Modeling Reminder System for Dementia by Reinforcement Learning

Prospective memory refers to preparing, remembering and recalling plans that have been conceived in an intended manner. Various busyness and distractions can make people forget the activities that must be done the next time, especially for people with cognitive memory problems such as dementia. In this paper, we propose a reminder system with the idea of taking time and response into consideration to assist in remembering activities. Using the reinforcement learning method, this idea predicts the right time to remind users through notifications on smartphones. The notification delivery time will be adjusted to the user’s response history, which becomes feedback at any available time. Thus, users will get notifications based on the ideal time for each individual either, either with repetition or without repetition, so as not to miss the planned activity. By evaluating the dataset, the results show that our proposed modelling is able to optimize the time to send notifications. The eight alternative times to send notifications can be optimized to get the best time to notify the user with dementia. This implies that our algorithm propose can adjust to individual personality characteristics, which might be a stumbling block in dementia patient care, and solve multi-routine plan problems. Our propose can be useful for users with dementia because we can remind very well that the execution time of notifications is right on target, so it can prevent users with dementia from stressing out over a lot of notifications, but those who miss notifications can receive them back at a later time step, with the result that information on activities to be completed is still available.3rd International Conference on Activity and Behavior Computing, ABC 2021, 22 October 2021 through 23 October 2021, Onlinejournal articl

Production of Prompt Charmonia in e+e- Annihilation at sqrt[s] ≈ 10.6 GeV

journal articl

21セイキ ノ トショカンゾウ オ カタル

video/mp4vide

特集2 : 研究解説 : シアル酸とその誘導体

最近その生理作用から注員されているシアル酸の工業的利用の目的で、これまでに行われているシアル酸の化学変換による誘導体について概観し、我々が行っているシアリルリン脂質の合成について述べる。シアリルリン脂質はホスファチジルコリンのリポソームに組み込まれ、シアル酸残基を表面にもつリポソームが合成された小特集　バイオテクノロジーdepartmental bulletin pape

sj-docx-1-car-10.1177_19476035221074009 – Supplemental material for Automatic Detection of Medial and Lateral Compartments from Histological Sections of Mouse Knee Joints Using the Single-Shot Multibox Detector Algorithm

Supplemental material, sj-docx-1-car-10.1177_19476035221074009 for Automatic Detection of Medial and Lateral Compartments from Histological Sections of Mouse Knee Joints Using the Single-Shot Multibox Detector Algorithm by Yoshifumi Mori, Takeshi Oichi, Motomi Enomoto-Iwamoto and Taku Saito in CARTILAGE</p

