Out-of-band exclusive frequency-domain MIMO equalization with the reduced-overlap-and-save method for scalable mode multiplexed signal transmission.

We present computationally-efficient implementation techniques of multiple-input multiple-output (MIMO) frequency-domain equalization (FDE) that deals with a modal dispersion effect underlying in long-haul mode-division-multiplexed (MDM) signal transmission. Computational complexity reduction comes from twofold approaches: the first is out-of-band-exclusive (OBE) FDE for removing redundant computations in MIMO-FDE processing by taking a practical signal bandwidth occupation into account. A second appoarch, referred to as overlapping-reduced (OR) FDE, further reduces the complexity by modifying an overlapping ratio in the overlap-and-save FDE method to below 0.5. We show that OBE-FDE reduces complexity for processing with a larger number of spatial channels compared with the conventional FDE, and that the overlapping ratio is minimized up to 0.25 by the OR-FDE approach. Also shown is an experimental demonstration using the results of three-mode MDM transmission with different inter-mode coupling scenarios, verifying that the complexity is decreased by up to 37 % with negligible deterioration in signal performance by using the proposed method.

Over-30-dB gain and 1-dB noise figure phase-sensitive amplification using a pump-combiner-integrated fiber I/O PPLN module.

Phase-sensitive amplifiers (PSAs) via the optical parametric amplification (OPA) process are capable of near-noiseless amplification, which can improve the performance of optical communications systems. OPA based on periodically poled lithium niobate (PPLN) waveguides is a proven means to implement a PSA with low additional nonlinear effects, such as frequency chirp, stimulated Brillouin scattering, and parametric crosstalk due to unwanted nonlinear interactions among pump and other signal waves. However, fiber compatibility is a challenge because optical coupling loss between a fiber and PPLN waveguide limits essential performance such as the gain and noise figure (NF), which makes PSAs still far from being practical. In this work, we developed a PPLN-waveguide-based pump-combiner-integrated OPA module with fiber input and output ports. With our recent development and optimization of the OPA module, we demonstrated high-performance phase-sensitive amplification with a gain of over 30 dB and an NF of 1.0 dB. In addition, we observed a 3-dB gain bandwidth of over 65 nm and flat NF characteristics in that wavelength band. The high conversion efficiency and high damage resistance of the PPLN waveguide, obtained by employing direct bonding and dry etching techniques, provide a high parametric gain. The low-loss coupling for the signal and pump between the fiber and a spot-size-converter-integrated PPLN waveguide through the dichroic beam combiner improve not only the gain but also the NF of the amplifier. Using the PSA as a preamplifier, the low-noise characteristics were confirmed by the sensitivity improvement provided by the low NF value.

MIMO carrier phase recovery for carrier-asynchronous SDM-MIMO reception based on the extended Kalman filter.

We propose a novel phase recovery scheme designed for coherent space division multiplexing (SDM) systems with independently-operated asynchronous light sources. The proposed scheme is based on the approach of the extended Kalman filter and is referred to as multiple-input multiple-output carrier phase recovery (MIMO-CPR). In the minimum mean squared error (MMSE) sense, it simultaneously and optimally obtains estimates of the multiple phase errors arising from phase-unlocked asynchronous light sources. To ensure the scheme's application for SDM fibers with a time-varying property, we also describe a modification to incorporate a MIMO equalization scheme and analyze the computational complexity. The performance of the proposed MIMO-CPR scheme is investigated through numerical simulation, which shows that it has a tolerance for the sum linewidth symbol duration product of up to 3.4 × 10-4, 1.0 × 10-4 and 2.2 × 10-5 for QPSK, 16QAM, and 64QAM signals, respectively, if 1-dB optical signal-to-noise ratio (OSNR) penalty is allowable to achieve BER of 10-3. Transmission experimental results using three spatial modes in a 51-km-long few-mode fiber (FMF) also verify the applicability of the MIMO-CPR scheme to carrier-asynchronous coherent SDM-MIMO systems.

Non-degenerate phase-sensitive amplification scheme using digital dispersion pre-equalization for unrepeated transmission.

