THE APODEME COMPLEX OF THE FEMORAL CHORDOTONAL ORGAN IN THE METATHORACIC LEG OF THE LOCUST SCHISTOCERCA GREGARIA

1992 ◽  
Vol 163 (1) ◽  
pp. 345-358 ◽  
Author(s):  
P. M.J. SHELTON ◽  
R. O. STEPHEN ◽  
J. J.A. SCOTT ◽  
A. R. TINDALL

The mechanical connections of the metathoracic femoral chordotonal organ (mtFCO) with its insertion at the femoro-tibial joint are described. The apodeme complex is shown to consist of a distal cuticular rod that is replaced proximally by dorsal and ventral ligaments. The dorsal ligament is a direct continuation of the distal rod but proximally it is replaced by ligamentous cells. The ventral ligament has no cuticular core and consists of ligamentous cells throughout its length. The ligaments are composed of bundles of connective tissue cells that are each enclosed in an extracellular matrix containing acid-fuchsin-staining fibrils. Internally the cells are packed with microtubules. During extension and flexion of the joint, the two ligaments move differentially. During passive extension of the tibia, the ventral ligament remains taut but the dorsal one buckles to form a slack loop. Direct observation of living preparations shows that the loop is first detectable during extension of the tibia at joint angles greater than about 51°. During flexion, the loop gradually tightens and disappears. It has completely disappeared at joint angles of less than about 36°. Changes in loop shape were demonstrable using preparations in which the tibia was moved sinusoidally ±10° about a mean femoro-tibial angle of 90° and photographs were taken using phase-locked illumination. Other details of the apodeme complex are described and the significance of the findings is discussed in relation to mtFCO function.

Connective tissue cells are capable of both synthesizing and degrading the macromolecular components of the extracellular matrix. The degradation of proteoglycan and collagen has been shown to be associated with the extracellular release of proteolytic enzymes, some of which are of lysosomal origin. The identity in cartilage of two previously unrecognized proteases, capable of proteoglycan breakdown (CPGases), has recently been achieved by the use of a new assay for proteoglycan degradation. These enzymes have been shown to be synthesized and released in response to vitamin A. The third proteoglycan degrading enzyme of connective tissue cells, cathepsin D, has been located in the pericellular environment by trapping with specific antibody and the pattern of release studied in organ culture, experimental arthritis and in human rheumatoid tissues. The secretion of this enzyme and possibly also of the other CPGases is thought to be of importance in the local (pericellular) turnover of matrix macromolecules and, in association with collagenase, to be the cause of the excessive degradation in the pannus erosion of articular cartilage in rheumatoid arthritis.


Diabetes ◽  
1991 ◽  
Vol 40 (5) ◽  
pp. 605-611 ◽  
Author(s):  
P. Muona ◽  
J. Peltonen ◽  
S. Jaakkola ◽  
J. Uitto

2021 ◽  
Vol 22 (3) ◽  
pp. 1411
Author(s):  
Caterina Fede ◽  
Carmelo Pirri ◽  
Chenglei Fan ◽  
Lucia Petrelli ◽  
Diego Guidolin ◽  
...  

The fascia can be defined as a dynamic highly complex connective tissue network composed of different types of cells embedded in the extracellular matrix and nervous fibers: each component plays a specific role in the fascial system changing and responding to stimuli in different ways. This review intends to discuss the various components of the fascia and their specific roles; this will be carried out in the effort to shed light on the mechanisms by which they affect the entire network and all body systems. A clear understanding of fascial anatomy from a microscopic viewpoint can further elucidate its physiological and pathological characteristics and facilitate the identification of appropriate treatment strategies.


2004 ◽  
Vol 15 (3) ◽  
pp. 165-175 ◽  
Author(s):  
P. C. Trackman ◽  
A. Kantarci

Gingival overgrowth occurs mainly as a result of certain anti-seizure, immunosuppressive, or antihypertensive drug therapies. Excess gingival tissues impede oral function and are disfiguring. Effective oral hygiene is compromised in the presence of gingival overgrowth, and it is now recognized that this may have negative implications for the systemic health of affected patients. Recent studies indicate that cytokine balances are abnormal in drug-induced forms of gingival overgrowth. Data supporting molecular and cellular characteristics that distinguish different forms of gingival overgrowth are summarized, and aspects of gingival fibroblast extracellular matrix metabolism that are unique to gingival tissues and cells are reviewed. Abnormal cytokine balances derived principally from lymphocytes and macrophages, and unique aspects of gingival extracellular matrix metabolism, are elements of a working model presented to facilitate our gaining a better understanding of mechanisms and of the tissue specificity of gingival overgrowth.


