178 research outputs found

    Diagnosing Small Hepatic Cysts on Multidetector CT: an Additional Merit of Thinner Coronal Reformations

    Get PDF
    OBJECTIVE: We wanted to validate the additional merit of the thinner coronal reformation images from multidetector CT (MDCT) for making the diagnosis of hepatic cysts. MATERIALS AND METHODS: For the 90 benign hepatic cysts confirmed on MRI, the transverse (5-mm thickness) and additional coronal (2-mm thickness) reformation images from MDCT were compared with each other in terms of the Hounsfield units (HUs) and the size of each hepatic cyst. RESULTS: THE ATTENUATIONS (MEAN: 17.2 HUs, standard deviation: ± 14.4) on the thinner coronal images were significantly lower than those (mean: 40.7 HUs; standard deviation: ± 20.6) on the thicker transverse images for the small hepatic cysts (≤ 10 mm on the transverse image, p < 0.01). Twenty-three (79%) of the 29 cysts between 5 mm and 10 mm and 21 (51%) of 41 lesions up to 5 mm showed a mean HU value of 20 or less on the coronal reformation images. CONCLUSION: By reducing the partial volume effect, routine coronal reformation of MDCT with a thinner section thickness can provide another merit for making a confidential diagnosis of many small sub-centimeter hepatic cysts, and these small cysts are not easily characterized on the conventional transverse images.ope

    Clinicopathologic Features of Metachronous or Synchronous Gastric Cancer Patients with Three or More Primary Sites

    Get PDF
    PURPOSE: We investigated the clinicopathologic information of patients with gastric cancer with multiple primary cancers (GC-MPC) of three or more sites. MATERIALS AND METHODS: Between 1995 and 2009, 105,908 patients were diagnosed with malignancy at Severance Hospital, Yonsei University Health System. Of these, 113 (0.1%) patients with MPC of three or more sites were registered, and 41 (36.3%) of these were GC-MPC. We retrospectively reviewed the clinical data and overall survival using the medical records of these 41 GC-MPC patients. We defined synchronous cancers as those occurring within 6 months of the first primary cancer, while metachronous cancers were defined as those occurring more than 6 months later. RESULTS: Patients with metachronous GC-MPC were more likely to be female (p=0.003) and young than patients with synchronous GC-MPC (p=0.013). The most common cancer sites for metachronous GC-MPC patients were the colorectum, thyroid, lung, kidney and breast, while those for synchronous GC-MPC were the head and neck, esophagus, lung, and kidney. Metachronous GC-MPC demonstrated significantly better overall survival than synchronous GC-MPC, with median overall survival durations of 4.7 and 14.8 years, respectively, and 10-year overall survival rates of 48.2% and 80.7%, respectively (p<0.001). CONCLUSION: Multiplicity of primary malignancies itself does not seem to indicate a poor prognosis. The early detection of additional primary malignancies will enable proper management with curative intentope

