An Energy-Efficient Elevator Operating System that Considers Sensor Information and Electricity Price Changes in Smart Green Buildings

In modern smart buildings, the energy consumption of a building is monitored every time. Smart buildings are also equipped with sensors that can collect various physical data such as temperature, motion, and light. In this paper, we use smart sensor technologies in the design of an efficient elevator operating system (EOS). Specifically, multiple sensor devices are used together to detect elevator passengers’ behavior before they arrive at the elevator door and press the elevator call button. The detected information is then delivered to EOS through building networks and the scheduling system utilizes this information for the efficient control of the elevator cars. Specifically, when the number of passengers becomes large, EOS increases the number of working elevator cars to reduce the waiting time of passengers. In contrast, when the elevator traffic lessens, EOS reduces the number of working elevator cars in order to save the energy consumption. Experimental results with a wide range of configurations show that our EOS outperforms the conventional elevator scheduling system that does not consider sensor information or electricity price changes

Double-stranded RNA induces inflammatory gene expression in schwann cells: Implication in the Wallerian degeneration

Schwann cells play an important role in peripheral nerve regeneration. Upon neuronal injury, activated Schwann cells clean up the myelin debris by phagocytosis, and promote neuronal survival and axon outgrowth by secreting various neurotrophic factors. However, it is unclear how the nerve injury induces Schwann cell activation. Recently, it was reported that certain cytoplasmic molecules, which are secreted by cells undergoing necrotic cell death, induce immune cell activation via the toll-like receptors (TLRs). This suggests that the TLRs expressed on Schwann cells may recognize nerve damage by binding to the endogenous ligands secreted by the damaged nerve, thereby inducing Schwann cell activation. Accordingly, this study was undertaken to examine the expression and the function of the TLRs on primary Schwann cells and iSC, a rat Schwann cell line. The transcripts of TLR2, 3, 4, and 9 were detected on the primary Schwann cells as well as on iSC. The stimulation of iSC with poly (I：C), a synthetic ligand for the TLR3, induced the expression of TNF-α and RANTES. In addition, poly (I：C) stimulation induced the iNOS expression and nitric oxide secretion in iSC. These results suggest that the TLRs may be involved in the inflammatory activation of Schwann cells, which is observed during Wallerian degeneration after a peripheral nerve injury.This work was supported by the Korea Research Foundation Grant (KRF-2003-003-E00178)

An Exploration of Robot-Mediated Tai Chi Exercise for Older Adults

In this fast-aging society, many older adults fail to meet the required level of exercise due to trainer shortages. Therefore, we developed a robot tutor to investigate the feasibility of robot-mediated exercise for older adults. Twenty older adults participated in an experimental study. A pre-exercise survey was used to assess their background. Each participant experienced a 30-min robot-led Tai Chi exercise followed by a post-exercise survey to evaluate the easiness of following the robot and expectations for future robot design. Participants’ Tai Chi performances were evaluated in terms of completion and accuracy. Associations between the surveys and the performance were also analyzed. All participants completed the study. Fifteen out of the twenty subjects had at least one chronic condition, and most practiced Tai Chi before the study but had never interacted with a robot. On average, the participants scored 93.09 and 85.21 out of 100 for movement completion and accuracy, respectively. Their initial movement accuracy was correlated with their attitude towards exercise. Most subjects reported that they could follow the robot’s movements and speeches well and were interested in using a robot tutor in the community. The study demonstrated the initial feasibility of robot-led Tai Chi exercise for older adults

Necrotic neuronal cells induce inflammatory Schwann cell activation via TLR2 and TLR3: Implication in Wallerian degeneration

Schwann cells play an important role in peripheral nerve regeneration. Upon nerve injury, Schwann cells are activated and produce various proinflammatory cytokines and chemokines, resulting in the recruitment of macrophages and the phagocytosis of myelin debris. However, it is unclear how nerve injury induces Schwann cell activation. Recently, it was reported that necrotic cells induce immune cell activation via toll-like receptors (TLRs). This suggests that the TLRs expressed on Schwann cells may recognize nerve injury by binding to the endogenous ligands secreted by the damaged nerve, thereby inducing Schwann cell activation. To explore such a possibility, we stimulated rat Schwann cells with necrotic neuronal cells (NNC). The stimulation of Schwann cells with NNC induced the expression of various inflammatory mediators, including TNF-α and iNOS. Studies on the NNC-mediated intracellular signaling pathways revealed that p38 and JNK are involved in the NNC-mediated Schwann cell activation. In addition, NNC-induced proinflammatory gene expression was reduced in mouse Schwann cells derived from TLR2 or TLR3 knockout mice. In summary, these results suggest that necrotic neuronal cells induce inflammatory Schwann cell activation via TLR2 and TLR3, which might be involved in Wallerian degeneration upon peripheral nerve injury

IKKβ-mediated inflammatory myeloid cell activation exacerbates experimental autoimmune encephalomyelitis by potentiating Th1/Th17 cell activation and compromising blood brain barrier

