Intelligent Reflecting Surface (IRS) significantly improves the energy utilization efficiency in 6th generation cellular communication systems. Here, we consider a system with multiple IRS and users, ...with one user communicating via several IRSs. In such a system, the user to which an IRS is assigned for each unit time must be determined to realize efficient communication. The previous studies on the optimization of various parameters for IRS based wireless systems did not consider the optimization of such IRS allocation scheduling. Therefore, we propose an IRS allocation scheduling method that limits the number of users who allocate each IRS to one unit time and sets the reflection coefficients of the IRS specifically to the assigned user resulting in the maximum IRS array gain. Additionally, as the proposed method is a combinatorial optimization problem, we develop a quadratic unconstrained binary optimization formulation to solve this using quantum computing. This will lead to the optimization of the entire system at a high speed and low power consumption in the future. Using computer simulation, we clarified that the proposed method realizes a more efficient communication compared to the method where one IRS is simultaneously used by multiple users.
Intelligent reflecting surface (IRS) enables the control of propagation characteristics and is attracting considerable attention as a technology to improve energy utilization efficiency in 6th ...generation mobile communication systems. As cell-free networks with multiple distributed base stations (BSs) can communicate in a coordinated manner, they are being actively researched as a new network architecture to resolve the problem of inter-cell interference in conventional cellular networks. The introduction of the IRS into the cell-free network can avoid shadowing at a lower cost with less power consumption. Thus, in this study, we considered the case of communication with user equipment (UE) in a shadowing environment using IRS in a cell-free network that contained distributed BSs with a single antenna. Moreover, the selection of multiple access methods was derived according to the numbers of BSs, IRSs, and UEs. In addition, we proposed a quadratic unconstrained binary optimization formulation to optimize the IRS reflection coefficient using quantum computing. The simulation results verified that the application of the proposed method resulted in a more efficient communication. Thus, this study clarifies that the optimum control method in every communication environment and aims to act as a stepping stone to optimize the entire cell-free system.
In binary optimization problems, where the goal is to find the input <inline-formula> <tex-math notation="LaTeX">\boldsymbol {x} </tex-math></inline-formula> that minimizes a given objective ...function, Grover adaptive search (GAS) is a well-known quantum algorithm that provides quadratic speedup when compared with the brute-force approaches of classical computers. GAS calls a renowned quantum search algorithm, Grover search (GS), as a subroutine to search for inputs with function values less than the threshold value. If such an input is found, the threshold value is updated with the function value and the search targets are narrowed. To search efficiently for a solution, an appropriate number of queries must be selected to amplify the desired state of the GS in each step. This paper discusses this issue and proposes a new method for selecting the number of queries and provides proof that our method achieves quadratic speedup as well as the original GAS. Furthermore, the simulation results for 40-bit problems confirm that our method allows an optimal solution with 22% fewer queries than the standard method, thus offering the possibility of significantly reduced computation times for combinatorial optimization problems.
Metalloporphyrin-based nanostructures were fabricated on 3-aminopropylmethoxysilane-modified indium tin oxide (ITO) surface. UV-visible spectroscopy and cyclic voltammetry are used for investigating ...electronic absorption spectra and catalytic activity in oxygen reduction reactions as alternative cathode electrochemical catalysts for polymer electrolyte membrane fuel cells (PEMFCs). Using of 5,10,15,20-tetrakis-(4-amiophenyl)-porphyrin-Co (II) as a building block and 1,4-phenylene diisocyanate as a linker, the mixed toluene/chloroform solution-based layer-by-layer process can produce linear growth of 5,10,15,20-tetrakis-(4-amiophenyl)-porphyrin-Co (II) up to 30 layers through urea bonds. The vacuum thermal annealing process demonstrated the improvement of catalytic activity in oxygen reduction reaction.
