Background: The effect of sarcopenia on depressive mood during geriatric rehabilitation remains unclear. This study investigated the potential influence of sarcopenia on depressive mood among geriatric patients in a rehabilitation setting. Methods: This observational cohort study enrolled 204 patients aged ≥65 years (mean age, 78.8±7.6 years; women, 45.1%) admitted to a rehabilitation unit between April 2020 and July 2021. Sarcopenia was diagnosed based on the Asian Working Group for Sarcopenia: 2019 Consensus Update on Sarcopenia Diagnosis and Treatment criteria, which include low handgrip strength and muscle mass. Depressive mood was defined as a 15-item Geriatric Depression Scale score of ≥6 points. We applied logistic regression models to examine the influence of sarcopenia on depressive mood at discharge. Results: We observed sarcopenia in 58.3% of patients. The logistic regression model showed that sarcopenia negatively influenced depressive mood at discharge (odds ratio=5.460; 95% confidence interval, 2.344–13.415). Of the 68 patients without depressive mood at admission, those with sarcopenia (n=31) had a significantly higher incidence of depressive mood at discharge compared with patients without sarcopenia (n=37) (41.9% vs. 16.2%, p=0.037). Conclusion Sarcopenia at admission negatively affected depressive mood at discharge from geriatric rehabilitation. Thus, early and routine assessment of sarcopenia is vital for patients undergoing geriatric rehabilitation.

Background: The effect of sarcopenia on depressive mood during geriatric rehabilitation remains unclear. This study investigated the potential influence of sarcopenia on depressive mood among geriatric patients in a rehabilitation setting. Methods: This observational cohort study enrolled 204 patients aged ≥65 years (mean age, 78.8±7.6 years; women, 45.1%) admitted to a rehabilitation unit between April 2020 and July 2021. Sarcopenia was diagnosed based on the Asian Working Group for Sarcopenia: 2019 Consensus Update on Sarcopenia Diagnosis and Treatment criteria, which include low handgrip strength and muscle mass. Depressive mood was defined as a 15-item Geriatric Depression Scale score of ≥6 points. We applied logistic regression models to examine the influence of sarcopenia on depressive mood at discharge. Results: We observed sarcopenia in 58.3% of patients. The logistic regression model showed that sarcopenia negatively influenced depressive mood at discharge (odds ratio=5.460; 95% confidence interval, 2.344–13.415). Of the 68 patients without depressive mood at admission, those with sarcopenia (n=31) had a significantly higher incidence of depressive mood at discharge compared with patients without sarcopenia (n=37) (41.9% vs. 16.2%, p=0.037). Conclusion Sarcopenia at admission negatively affected depressive mood at discharge from geriatric rehabilitation. Thus, early and routine assessment of sarcopenia is vital for patients undergoing geriatric rehabilitation.

Background: The effect of sarcopenia on depressive mood during geriatric rehabilitation remains unclear. This study investigated the potential influence of sarcopenia on depressive mood among geriatric patients in a rehabilitation setting. Methods: This observational cohort study enrolled 204 patients aged ≥65 years (mean age, 78.8±7.6 years; women, 45.1%) admitted to a rehabilitation unit between April 2020 and July 2021. Sarcopenia was diagnosed based on the Asian Working Group for Sarcopenia: 2019 Consensus Update on Sarcopenia Diagnosis and Treatment criteria, which include low handgrip strength and muscle mass. Depressive mood was defined as a 15-item Geriatric Depression Scale score of ≥6 points. We applied logistic regression models to examine the influence of sarcopenia on depressive mood at discharge. Results: We observed sarcopenia in 58.3% of patients. The logistic regression model showed that sarcopenia negatively influenced depressive mood at discharge (odds ratio=5.460; 95% confidence interval, 2.344–13.415). Of the 68 patients without depressive mood at admission, those with sarcopenia (n=31) had a significantly higher incidence of depressive mood at discharge compared with patients without sarcopenia (n=37) (41.9% vs. 16.2%, p=0.037). Conclusion Sarcopenia at admission negatively affected depressive mood at discharge from geriatric rehabilitation. Thus, early and routine assessment of sarcopenia is vital for patients undergoing geriatric rehabilitation.

We report the case of a patient with severe tricuspid regurgitation and severe liver dysfunction who was successfully treated by tricuspid valve repair with spiral suspension and perioperative management of high cardiac output. The patient was a 77-year-old woman who presented with chronic atrial fibrillation with bradycardia (heart rate approximately 50 bpm). She had been diagnosed with severe tricuspid valve and mitral valve regurgitation at the age of 74. As her heart failure and hepatic failure grew worse, and hepatic encephalopathy also occurred, she was admitted to the hospital. Her Child-Pugh score for liver disease was Grade C at the preoperative assessment, suggesting that she was in the high-risk category for open heart surgery. Therefore, further medical treatment was required before selecting the surgical treatment. After the implantation of a pacemaker (VVI mode, 80 bpm), the cardiac output increased with a cardiac index of 5.17 L/min/m2 compared with 2.97 L/min/m2 prior to pacemaker implantation. Furthermore, the symptoms of heart failure improved and total bilirubin decreased from 3.9 mg/dl to 1.7 mg/dl, and surgery was performed. Tricuspid regurgitation was treated with spiral suspension, and mitral regurgitation due to annular dilation was treated with annuloplasty. Following the surgery, the cardiac index was maintained from 4.3 L/min/m2 to 5.8 L/min/m2 with central venous pressure below 10 mmHg by the assistance of intra-aortic balloon pumping. The patient was extubated 30 h after surgery, and was discharged on postoperative day 54. At the time of discharge, total bilirubin was 1.5 mg/dl. At 1.5 post-operative years, the patient is New York Heart Association functional Class II and tricuspid valve regurgitation is mild.

