手部の重心補正に基づく手洗い支援システム

Aiming at solving the problem of recognition accuracy decrease during hand-washing in existing systems due to noise produced by hand-shaking, lighting changes, and so on, we develop a novel system. The system focuses on proper hand-washing patterns to examine whether hands are being washed correctly. By comparing videos of hand-washing captured at sinks and learning model videos, the system informs users in real time whether they are using proper hand-washing patterns. Optical flows and skin-color areas are used as data features to recognize proper hand-washing patterns. Support vector machine is used as the recognition model in this system. The hand-washing pattern recognition accuracy is improved by removing noise sources and capturing pattern characteristics by labeling and using a correction that considers the center of gravity in hand

Angiotensin-Converting-Enzyme Inhibitor, Lisinopril, Reduces Lipopolysaccharide-Induced Expression of Splenic Interleukin-6 mRNA in Dehydrated Rats

Angiotensin II (ANG II) has been shown to have proinflammatory properties. To investigate whether ANG II is involved in the lipopolysaccharide (LPS)-induced production of a pyrogenic/proinflammatory cytokine, interleukin-6 (IL-6), we examined the effects of an angiotensin-converting-enzyme (ACE) inhibitor, lisinopril, on LPS-induced fever and on the expression of IL-6 mRNA in the spleen of dehydrated rats (in which the secretion of ANG II increases). The results showed that the ACE inhibitor significantly inhibited LPS-induced fever as well as the splenic expression of IL-6 mRNA in dehydrated rats. It is suggested that endogenous ANG II may be involved in the production of IL-6 that occurs in response to LPS, and thereby contribute to the LPS-induced febrile response in dehydrated rats

High Level Estradiol Induces EBV Reactivation and EBV gp350/220(+)CD138(+) Double-positive B Cell Population in Graves’ Disease Patients and Healthy Controls

Graves’ disease occurs predominantly in women. Epstein-Barr virus (EBV) mainly persists in human B lymphocytes, and its reactivation stimulates antibody production. We previously suggested that the EBV reactivation-induced production of TRAb and IgM at 100 nM estradiol (pregnant level) was lower than that at 0 nM estradiol and that class switch recombination may be increased by estradiol. In this study, we examined the effect of estradiol on EBV reactivation. We identified the expression of EBV-glycoprotein 350/220 (gp350/220) in the late phase of reactivation and plasma cell differentiation of EBV-infected cells using 72A1 antibody and CD138 antibody, respectively. We found the mean ratio of gp 350/220(+) CD138(+) cells at 100 nM estradiol was higher than that at 0 nM estradiol. These results suggested that EBV-infected cells could survive with keeping the ability of antibody production in 100 nM estradiol, which is consistent with the improvement of Graves’ disease during maternity and exacerbation postpartum

Low-dose Warfarin Functions as an Immunomodulator to Prevent Cyclophosphamide-induced NOD Diabetes

