Purpose: This study aimed to develop an educational informatics system for nursing faculty to improve their competencies in teaching patient safety and to evaluate the effectiveness of the system. Methods: We developed a system called, ‘Resource to Enhance Safety Competency and Utilize for Education’ (RESCUE) based on the World Health Organization Multi-professional Patient Safety Curriculum Guide, and it was implemented with full-time nursing faculty in 4-year nursing schools. A one-group pretest-posttest design was used for evaluation. A total of 46 nursing faculty members used the system during a 3-month period. The effects of the RESCUE were measured using a survey including patient safety teaching competency, system usability and user satisfaction. Data were analyzed using descriptive statistics and the Wilcoxon signed-rank test. Results: After using the RESCUE, participants showed a significant increase in self-confidence in teaching patient safety during lectures (Z=-3.61, p<.001) and practica (Z=-3.14, p=.002). Conclusion The developed informatics system was shown to be effective in improving the self-confidence of nursing faculty in teaching patient safety. To effectively integrate patient safety topics into the curriculum, it can be helpful to utilize the educational materials provided in this study with various clinical cases.

PURPOSE: The purpose of this study was to investigate patient safety teaching competency of nursing faculty and the extent of teaching patient safety topics in the nursing curriculum. METHODS: A national survey was conducted with full-time nursing faculty in 4-year nursing schools. Regional quota sampling method was used. An online survey was sent to 1,028 nursing faculty and 207 of them were completed. Among the 207, we analyzed data from 184 participants. The revised Health Professional Education in Patient Safety Survey was used. Data were analyzed using descriptive statistics, independent t-test, one-way ANOVA, Pearson's correlation analysis, and multiple linear regression analyses. RESULTS: The faculty's self-confidence was lower than their perceived importance of patient safety education. The mean score of teaching patient safety was 3.52±0.67 out of 5, and the contents were mostly delivered through lectures. The extent of faculty's teaching varied depending on faculty's clinical career, teaching subjects, participation in practicum courses, and previous experience of patient safety education. The significant predictors of the extent of teaching patient safety were the faculty's self-confidence in teaching patient safety (β=.39) during clinical practicum, their perceived importance of patient safety education during lectures (β=.23), and the teaching subject (β=.15). CONCLUSION: To enhance the competency of nursing faculty for effective patient safety education, a patient safety education program tailored to faculty characteristics should be developed and continuously provided for faculty. In addition, it is necessary to improve patient safety curriculum, strengthen clinical and school linkages, and utilize various education methods in patient safety education.
Curriculum ; Education ; Education, Nursing ; Faculty, Nursing* ; Health Occupations ; Humans ; Lectures ; Linear Models ; Methods ; Nursing* ; Patient Safety* ; Preceptorship ; Professional Competence ; Schools, Nursing

The purpose of this study was to analyze the accessibility to dental facilities and the differences in chief complaints of new patients who visited Pusan National University Dental Hospital. We collected information from electronic medical records for 1,820 new patients. The accessibility was analyzed by measuring the distance from the patient’s house to the dental facilities. The distance was categorized into 10 km sections, and the presence or absence of a local pediatric dental clinic within 10 km of the patient’s house was also categorized. As the distance between the house and Pusan National University Dental Hospital increased, the proportion of patients who visited for dental caries decreased, and orthodontic treatment increased. Dental caries accounts for 27.9% of less than 10 km and 20.5% over 30 km. Orthodontic treatment accounts for 25.4% within 10 km and 27.3% more than 30 km away. The presence or absence of a local pediatric dental clinic within 10 km did not significantly affect the distribution of chief complaints. This study can be used as basic research data to establish effective treatment measures that can improve the physical and geographical accessibility of patients visiting pediatric dentistry.

The mammalian intestines harbor trillions of commensal microorganisms composed of thousands of species that are collectively called gut microbiota. Among the microbiota, bacteria are the predominant microorganism, with viruses, protozoa, and fungi (mycobiota) making up a relatively smaller population. The microbial communities play fundamental roles in the maturation and orchestration of the immune landscape in health and disease.Primarily, the gut microbiota modulates the immune system to maintain homeostasis and plays a crucial role in regulating the pathogenesis and pathophysiology of inflammatory, neuronal, and metabolic disorders. The microbiota modulates the host immune system through direct interactions with immune cells or indirect mechanisms such as producing short-chain acids and diverse metabolites. Numerous researchers have put extensive efforts into investigating the role of microbes in immune regulation, discovering novel immunomodulatory microbial species, identifying key effector molecules, and demonstrating how microbes and their key effector molecules mechanistically impact the host immune system. Consequently, recent studies suggest that several microbial species and their immunomodulatory molecules have therapeutic applicability in preclinical settings of multiple disorders. Nonetheless, it is still unclear why and how a handful of microorganisms and their key molecules affect the host immunity in diverse diseases. This review mainly discusses the role of microbes and their metabolites in T helper cell differentiation, immunomodulatory function, and their modes of action.

