PubMed Health⌕ Search

Biomedical subjects

W H Cheng

Publications and source records attributed to W H Cheng.

At least 19 recordsLinked to original sources
PubMed2006

Crystalline style and tissue redistribution in Perna viridis as indicators of Cu and Pb bioavailabilities and contamination in coastal waters.

The concentrations of Cu, Pb, and Zn in the crystalline style (CS) and in the remaining soft tissues (ST) of the green-lipped mussel Perna viridis from 10 geographical sites along the coastal waters off peninsular Malaysia were determined. The CS, compared with the remaining ST, accumulated higher levels of Cu in both contaminated and uncontaminated samples, indicating that the style has a higher affinity for the essential Cu to bind with metallothioneins. The similar pattern of Cu accumulation in the different ST of mussels collected from clean and Cu-contaminated sites indicated that the detoxification capacity of the metallothioneins had not been overloaded. For Pb, higher levels of the metal in the CS than in the remaining ST were found only in mussels collected from a contaminated site at Kg. Pasir Puteh. This indicated a tissue redistribution of Pb due to its binding to metallothioneins for Pb detoxification and the potential of the CS as an indicator organ of Pb bioavailability and contamination. For Zn, the above two phenomena were not found since no obvious patterns were observed (lower levels of Zn in the CS than in the remaining ST) in contaminated and uncontaminated samples due to the mechanism of partial regulation. Generally, all the different STs studied (foot, mantle, gonad, CS, gill, muscle, and byssus) are good biomonitoring tissues for Cu and Pb bioavailabilities and contamination. Among these organs, the CS was found to be the best organ for biomonitoring Cu. The present data also suggest the use of the tissue redistribution of Pb in P. viridis as an indicator of Pb bioavailability and contamination in coastal waters.

Animals↗
PubMed2000

Performance characteristics of a regenerative catalytic oxidizer for treating VOC-contaminated airstreams.

A pilot apparatus of a regenerative catalytic oxidizer (RCO) equipped with two electrical heaters and two 20-cm i.d. x 200-cm height regenerative beds was used to treat methyl ethyl ketone (MEK) and toluene, respectively, in an airstream. The regenerative beds were packed with gravel (approximate particle size 1.25 cm, specific area 205 m2/m3, and specific heat capacity 840 J/kg degree C) as a solid regenerative material and K-type thermal couples for measuring solid and gas temperatures, respectively. The catalyst bed temperature was kept around 400 degrees C and the gas superficial velocity was operated at 0.234 m/sec. This investigation measured and analyzed distributions of solid and gas temperatures with operating time and variations of volatile organic compound (VOC) concentrations in the regenerative beds. The overall VOC removal efficiency exceeded 98% for MEK and 95% for toluene. Degradation of VOCs will exist for MEK on the surface of solid material (gravel) in the temperature range of 330-400 degrees C, but toluene does not exhibit this phenomenon.

Air Movements↗
PubMed1999

Sugars modulate an unusual mode of control of the cell-wall invertase gene (Incw1) through its 3' untranslated region in a cell suspension culture of maize.

We show here that a cell-wall invertase encoded by the Incw1 gene is regulated at both the transcriptional and posttranscriptional levels by sugars in a heterotrophic cell suspension culture of maize. The Incw1 gene encoded two transcripts: Incw1-S (small) and Incw1-L (large); the size variation was attributable to different lengths in the 3' untranslated region. Both metabolizable and nonmetabolizable sugars induced Incw1-L RNA apparently by default. However, only the metabolizable sugars, sucrose and D-glucose, were associated with the increased steady-state abundance of Incw1-S RNA, the concomitant increased levels of INCW1 protein and enzyme activity, and the downstream metabolic repression of the sucrose synthase gene, Sh1. Conversely, nonmetabolizable sugars, including the two glucose analogs 3-O-methylglucose and 2-deoxyglucose, induced greater steady-state levels of the Incw1-L RNA, but this increase did not lead to either an increase in the levels of the INCW1 protein/enzyme activity or the repression of the Sh1 gene. We conclude that sugar sensing and the induction of the Incw1 gene is independent of the hexokinase pathway. More importantly, our results also suggest that the 3' untranslated region of the Incw1 gene acts as a regulatory sensor of carbon starvation and may constitute a link between sink metabolism and cellular translation in plants.

3' Untranslated Regions↗
PubMed1999

Technology development in breath microanalysis for clinical diagnosis.

