likewise, IGF I concentration of CC group(101.76$\pm$15.90 ng/ml) was significantly higher than that of CCHE group(38.50$\pm$ 11.20ng/ml; p<0.05). By western immunoblot analysis, especially IGFBP 1, 2 levels are increased, whereas IGFBP 3 level was de creased in CCHE group. After extraction of browning material from each samples, the extractive was filtered and absorbance at 420nm was measured. The absorbance of CCHE group was significantly higher than that of CC group. These results suggest that IGF I can be employed as an index of protein metabolism, particulary as a simple index in the assessing the status of protein nutrition.

• Journal of Pathology and Translational Medicine
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• v.52 no.6
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• pp.363-368
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• 2018

Background: Vitiligo is a chronic autoimmune disease in which the destruction of melanocytes causes white spots on the affected skin. Janus kinase (JAK) is a family of intracellular, non-receptor tyrosine kinases that transduce cytokine-mediated signals via the JAK-signal transducer and activator of transcription pathway. The aim of the present study is to explore the possible role of JAK1 in the pathogenesis of vitiligo using immunohistochemical methods. Methods: The current study was conducted in a sample of 39 patients who presented with vitiligo and 22 healthy individuals who were age and sex matched as a control group. We used immunohistochemistry to evaluate JAK1 status (intensity and distribution) and assess the percentage of residual melanocytes using human melanoma black 45 (HMB45). Results: Intense and diffuse JAK1 expression was significantly more likely to indicate vitiliginous skin compared to normal skin (p<.001). Strong and diffuse JAK1 expression was associated with short disease duration, female sex, and lower percentage of melanocytes (detected by HMB45) (p<.05). Conclusions: JAK1 may be involved in the pathogenesis of vitiligo, as indicated by intense and diffuse expression compared to control and association with lower percentage of melanocytes detected by HMB45 immunostaining.

• Journal of Interdisciplinary Genomics
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• v.3 no.2
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• pp.41-46
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• 2021

Inherited platelet function disorders (IPFDs) are a disease group of heterogeneous bleeding disorders associated with congenital defects of platelet functions. Normal platelets essential role for primary hemostasis by adhesion, activation, secretion of granules, aggregation, and procoagulant activity of platelets. The accurate diagnosis of IPFDs is challenging due to unavailability of important testing methods, including light transmission aggregometry and flow cytometry, in several medical centers in Korea. Among several IPFDs, Glanzmann thrombasthenia (GT) is a most representative IPFD and is relatively frequently found compare to the other types of rarer IPFDs. GT is an autosomal recessive disorder caused by mutations of ITGA2B or ITGB3. There are quantitative or qualitative defects of the GPIIb/IIIa complex in platelet, which is the binding receptor for fibrinogen, von Willbrand factor, and fibronectin in GT patients. Therefore, patients with GT have normal platelet count and normal platelet morphology, but they have severely decreased platelet aggregation. Thus, GT patients have a very severe hemorrhagic phenotypes that begins at a very early age and persists throughout life. In this article, the general contents about platelet functions and respective IPFDs, the overall contents of GT, and the current status of genetic diagnosis of GT in Korea will be reviewed.

• Journal of Neurocritical Care
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• v.7 no.2
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• pp.104-110
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• 2014

Background: Cefepime is a fourth-generation cephalosporin widely used for empiric treatment of severe infections. Neurotoxicity by cefepime have been reported due to γ-aminobutyric acid A receptor inhibition or other mechanisms. The aim of this study was to evaluate the risk factors for cefepime-induced neurotoxicity between group showing cefepime-induced neurotoxicity and group without neurotoxicity. Methods: From Jan 2005 to June 2010, a total of 2,461 patients (older than 20) who used cefepime were considered in this study. We compared patients who developed cefepime-induced neurotoxicity (patient group, n=21) to patients who had no cefepime-induced neurotoxicity (control group, n=31). We analyzed demographic, underlying diseases, and metabolic parameters before cefepime treatment and during cefepime treatment between the two groups. Statistical analysis was performed using SPSS 18 software. Results: Of the total 2461 patients, 21 (0.85%) were diagnosed with cefepime-induced neurotoxicity. Impaired glomerular filtration rate (GFR at 15-30 ml/min) before cefepime use were significantly (P<0.05) higher risk for developing cefepime-induced neurotoxicity in patient group compared to that in the control group. Age, sex, and other metabolic parameters except GFR before and during, usage of cefepime did not show any statistical difference between the two groups. Conclusion: The present study revealed that cefepime-induced neurotoxicity was prone to develop in patients with impaired renal function before cefepime usage.

• Anatomy and Cell Biology
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• v.56 no.1
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• pp.94-108
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• 2023

Cancer cell heterogeneity is a serious problem in the control of tumor progression because it can cause chemoresistance and metastasis. Heterogeneity can be generated by various mechanisms, including genetic evolution of cancer cells, cancer stem cells (CSCs), and niche heterogeneity. Because the genetic heterogeneity of CSCs has been poorly characterized, the genetic mutation status of CSCs was examined using Exome-Seq and RNA-Seq data of liver cancer. Here we show that different surface markers for liver cancer stem cells (LCSCs) showed a unique propensity for genetic mutations. Cluster of differentiation 133 (CD133)-positive cells showed frequent mutations in the IRF2, BAP1, and ERBB3 genes. However, leucine-rich repeat-containing G protein-coupled receptor 5-positive cells showed frequent mutations in the CTNNB1, RELN, and ROBO1 genes. In addition, some genetic mutations were frequently observed irrespective of the surface markers for LCSCs. BAP1 mutations was frequently observed in CD133-, CD24-, CD13-, CD90-, epithelial cell adhesion molecule-, or keratin 19-positive LCSCs. ASXL2, ERBB3, IRF2, TLX3, CPS1, and NFATC2 mutations were observed in more than three types of LCSCs, suggesting that common mechanisms for the development of these LCSCs. The present study provides genetic heterogeneity depending on the surface markers for LCSCs. The genetic heterogeneity of LCSCs should be considered in the development of LCSC-targeting therapeutics.

• IMMUNE NETWORK
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• v.20 no.1
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• pp.6.1-6.20
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• 2020

IL-17 is produced by RAR-related orphan receptor gamma t (RORγt)-expressing cells including Th17 cells, subsets of γδT cells and innate lymphoid cells (ILCs). The biological significance of IL-17-producing cells is well-studied in contexts of inflammation, autoimmunity and host defense against infection. While most of available studies in tumor immunity mainly focused on the role of T-bet-expressing cells, including cytotoxic CD8⁺ T cells and NK cells, and their exhaustion status, the role of IL-17-producing cells remains poorly understood. While IL-17-producing T-cells were shown to be anti-tumorigenic in adoptive T-cell therapy settings, mice deficient in type 17 genes suggest a protumorigenic potential of IL-17-producing cells. This review discusses the features of IL-17-producing cells, of both lymphocytic and myeloid origins, as well as their suggested pro- and/or anti-tumorigenic functions in an organ-dependent context. Potential therapeutic approaches targeting these cells in the tumor microenvironment will also be discussed.