PURPOSE: Reduced heart rate variability significantly increases cardiovascular mortality. Metabolic syndrome increases the cardiac autonomic dysfunction. Recently, increasing cardiovascular mortality has been reported in patients with schizophrenia. This study was done to compare heart rate variability between adults with and without schizophrenia and to compare the relationship of heart rate variability to metabolic syndrome in hospitalized patients with schizophrenia. METHODS: This was a descriptive and correlational study in which 719 adults without schizophrenia and 308 adults with schizophrenia took part between May and June 2008. We measured the following: five-minute heart rate variability; high-frequency, low-frequency, the ratio of low-frequency to high-frequency, and the Standard Deviation of all the normal RR intervals. Data was also collected on metabolic syndrome, abdominal obesity, triglycerides, HDL cholesterol, blood pressure and fasting glucose. RESULTS: The Standard Deviation of all the normal RR intervals values of heart rate variability indices were 1.53+/-0.18. The low-frequency and high-frequency values of heart rate variability indices were significantly higher in hospitalized patients with schizophrenia (3.89+/-1.36; 3.80+/-1.20) than those in the healthy participants (2.20+/-0.46; 2.10+/-0.46). There were no significant differences between the schizophrenic patients with and without metabolic syndrome. CONCLUSION: The results of this study indicate that schizophrenia patients have significantly lower cardiac autonomic control, but they have significantly higher low-frequency and high-frequency values than those of healthy adults. Use of antipsychotic drug may affect the autonomic nervous system in schizophrenic patients. Metabolic syndrome was not associated with cardiac autonomic control in schizophrenia patients.
Adult ; Autonomic Nervous System/physiopathology ; Blood Glucose/analysis ; Blood Pressure ; Cardiovascular Diseases/complications/diagnosis/mortality ; Cholesterol, HDL/blood ; Female ; *Heart Rate ; Hospitalization ; Humans ; Male ; Metabolic Syndrome X/*complications/*physiopathology ; Middle Aged ; Obesity/etiology ; Schizophrenia/*complications/mortality/*physiopathology ; Triglycerides/blood

Gitelman's syndrome (GS), a hereditary disease characterized by hypokalemia, hypomagnesemia, and hypocalciuria, is a salt-losing renal tubulopathy. Herein, we describe a case of a 28-year-old woman diagnosed with atypical GS accompanying chondrocalcinosis. One year ago, she presented with vomiting, hypokalemic metabolic alkalosis, and hypocalciuria, and was tested by diuretic challenge test. As a result, she was diagnosed with atypical GS with normomagnesemia and treated with spironolactone and potassium supplementation. Meanwhile, acute arthritis of the right 1st metatarsophalangeal joint occurred. On the radiographies of the knees, chondrocalcinosis was observed. To the best of our knowledge, this is the first report in Korea of GS with chondrocalcinosis. Antialdosterone therapy or magnesium supplementation is effective in preventing the progression of chondrocalcinosis; thus, early diagnosis and treatment of GS are important.
Adult ; Alkalosis ; Arthritis ; Chondrocalcinosis* ; Early Diagnosis ; Female ; Genetic Diseases, Inborn ; Gitelman Syndrome* ; Humans ; Hypokalemia ; Knee ; Korea ; Magnesium ; Metatarsophalangeal Joint ; Potassium ; Spironolactone ; Vomiting

Background: Despite the lack of official COVID-19 statistics, various workplaces and occupations have been at the center of COVID-19 outbreaks. We aimed to compare legal measures and governance established for managing COVID-19 infection risks at workplaces in nine Asia and Pacific countries and to recommend key administrative measures. Methods: We collected information on legal measures and governance from both general citizens and workers regarding infection risks such as COVID-19 from industrial hygiene professionals in nine countries (Indonesia, India, Japan, Malaysia, New Zealand, Republic of the Philippines, Republic of Korea, Taiwan, and Thailand) using a structured questionnaire. Results: A governmental body overseeing public health and welfare was in charge of containing the spread and occurrence of infectious diseases under an infectious disease control and prevention act or another special act, although the name of the pertinent organizations and legislation vary among countries. Unlike in the case of other traditional hazards, there have been no specific articles or clauses describing the means of mitigating virus risk in the workplace that are legally required of employers, making it difficult to define the responsibilities of the employer. Each country maintains own legal systems regarding access to the duration, administration, and financing of paid sick leave. Many workers may not have access to paid sick leave even if it is legally guaranteed. Conclusion Specific legal measures to manage infectious disease risks, such as providing proper personal protective equipment, education, engineering control measures, and paid sick leave are recommended to be stipulated in Industrial safety and health-related acts.