We experimentally demonstrate an ultra-low-noise pre-amplification using a non-degenerate phase-sensitive amplifier (ND-PSA) with an optically dispersion-unmanaged link. Chromatic dispersion (CD) compensation is required for phase-sensitive amplification after fiber transmission. In the conventional transmitter configuration for ND-PSAs in which phase-conjugated light (idler light) is optically generated, it is necessary to optically compensate for the CD, for example, by using dispersion-compensating fibers. In this work, we propose an ND-PSA scheme using a digitally generated idler and CD pre-equalization by means of digital signal processing. We conduct an unrepeated transmission over a 200-km single-mode fiber with a 10-Gbaud 64QAM signal using the periodically poled LiNbO3-based PSA. The experimental results demonstrate that the proposed ND-PSA scheme provides a low-noise pre-amplification that outperforms the EDFA without optical CD compensation.

Stable deep bite correction with true mandibular incisor intrusion in a late adolescent patient with skeletal deep bite: A case report.

The treatment of skeletal deep bite does not remain stable. The patient was a Japanese woman aged 16 years and 10 months. Her chief complaint was maxillary protrusion. The degree of overjet was + 10.5 mm and overbite was + 5.0 mm; the intermolar relationship was Angle Class II. An excessive curve of Spee was observed in the mandibular arch. A hypodivergent skeletal pattern was indicated by a small mandibular plane angle and gonial angle. The maxillary incisors were proclined and the mandibular incisors were retroclined. Based on the above findings, the patient was diagnosed with Angle Class II maxillary protrusion and deep bite with hypodivergency. Both maxillary first premolars were extracted and orthodontic treatment was performed using multi-bracket appliances. A proper overbite was achieved by 5.0 mm intrusion of the mandibular incisors. The maxillary incisors were retracted by 11.2 mm and a proper overjet was achieved. Good treatment results were obtained without apical root resorption. After 2 years of retention, the occlusion has been well maintained. This report may constitute a remarkable suggestion for treatment of an unstable deep bite.

Net-400-Gbps PS-PAM transmission using integrated AMUX-MZM.

Simple high-speed optical transmission technologies are desired for use in intra-and inter-datacenter networks. In this study, we demonstrate simple single-carrier intensity-modulated direct-detection (IMDD) transmissions at a net data rate of 400 Gbps (516.7 Gbps gross) over 20 km with a compact transmitter subassembly. The subassembly consists of a 2:1 analog multiplexer (AMUX) and an InP Mach-Zehnder modulator (MZM) placed close to each other and connected via wires. We employed 162-Gbaud single-carrier probabilistically shaped pulsed amplitude modulation (PS-PAM). The baseband signals with a bandwidth of around 81 GHz to drive the MZM were generated by a super-digital-to-analog converter (super-DAC) consisting of two sub-DACs and the AMUX. Digital nonlinear pre-distortion enabled us to transmit the signals with normalized generalized mutual information (NGMI) larger than the threshold of a soft-decision forward error correction (SD-FEC) code of 0.857. Truncation of the PS-PAM symbol distribution further enhanced performance. To the best of our knowledge, this is the first net-400-Gbps single-carrier IMDD transmission using a compact transmitter subassembly.

Compression and tension variably alter Osteoprotegerin expression via miR-3198 in periodontal ligament cells.

BACKGROUND: Osteoclasts play a critical role in bone resorption due to orthodontic tooth movement (OTM). In OTM, a force is exerted on the tooth, creating compression of the periodontal ligament (PDL) on one side of the tooth, and tension on the other side. In response to these mechanical stresses, the balance of receptor activator of nuclear-factor kappa-B ligand (RANKL) and osteoprotegerin (OPG) shifts to stimulate osteoclastogenesis. However, the mechanism of OPG expression in PDL cells under different mechanical stresses remains unclear. We hypothesized that compression and tension induce different microRNA (miRNA) expression profiles, which account for the difference in OPG expression in PDL cells. To study miRNA expression profiles resulting from OTM, compression force (2 g/cm2) or tension force (15% elongation) was applied to immortalized human PDL (HPL) cells for 24 h, and miRNA extracted. The miRNA expression in each sample was analyzed using a human miRNA microarray, and the changes of miRNA expression were confirmed by real-time RT-PCR. In addition, miR-3198 mimic and inhibitor were transfected into HPL cells, and OPG expression and production assessed. RESULTS: We found that certain miRNAs were expressed differentially under compression and tension. For instance, we observed that miR-572, - 663, - 575, - 3679-5p, UL70-3p, and - 3198 were upregulated only by compression. Real-time RT-PCR confirmed that compression induced miR-3198 expression, but tension reduced it, in HPL cells. Consistent with previous reports, OPG expression was reduced by compression and induced by tension, though RANKL was induced by both compression and tension. OPG expression was upregulated by miR-3198 inhibitor, and was reduced by miR-3198 mimic, in HPL cells. We observed that miR-3198 inhibitor rescued the compression-mediated downregulation of OPG. On the other hand, miR-3198 mimic reduced OPG expression under tension. However, RANKL expression was not affected by miR-3198 inhibitor or mimic. CONCLUSIONS: We conclude that miR-3198 is upregulated by compression and is downregulated by tension, suggesting that miR-3198 downregulates OPG expression in response to mechanical stress.

