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9 result(s) for "interzone"
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Mechanisms of synovial joint and articular cartilage development
Articular cartilage is formed at the end of epiphyses in the synovial joint cavity and permanently contributes to the smooth movement of synovial joints. Most skeletal elements develop from transient cartilage by a biological process known as endochondral ossification. Accumulating evidence indicates that articular and growth plate cartilage are derived from different cell sources and that different molecules and signaling pathways regulate these two kinds of cartilage. As the first sign of joint development, the interzone emerges at the presumptive joint site within a pre-cartilage tissue. After that, joint cavitation occurs in the center of the interzone, and the cells in the interzone and its surroundings gradually form articular cartilage and the synovial joint. During joint development, the interzone cells continuously migrate out to the epiphyseal cartilage and the surrounding cells influx into the joint region. These complicated phenomena are regulated by various molecules and signaling pathways, including GDF5, Wnt, IHH, PTHrP, BMP, TGF-β, and FGF. Here, we summarize current literature and discuss the molecular mechanisms underlying joint formation and articular development.
Unique Spatial Transcriptomic Profiling of the Murine Femoral Fracture Callus: A Preliminary Report
Fracture callus formation is a dynamic stage of bone activity and repair with precise, spatially localized gene expression. Metastatic breast cancer impairs fracture healing by disrupting bone homeostasis and imparting an altered genomic profile. Previous sequencing techniques such as single-cell RNA and in situ hybridization are limited by missing spatial context and low throughput, respectively. We present a preliminary approach using the Visium CytAssist spatial transcriptomics platform to provide the first spatially intact characterization of genetic expression changes within an orthopedic model of impaired fracture healing. Tissue slides prepared from BALB/c mice with or without MDA-MB-231 metastatic breast cancer cells were used. Both unsupervised clustering and histology-based annotations were performed to identify the hard callus, soft callus, and interzone for differential gene expression between the wild-type and pathological fracture model. The spatial transcriptomics platform successfully localized validated genes of the hard (Dmp1, Sost) and soft callus (Acan, Col2a1). The fibrous interzone was identified as a region of extensive genomic heterogeneity. MDA-MB-231 samples demonstrated downregulation of the critical bone matrix and structural regulators that may explain the weakened bone structure of pathological fractures. Spatial transcriptomics may represent a valuable tool in orthopedic research by providing temporal and spatial context.
Synovial Joints: from Development to Homeostasis
Synovial joint morphogenesis occurs through the condensation of mesenchymal cells into a non-cartilaginous region known as the interzone and the specification of progenitor cells that commit to the articular fate. Although several signaling molecules are expressed by the interzone, the mechanism is poorly understood. For treatments of cartilage injuries, it is critical to discover the presence of joint progenitor cells in adult tissues and their expression gene pattern. Potential stem cell niches have been found in different joint regions, such as the surface zone of articular cartilage, synovium, and groove of Ranvier. Inherited joint malformations as well as joint-degenerating conditions are often associated with other skeletal defects and may be seen as the failure of morphogenic factors to establish the correct microenvironment in cartilage and bone. Therefore, exploring how joints form can help us understand how cartilage and bone are damaged and develop drugs to reactivate this developing mechanism.
Modelling of Failure of Woven Composites. Part 1: Nomenclature Defining the Interzone Concept
The failure of woven composites has been examined. This study is presented in two parts: Modelling of failure of woven composites. Part 1: nomenclature defining the interzone concept ; Modelling of failure of woven composites. Part 2: experimental and numerical justification of the interzone concept . In the first part, the concepts of the interzone and the geometry of an interzone have been defined in a general way for a large panel of woven composites. In the second part, it has been shown that the failure of woven composites is well described by using the interzone concept. The load transfer between intact interzones and broken interzones has been evaluated for two types of loadings (tensile loading and loading in bending). The analysis of these load transfers explains why in the case of a tensile loading the failure is of a sudden-death type whereas in the case of bending loading the failure is progressive. The concept of failure of an interzone has been also defined.
Modelling of Failure of Woven Composites. Part 2: Experimental and Numerical Justification of the Interzone Concept
The failure of woven composites has been examined. This study is presented in two parts: Modelling of failure of woven composites. Part 1: nomenclature defining the interzone concept ; Modelling of failure of woven composites. Part 2: experimental and numerical justification of the interzone concept . In the first part, the concepts of the interzone and the geometry of an interzone have been defined in a general way for a large panel of woven composites. In the second part, it has been shown that the failure of woven composites is well described by using the interzone concept. The load transfer between intact interzones and broken interzones has been evaluated for two types of loadings (tensile loading and loading in bending). The analysis of these load transfers explains why in the case of a tensile loading the failure is of a sudden-death type whereas in the case of bending loading the failure is progressive. The concept of failure of an interzone has been also defined.
Formation of synovial joints and articular cartilage
Chondrocytes differentiate from mesenchymal progenitors and produce templates(anlagen) for the developing bones. Chondrocyte differentiation is controlled by Sox transcription factors. Templates for the neighbour bones are subsequently separated by conversion of differentiated chondrocytes into non-chondrogenic cells and emergence of interzone in which joints cavitation occurs. A central role in initiating synovial joint formation plays Wnt-14/beta-catenin signalling pathway.Moreover, bone morphogenetic proteins and growth and differentiation factors are expressed at the site of joint formation. Joint cavitation is associated with increased hyaluronic acid synthesis. Hyaluronic acid facilitates tissue separation and creation of a functional joint cavity. According to the traditional view articular cartilage represents part of cartilage anlage that is not replaced by bone through endochondral ossification. Recent studies indicate, however, that peri-joint mesenchymal cells take part in interzone formation and that these interzone cells subsequently differentiate into articular chondrocytes and synovial cells. Thus,anlage chondrocytes have a transient character and disappear after cessation of growth plate function while articular chondrocytes have stable and permanent phenotype and function throughout life.
'Signalling' between chromosomes in crane-fly spermatocytes studied using ultraviolet microbeam irradiation
The present article deals with signals from kinetochores in anaphase crane-fly spermatocytes: when a half-bivalent's kinetochore is irradiated with an ultraviolet microbeam during anaphase, all half-bivalents in the cell stop moving to both poles. Movement blockage is temporary, and different half-bivalent pairs resume movement at different times. Movement stoppage presumably is due to signals arising from the irradiated kinetochores and transmitted to the 'motors' of the other chromosomes. We used a second irradiation (of the interzone) to determine the path of the signal. We reasoned that if irradiation of the interzone blocked transmission of the putative signal, then those chromosomes not receiving the signal should continue to move after irradiation of a kinetochore. Interzone irradiation interfered with the signal in about 20% of the 51 cells irradiated doubly, in that chromosome(s) moving to one pole stopped while chromosome(s) moving to the other pole continued. There was a second indication that interzonal irradiation blocked the signal: in about 30% of the cells in which the kinetochore was irradiated first and interzone second, all half-bivalents resumed movement immediately after the second irradiation.
Science Fiction and Fantasy after 1945: Beyond Pulp Fiction
This chapter contains sections titled: Arthur C. Clarke and Genre SF New Wave SF and the Mainstream Michael Moorcock and Dark Fantasy Interzone References and Further Reading