Purpose: Erectile dysfunction (ED) is considered a microvascular disorder and serves as an indicator for the potential development of cardiovascular disease (CVD). Although left ventricular diastolic dysfunction (LVDD) reflects early myocardial damage caused by microvascular disorders, the association between ED and LVDD remains poorly elucidated. Materials and Methods: A cross-sectional study was conducted on 123 patients with ED. They underwent RigiScan, and conventional echocardiography, and attempted International Index of Erectile Function (IIEF) questionnaire. ED severity was evaluated by measuring changes in the penile base circumference and duration of penile rigidity (≥70%) during erection. The early diastolic velocity of mitral inflow (E) and early diastolic velocity of the mitral annulus (e′) were measured using echocardiography. The patients were grouped based on the presence of CVD. Results: Among 123 patients, 29 had CVD and 94 did not. Patients with CVD exhibited more pronounced ED and more severe LVDD. Associations between increased penile circumference with echocardiographic parameters were more prominent in patients with CVD than in those without CVD (ΔTtop and e′ wave, r=0.508 and r=0.282, respectively, p for interaction=0.033; ΔTbase and E/e′ ratio, r=-0.338 and r=-0.293, respectively, p for interaction <0.001). In the multivariate linear regression, the increase of penile base circumference was an independent risk factor for LVDD (e′, B=0.503; E/e′ ratio, B=-1.416, respectively, p<0.001). Conclusions ED severity correlated well with LV diastolic dysfunction, particularly in the presence of CVD. This study highlighted the potential role of ED assessment as early indicator of CVD development.

Background: Diabetic nephropathy (DN) is a progressive complication among patients with diabetes and the most common cause of end-stage kidney disease. Neutrophil extracellular traps (NETs) are known to play a role in kidney disease, thus this study aimed to determine their role in the development of diabetic kidney disease using diabetic murine models. Results: Protein and histological analyses revealed that db/db mice and streptozotocin DN models expressed no significant NET-related proteins, myeloperoxidase, citrullinated histone H3 (citH3), neutrophil elastase, and lymphocyte antigen 6 complex locus G6D (Ly6G). However, the inflamed individuals in the DN model showed that citH3 and Ly6G were highly deposited in the renal system based on immunohistochemistry images. In vitro, NET treatment did not induce apoptosis in glomerular endothelial and renal tubular epithelial cells. NET inhibition by DNase administration demonstrated no significant changes in cell apoptosis. Conclusions NET-related proteins were only expressed in the DN model with tubulointerstitial inflammation. Our study revealed that NETs are only induced in mice with hyperglycemia-induced inflammation.

Background: Diabetic nephropathy (DN) is a progressive complication among patients with diabetes and the most common cause of end-stage kidney disease. Neutrophil extracellular traps (NETs) are known to play a role in kidney disease, thus this study aimed to determine their role in the development of diabetic kidney disease using diabetic murine models. Results: Protein and histological analyses revealed that db/db mice and streptozotocin DN models expressed no significant NET-related proteins, myeloperoxidase, citrullinated histone H3 (citH3), neutrophil elastase, and lymphocyte antigen 6 complex locus G6D (Ly6G). However, the inflamed individuals in the DN model showed that citH3 and Ly6G were highly deposited in the renal system based on immunohistochemistry images. In vitro, NET treatment did not induce apoptosis in glomerular endothelial and renal tubular epithelial cells. NET inhibition by DNase administration demonstrated no significant changes in cell apoptosis. Conclusions NET-related proteins were only expressed in the DN model with tubulointerstitial inflammation. Our study revealed that NETs are only induced in mice with hyperglycemia-induced inflammation.