A new generation of breath tests detects trace amounts of endogenous volatile organic compounds (VOCs) present in the breath. The breath microanalysis is potentially fast and convenient. It opens up a new promising area of using the breath test as a noninvasive diagnostic tool for a variety of diseases. Recent developments in microanalysis technology are expected to greatly facilitate the use of the breath test in clinical evaluations and applications, and these developments are described in the present review.

Breath Tests↗
PubMed1999

Knockout of cellular glutathione peroxidase gene renders mice susceptible to diquat-induced oxidative stress.

Two experiments were conducted to determine the protection and the underlying mechanisms of cellular glutathione peroxidase (GPX1) against lethal, acute oxidative stress induced by an intraperitoneal injection of 24 mg diquat/kg body weight. In experiment 1, mortality and survival times were compared among selenium (Se)-adequate or deficient GPX1 knockout mice [GPX1(-/-)] and wild-type mice (WT). In experiment 2, mice from these four groups were euthanized at 0, 1, 2, and 3 h after the injection of diquat to elucidate the time course of oxidative events. The stress produced 100% mortality in all of the groups except for the Se-adequate WT, which were euthanized on day 7 for analysis. The Se-deficient WT and the Se-adequate GPX1(-/-) had similar survival times (4.1 and 3.9 h), which were longer (p < .05) than that of the Se-deficient GPX1(-/-) (2.4 h). However, these three GPX1-deficient groups had higher levels (p < .05) of hepatic F2-isoprostanes and carbonyl contents and/or plasma alanine aminotransferase activities than those of the Se-adequate WT. The diquat-induced formations of hepatic F2-isoprostanes in these animals peaked at 1 h and preceded the rise of plasma alanine aminotransferase in the Se-adequate GPX1(-/-). Responses of hepatic superoxide dismutase activities to the diquat treatment were affected by the GPX1 level. In conclusion, GPX1 is the major selenoprotein to protect mice against the lethal oxidative stress induced by diquat.

Alanine Transaminase↗
PubMed1999

Cellular glutathione peroxidase protects mice against lethal oxidative stress induced by various doses of diquat.

This study was to determine if cellular glutathione peroxidase (GPX1) protects against acute oxidative stress induced by diquat. Lethality and hepatic biochemical indicators in GPX1 knockout mice [GPX1(-/-)] were compared with those of wild-type mice (WT) after an intraperitoneal injection of diquat at 6, 12, 24, or 48 mg/kg of body weight. Although the WT survived all the doses, the GPX1(-/-) survived only 6 mg diquat/kg and were killed by 12, 24, and 48 mg diquat/kg at 52, 4.4 and 3.9 hr, respectively. Compared with those of surviving mice that were sacrificed on Day 7, the dead GPX1(-/-) had diquat dose-dependent increases (P < 0.05) in plasma alanine aminotransferase (ALT) activities. The GPX1(-/-) also had higher (P < 0.05) liver carbonyl contents than those of the WT, but the differences were irrespective of diquat doses. Whereas hepatic total GPX and phospholipid hydroperoxide glutathione peroxidase activities or hepatic GPX1 protein was not significantly affected by the diquat treatment, liver thioredoxin reductase and catalase activities were lower (P < 0.05) in the GPX1(-/-) injected with 12 mg diquat/kg than those of other groups. In conclusion, normal GPX1 expression is necessary to protect mice against the lethality, hepatic protein oxidation, and elevation of plasma ALT activity induced by 12-48 mg diquat/kg.

Animals↗
PubMed1999

Dietary intrinsic phytate protects colon from lipid peroxidation in pigs with a moderately high dietary iron intake.

