The research on the problems of health care and living of the aged (Pursuing the cases of home treatment given to the elderly patients for one year after their discharge)

退院後の生活に目を向けた適切な退院指導がなされることは、高齢患者が安心して在宅療養を送る上で、重要な意味を持つ。そこで病院から在宅療養に移行した70歳以上の高齢者の抱える問題を4回に渡って1年間調査し、これまでに退院時、3ヵ月後、6ヵ月後の調査結果を報告した。本稿では1年を通じて回答のあった53名について健康と生活上の問題の変化を分析し、考察した。在宅療養に移行した高齢者の健康状態と生活上の問題は、ほぼ一致して退院後6ヵ月から1年後までに変化を認め、特に日常生活上の問題は著しく増加した。その原因として病状の悪化との関連が考えられた。また、高齢者の問題についての意識は、研究者の専門的な問題意識に比べて低かった。従って入院中に退院後の生活を予測することには限界があり、今後は退院指導の充実と伴に在宅サービスとの連携が重要であることを認めた。We planned to make emerge the problems felt by the elderly patients of 70 years and over given home treatment. As a means of our research, four times a year we sent a questinnaire to the aged who had been discharged. After collecting the answers of the questionnaires, we decided to focus on the 53 elderly patients who answered all four questionnaires, and then tried to make their problems emerge. The contents of the questionnaires were about their health care in a year and how their daily life changed. We can see that the condition of the elderly patients under home treatment and their living problems have changed almost without exceptions six months to a year after their discharge. Especially the number of the problems in their daily life increased remarkably. These results might be considered to be caused by the aggravation of their diseases. In addition, the elderly patients are not as conscious of their own problems as a specialist with a critical mind. Therefore, there is a limit to estimating the change in lifestyle of a discharged patient while they remain hospitalized. We consider it essential to get full discharge-care closely connected with home service for elderly patients

Morphologic studies of bone marrow cells exposed to the phospholipid fraction from the liver of irradiated animal, an experiment in vitro

With the purpose of revealing the biological effects of the X-ray irradiation the authors extracted phospholipids from the liver of irradiated animals and proved that this substance has the action to inhibit the growth of the bone marrow cells, the motility of pseudo-eosinophilis and the erythropoiesis in tissue culture, suggesting that the injury will mainly be induced by the toxic substances produced by irradiation.</p

Characteristics of Rhetorical Use by Japanese Learners of English

departmental bulletin pape

Glucocorticoid induced osteoporosis and mechanisms of intervention

Indiana University-Purdue University Indianapolis (IUPUI)Glucocorticoid excess is a leading cause of osteoporosis. The loss of bone mass and strength corresponds to the increase in fractures exhibited after three months of glucocorticoid therapy. Glucocorticoids induce the bone cellular responses of deceased bone formation, increased osteoblast/osteocyte apoptosis, and transient increased bone resorption, which result in rapid bone loss and degradation of bone microarchitecture. The current standard of care for osteoporosis is bisphosphonate treatment; however, these agents further suppress bone formation and increase osteonecrosis and low energy atypical fracture risks. Thus, there is an unmet need for interventions that protect from glucocorticoid therapy. The purpose of these studies was to investigate novel mechanisms that potentially interfere with glucocorticoid-induced bone loss. We chose to explore pathways that regulate endoplasmic reticulum stress, the canonical Wnt pathway, and Pyk2 activity. Pharmacologic reduction of endoplasmic reticulum stress through salubrinal administration protected against glucocorticoid-induced bone loss by preservation of bone formation and osteoblast/osteocyte viability. In contrast, inhibition of Wnt antagonist Sost/sclerostin and inhibition of Pyk2 signaling did not prevent glucocorticoid-induced reductions in bone formation; however, both Sost/sclerostin and Pyk2 deficiency protected against bone loss through inhibition of increases in resorption. Overall, these studies demonstrate the significant contributions of reductions in bone formation, increased osteoblast/osteocyte apoptosis, and elevations in resorption to the rapid 6-12% bone loss exhibited during the first year of glucocorticoid therapy. However, glucocorticoid excess also induces skeletal muscle weakness, which is not reversed by bisphosphonate treatment or the interventions reported here of salubrinal, Sost/sclerostin inhibition, or Pyk2 deficiency. Further, the novel finding of increased E3 ubiquitin ligase atrophy signaling induce by glucocorticoids in both bone and muscle, by tissue-specific upstream mechanisms, provides opportunities for therapeutic combination strategies. Thus, future studies are warranted to investigate the role of E3 ubiquitin ligase signaling in the deleterious glucocorticoid effects of bone and muscle

