K Takahashi
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Publication
Journal: Annals of Oncology
March/6/2020
Publication
Journal: The Journal of frailty & aging
October/22/2019
Abstract
Eating alone is related to depression, nutritional risk, and mortality. These effects are also influenced by living status. However, little is known about the relationship between eating alone despite living with family and frailty. This study explores the relationship of eating alone and living status with frailty in community-dwelling older adults.Cross-sectional study.Kashiwa city, Chiba prefecture, Japan; randomly selected community-dwelling older adults (aged 65 years and over).Eating status was assessed by the question, "Do you eat meals with anyone, at least once a day: yes or no?" Frailty was defined by Kihon Checklist (KCL) score 8 or over. Domains of frailty were divided into instrumental activities of daily living (IADL), physical strength, nutrition, eating, socialization, memory, and mood, based on KCL categories. Binary logistic regression analysis was used, adjusting for age, years of education, chronic diseases, number of teeth and cognitive function.Among the total of 1,914 participants, 49.8% were male, and the overall mean age was 72.9 ± 5.5 years. Of all participants, 56 (5.9%) of men and 112 (11.7%) of women were frail. Older adults who ate alone despite living with others were more likely to be frail (OR 2.49, 95%CI 1.1-5.5 for men and OR 2.16, 95%CI 1.0-4.5 for women). Of particular note, eating and living status were associated with lower physical strength and mood in men, whereas in women these statuses were associated with lower scores for IADL, socialization, memory, and mood.Eating alone despite living with others was associated with high frailty in both genders; however, the pathways were different between genders. These results might help yield a simple, fundamental intervention approach to multifaceted frailty, reflecting gender and associated high-risk domains.
Publication
Journal: Anaesthesia
September/26/2019
Abstract
The inflationary non-invasive blood pressure monitor (iNIBP™) uses a new measurement method, whereby the cuff is slowly inflated whilst simultaneously sensing oscillations, to determine the diastolic blood pressure first and then the systolic pressure. It may measure blood pressure more quickly than the conventional non-invasive blood pressure monitor. We studied 66 patients undergoing general anaesthesia, comparing the time taken to measure the blood pressure between the two monitors at times when there were marked changes (increases or decreases by 30 mmHg or greater) in the systolic blood pressure. The median (IQR) [range]) time was significantly longer for the non-invasive blood pressure monitor (38.8 (31.5-44.7) [18.0-130.0] s) than for the iNIBP (14.6 (13.7-16.4) [11.5-35.5] s), p = 0.001, 95%CI for difference 22-25 s). We also studied 30 volunteers to evaluate the accuracy of the iNIBP, comparing it with the mercury sphygmomanometer. There was good agreement between the two monitors, with a mean difference of 0 (95% limit of agreement -12 to 11) mmHg for the systolic blood pressure. We also compared the degree of pain during cuff inflation between the automated non-invasive blood pressure and iNIBP monitors. Pain was significantly more for the non-invasive blood pressure monitor (22 of 30 volunteers had less pain with the iNIBP). We have shown that the iNIBP measured the blood pressure quicker than the conventional non-invasive blood pressure monitor and the speed of measurement was not significantly affected by marked changes in the blood pressure.
Publication
Journal: Anaesthesia
September/19/2019
Abstract
Thoracic interfascial plane blocks are effective for post-mastectomy acute analgesia. However, their effects on chronic pain are uncertain. We randomly allocated 80 women equally to pectoral nerve-2 (PECS 2) block or serratus plane block. The pectoral nerve-2 block reduced the rate of moderate or severe chronic pain from 13/40 (33%) with the serratus plane block to 4/40 (10%), p = 0.03, adjusted odds ratio (95%CI) 0.23 (0.07-0.80), p = 0.02. The rates of pain-free women at six postoperative months were indeterminate, 10/40 (25%) after serratus plane block vs. 19/40 (48%) after pectoral nerve-2 block, p = 0.06, adjusted odds ratio (95%CI) 2.9 (1.1-7.5), p = 0.03. Health-related quality of life at six postoperative months was similar after serratus plane and pectoral nerve-2 blocks, mean (SD) EQ-5D-3L scores 0.87 (0.15) vs. 0.91 (0.14), respectively, p = 0.21. The pectoral nerve-2 block reduced median (IQR [range]) morphine consumption in the first 24 postoperative hours from 6 (3-9 [1-25]) mg to 4 (2-7 [0-37]) mg, p = 0.04. However, acute pain scores after serratus plane and pectoral nerve-2 blocks were similar, median (IQR [range]) 23 (11-35 [0-70]) mm vs. 18 (11-27 [0-61]) mm, respectively, p = 0.44. Pectoral nerve-2 block reduced chronic pain 6 months after mastectomy compared with serratus plane block.