High iron consumption has been proposed to relate to an increase in the risk of colon cancer, whereas high levels of supplemental sodium phytate effectively reduce iron-induced oxidative injury and reverse iron-dependent augmentation of colorectal tumorigenesis. However, the protective role of intrinsic dietary phytate has not been determined. In this study, we examined the impact of removing phytate present in a corn-soy diet by supplemental microbial phytase on susceptibility of pigs to the oxidative stress caused by a moderately high dietary iron intake. Thirty-two weanling pigs were fed the corn-soy diets containing two levels of iron (as ferrous sulfate, 80 or 750 mg/kg diet) and microbial phytase (as Natuphos, BASF, Mt. Olive, NJ, 0 or 1200 units/kg). Pigs fed the phytase-supplemented diets did not receive any inorganic phosphorus to ensure adequate degradation of phytate. After 4 months of feeding, liver, colon, and colon mucosal scrapings were collected from four pigs in each of the four dietary groups. Colonic lipid peroxidation, measured as thiobarbituric acid reacting substances (TBARS), was increased by both the high iron (P< 0.0008) and phytase (P< 0.04) supplementation. Both TBARS and F2-isoprostanes, an in vivo marker of lipid peroxidation, in colonic mucosa were affected by dietary levels of iron (P< 0.03). Mean hepatic TBARS in pigs fed the phytase-supplemented, high iron diet was 43%-65% higher than that of other groups although the differences were nonsignificant. Moderately high dietary iron induced hepatic glutathione peroxidase activity (P= 0.06) and protein expression, but decreased catalase (P< 0.05) in the colonic mucosa. In conclusion, intrinsic phytate in corn and soy was protective against lipid peroxidation in the colon associated with a moderately high level of dietary iron.

Animals↗
PubMed1999

High levels of dietary vitamin E do not replace cellular glutathione peroxidase in protecting mice from acute oxidative stress.

Our objective was to determine whether high levels of dietary vitamin E replaced the protection of the Se-dependent cellular glutathione peroxidase (GPX1) against paraquat- or diquat-induced acute oxidative stress in mice. Two experiments were conducted using GPX1 knockout [GPX1(-/-)] mice and wild-type (WT) mice (n = 78/group). In Experiment 1, mice were fed torula yeast-based, Se-adequate (0.4 mg/kg as sodium selenite) diets + 0, 75, 750 or 7,500 mg all-rac-alpha-tocopheryl acetate for 5 wk before an intraperitoneal injection of 50 mg paraquat/kg body weight. In Experiment 2, mice were fed the diet + 0 or 750 mg all-rac-alpha-tocopheryl acetate for 5 wk and were killed 1 or 3 h after an injection of diquat at 12, 24 or 48 mg/kg. In Experiment 1, all mice died of the injection and there were 8- to 15-fold differences (P < 0.001) in survival times between the GPX1(-/-) and the WT mice. Although increasing tocopheryl acetate from 0 to 750 mg/kg extended the survival time of the GPX1(-/-) mice for 2 h (P = 0.06), the highest tocopheryl acetate level resulted in a decrease (P < 0.05) in survival time in the WT mice. The vitamin E-deficient GPX1(-/-) mice had the highest concentration of hepatic thiobarbituric acid reacting substances. In Experiment 2, the diquat-induced formation of hepatic F(2)-isoprostanes was accelerated (P < 0.05) by vitamin E deficiency and was also affected by the GPX1 knockout. Diquat produced much greater (P < 0.01) dose-dependent increases in plasma alanine transaminase (ALT) activities in the GPX1(-/-) than in the WT mice. Hepatic phospholipid hydroperoxide GPX activities were decreased (P < 0.05) by the diquat injection only in the vitamin E-deficient GPX1(-/-) mice. Despite a potent inhibition of hepatic lipid peroxidation, high levels of dietary vitamin E do not replace the protection of GPX1 against the paraquat-induced lethality or the diquat-induced plasma ALT activity increase in mice.

Animals↗
PubMed1998

Knockout of cellular glutathione peroxidase affects selenium-dependent parameters similarly in mice fed adequate and excessive dietary selenium.

This study was to determine whether or not effects of the cellular glutathione peroxidase (GPX1) knockout on several Se-dependent parameters in mice were tissue, dietary Se concentration, and selenoprotein specific. A 2 x 3 factorial experiment was conducted with 18 GPX1 knockout mice [GPX1(-)] and 18 controls (3 weeks old, half males and females). These mice were fed a torula yeast diet supplemented with all-rac-alpha-tocopheryl acetate (50 mg/kg of feed) and Se (sodium selenite) at 0, 0.5, or 3.0 mg/kg of feed for 6 weeks. Both kidney GPX1 mRNA levels and liver, kidney, lung, and testis total GPX activities, assayed using hydrogen peroxide, were affected (p < 0.001) by the GPX1 knockout and dietary Se concentrations, whereas kidney extracellular or plasma GPX (GPX3) mRNA levels and phospholipid hydroperoxide GPX (GPX4) activities in the four tissues were affected (p < 0.001) by only dietary Se concentrations. Total GPX activity in testis was reduced approximately 90% (p < 0.01) by the GPX1 knockout. Neither the GPX1 knockout nor the dietary Se concentrations affected mRNA levels of GPX4 in testis or selenoprotein P in kidney. Total liver Se concentrations were not different between the GPX1(-) and control mice at 0 mg Se/kg of feed, but were reduced (p < 0.01) by 61 and 64% in the GPX1(-) mice at 0.5 and 3.0 mg Se/kg of feed, respectively. These results not only confirm the independent expression of GPX3, GPX4, and selenoprotein P from that of GPX1, but also show similar effects of the GPX1 knockout on Se-dependent parameters in mice between different dietary Se concentrations, tissues, and selenoproteins.

