scholarly journals Interstitial spaces are continuous across tissue and organ boundaries in humans

2020 ◽  
Author(s):  
Odise Cenaj ◽  
Douglas H. R. Allison ◽  
R Imam ◽  
Briana Zeck ◽  
Lilly M. Drohan ◽  
...  
Keyword(s):  
Fibrous Tissue ◽  
The Body ◽  
Cell Trafficking ◽  
Molecular Signaling ◽  
Extracellular Matrix Components ◽  
Tattoo Pigment ◽  
Flow Through ◽  
Macromolecular Component ◽  
Fibrous Tissues ◽  
Organ Boundaries

AbstractBodies have “reticular networks” comprising collagens, elastin, glycosaminoglycans, and other extracellular matrix components, that are continuous within and around all organs. Fibrous tissue coverings of nerves and blood vessels create structural continuity beyond organ boundaries. We recently described fluid flow through such human fibrous tissues. It remains unclear whether these interstitial spaces are continuous through the body or are discontinuous, confined within individual organs. We investigated IS continuity using two approaches. Non-biological particles (tattoo pigment, colloidal silver) were tracked within colon and skin interstitial spaces and into adjacent fascia. We also exploited hyaluronic acid, a macromolecular component of interstitial spaces. Both techniques demonstrate continuity of interstitial spaces within and across organ boundaries, including within perineurium and vascular adventitia traversing organs and the spaces between them. We suggest a body-wide network of fluid-filled interstitial spaces with significant implications for molecular signaling, cell trafficking, and the spread of malignant and infectious disease.

scholarly journals Evidence for continuity of interstitial spaces across tissue and organ boundaries in humans

2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Odise Cenaj ◽  
Douglas H. R. Allison ◽  
Rami Imam ◽  
Briana Zeck ◽  
Lilly M. Drohan ◽  
...  
Keyword(s):  
The Body ◽  
Cell Trafficking ◽  
Molecular Signaling ◽  
Extracellular Matrix Components ◽  
Show Evidence ◽  
Tattoo Pigment ◽  
Flow Through ◽  
Macromolecular Component ◽  
Fibrous Tissues ◽  
Organ Boundaries

AbstractBodies have continuous reticular networks, comprising collagens, elastin, glycosaminoglycans, and other extracellular matrix components, through all tissues and organs. Fibrous coverings of nerves and blood vessels create structural continuity beyond organ boundaries. We recently validated fluid flow through human fibrous tissues, though whether these interstitial spaces are continuous through the body or discontinuous, confined within individual organs, remains unclear. Here we show evidence for continuity of interstitial spaces using two approaches. Non-biological particles (tattoo pigment, colloidal silver) were tracked within colon and skin interstitial spaces and into adjacent fascia. Hyaluronic acid, a macromolecular component of interstitial spaces, was also visualized. Both techniques demonstrate interstitial continuity within and between organs including within perineurium and vascular adventitia traversing organs and the spaces between them. We suggest that there is a body-wide network of fluid-filled interstitial spaces that has significant implications for molecular signaling, cell trafficking, and the spread of malignant and infectious disease.

scholarly journals High-resolution 3D tractography of fibrous tissue based on polarization-sensitive optical coherence tomography

2019 ◽  
Vol 245 (4) ◽  
pp. 273-281 ◽  
Author(s):  
Gang Yao ◽  
Dongsheng Duan
Keyword(s):  
Optical Coherence Tomography ◽  
High Resolution ◽  
Fibrous Tissue ◽  
The Body ◽  
Great Promise ◽  
Imaging Method ◽  
Optical Coherence ◽  
Fiber Architecture ◽  
Fibrous Tissues ◽  
Fiber Organization

Fibrous tissues play important roles in many parts of the body. Their highly organized directional structure is essential in achieving their normal biomechanical and physiological functions. Disruption of the typical fiber organization in these tissues is often linked to pathological changes and disease progression. Tractography is a specialized imaging method that can reveal the detailed fiber architecture. Here, we review recent developments in high-resolution optical tractography using Jones matrix polarization-sensitive optical coherence tomography. We also illustrate the use of this new tractography technology for visualizing depth-resolved, three-dimensional fibrous structures and quantifying tissue damages in several major fibrous tissues. Impact statement Organized fiber structure plays an essential role in realizing normal biological functions in fibrous tissues. A thorough understanding of the structure–function relationship in these tissues is crucial for developing effective technology to diagnose and treat diseases. Tractography imaging is an effective tool in visualizing and quantifying fiber architecture in fibrous tissues. This review describes a recently developed tractography technology that has shown great promise for fast image of 3D fiber organization with microscopic details.

