Biomedical subjects

X Deng

Publications and source records attributed to X Deng.

At least 73 records · Page 4Linked to original sources

PubMed2000

Influence of process parameters on the protein stability encapsulated in poly-DL-lactide-poly(ethylene glycol) microspheres.

Glucose oxidase (GOD) has been encapsulated as a model protein within poly-DL-lactide-poly(ethylene glycol) (PELA) microspheres to evaluate the activity retention during microencapsulation process. This paper was aimed to investigate the effect of process parameters, such as the preparation method, the used matrix polymer with different compositions, the solvent system and the addition of stabilizer on the structural integrity and activity retention of encapsulated protein. The stability of the protein released during in vitro assay was also assessed. The obtained results showed that the solvent extraction/evaporation method based on the formation of double emulsion w(1)/o/w(2) benefited the activity retention compared with the phase separation method based on the formation of w/o(1)/o(2). And in the emulsion-evaporation system most of the protein activity was lost during the first emulsification procedure to form primary emulsion w(1)/o (ca. 28%) and the second emulsification procedure to form the double emulsion w(1)/o/w(2) (ca. 20%), in contrast to other processes occurring during microspheres preparation. The matrix polymer and the solvent system in the oil phase had an impressive impact on the activity retention, while the addition of gelatin in the internal aqueous phase resulted in no major reduction of activity loss. GOD release from PELA microspheres exhibited a triphasic profile, that is, the initial burst release during the first day, the gradual release over about 1 month, and then the second burst release. The encapsulation of GOD in PELA microspheres was effective in reducing its specific activity loss. Sixty-seven per cent of the initial specific activity retention was detected for the released GOD from microspheres formulation during 1 week of incubation, but nearly all the activity was lost for GOD in solution incubated under the same condition. SDS-PAGE results showed that, although the activity loss was detected, no rough changes of molecular weight of GOD was observed during encapsulation procedure and the initial days of incubation into the in vitro release medium.

Absorbable Implants↗

PubMed2000

Mirk protein kinase is a mitogen-activated protein kinase substrate that mediates survival of colon cancer cells.

We have cloned a novel gene mirk (minibrain-related kinase) encoding a protein kinase that enables colon carcinoma cells to survive under certain stress conditions. Mirk is a mitogen-activated protein kinase substrate but is down-regulated by activated extracellular signal-regulated kinases (erks) in vivo. Mirk contains a PEST region characteristic of rapidly turned over proteins and is broken down to a Mr 57,000 form only in the nucleus. In each of three colon carcinoma cell lines, mirk levels were increased 20-fold when erk activation was blocked by the MEK inhibitor PD98059 in serum-free medium. Addition of IGF-I to activate erks blocked this increase. Mirk was stably overexpressed in two colon carcinoma cell lines to attain levels seen in colon cancers. Each of five mirk transfectants proliferated when switched to serum-free medium and regained rapid growth when serum was restored, whereas five vector control transfectants and three kinase-dead mutant mirk transfectants did not. mirk mRNA levels were elevated in several types of carcinomas, and mirk protein was detected in each of seven colon carcinoma cell lines. mirk was expressed at a higher protein level in Western blots from three of eight colon cancers compared with paired normal colon tissue, suggesting that mirk plays a role in the evolution of a subset of colon cancers. mirk is not mutated in colon carcinomas. Mirk may mediate tumor cell survival in mitogen-poor environments or early in colon cancer development before many autocrine growth factors have been induced.

Amino Acid Sequence↗

PubMed2000

Survival function of ERK1/2 as IL-3-activated, staurosporine-resistant Bcl2 kinases.