Publication
Journal: Acta Virologica
September/11/2019
Abstract
Influenza virus is activated by proteolytic cleavage of hemagglutinin by trypsin. After determining the optimal trypsin concentration, intracellular and extracellular influenza A/PR/8/34 (H1N1) and A/Victoria/361/2011 (H3N2) virus productions were compared in cultures treated with T-705 (favipiravir) and GS 4071 (an active form of oseltamivir). Although both drugs efficiently inhibited extracellular viral RNA release in a dose-dependent manner, T-705 inhibited it to the level of the inoculum without trypsin treatment, while GS 4071 inhibited it to a final level 10 times higher than that without trypsin. T-705 inhibited intracellular viral RNA production to the level of input virus in both trypsin-treated and untreated cells. In contrast, GS 4071 dose-dependently inhibited intracellular viral RNA production in cells treated with trypsin but allowed viral RNA synthesis. The level of maximum inhibition by GS 4071was 10 times higher than that of cells without trypsin and 1,000 times greater than the inoculum titer in cells without trypsin. T-705 inhibited both intracellular and extracellular virus production 1,000 and 10 times more strongly, respectively, than GS 4071. T-705 has powerful anti-influenza activity in the absence of trypsin and even in the trypsin-optimized growth condition, suggesting the therapeutic advantage in treatment of influenza complicated with bacterial pneumonia. Keywords: influenza; T-705; Tamiflu; trypsin; bacterial trypsin-like protease.
Publication
Journal: Science of the Total Environment
July/21/2019
Abstract
High emissions of air pollutants from Northeast Asia are strongly influenced by air quality as well as by ecosystems. This study investigated the spatiotemporal variations in the sulfur isotopic ratio (δ34S) in atmospheric deposition at eleven monitoring stations in Japan from 2011 to 2016 and estimated the amount of transboundary transported anthropogenic sulfate (TRB) deposition using mass balance calculations. The δ34S of sulfate in precipitation ranged from -0.42 to +22.7‰. Sea salt (SS), TRB, and domestic anthropogenic sources (DOM) were the dominant sources of sulfate deposition in Japan. TRB sulfate deposition was largest on the Sea of Japan side, with an annual average value of 1.5 ± 0.3-6.9 ± 0.5 mg m-2 d-1 (36-44%), followed by Mt. Happo (4.5 ± 0.1 mg m-2 d-1; 88%), the Pacific Ocean side (1.5 ± 0.8, 4.3 ± 0.9 mg m-2 d-1; 24-50%), and the remote islands in the North Pacific Ocean (1.1 ± 0.2, 2.0 ± 0.8 mg m-2 d-1; 19-32%). TRB sulfate deposition on the Sea of Japan side was 2-12 times higher in winter and 1-2 times higher in summer than that of DOM. In contrast, TRB sulfate deposition on the Pacific Ocean side was 1.5-3 times higher in summer than in winter due to high precipitation levels. In Tokyo, the annual contribution from DOM sulfate deposition is approximately three times higher than that from TRB. Annual TRB sulfate deposition is lowest at Ogasawara at 1.1 ± 0.2 mg m-2 d-1, and the annual oceanic DMS contribution to sulfate deposition is high, accounting for 1.3 mg m-2 d-1 (20 ± 6%). The contribution of Asian dust was estimated to be 1-5.2 mg m-2 d-1(3-6%), which occurred in a single Asian dust event on the Sea of Japan side.