Nutritional supplementation with myo-inositol in growing mice specifically augments mandibular endochondral growth.

INTRODUCTION: The purpose of this study was to examine growth-promoting effects of myo-inositol nutritional supplementation on the mandible in experimental animals. METHODS: Mice were fed on diets that contained various concentration of myo-inositol for 3 to 12 weeks. The length of the mandible, maxilla, and femur were measured on µCT images. The mandible and tibia were examined histologically and immunohistochemically. The effects of myo-inositol on cell proliferation and chondrocytic differentiation were examined using ATDC5 cells. RESULTS: Myo-inositol supplementation had no effects on body weight, length, and maxilla and femur lengths. However, the length of mandible and the thickness of the mandibular condylar cartilage (MCC) were increased by myo-inositol supplement. Microarray analysis revealed that Pik3cd was highly expressed in MCC as compared to that in the cartilage of the tibial growth plate, which was confirmed by real-time RT-PCR and immunohistochemistry. ATDC5 cells also highly expressed Pik3CD. Myoinositol induced increases in cell proliferation and chondrocytic differentiation in ATDC5 cells. The addition of a PIK3CD inhibitor blocked the induction of cell proliferation by myo-inositol in ATDC5 cells. CONCLUSIONS: Nutritional supplementation with myo-inositol in growing mice augmented mandibular endochondral growth without any systemic effects. The specific promotion of mandibular growth by myoinositol is primarily dependent on the specific intensive expression of PIK3CD in the MCC.

Orthodontic treatment of acquired open bite accompanied with extreme mesially inclined mandibular molars.

Acquired open bite mainly occurs after adolescence and is caused by a pathological or biological process. We herein report the case of an 18-year and 10-month-old Japanese woman. Her chief complaint was difficulty with mastication. Only distal cusps of first molars and second molars had contact. An angle class II molar relationship and extreme mesially inclined mandibular first molars were observed. The degree of overjet was +6.1mm and overbite was -2.0mm. There were no symptoms or abnormal findings in temporomandibular joints by radiography and magnetic resonance imaging. A skeletal class II jaw relationship was indicated. Therefore, the patient was diagnosed with a skeletal class II acquired open bite malocclusion accompanied with extreme mesial inclination of mandibular first molars. Orthodontic treatment with extraction of maxillary first premolars was performed. After stabilizing the maxillary dental arch, mandibular molars were uprighted and intruded by class III elastics. After treatment, overjet was +3.0mm and overbite was +2.3mm. Occlusal cusp-fossa relationships were established and canine relationships were class I. The lower occlusal plane and mandible were rotated counterclockwise, which helped to achieve proper overbite. After 2 years of retention, occlusion was well maintained.

Hybrid cladding-pumped multicore EDFA/Raman amplification for space division multiplexing transmission systems.

We propose and demonstrate a hybrid cladding-pumped multicore erbium-doped fiber amplifier (EDFA) and distributed Raman amplification for space division multiplexing transmission systems. The cladding-pumped multicore EDFA is used to efficiently amplify signals in multiple cores simultaneously, while Raman pumping is used to control loss in each core individually. We construct an in-line amplified 7-core transmission line, and show that distributed Raman amplification can compensate loss variation between cores. Furthermore, we transmit 46 WDM PDM-16QAM signals over a long distance of greater than 1000 km and demonstrate good transmission performance.

Dimethyl fumarate inhibits osteoclasts via attenuation of reactive oxygen species signalling by augmented antioxidation.