scholarly journals MiR-140-3p inhibits the cell viability and promotes apoptosis of synovial fibroblasts in rheumatoid arthritis through targeting sirtuin 3

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Beibei Zu ◽  
Lin Liu ◽  
Jingya Wang ◽  
Meirong Li ◽  
Junxia Yang
Keyword(s):  
Rheumatoid Arthritis ◽  
Cell Viability ◽  
Cell Apoptosis ◽  
Caspase 3 ◽  
Pearson Correlation ◽  
Fibrous Tissue ◽  
Synovial Fibroblasts ◽  
Cell Counting ◽  
Sirtuin 3 ◽  
Fibrous Tissues

Abstract Background Synovial fibroblasts (SFs) with the abnormal expressions of miRNAs are the key regulator in rheumatoid arthritis (RA). Low-expressed miR-140-3p was found in RA tissues. Therefore, we attempted to investigate the effect of miR-140-3p on SFs of RA. Methods RA and normal synovial fibrous tissue were gathered. The targets of miR-140-3p were found by bioinformatics and luciferase analysis. Correlation between the expressions of miR-140-3p with sirtuin 3 (SIRT3) was analyzed by Pearson correlation analysis. After transfection, cell viability and apoptosis were detected by cell counting kit-8 and flow cytometry. The expressions of miR-140-3p, SIRT3, Ki67, Bcl-2, Bax, and cleaved Caspase-3 were detected by RT-qPCR or western blot. Results Low expression of miR-140-3p and high expression of SIRT3 were found in RA synovial fibrous tissues. SIRT3 was a target of miR-140-3p. SIRT3 expression was negatively correlated to the expression of miR-140-3p. MiR-140-3p mimic inhibited the MH7A cell viability and the expressions of SIRT3, Ki67, and Bcl-2 and promoted the cell apoptosis and the expressions of Bax and cleaved Caspase-3; miR-140-3p inhibitor showed an opposite effect to miR-140-3p mimic on MH7A cells. SIRT3 overexpression not only promoted the cell viability and inhibited cell apoptosis of MH7A cells but also reversed the effect of miR-140-3p mimic had on MH7A cells. Conclusions The results in this study revealed that miR-140-3p could inhibit cell viability and promote apoptosis of SFs in RA through targeting SIRT3.

scholarly journals Keloidal pathophysiology: Current notions

2021 ◽  
Vol 7 ◽  
pp. 205951312098032
Author(s):  
Chenyu Huang ◽  
Rei Ogawa
Keyword(s):  
Web Of Science ◽  
English Literature ◽  
The Body ◽  
Mechanical Forces ◽  
Healthy Skin ◽  
Level Of Evidence ◽  
Extracellular Matrix Components ◽  
Keloid Formation ◽  
Mechanical Factors ◽  
Pathological Scar

Introduction: Keloids are pathological scars that are notorious for their chronic and relentless invasion into adjacent healthy skin, with commonly seen post-therapeutic recurrence after monotherapies. Methods: An English literature review on keloid pathophysiology was performed by searching the PubMed, Embase and Web of Science databases, to find out the up-to-date relevant articles. The level of evidence was evaluated based on the included studies with the highest level of evidence first. Results: Keloid morphology, signs, symptoms and the histopathological changes that occur in the local cells and extracellular matrix components are described. The theories on the pathophysiology of keloidogenesis that have been proposed to date are also covered; these include endocrinological, nutritional, vascular, and autoimmunological factors. In addition, we describe the local mechanical forces (and the mechanosignalling pathways by which these forces shape keloid cell activities) that promote keloid formation and determine the direction of invasion of keloids and the body sites that are prone to them. Conclusion: A better understanding of this pathological entity, particularly its mechanobiology, will aid the development of new diagnostic and therapeutic strategies for use in the clinic to prevent, reduce or even reverse the growth of this pathological scar. Lay Summary Keloids are skin scars that are famous for their chronic invasion into healthy skin, with commonly seen recurrence after surgeries. Cells such as lymphocytes, macrophages, mast cells and endothelial cells are involved in keloid growth. Particularly, endocrinological, nutritional, vascular, autoimmunological and mechanical factors actively take part in keloid progression.

