Статті в журналах: "Muscle Cytoarchitecture"

1

Iskratsch, Thomas, and Elisabeth Ehler. "Formin-g muscle cytoarchitecture." BioArchitecture 1, no. 2 (March 2011): 66–68. http://dx.doi.org/10.4161/bioa.1.2.15467.

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2

CARTER, A.-J., F. KRISTMUNDSDOTTIR, J. GILMOUR, and M. A. GLASBY. "Changes in Muscle Cytoarchitecture after Peripheral Nerve Injury and Repair." Journal of Hand Surgery 23, no. 3 (June 1998): 365–69. http://dx.doi.org/10.1016/s0266-7681(98)80059-4.

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The aim of this study was to assess the changes which occurred in the rat in target muscles after the injury and repair of a specific peripheral nerve, using several clinically-appropriate surgical techniques. There were alterations in the size, shape, morphology and cytochemical architecture of the fibres of the target muscles. These changes were marked when transection and repair of the nerve was compared with the less-severe crush injury. The method of repair did not correlate significantly with the occurrence of changes in muscle cytoarchitecture. The results suggest that the extent of cell loss and the changes in muscle fibre architecture were influenced by the type of injury, rather than by the method of repair.

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3

Schäfer, B. W., and J. C. Perriard. "Intracellular targeting of isoproteins in muscle cytoarchitecture." Journal of Cell Biology 106, no. 4 (April 1, 1988): 1161–70. http://dx.doi.org/10.1083/jcb.106.4.1161.

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Part of the muscle creatine kinase (MM-CK) in skeletal muscle of chicken is localized in the M-band of myofibrils, while chicken heart cells containing myofibrils and BB-CK, but not expressing MM-CK, do not show this association. The specificity of the MM-CK interaction was tested using cultured chicken heart cells as "living test tubes" by microinjection of in vitro generated MM-CK and hybrid M-CK/B-CK mRNA with SP6 RNA polymerase. The resulting translation products were detected in injected cells with isoprotein-specific antibodies. M-CK molecules and translation products of chimeric cDNA molecules containing the head half of the B-CK and the tail half of the M-CK coding regions were localized in the M-band of the myofibrils. The tail, but not the head portion of M-CK is essential for the association of M-CK with the M-band of myofibrils. We conclude that gross biochemical properties do not always coincide with a molecule's specific functions like the participation in cell cytoarchitecture which may depend on molecular targeting even within the same cellular compartment.

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4

Ontell, Marcia, Dianna Bourke, and Donna Hughes. "Cytoarchitecture of the fetal murine soleus muscle." American Journal of Anatomy 181, no. 3 (March 1988): 267–78. http://dx.doi.org/10.1002/aja.1001810305.

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5

Ushiwata, Issei, and Tatsuo Ushiki. "Cytoarchitecture of the smooth muscles and pericytes of rat cerebral blood vessels." Journal of Neurosurgery 73, no. 1 (July 1990): 82–90. http://dx.doi.org/10.3171/jns.1990.73.1.0082.

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✓ The three-dimensional cytoarchitecture of the smooth muscles and pericytes of rat cerebral blood vessels was studied by scanning electron microscopy after removing extracellular connective tissue matrices with the KOH-collagenase digestion method. The tunica media of major intracranial arteries such as the internal carotid, vertebral, basilar, and other cerebral arteries measuring more than 100 µm in outer diameter consisted of spindle-shaped smooth-muscle cells arranged circularly to the long axis of the vessel. Muscle cells at the branching points, however, showed a variety of shapes, sizes, and arrangements. As the vessel size decreased, smooth-muscle cells showed bi- or trifurcations at the cell poles. In the precapillary arterioles, smooth-muscle cells which had helically surrounded the endothelial tubes had bulging cell bodies with various cytoplasmic processes extending from the cell poles. Distinct specializations presumed to be sphincters were not found on the arteries or arterioles. Pericytes of the capillary had become extended along the vessel axis, having fusiform cell bodies with longitudinally oriented long cytoplasmic processes. Cells located periendothelially in the venules and veins were stellate in shape with many cytoplasmic processes which were interwoven to form complicated cellular networks around the endothelial tube.

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6

Clark, Kathleen A., Abigail S. McElhinny, Mary C. Beckerle, and Carol C. Gregorio. "Striated Muscle Cytoarchitecture: An Intricate Web of Form and Function." Annual Review of Cell and Developmental Biology 18, no. 1 (November 2002): 637–706. http://dx.doi.org/10.1146/annurev.cellbio.18.012502.105840.

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7

Feczko, John D., and Kathleen M. Klueber. "Cytoarchitecture of muscle in a genetic model of murine diabetes." American Journal of Anatomy 182, no. 3 (July 1988): 224–40. http://dx.doi.org/10.1002/aja.1001820304.

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8

Dalpé, Gratien, Martine Mathieu, Alain Comtois, Ercheng Zhu, Sylwia Wasiak, Yves De Repentigny, Nicole Leclerc, and Rashmi Kothary. "Dystonin-Deficient Mice Exhibit an Intrinsic Muscle Weakness and an Instability of Skeletal Muscle Cytoarchitecture." Developmental Biology 210, no. 2 (June 1999): 367–80. http://dx.doi.org/10.1006/dbio.1999.9263.

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9

Zhang, Jianlin, Marie-Louise Bang, David S. Gokhin, Yingchun Lu, Li Cui, Xiaodong Li, Yusu Gu, et al. "Syncoilin is required for generating maximum isometric stress in skeletal muscle but dispensable for muscle cytoarchitecture." American Journal of Physiology-Cell Physiology 294, no. 5 (May 2008): C1175—C1182. http://dx.doi.org/10.1152/ajpcell.00049.2008.

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Syncoilin is a striated muscle-specific intermediate filament-like protein, which is part of the dystrophin-associated protein complex (DPC) at the sarcolemma and provides a link between the extracellular matrix and the cytoskeleton through its interaction with α-dystrobrevin and desmin. Its upregulation in various neuromuscular diseases suggests that syncoilin may play a role in human myopathies. To study the functional role of syncoilin in cardiac and skeletal muscle in vivo, we generated syncoilin-deficient ( syncoilin−/−) mice. Our detailed analysis of these mice up to 2 yr of age revealed that syncoilin is entirely dispensable for cardiac and skeletal muscle development and maintenance of cellular structure but is required for efficient lateral force transmission during skeletal muscle contraction. Notably, syncoilin−/− skeletal muscle generates less maximal isometric stress than wild-type (WT) muscle but is as equally susceptible to eccentric contraction-induced injury as WT muscle. This suggests that syncoilin may play a supportive role for desmin in the efficient coupling of mechanical stress between the myofibril and fiber exterior. It is possible that the reduction in isometric stress production may predispose the syncoilin skeletal muscle to a dystrophic condition.