Publication
Journal: British Journal of Anaesthesia
June/29/2019
Abstract
The long-term use of opioid analgesics is limited by the development of unwanted side-effects, such as tolerance. The molecular mechanisms of morphine anti-nociceptive tolerance are still unclear. The mitochondrial calcium uniporter (MCU) is involved in painful hyperalgesia, but the role of MCU in morphine tolerance has not been uncharacterised.Rats received intrathecal injection of morphine for 7 days to induce morphine tolerance. The mechanical withdrawal threshold was measured using von Frey filaments, and thermal latency using the hotplate test. The effects of an MCU inhibitor, antisense oligodeoxynucleotide against cyclic adenosine monophosphate response element (CRE)-binding protein (CREB) or cytoplasmic polyadenylation element-binding protein 1 (CPEB1) in morphine tolerance were examined.Spinal morphine tolerance was associated with an increased expression of neuronal MCU, phospho-CREB (pCREB), and CPEB1 in the spinal cord dorsal horn. MCU inhibition increased the mechanical threshold and thermal latency, and reduced the accumulation of mitochondrial calcium in morphine tolerance. Intrathecal antisense oligodeoxynucleotide against CREB or CPEB1 restored the anti-nociceptive effects of morphine compared with mismatch oligodeoxynucleotide in von Frey test and hotplate test. Chromatin immunoprecipitation with quantitative PCR assay showed that CREB knockdown reduced the interaction of pCREB with the ccdc109a gene (encoding MCU expression) promoter and decreased the MCU mRNA transcription. RNA immunoprecipitation assay suggested that CPEB1 binds to the MCU mRNA 3' untranslated region. CPEB1 knockdown decreased the expression of MCU protein.These findings suggest that spinal MCU is regulated by pCREB and CPEB1 in morphine tolerance, and that inhibition of MCU, pCREB, or CPEB1 may be useful in preventing the development of opioid tolerance.
Authors
Publication
Journal: Journal of Dental Research
June/25/2019
Abstract
While the prevalence of supernumerary teeth (ST) is high in permanent dentition, the etiology of ST in humans remains unclear. However, multiple murine models of ST have elaborated on dated mechanisms traditionally ascribed to ST etiology: one involves the rescue of rudimental teeth, and the second considers the contribution of odontogenic epithelial stem cells. It remains unclear whether these mechanisms of ST formation in mice are applicable to humans. The third dentition is usually regressed apoptotic-that is, the teeth do not completely form in humans. Recently, it was suggested that ST result from the rescue of regression of the third dentition in humans. The present investigation evaluates the proportion of collected general ST cases that evinced a third dentition based on the clinical definition of ST derived from the third dentition. We also investigated the contribution of SOX2-positive odontogenic epithelial stem cells to ST formation in humans. We collected 215 general ST cases from 15,008 patients. We confirmed that the general characteristics of the collected ST cases were similar to the results from previous reports. Of the 215 cases, we narrowed our analysis to the 78 patients who had received a computed tomography scan. The frequency of ST considered to have been derived from the third dentition was 26 out of 78 cases. Evidence of a third dentition was especially apparent in the premolar region, was more common in men, and was more likely among patients with ≥3 ST. SOX2-positive odontogenic epithelial stem cells within the surrounding epithelial cells of developing ST were observed in non-third dentition cases and not in third dentition cases. In conclusion, the third dentition is the main cause of ST in humans. The odontogenic epithelial stem cells may contribute to ST formation in cases not caused by a third dentition.
Publication
Journal: Journal of Comparative Pathology
January/29/2019
Abstract
A 13-year-old neutered female mixed-breed dog with a clinical history of emaciation, inappetence and vomiting for 2 months was presented. Blood tests showed marked leucocytosis with increased neutrophil and basophil count, mild thrombocytosis and anaemia. Seven days after the initial visit, the dog died and was submitted for necropsy examination. Grossly, the bone marrow was red in colour and hepatomegaly and splenomegaly with discolouration were observed. A bone marrow smear showed an increased proportion of basophilic lineage cells. Histologically, the bone marrow showed high cellular density and numerous basophilic lineage cells with a round or segmented nucleus. The cytoplasm contained basophilic granules exhibiting metachromasia on toluidine blue staining. Immunohistochemically, the neoplastic basophils were diffusely positive for vimentin and myeloperoxidase, but negative for CD3, BLA36, CD163, CD204 and c-kit. The immunohistochemical features of neoplastic basophils that had invaded the liver and spleen were similar to those of the basophils in the bone marrow. Based on the clinicopathological and histopathological findings, chronic basophilic leukaemia was diagnosed. The present case study provides insights into the pathological features of chronic basophilic leukaemia in dogs.
Publication
Journal: Journal of Gastroenterology and Hepatology
January/21/2019
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