Myiasis in Bufo regularis caused by a Tabanid Larva

Parasitology ◽  
1924 ◽  
Vol 16 (1) ◽  
pp. 111-112
Author(s):  
Edward Hindle
Keyword(s):  
Fibrous Tissue ◽  
Dorsal Surface ◽  
Body Cavity ◽  
The Body ◽  
Careful Examination ◽  
Large Female ◽  
Considerable Time ◽  
Ventral Region ◽  
Cylindrical Structure ◽  
The Right

In December, 1922, whilst dissecting a large female example of Bufo regularis, one of my students noticed a cylindrical structure extending along the ventral region of the body-cavity. A careful examination showed that this structure consisted of an elongated sac-like diverticulum of the right lung, containing an almost full-grown specimen of a dipterous larva, which could be seen through the membraneous wall of the diverticulum. The base of the latter, in addition to its point of origin from the lung, was also connected to the dorsal surface of the liver by strands of fibrous tissue, suggesting that the growth had been in existence some considerable time in order to cause such adhesions. Posteriorly, the diverticulum hung freely in the body cavity and extended to the extreme hinder end. Its dimensions were 5·5 cm. in length, by 0·5 cm. in diameter, but tapering towards each extremity.

Pressure-flow relations in coronary circulation

1990 ◽  
Vol 70 (2) ◽  
pp. 331-390 ◽  
Author(s):  
J. I. Hoffman ◽  
J. A. Spaan
Keyword(s):  
Coronary Vessels ◽  
Good Evidence ◽  
The Body ◽  
Vascular Compression ◽  
Exact Nature ◽  
Coronary Veins ◽  
Collapsible Tubes ◽  
External Pressures ◽  
Flow Through

The blood vessels that run on the surface of the heart and through its muscle are compliant tubes that can be affected by the pressures external to them in at least two ways. If the pressure outside these vessels is higher than the pressure at their downstream ends, the vessels may collapse and become Starling resistors or vascular waterfalls. If this happens, the flow through these vessels depends on their resistance and the pressure drop from their inflow to the pressure around them and is independent of the actual downstream pressure. In the first part of this review, the physics of collapsible tubes is described, and the possible occurrences of vascular waterfalls in the body is evaluated. There is good evidence that waterfall behavior is seen in collateral coronary arteries and in extramural coronary veins, but the evidence that intramural coronary vessels act like vascular waterfalls is inconclusive. There is no doubt that in systole there are high tissue pressures around the intramyocardial vessels, particularly in the subendocardial muscle of the left ventricle. The exact nature and values of the forces that act at the surface of the small intramural vessels, however, are still not known. We are not certain whether radial (compressive) or circumferential and longitudinal (tensile) stresses are the major causes of vascular compression; the role of collagen struts in modifying the reaction of vessel walls to external pressures is unknown but possibly important; direct examination of small subepicardial vessels has failed to show vascular collapse. One of the arguments in favor of intramyocardial vascular waterfalls has been that during a long diastole the flow in the left coronary artery decreases and reaches zero when coronary arterial pressure is still high: it can be as much as 50 mmHg in the autoregulating left coronary arterial bed and approximately 15-20 mmHg even when the vessels have been maximally dilated. These high zero flow pressures, especially during maximal vasodilatation, have been regarded as indicating a high back pressure to flow that is due to waterfall behavior of vessels that are exposed to tissue pressures.(ABSTRACT TRUNCATED AT 400 WORDS)

Rack Level Modeling of Air Flow Through Perforated Tile in a Data Center

2012 ◽  
Author(s):  
Vaibhav K. Arghode ◽  
Pramod Kumar ◽  
Yogendra Joshi ◽  
Thomas S. Weiss ◽  
Gary Meyer
Keyword(s):  
Data Center ◽  
Body Force ◽  
Air Flow ◽  
The Body ◽  
Physical Models ◽  
Cfd Modeling ◽  
Computational Time ◽  
Force Model ◽  
Flow Through ◽  
Tile Surface

Effective air flow distribution through perforated tiles is required to efficiently cool servers in a raised floor data center. We present detailed computational fluid dynamics (CFD) modeling of air flow through a perforated tile and its entrance to the adjacent server rack. The realistic geometrical details of the perforated tile, as well as of the rack are included in the model. Generally models for air flow through perforated tiles specify a step pressure loss across the tile surface, or porous jump model based on the tile porosity. An improvement to this includes a momentum source specification above the tile to simulate the acceleration of the air flow through the pores, or body force model. In both of these models geometrical details of tile such as pore locations and shapes are not included. More details increase the grid size as well as the computational time. However, the grid refinement can be controlled to achieve balance between the accuracy and computational time. We compared the results from CFD using geometrical resolution with the porous jump and body force model solution as well as with the measured flow field using Particle Image Velocimetry (PIV) experiments. We observe that including tile geometrical details gives better results as compared to elimination of tile geometrical details and specifying physical models across and above the tile surface. A modification to the body force model is also suggested and improved results were achieved.