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10

Diermeier, Stefanie, Andreas Buttgereit, Sebastian Schürmann, Lilli Winter, Hongyang Xu, Robyn M. Murphy, Christoph S. Clemen, Rolf Schröder, and Oliver Friedrich. "Preaged remodeling of myofibrillar cytoarchitecture in skeletal muscle expressing R349P mutant desmin." Neurobiology of Aging 58 (October 2017): 77–87. http://dx.doi.org/10.1016/j.neurobiolaging.2017.06.001.

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11

Gokhin, David S., and Velia M. Fowler. "Tropomodulin Capping of Actin Filaments in Striated Muscle Development and Physiology." Journal of Biomedicine and Biotechnology 2011 (2011): 1–16. http://dx.doi.org/10.1155/2011/103069.

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Efficient striated muscle contraction requires precise assembly and regulation of diverse actin filament systems, most notably the sarcomeric thin filaments of the contractile apparatus. By capping the pointed ends of actin filaments, tropomodulins (Tmods) regulate actin filament assembly, lengths, and stability. Here, we explore the current understanding of the expression patterns, localizations, and functions of Tmods in both cardiac and skeletal muscle. We first describe the mechanisms by which Tmods regulate myofibril assembly and thin filament lengths, as well as the roles of closely related Tmod family variants, the leiomodins (Lmods), in these processes. We also discuss emerging functions for Tmods in the sarcoplasmic reticulum. This paper provides abundant evidence that Tmods are key structural regulators of striated muscle cytoarchitecture and physiology.

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12

Hughes, Donna S., Robert R. Schade, and Marcia Ontell. "Ablation of the fetal mouse spinal cord: The effect on soleus muscle cytoarchitecture." Developmental Dynamics 193, no. 2 (February 1992): 164–74. http://dx.doi.org/10.1002/aja.1001930208.

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13

von Arx, P., S. Bantle, T. Soldati, and J. C. Perriard. "Dominant negative effect of cytoplasmic actin isoproteins on cardiomyocyte cytoarchitecture and function." Journal of Cell Biology 131, no. 6 (December 15, 1995): 1759–73. http://dx.doi.org/10.1083/jcb.131.6.1759.

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The intracompartmental sorting and functional consequences of ectopic expression of the six vertebrate actin isoforms was investigated in different types of cultured cells. In transfected fibroblasts all isoactin species associated with the endogenous microfilament cytoskeleton, even though cytoplasmic actins also showed partial localization to peripheral submembranous sites. Functional and structural studies were performed in neonatal and adult rat cardiomyocytes. All the muscle isoactin constructs sorted preferentially to sarcomeric sites and, to a lesser extent, also to stress-fiber-like structures. The expression of muscle actins did not interfere with cell contractility, and did not disturb the localization of endogenous sarcomeric proteins. In sharp contrast, ectopic expression of the two cytoplasmic actin isoforms resulted in rapid cessation of cellular contractions and induced severe morphological alterations characterized by an exceptional outgrowth of filopodia and cell flattening. Quantitative analysis in neonatal cardiomyocytes indicated that the levels of accumulation of the different isoactins are very similar and cannot be responsible for the observed isoproteins-specific effects. Structural analysis revealed a remodeling of the cytoarchitecture including a specific alteration of sarcomeric organization; proteins constituting the sarcomeric thin filaments relocated to nonmyofibrillar sites while thick filaments and titin remained unaffected. Experiments with chimeric proteins strongly suggest that isoform specific residues in the carboxy-terminal portion of the cytoplasmic actins are responsible for the dominant negative effects on function and morphology.

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14

Klueber, Kathleen M., and David J. Porta. "Cytoarchitecture of diabetic myopathy during the pathogenesis of the disease: Fast versus slow muscle." Clinical Anatomy 7, no. 6 (1994): 335–51. http://dx.doi.org/10.1002/ca.980070606.

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15

Tamaki, Tetsuro, Tadashi Sekine, Akira Akatsuka, Shuichi Uchiyama, and Shoichi Nakano. "Three-dimensional cytoarchitecture of complex branched fibers in soleus muscle from mdx mutant mice." Anatomical Record 237, no. 3 (November 1993): 338–44. http://dx.doi.org/10.1002/ar.1092370307.

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16

Sarnat, Harvey B. "Myotubular Myopathy: Arrest of Morphogenesis of Myofibres Associated with Persistence of Fetal Vimentin and Desmin Four cases compared with fetal and neonatal muscle." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 17, no. 2 (May 1990): 109–23. http://dx.doi.org/10.1017/s0317167100030304.

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ABSTRACT:Vastus lateralis muscle biopsies of four unrelated male neonates showing myotubular (i.e. centronuclear) myopathy (MM) were compared with muscle from four human fetuses in the myotubular stage of development, a 31 week preterm infant and four term neonates. The perimysium, blood vessels, spindles, myelinated intramuscular nerves, and motor end-plates in MM are as well developed as in term neonatal muscle. The cytoarchitecture of myofibres in MM is more mature than that of fetal myotubes in the spacing of central nuclei, Z-band registry, development of the sarcotubular system, and in the condensation of nuclear chromatin and nucleoli. Triads in MM may retain an immature oblique or longitudinal orientation. Myofibrillar ATPase shows normal differentiation of fibre types, consistent with nonnal innervation. Spinal motor neurons are nonnal in number and in RNA fluorescence. Immunoreactivity for vimentin and desmin in myofibres of MM is uniformly strong, as in fetal myotubes and unlike mature neonatal muscle. Maternal muscle biopsies of two cases also showed scattered small centronuclear myofibres reactive for vimentin and desmin. The arrest in morphogenesis of fibre architecture in MM is not a general arrest in muscle development. Persistence of fetal cytoskeletal proteins that preserve the immature central positions of nuclei and mitochondria may be important in pathogenesis. Vimentin/desmin studies of the infant and maternal muscle biopsies are useful in establishing the diagnosis.

