Methods: Nineteen volunteers (16 men, three women) lifted a 60-kg doll from a seated position to a standing position. The first transfer was performed without the HAL for Care Support, and the second was performed with the HAL for Care Support assistive robot. We evaluated transfer performance, the visual analog scale (VAS) score for lumbar fatigue, and electromyogram analyses of the trunk and hip. Results: Four participants (two men, two women) succeeded with the HAL for Care Support even though they were unable to perform the task without it. The mean lumbar fatigue VAS score for all participants without the HAL for Care Support was 62 mm, while that with it was 43 mm. With lumbar assistance from the HAL for Care Support, subjective lumbar fatigue during the transfer decreased significantly. A power analysis indicated adequate statistical power to detect a difference in the VAS score for lumbar fatigue (0.99). The activity of the left gluteus maximus alone increased significantly during transfers with the HAL for Care Support. No adverse events occurred during use of the HAL for Care Support for transfers. Conclusions The HAL for Care Support was able to reduce lumbar load in a simulated patient transfer.

Objective: The utility of topotecan monotherapy for relapsed small-cell lung cancer (SCLC) after failure of amrubicin monotherapy has not been evaluated. We aimed to investigate the efficacy and safety of topotecan monotherapy in patients with relapsed SCLC after amrubicin monotherapy.Patients and Methods: We retrospectively analyzed data from 16 patients with relapsed SCLC who were treated with topotecan monotherapy after amrubicin monotherapy at our hospital.Results: The response rate, progression-free survival, and overall survival were 0%, 32.5 days (95% confidence interval [CI] = 18–51), and 112 days (95% CI = 55–267), respectively. The most common adverse events (grade ≥3) were leukopenia (31.3%) and thrombocytopenia (31.3%), followed by anemia, anorexia, edema, and lung infections.Conclusion: The efficacy of topotecan monotherapy for relapsed SCLC after amrubicin monotherapy is inconclusive. Therefore, further studies are warranted.

Liver fibrosis reflects tissue scarring in the liver due to the accumulation of excessive extracellular matrix in response to chronically persistent liver injury. Hepatocyte cell death can trigger capillarization of liver sinusoidal endothelial cells, stimulation of immune cells including macrophages and Kupffer cells, and activation of hepatic stellate cells (HSCs), resulting in progression of liver fibrosis. Liver cirrhosis is the terminal state of liver fibrosis and is associated with severe complications, such as liver failure, portal hypertension, and liver cancer. Nevertheless, effective therapy for cirrhosis has not yet been established, and liver transplantation is the only radical treatment for severe cases. Studies investigating HSC activation and regulation of collagen production in the liver have made breakthroughs in recent decades that have advanced the knowledge regarding liver fibrosis pathophysiology. In this review, we summarize molecular mechanisms of liver fibrosis and discuss the development of novel anti-fibrotic therapies.

Liver fibrosis reflects tissue scarring in the liver due to the accumulation of excessive extracellular matrix in response to chronically persistent liver injury. Hepatocyte cell death can trigger capillarization of liver sinusoidal endothelial cells, stimulation of immune cells including macrophages and Kupffer cells, and activation of hepatic stellate cells (HSCs), resulting in progression of liver fibrosis. Liver cirrhosis is the terminal state of liver fibrosis and is associated with severe complications, such as liver failure, portal hypertension, and liver cancer. Nevertheless, effective therapy for cirrhosis has not yet been established, and liver transplantation is the only radical treatment for severe cases. Studies investigating HSC activation and regulation of collagen production in the liver have made breakthroughs in recent decades that have advanced the knowledge regarding liver fibrosis pathophysiology. In this review, we summarize molecular mechanisms of liver fibrosis and discuss the development of novel anti-fibrotic therapies.

To determine the physical symptoms and ki, ketsu and sui (qi, blood and fluid) factors associated with the presence of hie-sho (chill syndrome). Total 118 healthy university students (66 males and 52 females, median age 22 years, range 21­-29) were enrolled. A cross-­sectional study about the presence of chill syndrome in par­ticipants was performed. Terasawa's ki, ketsu and sui diagnostic score was used to identify the presence of physical symptoms. Number rating scale (NRS) was used to classify the chill and NRS more than 5 was de­fined as chill syndrome based on Furuya's report. Eighteen students (4 males and 14 females) were docu­mented as chill syndrome. The multivariate analysis of physical symptoms identified female (OR 4.65, p = 0.0427), heavy sensation of head (OR 2.98, p = 0.0190) and chill of extremities (OR 1.94, p = 0.0480) as sig­nificantly associated factors with chill syndrome. The score of ki-kyo (qi deficiency), ketsu-kyo (blood defi­ciency) and suitai (fluid retention) showed higher score in students with chill syndrome compared to students without chill syndrome in univariate analysis. Being female and two indicators of qi abnormalities including heavy sensation of head and chill of extremities were associated with the presence of chill syndrome in univer­sity students.

