We investigated whether endurance exercise training (EXT) ameliorates circadian rhythm (CR)-induced risk factors by improving skeletal muscle (SKM) mitochondrial biogenesis, reducing oxidative stress, and modulating apoptotic protein expression. We distinguished between regular and shift workers using the National Health and Nutrition Examination Survey (NHANES) and investigated the health problems caused by shift work (CR disturbance) and the potential therapeutic effects of exercise. In our animal study, 36 rats underwent 12 weeks of CR disturbance, divided into regular and irregular CR groups. These groups were further split into EXT (n = 12) and sedentary (n = 12) for an additional 8 weeks. We analyzed SKM tissue to understand the molecular changes induced by CR and EXT. NHANES data were analyzed using SAS 9.4 and Prism 8 software, while experimental animal data were analyzed using Prism 8 software. The statistical procedures used in each experiment are indicated in the figure legends. Our studies showed that CR disturbance increases dyslipidemia, alters circadian clock proteins (BMAL1, PER2), raises apoptotic protein levels, and reduces mitochondrial biogenesis in SKM. EXT improved LDL-C and HDLC levels without affecting muscle BMAL1 expression. It also enhanced mitochondrial biogenesis (AMPK, PGC-1α, Tfam, NADH-UO, COX-I), antioxidant levels (Catalase, SOD1, SOD2), and apoptotic protein (p53, Bax/Bcl2) expression or activity in SKM. We demonstrated that shift work-induced CR disturbance leads to dyslipidemia, diminished mitochondrial biogenesis, and reduced antioxidant capacity in SKM. However, EXT can counteract dyslipidemia under CR disturbance, potentially lowering the risk of cardiovascular disorders.

We investigated whether endurance exercise training (EXT) ameliorates circadian rhythm (CR)-induced risk factors by improving skeletal muscle (SKM) mitochondrial biogenesis, reducing oxidative stress, and modulating apoptotic protein expression. We distinguished between regular and shift workers using the National Health and Nutrition Examination Survey (NHANES) and investigated the health problems caused by shift work (CR disturbance) and the potential therapeutic effects of exercise. In our animal study, 36 rats underwent 12 weeks of CR disturbance, divided into regular and irregular CR groups. These groups were further split into EXT (n = 12) and sedentary (n = 12) for an additional 8 weeks. We analyzed SKM tissue to understand the molecular changes induced by CR and EXT. NHANES data were analyzed using SAS 9.4 and Prism 8 software, while experimental animal data were analyzed using Prism 8 software. The statistical procedures used in each experiment are indicated in the figure legends. Our studies showed that CR disturbance increases dyslipidemia, alters circadian clock proteins (BMAL1, PER2), raises apoptotic protein levels, and reduces mitochondrial biogenesis in SKM. EXT improved LDL-C and HDLC levels without affecting muscle BMAL1 expression. It also enhanced mitochondrial biogenesis (AMPK, PGC-1α, Tfam, NADH-UO, COX-I), antioxidant levels (Catalase, SOD1, SOD2), and apoptotic protein (p53, Bax/Bcl2) expression or activity in SKM. We demonstrated that shift work-induced CR disturbance leads to dyslipidemia, diminished mitochondrial biogenesis, and reduced antioxidant capacity in SKM. However, EXT can counteract dyslipidemia under CR disturbance, potentially lowering the risk of cardiovascular disorders.