Positioning and maintenance of embryonic body wall muscle attachments in C. elegans requires the mup-1 gene

Development ◽  
1991 ◽  
Vol 111 (3) ◽  
pp. 667-681 ◽  
Author(s):  
P.Y. Goh ◽  
T. Bogaert
Keyword(s):  
Extracellular Matrix ◽  
Body Wall ◽  
Early Stage ◽  
Muscle Growth ◽  
The Body ◽  
Body Wall Muscle ◽  
C Elegans ◽  
Extracellular Matrix Molecule ◽  
Extracellular Matrix Components ◽  
Body Wall Muscles

As part of a general study of genes specifying a pattern of muscle attachments, we identified and genetically characterised mutants in the mup-1 gene. The body wall muscles of early stage mup-1 embryos have a wild-type myofilament pattern but may extend ectopic processes. Later in embryogenesis, some body wall muscles detach from the hypodermis. Genetic analysis suggests that mup-1 has both a maternal and a zygotic component and is not required for postembryonic muscle growth and attachment. mup-1 mutants are suppressed by mutations in several genes that encode extracellular matrix components. We propose that mup-1 may encode a cell surface/extracellular matrix molecule required both for the positioning of body wall muscle attachments in early embryogenesis and the subsequent maintenance of these attachments to the hypodermis until after cuticle synthesis.

Memoirs: On the Structure of the Nephridia and ‘funnels’ of the Indian Leech Hirudinaria with remarks on these organs in Hirudo

1938 ◽  
Vol s2-81 (321) ◽  
pp. 27-80
Author(s):  
M. L. BHATIA
Keyword(s):  
Early Stage ◽  
Fibrous Tissue ◽  
Outer Wall ◽  
Central Canal ◽  
The Body ◽  
Main Lobe ◽  
Excretory Function ◽  
Ciliary Action ◽  
Apical Lobe ◽  
Discrete Structures

1. The nephridial system of Hirudinaria consists of a series of seventeen pairs of nephridia metamerically arranged in somites VI to XXII. The first sis pairs occur in the pretesticular segments (VI-XI), while the remaining eleven pairs lie in the testicular segments (XII-XXII). 2. A typical nephridium consists of the following parts: (i) the initial lobe, (ii) the apical lobe, (iii) the inner lobe, (iv) the main lobe, (v) the vesicle-duct and the vesicle. All the nephridia in the testicular region possess ‘funnels’ (ciliated organs) which are enclosed within the ampullae of the perinephrostoniial sinus. There is no continuity or connexion of these ‘funnels’ with the nephridia in the adult leech. 3. The inner end of the initial lobe is directed towards the testis-sac and either ends freely within the connective tissue without coming in contact with the testis-sac, o r- is embedded in fibrous tissue in external contact with the wall of the sac, or becomes incorporated within the outer wall of the perinephrostomial sinus. 4. The initial lobe (testis-lobe) forms a very long coiled string of cells round the apical lobe and part of the inner lobe. The inner lobe (the ‘recurrent lobe’ of Bourne) forms a distinct strip of nephridial tissue enclosed between the two limbs of the main lobe besides a small piece which runs alongside the apical lobe. The inner lobe canals serve to connect the intra-cellular canals of all the lobes with one another. 5. The cells of the different lobes of the nephridium are tunnelled through by intra-cellular canals and canaliculi which form a continuous branching network throughout the body of the nephridium. Besides, there is an intra-cellular central canal which makes 1 3/4 ‘rounds’ through the various lobes of the nephridium and opens into the vesicle. The intra-cellular canals and canaliculi open directly or indirectly into the central canal. 6. The vesicle has no muscular layer, and its wall is not contractile. The evacuation of the contents of the vesicle is brought about by the contraction of ventro-lateral mameles of the bodywall that extend across all the resides. The vesicle and the terminal excretory duet do not develop from the rudiments of the true nepfaritliam, but are formed from an ingrowth of the epidermis. 7. A fully developed adult ‘funnel’ (ciliated organ) is a compound structure consisting of (1) a central reservoir and (2) a large number of small independent funnels set on the reservoir and opening into it. The funnels are profusely dilated. Each funnel is composed of five to six cells, and has the appearance of an ear-lobe with a broad distal and a narrow proximal end. 8. The reservoir is the seat of manufacture of corpuscles which are thrown out of the reservoir through the funnels into the surrounding sinus by the active movements of the cilia of the numerous funnels. 9. The ‘funnel’ is not a degenerate structure. It has, infact, multiplied into numerous small ciliated funnels, which, are much more effective in their ciliary action than a single funnel, even of a large size, could be. Cilia of the funnels show very vigorous movements which keep the fluid in the sinus in constant active circulation. The ciliated organ, instead of serving a renal excretory function, has here become subservient to the sinus-system. 10. The botryoidal vessels are in direct communication with the perinephrostomial sinus. Possibly the corpuscles take up pigment and become the chloragogen cells in the botryoidal vessels. 11. In the embryonic condition the ‘funnel’ is a solid mass of cells which is distinctly continuous with the nephridinm by means of a delicate strand of cells. This connexion of the ‘funnel’ with the nephridium snaps later, and the two become discontinuous and discrete structures. In the embryonic solid ciliated organ the funnel-forming cells can be clearly distinguished from the cells of the reservoir. The ‘funnel’ becomes enclosed at an early stage in the perinephrostomial sinus, which is a part of the reduced coelom. 12. The nephridial system of Hirudo is essentially similar to that of Hirudinaria. In Hirudo the initial lobe does not coil round the apical lobe, but forms one mass round the ampullae of the perinephrostomial sinus and another between the apical and main lobes. The inner end of the nephridium is closed as in Hiradinaria. The ‘funnels’ have the same structure and perform the same function as in Hirudinaria.