Warfarin has been used as an anticoagulant for a long time. Recently, the pleiotropic effect of warfarin has been investigated. As low-dose warfarin has been reported to have anti-inflammatory effect through suppression of IL-6 secretion and inhibit the immune-associated signal between Tyro3 and its ligand, Gas6, the effect of low-dose warfarin on autoimmune diabetes in NOD mice was examined. To investigate the anti-inflammatory effect of warfarin, IL-6 secretion by splenocytes was examined in the presence of various concentrations of warfarin. Low concentration of warfarin inhibited IL-6 secretion. mRNA expression of Rse, one of the Tyro3 receptor family members, and Gas6 were analyzed in NOD mice. It was detected in islets, splenocytes and bone-marrow derived dendritic cells. 0.25 mg/l or 0.50 mg/l of warfarin was orally administered to NOD mice as a cyclophosphamide-induced diabetes model. Oral administration of warfarin at much lower doses than those clinically used as an anticoagulant significantly reduced the degree of insulitis and diabetes incidence in this model. We previously demonstrated that anti-FasL Ab-treatment led to complete prevention of autoimmune diabetes in NOD mice. As Fas/FasL signaling is reported to be essential for cyclophosphamide-induced diabetes model, we extracted RNA from lymphocytes of the inguinal lymph nodes of anti-FasL Ab-treated NOD mice and performed real-time PCR to determine expression of Rse gene. Interestingly, the expression of Rse gene related to the blockade of Fas/FasL signaling was reduced to less than half the level of untreated mice. In conclusion, low-dose warfarin is a potential immunomodulator which can prevent autoimmune diabetes. Type 1 diabetes is a chronic autoimmune disease caused by autoreactive T cells promoting the specific destruction of insulin-producing β cells of the pancreatic islets (1,6). Nonobese diabetic (NOD) mouse is an animal model of human autoimmune diabetes (19). In the NOD mouse, diabetes develops as the result of a chronic inflammation that starts with leukocytic infiltration of islets from 3-5 weeks of age and gradually exacerbates until hyperglycemia develops after 16 weeks of age in a high percentage of female mice. Warfarin has been widely used for a long time as an oral anticoagulant agent. In addition, Kater et al. reported the pleiotropic effect of low-dose warfarin related with inflammation, demonstrating that low-dose warfarin inhibited inflammatory signal transduction through suppression of TNF-α induced IL-6 secretion from murine macrophages (12)

Virological characteristics of the SARS-CoV-2 Omicron BA.2.75 variant

SARS-CoV-2オミクロンBA.2.75株（通称ケンタウロス）のウイルス学的性状の解明. 京都大学プレスリリース. 2022-10-12.The SARS-CoV-2 Omicron BA.2.75 variant emerged in May 2022. BA.2.75 is a BA.2 descendant but is phylogenetically distinct from BA.5, the currently predominant BA.2 descendant. Here, we show that BA.2.75 has a greater effective reproduction number and different immunogenicity profile than BA.5. We determined the sensitivity of BA.2.75 to vaccinee and convalescent sera as well as a panel of clinically available antiviral drugs and antibodies. Antiviral drugs largely retained potency but antibody sensitivity varied depending on several key BA.2.75-specific substitutions. The BA.2.75 spike exhibited a profoundly higher affinity for its human receptor, ACE2. Additionally, the fusogenicity, growth efficiency in human alveolar epithelial cells, and intrinsic pathogenicity in hamsters of BA.2.75 were greater than those of BA.2. Our multilevel investigations suggest that BA.2.75 acquired virological properties independent of BA.5, and the potential risk of BA.2.75 to global health is greater than that of BA.5

DHMEQ, a novel NF-kappaB inhibitor, suppresses growth and type I collagen accumulation in keloid fibroblasts

Background:Keloid is a benign dermal tumor characterized by proliferation of dermal fibroblasts and overproduction of extracellular matrix (ECM). Nuclear factor kappaB (NF-κB) plays an important role in regulation of inflammation, immune response and cell proliferation. Activation of the NF-κB pathway is thought to be closely linked to abnormal cell proliferation and ECM production in keloid fibroblasts. Objective:This study was set out to investigate the effects of a novel selective NF-κB inhibitor, dehydroxymethylepoxyquinomicin (DHMEQ), on keloid fibroblasts. Methods:Primary normal and keloid dermal fibroblasts were used for this study. NF-κB activity was assessed by DNA-binding assay and immunohistochemistry. The effect of DHMEQ was evaluated by cell viability, cell growth and type I collagen accumulation. Results:Basal NF-κB activity was constitutively elevated in keloid fibroblasts, indicating that this pathway is involved in keloid pathogenesis. DHMEQ markedly reduced cell proliferation and type I collagen accumulation in keloid fibroblasts. Conclusion:The inhibition of NF-κB by DHMEQ may be an attractive therapeutic approach for keloids