This manuscript represents the official position of the Korean Society of Echocardiography on valvular heart diseases.This position paper focuses on the clinical management of valvular heart diseases with reference to the guidelines recently published by the American College of Cardiology/American Heart Association and the European Society of Cardiology. The committee tried to reflect the recently published results on the topic of valvular heart diseases and Korean data by a systematic literature search based on validity and relevance. In part I of this article, we will review and discuss the current position of aortic valve disease in Korea.

BACKGROUND: The genicular arteries (GAs) can be utilized for genicular nerve block. We aimed to evaluate the ability to localize GAs under ultrasound in patients with chronic knee pain. METHODS: Twenty-four knees from 14 osteoarthritic patients were enrolled. The target GAs included the superomedial GA (SMGA), superolateral GA (SLGA), and inferomedial GA (IMGA). GAs were observed at the relevant adductor tubercle and epicondyle-shaft transition under ultrasound. Distribution of the SMGA at the adductor tubercle was evaluated using defined zones in transverse and longitudinal ultrasound images. SLGA and IMGA were also categorized using defined zones in longitudinal images. Distance from bony cortex to the relevant GA was then estimated. RESULTS: Among 24 knees, 91.7% of SMGAs were located at the upper part of the adductor tubercle. The distances between the SMGA and bony cortex on transverse view (dSMGAt) and on longitudinal view (dSMGAl) were directly correlated (rs = 0.6539, P = 0.0005). CONCLUSIONS: Under ultrasound guidance, the SMGA was found to be mainly localized to the upper part of the adductor tubercle. Likewise, the SLGA and IMGA were mainly localized at the distal and proximal parts of the epicondyle-shaft transition, respectively. Our results support the feasibility of ultrasound guidance for GA localization in patients with knee osteoarthritis.
Arteries* ; Humans ; Knee ; Nerve Block ; Osteoarthritis, Knee ; Ultrasonography*

BACKGROUND: We examined the association between salivary mitochondrial DNA (mtDNA) copy number and chronic fatigue combined with depression and insomnia. METHODS: This cross-sectional study included 58 healthy adults with moderate to severe fatigue (Brief Fatigue Inventory [BFI] ≥4) for longer than 6 months. Subjects were classified as those without combined symptoms, with either depression (Beck Depression Inventory [BDI] ≥13) or insomnia (Pittsburgh Sleep Quality Index [PSQI] ≥5), or with both depression and insomnia. Salivary mtDNA copy number was measured by real-time quantitative polymerase chain reaction. The association was evaluated using a general linear model. RESULTS: About 76% of participants had either depression or insomnia as additional symptoms. These subjects were predominately female, drank more alcohol, and exercised less than those without combined symptoms (P<0.05). The group with both depression and insomnia exhibited significantly higher BFI and lower mtDNA copy number than those without combined symptoms (P<0.05). After adjusting for confounding factors, significant negative associations between mtDNA copy number and usual fatigue were found in the group without combined symptoms, whereas the negative associations in the group with combined symptoms were attenuated. BDI and PSQI were not associated with mtDNA copy number. CONCLUSION: Chronic fatigue is negatively associated with salivary mtDNA copy number. Salivary mtDNA copy number may be a biological marker of fatigue with or without combined symptoms, indicating that a separate approach is necessary.
Adult* ; Biomarkers ; Cross-Sectional Studies ; Depression ; Depressive Disorder ; DNA, Mitochondrial* ; Fatigue* ; Female ; Humans ; Linear Models ; Mental Fatigue ; Polymerase Chain Reaction ; Sleep Initiation and Maintenance Disorders ; Sleep Wake Disorders

PURPOSE: Reactive oxygen species modulator 1 (Romo1) is a key mediator of intracellular reactive oxygen species production. However, examination of the clinical usefulness of Romo1 in cancers has been limited. We evaluated the association of Romo1 expression with clinical outcomes in advanced non-small cell lung cancer (NSCLC) patients treated with platinum-based chemotherapy. MATERIALS AND METHODS: Romo1 expression in tumor tissue was examined by immunohistochemistry and evaluated by histological score. Survival analyses were performed according to Romo1 expression and the association between Romo1 expression and clinical parameters was evaluated. RESULTS: A total of 88 tumor specimens were analyzed. Significantly shorter median progression-free survival (PFS) was observed in the high Romo1 group compared with the low Romo1 group (4.5 months vs. 9.8 months, p < 0.001), and the median overall survival (OS) of the high Romo1 group was also significantly shorter than that of the low Romo1 group (8.4 months vs. 15.5 months, p < 0.001). Results of multivariate analyses showed significant association of high Romo1 expression with both poor PFS (hazard ratio [HR], 2.75; 95% confidence interval [CI], 1.71 to 4.44) and poor OS (HR, 3.99; 95% CI, 2.36 to 6.74). Results of the subgroup analysis showed a similar association regardless of tumor histology. Romo1 expression showed no association with any clinical parameter including age, sex, smoking status, stage, differentiation, or tumor histology. CONCLUSION: Romo1 overexpression was associated with poor response to treatment and shorter survival in advanced NSCLC patients treated with platinum-based chemotherapy. Romo1 could be a potential adverse predictive marker in this setting.
Biomarkers ; Carcinoma, Non-Small-Cell Lung* ; Disease-Free Survival ; Drug Therapy* ; Humans ; Immunohistochemistry ; Lung Neoplasms ; Multivariate Analysis ; Platinum ; Prognosis ; Reactive Oxygen Species* ; Smoke ; Smoking

