scholarly journals Plausible Biomedical Consequences of Acupuncture Applied at Sites Characteristic of Acupoints in the Connective-Tissue-Interstitial-Fluid System

Author(s):  
Peter Chin Wan Fung
2017 ◽  
Vol 19 (5) ◽  
pp. 305-314 ◽  
Author(s):  
Katrin Tiffner ◽  
Beate Boulgaropoulos ◽  
Christian Höfferer ◽  
Thomas Birngruber ◽  
Niels Porksen ◽  
...  

1941 ◽  
Vol 73 (1) ◽  
pp. 85-108 ◽  
Author(s):  
Philip D. McMaster

Minute amounts of Locke's or Tyrode's solution have been brought into contact with the interstitial connective tissue of the skin of the living mouse, at atmospheric pressure, in such a manner that the blood or lymphatic vessels are not entered directly. Under such circumstances these absorbable fluids enter the tissue spontaneously. Entrance is strikingly intermittent, not continuous, and so too when very slight pressures are brought to bear on the fluids (1). Hyperemia of the tissues, with accompanying dilatation of the blood vessels, increases the entrance of fluids at atmospheric pressure but it is still intermittent. By contrast, venous obstruction leads to intermittent backflow into the apparatus, but reflex hyperemia, following release of the obstruction, is attended by an increase of flow into the tissues in spite of the great reactive dilatation of vessels. The inflow is also intermittent. If the skin is deprived of circulation, fluid does not enter it at all at atmospheric pressure, though it moves in regularly and continuously if slight pressure is put upon it. Edema-forming fluids, described in the text, also enter in a continuous manner when forced into the skin of either living or dead animals. So too do serum and sperm oil. The findings indicate that the passage of interstitial fluid into the blood vessels may be intermittent under normal circumstances and its escape from them as well. The observed occurrence of intermittent flow in the blood vessels of several tissues (9, 15–25) will go far to account for the intermittent entrance of fluid into the skin.


Some solutions of proteins, under certain conditions of temperature, protein concentration and hydrogen ion concentration, slowly set to a gel. The most familiar example of this phenomenon is the gelation of the heat reversible gelatin gel. Many theories of the mechanism of gel formation have been brought forward. The theory of a framework of hydrated gelatin was originally suggested by Hardy and further developed by Jordan Lloyd.This theory states that "gels are two-phase structures, which can only be formed in the first place from a fluid system ( i. e., by cooling). They consist (1) of a solid framework of precipitated neutral gelatin, with which is combined a certain amount of water; (2) of an interstitial fluid, which is a solution of gelatin in the salt form (either acid or basic). The volume of any system in the gel condition is determined by the equilibrium between two opposing sets of forces. These are (1) the elastic forces of the solid framework which tend to make the volume contract; (2) the osmotic forces of the ionised gelatin salts dissolved in the interstitial fluids which tend to make the volume expand. Neutral gelatin at the iso-electric point cannot make a stable gel, since the constituent of only one phase is present. The gel formed on cooling will be free to contract till it is solid throughout, i. e., it will no longer be a gel. Gelatin in the salt form cannot make a gel, since the constituent of only one phase is present. Gelatin in this form will form only sols with water. The proportion of neutral gelatin to gelatin salts in any system is determined by the reaction of the system."


Infection ◽  
1976 ◽  
Vol 4 (S2) ◽  
pp. S97-S104 ◽  
Author(s):  
H. -U. Eickenberg ◽  
L. Scharfenberger ◽  
N. G. Waterman

Physiology ◽  
1997 ◽  
Vol 12 (1) ◽  
pp. 42-49 ◽  
Author(s):  
RK Reed ◽  
K Woie ◽  
K Rubin

The present review summarizes recent information on the physiology of connective tissues, in particular, control of interstitial fluid pressure (Pif) and, thereby, interstitial volume. A combination of classic physiological techniques and techniques from cellular and molecular biology have provided new insights into control of Pif by connective tissue cells and the adhesion receptors anchoring them to structural connective tissue components.


2020 ◽  
Author(s):  
Shahar Ben-Zeev ◽  
Einat Aharonov ◽  
Liran Goren ◽  
Renaud Toussaint ◽  
Stanislav Parez

<p>Soil liquefaction is one of the most impactful secondary hazards of earthquakes. For example, it played a crucial role in driving the devastating landslides following the 2018 Palu earthquake, Indonesia. While traditionally, the initiation of liquefaction is treated as an undrained phenomenon, evidence shows that a well-drained end-member exists.</p><p>We develop a theory for the coupled grains - pore fluid system, and conduct numerical discrete element – fluid dynamics simulations and lab experiments under well-drained conditions. Here, a well-drained layer means that the interstitial fluid can flow out of the layer faster than a single earthquake shaking period. Theory, simulations, and experiments, all suggest that a saturated granular layer, although well-drained, can liquefy when subjected to horizontal cyclic shear. The liquefaction event, evident by high pore pressure, loss of shear strength, and dissipation of shear waves is spatially and temporally controlled by a compaction front that swipes upward through the layer. The compaction front separates the grain-fluid system into two sub-layers: The bottom sub-layer, below the front, is fully-compacted, and the pore pressure gradient across it is hydrostatic. The top sub-layer, above the front, is actively subsiding, and its pore pressure gradient reaches the total solid stress gradient. I.e., the fluid fully supports the granular skeleton. The velocity of the compaction front depends on the permeability of the soil layer and the viscosity of the interstitial fluid. Analytic considerations of the propagation rate of the compaction front allows us to evaluate the duration of a liquefaction event, the magnitude of soil subsidence, and the timing of water seepage at the surface level, which are all independent of the time scales related to the earthquake shaking. Our approach, when combined with field stratigraphy and groundwater level data, could explain and predict the occurrence and duration of soil liquefaction when the soil layer is effectively drained.</p>


2007 ◽  
Vol 283 (3) ◽  
pp. 1234-1242 ◽  
Author(s):  
Åsa Lidén ◽  
Tijs van Wieringen ◽  
Jonas Lannergård ◽  
Anja Kassner ◽  
Dick Heinegård ◽  
...  

Fibroblast-mediated collagen gel contraction depends on collagen-binding β1 integrins. Perturbation of these integrins reveals an alternative contraction process that is integrin αVβ3-dependent and platelet-derived growth factor (PDGF) BB-stimulated. Connective tissue cells actively control interstitial fluid pressure (IFP), and inflammation-induced lowering of IFP provides a driving force for edema formation. PDGF-BB normalizes a lowered IFP by an αVβ3-dependent process. A potential modulation of IFP by extracellular matrix-binding bacterial proteins has previously not been addressed. The fibronectin (FN)-binding protein FNE is specifically secreted by the highly virulent Streptococcus equi subspecies equi. FNE bound FN and native collagen type I with Kd values of ∼20 and ∼50 nm determined by solid-phase binding assays. Rotary shadowing revealed a single FNE binding site located at on average 122 nm from the C terminus of procollagen type I. FNE induced αVβ3-mediated contraction by C2C12 cells in a concentration-dependent manner having a maximal effect at ∼100 nm. This activity of FNE required cellular FN, and FNE acted synergistically to added plasma FN or PDGF-BB. FNE enhanced binding of soluble FN to immobilized collagen, and conversely the binding of collagen to immobilized FN. Marked bell-shaped concentration dependences for these interactions suggest that FNE forms a bridge between FN and collagen. Finally, FNE normalized dermal IFP lowered by anaphylaxis. Our data suggest that secreted FNE normalized lowering of IFP by stimulating connective tissue cell contraction.


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