We investigated whether endurance exercise training (EXT) ameliorates circadian rhythm (CR)-induced risk factors by improving skeletal muscle (SKM) mitochondrial biogenesis, reducing oxidative stress, and modulating apoptotic protein expression. We distinguished between regular and shift workers using the National Health and Nutrition Examination Survey (NHANES) and investigated the health problems caused by shift work (CR disturbance) and the potential therapeutic effects of exercise. In our animal study, 36 rats underwent 12 weeks of CR disturbance, divided into regular and irregular CR groups. These groups were further split into EXT (n = 12) and sedentary (n = 12) for an additional 8 weeks. We analyzed SKM tissue to understand the molecular changes induced by CR and EXT. NHANES data were analyzed using SAS 9.4 and Prism 8 software, while experimental animal data were analyzed using Prism 8 software. The statistical procedures used in each experiment are indicated in the figure legends. Our studies showed that CR disturbance increases dyslipidemia, alters circadian clock proteins (BMAL1, PER2), raises apoptotic protein levels, and reduces mitochondrial biogenesis in SKM. EXT improved LDL-C and HDLC levels without affecting muscle BMAL1 expression. It also enhanced mitochondrial biogenesis (AMPK, PGC-1α, Tfam, NADH-UO, COX-I), antioxidant levels (Catalase, SOD1, SOD2), and apoptotic protein (p53, Bax/Bcl2) expression or activity in SKM. We demonstrated that shift work-induced CR disturbance leads to dyslipidemia, diminished mitochondrial biogenesis, and reduced antioxidant capacity in SKM. However, EXT can counteract dyslipidemia under CR disturbance, potentially lowering the risk of cardiovascular disorders.

We investigated whether endurance exercise training (EXT) ameliorates circadian rhythm (CR)-induced risk factors by improving skeletal muscle (SKM) mitochondrial biogenesis, reducing oxidative stress, and modulating apoptotic protein expression. We distinguished between regular and shift workers using the National Health and Nutrition Examination Survey (NHANES) and investigated the health problems caused by shift work (CR disturbance) and the potential therapeutic effects of exercise. In our animal study, 36 rats underwent 12 weeks of CR disturbance, divided into regular and irregular CR groups. These groups were further split into EXT (n = 12) and sedentary (n = 12) for an additional 8 weeks. We analyzed SKM tissue to understand the molecular changes induced by CR and EXT. NHANES data were analyzed using SAS 9.4 and Prism 8 software, while experimental animal data were analyzed using Prism 8 software. The statistical procedures used in each experiment are indicated in the figure legends. Our studies showed that CR disturbance increases dyslipidemia, alters circadian clock proteins (BMAL1, PER2), raises apoptotic protein levels, and reduces mitochondrial biogenesis in SKM. EXT improved LDL-C and HDLC levels without affecting muscle BMAL1 expression. It also enhanced mitochondrial biogenesis (AMPK, PGC-1α, Tfam, NADH-UO, COX-I), antioxidant levels (Catalase, SOD1, SOD2), and apoptotic protein (p53, Bax/Bcl2) expression or activity in SKM. We demonstrated that shift work-induced CR disturbance leads to dyslipidemia, diminished mitochondrial biogenesis, and reduced antioxidant capacity in SKM. However, EXT can counteract dyslipidemia under CR disturbance, potentially lowering the risk of cardiovascular disorders.

We investigated whether endurance exercise training (EXT) ameliorates circadian rhythm (CR)-induced risk factors by improving skeletal muscle (SKM) mitochondrial biogenesis, reducing oxidative stress, and modulating apoptotic protein expression. We distinguished between regular and shift workers using the National Health and Nutrition Examination Survey (NHANES) and investigated the health problems caused by shift work (CR disturbance) and the potential therapeutic effects of exercise. In our animal study, 36 rats underwent 12 weeks of CR disturbance, divided into regular and irregular CR groups. These groups were further split into EXT (n = 12) and sedentary (n = 12) for an additional 8 weeks. We analyzed SKM tissue to understand the molecular changes induced by CR and EXT. NHANES data were analyzed using SAS 9.4 and Prism 8 software, while experimental animal data were analyzed using Prism 8 software. The statistical procedures used in each experiment are indicated in the figure legends. Our studies showed that CR disturbance increases dyslipidemia, alters circadian clock proteins (BMAL1, PER2), raises apoptotic protein levels, and reduces mitochondrial biogenesis in SKM. EXT improved LDL-C and HDLC levels without affecting muscle BMAL1 expression. It also enhanced mitochondrial biogenesis (AMPK, PGC-1α, Tfam, NADH-UO, COX-I), antioxidant levels (Catalase, SOD1, SOD2), and apoptotic protein (p53, Bax/Bcl2) expression or activity in SKM. We demonstrated that shift work-induced CR disturbance leads to dyslipidemia, diminished mitochondrial biogenesis, and reduced antioxidant capacity in SKM. However, EXT can counteract dyslipidemia under CR disturbance, potentially lowering the risk of cardiovascular disorders.

