Purpose: This study aimed to investigate healthcare consumers’ interest in patient safety on social media using structural topic modeling (STM) and to identify changes in interest over time. Methods: Analyzing 105,727 posts from Naver news comments, blogs, internet cafés, and Twitter between 2010 and 2022, this study deployed a Python script for data collection and preprocessing. STM analysis was conducted using R, with the documents’ publication years serving as metadata to trace the evolution of discussions on patient safety. Results: The analysis identified a total of 13 distinct topics, organized into three primary communities: (1) “Demand for systemic improvement of medical accidents,” underscoring the need for legal and regulatory reform to enhance accountability; (2) “Efforts of the government and organizations for safety management,” highlighting proactive risk mitigation strategies; and (3) “Medical accidents exposed in the media,” reflecting widespread concerns over medical negligence and its repercussions. These findings indicate pervasive concerns regarding medical accountability and transparency among healthcare consumers. Conclusion The findings emphasize the importance of transparent healthcare policies and practices that openly address patient safety incidents. There is clear advocacy for policy reforms aimed at increasing the accountability and transparency of healthcare providers. Moreover, this study highlights the significance of educational and engagement initiatives involving healthcare consumers in fostering a culture of patient safety. Integrating consumer perspectives into patient safety strategies is crucial for developing a robust safety culture in healthcare.

BACKGROUND: Hydrocarbon is used frequently in the home in places such as the kitchen, garage, and basement. Accidental ingestion of hydrocarbons occurs generally in infants and children in the home. In cases of accidental ingestion, the amount is usually too small to cause medical problems, but can bring about diseases such as chemical pneumonitis. CASE REPORT: After ingesting organic solvent mistaken for mineral water, a 53-year-old male complained of cough, fever, and pain in the right upper abdomen, back, and right chest. Simple chest x-ray revealed focal chemical pneumonitis mainly involving the right middle lobe. The resulting lung abscess did not resolve until after treatment with drainage accompanied with antibiotics therapy. The ingested solution was analyzed and found to be a C11~C13 hydrocarbon mixture which has low viscosity. CONCLUSION: Chemical pneumonitis occurred after ingestion of hydrocarbon solution, and there is evidence of aspiratory mechanism.
Abdomen ; Anti-Bacterial Agents ; Child ; Cough ; Drainage ; Eating ; Fever ; Humans ; Hydrocarbons ; Infant ; Lung Abscess ; Male ; Middle Aged ; Mineral Waters ; Pneumonia ; Thorax

PURPOSE: The purpose of this descriptive study was to investigate the pattern of physical restraints used in ICUs and to identify influencing factors of application and removal of restraints. METHOD: The subjects of this study were 90 restrained patients out of 215 patients over 6 years old who were admitted to 6 ICUs in SMC during a 2 weeks period. The data was collected through a questionnaire of characte-ristics, guidelines and nursing care of restraint uses. The data were analyzed by non-parametric statistic with the use of the SAS program. RESULTS: The restraints were applied to 31.4% of subjects. Mean time of physical restraint was 36.76 55.7 hours. There were significant difference with mean time and frequency according to duty shift. GCS, restless behavior and discomfort factors, medical devices, and life sustaining devices had significant relation with application of restraints. In addition, the mean time of restraints used were related significantly with GCS, restless behavior, and discomfort factors. CONCLUSION: The used of restraints were dependent on mainly the nurses' decision. Thus ICU nurses have to develop the guidelines to applying restraints and removal of restraints in regard to patients rights and ethics. Continuous monitoring and evaluation of application of the restraints is essential in professional nursing.
Child ; Ethics ; Humans ; Intensive Care Units ; Nursing ; Nursing Care ; Patient Rights ; Restraint, Physical* ; Surveys and Questionnaires