A 38-year-old man was admitted to our hospital with fever and skin rash, and he was diagnosed as having dermatomyositis. He was treated with anti-inflammatory steroid and immunosuppressive agents. On hospital day 48, chest computed tomography (CT) revealed a nodule measuring approximately 2 cm in size in the lower lobe of the right lung (S9). Bacterial and/or fungal infection was suspected, but there was no response to antibiotic or antifungal treatment. A week later, repeat chest CT revealed the tumor now measuring approximately 6 cm in size in the lower lobe of the right lung. We performed bronchoscopy, and bacteriological examination of the transbronchial biopsy specimen revealed pulmonary tuberculosis. Interferongamma release assay (IGRA) before the initiation of immunosuppressive treatment was negative, so we did not administer treatment for latent tuberculosis infection. He was, however, treated with isoniazid, rifampicin, ethambutol, and pyrazinamide for 9 months, following which radiological features improved gradually. Here we describe in detail this rare case of a negative IGRA result before immunosuppressive therapy in a relatively young Japanese man who went on to develop active tuberculosis with a rapidly-growing pulmonary lesion during hospitalization.

A 68-year-old man was admitted to our hospital with complaints of fatigue, polyuria, and loss of appetite, and was diagnosed with diabetic ketosis. Chest and abdominal computed tomography (CT) showed a pulmonary tumor on the right S3 and multiple liver tumors. Blood chemistry revealed elevated levels of amylase and hepatobiliary enzymes. Pathological examination of a biopsy specimen from the liver tumor showed a small cell carcinoma. Based on the imaging and pathological findings, we made a diagnosis of extensive disease small-cell lung cancer (ED-SCLC), cT1aN3M1b (HEP, ADR). Treatment with carboplatin and etoposide evoked partial response and the serum level of amylase decreased. Immunohistochemical staining of liver biopsy specimen was positive for amylase, leading to a diagnosis of SCLC with amylase production. About 22 months after the diagnosis of SCLC, he was admitted to our hospital with fatigue, muscular weakness, edema, and hyperpigmentation. Laboratory findings showed elevated serum levels of hepatobiliary enzymes, adrenocorticotropic hormone (ACTH), and cortisol, and a decreased serum potassium level. Urinary potassium level was elevated. Pituitary magnetic resonance imaging showed a normal morphology. We made a diagnosis of SCLC complicated by Cushing’s syndrome. We report this rare case of SCLC with amylase and ACTH production, which was detected in the course of treatment of SCLC.

Calcified amorphous tumor (CAT) is a non-neoplastic mass characterized by calcified nodules that was first reported in 1997. It is often associated with dialysis or mitral annular calcification (MAC). CAT is considered a risk factor for systemic embolism, but there has been no report of CAT damaging the native valve tissue and leading to valvular disease. An 81-year-old woman had shortness of breath on exertion starting 1 year previously, and was referred to our hospital with cardiac murmur detected on physical examination. Echocardiography showed evidence of severe mitral valve regurgitation with ruptured chordae tendineae of the posterior leaflet and a poorly mobile club-shaped structure protruding into the left ventricle and appearing to be continuous with MAC. She underwent elective mitral valve repair. A club-shaped calcification originating from MAC was found under the P2 segment, with ruptured P2 chordae tendineae immediately above it and mitral perforation in the contralateral A2 segment, which were likely to have resulted from direct damage by the hard structure. Mitral valve repair was successful with mass resection, triangular resection of the posterior leaflet P2 segment, and closure of the perforation. Histopathological findings of the mass were consistent with CAT, with no evidence of infection or malignancy. CAT may not only cause embolism but also grow while damaging the native valve tissue. It is important to closely follow-up and perform surgery in proper timing.

In patients with epidermal growth factor receptor (EGFR) mutation-positive lung cancer (LC) who have acquired resistance to first and/or second-generation EGFR-tyrosine kinase inhibitors (EGFR-TKIs), detection of EGFR T790M (T790M) mutation is essential before administration of osimertinib. Tissue sample is the main specimen used to detect the T790M mutation, and so cell block preparation using pleural or pericardial fluid should be considered. The utility of body cavity effusion cell block methods in T790M mutation detection have not yet been fully evaluated. This study aimed to evaluate the clinical background and treatment course of LC patients harboring the T790M mutation by using body cavity effusion cell block methods at our hospital. All patients were treated with first and/or second-generation EGFR-TKIs and had developed malignant pleural or pericardial fluid as a result of progressive disease. T790M mutation status was evaluated using body cavity effusion cell block method in 9 patients, from April 2016 to August 2017. We retrospectively evaluated the clinical characteristics and treatment course of these 9 patients (3 males and 6 females; median age 76 years). At the first diagnosis of LC, 7 patients had stage IV cancer; 4 patients were diagnosed by bronchial fibroscopy and 3 were diagnosed from pleural fluid examination. Regarding EGFR mutation, 3 and 6 patients carried the exon 19 deletion and L858R mutation, respectively. Median time interval between the first diagnosis of LC and T790M mutation evaluation was 30.8 months; 7 patients were diagnosed with positive T790M mutation by using body cavity effusion cell block methods. The T790M mutation was highly detected by examination of body cavity effusion cell blocks. Further evaluation is necessary with respect to variations in T790M detection rate based on the specimen collection site and/or progressive disease pattern in different patients.

　　A 56-year-old woman was referred to our hospital because of an abnormal finding in the right pulmonary hilum on chest X-ray. Enhanced chest computed tomography showed hyperplastic bronchial arteries dilating and winding around the trachea and bronchi. A racemose hemangioma of the bronchial artery with multiple bronchial artery aneurysms (diameter <20mm) was seen displacing the trachea and both main bronchi. Bronchoscopy showed submucosal tumor-like lesions at the distal trachea and in both main bronchi, and a dusky-red elevated pulsatile lesion at the orifice of the left B3b＋c. We performed coil embolization of the bronchial artery aneurysm to prevent abrupt rupture of the bronchial aneurysm.