OBJECTIVE: To assess the frequency and severity of sleep-disordered breathing (SDB) in subacute stroke patients in Korea. METHODS: We consecutively enrolled subacute stroke patients who were transferred to the Department of Rehabilitation Medicine from February 2016 to August 2016. The inclusion criteria were as follows: diagnosis of the first onset of cerebral infarction or hemorrhage in the brain by computed tomography or magnetic resonance imaging; patients between 18 and 80 years old; and patients admitted within 7 days to 6 months after stroke onset. We evaluated baseline clinical data on patients' admission to the Department of Rehabilitation Medicine. We assessed demographic data, stroke severity, neurologic impairment, cognition and quality of life. We used the Epworth Sleepiness Scale to assess quality of sleep. We used a portable polysomnography to detect SDB. RESULTS: Of the 194 stroke patients, 76 patients enrolled in this study. We evaluated and included 46 patients in the outcome analysis. The mean apnea-hypopnea index (AHI) was 24.2±17.0 and 31 patients (67.4%) exhibited an AHI ≥15. Those in the SDB group showed a higher National Institutes of Health Stroke Scale, lower Functional Ambulation Category, lower Korean version of Modified Barthel Index, and lower EuroQol five dimensions questionnaire (EQ-5D) at admission. Prevalence and clinical characteristics of SDB did not show significant differences among stroke types or locations. CONCLUSION: SDB is common in subacute stroke patients. SDB must be evaluated after a stroke, particularly in patients presenting severe neurologic impairment.
Brain ; Cerebral Infarction ; Cognition ; Diagnosis ; Hemorrhage ; Humans ; Korea ; Magnetic Resonance Imaging ; National Institutes of Health (U.S.) ; Polysomnography ; Prevalence ; Quality of Life ; Rehabilitation ; Sleep Apnea Syndromes* ; Stroke* ; Walking

Indoleamine 2,3-dioxygenase 1 (IDO1) is an enzyme that plays a pivotal role in immune regulation by metabolizing tryptophan into kynurenine, leading to T cell suppression and promoting immune tolerance. However, persistent activation of IDO1 can lead to prolonged immune stimulation in inflammatory conditions such as skin diseases and chronic inflammation. In this study, we developed modified peptide nucleic acids (PNAs) conjugated with cationic lipid chains to target IDO1 pre-mRNA and evaluated their anti-inflammatory effects in human keratinocytes. The modified PNAs demonstrated enhanced solubility, robust binding affinity, and effective penetration into keratinocytes. Quantitative PCR results showed significant downregulation of IDO1 and pro-inflammatory cytokines such as IL-6, IL-8, and PTGS2 in interferon γ (IFNγ)-treated keratinocytes. These findings suggest that cell-penetrating PNAs targeting IDO1 hold potential as a therapeutic approach for inflammatory skin disorders and chronic inflammation.

Indoleamine 2,3-dioxygenase 1 (IDO1) is an enzyme that plays a pivotal role in immune regulation by metabolizing tryptophan into kynurenine, leading to T cell suppression and promoting immune tolerance. However, persistent activation of IDO1 can lead to prolonged immune stimulation in inflammatory conditions such as skin diseases and chronic inflammation. In this study, we developed modified peptide nucleic acids (PNAs) conjugated with cationic lipid chains to target IDO1 pre-mRNA and evaluated their anti-inflammatory effects in human keratinocytes. The modified PNAs demonstrated enhanced solubility, robust binding affinity, and effective penetration into keratinocytes. Quantitative PCR results showed significant downregulation of IDO1 and pro-inflammatory cytokines such as IL-6, IL-8, and PTGS2 in interferon γ (IFNγ)-treated keratinocytes. These findings suggest that cell-penetrating PNAs targeting IDO1 hold potential as a therapeutic approach for inflammatory skin disorders and chronic inflammation.

Indoleamine 2,3-dioxygenase 1 (IDO1) is an enzyme that plays a pivotal role in immune regulation by metabolizing tryptophan into kynurenine, leading to T cell suppression and promoting immune tolerance. However, persistent activation of IDO1 can lead to prolonged immune stimulation in inflammatory conditions such as skin diseases and chronic inflammation. In this study, we developed modified peptide nucleic acids (PNAs) conjugated with cationic lipid chains to target IDO1 pre-mRNA and evaluated their anti-inflammatory effects in human keratinocytes. The modified PNAs demonstrated enhanced solubility, robust binding affinity, and effective penetration into keratinocytes. Quantitative PCR results showed significant downregulation of IDO1 and pro-inflammatory cytokines such as IL-6, IL-8, and PTGS2 in interferon γ (IFNγ)-treated keratinocytes. These findings suggest that cell-penetrating PNAs targeting IDO1 hold potential as a therapeutic approach for inflammatory skin disorders and chronic inflammation.

Adrenal insufficiency during the treatment of pulmonary tuberculosis is a troublesome condition and can at times be lifethreatening if untreated. Rifampin is one of the most widely prescribed anti-tuberculosis agents. Furthermore, rifampin has been known to be capable of affecting the metabolism of various medications, including glucocorticoids. In this paper, a case of recurrent adrenal insufficiency induced by rifampin during the treatment of pulmonary tuberculosis is reported. The patient was a 63-year-old man who was diagnosed with Addison's disease 17 years earlier and had been undergoing glucocorticoid replacement therapy. Five months before, the patient manifested pulmonary tuberculosis and was immediately given anti-tuberculosis medication that included rifampin. After one week of medication, general weakness and hyponatremia occurred. Despite the increased dose of the glucocorticoid medication, the adrenal insufficiency recurred many times. Since the substitution of levofloxacin for rifampin, the episodes of adrenal insufficiency have not recurred so far.
Addison Disease ; Adrenal Insufficiency ; Glucocorticoids ; Humans ; Hyponatremia ; Middle Aged ; Ofloxacin ; Rifampin ; Tuberculosis, Pulmonary