The aim of the present study is to investigate the contribution of Ca2+-activated K+ (KCa) channels and delayed rectifier K+ (KV) channels to the resting membrane potential (RMP) in rabbit middle cerebral arterial smooth muscle cells. The RMP and membrane currents were recorded using the whole-cell patch configuration and single KCa channel was recorded using the outside-out patch configuration. Using the pipette solution containing 0.05 mM EGTA, the RMP was -25.76+/-5.08 mV (n=12) and showed spontaneous transient hyperpolarizations (STHPs). The membrane currents showed time- and voltage-dependent outward currents with spontaneous transient outward currents (STOCs). When we recorded the membrane potential using the pipette solution containing 10 mM EGTA, the RMP was depolarized and did not show STHPs. The membrane currents showed no STOCs but only showed slowly inactivating outward currents. External TEA (1 mM) reversibly inhibited the STHPs, depolarized the RMP, reduced the membrane currents, abolished STOCs, and decreased the open probability of single KCa channel. When KV currents were isolated, the application of 4-AP (5 mM) depolarized the RMP. The important aspect of our results is that KCa channel is responsible for the generation of the STHPs in the membrane potential and plays an important role in the regulation of the RMP and KV channel is also responsible for the regulation of the RMP in rabbit middle cerebral arterial smooth muscle cells.
Egtazic Acid ; Membrane Potentials* ; Membranes ; Muscle, Smooth* ; Myocytes, Smooth Muscle* ; Tea

BACKGROUND: Postoperative delirium has been suggested as a significant predictor of postoperative morbidity and mortality in elderly patients. They usually have multiple comorbidities, including cardiovascular, respiratory, renal, and neurologic disease. We aimed to determine the incidence rate and modifiable risk factors of postoperative delirium following total knee arthroplasty in elderly. METHODS: We reviewed the medical records of 318 elderly patients (age >65 years) underwent unilateral total knee arthroplasty between 2009 and 2016. Patient demographics, American Society of Anesthesiologists physical status, preoperative comorbidities, type and duration of anesthesia and surgery, length of hospital stay, ambulation ability, frequency of intraoperative hypotension, frequency of hypothermia, whether the patient was transfused or heparinized, and perioperative laboratory results were evaluated. Univariate and multivariate logistic regression analyses were used to identify significant independent predictors of postoperative delirium. RESULTS: The incidence rate of postoperative delirium was 6% in this study. Univariate analysis showed that postoperative delirium was significantly associated with age, body mass index, general anesthesia, anesthesia time, preoperative dementia, intraoperative hypotension, preoperative hemoglobin, blood transfusion, and intraoperative hypothermia. Preoperative dementia (odds ratio [OR] = 8.80), intraoperative hypotension (OR = 1.06), and preoperative hemoglobin (OR = 0.66) were significant independent risk factors of postoperative delirium. CONCLUSIONS: Preoperative dementia is the most important risk factor of postoperative delirium. High-risk patients undergoing total knee arthroplasty should be thoroughly evaluated and their dementia should be managed preoperatively. Adequate management of preoperative hemoglobin and intraoperative hypotension might also be helpful in reducing the incidence of postoperative delirium in this population.
Aged* ; Anesthesia ; Anesthesia, General ; Arthroplasty, Replacement, Knee* ; Blood Transfusion ; Body Mass Index ; Comorbidity ; Delirium* ; Dementia ; Demography ; Heparin ; Humans ; Hypotension ; Hypothermia ; Incidence ; Length of Stay ; Logistic Models ; Medical Records ; Mortality ; Postoperative Complications ; Risk Factors* ; Walking

Recent studies indicated that cancer cells become resistant to ionizing radiation (IR) and chemotherapy drugs by enhanced DNA repair of the lesions. Therefore, it is expected to increase the killing of cancer cells and reduce drug resistance by inhibiting DNA repair pathways that tumor cells rely on to escape chemotherapy. There are a number of key human DNA repair pathways which depend on multimeric polypeptide activities. For example, Ku heterodimer regulatory DNA binding subunits (Ku70/Ku80) on binding to double strand DNA breaks (DSBs) are able to interact with 470-kDa DNA-dependent protein kinase catalytic subunit (DNA-PKcs), and are essential for DNA-dependent protein kinase (DNA-PK) activity. It has been known that DNA-PK is an important factor for DNA repair and also is a sensor-transmitting damage signal to downstream targets, leading to cell cycles arrest. Our ultimate goal is to develop a treatment of breast tumors by targeting proteins involved in damage-signaling pathway and/or DNA repair. This would greatly facilitate tumor cell cytotoxic activity and programmed cell death through DNA damaging drug treatment. Therefore, we designed a domain of Ku80 mutants that binds to Ku70 but not DNA end binding activity and used the peptide in co-therapy strategy to see whether the targeted inhibition of DNA-PK activity sensitized breast cancer cells to irradiation or chemotherapy drug. We observed that the synthesized peptide (HNI-38) prevented DNA-PKcs from binding to Ku70/Ku80, thus resulting in inactivation of DNA-PK activity. Consequently, the peptide treated cells exhibited poor to no DNA repair, and became highly sensitive to IR or chemotherapy drugs, and the growth of breast cancer cells was inhibited. Additionally, the results obtained in the present study also support the physiological role of resistance of cancer cells to IR or chemotherapy.
Breast Neoplasms ; Catalytic Domain* ; Cell Cycle ; Cell Death ; DNA ; DNA Breaks, Double-Stranded ; DNA Repair ; DNA-Activated Protein Kinase* ; Drug Resistance ; Drug Therapy ; Homicide ; Humans ; Radiation, Ionizing ; United Nations