Background: Diabetic nephropathy (DN) is a progressive complication among patients with diabetes and the most common cause of end-stage kidney disease. Neutrophil extracellular traps (NETs) are known to play a role in kidney disease, thus this study aimed to determine their role in the development of diabetic kidney disease using diabetic murine models. Results: Protein and histological analyses revealed that db/db mice and streptozotocin DN models expressed no significant NET-related proteins, myeloperoxidase, citrullinated histone H3 (citH3), neutrophil elastase, and lymphocyte antigen 6 complex locus G6D (Ly6G). However, the inflamed individuals in the DN model showed that citH3 and Ly6G were highly deposited in the renal system based on immunohistochemistry images. In vitro, NET treatment did not induce apoptosis in glomerular endothelial and renal tubular epithelial cells. NET inhibition by DNase administration demonstrated no significant changes in cell apoptosis. Conclusions NET-related proteins were only expressed in the DN model with tubulointerstitial inflammation. Our study revealed that NETs are only induced in mice with hyperglycemia-induced inflammation.

Background: Diabetic nephropathy (DN) is a progressive complication among patients with diabetes and the most common cause of end-stage kidney disease. Neutrophil extracellular traps (NETs) are known to play a role in kidney disease, thus this study aimed to determine their role in the development of diabetic kidney disease using diabetic murine models. Results: Protein and histological analyses revealed that db/db mice and streptozotocin DN models expressed no significant NET-related proteins, myeloperoxidase, citrullinated histone H3 (citH3), neutrophil elastase, and lymphocyte antigen 6 complex locus G6D (Ly6G). However, the inflamed individuals in the DN model showed that citH3 and Ly6G were highly deposited in the renal system based on immunohistochemistry images. In vitro, NET treatment did not induce apoptosis in glomerular endothelial and renal tubular epithelial cells. NET inhibition by DNase administration demonstrated no significant changes in cell apoptosis. Conclusions NET-related proteins were only expressed in the DN model with tubulointerstitial inflammation. Our study revealed that NETs are only induced in mice with hyperglycemia-induced inflammation.

Next-generation sequencing (NGS) allows high-throughput detection of molecular changes in tumors. Over the past 15 years, NGS has rapidly evolved from a promising research tool to a core component of the clinical labo‑ ratory. Sequencing of tumor cells provides an important step in detecting somatic driver mutations that not only characterize the disease but also influence treatment decisions. For patients with hematologic malignancies, NGS has been used for accurate classification and diagnosis based on genetic alterations. The recently revised World Health Organization classification and the European LeukemiaNet recommendations for acute myeloid leukemia con‑ sider genetic abnormalities as a top priority for diagnosis, prognostication, monitoring of measurable residual disease, and treatment choice. This review aims to present the role and utility of various NGS approaches for the diagnosis, treatment, and follow-up of hemato-oncology patients.

Background and Objectives: Oropharyngeal squamous cell carcinoma (OPSCC) can be caused by human papilloma virus (HPV) infection or other factors like smoking. The 8th Edition of the AJCC Cancer Staging Manual recommends different staging and treatment approaches based on etiology. Despite criticisms of its low specificity, the current guidelines suggest using p16 immunohistochemistry (IHC) as a surrogate marker for the HPV-related OPSCC. This study assessed the reliability of p16 as a surrogate marker by correlating the survival rates of OPSCC patients with the results of p16 IHC and HPV-DNA testing.Subjects and Method A retrospective analysis was performed on patients treated for tonsil squamous cell carcinoma at a tertiary medical institution between 1994 and 2018. All patients underwent p16 immunostaining and HPV-DNA chip tests. Out of 88 patients, 17 were excluded due to insufficient data or secondary primary cancer, leaving 71 patients. Results: Among the 71 patients, 51 were p16 positive and 49 were HPV-DNA positive; both tests were associated with extended survival. However, discrepancies were noted in 18 patients: specifically, 11 patients were p16 positive but HPV-DNA negative, displaying a different survival pattern compared to HPV-associated and non-HPV-associated patients. Conclusion Both p16 immunostaining and HPV-DNA testing have their pros and cons. p16 immunostaining is cost-effective but has lower specificity. The study found discrepancies in 18 patients, suggesting that relying solely on p16 immunostaining may have limitations. It would be advisable to complement it with additional tests like the HPV-DNA chip test to predict the disease’s prognosis more accurately.

