Interdisciplinary Stroke Rehabilitation Delivered by a Humanoid Robot: Simultaneous vs. Alternating Therapy Schedules

A great number of stroke survivors experience disabilities in multiple domains (e.g., aphasia, hemiparesis). However, no previous research has investigated how treatment in one domain (e.g., speech therapy) affects the progress in other areas (e.g., physical recovery). The current study is comparing two therapy schedules: simultaneous where a patient receives speech AND physical therapy services for four weeks; and alternating where a patient receives speech therapy for four weeks and then receives physical therapy for four weeks. This interdisciplinary intervention is delivered by a humanoid robot that can potentially enhance the intensity and accessibility of stroke rehabilitation

SIRT6 Depletion Suppresses Tumor Growth by Promoting Cellular Senescence Induced by DNA Damage in HCC

The role of Sirtuin 6 (SIRT6) as a tumor suppressor or oncogene in liver cancer remains controversial. Thus, we identified the specific role of SIRT6 in the progression of hepatocellular carcinoma (HCC). SIRT6 expression was significantly higher in HCC cell lines and HCC tissues from 138 patients than in an immortalized hepatocyte cell line, THLE-2 and non-tumor tissues, respectively. SIRT6 knockdown by shRNA suppressed the growth of HCC cells and inhibited HCC tumor growth in vivo. In addition, SIRT6 silencing significantly prevented the growth of HCC cell lines by inducing cellular senescence in the p16/Rb- and p53/p21-pathway independent manners. Microarray analysis revealed that the expression of genes involved in nucleosome assembly was apparently altered in SIRT6-depleted Hep3B cells. SIRT6 knockdown promoted G2/M phase arrest and downregulation of genes encoding histone variants associated with nucleosome assembly, which could be attributed to DNA damage. Taken together, our findings suggest that SIRT6 acts as a tumor promoter by preventing DNA damage and cellular senescence, indicating that SIRT6 represents a potential therapeutic target for the treatment of HCC.11137Ysciescopu

The Korean Mistletoe (Viscum album coloratum) Extract Has an Antiobesity Effect and Protects against Hepatic Steatosis in Mice with High-Fat Diet-Induced Obesity

This study investigates the inhibitory effects of Korean mistletoe extract (KME) on adipogenic factors in 3T3-L1 cells and obesity and nonalcoholic fatty liver disease (NAFLD) in mice fed a high-fat diet. Male C57Bl/6 mice fed a high-fat diet were treated with KME (3 g/kg/day) for 15 weeks for the antiobesity and NAFLD experiments. Body weight and daily food intake were measured regularly during the experimental period. The epididymal pad was measured and liver histology was observed. The effects of KME on thermogenesis and endurance capacity were measured. The effects of KME on adipogenic factors were examined in 3T3-L1 cells. Body and epididymal fat pad weights were reduced in KME-treated mice, and histological examination showed an amelioration of fatty liver in KME-treated mice, without an effect on food consumption. KME potently induces mitochondrial activity by activating thermogenesis and improving endurance capacity. KME also inhibited adipogenic factors in vitro. These results demonstrate the inhibitory effects of KME on obesity and NAFLD in mice fed a high-fat diet. The effects appear to be mediated through an enhanced mitochondrial activity. Therefore, KME may be an effective therapeutic candidate for treating obesity and fatty liver caused by a high-fat diet

Adenocarcinoma Arising in a Duplication of the Cecum

Intestinal duplications are rare developmental abnormalities that may occur anywhere in the gastrointestinal tract. The possibility of a malignant change occurring in these duplications is very low. We present a case of adenocarcinoma arising in a duplication of the cecum. A 41-year-old male patient was admitted because of a palpable abdominal mass. Abdominal computed tomography revealed a 6-cm, peripheral wall-enhanced, round, cystic mass in the cecal area. Excision of the mesenteric mass and a right hemicolectomy was performed. Upon histologic examination, the patient was diagnosed with adenocarcinoma arising in a duplication of the cecum

Factors associated with hospitalization via emergency department in children with acute bronchiolitis