BACKGROUND: We have previously reported that not only cGMP but also 8-Br-cGMP or 8-pCPT-cGMP, specific and potent stimulators of cGMP-dependent protein kinase (cGMP-PK), increased basal L-type calcium current (ICa) in rabbit ventricular myocytes. Our findings in rabbit ventricular myocytes were entirely different from the earlier findings in different species, suggesting that the activation of cGMP-PK is involved in the facilitation of ICa by cGMP. However, there is no direct evidence that cGMP-PK can stimulate ICa in rabbit ventricular myocytes. In this report, we focused on the direct effect of cGMP-PK an ICa in rabbit ventricular myocytes. METHODS AND RESULTS: We isolated single ventricular myocytes of rabbit hearts by using enzymatic dissociation. Regulation of ICa by cGMP-PK was investigated in rabbit ventricular myocytes using whole-cell voltage clamp method. ICa was elicited by a depolarizing pulse to +10 mV from a holding potential of -40 mV. Extracellular 8-(4-Chlorophenylthio)-guanosine-3',5'-cyclic monophosphate (8-pCPT-cGMP), potent stimulator of cGMP-dependent protein kinase (cGMP-PK), increased basal ICa. cGMP-PK also increased basal ICa. The stimulation of basal ICa by cGMP-PK required both 8-Br-cGMP in low concentration and intracellular ATP to be present. The stimulation of basal ICa by cGMP-PK was blocked by heat inactivation of the cGMP-PK and by bath application of 8-(4-chlorophenylthio)-guanosine-3',5'-cyclic monophosphate, Rp-isomer (Rp-pCPT-cGMP), a phosphodiesterase-resistant cGMP-PK inhibitor. When ICa was increased by internal application of cGMP-PK, IBMX resulted in an additional stimulation of ICa. In the presence of cGMP-PK, already increased ICa was potentiated by bath application of isoprenaline or forskolin or intracellular application of cAMP. CONCLUSIONS: We present evidence that cGMP-PK stimulated basal ICa by a direct phosphorylation of L-type calcium channel or associated regulatory protein in rabbit ventricular myocytes.
1-Methyl-3-isobutylxanthine ; Adenosine Triphosphate ; Baths ; Calcium Channels, L-Type ; Calcium* ; Colforsin ; Heart ; Hot Temperature ; Isoproterenol ; Muscle Cells* ; Phosphorylation ; Protein Kinases*

The purpose of our investigation was to examine the effects of prostaglandin F2alpha (PGF2alpha) on membrane potentials, Ca2+-activated K+ (KCa) channels, and delayed rectifier K+ (KV) channels using the patch-clamp technique in single rabbit middle cerebral arterial smooth muscle cells. PGF2alpha significantly hyperpolarized membrane potentials and increased outward whole-cell K+ currents. PGF2alpha increased open-state probability of KCa channels without the change of the open and closed kinetics. PGF2alpha increased the amplitudes of KV currents with a leftward shift of activation and inactivation curves and a decrease of activation time constant. Our results suggest that the activation of KCa and KV channels, at least in part, may lead to attenuate or counteract vasoconstriction by PGF2alpha in middle cerebral artery.
Dinoprost* ; Kinetics ; Membrane Potentials* ; Membranes* ; Middle Cerebral Artery ; Myocytes, Smooth Muscle ; Patch-Clamp Techniques ; Vasoconstriction

