This study aims to correct the Chinese characters of 普救女館 (Po Goo Nyo Goan) and its Korean pronunciation by re-examining the circumstances around the establishment of this hospital, and to discover its naming principle which is associated with the Confucian political philosophy of the Joseon Dynasty. Although 普救女館 is the first modern women's hospital in Korea, most historical studies of this institute have been conducted on limited documents and records. Many published studies use the incorrect names in many ways, so the correct name of the hospital is still in confusion.普救女館, however, was named with four or five of the Chinese characters given by the Joseon government (King Gojong (高宗)) at the time of its establishment. The Joseon government gave the name of Seonnyeoboguwon (善女普救院) to the first modern women's hospital established by Mary Scranton, the name of which was changed to 普救女館.Some records left by the female missionary doctors who worked in 普救女館 show the romanization and meaning of the name of the hospital. The romanization of 普救女館 clarified the Korean pronunciation of “女 (nyeo)” at that time. English translation name of the hospital has always shown that the place provided “extensive” medical treatment to women. It proves the fact that the first Chinese character of the name is “普”, not “保” which is expressed in many documents today.The hospital was named according to Confucian ideals just like the other modern hospitals established around the same time, such as Jejungwon (濟衆院), Gwangjewon (廣濟院), Gwanghyeyeowon (廣惠女院). The Joseon government commonly used similar Chinese characters during the naming of these hospitals, characters that imply the ideal of the good Confucian king's favor for many people of Joseon. 普救女館 was unique in having the character “館(gwan)” in its name, not “院(won)” as in other hospitals. It seems to stem from the characteristic of “women's hospital.” Po Gu Nyo Goan, the unprecedented women's hospital, was probably imagined as a hospitable accommodation where women provided kindness to people in need. This may have been the reason why “館”, which has the meaning of accommodation, was chosen instead of “院” that primarily meant medical facilities.Correcting the name of 普救女館 helps to eliminate the confusion in current historiography and to promote the understanding of the historical significance of this hospital.

Background: The Harris-Galante (HG) prosthesis is a first-generation, cementless total hip arthroplasty (THA) prosthesis. Considering the recent increase in the demand for THA in young patients and their life expectancy, a study with a follow-up duration of longer than 20 years in a young population is needed. Therefore, we evaluated the long-term clinical and radiographic results after cementless THA using the HG prosthesis in patients younger than 50 years. Methods: A total of 61 THAs performed using the HG with a minimum follow-up of 10 years were included. There were 38 men and 11 women with an average age of 46 years and the mean follow-up duration was 22 years. Clinical evaluation included modified Harris Hip Score (HHS) and radiographic analysis consisted of cup inclination, anteversion angle, component stability, osteolysis, liner wear rate, wear-through, liner dissociation, and heterotopic ossification. Complications included recurrent dislocation, periprosthetic femoral fracture, and periprosthetic joint infection. Survivorship analysis included cup and stem revision for aseptic loosening, as well as any revision. Results: The HHS improved from 46.5 preoperatively to 81.8 postoperatively (p < 0.001). The average linear wear rate was 0.36 mm/yr. A total of 34 hips (56%) were revised: stem revision in 10 (16.4%), cup revision in 9 (14.8%), exchange limited to bearing surface in 8 (13.1%), and revision of all components in 7 (11.5%). Estimated survivorship at 34 years postoperatively was 90.9% for cup revision for aseptic loosening, 80.5% for stem revision for aseptic loosening, and 22.1% for any revision. Conclusions THA using the HG prosthesis showed satisfactory estimated survivorship of the acetabular and femoral components at 34 years postoperatively with good clinical outcomes. Bearing-related problems, such as osteolysis and liner dissociation, accounted for 56% of revision operations and were concerns in patients younger than 50 years.