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17

Stronach, Beth E., Patricia J. Renfranz, Brenda Lilly, and Mary C. Beckerle. "Muscle LIM Proteins Are Associated with Muscle Sarcomeres and Require dMEF2 for Their Expression during DrosophilaMyogenesis." Molecular Biology of the Cell 10, no. 7 (July 1999): 2329–42. http://dx.doi.org/10.1091/mbc.10.7.2329.

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A genetic hierarchy of interactions, involving myogenic regulatory factors of the MyoD and myocyte enhancer-binding 2 (MEF2) families, serves to elaborate and maintain the differentiated muscle phenotype through transcriptional regulation of muscle-specific target genes. Much work suggests that members of the cysteine-rich protein (CRP) family of LIM domain proteins also play a role in muscle differentiation; however, the specific functions of CRPs in this process remain undefined. Previously, we characterized two members of the Drosophila CRP family, the muscle LIM proteins Mlp60A and Mlp84B, which show restricted expression in differentiating muscle lineages. To extend our analysis ofDrosophila Mlps, we characterized the expression of Mlps in mutant backgrounds that disrupt specific aspects of muscle development. We show a genetic requirement for the transcription factor dMEF2 in regulating Mlp expression and an ability of dMEF2 to bind, in vitro, to consensus MEF2 sites derived from those present inMlp genomic sequences. These data suggest that theMlp genes may be direct targets of dMEF2 within the genetic hierarchy controlling muscle differentiation. Mutations that disrupt myoblast fusion fail to affect Mlp expression. In later stages of myogenic differentiation, which are dedicated primarily to assembly of the contractile apparatus, we analyzed the subcellular distribution of Mlp84B in detail. Immunofluorescent studies revealed the localization of Mlp84B to muscle attachment sites and the periphery of Z-bands of striated muscle. Analysis of mutations that affect expression of integrins and α-actinin, key components of these structures, also failed to perturb Mlp84B distribution. In conclusion, we have used molecular epistasis analysis to position Mlp function downstream of events involving mesoderm specification and patterning and concomitant with terminal muscle differentiation. Furthermore, our results are consistent with a structural role for Mlps as components of muscle cytoarchitecture.

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18

Andra, K., H. Lassmann, R. Bittner, S. Shorny, R. Fassler, F. Propst, and G. Wiche. "Targeted inactivation of plectin reveals essential function in maintaining the integrity of skin, muscle, and heart cytoarchitecture." Genes & Development 11, no. 23 (December 1, 1997): 3143–56. http://dx.doi.org/10.1101/gad.11.23.3143.

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19

Berchtold, Martin W., Heinrich Brinkmeier, and Markus Müntener. "Calcium Ion in Skeletal Muscle: Its Crucial Role for Muscle Function, Plasticity, and Disease." Physiological Reviews 80, no. 3 (July 1, 2000): 1215–65. http://dx.doi.org/10.1152/physrev.2000.80.3.1215.

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Mammalian skeletal muscle shows an enormous variability in its functional features such as rate of force production, resistance to fatigue, and energy metabolism, with a wide spectrum from slow aerobic to fast anaerobic physiology. In addition, skeletal muscle exhibits high plasticity that is based on the potential of the muscle fibers to undergo changes of their cytoarchitecture and composition of specific muscle protein isoforms. Adaptive changes of the muscle fibers occur in response to a variety of stimuli such as, e.g., growth and differentition factors, hormones, nerve signals, or exercise. Additionally, the muscle fibers are arranged in compartments that often function as largely independent muscular subunits. All muscle fibers use Ca2+ as their main regulatory and signaling molecule. Therefore, contractile properties of muscle fibers are dependent on the variable expression of proteins involved in Ca2+ signaling and handling. Molecular diversity of the main proteins in the Ca2+ signaling apparatus (the calcium cycle) largely determines the contraction and relaxation properties of a muscle fiber. The Ca2+ signaling apparatus includes 1) the ryanodine receptor that is the sarcoplasmic reticulum Ca2+ release channel, 2) the troponin protein complex that mediates the Ca2+ effect to the myofibrillar structures leading to contraction, 3) the Ca2+pump responsible for Ca2+ reuptake into the sarcoplasmic reticulum, and 4) calsequestrin, the Ca2+storage protein in the sarcoplasmic reticulum. In addition, a multitude of Ca2+-binding proteins is present in muscle tissue including parvalbumin, calmodulin, S100 proteins, annexins, sorcin, myosin light chains, β-actinin, calcineurin, and calpain. These Ca2+-binding proteins may either exert an important role in Ca2+-triggered muscle contraction under certain conditions or modulate other muscle activities such as protein metabolism, differentiation, and growth. Recently, several Ca2+signaling and handling molecules have been shown to be altered in muscle diseases. Functional alterations of Ca2+ handling seem to be responsible for the pathophysiological conditions seen in dystrophinopathies, Brody's disease, and malignant hyperthermia. These also underline the importance of the affected molecules for correct muscle performance.

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20

Konieczny, Patryk, Peter Fuchs, Siegfried Reipert, Wolfram S. Kunz, Anikó Zeöld, Irmgard Fischer, Denise Paulin, Rolf Schröder, and Gerhard Wiche. "Myofiber integrity depends on desmin network targeting to Z-disks and costameres via distinct plectin isoforms." Journal of Cell Biology 181, no. 4 (May 19, 2008): 667–81. http://dx.doi.org/10.1083/jcb.200711058.

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Dysfunction of plectin, a 500-kD cytolinker protein, leads to skin blistering and muscular dystrophy. Using conditional gene targeting in mice, we show that plectin deficiency results in progressive degenerative alterations in striated muscle, including aggregation and partial loss of intermediate filament (IF) networks, detachment of the contractile apparatus from the sarcolemma, profound changes in myofiber costameric cytoarchitecture, and decreased mitochondrial number and function. Analysis of newly generated plectin isoform–specific knockout mouse models revealed that IF aggregates accumulate in distinct cytoplasmic compartments, depending on which isoform is missing. Our data show that two major plectin isoforms expressed in muscle, plectin 1d and 1f, integrate fibers by specifically targeting and linking desmin IFs to Z-disks and costameres, whereas plectin 1b establishes a linkage to mitochondria. Furthermore, disruption of Z-disk and costamere linkages leads to the pathological condition of epidermolysis bullosa with muscular dystrophy. Our findings establish plectin as the major organizer of desmin IFs in myofibers and provide new insights into plectin- and desmin-related muscular dystrophies.