    A Validation Study of the Korean Version of SPAN

    Get PDF
    Purpose: The SPAN, which is acronym standing for its four components: Startle, Physiological arousal, Anger, and Numbness, is a short post-traumatic stress disorder (PTSD) screening scale. This study sought to develop and validate a Korean version of the SPAN (SPAN-K). Materials and Methods: Ninety-three PTSD patients (PTSD group), 73 patients with non-psychotic psychiatric disorders (psychiatric control group), and 88 healthy participants (normal control group) were recruited for this study. Participants completed a variety of psychiatric assessments including the SPAN-K, the Davidson Trauma Scale (DTS), the Clinician-Administered PTSD Scale (CAPS), and the State-Trait Anxiety Inventory (STAI). Results: Cronbach&#39;s alpha and test-retest reliability values for the SPAN-K were both 0.80. Mean SPAN-K scores were 10.06 for the PTSD group, 4.94 for the psychiatric control group, and 1.42 for the normal control group. With respect to concurrent validity, correlation coefficients were 0.87 for SPAN-K vs. CAPS total scores (p&lt;0.001) and 0.86 for SPAN-K vs. DTS scores (p&lt;0.001). Additionally, correlation coefficients were 0.31 and 0.42 for SPAN-K vs. STAI-S and STAI-T, respectively. Receiver operating characteristic analysis of SPAN-K showed good diagnostic accuracy with an area under the curve (AUC) of 0.87. The SPAN-K showed the highest efficiency at a cutoff score of 7, with a sensitivity of 0.83, a specificity of 0.81, positive predictive value (PPV) of 0.88, and negative predictive value (NPV) of 0.73. Conclusion: These results suggest that the SPAN-K had good psychometric properties and may be a useful instrument for rapid screening of PTSD patients.This study was supported by a grant of the Korean Academy of Anxiety Disorders, Korean Neuropsychiatric Association, and Korean Research Foundation (2006-2005152), Republic of Korea

    The Prevalence and Clinical Characteristics of Reflux Esophagitis in Koreans and Its Possible Relation to Metabolic Syndrome

    Get PDF
    The prevalence of reflux esophagitis is increasing in Korea. To estimate the prevalence and clinical characteristics of reflux esophagitis in healthy subjects, we retrospectively examined the medical records of healthy subjects undergoing a routine check-up from October 2004 to September 2005. A total of 6,082 (3,590 men, mean age 44±10 yr) subjects were enrolled in this study. The prevalence of reflux esophagitis in healthy subjects was 10.5%. According to the univariate analysis, male sex (odds ratio [OR] 3.49, 95% confidence interval [CI] 2.84-4.30), smoking history (OR 1.91, 95% CI 1.60-2.28), body mass index (BMI) >30 kg/m2 (OR 2.13, 95% CI 1.37-3.33), total cholesterol >250 mg/dL (OR 1.50, 95% CI 1.05-2.14), low-density lipoprotein (LDL) cholesterol ≥160 mg/dL (OR 1.52, 95% CI 1.08-2.14), triglyceride ≥150 mg/dL (OR 1.92, 95% CI 1.61-2.30), high blood pressure (BP) (OR 1.46, 95% CI 1.20-1.76), and fasting glucose ≥110 mg/dL (OR 1.45, 95% CI 1.13-1.86) were significantly associated with reflux esophagitis (all p<0.05). However, age, alcohol drinking and Helicobacter pylori infection were not associated with reflux esophagitis. In conclusiosn, significant relationships of reflux esophagitis with obesity, low high-density lipoprotein (HDL) cholesterol, high triglyceride, high BP, and elevated fasting glucose suggested that reflux esophagitis might represent the disease spectrum of the metabolic syndrome

    Phosphorylation of Nrf2 at Multiple Sites by MAP Kinases Has a Limited Contribution in Modulating the Nrf2-Dependent Antioxidant Response

    Get PDF
    The bZIP transcription factor Nrf2 has emerged as a pivotal regulator of intracellular redox homeostasis by controlling the expression of many endogenous antioxidants and phase II detoxification enzymes. Upon oxidative stress, Nrf2 is induced at protein levels through redox-sensitive modifications on cysteine residues of Keap1, a component of the E3 ubiquitin ligase that targets Nrf2 for ubiquitin-dependent degradation. The mitogen activated protein kinases (MAPKs) have previously been proposed to regulate Nrf2 in response to oxidative stress. However, the exact role of MAPKs and the underlying molecular mechanism remain poorly defined. Here we report the first evidence that Nrf2 is phosphorylated in vivo by MAPKs. We have identified multiple serine/threonine residues as major targets of MAPK-mediated phosphorylation. Combined alanine substitution on those residues leads to a moderate decrease in the transcriptional activity of Nrf2, most likely due to a slight reduction in its nuclear accumulation. More importantly, Nrf2 protein stability, primarily controlled by Keap1, is not altered by Nrf2 phosphorylation in vivo. These data indicate that direct phosphorylation of Nrf2 by MAPKs has limited contribution in modulating Nrf2 activity. We suggest that MAPKs regulate the Nrf2 signaling pathway mainly through indirect mechanisms