Animals↗
PubMed1998

Dietary selenium supplementation is required to support full expression of three selenium-dependent glutathione peroxidases in various tissues of weanling pigs.

The current dietary allowance for selenium (Se) for pigs does not consider Se requirements for expression of several newly discovered Se-dependent enzymes and has raised environmental concerns. Our objective was to determine dietary Se requirements of young pigs for the full expression of cellular (GPX1), plasma (GPX3) and phospholipid hydroperoxide (GPX4) glutathione peroxidases. In Experiment 1, 18 weanling male pigs (4 wk old) were fed a corn-soybean meal basal diet (BD, 0.03 mg Se/kg) with the addition of 0, 0.1 or 0.3 mg Se/kg (Na2SeO3). In Experiment 2, 24 weanling barrows (6 wk old) were fed a similar BD with the addition of 0, 0.2, 0.3 or 0.5 mg Se/kg. Both experiments lasted for 5 wk. Pigs fed the BD had lower (P < 0.05) tissue GPX1 and GPX4 activities, plasma GPX activity, and(or) plasma Se concentrations than those fed the Se-supplemented diets. In Experiment 1, GPX1 and GPX4 activities in liver, heart and lung were lower (P < 0.05) in pigs fed 0.1 mg Se/kg than in those fed 0.3 mg Se/kg, although no such differences existed in thyroid or pituitary. Pigs fed 0.1 mg Se/kg also had lower (P < 0.05) plasma GPX3 activity at wk 5 and higher (P < 0.05) hepatic glutathione S-transferase activity than pigs fed 0.3 mg Se/kg. In Experiment 2, GPX1 and GPX4 activities in liver and heart, GPX1 and GPX4 mRNA levels in liver and GPX3 activity in plasma exhibited plateaus at 0.2 mg Se/kg. Pigs fed the BD had greater concentrations of F2-isoprostanes (a marker of in vivo lipid peroxidation) than those fed 0.2 mg Se/kg in plasma (P < 0.03) and liver (P < 0.04). We conclude that supplemental Se at 0.2 mg Se/kg of diet is required to support the full expression of three Se-dependent glutathione peroxidases in young pigs.

Animals↗
PubMed1998

Cellular glutathione peroxidase is the mediator of body selenium to protect against paraquat lethality in transgenic mice.

The antioxidative role of Se-dependent cellular glutathione peroxidase (EC 1.11.1.9, GPX1) in vivo has not been established. Our objective was to determine the effects of GPX1 knockout or overexpression on the susceptibility of mice to paraquat toxicity and the contributions of GPX1, compared with other selenoproteins and vitamin E, to body defenses against such acute oxidative stress. Four experiments were conducted using 111 GPX1 knockout or overexpressing mice and the respective controls. Mice were fed diets supplemented with Se (as sodium selenite) at 0-0.4 mg/kg and/or all-rac-alpha-tocopheryl acetate at 0-75 mg/kg before intraperitoneal injections of 12.5, 50 or 125 mg paraquat/kg body weight. All mice that received 50 or 125 mg paraquat/kg died spontaneously, and the survival time of mice was (independent of dietary levels of Se per se or alpha-tocopheryl acetate) solely a function of tissue GPX1 activity (P < 0.001). Severe acute pulmonary interstitial necrosis was found only in the GPX1 overexpressing mice and the controls that had extended survival time. Thiobarbituric acid reacting substances in postmortem liver inversely correlated with the tissue GPX1 activity and dietary levels of Se and/or alpha-tocopheryl acetate. In contrast, all mice that received 12.5 mg paraquat/kg survived and were killed 2 wk after the injection for tissue collection. Compared with the saline injection, this low dose of paraquat resulted in greater (P < 0.001) liver and lung F2-isoprostanes in both the GPX1 knockout mice and the controls. However, there was no difference in plasma alanine transaminase (EC 2.6.1.2) activity or overt injuries in liver, lung and kidney in either group. Our data indicate that GPX1 is the major, if not the only, metabolic form of body Se that protects mice against the lethal oxidative stress caused by high levels of paraquat; it seems less important, however, in protecting mice against the moderate oxidative stress by the low level of paraquat.

