Inhibition of SOD1 trimerization is a novel drug target for ALS disease.

Background: Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease that begins with motor neuron death in the spinal cord and cerebral cortex, ultimately resulting in death from respiratory distress (breathing failure). About 90% of ALS cases are sporadic, and 10% of ALS cases are of the inherited type with a genetic cause. About 150 different gene mutations have been reported so far.

Therapeutic effect of novel drug candidate, PRG-N-01, on NF2 syndrome-related tumor.

Background: NF2-related schwannomatosis (NF2-SWN) is associated with multiple benign tumors in the nervous system. NF2-SWN, caused by mutations in the NF2 gene, has developed into intracranial and spinal schwannomas. Because of the high surgical risk and frequent recurrence of multiple tumors, targeted therapy is necessary.

Progerin, an Aberrant Spliced Form of Lamin A, Is a Potential Therapeutic Target for HGPS.

Hutchinson-Gilford progeria syndrome (HGPS) is an extremely rare genetic disorder caused by the mutant protein progerin, which is expressed by the abnormal splicing of the gene. HGPS affects systemic levels, with the exception of cognition or brain development, in children, showing that cellular aging can occur in the short term. Studying progeria could be useful in unraveling the causes of human aging (as well as fatal age-related disorders).

Dysfunction in parkin aggravates inflammatory bone erosion by reinforcing osteoclast activity.

Background: Parkin dysfunction associated with the progression of parkinsonism contributes to a progressive systemic skeletal disease characterized by low bone mineral density. However, the role of parkin in bone remodeling has not yet been elucidated in detail.

Result: We observed that decreased parkin in monocytes is linked to osteoclastic bone-resorbing activity.

Inflammatory conversion of quiescent osteoblasts by metastatic breast cancer cells through pERK1/2 aggravates cancer-induced bone destruction.

Disruption of bone homeostasis caused by metastatic osteolytic breast cancer cells increases inflammatory osteolysis and decreases bone formation, thereby predisposing patients to pathological fracture and cancer growth. Alteration of osteoblast function induces skeletal diseases due to the disruption of bone homeostasis. We observed increased activation of pERK1/2 in osteolytic breast cancer cells and osteoblasts in human pathological specimens with aggressive osteolytic breast cancer metastases.

Artificial neural network estimation of data and channel characteristics in free-space ultraviolet communications.

In this paper, we develop an artificial neural network (ANN)-based algorithm for signal classification, i.e., data demodulation, and the estimation of channel characteristics, such as channel DC gain and turbulence distribution parameters, in free-space ultraviolet (UV) communication systems.

Systemic Parathyroid Hormone Enhances Fracture Healing in Multiple Murine Models of Type 2 Diabetes Mellitus.

Type 2 diabetes mellitus (T2DM) is a multisystemic disease that afflicts more than 415 million people globally-the incidence and prevalence of T2DM continues to rise. It is well-known that T2DM has detrimental effects on bone quality that increase skeletal fragility, which predisposes subjects to an increased risk of fracture and fracture healing that results in non- or malunion. Diabetics have been found to have perturbations in metabolism, hormone production, and calcium homeostasis-particularly PTH expression-that contribute to the increased risk of fracture and decreased fracture healing.

Optical extra-body communication using smartphone cameras for human vital sign transmission.

This paper presents an optical extra-body communication (OEBC) for the transmission of human vital signs in an optical camera communication link. The primary vital signs, such as pulse rate, respiratory rate, body temperature, blood pressure, and peripheral capillary oxygen saturation, are captured from the patient's body. The proposed OEBC system has body sensors installed on various parts of the body for detecting, processing, and communicating the vital sign data.

Patient Mobility Support for Indoor Non-Directed Optical Body Area Networks.

In this paper, a patient mobility support scheme for indoor non-directed optical body area networks (OBAN) is presented. The OBAN is an optical healthcare system where medical sensors are installed on various parts of the patient's body and are connected to an optical coordinator for transmitting the physiological signals via optical wireless links. In the proposed scheme, a white light-emitting diode (LED) was employed as the optical coordinator that was mounted on the patient body, while a photodetector (PD) was used as the receiver installed at the ceiling.

Suppression of Syk activation by resveratrol inhibits MSU crystal-induced inflammation in human monocytes.

Monosodium urate (MSU) crystals are an endogenous sterile particulate that has been identified as a potent damage-associated molecular pattern (DAMP). In humans, the induction of IL-1β production through MSU-induced NLRP3 inflammasome activation in monocytes/macrophages is responsible for pathogenesis of gouty arthritis. It was recently reported that in a murine model of this disease, resveratrol decreases MSU-induced recurrent attacks of gouty arthritis.

Experimental demonstration of indoor uplink near-infrared LED camera communication.

In this paper, we present experimental demonstration of an indoor uplink near-infrared LED camera communication (ICC) that employs near-infrared (IR) light as a communication medium and a camera as the receiver. The proposed ICC exploits advantages of the camera receiver to provide wider coverage and accurate indoor positioning in IR communications. Since near-IR light is the communication medium, ICC can safely increase the light intensity compared with other visible light based wireless communication schemes.

Interleukin-32 Gamma Stimulates Bone Formation by Increasing miR-29a in Osteoblastic Cells and Prevents the Development of Osteoporosis.

