Objectives: To investigate the relationship between the psoas muscle cross-sectional area and physical performance in patients with liver cirrhosis. Methods: This study analyzed ambulatory patients with liver cirrhosis aged < 65 years, who underwent abdominal computed tomography (CT) and Short Physical Performance Battery (SPPB) tests from December 2018 to December 2019.A total of 46 patients (36 men, 10 women) were included. In abdominal CT scans, the psoas muscle cross-sectional area (mm2 ) was measured at the distal end-plate level of the L4 vertebral body and normalized by dividing by height (m).Physical performance was evaluated using SPPB. A correlation analysis between the psoas muscle cross-sectional area and SPPB was performed. Kruskal-Wallis test was used to determine differences in the psoas muscle cross-sectional area and SPPB according to the Child-Pugh classification. Multiple regression analysis was performed to determine factors affecting SPPB. Results: The correlation coefficient between the psoas muscle cross-sectional area and SPPB was 0.459 at the P < 0.01 level. No difference was observed in the psoas muscle cross-sectional area and SPPB according to the Child-Pugh classification. The psoas muscle cross-sectional area was a factor affecting SPPB in multiple regression analysis. Conclusions Abdominal CT is an essential diagnostic tool in patients with liver cirrhosis. Ambulatory patients with liver cirrhosis aged < 65 years could have reduced physical performance. In this study, the psoas muscle cross-sectional area was correlated with physical performance and was a factor affecting physical performance. The psoas muscle cross-sectional area and physical performance should be evaluated in patients with liver cirrhosis.

Objectives: To investigate the relationship between the psoas muscle cross-sectional area and physical performance in patients with liver cirrhosis. Methods: This study analyzed ambulatory patients with liver cirrhosis aged < 65 years, who underwent abdominal computed tomography (CT) and Short Physical Performance Battery (SPPB) tests from December 2018 to December 2019.A total of 46 patients (36 men, 10 women) were included. In abdominal CT scans, the psoas muscle cross-sectional area (mm2 ) was measured at the distal end-plate level of the L4 vertebral body and normalized by dividing by height (m).Physical performance was evaluated using SPPB. A correlation analysis between the psoas muscle cross-sectional area and SPPB was performed. Kruskal-Wallis test was used to determine differences in the psoas muscle cross-sectional area and SPPB according to the Child-Pugh classification. Multiple regression analysis was performed to determine factors affecting SPPB. Results: The correlation coefficient between the psoas muscle cross-sectional area and SPPB was 0.459 at the P < 0.01 level. No difference was observed in the psoas muscle cross-sectional area and SPPB according to the Child-Pugh classification. The psoas muscle cross-sectional area was a factor affecting SPPB in multiple regression analysis. Conclusions Abdominal CT is an essential diagnostic tool in patients with liver cirrhosis. Ambulatory patients with liver cirrhosis aged < 65 years could have reduced physical performance. In this study, the psoas muscle cross-sectional area was correlated with physical performance and was a factor affecting physical performance. The psoas muscle cross-sectional area and physical performance should be evaluated in patients with liver cirrhosis.

Objective: We investigated the usefulness of maximal expiratory pressure (MEP) in evaluating dysphagia subsequent to ischemic stroke. Methods: This study included patients with ischemic stroke who underwent MEP testing and videofluoroscopic swallowing study (VFSS), from October 2016 to February 2020. The VFSS findings were interpreted using the penetrationaspiration scale (PAS) and functional dysphagia scale (FDS). Patients were stratified into the non-aspiration (n=59) and aspiration (n=47) groups. Partial correlation analysis among MEP, PAS, and FDS was performed after adjusting for age. Binary logistic regression using PAS was conducted to investigate the risk factors predisposing patients to inclusion in the aspiration group. Multiple linear regression using FDS was conducted to investigate the risk factors according to dysphagia severity. Receiver operating characteristic (ROC) curve analysis was applied to investigate factors which could be useful for detecting aspiration. Results: Student’s t-test revealed a significant difference in MEP between the non-aspiration and aspiration groups.MEP showed a positive correlation with PAS and FDS. MEP was also determined to be a risk factor for inclusion into the aspiration group, and a risk factor according to the severity of dysphagia. In the ROC curve analysis, MEP showed good diagnostic properties to help classify patients with aspiration. Conclusion Our results indicate that swallowing assessment can predict and help prevent aspiration pneumonia in patients with ischemic stroke. In the present study, MEP showed significant association with aspiration and the severity of dysphagia. Thus, determining the MEP during swallowing assessment in patients with ischemic stroke is potentially a useful parameter to predict dysphagia.

Aldose reductase (AR) protein, a member of the NADPH-dependent aldo-keto reductase family, reduces a wide range of aldehydes and enhances cell survival by inhibition of oxidative stress. Oxidative stress is known as one of the major pathological factor in ischemia. Since the precise function of AR protein in ischemic injury is fully unclear, we examined the function of AR protein in hippocampal neuronal (HT-22) cells and in an animal model of ischemia in this study. Cell permeable Tat-AR protein was produced by fusion of protein transduction domain in Tat for delivery into the cells. Tat-AR protein transduced into HT-22 cells and significantly inhibited cell death and regulated the mitogen-activate protein kinases (MAPKs), Bcl-2, Bax, and Caspase-3 under oxidative stress condition. In an ischemic animal model, Tat-AR protein transduced into the brain tissues through the blood-brain barrier (BBB) and drastically decreased neuronal cell death in hippocampal CA1 region. These results indicate that transduced Tat-AR protein has protective effects against oxidative stress-induced neuronal cell death in vitro and in vivo, suggesting that Tat-AR protein could be used as potential therapeutic agent in ischemic injury.
Aldehyde Reductase ; Aldehydes ; Blood-Brain Barrier ; Brain ; CA1 Region, Hippocampal ; Caspase 3 ; Cell Death ; Cell Survival ; Humans ; In Vitro Techniques ; Ischemia ; Models, Animal ; Neurons ; Oxidative Stress ; Oxidoreductases ; Protein Kinases