Purpose: Moderate-intensity continuous training (MICT) improves exercise capacity with vascular benefits, but time constraints hinder consistent adherence. High-intensity interval training (HIIT) has emerged as a time-efficient alternative, with repeated sprint training (RST) being the shortest format. We hypothesized that RST would be as effective as MICT in improving vascular function and exercise capacity in young adults. Methods: Twenty-three adults (mean age, 26.2±3.8 years) were randomly assigned to either RST or MICT. RST involved 20 sets of 4-second cycling sprints followed by 30-second active recovery, totaling 11 minutes. MICT consisted of 30-minute cycling at 50% to 60% of heart rate reserve. Vascular function evaluated via brachial artery flow-mediated dilation. Exercise capacity (maximum oxygen uptake, total exercise load test time) and anaerobic capacity (maximum power, anaerobic threshold) were measured using maximum exercise tests. These variables were measured befre and after a 6-week training. Results: Both groups showed comparable improvements in flow-mediated dilation (p＜ 0.05). Maximum oxygen intake slightly improved, while total exercise time significantly increased for both (p＜ 0.05). Anaerobic threshold unchanged, while maximum power improved (p＜ 0.05). Conclusion These findings underscore that RST is a time-efficient exercise strategy, which improves vascular function and exercise capacity as effectively as MICT in young adults.

Purpose: Isometric handgrip exercise (IHE) has a favorable cardiovascular effect and improves hemodynamic responses. Whether IHE attenuates stress-related hemodynamic reactivity assessed during a sympathetic challenge remains unexplored. We tested the hypothesis that an acute bout of IHE would improve carotid arterial function and attenuate cardiovascular vasoreactivity response to sympathetic stress in healthy adults. Methods: In a randomized cross-over design, sixteen healthy adults (aged 21.8±3.1 years) were enrolled. Participants completed two testing sessions, separated by 1 week. Trials were either a control trial or performed IHE for two sets of 2 minutes at 30% of maximal voluntary contraction for each hand. The participant’s hand was immersed in an ice water bath (4 ℃ ) up to the wrist for 2 minutes. Carotid artery diameter, β-stiffness index, and compliance using ultrasound machine and brachial blood pressure (BP), heart rate (HR) were measured as indices of vasoreactivity at baseline, during, and recovery from cold pressor testing (CPT). Results: The BP, HR, carotid artery diameter, and β-stiffness index increased similarly during CPT in both trials (p＜ 0.001), without any interaction effect. Compared with the IHE trial, arterial compliance decreased in the control groups at 120 seconds during recovery with a significant interaction effect (p=0.02). Conclusion These findings suggest that an acute IHE did not attenuate BP, HR, carotid artery diameter and β-stiffness index vasoreactivity, but improved carotid artery compliance to sympathetic activation in healthy young adults.

Background: Patients with chronic obstructive pulmonary disease (COPD) expressing eosinophilia experience slightly fewer episodes of community-acquired pneumonia (CAP), than those without eosinophilia. However, the severity and burden of hospitalized pneumonia patients with COPD involving eosinophilia have not been assessed. Methods: We evaluated the differences in clinical characteristics between patients with CAP and COPD with or without eosinophilia by a post hoc analysis of a prospective, multi-center, cohort study data. Results: Of 349 CAP patients with COPD, 45 (12.9%) had eosinophilia (blood eosinophil ≥300 cells/μL). Patients with eosinophilia had a lower sputum culture percentile (8.1% vs. 23.4%, p<0.05), a lower percentile of neutrophils (70.3% vs. 80.2%, p<0.05), reduced C-reactive protein levels (30.6 mg/L vs. 86.6 mg/L, p<0.05), and a lower pneumonia severity index score (82.5 vs. 90.0, p<0.05), than those without eosinophilia. The duration of antibiotic treatment (8.0 days vs. 10.0 days, p<0.05) and hospitalization (7.0 days vs. 9.0 days, p<0.05) were shorter in eosinophilic patients. The cost of medical care per day (256.4 US$ vs. 291.0 US$, p<0.05), cost for the medication (276.4 US$ vs. 349.9 US$, p<0.05), and cost for examination (685.5 US$ vs. 958.1 US$, p<0.05) were lower in patients with eosinophilia than those without eosinophilia. Conclusion Eosinophilia serves as a favorable marker for the severity of pneumonia, health-care consumption, and cost of medical care in patients with CAP and COPD.