Sarcopenic Dysphagia and Simplified Rehabilitation Nutrition Care Process: An Update.

Sarcopenic dysphagia is characterized by weakness of swallowing-related muscles associated with whole-body sarcopenia. As the number of patients with sarcopenia increases with the aging of the world, the number of patients with sarcopenic dysphagia is also increasing. The prevalence of sarcopenic dysphagia is high in the institutionalized older people and in patients hospitalized for pneumonia with dysphagia in acute care hospitals. Prevention, early detection and intervention of sarcopenic dysphagia with rehabilitation nutrition are essential. The diagnosis of sarcopenic dysphagia is based on skeletal and swallowing muscle strength and muscle mass. A reliable and validated diagnostic algorithm for sarcopenic dysphagia is used. Sarcopenic dysphagia is associated with malnutrition, which leads to mortality and Activities of Daily Living (ADL) decline. The rehabilitation nutrition approach improves swallowing function, nutrition status, and ADL. A combination of aggressive nutrition therapy to improve nutrition status, dysphagia rehabilitation, physical therapy, and other interventions can be effective for sarcopenic dysphagia. The rehabilitation nutrition care process is used to assess and problem solve the patient's pathology, sarcopenia, and nutrition status. The simplified rehabilitation nutrition care process consists of a nutrition cycle and a rehabilitation cycle, each with five steps: assessment, diagnosis, goal setting, intervention, and monitoring. Nutrition professionals and teams implement the nutrition cycle. Rehabilitation professionals and teams implement the rehabilitation cycle. Both cycles should be done simultaneously. The nutrition diagnosis of undernutrition, overnutrition/obesity, sarcopenia, and goal setting of rehabilitation and body weight are implemented collaboratively.

Rehabilitation Nutrition and Exercise Therapy for Sarcopenia.

Sarcopenia is an age-related loss of skeletal muscle associated with adverse outcomes such as falls, fractures, disability, and increased mortality in older people and hospitalized patients. About half of older male nursing home residents have sarcopenia. The diagnostic criteria by the European Working Group on Sarcopenia in Older People (EWGSOP) and the Asian Working Group for Sarcopenia (AWGS) have led to increased interest in sarcopenia. Exercise and nutritional management are crucial for the prevention and treatment of sarcopenia. Nutritional therapy for sarcopenia that includes 20 g of whey protein and 800 IU of vitamin D twice a day improves lower limb strength. Exercise therapy for sarcopenia, such as resistance training and 6 months of home exercises, improves muscle strength and physical function. Combination therapy that includes both nutritional and exercise therapy improves gait speed and knee extension strength more than either exercise alone or nutrition therapy alone. Excessive bedrest and mismanagement of nutrition in medical facilities can lead to iatrogenic sarcopenia. Iatrogenic sarcopenia is sarcopenia caused by the activities of health care workers in health care facilities. Appropriate nutritional management and exercise programs through rehabilitation nutrition are important for prevention and treatment of iatrogenic sarcopenia. Nutritional and exercise therapy should be started very early after admission and adjusted to the level of inflammation and disease status. Repeated assessment, diagnosis, goal setting, interventions, and monitoring using the rehabilitation nutrition care process is important to maximize treatment effectiveness and improve patients' functional recovery and quality of life.

Dysregulation of MAP Kinase Signaling Pathways Including p38MAPK, SAPK/JNK, and ERK1/2 in Cultured Rat Cerebellar Astrocytes Exposed to Diphenylarsinic Acid.

Diphenylarsinic acid (DPAA) was a major compound found in the arsenic poisoning incident that occurred in Kamisu, Ibaraki, Japan in 2003. People exposed to DPAA via contaminated well water suffered from several neurological disorders, including cerebellar symptoms. We previously reported that DPAA induces cellular activation in cultured rat cerebellar astrocytes, dose-dependent promotion of cell growth (low DPAA), cell death (high DPAA), and increased phosphorylation of mitogen-activated protein (MAP) kinases (p38MAPK, SAPK/JNK, and ERK1/2). Moreover, DPAA induces up-regulation of oxidative stress-counteracting proteins, activation of CREB phosphorylation, increased protein expression of c-Jun and c-Fos, and aberrant secretion of brain-active cytokines (MCP-1, adrenomedullin, FGF2, CXCL1, and IL-6). Here, we explored the role of MAP kinases in DPAA-induced activation of astrocytes using specific MAP kinase signaling inhibitors [SB203580 (p38MAPK), SP600125 (SAPK/JNK), SCH772984 (ERK1/2), and U0126 (MEK1/2, a kinase for ERK1/2)]. DPAA-induced activation of MAP kinases had little contribution to DPAA-induced cell growth and death. On the other hand, a power relationship among MAP kinases was also observed, in which p38MAPK suppressed DPAA-induced SAPK/JNK and ERK1/2 activation, whereas ERK1/2 and MEK1/2 facilitated p38MAPK and SAPK/JNK activation. In addition, SAPK/JNK had minimal effects on the activation of other MAP kinases. DPAA-induced activation of transcription factors and secretion of brain-active cytokines were submissively but intricately dominated by MAP kinases. Collectively, our results indicate that DPAA-induced activation of MAP kinases is neither a cell growth-promoting response nor a cytoprotective one but leads to transcriptional disruption and aberrant secretion of brain-active cytokines in cerebellar astrocytes.