Recently, atypical femoral fractures (AFFs) have been found in patients who were prescribed bisphosphonate to prevent osteoporotic fractures. Although the occurrence of AFF is rare, there are some concerns, such as a higher risk of delayed or non-union of AFF. This paper reviews the treatment of AFF and suggests some considerations during surgery.
Femoral Fractures ; Humans ; Osteoporosis ; Osteoporotic Fractures ; Teriparatide

OBJECTIVE: Enteroviruses are major causes of aseptic meningitis in children. This study aimed to describe the clinical manifestations of enteroviral meningitis according to the presence of cerebrospinal fluid (CSF) pleocytosis, and to investigate the factors influencing the CSF pleocytosis in children with this condition. METHODS: Eighty children with enteroviral meningitis treated at Soonchunhyang University Hospitals in Seoul and Bucheon between July 2012 and August 2013 were enrolled. The patients were diagnosed by reverse transcription-polymerase chain reaction (RT-PCR), and the clinical variables were compared according to the presence of CSF pleocytosis. RESULTS: Of the 80 patients, 54 (67.5%) and 26 (32.5%) patients had and did not have CSF pleocytosis, respectively. Forty-eight (60%) patients were male, and the median age was 63 months (range, 2 to 192 months). Seventy-six (95%), 67 (83.7%), 51 (63.7), and 2 (2.5%) patients presented with fever, headache, vomiting, and seizure, respectively. Increased CSF protein and pressure were associated with CSF pleocytosis. However, age, peripheral white blood cell count, C-reactive protein, CSF glucose, CSF/serum glucose ratio, and onset-puncture time interval were not associated with the presence of CSF pleocytosis. CONCLUSION: This study demonstrated a high proportion of non-pleocytic enteroviral meningitis in children, and identified several clinical manifestations that were associated with CSF pleocytosis. The findings of this study may help us better understand the characteristics of the disease and facilitate early diagnosis and treatment of enteroviral meningitis. During the outbreak seasons of enteroviral meningitis, the importance of continuous surveillance of enteroviruses and rapid RT-PCR testing should be emphasized.
C-Reactive Protein ; Cerebrospinal Fluid* ; Child* ; Early Diagnosis ; Enterovirus ; Fever ; Glucose ; Gyeonggi-do ; Headache ; Hospitals, University ; Humans ; Leukocyte Count ; Leukocytosis* ; Male ; Meningitis* ; Meningitis, Aseptic ; Pediatrics ; Seasons ; Seizures ; Seoul ; Vomiting

Background: Particulate matter 10 (PM10; airborne particles <10 μm) inhalation has been demonstrated to induce airway and lung diseases. In this study, we investigate the effects of PM10 inhalation on RNA expression in lung tissues using a murine model. Methods: Female BALB/c mice were affected with PM10, ovalbumin (OVA), or both OVA and PM10. PM10 was administered intranasally while OVA was both intraperitoneally injected and intranasally administered. Treatments occurred 4 times over a 2-week period. Two days after the final challenges, mice were sacrificed. Full RNA sequencing using lung homogenates was conducted. Results: While PM10 did not induce cell proliferation in bronchoalveolar fluid or lead to airway hyper-responsiveness, it did cause airway inflammation and lung fibrosis. Levels of interleukin 1β, tumor necrosis factor-α, and transforming growth factor-β in lung homogenates were significantly elevated in the PM10-treated group, compared to the control group. The PM10 group also showed increased RNA expression of Rn45a, Snord22, Atp6v0c-ps2, Snora28, Snord15b, Snora70, and Mmp12. Generally, genes associated with RNA splicing, DNA repair, the inflammatory response, the immune response, cell death, and apoptotic processes were highly expressed in the PM10-treated group. The OVA/PM10 treatment did not produce greater effects than OVA alone. However, the OVA/PM10-treated group did show increased RNA expression of Clca1, Snord22, Retnla, Prg2, Tff2, Atp6v0c-ps2, and Fcgbp when compared to the control groups. These genes are associated with RNA splicing, DNA repair, the inflammatory response, and the immune response. Conclusion Inhalation of PM10 extensively altered RNA expression while also inducing cellular inflammation, fibrosis, and increased inflammatory cytokines in this murine mouse model.