Background The inflammatory myeloid cell activation is one of the hallmarks of experimental autoimmune encephalomyelitis (EAE), yet the in vivo role of the inflammatory myeloid cell activation in EAE has not been clearly resolved. It is well-known that IKK/NF-κB is a key signaling pathway that regulates inflammatory myeloid activation. Methods We investigated the in vivo role of inflammatory myeloid cell activation in myelin oligodendrocyte glycoprotein (MOG) peptides-induced EAE using myeloid cell type-specific ikkβ gene conditional knockout-mice (LysM-Cre/IkkβF/F). Results In our study, LysM-Cre/IkkβF/F mice had alleviated clinical signs of EAE corresponding to the decreased spinal demyelination, microglial activation, and immune cell infiltration in the spinal cord, compared to the wild-type mice (WT, IkkβF/F). Myeloid ikkβ gene deletion significantly reduced the percentage of CD4+/IFN-γ+ (Th1) and CD4+/IL-17+ (Th17) cells but increased the percentages of CD4+/CD25+/Foxp3+ (Treg) cells in the spinal cord and lymph nodes, corresponding to the altered mRNA expression of IFN-γ, IL-17, IL-23, and Foxp3 in the spinal cords of LysM-Cre/IkkβF/F EAE mice. Also, the beneficial effect of myeloid IKKβ deletion in EAE corresponded to the decreased permeability of the blood brain barrier (BBB). Conclusions Our findings strongly suggest that IKK/NF-kB-induced myeloid cell activation exacerbates EAE by activating Th1 and Th17 responses and compromising the BBB. The development of NF-κB inhibitory agents with high efficacy through specific targeting of IKKβ in myeloid cells might be of therapeutic potential in MS and other autoimmune disorders

Highly Pathogenic Avian Influenza A(H5N6) in Domestic Cats, South Korea

In December 2016, highly pathogenic avian influenza (HPAI) infection with systemic pathologic lesions was found in cats in South Korea. Genetic analyses indicated that the feline isolates were similar to HPAI H5N6 viruses isolated in chicken farms nearby. This finding highlights the need for monitoring of domestic mammals during HPAI outbreaks

Double-stranded RNA induces iNOS gene expression in Schwann cells, sensory neuronal death, and peripheral nerve demyelination

Inflammation in the peripheral nervous system (PNS) is one of the characteristics of virus-induced peripheral neuropathy. In this inflammatory response, Schwann cells are actively involved. Previously, toll-like receptor 3 (TLR3) was reported as a receptor for double-stranded RNA (dsRNA) that induces antiviral and inflammatory responses in cells of the innate immune system. In this study, we investigated the expression and putative role of TLR3 in Schwann cells. TLR3 was constitutively expressed in Schwann cells. Stimulation with polyinosinic-polycytidylic acid, a synthetic dsRNA analogue, induced the expression of inducible nitric oxide synthase (iNOS) gene in Schwann cells. Studies on the intracellular signal transduction pathways using iSC, an immortalized Schwann cell line, revealed that dsRNA induces the activation of NF-B, p38, and c-Jun N-terminal kinase (JNK). The activation of NF-B, p38, JNK, and dsRNA-dependent protein kinase is required for dsRNA-mediated iNOS gene expression. However, the activation of PI3 kinase and GSK-3 inhibited iNOS gene induction, a process mediated by their inhibitory effects on NF-B and p38 activation. dsRNA-induced NO production caused neuronal cell death in cultured dorsal root ganglion. Finally, the introduction of dsRNA into the rat sciatic nerve induced iNOS gene expression and peripheral nerve demyelination in vivo. Taken together, these data suggest that viral RNA may induce inflammatory Schwann cell activation via TLR3 and peripheral nerve damage in the PNS.Korea Research Foundation; Grant Number: KRF-2005-070-C00096 Korea Ministry of Science and Technology, Republic of Korea; Grant Number: M10412000014-06N1200-0141

Pathogenicity and Pathological Characteristics of African Swine Fever Virus Strains from Pig Farms in South Korea from 2022 to January 2023

Since the first African swine fever (ASF) outbreak occurred at a pig farm in South Korea in September 2019, as of 31 January 2023, 31 ASF cases have occurred at pig farms, while 2799 ASF virus (ASFV)-infected wild boars have been identified. The circulation of ASFV in wild boar populations poses a high risk of spillover to pig farms in the country. However, information on the changes in the pathogenicity of Korean ASFV strains from wild boars is not available. Investigating the pathogenicity of ASFV strains from pig farms is the only way to predict their alterations. In a previous study, no changes in the pathogenicity of ASFV strains circulating during 2019–2021 were identified through animal experiments. In this study, we chose two ASFV strains with potentially reduced pathogenicity among ten viruses obtained from pig premises from 2022 to January 2023 and estimated their pathogenicities and pathological characteristics. All the inoculated pigs died 8–10 days post–inoculation after showing pyrexia, depression, anorexia, and recumbency together with the common pathological lesions of enlarged hemorrhagic lymph nodes and splenomegaly with infarction. These results support that the pathogenicity among ASFV isolates in South Korea still remained unchanged during the study period