Bcl2 phosphorylation at Ser-70 may be required for the full and potent suppression of apoptosis in IL-3-dependent myeloid cells and can result from agonist activation of mitochondrial protein kinase C (PKC). Paradoxically, expression of exogenous Bcl2 can protect parental cells from apoptosis induced by the potent PKC inhibitor, staurosporine (stauro). High concentrations of stauro of up to 1 microM only partially inhibit IL-3-stimulated Bcl2 phosphorylation but completely block PKC-mediated Bcl2 phosphorylation in vitro. These data indicate a role for a stauro-resistant Bcl2 kinase (SRK). We show that aurintricarboxylic acid (ATA), a nonpeptide activator of cellular MEK/mitogen-activated protein kinase (MAPK) kinase, can induce Ser-70 phosphorylation of Bcl2 and support survival of cells expressing wild-type but not the phosphorylation-incompetent S70A mutant Bcl2. A role for a MEK/MAPK as a responsible SRK was implicated because the highly specific MEK/MAPK inhibitor, PD98059, also can only partially inhibit IL-3-induced Bcl2 phosphorylation, whereas the combination of PD98059 and stauro completely blocks phosphorylation and synergistically enhances apoptosis. p44MAPK/extracellular signal-regulated kinase 1 (ERK1) and p42 MAPK/ERK2 are activated by IL-3, colocalize with mitochondrial Bcl2, and can directly phosphorylate Bcl2 on Ser-70 in a stauro-resistant manner both in vitro and in vivo. These findings suggest a role for the ERK1/2 kinases as SRKs. Thus, the SRKs can serve to functionally link the IL-3-stimulated proliferative and survival signaling pathways and, in a novel capacity, may explain how Bcl2 can suppress stauro-induced apoptosis. In addition, although the mechanism of regulation of Bcl2 by phosphorylation is not yet clear, our results indicate that phosphorylation may functionally stabilize the Bcl2-Bax heterodimerization.

Animals↗

PubMed2000

Mechanism and rate of degradation of polyhydroxyoctanoate films in aqueous media: A long-term in vitro study.

The present study investigated the in vitro mechanism and degradation rate of polyhydroxyoctanoate (PHO). Solution-cast PHO films were incubated in either water or isoosmotic phosphate-buffered saline (PBS) for periods ranging from 1 to 24 months. Physical characterization included weight loss, water absorption, pH change, tensile strength, and scanning electron microscopy (SEM) studies. Analytical investigations including electron spectroscopy for chemical analysis, Fourier transform infrared (FTIR) spectroscopy, differential scanning calorimetry (DSC), wide-angle X-ray diffraction, and size exclusion chromatography were also performed to assess chemical and morphological changes to the structure of the PHO. The results show that the PHO-cast films incubated in either water or isoosmotic PBS underwent a simple hydrolytic degradation process characterized by water absorption, gradual molecular weight decrease, and negligible mass loss after 24 months of incubation. DSC results suggest that degradation occurred in the amorphous zone, followed by an attack in the crystalline domain. An increase in the vibration stretching of OH after 24 months of incubation, as revealed by FTIR, may indicate that the degradation process began internally, moving outwardly toward the surface of the PHO films. This process was more rapid in the films incubated in PBS than in those incubated in water. However, no significant changes in the morphology of the films were detected by SEM. This study demonstrated that the in vitro degradation of PHO in water or in PBS is a very slow hydrolytic process, exceeding 2 years. Our findings also suggest that the internal degradation mechanism is faster in PBS because of the ionic strength of the medium and that this internal process surface moves gradually toward the surface.

Biocompatible Materials↗

PubMed2000

The prognostic value of pretherapeutic tetranectin and CA-125 in patients with relapse of ovarian cancer.

OBJECTIVE: The aim of the study was to examine the prognostic values of, respectively, tetranectin (TN) and CA-125 measured in serum from patients presenting with relapse of ovarian cancer (OC). METHODS: TN and CA-125 were measured in serum samples from 75 patients with relapse of OC before the start of second-line chemotherapy. The endpoint used was death of OC. The variables were analyzed by univariate life table analysis and multivariate Cox analysis. RESULTS: A significantly shortened survival was found for patients with low serum TN values compared to patients with serum TN levels above one of the cutoff levels. The survivals are illustrated by life tables. No prognostic function was found for CA-125. TN and relapse </=12 months after primary treatment were the only significant independent prognostic variables among the following variables tested in the Cox analyses: primary and second-line treatment, CA-125, age, histology, performance score, tumor localization, and size. CONCLUSION: Serum TN determination may be valuable in the selection of patients with relapse of OC for new treatment strategies in future studies.

Biomarkers, Tumor↗

PubMed2000

Alternative blood conduits: assessment of whether the porosity of synthetic prostheses is the key to long-term biofunctionality.