2016 ◽  
Vol 31 (6) ◽  
pp. 844-850 ◽  
Author(s):  
Anne Schneider ◽  
Isabelle Talon ◽  
Eric Mathieu ◽  
Pierre Schaaf ◽  
François Becmeur ◽  
...  

Congenital diaphragmatic hernia is a severe disease requiring diaphragm replacement mostly with expanded polytetrafluoroethylene. Unfortunately, the recurrence rate is high due to prosthesis failure with significant morbidity for the child. To provide a better understanding of the integration and possible failure processes of the biomaterial implanted in humans, we conducted electron microscopical and mechanical assessments on a prosthesis explant from a child with congenital diaphragmatic hernia presenting a recurrence. Our findings show a major penetration of connective tissue into the expanded polytetrafluoroethylene on the rough side, whereas the smooth side presents few tissue colonization. This penetration is more important in the central area (area A) with large collagen bundles and layers, in comparison to the peripheral areas without prosthesis failure (area B), where few extracellular matrix is produced. The connective tissue penetrates the prosthesis in depth. In contrast, the peripheral areas with prosthesis failure (area C) show very few cells and extracellular matrix, with an oriented organization in comparison to areas A and B. Obviously, the forces applied on the implanted material modulate the cellular behavior of the newly developed tissues. Atomic force microscopic measurements of the biomaterials’ surfaces may explain some cellular behaviors according to areas with or without failure.


2006 ◽  
Vol 290 (1) ◽  
pp. L153-L161 ◽  
Author(s):  
Janette K. Burgess ◽  
Qi Ge ◽  
Maree H. Poniris ◽  
Sarah Boustany ◽  
Stephen M. Twigg ◽  
...  

Airway remodeling describes the structural changes that occur in the asthmatic airway that include airway smooth muscle hyperplasia, increases in vascularity due to angiogenesis, and thickening of the basement membrane. Our aim in this study was to examine the effect of transforming growth factor-β on the release of connective tissue growth factor and vascular endothelial growth factor from human airway smooth muscle cells derived from asthmatic and nonasthmatic patients. In addition we studied the immunohistochemical localization of these cytokines in the extracellular matrix after stimulating bronchial rings with transforming growth factor-β. Connective tissue growth factor and vascular endothelial growth factor were released from both cell types and colocalized in the surrounding extracellular matrix. Prostaglandin E2 inhibited the increase in connective tissue growth factor mRNA but augmented the release of vascular endothelial growth factor. Matrix metalloproteinase-2 decreased the amount of connective tissue growth factor and vascular endothelial growth factor, but not fibronectin deposited in the extracellular matrix. This report provides the first evidence that connective tissue growth factor may anchor vascular endothelial growth factor to the extracellular matrix and that this deposition is decreased by matrix metalloproteinase-2 and prostaglandin E2. This relationship has the potential to contribute to the changes that constitute airway remodeling, therefore providing a novel focus for therapeutic intervention in asthma.


1973 ◽  
Vol 57 (3) ◽  
pp. 743-759 ◽  
Author(s):  
Charles K. Jablecki ◽  
John E. Heuser ◽  
Seymour Kaufman

Work-induced growth of rat soleus muscle is accompanied by an early increase in new RNA synthesis. To determine the cell type(s) responsible for the increased RNA synthesis, we compared light autoradiographs of control and hypertrophying muscles from rats injected with tritiated uridine 12, 24, and 48 h after inducing hypertrophy. There was an increased number of silver grains over autoradiographs of hypertrophied muscle. This increase occurred over connective tissue cells; there was no increase in the number of silver grains over the muscle fibers. Quantitative studies demonstrated that between 70 and 80% of the radioactivity in the muscle that survived fixation and washing was in RNA. Pretreatment of the animals with actinomycin D reduced in parallel both the radioactivity in RNA and the number of silver grains over autoradiographs. Proliferation of the connective tissue in hypertrophying muscle was evident in light micrographs, and electron micrographs identified the proliferating cells as enlarged fibroblasts and macrophages; the connective tissue cells remained after hypertrophy was completed. Thus, proliferating connective tissue cells are the major site of the increase in new RNA synthesis during acute work-induced growth of skeletal muscle. It is suggested that in the analysis of physiological adaptations of muscle, the connective tissue cells deserve consideration as a site of significant molecular activity.


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