Incidental thyroid nodules are commonly detected on ultrasonography (US). This has contributed to the rapidly rising incidence of low-risk papillary thyroid carcinoma over the last 20 years. The appropriate diagnosis and management of these patients is based on the risk factors related to the patients as well as the thyroid nodules. The Korean Society of Thyroid Radiology (KSThR) published consensus recommendations for US-based management of thyroid nodules in 2011 and revised them in 2016. These guidelines have been used as the standard guidelines in Korea. However, recent advances in the diagnosis and management of thyroid nodules have necessitated the revision of the original recommendations. The task force of the KSThR has revised the Korean Thyroid Imaging Reporting and Data System and recommendations for US lexicon, biopsy criteria, US criteria of extrathyroidal extension, optimal thyroid computed tomography protocol, and US follow-up of thyroid nodules before and after biopsy. The biopsy criteria were revised to reduce unnecessary biopsies for benign nodules while maintaining an appropriate sensitivity for the detection of malignant tumors in small (1–2 cm) thyroid nodules. The goal of these recommendations is to provide the optimal scientific evidence and expert opinion consensus regarding US-based diagnosis and management of thyroid nodules.

PURPOSE: Splicing factors play important roles in tumorigenesis. Serine/arginine-rich splicing factors 2 (SRSF2) and SRSF4 proteins, the members of SR family proteins, are dysregulated in various cancers. However, their protein expression levels and diagnostic values are unclear in colorectal cancer.METHODS: We quantified the protein levels of SRSF2, SRSF4, and previously known colon cancer markers (heterogeneous nuclear ribonucleoprotein A1 [HNRNPA1] and carcinoembryonic antigen [CEA]) in tumor compared with adjacent normal-looking areas (non-tumor) of the colon in Korean patients with colon cancer using immunoblot analysis.RESULTS: The protein levels of HNRNPA1 and CEA were remarkably increased in tumor compared to non-tumor tissue and up-regulated in all of the tumor samples. However, the protein levels of SRSF2 and SRSF4 in tumor tissue were reduced in contrast with those of non-tumor tissue.CONCLUSION: None of the SRSF proteins were significantly different between the low (≤II) and high (>II) stages.
Carcinoembryonic Antigen ; Carcinogenesis ; Colon ; Colonic Neoplasms ; Colorectal Neoplasms ; Humans ; Ribonucleoproteins

Imatinib mesylate is a targeted therapy that acts by inhibiting tyrosine kinase of the bcr-abl fusion oncoprotein, which is specific to chronic myeloid leukemia (CML), and the c-transmembrane receptor, which is specific to gastrointestinal stromal tumors. Interstitial pneumonitis is a rare adverse event of imatinib therapy. It is clinically difficult to distinguish from infectious pneumonia, which can frequently occur due to the underlying disease. The standard treatment for imatinib-induced pneumonitis is to discontinue the medication and optionally administer corticosteroids. However, there are a few cases of successful retrial with imatinib. We describe a case of successful rechallenge of imatinib in a patient with imatinib-induced interstitial pneumonitis and CML without a recurrence of the underlying disease after 3 months of follow-up.
Adrenal Cortex Hormones ; Follow-Up Studies ; Gastrointestinal Stromal Tumors ; Humans ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive* ; Lung Diseases, Interstitial ; Mesylates* ; Pneumonia* ; Protein-Tyrosine Kinases ; Recurrence ; Imatinib Mesylate