Interleukin-32 gamma (IL-32γ) is a recently discovered cytokine that is elevated in inflamed tissues and contributes to pathogenic features of bone in human inflammatory rheumatic diseases. Nevertheless, the role of IL-32γ and its direct involvement in bone metabolism is unclear. We investigated the molecular mechanism of IL-32γ in bone remodeling and the hypothetical correlation between IL-32γ and disease activity in osteoporosis patients.

Monosodium urate crystal-induced pro-interleukin-1β production is post-transcriptionally regulated via the p38 signaling pathway in human monocytes.

IL-1β is a key mediator of sterile inflammation in response to endogenous particulates, a type of damage-associated molecular pattern (DAMPs) molecule derived from damaged cells. Despite the well-known role of sterile particulates such as monosodium urate (MSU) crystals as inflammasome inducers in monocytes/macrophages, little is known regarding how pro-IL-1β synthesis is induced under sterile inflammatory conditions. We provide evidence that MSU crystals post-transcriptionally induce the rapid production of pro-IL-1β in human primary monocytes.

Experimental demonstration of highway I2V using visible light communications.

A visible light communication (VLC)-based intelligent transportation system (ITS) has drawn much interest from telematics and automobile industries due to its enhanced safety and cost effectiveness. Within the framework of ITS, vehicle-to-vehicle and infrastructure-to-vehicle (I2V) communications have largely been considered. I2V can be viewed as an important ITS technology that broadcasts traffic information from fixed traffic infrastructure.

Preferential Induction of the T Cell Auxiliary Signaling Molecule B7-H3 on Synovial Monocytes in Rheumatoid Arthritis.

B7-H3, a newly identified B7 family member, has functional duality as a co-stimulator and co-inhibitor that fine-tunes T cell-mediated immune responses. Given that B7-H3 expression on human monocytes and dendritic cells is enhanced by inflammatory cytokines, its potential inmmunoregulatory role at sites of inflammation has been suggested. Further, monocytes play crucial roles in the pathophysiology of various inflammatory disorders including autoimmune diseases; however, the immunological role of B7-H3 in rheumatoid arthritis (RA) has not been defined.

Optical bidirectional beacon based visible light communications.

In an indoor bidirectional visible light communications (VLC), a line-of-sight (LOS) transmission plays a major role in obtaining adequate performance of a VLC system. Signals are often obstructed in the LOS transmission path, causing an effect called optical shadowing. In the absence of LOS, the performance of the VLC system degrades significantly and, in particular, at uplink transmission this degradation becomes severe due to design constraints and limited power at uplink devices.

Visible light communication based motion detection.

In this paper, a unique and novel visible light communication based motion detection is presented. The proposed motion detection is performed based on white light LEDs and an array of photodetectors from existing visible light communication (VLC) links, thus providing VLC with three functionalities of illumination, communication and motion detection. The motion is detected by observing the pattern created by intentional obstruction of the VLC link.

Smart LED allocation scheme for efficient multiuser visible light communication networks.

In a multiuser bidirectional visible light communication (VLC), a large number of LEDs or an LED array needs to be allocated in an efficient manner to ensure sustainable data rate and link quality. Moreover, in order to support an increasing or decreasing number of users in the network, the LED allocation is required to be performed dynamically. In this paper, a novel smart LED allocation scheme for efficient multiuser VLC networks is presented.

Functional phenotype of synovial monocytes modulating inflammatory T-cell responses in rheumatoid arthritis (RA).

Monocytes function as crucial innate effectors in the pathogenesis of chronic inflammatory diseases, including autoimmunity, as well as in the inflammatory response against infectious pathogens. Human monocytes are heterogeneous and can be classified into three distinct subsets based on CD14 and CD16 expression. Although accumulating evidence suggests distinct functions of monocyte subsets in inflammatory conditions, their pathogenic roles in autoimmune diseases remain unclear.

Interleukin-1β promotes the LC3-mediated secretory function of osteoclast precursors by stimulating the Ca²⁺-dependent activation of ERK.

Bone resorption by osteoclasts requires the release of secretory lysosomes containing cathepsin K, which degrades the organic bone matrix. The activity of this secretory function is determined by the level of lipidation of microtubule-associated protein 1 light chain 3 (LC3). Although the inflammatory cytokine IL-1β increases osteoclast activity, the underlying mechanism(s) remains undefined.

Beclin-1 is required for RANKL-induced osteoclast differentiation.

Beclin-1 plays a critical role in autophagy; however, it also contributes to other biological processes in a non-autophagic manner. Although studies have examined the non-autophagic role of autophagy proteins in the secretory function of osteoclasts (OC), the role of Beclin-1 is unclear. Here, we examined the role of Beclin-1 in OC differentiation, and found that mouse bone marrow macrophages (BMMs) showed increased expression of Beclin-1 upon RANKL stimulation in a p38- and NF-kappa B-dependent manner.

PTX3 stimulates osteoclastogenesis by increasing osteoblast RANKL production.

Pentraxin-3 (PTX3), also known as tumor necrosis factor-stimulated gene 14 (TSG-14), is produced by immune and vascular cells in response to pro-inflammatory signals and is therefore a multipotent inflammatory mediator. The present study showed that during human osteoblast (OB) differentiation, precursor OBs (pOBs), but not mature OB, highly expressed PTX3. TNFα treatment elevated the PTX3 expression of pOBs.