Oxidative stress plays a crucial role in the development of neuronal disorders including brain ischemic injury. Thioredoxin 1 (Trx1), a 12 kDa oxidoreductase, has anti-oxidant and anti-apoptotic functions in various cells. It has been highly implicated in brain ischemic injury. However, the protective mechanism of Trx1 against hippocampal neuronal cell death is not identified yet. Using a cell permeable Tat-Trx1 protein, protective mechanism of Trx1 against hydrogen peroxide-induced cell death was examined using HT-22 cells and an ischemic animal model. Transduced Tat-Trx1 markedly inhibited intracellular ROS levels, DNA fragmentation, and cell death in H 2O 2-treatment HT-22 cells. Tat-Trx1 also significantly inhibited phosphorylation of ASK1 and MAPKs in signaling pathways of HT-22 cells. In addition, Tat-Trx1 regulated expression levels of Akt, NF-κB, and apoptosis related proteins. In an ischemia animal model, Tat-Trx1 markedly protected hippocampal neuronal cell death and reduced astrocytes and microglia activation. These findings indicate that transduced Tat-Trx1 might be a potential therapeutic agent for treating ischemic injury.

Oxidative stress plays a crucial role in the development of neuronal disorders including brain ischemic injury. Thioredoxin 1 (Trx1), a 12 kDa oxidoreductase, has anti-oxidant and anti-apoptotic functions in various cells. It has been highly implicated in brain ischemic injury. However, the protective mechanism of Trx1 against hippocampal neuronal cell death is not identified yet. Using a cell permeable Tat-Trx1 protein, protective mechanism of Trx1 against hydrogen peroxide-induced cell death was examined using HT-22 cells and an ischemic animal model. Transduced Tat-Trx1 markedly inhibited intracellular ROS levels, DNA fragmentation, and cell death in H 2O 2-treatment HT-22 cells. Tat-Trx1 also significantly inhibited phosphorylation of ASK1 and MAPKs in signaling pathways of HT-22 cells. In addition, Tat-Trx1 regulated expression levels of Akt, NF-κB, and apoptosis related proteins. In an ischemia animal model, Tat-Trx1 markedly protected hippocampal neuronal cell death and reduced astrocytes and microglia activation. These findings indicate that transduced Tat-Trx1 might be a potential therapeutic agent for treating ischemic injury.

The survival rate of gastric cancer is mainly affected by lymph node metastasis and depth of invasion. It is now recognized that in early gastric cancer submucosal invasion and lymph node metastasis depend on the size of tumor. A 71-year-old man with epigastric discomfort for 1 month was admitted. Endoscopy showed a huge polypoid tumor with friable and nodular surface occupying the whole lumen of stomach. We suspected a Borrmann type 1 advanced gastric cancer, but we confirmed the gastric cancer confined to only mucosa without lymph node metastasis after operation. So we report a case of huge polypoid early gastric cancer mimicking advanced gastric cancer with a review of relevant literatures.
Aged ; Endoscopy ; Humans ; Lymph Nodes ; Mucous Membrane ; Neoplasm Metastasis ; Stomach ; Stomach Neoplasms* ; Survival Rate

No abstract available.

Reactive oxygen species (ROS) contribute to the development of a number of neuronal diseases including ischemia. DJ-1, also known to PARK7, plays an important role in transcriptional regulation, acting as molecular chaperone and antioxidant. In the present study, we investigated whether DJ-1 protein shows a protective effect against oxidative stress-induced neuronal cell death in vitro and in ischemic animal models in vivo. To explore DJ-1 protein's potential role in protecting against ischemic cell death, we constructed cell permeable Tat-DJ-1 fusion proteins. Tat-DJ-1 protein efficiently transduced into neuronal cells in a dose- and time-dependent manner. Transduced Tat-DJ-1 protein increased cell survival against hydrogen peroxide (H2O2) toxicity and also reduced intracellular ROS. In addition, Tat-DJ-1 protein inhibited DNA fragmentation induced by H2O2. Furthermore, in animal models, immunohistochemical analysis revealed that Tat-DJ-1 protein prevented neuronal cell death induced by transient forebrain ischemia in the CA1 region of the hippocampus. These results demonstrate that transduced Tat-DJ-1 protein protects against cell death in vitro and in vivo, suggesting that the transduction of Tat-DJ-1 may be useful as a therapeutic agent for ischemic injuries related to oxidative stress.
Animals ; Blood-Brain Barrier/metabolism ; Brain Ischemia/*metabolism/pathology/prevention & control ; CA1 Region, Hippocampal/drug effects/metabolism/pathology ; Cell Line, Tumor ; Cell Survival/drug effects ; Gerbillinae ; Intracellular Signaling Peptides and Proteins/*administration & dosage/biosynthesis/pharmacokinetics ; Lipid Peroxidation ; Malondialdehyde/metabolism ; Mice ; Neuroprotective Agents/*administration & dosage/pharmacokinetics ; Oncogene Proteins/*administration & dosage/biosynthesis/pharmacokinetics ; *Oxidative Stress ; Prosencephalon/drug effects/metabolism/pathology ; Rats ; Recombinant Fusion Proteins/*administration & dosage/biosynthesis/pharmacokinetics ; tat Gene Products, Human Immunodeficiency Virus/*administration & dosage/biosynthesis/pharmacokinetics