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21

KITAMURA, MASANORI. "The Antioxidant N-Acetylcysteine Induces Mesangial Cells to Create Three-Dimensional Cytoarchitecture That Underlies Cellular Differentiation." Journal of the American Society of Nephrology 10, no. 4 (April 1999): 746–51. http://dx.doi.org/10.1681/asn.v104746.

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Abstract. Prolonged culture of mesangial cells produces multifocal nodular structures, i.e., “hillocks,” consisting of cells and extracellular matrix. Hillock formation is associated with induction of a differentiated phenotype of mesangial cells, with suppressed mitogenesis and downregulation of α-smooth muscle actin (α-SMA). Currently, little is understood regarding physiologically relevant factors that facilitate this cytodifferentiation. This study explores whether and how the cellular redox state modulates hillock formation. Exposure of confluent rat mesangial cells to the antioxidant N-acetylcysteine (NAC), an inducer of glutathione, dramatically facilitated hillock formation. This effect was mimicked by external addition of the reduced form of glutathione ethyl ester. In contrast, the oxidizing agents diamide and menadione inhibited the development of hillocks triggered by either NAC, glutathione, or prolonged culture. The induction of hillocks by NAC was correlated with downregulation of α-SMA as well as attenuated activity of the CArG box element (the cis-element relevant to the expression of the α-SMA gene and growth-associated genes). These results indicate that, by a redox-sensitive mechanism, NAC induces mesangial cells to create three-dimensional cytoarchitecture that underlies cellular differentiation.

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22

Ehler, Elisabeth, Robert Horowits, Christian Zuppinger, Robert L. Price, Evelyne Perriard, Martin Leu, Pico Caroni, Mark Sussman, Hans M. Eppenberger, and Jean-Claude Perriard. "Alterations at the Intercalated Disk Associated with the Absence of Muscle Lim Protein." Journal of Cell Biology 153, no. 4 (May 14, 2001): 763–72. http://dx.doi.org/10.1083/jcb.153.4.763.

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In this study, we investigated cardiomyocyte cytoarchitecture in a mouse model for dilated cardiomyopathy (DCM), the muscle LIM protein (MLP) knockout mouse and substantiated several observations in a second DCM model, the tropomodulin-overexpressing transgenic (TOT) mouse. Freshly isolated cardiomyocytes from both strains are characterized by a more irregular shape compared with wild-type cells. Alterations are observed at the intercalated disks, the specialized areas of mechanical coupling between cardiomyocytes, whereas the subcellular organization of contractile proteins in the sarcomeres of MLP knockout mice appears unchanged. Distinct parts of the intercalated disks are affected differently. Components from the adherens junctions are upregulated, desmosomal proteins are unchanged, and gap junction proteins are downregulated. In addition, the expression of N-RAP, a LIM domain– containing protein located at the intercalated disks, is upregulated in MLP knockout as well as in TOT mice. Detailed analysis of intercalated disk composition during postnatal development reveals that an upregulation of N-RAP expression might serve as an early marker for the development of DCM. Altered expression levels of cytoskeletal proteins (either the lack of MLP or an increased expression of tropomodulin) apparently lead to impaired function of the myofibrillar apparatus and to physiological stress that ultimately results in DCM and is accompanied by an altered appearance and composition of the intercalated disks.

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23

Clark, Kathleen A., and Julie L. Kadrmas. "Drosophila melanogastermuscle LIM protein and alpha-actinin function together to stabilize muscle cytoarchitecture: A potential role for Mlp84B in actin-crosslinking." Cytoskeleton 70, no. 6 (April 18, 2013): 304–16. http://dx.doi.org/10.1002/cm.21106.

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Kinose, F., S. X. Wang, U. S. Kidambi, C. L. Moncman, and D. A. Winkelmann. "Glycine 699 is pivotal for the motor activity of skeletal muscle myosin." Journal of Cell Biology 134, no. 4 (August 15, 1996): 895–909. http://dx.doi.org/10.1083/jcb.134.4.895.

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Myosin couples ATP hydrolysis to the translocation of actin filaments to power many forms of cellular motility. A striking feature of the structure of the muscle myosin head domain is a 9-nm long "lever arm" that has been postulated to produce a 5-10-nm power stroke. This motion must be coupled to conformational changes around the actin and nucleotide binding sites. The linkage of these sites to the lever arm has been analyzed by site-directed mutagenesis of a conserved glycine residue (G699) found in a bend joining two helices containing the highly reactive and mobile cysteine residues, SH1 and SH2. Alanine mutagenesis of this glycine (G699A) dramatically alters the motor activity of skeletal muscle myosin, inhibiting the velocity of actin filament movement by > 100-fold. Analysis of the defect in the G699A mutant myosin is consistent with a marked slowing of the transition within the motor domain from a strong binding to a weak binding interaction with actin. This result is interpreted in terms of the role of this residue (G699) as a pivot point for motion of the lever arm. The recombinant myosin used in these experiments has been produced in a unique expression system. A shuttle vector containing a regulated muscle-specific promoter has been developed for the stable expression of recombinant myosin in C2C12 cells. The vector uses the promoter/enhancer region, the first two and the last five exons of an embryonic rat myosin gene, to regulate the expression of an embryonic chicken muscle myosin cDNA. Stable cell lines transfected with this vector express the unique genetically engineered myosin after differentiation into myotubes. The myosin assembles into myofibrils, copurifies with the endogenous myosin, and contains a complement of muscle-specific myosin light chains. The functional activity of the recombinant myosin is readily analyzed with an in vitro motility assay using a species-specific anti-S2 mAb to selectively assay the recombinant protein. This expression system has facilitated manipulation and analysis of the skeletal muscle myosin motor domain and is also amenable to a wide range of structure-function experiments addressing questions unique to the muscle-specific cytoarchitecture and myosin isoforms.