OBJECTIVE: To determine whether pretreatment evaluation with contrast-enhanced ultrasonography (CEUS) is effective for percutaneous radiofrequency ablation (RFA) of hepatocellular carcinoma (HCC) with poor conspicuity on conventional ultrasonography (US). MATERIALS AND METHODS: This retrospective study was approved by the institutional review board and informed consent was waived. From June 2008 to July 2011, 82 patients having HCCs (1.2 +/- 0.4 cm) with poor conspicuity on planning US for RFA were evaluated with CEUS prior to percutaneous RFA. We analyzed our database, radiologic reports, and US images in order to determine whether the location of HCC candidates on planning US coincide with that on CEUS. To avoid incomplete ablation, percutaneous RFA was performed only when HCC nodules were identified on CEUS. The rate of technical success was assessed. The cumulative rate of local tumor progression was estimated with the use of the Kaplan-Meier method (mean follow-up: 24.0 +/- 13.0 months). RESULTS: Among 82 patients, 73 (89%) HCCs were identified on CEUS, whereas 9 (11%) were not. Of 73 identifiable HCCs on CEUS, the location of HCC on planning US corresponded with that on CEUS in 64 (87.7%), whereas the location did not correspond in 9 (12.3%) HCCs. Technical success was achieved for all 73 identifiable HCCs on CEUS in a single (n = 72) or two (n = 1) RFA sessions. Cumulative rates of local tumor progression were estimated as 1.9% and 15.4% at 1 and 3 years, respectively. CONCLUSION: Pretreatment evaluation with CEUS is effective for percutaneous RFA of HCCs with poor conspicuity on conventional US.
Carcinoma, Hepatocellular/surgery/*ultrasonography ; Catheter Ablation/*methods ; Contrast Media/*diagnostic use ; Female ; Follow-Up Studies ; Humans ; Liver Neoplasms/surgery/*ultrasonography ; Male ; Middle Aged ; Neoplasm Staging ; Preoperative Period ; Retrospective Studies

PURPOSE: The purpose of this study was to investigate the microstructural changes according to aging on the thickness and signal intensity (SI) of the cortical gray matter (GM) and white matter (WM) on the T2-, fluid-attenuated inversion recovery (FLAIR) and T1-weighted MR images in normal subjects. MATERIALS AND METHODS: The 10, 20, 30, 40, 50, 60, 70, 80 and 90 year age groups of men and women (each 10 individuals) who underwent routine brain MRI, including the T2-, FLAIR and T1-weighted images, were selected for this study. We measured the thickness and the SI of the cortical GM and WM at the postcentral gyrus, which has an even thickness at the level of centrum semiovale, on the axial scans and we calculated the mean values of the thickness ratio of the gray/white matter (TRGW) and the signal intensity ratio of the gray/white matter (SRGW), and we compared the ratios of each age group. RESULTS: On the T2-weighted images, the TRGWs were 0.81 and 0.79 at the age of 10 and they were 0.73 and 0.71 at the age of 90 in the men and women, respectively. So, the GM thickness was decreased more than the WM thickness was with aging. On the FLAIR images, the TRGWs were 1.09 and 1.00 at the age of 10 and they were 1.11 and 0.95 at the age of 70 in the men and women, respectively. On the T1-weighted images, the TRGWs were 0.66 and 0.80 at the age of 10, and the ratio was changed to 0.90 and 0.78 at the age of 90 in the men and women, respectively. On the T2-weighted image, the SRGWs were 1.53 and 1.43 at the age of 10, and they were 1.23 and 1.27 at the age of 90 in the men and women, respectively. On the FLAIR images, the SRGWs were 1.23 and 1.25 at the age of 10 and they were 1.06 and 1.05 at the age of 90 in the men and women, respectively. On the T1-weighted images, the SRGWs were 0.86 and 0.85 at the age of 10, and they were 0.90 and 0.87 at the age of 90 in the men and women, respectively. CONCLUSION: We suggest that the age-related microstructural changes of the thickness and the SI of the cortical GM and WM on the T2-, FLAIR and T1-weighted images are unique, and so this knowledge will be helpful to differentiate neurodegenerative disease from normal aging of the brain.
Aging ; Brain ; Female ; Humans ; Male ; Neurodegenerative Diseases