The paper examines the effects of water permeability on solid particle (platelet) adhesion and lipid transport through the wall of a blood conduit. Also tested is the capacity of external supports to reduce lipid infiltration into venous grafts. The results indicate that water permeability not only facilitates particle adhesion, but also affects the spatial distribution of the adhesion. The presence of filtration flow leads to a concentration polarisation of atherogenic lipids at the blood/wall interface, with increased lipid concentration from the bulk value towards the interface, thus enhancing the drive potential for lipid infiltration into the vessel wall. An external support to a venous graft guards against excessive distention and significantly reduces lipid infiltration into the venous wall. These results strongly suggest that too high a water permeability or porosity can lead to the late failure of arterial grafting by affecting blood cell interaction with the graft and lipid infiltration into the wall. Therefore the pore structure of an arterial prosthesis is crucial to its long-term biofunctionality. Ideally, a synthetic prosthesis should display pores of adequate size and a structural network that promotes tissue ingrowth, while maintaining water porosity at a physiological level.

Blood Platelets↗

PubMed2000

Study on the relationship between plasma homocysteine and acute cerebral vascular disease.

The levels of plasma homocysteine were determined by using high-performance liquid chromatographic method. It was found that plasma homocysteine levels were significantly higher in the patients with stroke than that in the controls. There was no correlation between plasma homocysteine levels and hypertension, smoking, concentrations of blood glucose or hypertriglyceridesemia. It was suggested that hyperhomocysteinemia may be an independent risk factor for acute cerebral vascular disease.

Cerebral Hemorrhage↗

PubMed2000

PYY regulates pancreatic exocrine secretion through multiple receptors in the awake rat.

Peptide YY (PYY) is one of several regulatory peptides reported to modulate pancreatic secretion. PYY circulates in two forms, PYY1-36 and PYY3-36, and binds to multiple receptor subtypes. We sought to determine if PYY1-36 or PYY3-36 regulates neurally mediated pancreatic secretion through the Y1, Y2, and/or Y5 receptor subtypes. Experiments were conducted in awake, surgically recovered rats. In order to determine the effects of the PYYs on basal pancreatic secretion, either PYY1-36, [Pro34] PYY1-36 (a Y1/Y5 agonist), or PYY3-36 (a Y2/Y5 agonist) were infused for 40 min at doses of 0, 12.5, 25, or 50 pmol/kg/hr while measuring pancreatic juice volume and protein. PYY1-36 increased pancreatic protein secretion at 25 and 50 pmol/kg/hr (P < 0.05) in a dose-dependent manner (P < 0.001, R2 = 0.990). The Y2/Y5 receptor agonist PYY3-36 significantly inhibited pancreatic juice volume and protein at 12.5 and 25 pmol/kg/hr, but stimulated protein secretion at higher doses (P < 0.001, R2 = 0.995). The Y1/Y5 agonist, [Pro34] PYY1-36, had no significant effect on basal pancreatic exocrine secretion. Therefore, PYY1-36, PYY3-36 and [Pro34] PYY1-36 produced different, dose-dependent changes on basal pancreatic exocrine secretion. Inhibition of pancreatic secretion by circulating PYY1-36 and PYY3-36 are primarily mediated by the Y2 receptor. Since [Pro34] PYY1-36 did not change pancreatic secretion, it can be concluded that circulating PYY1-36 or PYY3-36 does not modulate pancreatic secretion through the Y1 or Y5 receptors. Since the stimulatory effects of PYY1-36 on pancreatic secretion could not be explained by the actions of PYY3-36 or [Pro34] PYY1-36 on Y1 or Y2 receptors, and since PYY1-36 fails to bind to Y3 or Y4 receptors, we also conclude that PYY1-36 may stimulate pancreatic secretion in a dose-dependent mechanism through a PYY receptor subtype different from Y1, Y2, Y3, Y4 or Y5.

Animals↗

PubMed2000

Phagocytic and intestinal endothelial and epithelial barrier function during the early stage of small intestinal ischemia and reperfusion injury.

The effects of intestinal ischemia and reperfusion (I/R) on small intestinal mucosal endothelial and epithelial barrier integrity and phagocytic function were assessed in rats subjected to 20- or 40-min mesenteric ischemia and a 3-h reperfusion. The results showed that human serum albumin (125I-HSA) flux through the endothelial layer to the interstitial space increased as did 125I-HSA clearance from blood to the gut lumen and 131I-HSA flux from the gut lumen to the interstitial space in rats with I/R. E. coli adhering to microvilli, invading and passing into the microvessels, were noted on the small intestinal mucosa in animals subjected to 40-min ischemia and a 3-h reperfusion. Phagocytic function increased, especially in the small intestinal wall, lungs, liver, and spleen in the groups with I/R, correlating with the length of ischemia. The results imply that both endothelial and epithelial barrier integrity is impaired in the early phase after I/R and that the epithelial barrier more effectively restricts macromolecular leakage compared with the endothelial barrier. I/R impairs the intestinal barrier not only by causing tissue hypoxia but also by activating the phagocytic system and aggravating barrier damage, which finally may result in bacterial translocation and remote organ dysfunction.