The mammalian inner ear detects sound with the organ of Corti, an intricately patterned region of the cochlea in which one row of inner hair cells and three rows of outer hair cells are surrounded by ...specialized supporting cells. The organ of Corti derives from a prosensory domain that runs the length of the cochlear duct and is bounded by two nonsensory domains, Kölliker's organ on the neural side and the outer sulcus on the abneural side. Although much progress has been made in identifying the signals regulating organ of Corti induction and differentiation, less is known about the mechanisms that establish sensory and nonsensory territories in the cochlear duct. Here, we show that a gradient of bone morphogenetic protein (BMP) signaling is established in the abneural-neural axis of the cochlea. Analysis of compound mutants of Alk3/6 type I BMP receptors shows that BMP signaling is necessary for specification of the prosensory domain destined to form the organ of Corti. Reduction of BMP signaling in Alk3/6 compound mutants eliminates both the future outer sulcus and the prosensory domain, with all cells expressing markers of Kölliker's organ. BMP4 upregulates markers of the future outer sulcus and downregulates marker genes of Kölliker's organ in cochlear organ cultures in a dose-dependent manner. Our results suggest BMP signaling is required for patterning sensory and nonsensory tissue in the mammalian cochlea.
Age-related hearing loss (ARHL) is a common sensory impairment with complex underlying mechanisms. In our previous study, we performed a meta-analysis of genome-wide association studies (GWAS) in ...mice and identified a novel locus on chromosome 18 associated with ARHL specifically linked to a 32 kHz tone burst stimulus. Consequently, we investigated the role of Formin Homology 2 Domain Containing 3 (Fhod3), a newly discovered candidate gene for ARHL based on the GWAS results. We observed Fhod3 expression in auditory hair cells (HCs) primarily localized at the cuticular plate (CP). To understand the functional implications of Fhod3 in the cochlea, we generated Fhod3 overexpression mice (Pax2-Cre+/-; Fhod3Tg/+) (TG) and HC-specific conditional knockout mice (Atoh1-Cre+/-; Fhod3fl/fl) (KO). Audiological assessments in TG mice demonstrated progressive high-frequency hearing loss, characterized by predominant loss of outer hair cells, and a decreased phalloidin intensities of CP. Ultrastructural analysis revealed loss of the shortest row of stereocilia in the basal turn of the cochlea, and alterations in the cuticular plate surrounding stereocilia rootlets. Importantly, the hearing and HC phenotype in TG mice phenocopied that of the KO mice. These findings suggest that balanced expression of Fhod3 is critical for proper CP and stereocilia structure and function. Further investigation of Fhod3 related hearing impairment mechanisms may lend new insight towards the myriad mechanisms underlying ARHL, which in turn could facilitate the development of therapeutic strategies for ARHL.
The inner ear develops from the otic placode, one of the cranial placodes that arise from a region of ectoderm adjacent to the anterior neural plate called the pre-placodal domain. We have identified ...a Forkhead family transcription factor, Foxi3, that is expressed in the pre-placodal domain and down-regulated when the otic placode is induced. We now show that Foxi3 mutant mice do not form otic placodes as evidenced by expression changes in early molecular markers and the lack of thickened placodal ectoderm, an otic cup or otocyst. Some preplacodal genes downstream of Foxi3-Gata3, Six1 and Eya1-are not expressed in the ectoderm of Foxi3 mutant mice, and the ectoderm exhibits signs of increased apoptosis. We also show that Fgf signals from the hindbrain and cranial mesoderm, which are necessary for otic placode induction, are received by pre-placodal ectoderm in Foxi3 mutants, but do not initiate otic induction. Finally, we show that the epibranchial placodes that develop in close proximity to the otic placode and the mandibular division of the trigeminal ganglion are missing in Foxi3 mutants. Our data suggest that Foxi3 is necessary to prime pre-placodal ectoderm for the correct interpretation of inductive signals for the otic and epibranchial placodes.
•Foxi3 is an early marker of non-neural ectoderm and the pre-placodal domain.•Foxi3 can regulate non-neural ectoderm and pre-placodal transcription factors.•Foxi3 is necessary for otic placode induction in response to FGF.•Foxi3 is necessary for the development of epibranchial placodes.•However, Foxi3 is not necessary for ectoderm to receive FGF signals.