Polyploidization is a process by which cells are induced to possess more than two sets of chromosomes. Although polyploidization is not frequent in mammals, it is closely associated with development and differentiation of specific tissues and organs. The liver is one of the mammalian organs that displays ploidy dynamics in physiological homeostasis during its development. The ratio of polyploid hepatocytes increases significantly in response to hepatic injury from aging, viral infection, iron overload, surgical resection, or metabolic overload, such as that from non-alcoholic fatty liver diseases (NAFLDs). One of the unique features of NAFLD is the marked heterogeneity of hepatocyte nuclear size, which is strongly associated with an adverse liver-related outcome, such as hepatocellular carcinoma, liver transplantation, and liver-related death. Thus, hepatic polyploidization has been suggested as a potential driver in the progression of NAFLDs that are involved in the control of the multiple pathogenicity of the diseases. However, the importance of polyploidy in diverse pathophysiological contexts remains elusive. Recently, several studies reported successful improvement of symptoms of NAFLDs by reducing pathological polyploidy or by controlling cell cycle progression in animal models, suggesting that better understanding the mechanisms of pathological hepatic polyploidy may provide insights into the treatment of hepatic disorders.

Uncontrolled inflammation is considered the pathophysiological basis of many prevalent metabolic disorders, such as nonalcoholic fatty liver disease, diabetes, obesity, and neurodegenerative diseases. The inflammatory response is a self-limiting process that produces a superfamily of chemical mediators, called specialized proresolving mediators (SPMs). SPMs include the ω-3-derived family of molecules, such as resolvins, protectins, and maresins, as well as arachidonic acid-derived (ω-6) lipoxins that stimulate and promote resolution of inflammation, clearance of microbes, and alleviation of pain and promote tissue regeneration via novel mechanisms. SPMs function by binding and activating G protein-coupled receptors, such as FPR2/ALX, GPR32, and ERV1, and nuclear orphan receptors, such as RORα. Recently, several studies reported that SPMs have the potential to attenuate lipid metabolism disorders. However, the understanding of pharmacological aspects of SPMs, including tissue-specific biosynthesis, and specific SPM receptors and signaling pathways, is currently limited. Here, we summarize recent advances in the role of SPMs in resolution of inflammatory diseases with metabolic disorders, such as nonalcoholic fatty liver disease and obesity, obtained from preclinical animal studies. In addition, the known SPM receptors and their intracellular signaling are reviewed as targets of resolution of inflammation, and the currently available information on the therapeutic effects of major SPMs for metabolic disorders is summarized.

Uncontrolled inflammation is considered the pathophysiological basis of many prevalent metabolic disorders, such as nonalcoholic fatty liver disease, diabetes, obesity, and neurodegenerative diseases. The inflammatory response is a self-limiting process that produces a superfamily of chemical mediators, called specialized proresolving mediators (SPMs). SPMs include the ω-3-derived family of molecules, such as resolvins, protectins, and maresins, as well as arachidonic acid-derived (ω-6) lipoxins that stimulate and promote resolution of inflammation, clearance of microbes, and alleviation of pain and promote tissue regeneration via novel mechanisms. SPMs function by binding and activating G protein-coupled receptors, such as FPR2/ALX, GPR32, and ERV1, and nuclear orphan receptors, such as RORα. Recently, several studies reported that SPMs have the potential to attenuate lipid metabolism disorders. However, the understanding of pharmacological aspects of SPMs, including tissue-specific biosynthesis, and specific SPM receptors and signaling pathways, is currently limited. Here, we summarize recent advances in the role of SPMs in resolution of inflammatory diseases with metabolic disorders, such as nonalcoholic fatty liver disease and obesity, obtained from preclinical animal studies. In addition, the known SPM receptors and their intracellular signaling are reviewed as targets of resolution of inflammation, and the currently available information on the therapeutic effects of major SPMs for metabolic disorders is summarized.