Achievement of over 1.4 V photovoltage in a dye-sensitized solar cell by the application of a silyl-anchor coumarin dye.

A dye-sensitized solar cell (DSSC) fabricated by using a novel silyl-anchor coumarin dye with alkyl-chain substitutes, a Br3-/Br- redox electrolyte solution containing water, and a Mg2+-doped anatase-TiO2 electrode with twofold surface modification by MgO and Al2O3 exhibited an open-circuit photovoltage over 1.4 V, demonstrating the possibility of DSSCs as practical photovoltaic devices.

Diphenylarsinic Acid Induced Activation of Cultured Rat Cerebellar Astrocytes: Phosphorylation of Mitogen-Activated Protein Kinases, Upregulation of Transcription Factors, and Release of Brain-Active Cytokines.

Diphenylarsinic acid (DPAA) was detected as the primary compound responsible for the arsenic poisoning that occurred in Kamisu, Ibaraki, Japan, where people using water from a well that was contaminated with a high level of arsenic developed neurological (mostly cerebellar) symptoms and dysregulation of regional cerebral blood flow. To understand the underlying molecular mechanism of DPAA-induced cerebellar symptoms, we focused on astrocytes, which have a brain-protective function. Incubation with 10 µM DPAA for 96 h promoted cell proliferation, increased the expression of antioxidative stress proteins (heme oxygenase-1 and heat shock protein 70), and induced the release of cytokines (MCP-1, adrenomedullin, FGF2, CXCL1, and IL-6). Furthermore, DPAA overpoweringly increased the phosphorylation of three major mitogen-activated protein kinases (MAPKs) (ERK1/2, p38MAPK, and SAPK/JNK), which indicated MAPK activation, and subsequently induced expression and/or phosphorylation of transcription factors (Nrf2, CREB, c-Jun, and c-Fos) in cultured rat cerebellar astrocytes. Structure-activity relationship analyses of DPAA and other related pentavalent organic arsenicals revealed that DPAA at 10 µM activated astrocytes most effective among organic arsenicals tested at the same dose. These results suggest that in a cerebellum exposed to DPAA, abnormal activation of the MAPK-transcription factor pathway and irregular secretion of these neuroactive, glioactive, and/or vasoactive cytokines in astrocytes can be the direct/indirect cause of functional abnormalities in surrounding neurons, glial cells, and vascular cells: This in turn might lead to the onset of cerebellar symptoms and disruption of cerebral blood flow.

Highly-efficient dye-sensitized solar cells with collaborative sensitization by silyl-anchor and carboxy-anchor dyes.

In dye-sensitized solar cells co-photosensitized with an alkoxysilyl-anchor dye ADEKA-1 and a carboxy-anchor organic dye LEG4, LEG4 was revealed to work collaboratively by enhancing the electron injection from the light-excited dyes to the TiO2 electrodes, and the cells exhibited a high conversion efficiency of over 14% under one sun illumination.

Fabrication of a high-performance dye-sensitized solar cell with 12.8% conversion efficiency using organic silyl-anchor dyes.

The co-sensitization of organic silyl-anchor dyes in dye-sensitized solar cells (DSSCs) using carbazole and coumarin dyes with organosilicon tethers for binding to titanium dioxide has been examined. We have succeeded in fabricating a high-performance DSSC with a light-to-electric energy conversion efficiency of 12.8% under one sun simulated solar irradiation.

An achievement of over 12 percent efficiency in an organic dye-sensitized solar cell.

Dye-sensitized solar cells fabricated by using a novel metal-free alkoxysilyl carbazole as a sensitizing dye and a Co(3+/2+)-complex redox electrolyte exhibited light-to-electric energy conversion efficiencies of over 12% with open-circuit photovoltages higher than 1 V by applying a hierarchical multi-capping treatment to the photoanode.

Asymmetric autocatalysis induced by chiral hydrocarbon [2.2]paracyclophanes.

Chiral hydrocarbon [2.2]paracyclophanes act as chiral initiators in asymmetric autocatalysis in the addition of diisopropylzinc to pyrimidine-5-carbaldehyde and give highly enantiomerically enriched 5-pyrimidyl alkanol with a reversed sense of the enantioselectivity to that of other [2.2]paracyclophanes with heteroatoms.