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Although early identification and management services for dementia have become more widespread, their efficacy and the clinical characteristics of service have yet to be fully evaluated. Therefore, the objective of this study is to clarify these issues.
The subjects were 164 Japanese users of an early identification and management program for dementia, known as the Initial-phase Intensive Support Team (IPIST), between 2013 and 2015. Nonhierarchical cluster analysis was used to derive subgroups based on cognitive status and ability in activities of daily living (ADL) and behavioral and psychological symptoms of dementia (BPSD). One-way analysis of variance was performed to evaluate differences among the groups derived by the cluster analysis. A paired t test was used to assess how the clinical status of the groups changed between baseline and follow-up.
Four groups were identified by cluster analysis, i.e. a mild group, a moderate group, a BPSD group with moderate cognitive impairment and severe BPSD, and a severe group with severe cognitive impairment and severe BPSD. Although there were no significant improvements in cognitive impairment or ADL in any group, significant improvements were found in BPSD in the BPSD and severe BPSD groups. Caregiver burden was significantly lessened in all groups. Clinical diagnosis and long-term care insurance service utilization rates were significantly improved overall.
The users of IPIST were classified into four subgroups based on their clinical characteristics. The IPIST program could improve the quality of life of people with dementia and their caregivers.
In this paper, we propose a reversible color transform (RCT) for color images acquired through a Bayer pattern color filter array. One existing RCT with fixed coefficients is simple to implement. However, it is not adaptive to each of input images. Another existing RCT based on eigenvector of covariance matrix of color components, which is equivalent to Karhunen–Loève transform (KLT), is adaptive. However, it requires heavy computational load. We remove a redundant part of this existing method, utilizing fixed statistical relation between two green components at different locations. Comparing to the KLT-based existing RCT, it was observed that the proposed RCT keeps adaptability and has better coding performance, even though its computational load is reduced.
Muscle atrophy increases the production of reactive oxygen species and the expression of atrophy-related genes, which are involved in the ubiquitin–proteasome system. In the present study, we investigated the effects of β-carotene on oxidative stress (100 μm-H2O2)-induced muscle atrophy in murine C2C12 myotubes. β-Carotene (10 μm) restored the H2O2-induced decreased levels of myosin heavy chain and tropomyosin (P< 0·05, n 3) and decreased the H2O2-induced increased levels of ubiquitin conjugates. β-Carotene reduced the H2O2-induced increased expression levels of E3 ubiquitin ligases (Atrogin-1 and MuRF1) and deubiquitinating enzymes (USP14 and USP19) (P< 0·05, n 3) and attenuated the H2O2-induced nuclear localisation of FOXO3a. Furthermore, we determined the effects of β-carotene on denervation-induced muscle atrophy. Male ddY mice (8 weeks old, n 30) were divided into two groups and orally pre-administered micelle with or without β-carotene (0·5 mg once daily) for 2 weeks, followed by denervation in the right hindlimb. β-Carotene was further administered once daily until the end of the experiment. At day 3 after denervation, the ratio of soleus muscle mass in the denervated leg to that in the sham leg was significantly higher in β-carotene-administered mice than in control vehicle-administered ones (P< 0·05, n 5). In the denervated soleus muscle, β-carotene administration significantly decreased the expression levels of Atrogin-1, MuRF1, USP14 and USP19 (P< 0·05, n 5) and the levels of ubiquitin conjugates. These results indicate that β-carotene attenuates soleus muscle loss, perhaps by repressing the expressions of Atrogin-1, MuRF1, USP14 and USP19, at the early stage of soleus muscle atrophy.
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