The concept of cognitive frailty has recently been proposed by an International Consensus Group as the presence of physical frailty and cognitive impairment [defined using the Clinical Dementia Ratings (CDR)=0.5], without concurrent dementia. However, CDR is difficult to implement and not often available in epidemiologic studies or busy clinical settings, and an alternative to CDR is required. We suggest an alternative definition of cognitive frailty as: 1) physical frailty, 2) more than 1.5 standard deviation below the mean for age-, gender-, and education-adjusted norms on any cognitive function test (e.g., the Montreal Cognitive assessment test, the Alzheimer’s disease assessment scale-cognitive subscale, verbal learning test, Digit Span, Boston Naming Test, Trail Making Test, and Frontal Assessment Battery), and 3) no dependency in instrumental activities of daily living. The redefined criteria for cognitive frailty would be more feasible to implement and thus more applicable in epidemiologic studies and busy clinical settings.
Activities of Daily Living ; Cognition ; Cognition Disorders ; Consensus ; Dementia ; Epidemiologic Studies ; Mild Cognitive Impairment ; Trail Making Test ; Verbal Learning

Early detection and proper management of kidney rejection are crucial for the long-term health of a transplant recipient. Recipients are normally monitored by serum creatinine measurement and sometimes with graft biopsies. Donor-derived cell-free deoxyribonucleic acid (cfDNA) in the recipient's plasma and/or urine may be a better indicator of acute rejection. We evaluated digital PCR (dPCR) as a system for monitoring graft status using single nucleotide polymorphism (SNP)-based detection of donor DNA in plasma or urine. We compared the detection abilities of the QX200, RainDrop, and QuantStudio 3D dPCR systems. The QX200 was the most accurate and sensitive. Plasma and/or urine samples were isolated from 34 kidney recipients at multiple time points after transplantation, and analyzed by dPCR using the QX200. We found that donor DNA was almost undetectable in plasma DNA samples, whereas a high percentage of donor DNA was measured in urine DNA samples, indicating that urine is a good source of cfDNA for patient monitoring. We found that at least 24% of the highly polymorphic SNPs used to identify individuals could also identify donor cfDNA in transplant patient samples. Our results further showed that autosomal, sex-specific, and mitochondrial SNPs were suitable markers for identifying donor cfDNA. Finally, we found that donor-derived cfDNA measurement by dPCR was not sufficient to predict a patient's clinical condition. Our results indicate that donor-derived cfDNA is not an accurate predictor of kidney status in kidney transplant patients.
Biopsy ; Creatinine ; DNA ; Humans ; Kidney Transplantation* ; Kidney* ; Monitoring, Physiologic ; Plasma ; Polymerase Chain Reaction* ; Polymorphism, Single Nucleotide ; Tissue Donors ; Transplant Recipients ; Transplants

BACKGROUND: The plasma levels of cell-free DNA (cfDNA) are known to be elevated under inflammatory or apoptotic conditions. Increased cfDNA levels have been reported in hemodialysis (HD) patients. The aim of this study was to investigate the clinical significance of cfDNA in HD patients. METHODS: A total of 95 patients on HD were enrolled. We measured their predialysis cfDNA levels using real-time EIF2C1 gene sequence amplification and analyzed its association with certain clinical parameters. RESULTS: The mean plasma cfDNA level in the HD patients was 3,884 +/- 407 GE/mL, and the mean plasma cfDNA level in the control group was 1,420 +/- 121 GE/mL (P < 0.05). Diabetic patients showed higher plasma cfDNA levels compared with nondiabetic patients (P < 0.01). Patients with cardiovascular complications also showed higher plasma cfDNA levels compared with those without cardiovascular complication (P < 0.05). In univariable analysis, the cfDNA level was associated with 3-month mean systolic blood pressure (SBP), white blood cell, serum albumin, creatinine (Cr), normalized protein catabolic rate in HD patients. In diabetic patients, it was significantly correlated with SBP, hemoglobin A1c, and serum albumin. In multivariate analysis, SBP was the independent determinant for the cfDNA level. In diabetic patients, cfDNA level was independently associated with hemoglobin A1c and SBP. CONCLUSIONS: In patients with HD, cfDNA is elevated in diabetic patients and patients with cardiovascular diseases. Uncontrolled hypertension and poor glycemic control are independent determinants for the elevated cfDNA. Our data suggest that cfDNA might be a marker of vascular injury rather than proinflammatory condition in HD patients.
Blood Pressure* ; Cardiovascular Diseases ; Creatinine ; Diabetes Mellitus ; DNA* ; Humans ; Hypertension ; Leukocytes ; Multivariate Analysis ; Plasma* ; Renal Dialysis* ; Serum Albumin ; Vascular System Injuries