• Archives of Craniofacial Surgery
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• v.23 no.2
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• pp.71-76
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• 2022

Background: Xanthelasma palpebrarum (XP) is a benign periorbital lesion. The relationship between xanthelasma lesion size and serum cholesterol levels has been poorly studied. In this study, we investigated this relationship in the context of the clinical etiology of XP. Methods: We retrospectively reviewed medical records and pathology reports of all patients treated for XP at our hospital between June 2014 and June 2021; the data were used to analyze lesion size, underlying disease, serum cholesterol, and disease recurrence. Results: The mean values for patient age, serum cholesterol, and lesion size were 53.0 years, 235.0 mg/dL, and 69.2 mm², respectively. XP mainly occurred in women (64.7%); furthermore, the incidence of XP and lesion size was greatest among patients in their 5th decade of life (41.2%). There was no statistically significant relationship between xanthelasma lesion size and serum cholesterol level. Conclusion: This study compared lesion size with various clinical features in XP patients. In patients who underwent surgery for XP, serum cholesterol levels tended to be higher than those in the general population. However, the trend between the size of XP and serum cholesterol level was unclear. Therefore, if a patient with XP visits the hospital for surgery, it is recommended to check the lipid profile to confirm underlying dyslipidemia regardless of the size.

• Journal of Veterinary Science
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• v.24 no.1
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• pp.2.1-2.14
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• 2023

Background: Hypothermia is a crucial environmental factor that elevates the risk of cardiovascular disease, but the underlying effect is unclear. Objectives: This study examined the role of cold stress (CS) in cardiac injury and its underlying mechanisms. Methods: In this study, a chronic CS-induced myocardial injury model was used; mice were subjected to chronic CS (4℃) for three hours per day for three weeks. Results: CS could result in myocardial injury by inducing the levels of heat shock proteins 70 (HSP70), enhancing the generation of creatine phosphokinase-isoenzyme (CKMB) and malondialdehyde (MDA), increasing the contents of tumor necrosis factor-α (TNF-α), high mobility group box 1 (HMGB1) interleukin1b (IL-1β), IL-18, IL-6, and triggering the depletion of superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH). Multiple signaling pathways were activated by cold exposure, including pyroptosis-associated NOD-like receptor 3 (NLRP3)-regulated caspase-1-dependent/Gasdermin D (GSDMD), inflammation-related toll-like receptor 4 (TLR4)/myeloid differentiation factor 88 (MyD88)-mediated nuclear factor kappa B (NF-κB), and mitogen-activated protein kinase (MAPK), as well as oxidative stressinvolved thioredoxin-1/thioredoxin-interacting protein (Txnip) signaling pathways, which play a pivotal role in myocardial injury resulting from hypothermia. Conclusions: These findings provide new insights into the increased risk of cardiovascular disease at extremely low temperatures.

• Journal of Ginseng Research
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• v.47 no.2
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• pp.291-301
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• 2023

Introduction: Non-small cell lung cancer (NSCLC) patients are particularly vulnerable to the Coronavirus Disease-2019 (COVID-19). Currently, no anti-NSCLC/COVID-19 treatment options are available. As ginsenoside Rg3 is beneficial to NSCLC patients and has been identified as an entry inhibitor of the virus, this study aims to explore underlying pharmacological mechanisms of ginsenoside Rg3 for the treatment of NSCLC patients with COVID-19. Methods: Based on a large-scale data mining and systemic biological analysis, this study investigated target genes, biological processes, pharmacological mechanisms, and underlying immune implications of ginsenoside Rg3 for NSCLC patients with COVID-19. Results: An important gene set containing 26 target genes was built. Target genes with significant prognostic value were identified, including baculoviral IAP repeat containing 5 (BIRC5), carbonic anhydrase 9 (CA9), endothelin receptor type B (EDNRB), glucagon receptor (GCGR), interleukin 2 (IL2), peptidyl arginine deiminase 4 (PADI4), and solute carrier organic anion transporter family member 1B1 (SLCO1B1). The expression of target genes was significantly correlated with the infiltration level of macrophages, eosinophils, natural killer cells, and T lymphocytes. Ginsenoside Rg3 may benefit NSCLC patients with COVID-19 by regulating signaling pathways primarily involved in anti-inflammation, immunomodulation, cell cycle, cell fate, carcinogenesis, and hemodynamics. Conclusions: This study provided a comprehensive strategy for drug discovery in NSCLC and COVID-19 based on systemic biology approaches. Ginsenoside Rg3 may be a prospective drug for NSCLC patients with COVID-19. Future studies are needed to determine the value of ginsenoside Rg3 for NSCLC patients with COVID-19.