Bone destructive diseases are common worldwide and are caused by dysregulation of osteoclast formation and activation. During osteoclastogenesis, reactive oxygen species (ROS) play a role in the intracellular signalling triggered by receptor activator of nuclear factor-κB ligand (RANKL) stimulation. Previously, we demonstrated that induction of antioxidant enzymes by Nrf2 activation using Nrf2-gene transfer, an ETGE-peptide or polyphenols, successfully ameliorated RANKL-dependent osteoclastogenesis. Dimethyl fumarate (DMF) has been shown to activate Nrf2 signalling and has been lately used in clinical trials for neurodegenerative diseases. In this study, we hypothesized that Nrf2 activation by DMF would inhibit osteoclastogenesis and bone destruction via attenuation of intracellular ROS signalling through antioxidant mechanisms. RAW 264.7 cells were used as osteoclast progenitor cells. We found that DMF induced Nrf2 translocation to the nucleus, augmented Nrf2 promoter-luciferase reporter activity and increased antioxidant enzyme expression. Using flow cytometry, we found that DMF attenuated RANKL-mediated intracellular ROS generation, which resulted in the inhibition of RANKL-mediated osteoclastogenesis. Local DMF injection into the calvaria of male BALB/c mice resulted in attenuated bone destruction in lipopolysaccharide-treated mice. In conclusion, we demonstrated in a preclinical setting that DMF inhibited RANKL-mediated osteoclastogenesis and bone destruction via induction of Nrf2-mediated transcription of antioxidant genes and consequent decrease in intracellular ROS levels. Our results suggest that DMF may be a promising inhibitor of bone destruction in diseases like periodontitis, rheumatoid arthritis and osteoporosis.

Single Local Injection of Epigallocatechin Gallate-Modified Gelatin Attenuates Bone Resorption and Orthodontic Tooth Movement in Mice.

Osteoclastic bone resorption enables orthodontic tooth movement (OTM) in orthodontic treatment. Previously, we demonstrated that local epigallocatechin gallate (EGCG) injection successfully slowed the rate of OTM; however, repeat injections were required. In the present study, we produced a liquid form of EGCG-modified gelatin (EGCG-GL) and examined the properties of EGCG-GL with respect to prolonging EGCG release, NF-E2-related factor 2 (Nrf2) activation, osteoclastogenesis inhibition, bone destruction, and OTM. We found EGCG-GL both prolonged the release of EGCG and induced the expression of antioxidant enzyme genes, such as heme oxygenase 1 (Hmox1) and glutamate-cysteine ligase (Gclc), in the mouse macrophage cell line, RAW264.7. EGCG-GL attenuated intracellular reactive oxygen species (ROS) levels were induced by the receptor activator of nuclear factor-kB ligand (RANKL) and inhibited RANKL-mediated osteoclastogenesis in vitro. An animal model of bone destruction, induced by repeat Lipopolysaccharide (LPS)-injections into the calvaria of male BALB/c mice, revealed that a single injection of EGCG-GL on day-1 could successfully inhibit LPS-mediated bone destruction. Additionally, experimental OTM of maxillary first molars in male mice was attenuated by a single EGCG-GL injection on day-1. In conclusion, EGCG-GL prolongs the release of EGCG and inhibits osteoclastogenesis via the attenuation of intracellular ROS signaling through the increased expression of antioxidant enzymes. These results indicate EGCG-GL would be a beneficial therapeutic approach both in destructive bone disease and in controlling alveolar bone metabolism.

Possible alternative treatment for mandibular asymmetry by local unilateral IGF-1 injection into the mandibular condylar cavity: Experimental study in mice.

INTRODUCTION: The purpose of this study was to investigate whether a local unilateral IGF-1 injection into the mandibular condylar cavity can induce unilateral endochondral mandibular growth without any systemic adverse effects. METHODS: Seventy-five 3-week-old male Jcl:ICR mice were used in this study. The mice were divided into 2 groups: control group (n = 22) and IGF-1 group (n = 53). In the IGF-1 group, human IGF-1 was injected into the right mandibular condylar cavity, and phosphate-buffered saline solution was injected into the left cavity, 3 times per week for 10 weeks. RESULTS: There was no significant difference in body weight, serum human IGF-1 concentration, and soft tissue thickness of the cheeks including the masseter muscles between the 2 groups. Unilateral IGF-1 injection induced a lateral shift of the mandible to the contralateral side, and microcomputed tomogtraphy analysis showed that unilateral IGF-1 injection induced endochondral growth in the condyle. Col2, Ihh, and Runx2 were extensively upregulated by the local unilateral IGF-1 injection in real-time reverse transcription polymerase chain reaction analysis. Proliferation marker KI67, IGF-1 signaling molecule AKT1, and chondrogenic differentiation marker Col2 were strongly expressed in the IGF-1 injected condyle by immunohistochemistry. Vital labeling showed that the distance between the labels was increased in the IGF-1 injection group compared with that of the control group. CONCLUSIONS: The results verified in this study indicated that local unilateral IGF-1 injection into the mandibular condylar cavity successfully induced unilateral endochondral mandibular growth in mice without any systemic adverse effects. Thus, local unilateral IGF-1 injection into the mandibular condylar cavity could be a useful alternative for mandibular asymmetry therapy during the growth period. However, additional experimental and clinical studies will be necessary to prove the real effect of this new therapy.