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Fernandes-Lima, Flávia, Bianca M. Gregório, Fernanda A. M. Nascimento, Waldemar S. Costa, Carla B. M. Gallo, and Francisco J. B. Sampaio. "Effects of Vitamin D Restricted Diet Administered during Perinatal and Postnatal Periods on the Penis of Wistar Rats." BioMed Research International 2018 (2018): 1–9. http://dx.doi.org/10.1155/2018/6030646.

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Vitamin D deficiency is common in pregnant women and infants. The present study aimed to investigate the effects of vitamin D restricted diet on the Wistar rats offspring penis morphology. Mother rats received either standard diet (SC) or vitamin D restricted (VitD) diet. At birth, offspring were divided into SC/SC (from SC mothers, fed with SC diet) and VitD/VitD (from VitD mothers, fed with VitD diet). After euthanasia the penises were processed for histomorphometric analysis. The VitD/VitD offspring displayed metabolic changes and reduction in the cross-sectional area of the penis, corpus cavernosum, tunica albuginea, and increased area of the corpus spongiosum. The connective tissue, smooth muscle, and cell proliferation percentages were greater in the corpus cavernosum and corpus spongiosum in the VitD/VitD offspring. The percentages of sinusoidal spaces and elastic fibers in the corpus cavernosum decreased. The elastic fibers in the tunica albuginea of the corpus spongiosum in the VitD/VitD offspring were reduced. Vitamin D restriction during perinatal and postnatal periods induced metabolic and structural changes and represented important risk factors for erectile dysfunction in the penis of the adult offspring. These findings suggest that vitamin D is an important micronutrient in maintaining the cytoarchitecture of the penis.

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Meyer zum Gottesberge, A. M., and S. Hansen. "The collagen receptor DDR1 co-localizes with the non-muscle myosin IIA in mice inner ear and contributes to the cytoarchitecture and stability of motile cells." Cell and Tissue Research 358, no. 3 (October 12, 2014): 729–36. http://dx.doi.org/10.1007/s00441-014-2009-3.

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27

Racker, Darlene K. "The AV junction region of the heart: a comprehensive study correlating gross anatomy and direct three-dimensional analysis. Part II. Morphology and cytoarchitecture." American Journal of Physiology-Heart and Circulatory Physiology 286, no. 5 (May 2004): H1853—H1871. http://dx.doi.org/10.1152/ajpheart.01205.2003.

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This “Part II morphology and cytoarchitecture” study is based on paraffin-embedded specimens in which the extracellular and intracellular matrix are preserved; single parallel, perpendicular, and transverse serial sections of the entire atrioventricular (AV) junction region (AVJR) and their correlation with photographs of the tissue blocks. As in Part I, the same major new findings are: 1) a coronary sinus fossa is formed by the superoposterior right medial atria wall (MAW), the left atrium, and the coronary sinus roof; 2) the posterior MAW forms two myocardial bridges and is isolated from the sinus venarum by the floor of the inferior vena cava; 3) the tendon of Todaro terminates in the superior lip of the coronary sinus ostium; 4) only ordinary myocardium contacts the annulus fibrosus, and there is little to no collagen separating its myofibers and tissues; 5) the ventricular septum shoulder is humped shaped, completely overlaid by annular myocardium, and joined by struts of papillary muscle; 6) the membranous septum joining the ventricular septum shoulder to the crista supraventricularis forms part of the aortic valve sinus walls; and 7) myocardium of the atrionodal bundles is aggregated into numerous small fascicles encased by collagen and is outside of the MAW as are the other specialized tissues. The proximal AV bundle and medial atrionodal bundle are aligned to the medial leg of Koch's triangle and the tendon of Todaro. These data show, therefore, that the AVJR contains two overlapping atrial circuits. In the MAW, acivation of the posterior region is delayed because of the two myocardial bridges. Puncture of the AVJR can produce communication with an extracardiac space, posteriorly and medially, and with the aorta, anteriorly.

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Borthakur, Dibakar, Rajesh Kumar, and Rima Dada. "Myocardial bridge over coronary arteries and myocardial coat lining coronary sinus: clinical implications." European Journal of Anatomy 27 (January 2023): 47–56. http://dx.doi.org/10.52083/yqfo7375.

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Myocardial Bridge (MB) on the coronary artery and myocardial coat (MC) on the cardiac veins are usually detected in angiography and cadaveric dissection. Left anterior descending branch (LAD) of the left coronary artery is the most frequent site of MB. Rarely MB is also seen over the right coronary arterial branches. MB has proven association with ischemic heart disease and other critical cardiac consequences like myocardial infarction (MI) (Alegria et al., 2000; Soran et al., 2000). MC, on the other hand has not gained enough attention in previous studies. Large MB can be readily identified in angiograms, but minutes MB can be picked up by newer imaging studies like multidetector computed tomography (MDCT) and optical coherence tomography (OCT) scan (Tiryakioglu and Aliyu, 2020). Cadaveric dissection, however, holds its unique place in direct visualization and studying the macro and micro-anatomical characteristics. To study the prevalence and anatomical attributes of MB and MC in Indian population, ten adult cadaveric hearts (6 male and 4 female) were dissected as part of a routine undergraduate teaching at the Anatomy Department, All India Institute of Medical Sciences, New Delhi, India. MB over the coronary artery and MC over the cardiac vein were identified. Data pertaining to the MB and MC dimensions were measured with a digital vernier calliper. Histology of the MC was carried out to confirm its presence and observe the cytoarchitecture pattern. Relevant gross macroscopic and microscopic images were photographed and photomicrographed. 20% of the dissected cadavers revealed MB involving LAD in first heart while LAD and RCA both in second heart with lengths 5 mm, 18 mm and 2 mm respectively. MC was noted over coronary sinus and proximal few millimeters of great and middle cardiac veins. Histological examination revealed cardiac striated muscle in MC with typical cyto- architecture. The mean myocardial muscle index (MMI) of MBs ranged from 1.6 to 21.6. The present study highlights 20% prevalence of MBs in Indian population involving both right and left coronary artery. 10% of the subjects had histologically confirmed MC over cardiac veins. MC over the coronary sinus and other cardiac veins need more elaborate explorative studies to quantify the anatomic properties and to examine the possible association with cardiovascular disease. Nevertheless, anatomic attributes should be kept in mind to better appreciate MI in evolution and MI at evaluation in a case with MB.