The main pathogenic mechanism of diabetes consists of an increase in insulin resistance and a decrease in insulin secretion from pancreatic β-cells. The number of diabetic patients has been increasing dramatically worldwide, especially in Asian people whose capacity for insulin secretion is inherently lower than that of other ethnic populations. Causally, changes of environmental factors in addition to intrinsic genetic factors have been considered to have an influence on the increased prevalence of diabetes. Particular focus has been placed on “gene-environment interactions” in the development of a reduced pancreatic β-cell mass, as well as type 1 and type 2 diabetes mellitus. Changes in the intrauterine environment, such as intrauterine growth restriction, contribute to alterations of gene expression in pancreatic β-cells, ultimately resulting in the development of pancreatic β-cell failure and diabetes. As a molecular mechanism underlying the effect of the intrauterine environment, epigenetic modifications have been widely investigated. The association of diabetes susceptibility genes or dietary habits with gene-environment interactions has been reported. In this review, we provide an overview of the role of gene-environment interactions in pancreatic β-cell failure as revealed by previous reports and data from experiments.

A 24-year-old man was admitted to another hospital due to fever and chest and back pain. Enhanced chest computed tomography showed an aneurysm between the distal aortic arch and left pulmonary artery. The patient was transferred to our hospital for surgery. Because of suspicion of an infectious ductus arteriosus aneurysm, antibiotic therapy was started. Urgent graft replacement of the descending aorta was performed on the third day due to the enlargement of the aneurysm. All blood cultures including the preoperative examination, and the aneurysmal culture were negative. The histopathological study showed non-specific inflammatory response with plasma cell, T lymphocyte, and B lymphocyte infiltrations. There was no evidence of infection. Eventually we diagnosed this patient as having a ductus arteriosus aneurysm with non-specific inflammation. The antibiotic therapy was terminated on postoperative day 10, and the postoperative course was uneventful.

A novel coronavirus, severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), caused a worldwide pandemic. Our aim in this study is to produce new fusion inhibitors against SARS-CoV-2, which can be the basis for developing new antiviral drugs. The fusion core comprising the heptad repeat domains (HR1 and HR2) of SARS-CoV-2 spike (S) were used to design the peptides. A total of twelve peptides were generated, comprising a short or truncated 24-mer (peptide #1), a long 36-mer peptide (peptide #2), and ten peptide #2 analogs. In contrast to SARS-CoV, SARS-CoV-2 S-mediated cell-cell fusion cannot be inhibited with a minimal length, 24-mer peptide. Peptide #2 demonstrated potent inhibition of SARS-CoV-2 S-mediated cell-cell fusion at 1 µM concentration. Three peptide #2 analogs showed IC50 values in the low micromolar range (4.7-9.8 µM). Peptide #2 inhibited the SARSCoV-2 pseudovirus assay at IC50=1.49 µM. Given their potent inhibition of viral activity and safety and lack of cytotoxicity, these peptides provide an attractive avenue for the development of new prophylactic and therapeutic agents against SARS-CoV-2.

A novel coronavirus, severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), caused a worldwide pandemic. Our aim in this study is to produce new fusion inhibitors against SARS-CoV-2, which can be the basis for developing new antiviral drugs. The fusion core comprising the heptad repeat domains (HR1 and HR2) of SARS-CoV-2 spike (S) were used to design the peptides. A total of twelve peptides were generated, comprising a short or truncated 24-mer (peptide #1), a long 36-mer peptide (peptide #2), and ten peptide #2 analogs. In contrast to SARS-CoV, SARS-CoV-2 S-mediated cell-cell fusion cannot be inhibited with a minimal length, 24-mer peptide. Peptide #2 demonstrated potent inhibition of SARS-CoV-2 S-mediated cell-cell fusion at 1 µM concentration. Three peptide #2 analogs showed IC50 values in the low micromolar range (4.7-9.8 µM). Peptide #2 inhibited the SARSCoV-2 pseudovirus assay at IC50=1.49 µM. Given their potent inhibition of viral activity and safety and lack of cytotoxicity, these peptides provide an attractive avenue for the development of new prophylactic and therapeutic agents against SARS-CoV-2.

Middle East Respiratory Syndrome Coronavirus (MERS-CoV) is a newly emerging viral disease with fatal outcomes. However, no MERS-CoV-specific treatment is commercially available. Given the absence of previous structure-based drug discovery studies targeting MERS-CoV fusion proteins, this set of compounds is considered the first generation of MERS-CoV small molecule fusion inhibitors. After a virtual screening campaign of 1.56 million compounds followed by cell-cell fusion assay and MERS-CoV plaques inhibition assay, three new compounds were identified. Compound numbers 22, 73, and 74 showed IC50 values of 12.6, 21.8, and 11.12 μM, respectively, and were most effective at the onset of spike-receptor interactions. The compounds exhibited safe profiles against Human embryonic kidney cells 293 at a concentration of 20 μM with no observed toxicity in Vero cells at 10 μM. The experimental results are accompanied with predicted favorable pharmacokinetic descriptors and drug-likeness parameters. In conclusion, this study provides the first generation of MERS-CoV fusion inhibitors with potencies in the low micromolar range.