    Kawasaki syndrome: an intriguing disease with numerous unsolved dilemmas

    Get PDF
    More than 40 years have passed since Kawasaki syndrome (KS) was first described. Yet KS still remains an enigmatic illness which damages the coronary arteries in a quarter of untreated patients and is the most common cause of childhood-acquired heart disease in developed countries. Many gaps exist in our knowledge of the etiology and pathogenesis of KS, making improvements in therapy difficult. In addition, many KS features and issues still demand further efforts to achieve a much better understanding of the disease. Some of these problem areas include coronary artery injuries in children not fulfilling the classic diagnostic criteria, genetic predisposition to KS, unpredictable ineffectiveness of current therapy in some cases, vascular dysfunction in patients not showing echocardiographic evidence of coronary artery abnormalities in the acute phase of KS, and risk of potential premature atherosclerosis. Also, the lack of specific laboratory tests for early identification of the atypical and incomplete cases, especially in infants, is one of the main obstacles to beginning treatment early and thereby decreasing the incidence of cardiovascular involvement. Transthoracic echocardiography remains the gold-standard for evaluation of coronary arteries in the acute phase and follow-up. In KS patients with severe vascular complications, more costly and potentially invasive investigations such as coronary CT angiography and MRI may be necessary. As children with KS with or without heart involvement become adolescents and adults, the recognition and treatment of the potential long term sequelae become crucial, requiring that rheumatologists, infectious disease specialists, and cardiologists cooperate to develop specific guidelines for a proper evaluation and management of these patients. More education is needed for physicians and other professionals about how to recognize the long-term impact of systemic problems related to KS

    Gene regulatory network reveals oxidative stress as the underlying molecular mechanism of type 2 diabetes and hypertension

    Get PDF
    <p>Abstract</p> <p>Background</p> <p>The prevalence of diabetes is increasing worldwide. It has been long known that increased rates of inflammatory diseases, such as obesity (OBS), hypertension (HT) and cardiovascular diseases (CVD) are highly associated with type 2 diabetes (T2D). T2D and/or OBS can develop independently, due to genetic, behavioral or lifestyle-related variables but both lead to oxidative stress generation. The underlying mechanisms by which theses complications arise and manifest together remain poorly understood. Protein-protein interactions regulate nearly every living process. Availability of high-throughput genomic data has enabled unprecedented views of gene and protein co-expression, co-regulations and interactions in cellular systems.</p> <p>Methods</p> <p>The present work, applied a systems biology approach to develop gene interaction network models, comprised of high throughput genomic and PPI data for T2D. The genes differentially regulated through T2D were 'mined' and their 'wirings' were studied to get a more complete understanding of the overall gene network topology and their role in disease progression.</p> <p>Results</p> <p>By analyzing the genes related to T2D, HT and OBS, a highly regulated gene-disease integrated network model has been developed that provides useful functional linkages among groups of genes and thus addressing how different inflammatory diseases are connected and propagated at genetic level. Based on the investigations around the 'hubs' that provided more meaningful insights about the cross-talk within gene-disease networks in terms of disease phenotype association with oxidative stress and inflammation, a hypothetical co-regulation disease mechanism model been proposed. The results from this study revealed that the oxidative stress mediated regulation cascade is the common mechanistic link among the pathogenesis of T2D, HT and other inflammatory diseases such as OBS.</p> <p>Conclusion</p> <p>The findings provide a novel comprehensive approach for understanding the pathogenesis of various co-associated chronic inflammatory diseases by combining the power of pathway analysis with gene regulatory network evaluation.</p
    corecore