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Vita, G., M. C. Monici, K. Owaribe, and C. Messina. "Expression of plectin in muscle fibers with cytoarchitectural abnormalities." Neuromuscular Disorders 13, no. 6 (August 2003): 485–92. http://dx.doi.org/10.1016/s0960-8966(03)00037-3.

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30

Yama, O. E., O. V. Adeteye, T. O. Kusemiju, O. M. Avidime, T. Danboyi, A. A. Odetola, and K. A. Mohammed. "Morphoanatomy of striated myofibers in streptozotocin-induced diabetic wistar rats: assuaging effect of combined doses of Vernonia amygdalina and Azadirachta indica." Research Journal of Health Sciences 8, no. 2 (July 10, 2020): 92–101. http://dx.doi.org/10.4314/rejhs.v8i2.5.

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Objective: This study aimed to evaluate the effects of Azadirachta indica and Vernonia amygdalina extracts on the morphoanatomy of striated myofibrils in diabetic rat models. Methodology: Thirty Wistar rats randomly assigned into 5 groups of 6 rats/group were used. Group A received distilled water only, B (herbal) received A. indica (500 mg/kg/day) and V. amygdalina (400 mg/kg/day) simultaneously, C were diabetic rats, D were diabetic rats treated with herbal extracts combined and E, diabetic rats treated with metformin. Diabetes was induced with streptozotocin (70 mg/kg). Muscles glutathione peroxidase (GPx) and blood glucose levels were determined. The rats were sacrificed at the end of 60days treatment. The quadriceps femoris muscle harvested for histology. Results: Diabetic herbal treated rats became euglycemic by the end of 8 weeks. GPx activity was significantly (p<0.05) elevated compared to control. The histology of skeletal muscle fibers of the diabetic rats treated with herbal formulation and metformin showed minimal level of damage.Conclusions: The findings in this study showed that the herbal formulation could be used in treatment of diabetes and in ameliorating the associated muscular cytoarchitectural alterations. Keywords: diabetic, extract, glutathione, peroxidase

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31

Djiwa, Toukilnan, Kossi Akomola Sabi, Panakinao Simgban, Mayi Bombonne, Bagassam Mézéwè Sama, Mazamaesso Tchaou, and Tchin Darré. "Renal Leiomyosarcoma, a Rare Presentation." Journal of Kidney Cancer and VHL 9, no. 1 (March 21, 2022): 51–54. http://dx.doi.org/10.15586/jkcvhl.v9i1.216.

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Renal sarcomas are very rare malignant tumours with a very poor prognosis. Renal leiomyosarcoma, a malignant tumour of smooth muscle origin, is the most common histological type. The article reports a case of leiomyosarcoma of renal location, with a review of the literature. A 38-year-old female patient, with no previous pathological history, consulted the nephrology department of the Teaching Hospital of Lomé for abdominal pain that had been present for 4 years. Histology showed a tumour proliferation of fasciculated architecture, made of spindle cells arranged in long bundles, with cytonuclear atypia and cytoarchitectural abnormalities. Immunohistochemical examination showed positive staining for smooth muscle actin, h-caldesmone, desmin and CD34 and negative for pancytokeratin (AE1/AE3), myogenin and PS100. Renal leiomyosarcoma is an exceptional malignancy. It remains the most common renal sarcoma, the differential diagnosis of which is based on immunohistochemical findings.

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Karam, Renuca, Rajshree Huidrom, Subhalakshmi Wahengbam, Damayanti Ningthoujam, and Saratchandra N. "Prostate Gland in Human Foetuses: A Study of its Histogenesis." International Journal of Anatomy and Research 11, no. 2 (June 5, 2023): 8600–8609. http://dx.doi.org/10.16965/ijar.2023.103.

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Background: To study the histogenesis of the prostate gland in human foetuses. ‘Prostates’ is a Greek word which literally means “one who stands before”, protector, guardian. It is important from a clinical point of view as it undergoes benign enlargement from the fifth decade, hence attracting the attention of males around this age and simultaneously the clinicians. Materials and Methods: 100 foetuses of different gestational ages ranging from 14 weeks (85 mm) to 40 weeks (440 mm), products of terminated pregnancies under Medical Termination of Pregnancy, MTP Act of India, 1971 and stillbirths were collected from the Department of Obstetrics and Gynaecology, RIMS, (Regional Institute of Medical Sciences), Imphal, Manipur and utilised for the present study with permission from the Institutional Ethical Committee. Results and Discussion: The first sign of differentiation is recognised as increased cellularity and denser mesenchymal cells. Cytoarchitecture at specific age period at different age groups are described. Conclusion: Cytoarchitecturally, differentiation of all the three components of the prostate gland was noted as the age changes. It is inferred that of the three components of the adult tissues, the glandular component is differentiated from the epithelial lining of the urethra. This further induces the early mesenchymal tissues to differentiate into muscles and fibrous components. And at term, it has all the three components of the adult tissues although it is not as mature as in adult. KEY WORDS: Prostate gland, human foetuses, histogenesis and cytoarchitecture.

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Lim, Seh Hong, Tsyr-Jiuan Wang, Guo-Fang Tseng, Yee Fun Lee, Yong-San Huang, Jeng-Rung Chen, and Chen-Li Cheng. "The Distribution of Muscles Fibers and Their Types in the Female Rat Urethra: Cytoarchitecture and Three-Dimensional Reconstruction." Anatomical Record 296, no. 10 (July 5, 2013): 1640–49. http://dx.doi.org/10.1002/ar.22740.

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Naito, Eiichi, Per E. Roland, Christian Grefkes, H. J. Choi, Simon Eickhoff, Stefan Geyer, Karl Zilles, and H. Henrik Ehrsson. "Dominance of the Right Hemisphere and Role of Area 2 in Human Kinesthesia." Journal of Neurophysiology 93, no. 2 (February 2005): 1020–34. http://dx.doi.org/10.1152/jn.00637.2004.