The biomechanics study of the hip is aims to understand and explore the dynamic principles of weight transfer through the hip joint. This basic science knowledge can be applied in a variety of areas, including degenerative joint diseases and hip replacement arthroplasty. In particular, understanding of the biomechanics of the hip has led to the development of materials, design and fixation of implants, and it can be applied in various areas, such as the selection of surgical methods and the location of the implant. Moreover, it is essential to have good knowledge of the biomechanics of the hip to achieve better clinical results for patients. Therefore, this paper introduces the basic knowledge and biomechanical characteristics of a normal hip and hip replacement arthroplasty, which are needed to approach the biomechanics of the hip.
Arthroplasty, Replacement, Hip ; Biomechanical Phenomena ; Hip Joint ; Hip ; Humans ; Joint Diseases

Purpose: Obesity and metabolic syndrome are acknowledged as key factors contributing to the development of non-alcoholic fatty liver disease (NAFLD). Vitamin D (VitD) is a multifaceted secosteroid hormone known for its anti-fibrotic and anti-inflammatory properties, with its deficiency often linked to obesity. Our study aimed to investigate whether VitD supplementation could mitigate the liver pathology associated with NAFLD. Materials and Methods: The NAFLD model was developed by subjecting male C57BL/6 mice to a high-fat diet (HFD) for 14 weeks.These mice were supplemented with VitD through intraperitoneal injection at a dosage of 7 μg/kg, administered three times per week for 7 weeks. Results: HFD resulted in VitD deficiency, insulin resistance, and increased liver weight. It elevated serum levels of liver aminotransferases and triglyceride, ultimately leading to steatohepatitis with fibrosis. This model exhibited increased levels of transforming growth factor (TGF)-β1, pro-inflammatory cytokines, HNF4α transcription factors, reactive oxygen species (ROS), renin-angiotensin system activity, and epithelial-mesenchymal transitions (EMT) within the liver. Supplementation with VitD resulted in the recovery of liver weight, improvement in histologic features associated with steatohepatitis, and reduction in alanine aminotransferases and triglyceride levels induced by the HFD. Additionally, it mitigated the HFD-induced over-expressions of TGF-β1 and fibrosis-related genes, along with pro-inflammatory cytokines and ROS. Notably, no adverse effect was found due to VitD supplementation in this model. Conclusion VitD ameliorates steatohepatitis within obesity-induced NAFLD through its multifaceted pathways. VitD supplementation emerges as a potentially safe, cost-effective, and direct treatment approach for NAFLD patients dealing with obesity or metabolic dysfunction.

Purpose: Obesity and metabolic syndrome are acknowledged as key factors contributing to the development of non-alcoholic fatty liver disease (NAFLD). Vitamin D (VitD) is a multifaceted secosteroid hormone known for its anti-fibrotic and anti-inflammatory properties, with its deficiency often linked to obesity. Our study aimed to investigate whether VitD supplementation could mitigate the liver pathology associated with NAFLD. Materials and Methods: The NAFLD model was developed by subjecting male C57BL/6 mice to a high-fat diet (HFD) for 14 weeks.These mice were supplemented with VitD through intraperitoneal injection at a dosage of 7 μg/kg, administered three times per week for 7 weeks. Results: HFD resulted in VitD deficiency, insulin resistance, and increased liver weight. It elevated serum levels of liver aminotransferases and triglyceride, ultimately leading to steatohepatitis with fibrosis. This model exhibited increased levels of transforming growth factor (TGF)-β1, pro-inflammatory cytokines, HNF4α transcription factors, reactive oxygen species (ROS), renin-angiotensin system activity, and epithelial-mesenchymal transitions (EMT) within the liver. Supplementation with VitD resulted in the recovery of liver weight, improvement in histologic features associated with steatohepatitis, and reduction in alanine aminotransferases and triglyceride levels induced by the HFD. Additionally, it mitigated the HFD-induced over-expressions of TGF-β1 and fibrosis-related genes, along with pro-inflammatory cytokines and ROS. Notably, no adverse effect was found due to VitD supplementation in this model. Conclusion VitD ameliorates steatohepatitis within obesity-induced NAFLD through its multifaceted pathways. VitD supplementation emerges as a potentially safe, cost-effective, and direct treatment approach for NAFLD patients dealing with obesity or metabolic dysfunction.