Purpose In infants and young children, acute bronchiolitis is a leading cause of hospitalization via emergency departments (EDs). We aimed to investigate factors associated with hospitalization via ED in children with acute bronchiolitis. Methods We reviewed medical records of children aged 36 months or younger with acute bronchiolitis who visited the ED from January to December 2017. The following clinical data were collected and analyzed: age, sex, premature birth history, symptoms, fever duration, presence of respiratory distress and radiographic lesion, and inflammatory markers. Results Of 780 children enrolled, 463 (59.4%) were hospitalized via the ED. The factor associated with the hospitalization were age ≤ 12 months (odd ratio [OR], 45.34; confidence interval [CI], 17.50-117.44), fever lasting ≥ 3 days (OR, 13.66; 95% CI, 6.46-28.87), respiratory rate ≥ 24 breaths per minute (OR, 6.88; 95% CI, 4.21-11.26), radiographic lesion (OR, 5.70; 95% CI 2.62-12.40), and chest retraction (OR, 2.45; 95% CI, 1.11-5.41). Conclusion In children with acute bronchiolitis who visit EDs, those having younger age, longer fever duration, respiratory distress or radiographic lesion may need hospitalization

Activation of PERK Signaling Attenuates Aβ-Mediated ER Stress

Alzheimer's disease (AD) is characterized by the deposition of aggregated beta-amyloid (Aβ), which triggers a cellular stress response called the unfolded protein response (UPR). The UPR signaling pathway is a cellular defense system for dealing with the accumulation of misfolded proteins but switches to apoptosis when endoplasmic reticulum (ER) stress is prolonged. ER stress is involved in neurodegenerative diseases including AD, but the molecular mechanisms of ER stress-mediated Aβ neurotoxicity still remain unknown. Here, we show that treatment of Aβ triggers the UPR in the SK-N-SH human neuroblastoma cells. Aβ mediated UPR pathway accompanies the activation of protective pathways such as Grp78/Bip and PERK-eIF2α pathway, as well as the apoptotic pathways of the UPR such as CHOP and caspase-4. Knockdown of PERK enhances Aβ neurotoxicity through reducing the activation of eIF2α and Grp8/Bip in neurons. Salubrinal, an activator of the eIF2α pathway, significantly increased the Grp78/Bip ER chaperone resulted in attenuating caspase-4 dependent apoptosis in Aβ treated neurons. These results indicate that PERK-eIF2α pathway is a potential target for therapeutic applications in neurodegenerative diseases including AD

2023 Korean Endocrine Society Consensus Guidelines for the Diagnosis and Management of Primary Aldosteronism

Primary aldosteronism (PA) is a common, yet underdiagnosed cause of secondary hypertension. It is characterized by an overproduction of aldosterone, leading to hypertension and/or hypokalemia. Despite affecting between 5.9% and 34% of patients with hypertension, PA is frequently missed due to a lack of clinical awareness and systematic screening, which can result in significant cardiovascular complications. To address this, medical societies have developed clinical practice guidelines to improve the management of hypertension and PA. The Korean Endocrine Society, drawing on a wealth of research, has formulated new guidelines for PA. A task force has been established to prepare PA guidelines, which encompass epidemiology, pathophysiology, clinical presentation, diagnosis, treatment, and follow-up care. The Korean clinical guidelines for PA aim to deliver an evidence-based protocol for PA diagnosis, treatment, and patient monitoring. These guidelines are anticipated to ease the burden of this potentially curable condition

Serum Neopterin Concentration and Impaired Glucose Metabolism: Relationship With β-Cell Function and Insulin Resistance

Aim: The purpose of this study was to measure the serum neopterin according to glucose metabolism and to evaluate neopterin as a predictor of type 2 diabetes (T2D) in a hospital-based cohort.Methods: A 75-g oral glucose tolerance test (OGTT) was performed by people who visited the outpatient clinic in Seoul National University Bundang Hospital for suspected abnormal glucose tolerance or a strong family history of T2D. Neopterin was measured using an enzyme-link immunosorbent assay with baseline samples from the OGTT.Results: Neopterin was measured in 184 participants. Indices related to glucose metabolism, such as the HOMA-IR, disposition index, etc. were calculated based on the results of the OGTT. The classifications for the 184 participants were: 24 (13%) had NGT, 89 (48.4%) prediabetes, and 60 (38.6%) T2D. Neopterin increased with deterioration of glucose metabolism (0.55 ± 0.25 vs. 0.58 ± 0.27 vs. 0.67 ± 0.27 ng/ml, p = 0.041; NGT, prediabetes, and T2D, respectively). Neopterin also correlated with fasting plasma glucose, 30-min and 120-min glucose of OGTT and HbA1c (r = 0.251, 0.259, 0.184, and 0.270, all p < 0.05). The HOMA-IR and disposition index correlated with neopterin (r = 0.291 and −0.170, respectively, both p < 0.05). When combined with C-peptide level, neopterin was as powerful as HOMA-IR in predicting future T2D.Conclusion: Serum neopterin appears to be related to impaired insulin secretion and insulin resistance in the development of T2D. Further investigation of the relationship between neopterin and glucose metabolism would be helpful to understand the pathophysiology for the development of T2D