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We have previously shown that motor areas are engaged when subjects experience illusory limb movements elicited by tendon vibration. However, traditionally cytoarchitectonic area 2 is held responsible for kinesthesia. Here we use functional magnetic resonance imaging and cytoarchitectural mapping to examine whether area 2 is engaged in kinesthesia, whether it is engaged bilaterally because area 2 in non-human primates has strong callosal connections, which other areas are active members of the network for kinesthesia, and if there is a dominance for the right hemisphere in kinesthesia as has been suggested. Ten right-handed blindfolded healthy subjects participated. The tendon of the extensor carpi ulnaris muscles of the right or left hand was vibrated at 80 Hz, which elicited illusory palmar flexion in an immobile hand (illusion). As control we applied identical stimuli to the skin over the processus styloideus ulnae, which did not elicit any illusions (vibration). We found robust activations in cortical motor areas [areas 4a, 4p, 6; dorsal premotor cortex (PMD) and bilateral supplementary motor area (SMA)] and ipsilateral cerebellum during kinesthetic illusions (illusion-vibration). The illusions also activated contralateral area 2 and right area 2 was active in common irrespective of illusions of right or left hand. Right areas 44, 45, anterior part of intraparietal region (IP1) and caudo-lateral part of parietal opercular region (OP1), cortex rostral to PMD, anterior insula and superior temporal gyrus were also activated in common during illusions of right or left hand. These right-sided areas were significantly more activated than the corresponding areas in the left hemisphere. The present data, together with our previous results, suggest that human kinesthesia is associated with a network of active brain areas that consists of motor areas, cerebellum, and the right fronto-parietal areas including high-order somatosensory areas. Furthermore, our results provide evidence for a right hemisphere dominance for perception of limb movement.

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"Cytoarchitecture and fibre connections of the Edinger-Westphal nucleus in the filefish." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 337, no. 1279 (July 29, 1992): 73–81. http://dx.doi.org/10.1098/rstb.1992.0085.

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Many teleosts have an intraocular lens muscle which causes lens movement for visual accommodation. Central pathways for visual accommodation were traced in the filefish ( Novodon modestus ) using horseradish peroxidase (HRP) tracing method. After HRP injection into the lens muscle, large cells were labelled in the ciliary ganglion. After HRP injections into the ciliary ganglion, a compact cell group was retrogradely labelled in an area rostrodorsal to the somatic oculomotor nuclei in the midbrain. The nucleus consisted of about 90 cells which were slightly smaller than the somatic oculomotor neurons. This nucleus was considered to be homologous with the mammalian Edinger-Westphal nucleus. After injections of HRP into the Edinger-Westphal nucleus, cells in the nucleus of the posterior commissure were retrogradely labelled. Because the nucleus of the posterior commissure receives retinal projections (Ito et al. 1984), it is considered that the cells in the nucleus of the posterior commissure are the first central neurons in the pathway for visual accommodation in teleosts.

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Donald, Lorenzo, and Edward G. Lakatta. "What makes the sinoatrial node tick? A question not for the faint of heart." Philosophical Transactions of the Royal Society B: Biological Sciences 378, no. 1879 (May 2023). http://dx.doi.org/10.1098/rstb.2022.0180.

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Even before the sinoatrial node (SAN) was discovered, cardiovascular science was engaged in an active investigation of when and why the heart would beat. After the electrochemical theory of bioelectric membrane potentials was formulated and the first action potentials were measured in contracting muscle cells, the field became divided: some investigators studied electrophysiology and ion channels, others studied muscle contraction. It later became known that changes in intracellular Ca 2+ cause contraction. The pacemaking field was reunited by the coupled-clock theory of pacemaker cell function, which integrated intracellular Ca 2+ cycling and transmembrane voltage into one rhythmogenic system. In this review, we will discuss recent discoveries that contextualize the coupled-clock system, first described in isolated SAN cells, into the complex world of SAN tissue: heterogeneous local Ca 2+ releases, generated within SAN pacemaker cells and regulated by the other cell types within the SAN cytoarchitecture, variably co-localize and synchronize to give rise to relatively rhythmic impulses that emanate from the SAN to excite the heart. We will ultimately conceptualize the SAN as a brain-like structure, composed of intercommunicating meshworks of multiple types of pacemaker cells and interstitial cells, intertwined networks of nerves and glial cells and more. This article is part of the theme issue ‘The heartbeat: its molecular basis and physiological mechanisms’.

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Win, Zaw, Justin M. Buksa, Kerianne E. Steucke, G. W. Gant Luxton, Victor H. Barocas, and Patrick W. Alford. "Cellular Microbiaxial Stretching to Measure a Single-Cell Strain Energy Density Function." Journal of Biomechanical Engineering 139, no. 7 (June 6, 2017). http://dx.doi.org/10.1115/1.4036440.

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The stress in a cell due to extracellular mechanical stimulus is determined by its mechanical properties, and the structural organization of many adherent cells suggests that their properties are anisotropic. This anisotropy may significantly influence the cells' mechanotransductive response to complex loads, and has important implications for development of accurate models of tissue biomechanics. Standard methods for measuring cellular mechanics report linear moduli that cannot capture large-deformation anisotropic properties, which in a continuum mechanics framework are best described by a strain energy density function (SED). In tissues, the SED is most robustly measured using biaxial testing. Here, we describe a cellular microbiaxial stretching (CμBS) method that modifies this tissue-scale approach to measure the anisotropic elastic behavior of individual vascular smooth muscle cells (VSMCs) with nativelike cytoarchitecture. Using CμBS, we reveal that VSMCs are highly anisotropic under large deformations. We then characterize a Holzapfel–Gasser–Ogden type SED for individual VSMCs and find that architecture-dependent properties of the cells can be robustly described using a formulation solely based on the organization of their actin cytoskeleton. These results suggest that cellular anisotropy should be considered when developing biomechanical models, and could play an important role in cellular mechano-adaptation.

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Mnuskina, Sofia, Julian Bauer, Anette Wirth-Hücking, Dominik Schneidereit, Stefanie Nübler, Paul Ritter, Nicola Cacciani, Meishan Li, Lars Larsson, and Oliver Friedrich. "Single fibre cytoarchitecture in ventilator-induced diaphragm dysfunction (VIDD) assessed by quantitative morphometry second harmonic generation imaging: Positive effects of BGP-15 chaperone co-inducer and VBP-15 dissociative corticosteroid treatment." Frontiers in Physiology 14 (June 27, 2023). http://dx.doi.org/10.3389/fphys.2023.1207802.