Melatonin, a pineal gland hormone, is believed to act as an antioxidant via the stimulation of radical detoxifying enzymes and scavenging of free radicals. In this study, effects of in vitro and in vivo treatments of melatonin on the cisplatin-induced lipid peroxidation, LDH release and plasma creatinine were determined in rabbit renal cortical cells. The level of malondialdehyde (MDA) was assayed as an index of lipid peroxidation and the level of LDH release as an indicator of cellular damage. In in vitro studies, cisplatin increased the levels of MDA and LDH release in a concentration-and time-dependent manner. Melatonin inhibited the cisplatin-induced lipid peroxidation and LDH release in a concentration-dependent manner. The minimal effective concentration of melatonin that significantly reduced the 300 muM cisplatin-induced lipid peroxidation and LDH release was 1 mM. In in vivo studies, the levels of lipid peroxidation and LDH release in renal cortical cells increased significantly 24 or 48 hours after a single injection of cisplatin (6 mg/kg). When the cisplatin-injected rabbits were pretreated with 10 mg/kg of melatonin, a significant reduction in both lipid peroxidation and LDH release was observed. The plasma creatinine level increased from 0.87+/-0.07 mg/dl in control to 6.33+/-0.54 mg/dl in cisplatin-injected rabbits (P<0.05). Melatonin partially prevented the increase in serum creatinine level (1.98+/-0.11 mg/dl) by cisplatin (P<0.05). In the proximal tubules from cisplatin-treated group, tubular cells had microvilli of variable heights. Necrotic debris was seen in tubular lumens. In most of cells, the mitochondria and lysosomes were increased in frequency. The endocytic vacuoles were not prominent and distribution of the brush border was irregular and shortened. These cisplatin-induced morphological changes were moderate in the melatonin-pretreated group. These results suggest that the toxicity of cisplatin is associated with the generation of reactive oxygen free radicals and that melatonin is a powerful antioxidant, which prevents some of the adverse effects of cisplatin.
Cisplatin ; Creatinine ; Free Radicals ; Lipid Peroxidation ; Lysosomes ; Malondialdehyde ; Melatonin* ; Microvilli ; Mitochondria ; Oxygen ; Pineal Gland ; Plasma ; Rabbits* ; Vacuoles

Adriamycin is a commonly used chemotherapeutic agent for cancer, including acute leukemia, lymphoma, and a number of solid human tumors. However, recent studies have recognized severe cardiotoxicity after an acute dose, which are likely the result of generation of free radicals and lipid peroxidation. Therefore, the clinical uses of adriamycin have been limited. Melatonin, the pineal gland hormone known for its ability to modulate circardian rhythm, has recently been studied in its several functions, including cancer growth inhibition, stimulating the immune system, and acting as an antioxidant and radical scavenging effects. In the present study, we evaluated the effect of melatonin administration on adriamycin-induced cardiotoxicity in rat. Heart slices were prepared using a Stadie-Riggs microtome for the measurement of malondialdehyde (MDA) content used as an index of lipid peroxidation and lactate dehydrogenase (LDH) release as an indicator of lethal cell injury. Serious adriamycin-induced lethality was observed in rat by a single intraperitoneal injection in a dose-dependent manner. A single injection of adriamycin (25 mg/kg, i.p.) induced a lethality rate of 86%, with melatonin (10 mg/kg s.c. for 6 days) treatment reducing the adriamycin-induced lethality rate to 20%. The severe body weight loss caused by adriamycin was also significantly attenuated by melatonin treatment. Treatment of melatonin marked reduced adriamycin-induced the levels of MDA formation and LDH release. A cell damage indicated by the loss of myofibrils, swelling of the mitochondria as well as cytoplasmic vacuolization was seen in adriamycin-treated group. Melatonin attenuated the adriamycin-induced structural alterations. These data provide evidence that melatonin prevents adriamycin-induced cardiotoxicity and might serve as a combination with adriamycin to limit free radical-mediated cardiotoxicity.
Animals ; Body Weight ; Cytoplasm ; Doxorubicin ; Free Radicals ; Heart ; Humans ; Immune System ; Injections, Intraperitoneal ; L-Lactate Dehydrogenase ; Leukemia ; Lipid Peroxidation ; Lymphoma ; Malondialdehyde ; Melatonin* ; Mitochondria ; Myofibrils ; Pineal Gland ; Rats*