SOX10 and S100B in Schwann cells

<p>Figure 1. Expression pattern of Sox10 and other differentiation markers in Schwann cells. (A and B) Comparison of expression level between Sox10 and Sox9 in primary rat sciatic nerve Schwann cells and primary rat rib chondrocytes. (C) Time course of mRNA levels of Schwann cell differentiation markers determined by real-time RT-PCR analysis during rat perinatal stages.</p> <p>Figure 2. Modulation of S100B expression by SOX10 in Schwann cells. (A) mRNA levels of Sox10 (top) and S100b (bottom) in stable lines of primary rat Schwann cells retrovirally transfected with SOX10 or control GFP. (B) Protein level of S100B and Sox10 in stable lines of primary rat Schwann cells retrovirally transfected with SOX10 or control GFP. (C) Modulation of S100b expression by SOX10 in ROS cells. mRNA levels of Sox10 (top) and S100b (bottom) in stable lines of rat non-neurogenic ROS cells retrovirally transfected with SOX10 or control GFP.</p> <p>Figure 3. Suppression of S100B and Mpz expression by SOX10 insufficiency in Schwann cells. (A) mRNA levels of Sox10 (top), S100b (middle) and Mpz (bottom) in stable lines of primary rat Schwann cells retrovirally transfected with shRNA specific for Sox10 or GFP. (B) Protein levels of SOX10 and S100B in stable lines of primary rat Schwann cells retrovirally transfected with shRNA specific for SOX10 or control GFP.</p> <p>Figure 4. Identification of putative SOX10-response elements in S100B. (A) Luciferase activities after transfection of putative Schwann cell-related transcription factors into HeLa cells with a reporter construct containing a fragment (−1,000 to +200 bp) of the S100B gene. (B) Deletion analysis using luciferase-reporter constructs containing a series of deletion fragments of the S100B gene in HeLa cells transfected with SOX10 or control GFP. (C) Comparison of human (Hs), rat (Rn), and mouse (Mm) sequences in three putative SOX motifs in the S100B promoter and mutated sequences (Mut A, Mut B, and Mut C), used in the following mutagenesis analysis. (D) Site-directed mutagenesis analysis using luciferase-reporter constructs containing –334 to +200 bp of the S100B gene with mutations as in Figure 3C within the three SOX motifs in the cells above.</p> <p>Figure 5. Identification of putative response elements in S100B intron 1 by SOX10 and direct binding of SOX10 to the response elements. (A) Comparison of human (Hs), rat (Rn) and mouse (Mm) sequences in the putative SOX motif of the S100B intron 1 and mutated sequence (Mut D), used in the following mutagenesis analysis. (B) Deletion and site-directed mutagenesis analysis using luciferase-reporter constructs containing –334 to +200 bp of the S100B gene in HeLa cells transfected with SOX10 or control GFP. (C) ChIP assay performed using cell lysates of Schwann cells that were amplified by a primer set spanning the identified regions; sites A & B (top), site A (second row), site B (third row), and site D (fourth row), or not spanning the region (bottom) before (input) and after immunoprecipitation with antibodies to Sox10 (a-Sox10) or non-immune IgG (IgG). Genomic DNA was amplified as a positive control.</p> <p>Figure 6. Suppressed Schwann cell proliferation by SOX10-S100B signaling. Comparison of Sox10 and S100b mRNA levels between conditions of proliferation and differentiation in rat sciatic nerve Schwann cells.</p> <p>Figure 7. Enhanced proliferation by knockdown of Sox10 or S100b in Schwann cells. (A, B) BrdU labeling of stable lines of Schwann cells retrovirally transfected with SOX10 or shRNA specific for SOX10 and GFP (A). Ratio of BrdU-positive cells to total cells was quantified after 3 d culture of stable lines of Schwann cells transfected with Sox10 expressing vector, shRNA vector specific for Sox10, and control GFP vector (B). (C) Growth curves using the CCK-8 assay of stable lines of Schwann cells retrovirally transfected with sh-Sox10 or control GFP. (D, E) BrdU labeling of stable lines of Schwann cells retrovirally transfected with S100b or shRNA specific for S100b and GFP (D). Ratio of BrdU-positive cells to total cells were quantified after 3-day-old cultures of stable lines of Schwann cells were transfected with S100b expressing vector, shRNA vector specific for S100b, and control GFP vector (E).</p> <p>Figure 8. Enhanced proliferation by knockdown of S100b or Sox10 in C3H10T1/2 cells. (A) mRNA levels of S100b determined by real-time RT-PCR in stable lines of mouse mesenchymal C3H10T1/2 cells retrovirally transfected with S100b, shRNA for S100b, or control GFP. (B) mRNA levels of Sox10 determined by real-time RT-PCR in stable lines of mouse mesenchymal C3H10T1/2 cells retrovirally transfected with Sox10, shRNA for Sox10, or control GFP. (C and D) Growth curves using the CCK-8 assay of stable lines of C3H10T1/2 cells as mentioned above.</p> <p>Figure 9. Impaired myelination by knockdown of S100b. (A) Immunocytochemistry of neurons and stable lines of Schwann cells retrovirally transfected with shRNA specific for S100b or control GFP in DRG dissociated cultures. Staining of Tuj1 (red), MBP (green) and Hoechst (blue) in neurons, Schwann cells, and nuclei, respectively. (B) The number of MBP-positive Schwann cells in a high-power field of the immunocytochemistry as in Figure 9A.</p

Additional file 2 of Enhancement of chondrogenic differentiation supplemented by a novel small compound for chondrocyte-based tissue engineering

Additional file 2: Supplemental Table 2. Taqman assay list

Additional file 3 of Enhancement of chondrogenic differentiation supplemented by a novel small compound for chondrocyte-based tissue engineering

Additional file 3

Histological analyses of <i>Zfp449</i> knockout mice.

<p>(A) Safranin-O staining and immunofluorescence of Sox9, Sox6, Col2a1 and Zfp449 in proximal tibia of <i>Zfp449</i> null (−/−) and WT littermate embryos (+/+) (E18.5). Enlarged immunofluorescence figures on the left are from the areas indicated in the yellow inset box on Safranin-O staining. The further magnified views on the right are from the areas indicated in the blue inset boxes. Scale bars, 100 µm (Safranin-O stainings and immunofluorescence images), 10 µm (maginified views of immunofluorescence). (B) mRNA levels of <i>Sox9</i>, <i>Sox6</i>, <i>Col2a1</i> and <i>Zfp449</i> in primary chondrocytes from <i>Zfp449</i> null and WT littermate mice (6 d). Data are expressed as means (bars) ± SDs (error bars) for three wells/group. ^#<i>P</i><0.01 versus WT. (C) Safranin-O staining of knee joints in <i>Zfp449</i> null mice and WT littermates 8 weeks after the surgical induction of OA. Scale bars, 100 µm. (D) Safranin-O staining of knee joints in 17-month-old <i>Zfp449</i> null mice and WT littermates. Scale bars, 100 µm. (E) Immunofluorescence of GFP and Zfp449 in elbow joints of <i>Zfp449</i> heterozygous mutant. Scale bars, 200 µm.</p

Additional file 1 of Enhancement of chondrogenic differentiation supplemented by a novel small compound for chondrocyte-based tissue engineering

Additional file 1: Supplemental Table 1. Group list