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Ventilator-induced diaphragm dysfunction (VIDD) is a common sequela of intensive care unit (ICU) treatment requiring mechanical ventilation (MV) and neuromuscular blockade (NMBA). It is characterised by diaphragm weakness, prolonged respirator weaning and adverse outcomes. Dissociative glucocorticoids (e.g., vamorolone, VBP-15) and chaperone co-inducers (e.g., BGP-15) previously showed positive effects in an ICU-rat model. In limb muscle critical illness myopathy, preferential myosin loss prevails, while myofibrillar protein post-translational modifications are more dominant in VIDD. It is not known whether the marked decline in specific force (force normalised to cross-sectional area) is a pure consequence of altered contractility signaling or whether diaphragm weakness also has a structural correlate through sterical remodeling of myofibrillar cytoarchitecture, how quickly it develops, and to which extent VBP-15 or BGP-15 may specifically recover myofibrillar geometry. To address these questions, we performed label-free multiphoton Second Harmonic Generation (SHG) imaging followed by quantitative morphometry in single diaphragm muscle fibres from healthy rats subjected to five or 10 days of MV + NMBA to simulate ICU treatment without underlying confounding pathology (like sepsis). Rats received daily treatment of either Prednisolone, VBP-15, BGP-15 or none. Myosin-II SHG signal intensities, fibre diameters (FD) as well as the parameters of myofibrillar angular parallelism (cosine angle sum, CAS) and in-register of adjacent myofibrils (Vernier density, VD) were computed from SHG images. ICU treatment caused a decline in FD at day 10 as well as a significant decline in CAS and VD from day 5. Vamorolone effectively recovered FD at day 10, while BGP-15 was more effective at day 5. BGP-15 was more effective than VBP-15 in recovering CAS at day 10 although not to control levels. In-register VD levels were restored at day 10 by both compounds. Our study is the first to provide quantitative insights into VIDD-related myofibrillar remodeling unravelled by SHG imaging, suggesting that both VBP-15 and BGP-15 can effectively ameliorate the structure-related dysfunction in VIDD.

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Roy, Mahua Guha, Sanghamitra Pal, Kaushik Sarkar, Mukti Mondal, and Goutam Paul. "Fluoride Facilitates Contraction of Duodenal Smooth Muscle in Rat by Inhibiting the Enzymatic Activity of Acetylcholinesterase and Promoting Oxidative Stress." International Journal of Pharmaceutical Sciences Review and Research, March 15, 2022, 69–76. http://dx.doi.org/10.47583/ijpsrr.2022.v73i01.013.

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The aim of the present study was to examine the effects of fluoride on the contraction of visceral smooth muscle of duodenum, the initial segment of small intestine, in rat model. We have observed significant potentiation of the movement of the duodenum ex vivo in a dose and duration dependent manner in sodium fluoride exposed rats compared to control group of rats (7.5 mgNaF/KgBW/Day, 15 mgNaF/KgBW/Day, 30 mgNaF/KgBW/Day for 14 and 28 days durations). This result indicates that fluoride potentiates the duodenal movement probably by promoting the contraction of visceral smooth muscle found in the wall structure of duodenum. Further, a significant inhibition of the enzymatic activity of acetylcholinesterase (AChE) in duodenal smooth muscle homogenate in fluoride exposed groups of rats has been observed. This result suggests that fluoride induced potentiation of the contraction of duodenal smooth muscle might be due to inhibition of the enzymatic activity of AChE. To examine the involvement of smooth muscular oxidative stress in fluoride induced potentiation of smooth muscle contraction of duodenum, the effects of fluoride on oxidative stress variables have been studied. We have observed significant inhibition of the enzymatic activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), glutathione S-transferase (GST) and increase in the level of malondialdehyde (MDA) in smooth muscle homogenate of duodenum in exposed groups of rats. These findings indicate that fluoride might facilitate smooth muscle contraction by inducing oxidative stress. We have also found significant cytoarchitectural changes in stained duodenal wall structure in exposed groups of rats. This result suggests that fluoride may promote structural degeneration of muscle probably by inducing oxidative stress. In conclusion, fluoride potentiates the contraction of duodenal visceral smooth muscle of rat probably by inhibiting the enzymatic activity of AChE and inducing cellular oxidative stress.

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Dey, Chaitali, and Goutam Paul. "Sodium Benzoate (NaB) Induced Impairment of the Functions of Duodenal Visceral Smooth Muscle (VSM) ex vivo in Rat." International Journal of Pharmaceutical Sciences Review and Research, July 15, 2022, 216–22. http://dx.doi.org/10.47583/ijpsrr.2022.v75i01.037.

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Sodium benzoate (NaB) is a versatile food additive used to preserve packaged foods and beverages. Thus, people are unknowingly consuming it above the WHO recommended daily intake limit which draws our attention to experimenting with the effects of NaB on contractile functions of visceral smooth muscle (VSM) of the small intestine, the primary target organ exposed to NaB during digestion and absorption of food, in the albino rat model. We have observed a significant (p<0.05) increase in amplitude and decrease in the frequency of the contraction of the duodenum, the initial part of the small intestine, in dose and duration response manner in NaB exposed groups of rats compared to control contractions. This result indicates that NaB probably impairs the contraction of duodenal VSM by promoting the activity of myenteric cholinergic and/or the activity of adrenergic and/or nitrergic efferents. We have also found, a significant (p<0.05) decrease in the activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and glutathione reductase (GR) and an increase in the level of malondialdehyde (MDA) in duodenal VSM homogenate of groups of exposed rats compared to control. These results suggest that NaB probably impairs the contractile function of VSM by altering the functions of myenteric intrinsic efferents by producing oxidative stress in VSM and/or in intrinsic neurons. Further, we have found significant degenerative lesions and altered tissue architecture in the muscularis externa layer of the wall of the duodenum in NaB exposed hematoxylin and eosin stained duodenal tissue sections. These findings reveal that NaB might impair the contractile function of duodenal VSM by inducing the oxidative stress induced degenerations of the architecture of muscle at tissue and cellular levels. Hence, it is concluded that NaB impairs the contraction of duodenal VSM probably by inducing the cytoarchitectural degenerations of VSM structure and/or altering the functions of myenteric intrinsic efferent through oxidative stress.

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