There has been no study reporting on the influence of sleep deprivation on the male reproductive system including sperm quality. In this study, we hypothesized that sleep deprivation could lead to adverse effect on the male reproductive system. The rats were divided into three groups: 1) control (home-cage, n = 10); 2) SD4 (sleep deprivation for 4 days, n = 10); and 3) SD7 (sleep deprivation for 7 days, n = 10). Sleep deprivation was performed by a modified multiple platform method. Sperm quality (sperm motion parameters and counts), hormone levels (corticosterone and testosterone), and the histopathology of testis were evaluated and compared between the three groups. A statistically significant reduction (P = 0.018) was observed in sperm motility in the SD7 group compared to those of the control group. However, there were no significant differences in other sperm motion parameters, or in sperm counts of the testis and cauda epididymis between three groups. Compared with the control group, the SD4 (P = 0.033) and SD7 (P = 0.002) groups exhibited significant increases of corticosterone levels, but significant decreases of testosterone levels were found in the SD4 (P = 0.001) and SD7 (P < 0.001) groups. Seminiferous tubular atrophy and/or spermatid retention was partially observed in the SD4 and SD7 groups, compared with the normal histopathology of the control group. Sleep deprivation may have an adverse effect on the male reproductive system in rats.
Animals ; Atrophy ; Corticosterone ; Epididymis ; Humans ; Male* ; Methods ; Rats* ; Sleep Deprivation* ; Sperm Count ; Sperm Motility ; Spermatids ; Spermatozoa ; Testis ; Testosterone

This study was performed to examine the role of transglutaminase 2 (TG2) in ventilator-induced lung injury (VILI). C57BL/6 mice were divided into six experimental groups: 1) control group; 2) lipopolysaccharide (LPS) group; 3) lung protective ventilation (LPV) group; 4) VILI group; 5) VILI with cystamine, a TG2 inhibitor, pretreatment (Cyst+VILI) group; and 6) LPV with cystamine pretreatment (Cyst+LPV) group. Acute lung injury (ALI) score, TG2 activity and gene expression, inflammatory cytokines, and nuclear factor-kappaB (NF-kappaB) activity were measured. TG2 activity and gene expression were significantly increased in the VILI group (P < 0.05). Cystamine pretreatment significantly decreased TG2 activity and gene expression in the Cyst+VILI group (P < 0.05). Inflammatory cytokines were higher in the VILI group than in the LPS and LPV groups (P < 0.05), and significantly lower in the Cyst+VILI group than the VILI group (P < 0.05). NF-kappaB activity was increased in the VILI group compared with the LPS and LPV groups (P < 0.05), and significantly decreased in the Cyst+VILI group compared to the VILI group (P = 0.029). The ALI score of the Cyst+VILI group was lower than the VILI group, but the difference was not statistically significant (P = 0.105). These results suggest potential roles of TG2 in the pathogenesis of VILI.
Acute Lung Injury/pathology ; Animals ; Cystamine/therapeutic use ; Cytokines/analysis ; Enzyme Inhibitors/therapeutic use ; Enzyme-Linked Immunosorbent Assay ; GTP-Binding Proteins/*antagonists & inhibitors/genetics/metabolism ; Gene Expression ; Lipopolysaccharides/toxicity ; Male ; Mice ; Mice, Inbred C57BL ; NF-kappa B/metabolism ; Respiration, Artificial ; Transglutaminases/*antagonists & inhibitors/genetics/metabolism ; Ventilator-Induced Lung Injury/*enzymology/pathology/prevention & control

Immunoglobulin (Ig) G4-related disease is a recently recognized systemic fibroinflammatory condition characterized by a lymphoplasmacytic infiltrate rich in IgG4-positive plasma cells with elevated circulating levels of IgG4. The disease can either be localized to one or two organs, or present as diffuse multi-organ disease. Furthermore, lesions in different organs can present simultaneously or metachronously. In the pulmonary manefestations, lesions associated with IgG4-related disease have been described in the lung parenchyma, airways and pleura, as well as the mediastinum. We report a case of IgG4-related disease presenting as massive pleural effusion and thrombophlebitis.
Immunoglobulin G ; Immunoglobulins ; Lung ; Mediastinum ; Plasma Cells ; Pleura ; Pleural Effusion* ; Thrombophlebitis*