Animals↗

PubMed2000

Methamphetamine-induced neurotoxicity is attenuated in transgenic mice with a null mutation for interleukin-6.

Increasing evidence implicates apoptosis as a major mechanism of cell death in methamphetamine (METH) neurotoxicity. The involvement of a neuroimmune component in apoptotic cell death after injury or chemical damage suggests that cytokines may play a role in METH effects. In the present study, we examined if the absence of IL-6 in knockout (IL-6-/-) mice could provide protection against METH-induced neurotoxicity. Administration of METH resulted in a significant reduction of [(125)I]RTI-121-labeled dopamine transporters in the caudate-putamen (CPu) and cortex as well as depletion of dopamine in the CPu and frontal cortex of wild-type mice. However, these METH-induced effects were significantly attenuated in IL-6-/- animals. METH also caused a decrease in serotonin levels in the CPu and hippocampus of wild-type mice, but no reduction was observed in IL-6-/- animals. Moreover, METH induced decreases in [(125)I]RTI-55-labeled serotonin transporters in the hippocampal CA3 region and in the substantia nigra-reticulata but increases in serotonin transporters in the CPu and cingulate cortex in wild-type animals, all of which were attenuated in IL-6-/- mice. Additionally, METH caused increased gliosis in the CPu and cortices of wild-type mice as measured by [(3)H]PK-11195 binding; this gliotic response was almost completely inhibited in IL-6-/- animals. There was also significant protection against METH-induced DNA fragmentation, measured by the number of terminal deoxynucleotidyl transferase-mediated dUTP nick-end-labeled (TUNEL) cells in the cortices. The protective effects against METH toxicity observed in the IL-6-/- mice were not caused by differences in temperature elevation or in METH accumulation in wild-type and mutant animals. Therefore, these observations support the proposition that IL-6 may play an important role in the neurotoxicity of METH.

Amphetamine↗

PubMed2000

Beneficial effects of lexipafant, a PAF antagonist on gut barrier dysfunction caused by intestinal ischemia and reperfusion in rats.

BACKGROUND: Platelet-activating factor (PAF) may play a pivotal role in the pathogenesis of intestinal ischemic injury. METHODS: The potential role of PAF in intestinal ischemia and reperfusion (I/R) and the development of gut endothelial and epithelial barrier dysfunction and distant organ injury were investigated by pretreatment with a PAF antagonist, lexipafant. Bidirectional permeability of the intestinal barrier, enteric bacterial translocation, protease-antiprotease balance and mucosal histology, and also changes in pulmonary and liver endothelial barrier permeability were measured following intestinal ischemia for 40 min with 6 h of reperfusion in rats. RESULTS: Intestinal mucosal endothelial and epithelial permeabilities significantly increased in animals with I/R. Lexipafant prevented the increase in albumin leakage from blood to the mucosal interstitium and the intestinal lumen during reperfusion, and the mucosal albumin leakage from the gut lumen to blood during I/R. Bacterial translocation was frequently noted in animals with I/R, while only a few positive cultures were obtained in animals with I/R administered lexipafant. Less leakage of fluorescein isothiocyanate dextran 70,000 into the interstitial space and gut lumen in I/R animals with lexipafant pretreatment was found under fluorescein microscopy. Lexipafant also partly prevented C1 inhibitor, prekallikrein, and factor X consumption in I/R animals and partly prevented changes in pulmonary and liver albumin leakage. CONCLUSIONS: PAF seems to play an important role in I/R-associated intestinal dysfunction and the development of distant organ dysfunction, probably by triggering endothelial and epithelial barrier dysfunction. Furthermore, PAF seems to be partly involved in activation of the protease-antiprotease system. The use of PAF antagonists may provide a mode of treatment against I/R-associated organ dysfunction.

Animals↗

PubMed2000

Effects of N-acetylcysteine on pulmonary macrophage activity after intestinal ischemia and reperfusion in rats / with invited commentaries.