The inner ear derives from a patch of ectoderm defined by expression of the transcription factor Pax2. We recently showed that this Pax2(+) ectoderm gives rise not only to the otic placode but also ...to the surrounding cranial epidermis, and that Wnt signaling mediates this placode-epidermis fate decision. We now present evidence for reciprocal interactions between the Wnt and Notch signaling pathways during inner ear induction. Activation of Notch1 in Pax2(+) ectoderm expands the placodal epithelium at the expense of cranial epidermis, whereas loss of Notch1 leads to a reduction in the size of the otic placode. We show that Wnt signaling positively regulates Notch pathway genes such as Jag1, Notch1 and Hes1, and we have used transgenic Wnt reporter mice to show that Notch signaling can modulate the canonical Wnt pathway. Gain- and loss-of-function mutations in the Notch and Wnt pathways reveal that some aspects of otic placode development - such as Pax8 expression and the morphological thickening of the placode - can be regulated independently by either Notch or Wnt signals. Our results suggest that Wnt signaling specifies the size of the otic placode in two ways, by directly upregulating a subset of otic genes, and by positively regulating components of the Notch signaling pathway, which then act to augment Wnt signaling.
The vertebrate inner ear is a morphologically complex sensory organ comprised of two compartments, the dorsal vestibular apparatus and the ventral cochlear duct, required for motion and sound ...detection, respectively. Fgf10, in addition to Fgf3, is necessary for the earliest stage of otic placode induction, but continued expression of Fgf10 in the developing otic epithelium, including the prosensory domain and later in Kolliker׳s organ, suggests additional roles for this gene during morphogenesis of the labyrinth. While loss of Fgf10 was implicated previously in semicircular canal agenesis, we show that Fgf10−/+ embryos also exhibit a reduction or absence of the posterior semicircular canal, revealing a dosage-sensitive requirement for FGF10 in vestibular development. In addition, we show that Fgf10−/− embryos have previously unappreciated defects of cochlear morphogenesis, including a somewhat shortened duct, and, surprisingly, a substantially narrower duct. The mutant cochlear epithelium lacks Reissner׳s membrane and a large portion of the outer sulcus–two non-contiguous, non-sensory domains. Marker gene analyses revealed effects on Reissner׳s membrane as early as E12.5-E13.5 and on the outer sulcus by E15.5, stages when Fgf10 is expressed in close proximity to Fgfr2b, but these effects were not accompanied by changes in epithelial cell proliferation or death. These data indicate a dual role for Fgf10 in cochlear development: to regulate outgrowth of the duct and subsequently as a bidirectional signal that sequentially specifies Reissner׳s membrane and outer sulcus non-sensory domains. These findings may help to explain the hearing loss sometimes observed in LADD syndrome subjects with FGF10 mutations.
Display omitted
•Fgf10 has a dosage-sensitive role in vestibular morphogenesis.•Fgf10 is required for cochlear morphogenesis.•Fgf10 null mutants lack Reissner׳s membrane and are deficient in outer sulcus tissue.•FGF10 signals sequentially and bi-directionally to specify these non-sensory domains.
Congenital abnormalities of the kidney and urinary tract are some of the most common defects detected in the unborn child. Kidney growth is controlled by the GDNF/RET signalling pathway, but the ...molecular events required for the activation of RET downstream targets are still poorly understood. Here we show that SOX9, a gene involved in campomelic dysplasia (CD) in humans, together with its close homologue SOX8, plays an essential role in RET signalling. Expression of SOX9 can be found from the earliest stages of renal development within the ureteric tip, the ureter mesenchyme and in a segment-specific manner during nephrogenesis. Using a tissue-specific knockout approach, we show that, in the ureteric tip, SOX8 and SOX9 are required for ureter branching, and double-knockout mutants exhibit severe kidney defects ranging from hypoplastic kidneys to renal agenesis. Further genetic analysis shows that SOX8/9 are required downstream of GDNF signalling for the activation of RET effector genes such as Sprouty1 and Etv5. At later stages of development, SOX9 is required to maintain ureteric tip identity and SOX9 ablation induces ectopic nephron formation. Taken together, our study shows that SOX9 acts at multiple steps during kidney organogenesis and identifies SOX8 and SOX9 as key factors within the RET signalling pathway. Our results also explain the aetiology of kidney hypoplasia found in a proportion of CD patients.
PDF