Asporin stably expressed in the surface layer of mandibular condylar cartilage and augmented in the deeper layer with age.

Mandibular condylar cartilage (MCC) exhibits dual roles both articular cartilage and growth center. Of many growth factors, TGF-ß has been implicated in the growth of articular cartilage including MCC. Recently, Asporin, decoy to TGF-ß, was discovered and it blocks TGF-ß signaling. Asporin is expressed in a variety of tissues including osteoarthritic articular cartilage, though there was no report of Asporin expression in MCC. In the present study, we investigated the temporal and spatial expression of Asporin in MCC. Gene expression profile of MCC and epiphyseal cartilage in tibia of 5 weeks old ICR mice were firstly compared with microarray analysis using the laser capture microdissected samples. Variance of gene expression was further confirmed by real-time RT-PCR and immunohistochemical staining at 1,3,10, and 20 weeks old. TGF-ß and its signaling molecule, phosphorylated Smad-2/3 (p-Smad2/3), were also examined by immunohistochemical staining. Microarray analysis revealed that Asporin was highly expressed in MCC. Real-time RT-PCR analysis confirmed that the fibrous layer of MCC exhibited stable higher Asporin expression at any time points as compared to epiphyseal cartilage. This was also observed in immunohistochemical staining. Deeper layer in MCC augmented Asporin expression with age. Whereas, TGF-ß was stably highly observed in the layer. The fibrous layer of MCC exhibited weak staining of p-Smad2/3, though the proliferating layer of MCC was strongly stained as compared to epiphyseal cartilage of tibia at early time point. Consistent with the increase of Asporin expression in the deeper layer of MCC, the intensity of p-Smad-2/3 staining was decreased with age. In conclusion, we discovered that Asporin was stably expressed at the fibrous layer of MCC, which makes it possible to manage both articular cartilage and growth center at the same time.

Pathways that Regulate ROS Scavenging Enzymes, and Their Role in Defense Against Tissue Destruction in Periodontitis.

Periodontitis, an inflammatory disease that affects the tissues surrounding the teeth, is a common disease worldwide. It is caused by a dysregulation of the host inflammatory response to bacterial infection, which leads to soft and hard tissue destruction. In particular, it is the excessive inflammation in response to bacterial plaque that leads to the release of reactive oxygen species (ROS) from neutrophils, which, then play a critical role in the destruction of periodontal tissue. Generally, ROS produced from immune cells exhibit an anti-bacterial effect and play a role in host defense and immune regulation. Excessive ROS, however, can exert cytotoxic effects, cause oxidative damage to proteins, and DNA, can interfere with cell growth and cell cycle progression, and induce apoptosis of gingival fibroblasts. Collectively, these effects enable ROS to directly induce periodontal tissue damage. Some ROS also act as intracellular signaling molecules during osteoclastogenesis, and can thus also play an indirect role in bone destruction. Cells have several protective mechanisms to manage such oxidative stress, most of which involve production of cytoprotective enzymes that scavenge ROS. These enzymes are transcriptionally regulated via NRF2, Sirtuin, and FOXO. Some reports indicate an association between periodontitis and these cytoprotective enzymes' regulatory axes, with superoxide dismutase (SOD) the most extensively investigated. In this review article, we discuss the role of oxidative stress in the tissue destruction manifest in periodontitis, and the mechanisms that protect against this oxidative stress.

Proposal and experimental demonstration of SDM node enabling path assignment to arbitrary wavelengths, cores, and directions.

