scholarly journals Modeling of temperature field inside the tissue with a blood vessel using the BEM-FDM algorithm

Author(s):  
Ewa Majchrzak ◽  
◽  
Jolanta Borowska ◽  
Joanna Klekot ◽  
Damian Tarasek ◽  
...  
Author(s):  
Ping Zhang ◽  
Wujun Sun ◽  
Yuanguang Zhu ◽  
Xiaojing Zhang ◽  
Mizuo Zhang ◽  
...  

1993 ◽  
Vol 115 (2) ◽  
pp. 175-179 ◽  
Author(s):  
L. X. Xu ◽  
M. M. Chen ◽  
K. R. Holmes ◽  
H. Arkin

The influence of a large blood vessel (larger than 500 μm in diameter) on the local tissue temperature decay following a point source heating pulse was determined numerically using a sink/source method. It was assumed that the vessel was large enough so that the temperature of blood flowing within it remained essentially constant and was unaffected by any local tissue temperature transients. After the insertion of a point source heating pulse, the vessel influence on the local tissue transient temperature field was estimated by representing the vessel as a set of negative fictitious instantaneous heat sources with strength just sufficient to maintain the vessel at a constant temperature. In the surrounding tissue, the Pennes’ tissue heat transfer equation was used to describe the temperature field. Computations have been performed for a range of vessel sizes, probe-vessel spacings and local blood perfusion rates. It was found that the influence of a large vessel on the local tissue temperature decay is more sensitive to its size and location rather than to the local blood perfusion rate. For a heating pulse of 3s duration and 5 mW of power, there is a critical probe-vessel center distance 7R (R, vessel radius) beyond which the larger vessel influence on tissue temperature at the probe can be neglected.


Author(s):  
T. M. Murad ◽  
E. von Haam

Pericytes are vascular satellites present around capillary blood vessels and small venules. They have been observed in almost every tissue of the body and are thought to be related to vascular smooth muscle cells. Morphologically pericytes have great similarity to vascular endothelial cells and also slightly resemble myoepithelial cells.The present study describes the ultrastructural morphology of pericytes in normal breast tissue and in benign tumor of the breast. The study showed that pericytes are ovoid or elongated cells separated from the endothelial cell of the capillary blood vessel by the basement membrane of endothelial cell. The nuclei of pericytes are often very distinctive. Although some are round, oval, or elongated, others show marked irregularity and infolding of the nuclear membrane. The cytoplasm shows mono-or bipolar extension in which the cytoplasmic organelles are located (Fig. 1). These cytoplasmic extensions embrace the capillary blood vessel incompletely. The plasma membrane exhibits multiple areas of focal condensation called hemidesmosomes (Fig. 2, arrow). A variable number of pinocytotic vesicles are frequently seen lining the outer plasma membrane. Normally pericytes are surrounded by a basement membrane which is found more consistently on the outer plasma membrane separating the pericytes from the stromal connective tissue.


Author(s):  
N. Tamura ◽  
T. Goto ◽  
Y. Harada

On account of its high brightness, the field emission electron source has the advantage that it provides the conventional electron microscope with highly coherent illuminating system and that it directly improves the, resolving power of the scanning electron microscope. The present authors have reported some results obtained with a 100 kV field emission electron microscope.It has been proven, furthermore, that the tungsten emitter as a temperature field emission source can be utilized with a sufficient stability under a modest vacuum of 10-8 ~ 10-9 Torr. The present paper is concerned with an extension of our study on the characteristics of the temperature field emitters.


Author(s):  
M.V. Parthasarathy ◽  
C. Daugherty

The versatility of Low Temperature Field Emission SEM (LTFESEM) for viewing frozen-hydrated biological specimens, and the high resolutions that can be obtained with such instruments have been well documented. Studies done with LTFESEM have been usually limited to the viewing of small organisms, organs, cells, and organelles, or viewing such specimens after fracturing them.We use a Hitachi 4500 FESEM equipped with a recently developed BAL-TEC SCE 020 cryopreparation/transfer device for our LTFESEM studies. The SCE 020 is similar in design to the older SCU 020 except that instead of having a dedicated stage, the SCE 020 has a detachable cold stage that mounts on to the FESEM stage when needed. Since the SCE 020 has a precisely controlled lock manipulator for transferring the specimen table from the cryopreparation chamber to the cold stage in the FESEM, and also has a motor driven microtome for precise control of specimen fracture, we have explored the feasibility of using the LTFESEM for multiple-fracture studies of the same sample.


1990 ◽  
Vol 64 (01) ◽  
pp. 091-096 ◽  
Author(s):  
W J Janssens ◽  
F J S Cools ◽  
L A M Hoskens ◽  
J M Van Nueten

SummaryRidogrel (6.3 × 10−6 to 10−4 M) inhibited contractions of isolated rat caudal arteries and rabbit femoral arteries caused by U-46619. The slope of an Arunlakshana-Schild plot (pA2-value: 3.4 × 10−6 M) on the caudal artery was slightly higher than one (1.14). This effect was maximal within}D min of incubation of the blood vessel with the compound and easily reversible. Ridogrel antagonised contractions of isolated rabbit femoral arteries caused by prostaglandin Fzo2α in the same concentration range. Ridogrel also inhibited contractions induced by aggregating rat platelets on isolated rat caudal arteries (itt the presence of ketanserin 4 × 10−7 M) and on isolated rabbit pulmonary and femoral arteries (in the absence of ketanserin). Ridogrel had no effect on Ca2+-induced contractions in depolarised isolated rabbit femoral arteries, and at 10−4 M antagonised serotonin-induced contractions in this blood vessel. Its effect on serotonin-induced contractions was statistically significant but very small on isolated rat caudal arteries. These observations indicate that ridogrel is an antagonist of prostaglandin endoperoxide/thromboxane A2 and prostaglandin F2α raCeptors on vascular smooth muscle.


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