Abstract 312: Regulation of Fibrotic Signaling Pathways by Desmosomal Armadillo Proteins in Cardiac Tissue

2014 ◽  
Vol 115 (suppl_1) ◽  
Author(s):  
Adi D Dubash ◽  
Kathleen J Green
Keyword(s):  
Gene Expression ◽  
Signaling Pathways ◽  
Cardiac Disease ◽  
Cardiac Tissue ◽  
Cardiac Fibroblasts ◽  
Fibrous Tissue ◽  
Tgf Beta ◽  
Extracellular Matrix Components ◽  
Different Types ◽  
P38mapk Signaling

The process of fibrosis, described as accumulation of myofibroblasts and excessive deposition of extracellular matrix components, is a key development in the progression of multiple different types of cardiac disease. Nevertheless, little is known about the molecular mechanisms which cause the onset of fibrosis in cardiac disease. Fibrosis is a significant component of arrhythmogenic cardiomyopathy (AC), a genetic disorder characterized by replacement of healthy cardiomyocytes (CMs) with fibrous tissue, leading to arrhythmia and in certain cases, sudden death. AC is often characterized as a “disease of the desmosome”, as mutations for all obligate desmosome proteins have been found in cases of AC, including the desmosome armadillo proteins Plakophilin-2 (PKP2) and Plakoglobin (PG). PKP2 and PG are multi-functional proteins involved in both mechanical stabilization of the cardiac area composita, as well as mediation of desmosome-related signaling pathways. We have determined that loss of PKP2 or PG in neonatal CMs causes an aberrant increase in gene expression of pro-fibrotic stimuli such as transforming growth factor beta 1 (TGF-beta1) and Interleukin-6 (IL-6). In addition, p38 MAPK, a known mediator of inflammatory fibrosis, is activated upon loss of PKP2/PG. We hypothesize that mutation or loss of PKP2 or PG cause the recruitment and activation of cardiac fibroblasts via pro-fibrotic TGF-beta and p38MAPK signaling, resulting in pathological fibrosis characteristic of AC. Indeed, conditioned media from PKP2-silenced CMs causes an increase in fibronectin gene expression by freshly isolated cardiac fibroblasts. Our future experiments will investigate whether inhibition of TGF-beta or p38MAPK signaling can alleviate fibrotic gene production. By highlighting a novel link between desmosome armadillo proteins and pro-fibrotic signaling in cardiac tissue, this study provides mechanistic insights into the pathogenesis of AC, as well as advances our knowledge of potential therapeutic targets for combating fibrosis in multiple different types of heart disease or injury.

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