We propose a novel simple space division multiplexing (SDM) node which is rearrangeble nonblocking, and effectively utilizes enhanced network resources through SDM. The proposed node can reduce a number of ports of wavelength selective switches (WSSs) and a number of WSS modules by modifying conventional multi-stage switches and employing integrated multiple arrayed WSSs. We experimentally actualized the newly proposed node, and demonstrate wavelength, core, and direction switching functions based on 127-Gbps Dual Polarization Quadrature Phase Shift Keying (DP-QPSK) signals. We also confirm the feasibility of the proposed SDM node through SDM transmission experiments using a 40-km multicore fiber and a multicore amplifier.

Analysis of plutonium isotope ratios including 238Pu/239Pu in individual U-Pu mixed oxide particles by means of a combination of alpha spectrometry and ICP-MS.

Isotope ratio analysis of individual uranium-plutonium (U-Pu) mixed oxide particles contained within environmental samples taken from nuclear facilities is proving to be increasingly important in the field of nuclear safeguards. However, isobaric interferences, such as 238U with 238Pu and 241Am with 241Pu, make it difficult to determine plutonium isotope ratios in mass spectrometric measurements. In the present study, the isotope ratios of 238Pu/239Pu, 240Pu/239Pu, 241Pu/239Pu, and 242Pu/239Pu were measured for individual Pu and U-Pu mixed oxide particles by a combination of alpha spectrometry and inductively coupled plasma mass spectrometry (ICP-MS). As a consequence, we were able to determine the 240Pu/239Pu, 241Pu/239Pu, and 242Pu/239Pu isotope ratios with ICP-MS after particle dissolution and chemical separation of plutonium with UTEVA resins. Furthermore, 238Pu/239Pu isotope ratios were able to be calculated by using both the 238Pu/(239Pu+240Pu) activity ratios that had been measured through alpha spectrometry and the 240Pu/239Pu isotope ratios determined through ICP-MS. Therefore, the combined use of alpha spectrometry and ICP-MS is useful in determining plutonium isotope ratios, including 238Pu/239Pu, in individual U-Pu mixed oxide particles.

RANKL induces Bach1 nuclear import and attenuates Nrf2-mediated antioxidant enzymes, thereby augmenting intracellular reactive oxygen species signaling and osteoclastogenesis in mice.

Reactive oxygen species (ROS) play a role in intracellular signaling during osteoclastogenesis. We previously reported that transcriptional factor nuclear factor E2-related factor 2 (Nrf2) was exported from the nucleus to the cytoplasm by receptor activator of nuclear factor-κB ligand (RANKL), and that Nrf2 negatively regulated osteoclastogenesis via antioxidant enzyme up-regulation. Knockout mice of BTB and CNC homology 1 (Bach1)-the competitor for Nrf2 in transcriptional regulation-was known to attenuate RANKL-mediated osteoclastogenesis, although the mechanism remains unclear. Therefore, we hypothesized that RANKL could be involved in the nuclear translocation of Bach1, which would attenuate Nrf2-mediated antioxidant enzymes, thereby augmenting intracellular ROS signaling in osteoclasts. RANKL induced Bach1 nuclear import and Nrf2 nuclear export. Induction of Bach1 nuclear export increased Nrf2 nuclear import, augmented antioxidant enzyme expression, and, thus, diminished RANKL-mediated osteoclastogenesis via attenuated intracellular ROS signaling. Finally, an in vivo mouse bone destruction model clearly demonstrated that induction of Bach1 nuclear export inhibited bone destruction. In this study, we report that RANKL favors osteoclastogenesis via attenuation of Nrf2-mediated antioxidant enzyme expression by competing with Bach1 nuclear accumulation. Of importance, induction of Bach1 nuclear export activates Nrf2-dependent antioxidant enzyme expression, thereby attenuating osteoclastogenesis. Bach1 nuclear export might be a therapeutic target for such bone destructive diseases as rheumatoid arthritis, osteoporosis, and periodontitis.-Kanzaki, H., Shinohara, F., Itohiya, K., Yamaguchi, Y., Katsumata, Y., Matsuzawa, M., Fukaya, S., Miyamoto, Y., Wada, S., Nakamura, Y. RANKL induces Bach1 nuclear import and attenuates Nrf2-mediated antioxidant enzymes, thereby augmenting intracellular reactive oxygen species signaling and osteoclastogenesis in mice.