Effects of Reminiscence Therapy Using Nostalgic SONGS on The Cognitive Function of The Elderly Living in The Community.

The study aimed to examine the effects of reminiscence therapy using nostalgic songs on the cognitive function of elderly people living in the community. The subjects were 34 people who had undergonea ssessment of their vital functions using a basic check list and stated that they had problems related to "withdrawal" or "cognitive functions". Their cognitive functions were assessed using the Hasegawa Dementia Scale-Revised (HDS-R) and Mini-Mental State Examination (MMSE) prior to and following the implementation of reminiscence intervention using nostalgic songs. The cognitive functions of the elderly were classified into three levels and assessed according to the judgment criteria of those scales. There were significant differences in the total HDS-R score and scores for the subscale items -"recital of numbers in reverse order" and "delayed recall"-received by all subjects. There were also significant differences in the total MMSE score and scores for the subscale items -"spatial orientation" and "delayed recall" -received by all subjects. Regarding cognitive function levels, there were significant differences in the total score and subscale score for "delayed recal" received by elderly people who had been determined as having "cognitive dysfunction" using the HDS-R and "mild cognitive dysfunction". That is, it is not possible to evaluate possible dementia, but there is a risk of transitioning to suspicion of dementia when it is left unattended, using the HDS-R and MMSE

Tree-to-Sequence Attentional Neural Machine Translation

Most of the existing Neural Machine Translation (NMT) models focus on the conversion of sequential data and do not directly use syntactic information. We propose a novel end-to-end syntactic NMT model, extending a sequence-to-sequence model with the source-side phrase structure. Our model has an attention mechanism that enables the decoder to generate a translated word while softly aligning it with phrases as well as words of the source sentence. Experimental results on the WAT'15 English-to-Japanese dataset demonstrate that our proposed model considerably outperforms sequence-to-sequence attentional NMT models and compares favorably with the state-of-the-art tree-to-string SMT system.Comment: Accepted as a full paper at the 54th Annual Meeting of the Association for Computational Linguistics (ACL 2016

Inheriting Perpetrator Trauma: Intergenerational memory of the Sino‑Japan War

The legacy of a perpetrator past has always occupied a troubling place in Japan’s national culture. As in many post-confict societies, remembering dark history has been shrouded in uneasy trepidation, reticence, and remorse. Almost eight decades after World War II ended, the task of remembering Japan’s perpetrator past has now passed to the postwar generations who have become the carrier groups of perpetrator trauma. This paper explores the cultural trauma of war inherited by the children of veterans who fought in the Sino-Japan War, whose lives were indelibly marked by their fathers’ legacy of violence and guilt. I examine three recent memoirs by the second generation that probe their fathers’ broken lives. The memory work of these writers—Murakami Haruki, Henmi Yō, and Itō Hideko—show that haunting legacies of war can be transmitted across generations even when they are shrouded in silence. This study points a new direction in cultural trauma research that foregrounds intergenerational memory in the cultural trauma process

Next generation sequencing to identify new genetic causes of familial craniosynostosis

Craniosynostosis, the premature fusion of one or more cranial sutures, is one of the most common craniofacial abnormalities. There is considerable genetic heterogeneity and the underlying pathophysiological mechanisms are diverse, occurring at multiple stages of cranial suture biogenesis. A genetic diagnosis, currently made in ~25% of cases, is an important aspect of the multidisciplinary approach to clinical management and genetic counselling. The aim of this thesis is to identify novel genetic causes of craniosynostosis in unsolved familial cases. Four families were selected and investigated using a combination of next generation sequencing and copy number analysis. Candidate changes were followed up through segregation and functional analysis to determine if they were causal. The most convincing finding was a homozygous deletion identified in the 5′ UTR (untranslated region) of dehydrogenase/reductase 3 (DHRS3) in a consanguineous family with syndromic coronal synostosis. This deletion was shown to lead to loss of DHRS3 activity and an increase of all-trans-retinoic acid (ATRA), a known teratogen that had previously been deduced to contribute to craniosynostosis. These findings are consistent with a novel embryopathy caused by excess ATRA, leading to skeletal and cardiac defects. In a second large family with syndromic metopic synostosis, a nonsynonymous variant in HIST1H2AD, encoding one of the canonical histone H2A components of the nucleosome, was identified. Although a link between histone mutation and craniosynostosis is unknown, we speculated that this variant could perturb gene expression during development of the metopic suture. To gain support for causality, two approaches were undertaken; 1. Search for additional patients with a variant in H2A genes including resequencing in a large cohort of patients with craniosynostosis. 2. Creation of Hist1h2ad mutant Embryonic Stem cells using CRISPR/CAS9; Generation of the mouse model is ongoing. Chromosomal rearrangements can be pathogenic through altering the topological associated domain (TAD) structure. A de novo tandem duplication on chromosome 4 including FGF5 and C4orf22 was identified in a third family (affected mother and daughter) with multiple suture synostosis. The duplication overlaps TAD boundaries, leading to the hypothesis that this may induce mis-expression of genes in or near the duplication. Gene expression analysis was undertaken. To investigate this further, work using Capture-C, a technique used to discover local chromatin structure and interactions, is ongoing. In summary, I have identified a new craniosynostosis disease gene, DHRS3, suggesting an additional aetiology in osteogenesis of the cranial suture caused by disruption of retinoic metabolism. In addition, two loci, HIST1H2AD and FGF5/C4orf22 duplication, are plausible candidates for craniosynostosis with possible roles in disturbing neural crest development and RAS/MAPK signalling, respectively. Finally, this work illustrates a combined genomic technology approach to resolve difficult cases that may be applicable apply to other diseases in which a genetic cause is suspected

