14 results match your criteria: "Tokyo Medical and Dental University Graduate School of Health Care Sciences.[Affiliation]"

Objectives: The study aimed to develop a machine learning (ML) model to predict early postdischarge falls in older adults using data that are easy to collect in acute care hospitals. This may reduce the burden imposed by complex measures on patients and health care staff.

Design: This prospective multicenter study included patients admitted to and discharged from geriatric wards at 3 university hospitals and 1 national medical center in Japan between October 2019 and July 2023.

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Introduction: The mental health status of nurses affects not only their well-being but also the organisational outcomes and the quality of patient care. Hence, stress management strategies are critical as a universal prevention measure that address an entire population and are not directed at a specific risk group to maintain nurses' mental health in the workplace. No systematic review or meta-analysis has been conducted to evaluate the effect of cognitive-behavioural therapy (CBT) that specifically focuses on universal prevention.

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Purpose: Although home care improves patients' quality of life (QOL), several studies have suggested that home care lowers the QOL of family caregivers and decreases their mortality. To alleviate the deleterious impact of home care on caregivers, the major burdens on caregivers and the clinical characteristics of the caregivers vulnerable to the major burden needs to be clarified.

Method: A survey questionnaire was distributed to 710 family caregivers of patients with cancer in Japan, and 342 valid responses were obtained (valid response rate: 48.

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Plasmacytoma is one of the most difficult types of leukemia to treat, and it often invades the bone down to the marrow resulting in the development of multiple myeloma. NF-κB is often constitutively activated, and promotes metastasis and drug resistance in neoplastic cells. The present study assessed the cellular anticancer activity of an NF-κB inhibitor, dehydroxymethylepoxyquinomicin (DHMEQ), on mouse plasmacytoma SP2/0 cells.

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Ethyl acetate extract of Kaempferia parviflora inhibits Helicobacter pylori-associated mammalian cell inflammation by regulating proinflammatory cytokine expression and leukocyte chemotaxis.

BMC Complement Med Ther

April 2020

Research Unit of Innovative Diagnosis of Antimicrobial Resistance, Department of Transfusion Medicine and Clinical Microbiology, Faculty of Allied Health Sciences, Chulalongkorn University, Pathumwan, Bangkok, Thailand.

Article Synopsis
  • Kaempferia parviflora (KP) has historically been used in Thai medicine to treat gastrointestinal issues, specifically targeting inflammation caused by Helicobacter pylori, which can lead to gastric diseases and cancer.
  • A study evaluated the effects of a crude ethyl acetate extract of KP (CEAE-KP) on AGS gastric cancer cells and found that it reduced cell viability in a dose- and time-dependent manner, with no toxicity at lower concentrations (8-16 μg/ml).
  • CEAE-KP significantly decreased interleukin-8 (IL-8) production and neutrophil chemotaxis, suggesting its potential as an effective alternative treatment to reduce inflammation from H. pylori infections.
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Family caregivers of patients with terminal-stage cancer have numerous roles as caregivers, which can influence their anticipatory grief. The purpose of this study was to clarify how talking to family caregivers of patients with terminal illness using the narrative approach can influence such caregivers' process of anticipatory grief. We conducted the narrative approach as an intervention with two family caregivers several times and qualitatively analyzed their narratives.

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Background: Lipoprotein-X (Lp-X) is an abnormal phospholipid-rich lipoprotein found in patients with cholestatic liver disease. Some patients exhibit skin xanthomas and severe hyperlipidemia.

Objective: We investigated whether Lp-X induces foam cell formation in human-derived macrophages.

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Epac1 Deficiency Attenuated Vascular Smooth Muscle Cell Migration and Neointimal Formation.

Arterioscler Thromb Vasc Biol

December 2015

From the Cardiovascular Research Institute (Y.K., U.Y., C.Y., M.U., T.F., Y.I.) and Department of Immunology (D.K., T.T.), Yokohama City University, Graduate School of Medicine, Yokohama, Japan; Department of Microbiology and Immunology, Tokyo Medical and Dental University Graduate School of Health Care Sciences, Tokyo, Japan (Y.K., R.I., T.K.); Department of Physiology, Tsurumi University School of Dental Medicine, Yokohama, Japan (S.O.); and Department of Cardiovascular Medicine, Institute of Health Biosciences, The University of Tokushima Graduate School, Tokushima, Japan (M.S.).

Objective: Vascular smooth muscle cell (SMC) migration causes neointima, which is related to vascular remodeling after mechanical injury and atherosclerosis development. We previously reported that an exchange protein activated by cAMP (Epac) 1 was upregulated in mouse arterial neointima and promoted SMC migration. In this study, we examined the molecular mechanisms of Epac1-induced SMC migration and the effect of Epac1 deficiency on vascular remodeling in vivo.

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Background: β2-glycoprotein I (β2GPI)-dependent antiphospholipid antibodies (aPLs) are considered to play a pivotal pathogenic role in antiphospholipid syndrome (APS) by inducing the expression of tissue factor, inflammatory cytokines, and chemokines, most of which are dependent upon the NF-κB pathway. Therefore, the NF-κB is regarded as a promising target for the development of a novel therapeutic strategy. However, progress has been limited owing to the fact that there are no widely-used in vivo models, or highly specific inhibitors.

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Objectives: Cryopyrin-associated periodic syndrome (CAPS) is caused by unrestricted IL-1β release due to mutation of the gene coding NLRP3. This study aimed to clarify whether NLRP3-related IL-1β release is dependent on the NF-κB pathway.

Methods: Peripheral blood mononuclear cells (PBMCs) from healthy subjects or patients with Muckle-Wells syndrome were primed with LPS and subsequently stimulated by ATP.

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Among the heterogeneous antiphospholipid antibodies, many studies suggest that those directed to beta2-glycoprotein I (beta2GPI) are the major pathogenic antibodies in antiphospholipid syndrome (APS). They have been shown to activate the coagulation pathway via several mechanisms, activate platelets via thrombin formation, and suppress fibrinolysis. Additionally, we propose another possible mechanism that involves certain chemokines and results in platelet activation.

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