BACKGROUND/AIMS: Intestinal ischemia and reperfusion (I/R) is considered to be a critical and triggering event in the development of distal organ dysfunction after a variety of insults. It appears that activated leukocytes, especially polymorphonuclear granulocytes (PMNs), and reactive oxygen species are important mediators in the process. In the present study, the aim was to evaluate the behavior of pulmonary macrophages, acute lung injury and pulmonary endothelial permeability after intestinal I/R, together with potential alterations in pulmonary endothelial and epithelial ultrastructure and cellular membrane system integrity. METHODS: Intestinal ischemia for 40 min was followed by reperfusion for 12 h in the rat. Macrophage uptake of radiolabeled bacteria, levels of pulmonary blood content assessed by radiolabeled red blood cells and pulmonary endothelial permeability of radiolabeled albumin, as well as pulmonary endothelial and epithelial ultrastructure and cellular membrane system integrity by the use of scanning electron microscopy and a tracer was evaluated after 12 h reperfusion. Treatment with the free radical scavenger N-acetylcysteine (NAC) administered prior to reperfusion was evaluated. RESULTS: Overactivation of pulmonary macrophages was noted after intestinal I/R, as was a significant decrease in pulmonary blood content. No increase in pulmonary albumin leakage or increase in pulmonary water content was found after intestinal I/R as compared to controls. Treatment with NAC prevented against intestinal I/R-induced overactivation of pulmonary macrophages and a decrease in pulmonary blood content. CONCLUSION: Reactive oxygen species may be involved in the regulation of pulmonary macrophage function and pulmonary circulation after intestinal I/R.

Acetylcysteine↗

PubMed2000

Body distribution of poly-DL-lactide-poly(ethylene glycol) microspheres with entrapped leptospira interrogans antigens following intravenous and oral administration to guinea-pigs.

Poly-DL-lactide-poly(ethylene glycol) (PELA) microspheres with entrapped antigens were administered intravenously and orally into guinea-pigs to quantitatively determine the in-vivo distribution and release profiles. PELA microspheres containing 125I-labelled outer-membrane protein Leptospira interrogans antigens (125I-OMP) were prepared by double-emulsion solvent extraction procedure, and characterized with respect to size, morphology and in-vitro release profiles. The fractured sections of liver and spleen were inspected by scanning electron microscopy, which indicated that microspheres had successfully been entrapped within the above tissues after intravenous injection and oral administration. At predetermined intervals, the blood and such tissues as the liver, spleen, kidney, thyroid, small intestine and mesentery were collected, and the radioactivity was measured by gamma scintillation counting. Following intravenous administration, 56.7% of administered microspheres were accumulated in immunization-related tissues, and 40.1% of microspheres were located in the liver and spleen. However, there was limited uptake efficiency (8.33%) following oral administration, and 49.5% of the absorbed microspheres were located in the intestinal mucosa. Compared with in-vitro release, the in-vivo release profiles of 125I-OMP from PELA microspheres, determined from the decreasing radioactivity in the above tissues, were much faster and the burst effect was higher. Antigen-loaded PELA microspheres were efficiently entrapped within immunization-related tissues after intravenous administration, but orally administered PELA microspheres showed limited uptake efficiency. Further investigation is needed to improve intestinal absorption.

Administration, Oral↗

PubMed2000

Fast algorithm for chirp transforms with zooming-in ability and its applications.

A general fast numerical algorithm for chirp transforms is developed by using two fast Fourier transforms and employing an analytical kernel. This new algorithm unifies the calculations of arbitrary real-order fractional Fourier transforms and Fresnel diffraction. Its computational complexity is better than a fast convolution method using Fourier transforms. Furthermore, one can freely choose the sampling resolutions in both x and u space and zoom in on any portion of the data of interest. Computational results are compared with analytical ones. The errors are essentially limited by the accuracy of the fast Fourier transforms and are higher than the order 10(-12) for most cases. As an example of its application to scalar diffraction, this algorithm can be used to calculate near-field patterns directly behind the aperture, 0 < or = z < d2/lambda. It compensates another algorithm for Fresnel diffraction that is limited to z > d2/lambdaN [J. Opt. Soc. Am. A 15, 2111 (1998)]. Experimental results from waveguide-output microcoupler diffraction are in good agreement with the calculations.

Algorithms↗

PubMed2000

Comparison of two PCR techniques used in amplification of microdissected plant chromosomes from rice and wheat.

Linker adaptor-mediated PCR (LAM-PCR) and degenerate oligonucleotide primed PCR (DOP-PCR) are major ways to generate chromosome-specific libraries. In this study, these two PCR techniques were used to amplify the microdissected mitotic and meiotic chromosomes from rice and wheat. The results of amplifications were compared, and the advantages and limitations between the two techniques are presented.