Differential remodelling of peroxisome function underpins the environmental and metabolic adaptability of diplonemids and kinetoplastids

The remodelling of organelle function is increasingly appreciated as a central driver of eukaryotic biodiversity and evolution. Kinetoplastids including Trypanosoma and Leishmania have evolved specialized peroxisomes, called glycosomes. Glycosomes uniquely contain a glycolytic pathway as well as other enzymes, which underpin the physiological flexibility of these major human pathogens. The sister group of kinetoplastids are the diplonemids, which are among the most abundant eukaryotes in marine plankton. Here we demonstrate the compartmentalization of gluconeogenesis, or glycolysis in reverse, in the peroxisomes of the free-living marine diplonemid, Diplonema papillatum. Our results suggest that peroxisome modification was already under way in the common ancestor of kinetoplastids and diplonemids, and raise the possibility that the central importance of gluconeogenesis to carbon metabolism in the heterotrophic free-living ancestor may have been an important selective driver. Our data indicate that peroxisome modification is not confined to the kinetoplastid lineage, but has also been a factor in the success of their free-living euglenozoan relatives

Incidence and Risk Factors for Infections Requiring Hospitalization, Including Pneumocystis Pneumonia, in Japanese Patients with Rheumatoid Arthritis

Objective. Rheumatoid arthritis (RA) may be complicated by different infections, but risk factors for these are not fully elucidated. Here, we assessed the incidence of and risk factors for infections requiring hospitalization (IRH) including pneumocystis pneumonia (PCP) in patients with RA. Methods. We retrospectively surveyed all RA patients treated at our hospital from 2009 to 2013, for whom data were available on demographic features, medications, comorbidities, and severity of RA. Multivariate logistic regression analysis was applied to calculate adjusted odds ratios (ORs) for factors associated with the occurrence of IRH. Results. In a total of 9210 patient-years (2688 patients), there were 373 IRH (3.7/100 patient-years). Respiratory tract infections were most frequent (, and additionally 16 PCP), followed by urinary tract infections (). Significant factors for PCP included higher age (≥70 years; OR 3.5), male sex (6.6), underlying lung disease (3.0), use of corticosteroids (4.8), and use of biologics (5.4). Use of methotrexate (5.7) was positively associated with PCP but negatively with total infections (0.7). Additionally, functional disorders and higher RA disease activity were also related to total infections. Conclusions. Risk factors for infection should be taken into account when deciding treatment for the individual RA patient

Proteolytic release of the carboxy-terminal fragment of proHB-EGF causes nuclear export of PLZF

Cleavage of membrane-anchored heparin-binding EGF-like growth factor (proHB-EGF) via metalloprotease activation yields amino- and carboxy-terminal regions (HB-EGF and HB-EGF-C, respectively), with HB-EGF widely recognized as a key element of epidermal growth factor receptor transactivation in G protein–coupled receptor signaling. Here, we show a biological role of HB-EGF-C in cells. Subsequent to proteolytic cleavage of proHB-EGF, HB-EGF-C translocated from the plasma membrane into the nucleus. This translocation triggered nuclear export of the transcriptional repressor, promyelocytic leukemia zinc finger (PLZF), which we identify as an HB-EGF-C binding protein. Suppression of cyclin A and delayed entry of S-phase in cells expressing PLZF were reversed by the production of HB-EGF-C. These results indicate that released HB-EGF-C functions as an intracellular signal and coordinates cell cycle progression with HB-EGF