Animals↗
PubMed1997

Screening of biofiltering material for VOC treatment.

Screening of biofiltering material for treatment of volatile organic compounds was performed by using a gas stream containing methyl ethyl ketone (MEK) as a target pollutant. Filtering media (FM) for screening were prepared by blending compost (such as pig and cow manure) and filling material (such as fern chips, wheat bran, and bagasse). Results show that a blend of pig manure/fern chips = 9:1 (wt basis) was superior with respect to the stability of the pH and the water-holding capacity of the FM and in the capacity for treating the target compound. Complete removal of the target compound was obtained at an organic loading of 100 g per cubic meter of filtering media per hour. By using the screened FM for treating MEK and toluene, long-term stability (> 1,200 hours) and complete removal can be obtained at an organic loading of 50 g per cubic meter of FM per hour for either compound.

Animals↗
PubMed1997

Overexpression of cellular glutathione peroxidase does not affect expression of plasma glutathione peroxidase or phospholipid hydroperoxide glutathione peroxidase in mice offered diets adequate or deficient in selenium.

Selenium-dependent cellular glutathione peroxidase (GPX1) overexpressing [GPX1(+)] mice were derived by microinjecting a 5.3-kb cloned entire mouse GPX1 genomic DNA into fertilized eggs. The objective of this study was to determine the effect of GPX1 overexpression and dietary selenium on the expression of selenoperoxidases and the status of lipid peroxidation of these transgenic animals. An experiment with a 2 x 2 factorial arrangement of treatments with 15 GPX1(+) and 15 control mice (2 mo old) was conducted for 8 wk. Ten mice of each group (half males and females) were fed a Se-deficient, Torula yeast basal diet (0.02 mg Se/kg, no supplemental vitamin E) and five mice (three males and two females) were fed the basal diet supplemented with 0.51 mg Se/kg as Na2SeO3. The GPX1(+) mice had greater GPX1 activities (one- to sixfold, P < 0.0001) than the control mice at both levels of dietary selenium in all tissues except for liver, in which such difference (100%, P < 0.05) was observed only in Se-deficient mice. The GPX1 mRNA level in kidney and in lung of the Se-deficient GPX1(+) mice was 81% and 7.5-fold greater (P < 0.003) than the respective control level. Overexpression of GPX1 did not alter phospholipid hydroperoxide glutathione peroxidase (GPX4) activities and mRNA levels or glutathione S-transferase (GST) activities in most of the tissues, plasma glutathione peroxidase (GPX3) activity or plasma Se concentrations. No differences in lipid peroxidation in kidney, lung or intestine were observed between the Se-deficient GPX1(+) and control mice. In conclusion, the overexpression of the GPX1 gene in these mice was tissue specific and did not affect the expression of GPX3, GPX4 or GST and plasma Se levels; dietary Se appeared to affect the GPX1 overexpression at its mRNA level.

Animals↗
PubMed1997

Cellular glutathione peroxidase knockout mice express normal levels of selenium-dependent plasma and phospholipid hydroperoxide glutathione peroxidases in various tissues.