The purpose of this study was to identify time-related changes in clinical, MRI, histopathologic, and immunohistochemical findings associated with ischemic stroke in dogs. Additionally, the association of cerebrospinal fluid (CSF) and tissue levels of interleukin (IL)-6 with clinical prognosis was assessed. Ischemic stroke was induced by permanent middle cerebral artery occlusion (MCAO) in nine healthy experimental dogs. The dogs were divided into three groups according to survival time and duration of the experimental period: group A (survived only 1 day), group B (1-week experimental period), and group C (2-week experimental period). Neurologic status was evaluated daily. Magnetic resonance imaging (MRI) was performed according to a predetermined schedule. Concentration of IL-6 in CSF was measured serially after ischemic stroke. Postmortem examination was performed for all experimental dogs. During histopathological examination, variable degrees of cavitation and necrosis due to neuronal cytopathic effects, such as pyknotic nuclei and cytoplasmic shrinkage, were observed on the affected side of the cerebral cortex in all dogs. Immunohistochemistry specific for IL-6 showed increased expression in the ischemic lesions. CSF IL-6 concentrations and ischemic lesion volumes 1 day after ischemic stroke were significantly higher in group A compared to groups B and C.
Animals ; Brain Ischemia/*etiology ; Dogs ; Female ; *Immunohistochemistry ; *Infarction, Middle Cerebral Artery ; *Magnetic Resonance Imaging ; Male ; Stroke/*pathology

Osteoclasts originated from hematopoietic stem cells are multi-nucleated cells that can resorb the bone matrix. Receptor activator of nuclear factor kappa-B (RANK)/RANK ligand (RANKL) signaling pathway is crucial for the differentiation and activation of osteoclasts. In this study, we investigated for the first time whether or not RANKL induced mitogen- and stress-activated kinase 1 (MSK1) phosphorylation at Ser 376. Activation of MSK1 was detected as soon as 5 min after RANKL stimulation and sparsely detected at 30 min after stimulation. RANKL-induced MSK1 phosphorylation occurred in a dose-dependent manner. MSK1 is known as a downstream signaling molecule of cAMP-dependent protein kinase (PKA). Treatment with the PKA inhibitor H89 significantly suppressed c-Fos and nuclear factor of activated T-cells, cytoplasmic 1 (NFATc1) induction upon RANKL stimulation. In addition, cAMP response element-binding protein (CREB) phosphorylation was extremely inhibited by H89 treatment. Mitogen-activated protein kinases (MAPKs) have been investigated for induction of MSK1 phosphorylation. Specific signaling pathway inhibitors for p38 and extracellular signal-regulated kinases (ERKs) significantly blocked RANKL-induced MSK1 activation. Finally, as a downstream effector of the p38-MSK1 pathway, c-Fos transcriptional activity was determined. RANKL-mediated elevation of c-Fos transcriptional activity was significantly suppressed by p38 inhibitor. Moreover, a dominant negative form of CREB suppressed activation of NFATc1. In conclusion, RANKL-stimulated MSK1 phosphorylation could play a role in induction of NFATc1 through CREB and c-Fos activation as a downstream molecule of p38, ERK MAPKs, and PKA. Our results support basic information for the development of osteoclast specific inhibitors.
Bone Matrix ; Cyclic AMP Response Element-Binding Protein ; Cyclic AMP-Dependent Protein Kinases ; Extracellular Signal-Regulated MAP Kinases ; Hematopoietic Stem Cells ; Mitogen-Activated Protein Kinases ; NFATC Transcription Factors ; Osteoclasts ; Phosphorylation ; Phosphotransferases

Background/Aims: We aimed to compare the effectiveness and safety of Janus kinase inhibitors (JAKi) vs. biologic disease- modifying antirheumatic drugs (bDMARD) in Korean patients with rheumatoid arthritis (RA) who had an inadequate response to conventional synthetic DMARDs. Methods: A quasi-experimental, multi-center, prospective, non-randomized study was conducted to compare response rates between JAKi and bDMARDs in patients with RA naïve to targeted therapy. An interim analysis was performed to estimate the proportion of patients achieving low disease activity (LDA) based on disease activity score (DAS)–28– erythroid sedimentation rate (ESR) (DAS28-ESR) at 24 weeks after treatment initiation and to evaluate the development of adverse events (AEs). Results: Among 506 patients enrolled from 17 institutions between April 2020 and August 2022, 346 (196 JAKi group and 150 bDMARD group) were included in the analysis. After 24 weeks of treatment, 49.0% of JAKi users and 48.7% of bDMARD users achieved LDA (p = 0.954). DAS28-ESR remission rates were also comparable between JAKi and bDMARD users (30.1% and 31.3%, respectively; p = 0.806). The frequency of AEs reported in the JAKi group was numerically higher than that in the bDMARDs group, but the frequencies of serious and severe AEs were comparable between the groups. Conclusions Our interim findings reveal JAKi have comparable effectiveness and safety to bDMARDs at 24 weeks after treatment initiation.