Purpose: Obesity and metabolic syndrome are acknowledged as key factors contributing to the development of non-alcoholic fatty liver disease (NAFLD). Vitamin D (VitD) is a multifaceted secosteroid hormone known for its anti-fibrotic and anti-inflammatory properties, with its deficiency often linked to obesity. Our study aimed to investigate whether VitD supplementation could mitigate the liver pathology associated with NAFLD. Materials and Methods: The NAFLD model was developed by subjecting male C57BL/6 mice to a high-fat diet (HFD) for 14 weeks.These mice were supplemented with VitD through intraperitoneal injection at a dosage of 7 μg/kg, administered three times per week for 7 weeks. Results: HFD resulted in VitD deficiency, insulin resistance, and increased liver weight. It elevated serum levels of liver aminotransferases and triglyceride, ultimately leading to steatohepatitis with fibrosis. This model exhibited increased levels of transforming growth factor (TGF)-β1, pro-inflammatory cytokines, HNF4α transcription factors, reactive oxygen species (ROS), renin-angiotensin system activity, and epithelial-mesenchymal transitions (EMT) within the liver. Supplementation with VitD resulted in the recovery of liver weight, improvement in histologic features associated with steatohepatitis, and reduction in alanine aminotransferases and triglyceride levels induced by the HFD. Additionally, it mitigated the HFD-induced over-expressions of TGF-β1 and fibrosis-related genes, along with pro-inflammatory cytokines and ROS. Notably, no adverse effect was found due to VitD supplementation in this model. Conclusion VitD ameliorates steatohepatitis within obesity-induced NAFLD through its multifaceted pathways. VitD supplementation emerges as a potentially safe, cost-effective, and direct treatment approach for NAFLD patients dealing with obesity or metabolic dysfunction.

Purpose: Obesity and metabolic syndrome are acknowledged as key factors contributing to the development of non-alcoholic fatty liver disease (NAFLD). Vitamin D (VitD) is a multifaceted secosteroid hormone known for its anti-fibrotic and anti-inflammatory properties, with its deficiency often linked to obesity. Our study aimed to investigate whether VitD supplementation could mitigate the liver pathology associated with NAFLD. Materials and Methods: The NAFLD model was developed by subjecting male C57BL/6 mice to a high-fat diet (HFD) for 14 weeks.These mice were supplemented with VitD through intraperitoneal injection at a dosage of 7 μg/kg, administered three times per week for 7 weeks. Results: HFD resulted in VitD deficiency, insulin resistance, and increased liver weight. It elevated serum levels of liver aminotransferases and triglyceride, ultimately leading to steatohepatitis with fibrosis. This model exhibited increased levels of transforming growth factor (TGF)-β1, pro-inflammatory cytokines, HNF4α transcription factors, reactive oxygen species (ROS), renin-angiotensin system activity, and epithelial-mesenchymal transitions (EMT) within the liver. Supplementation with VitD resulted in the recovery of liver weight, improvement in histologic features associated with steatohepatitis, and reduction in alanine aminotransferases and triglyceride levels induced by the HFD. Additionally, it mitigated the HFD-induced over-expressions of TGF-β1 and fibrosis-related genes, along with pro-inflammatory cytokines and ROS. Notably, no adverse effect was found due to VitD supplementation in this model. Conclusion VitD ameliorates steatohepatitis within obesity-induced NAFLD through its multifaceted pathways. VitD supplementation emerges as a potentially safe, cost-effective, and direct treatment approach for NAFLD patients dealing with obesity or metabolic dysfunction.