Blotting, Southern↗

PubMed2000

Correlation between bone mineral density and sexual hormones in healthy Chinese women.

Osteoporosis is a common disease in women, but not in men. It is usually induced by the deficiency of estrogen after menopause. The lumbar spine is most often affected. We examined 74 healthy Chinese women in whom we measured serum estradiol (E2), estriol (E3), and total testosterone (TTT) by radioimmunoassay (RIA). The bone mineral density (BMD) of the total lumbar spine in the anterior (TLS-A) and lateral (TLS-L) position, the region of interest (ROI) of lateral spine (M-IALS), the forearm, and the total hip (TH) were scanned by a dual-energy X-ray absorptiometer. We found that (1) E2 and all BMD determinations declined significantly after menopause (p < 0.05 for all), except the BMD of TH; (2) the BMD of TLS-L, TH, and forearm correlated significantly with E2 (r = 0.2986, p < 0.05), E3 (r = 0.3380, p < 0.05), and TTT (r = 0.2867, p < 0.05), respectively, by partial correlation analysis. In conclusion, BMD at different sites of the skeleton correlated with the level of different sex hormones. It seems that BMD at different sites of the body is controlled by different sex hormones. Whether this phenomenon should be considered in the choice of hormone replacement therapy, or in improving the BMD diagnostic standard, needs further study.

Adult↗

PubMed2000

Higher prevalence and viral load of TT virus in saliva than in the corresponding serum: another possible transmission route and replication site of TT virus.

Although TT virus (TTV) is transmissible by blood or blood products, many patients with no history of transfusion of blood and blood products have been shown to be infected, suggesting other possible routes of transmission. To investigate the transmission routes and replication sites of TTV, 85 paired saliva and serum samples were studied by semi-nested polymerase chain reaction. The prevalence of TTV DNA was 38% (32/85 samples) and 21% (18/85) in saliva and serum, respectively. Fifteen patients had TTV DNA both in saliva and serum. Six out of fifteen patients had significantly higher viral titers in saliva than in serum, but none had higher titer in serum than in saliva. When the 222 base-pair nucleotide sequences of PCR products amplified from the samples were analyzed, 12 patients had the same genotype/subtype in saliva and serum and exhibited high homology (96-100%). The other 3 had different genotypes/subtypes in saliva and serum, and the homology was 61.9-87.2%. Mixed infection was observed both in saliva and serum. Further studies are required to determine if a subgroup of TTV has tropism to saliva. The high prevalence and viral load of TTV in saliva suggest that salivary fluid may be a possible route of transmission of TTV and that TTV might replicate not only in liver tissue but also in other tissues such as oropharyngeal tissues and/or salivary glands.

Aged↗

PubMed2000

Secretory response of endothelin-1 in cultured human glomerular microvascular endothelial cells to shear stress.

The shear-induced secretory response of endothelin-1 (ET-1) by human microvascular endothelial cells was studied using paired human glomerular microvascular endothelial cell (HGMEC) cultured monolayers exposed to steady-state laminar shear stress for up to 10 hours. The first cell monolayer was subjected to a shear stress of 0.65 N m-2 and the second, 1.3 N m-2. ET-1 secretion was determined by radioimmunoassay. Over 10 hours of shear, the total cumulative secretion of ET-1 was 237.4 pg/cm2 for the monolayer exposed to 1.3 N m-2 and 143.6 pg/cm2 for the monolayer exposed to 0.65 N m-2. The average ET-1 secretion rate was 20.90 +/- 2.15 and 12.45 +/- 1.05 pg/cm2.h at 0.65 N m-2 and 1.3 N m-2, respectively. The results showed that ET-1 secretion varied with the time of shear in a nonlinear fashion. Although the level of shear stress affected the absolute value of ET-1 cumulative secretion and secretion rate, the major secretion period for both monolayers occurred between 2.0 and 8.0 hours, with the peak secretion rate occurring at approximately 5 hours. Thus, the response of cultured human microvascular endothelial cells to shear stress differed from that of large vessel endothelial cell cultures in terms of ET-1 secretion. In addition to the level of shear stress, the time of shear was also an important determinant of ET-1 secretion. Consequently, the heterogeneity of vascular endothelial cells and the time of shear should both be considered in future research on the secretion of vascular endothelial cell cultures.

Capillaries↗