Current Status of Working Environment and Chronic Fatigue for Nurses in Clinical Care

Nurses work 23.4 hours of overtime on average per month (Japanese Nursing Association, 2009) , which is 13.2 hours longer than the monthly average for general workers (The Ministry of Health, Labor and Welfare, 2013). The purpose of this study is to clarify the current status of the working environment and chronic fatigue for nurses in clinical care. The questionnaire was anonymous and self-administered. The contents of the question are attributes, working environment and chronic fatigue. A total of 1676 female nurses working at 117 diff erent general hospitals located in Japan, participated in our survey. It was found that nurses are not able to fully recover from fatigue and chronic fatigue is likely to accumulate when the following conditions are relevant: they are in their 20s, they work under the working environment with overtime (the time to leave work is irregular) for 20 hours or longer on average per month, or they work on a three-shift pattern. It is necessary to adjust the environment in an organization or society including working structure by paying attention to characteristics of individual fatigue.弘前医学. 65, 2014, p.43-54journal articl

Effect of Donepezil on Group II mGlu Receptor Agonist- or Antagonist-Induced Amnesia on Passive Avoidance in Mice

We examined the effect of the acetylcholinesterase (ACHE) inhibitor, donepezil hydrocloride (DONP), on group II metabotropic glutamate (mGlu) receptor agonist- or antagonist-induced amnesia in the step-through passive avoidance task in male mice. DCG-IV, a group II mGlu receptor agonist, at dose of 50 ng and LY341495, a group II mGlu receptor antagonist, at dose of 300 ng, significantly attenuated the latency on the step-through task. The subcutaneous injection of DONP at dose of 1 mg/kg 1 hour before passive avoidance performance ameliorated the amnesia induced by DCG-IV and LY341495, whereas donepezil alone did not affect task latency. The results suggest that activation of group II mGlu receptors and disinhibition of the cAMP/PKA signaling pathway (caused by group II mGlu receptor antagonist) have a negative action on step-through passive avoidance memory performance, and that group II mGlu receptors and ACh interact to modulate learning and memory function

Synthetic retinoid Am80 ameliorates chronic graft-versus-host disease by down-regulating Th1 and Th17.

Chronic GVHD (cGVHD) is a main cause of late death and morbidity after allogeneic hematopoietic cell transplantation, but its pathogenesis remains unclear. We investigated the roles of Th subsets in cGVHD with the use of a well-defined mouse model of cGVHD. In this model, development of cGVHD was associated with up-regulated Th1, Th2, and Th17 responses. Th1 and Th2 responses were up-regulated early after BM transplantation, followed by a subsequent up-regulation of Th17 cells. Significantly greater numbers of Th17 cells were infiltrated in the lung and liver from allogeneic recipients than those from syngeneic recipients. We then evaluated the roles of Th1 and Th17 in cGVHD with the use of IFN-γ-deficient and IL-17-deficient mice as donors. Infusion of IFN-γ(-/-) or IL-17(-/-) T cells attenuated cGVHD in the skin and salivary glands. Am80, a potent synthetic retinoid, regulated both Th1 and Th17 responses as well as TGF-β expression in the skin, resulting in an attenuation of cutaneous cGVHD. These results suggest that Th1 and Th17 contribute to the development of cGVHD and that targeting Th1 and Th17 may therefore represent a promising therapeutic strategy for preventing and treating cGVHD