• Journal of Medicine and Life Science
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• v.18 no.3
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• pp.61-65
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• 2021

Although re-expansion pulmonary edema (RPE) is rare (incidence rate <1%), it is associated with a mortality rate of >20%; therefore, early diagnosis and treatment are important. We report a case of RPE following chest tube insertion in a patient with spontaneous pneumothorax. We have specifically focused on the mechanism underlying RPE and the possible etiology. An 82-year-old man with a history of chronic anemia, chronic obstructive pulmonary disease, diabetes mellitus, and hypertension was referred to the emergency department for management of recurrent right-sided pneumothorax. We performed emergency closed thoracostomy for suspected tension pneumothorax, which led to stabilization of the patient's vital signs; however, he coughed up frothy pink sputum accompanied by severe right-sided chest pain 30 min postoperatively. The patient showed new-onset right pulmonary consolidation on chest radiography, as well as desaturation, tachycardia, and tachypnea and was diagnosed with RPE. He was transferred to the intensive care unit for mechanical ventilation and supportive treatment using diuretics, ionotropic agents, and prophylactic antibiotics. RPE gradually resolved, and the patient was extubated 3 days after admission. He has not experienced recurrent pneumothorax or pulmonary disease for 4 months. We emphasize the importance of RPE prevention and that aggressive ventilator care and supportive treatment can effectively treat RPE following an accurate understanding of the underlying pathogenetic mechanisms and risk factors.

• Molecules and Cells
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• v.46 no.4
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• pp.191-199
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• 2023

The Golgi apparatus modifies and transports secretory and membrane proteins. In some instances, the production of secretory and membrane proteins exceeds the capacity of the Golgi apparatus, including vesicle trafficking and the post-translational modification of macromolecules. These proteins are not modified or delivered appropriately due to the insufficiency in the Golgi function. These conditions disturb Golgi homeostasis and induce a cellular condition known as Golgi stress, causing cells to activate the 'Golgi stress response,' which is a homeostatic process to increase the capacity of the Golgi based on cellular requirements. Since the Golgi functions are diverse, several response pathways involving TFE3, HSP47, CREB3, proteoglycan, mucin, MAPK/ETS, and PERK regulate the capacity of each Golgi function separately. Understanding the Golgi stress response is crucial for revealing the mechanisms underlying Golgi dynamics and its effect on human health because many signaling molecules are related to diseases, ranging from viral infections to fatal neurodegenerative diseases. Therefore, it is valuable to summarize and investigate the mechanisms underlying Golgi stress response in disease pathogenesis, as they may contribute to developing novel therapeutic strategies. In this review, we investigate the perturbations and stress signaling of the Golgi, as well as the therapeutic potentials of new strategies for treating Golgi stress-associated diseases.

• Pediatric Infection and Vaccine
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• v.26 no.1
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• pp.1-10
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• 2019

Purpose: We investigated the distribution and antimicrobial resistance of pneumococcal isolates from hospitalized children at Asan Medical Center for recent 4 years, and aimed to recommend proper choice of empirical antibiotics for pneumococcal infection. Methods: From March 2014 to May 2018, children admitted to Asan Medical Center Childrens' Hospital with pneumococcal infection were subjected for evaluation of minimal inhibitory concentration (MIC) for ${\beta}-lactams$ and macrolide antibiotics. Patient's age, underlying disease, gender were retrospectively collected. Using Monte Carlo simulation model and MIC from our study, we predicted the rate of treatment success with amoxicillin treatment. Results: Sixty-three isolates were analyzed including 20.6% (n=13) of invasive isolates, and 79.4% (n=50) of non-invasive isolates; median age were 3.3 years old, and 87.3% of the pneumococcal infections occurred to children with underlying disease. Overall susceptibility rate was 49.2%, 68.2%, and 74.6% for amoxicillin, parenteral penicillin, and cefotaxime respectively. 23.8% and 9.5% of the isolates showed high resistance for amoxicillin, and cefotaxime. Only 4.8% (n=3) were susceptible to erythromycin. Monte Carlo simulation model revealed the likelihood of treatment success was 46.0% at the dosage of 90 mg/kg/day of amoxicillin. Conclusions: Recent pneumococcal isolates from pediatric patients with underlying disease revealed high resistance for amoxicillin and cefotaxime, and high resistance for erythromycin. Prudent choice of antibiotics based on the local data of resistance cannot be emphasized enough, especially in high risk patients with underlying disease, and timely vaccination should be implemented for prevention of the spread of resistant strains.