Selenium-dependent cellular glutathione peroxidase (GPX1) knockout [GPX1(-)] mice were derived from 129/SVJ x C57BL/6 hybrid mice by microinjecting C57BL/6 blastocysts with recombinant embryonic stem cells carrying a target mutation in the GPX1 gene. Experiment 1 was conducted to determine the effects of the GPX1 knockout on the susceptibility of mice to dietary vitamin E and Se deficiency and on the expression of the Se-dependent plasma glutathione peroxidase (GPX3) and phospholipid hydroperoxide glutathione peroxidase (GPX4), and the Se-independent glutathione S-transferase (GST). Eleven GPX1(-) and 11 control mice (5 wk old, six males and five females) were fed a Se-deficient, Torula yeast basal diet (0.02 mg Se/kg, no supplemental vitamin E) or the basal diet supplemented with 0.5 mg Se/kg (as Na2SeO3) for 13 wk. Experiment 2 was conducted to determine the effect of the GPX1 knockout on the total Se concentration in the liver of Se-adequate mice. Six GPX1(-) and four control mice (5 wk old, half males and females) were fed the basal diet supplemented with 0.2 mg Se/kg and 15 mg of all-rac-alpha-tocopheryl acetate/kg for 5 wk. There was no difference in body weight gain or apparent susceptibility to dietary vitamin E and Se deficiency between the GPX1(-) and control mice. Knockout of GPX1 resulted in almost complete abolishment of GPX1 activity in various tissues, but had no effect on the GPX3 or GPX4 mRNA level and activity or the GST activity in several tissues at either level of dietary Se. The liver total Se concentration in the Se-adequate GPX1(-) mice was only 42% of that in the controls (P < 0. 0001). These results indicate that GPX1 is expressed independently of GPX3 or GPX4 and represents approximately 60% of the total hepatic Se in Se-adequate mice.

Animals↗
PubMed1996

Studies on epoxy compound fixation.

Bioprostheses derived from collagenous tissues have to be fixed and subsequently sterilized before they can be implanted in humans. Clinically, the most commonly used fixative is glutaraldehyde. However, the tendency for glutaraldehyde to markedly alter tissue stiffness and promote tissue calcification are well-recognized drawbacks of this fixative. To address the deficiencies with the glutaraldehyde-fixed tissue, a new fixative, epoxy compound, was used to fix biological prostheses. The study was undertaken to investigate the fixation rates and crosslinking densities of biological tissues fixed with various epoxy compounds. These epoxy compounds are different in their chemical structures. Glutaraldehyde was used as a control. The fixation rates and crosslinking densities of the fixed tissues were determined by measuring their fixation indices and denaturation temperatures, respectively. Generally, the epoxy-fixed tissues were more pliable than the glutaraldehyde-fixed one. Furthermore, the tissues fixed with monofunctional epoxy compound were more pliable than those fixed with multifunctional epoxy compounds. With increasing pH or temperature, the fixation rate of epoxy compound increased. However, the number of epoxide functional groups did not seem to affect the fixation rate of the epoxy compound. The fixation rate of glutaraldehyde was faster than that of epoxy compounds. Additionally, the crosslinking density of the glutaraldehyde-fixed tissue was greater than that of the epoxy-fixed counterparts. Moreover, it was noted that the denaturation temperatures of the tissues fixed with glutaraldehyde or multifunctional epoxy compounds were significantly higher than the fresh ones (p < 0.05), while that fixed with monofunctional epoxy compound stayed roughly the same throughout the entire fixation process (p > 0.05). The results obtained in this study may be used to optimize the fixation process for developing bioprostheses fixed with epoxy compounds.

Animals↗
PubMed1985

Critical evaluation of results of extension of indication for surgery for primary bronchogenic carcinoma.

Among 3,120 surgically resected cases (1957-1983) in Shanghai Chest Hospital, 1,476 resections (47.3%) were performed under extended indication. Six categories--(1) aged 70-87 years (102), (2) associated with severe impairment of pulmonary function (25), (3) small-cell anaplastic type (143), (4) stage III lesion (1,145), (5) invading carina (29), (6) with disseminated pleural metastasis and effusion (32)--were critically evaluated. For the first four categories, long-term survival rates were very encouraging, whereas only technical advancement and short-term results were discussed for the last two. The authors present strategic points significant in availing higher overall operability and hence the overall survival rate, shedding light on the increase of curative potential for lung cancer.

Adult↗
PubMed1980

A theoretical description of phase diagrams for nonideal lipid mixtures.

A theoretical description of phase diagrams for nonideal lipid mixtures is presented. The phase diagrams in this model are constructed by a quasi-chemical approach for the calculations of enthalpies of the regular solutions and by van der Waals attractive energy of lipids which described the degree of nonideality in the solid and fluid phases. The results of theoretical calculations of phase diagrams for dimyristoyl phsophatidylcholine/dipalmitoyl phosphatidylcholine dimyristoyl phosphatidylcholine/distearoyl phosphatidylcholine, and dipalmitoyl phosphatidylcholine/distearoyl phosphatidylcholine mixtures are in good agreement with experimental data.

Chemical Phenomena↗