• Tuberculosis and Respiratory Diseases
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• v.80 no.2
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• pp.113-135
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• 2017

Asthma is traditionally regarded as a chronic airway disease, and recent literature proves its heterogeneity, based on distinctive clusters or phenotypes of asthma. In defining such asthma clusters, the nature of comorbidity among patients with asthma is poorly understood, by assuming no causal relationship between asthma and other comorbid conditions, including both communicable and noncommunicable diseases. However, emerging evidence suggests that the status of asthma significantly affects the increased susceptibility of the patient to both communicable and noncommunicable diseases. Specifically, the impact of asthma on susceptibility to noncommunicable diseases such as chronic systemic inflammatory diseases (e.g., rheumatoid arthritis), may provide an important insight into asthma as a disease with systemic inflammatory features, a conceptual understanding between asthma and asthma-related comorbidity, and the potential implications on the therapeutic and preventive interventions for patients with asthma. This review discusses the currently under-recognized clinical and immunological phenotypes of asthma; specifically, a higher risk of developing a systemic inflammatory disease such as rheumatoid arthritis and their implications, on the conceptual understanding and management of asthma. Our discussion is divided into three parts: literature summary on the relationship between asthma and the risk of rheumatoid arthritis; potential mechanisms underlying the association; and implications on asthma management and research.

• BMB Reports
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• v.53 no.2
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• pp.65-73
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• 2020

Life expectancy has dramatically increased around the world over the last few decades, and staying healthier longer, without chronic disease, has become an important issue. Although understanding aging is a grand challenge, our understanding of the mechanisms underlying the degeneration of cell and tissue functions with age and its contribution to chronic disease has greatly advanced during the past decade. As our immune system alters with aging, abnormal activation of immune cells leads to imbalance of innate and adaptive immunity and develops a persistent and mild systemic inflammation, inflammaging. With their unique therapeutic properties, such as immunomodulation and tissue regeneration, mesenchymal stem cells (MSCs) have been considered to be a promising source for treating autoimmune disease or as anti-aging therapy. Although direct evidence of the role of MSCs in inflammaging has not been thoroughly studied, features reported in senescent MSCs or the aging process of MSCs are associated with inflammaging; MSC niche-driven skewing of hematopoiesis toward the myeloid lineage or oncogenesis, production of pro-inflammatory cytokines, and weakening their modulative property on macrophage polarization, which plays a central role on inflammaging development. This review explores the role of senescent MSCs as an important regulator for onset and progression of inflammaging and as an effective target for anti-aging strategies.

• Journal of Pharmacopuncture
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• v.22 no.4
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• pp.210-224
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• 2019

Rheumatoid arthritis is a severe autoimmune disorder, related to joints. It is associated with serious cartilage destruction. This causes disability and reduces the excellence of life. Numerous treatments are existed to combat this disease, however, they are not very efficient and possess severe side effects, higher doses, and frequent administration. Therefore, newer therapies are developed to overcome all these limitations. These include different monoclonal antibodies, immunoglobulins, small molecules used for immunotherapy and transgenes for gene therapy. One of the main goals of these new generation therapeutics is to address the underlying distressing biological processes by specifically targeting the causative agents with fewer systemic side effects and greater patient console. It is very fortuitous that loads of progressive investigations are going on in this field and many of them have entered into the successful clinical trial. But till date, a limited molecule has got FDA clearance and entered the market for treating this devastating disease. This review highlights the overview of conventional therapy and advancements in newer therapeutics including immunotherapy and gene therapy for rheumatoid arthritis. Further, different novel techniques for the delivery of these therapeutics of active and passive targeting are also described.

• BMB Reports
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• v.49 no.3
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• pp.139-148
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• 2016

In the past decade, the incidence of type 2 diabetes (T2D) has rapidly increased, along with the associated cardiovascular complications. Therefore, understanding the pathophysiology underlying T2D, the associated complications and the impact of therapeutics on the T2D development has critical importance for current and future therapeutics. The prevailing feature of T2D is hyperglycemia due to excessive hepatic glucose production, insulin resistance, and insufficient secretion of insulin by the pancreas. These contribute to increased fatty acid influx into the liver and muscle causing accumulation of lipid metabolites. These lipid metabolites cause dyslipidemia and non-alcoholic fatty liver disease, which ultimately contributes to the increased cardiovascular risk in T2D. Therefore, understanding the mechanisms of hepatic insulin resistance and the specific role of liver lipids is critical in selecting and designing the most effective therapeutics for T2D and the associated co-morbidities, including dyslipidemia and cardiovascular disease. Herein, we review the effects and molecular mechanisms of conventional anti-hyperglycemic and lipid-lowering drugs on glucose and lipid metabolism.