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Biomedical subjects

C Y Lu

Publications and source records attributed to C Y Lu.

At least 163 records · Page 9Linked to original sources
PubMed1988

Application of hydroelastic waves of the Chinese traditional medicine solution to the traumatotherapy.

We have used hydroelastic waves to treat the closed trauma of the soft tissue. The Shu Huo Jiu (S. H. J.) which is the Chinese traditional medicine alcohol, was used as the fluid medium for generating the pressure waves. The biomechanical model was established and analysed. Both animal and human tests have been made. A practical system was designed, constructed and clinically tested to treat the closed trauma, such as the bruise, contusion, sprain etc.. This system was found to be effective.

Biomechanical Phenomena↗
PubMed1988

Defective anti-listerial responses in deciduoma of pseudopregnant mice.

Two different hormonal regimens to induce pseudopregnancy resulted in a pronounced increase in the susceptibility of the murine uterus to intraluminal injections of Listeria monocytogenes. Preimmunization, which profoundly augments systemic listeria resistance, had no effect on this increased uterine susceptibility. Anti-listerial responses in other organs were unaffected by pseudopregnancy. Animals manifesting increased susceptibility formed distinct uterine swellings in response to the combination of hormones and uterine listeria. These swellings correspond to previously described deciduoma and closely mimic the decidualized endometrium of pregnancy. The nature of the defective response to listeria was investigated by immunocytochemistry. Increased bacterial titers were correlated with an inability of macrophages and T lymphocytes to reach tissue listeria in discrete regions of deciduoma-bearing uteri. Control uteri showed a normal granulomatous pattern of inflammation. These findings closely parallel previous findings in the murine decidua basalis and suggest that properties of decidualized endometrial stromal cells regulate local immune responsiveness.

Animals↗
PubMed1987

In vitro plantlet formation from embryonic explants of eastern white cedar (Thuja occidentalis L.).

A protocol is described for the in vitro production of plantlets from embryonic explants of eastern white cedar (Thuja occidentalis L.). Bud induction was optimal when embryonic explants were cultured for 20-25 days on half-strength Quoirin and Le Poivre mineral salts containing equimolar concentrations (10(-6) M) of N(6)-benzyladenine and 2-isopentyl adenine. Bud development was achieved in phytohormone-free medium in the presence of activated charcoal. Maximal shoot elongation occurred on half-strength Quoirin and Le Poivre salts, whereas shoot multiplication was optimal on half-strength Bornman's MCM salts in the presence of cytokinin. Hardened shoots, dipped in commercial rooting powder containing indole-3-butyric acid, rooted optimally in mist under non-sterile greenhouse conditions. Both rooting and subsequent plantlet growth was best when Redi-Earth((R)) was used as a substrate. Over 250 plantlets per embryo can be produced annually by this technique.

Journal Article↗
PubMed1987

Role of local immunosuppression in murine fetoplacental listeriosis.

Recent evidence suggests that local immunoregulation may prevent rejection of the placenta by the mother. This local immunoregulation may also compromise the response to placental infection. Listeria monocytogenes infection in 121 pregnant mice and 1,050 fetoplacental units was examined and the kinetics of bacterial growth in various maternal and fetal tissues were determined. A subset of pregnant mice developed overwhelming placental listeria infections. Pregnancy did not impair the maternal immune response in the liver and spleen. Pregnant mice without placental infection had numbers of listeria equivalent to nonpregnant controls and mice immunized during pregnancy had significantly less listeria than nonimmunized controls. The secondary response in immunized pregnant mice had no effect on the development of placental infection and the histologic features of placental infection were distinct from those in other organs. Our data suggest that an ineffective local immune response may contribute to the pathogenicity of listeria for the placenta.

Animals↗
PubMed1987

Polyamines mediate uncontrolled calcium entry and cell damage in rat heart in the calcium paradox.

Brief perfusion of heart with calcium-free medium renders myocardial cells calcium-sensitive so that readmission of calcium results in uncontrolled Ca2+ entry and acute massive cell injury (calcium paradox). We investigated the hypothesis that polyamines may be involved in the mediation of abnormal Ca2+ influx and cell damage in the calcium paradox. The isolated perfused rat heart was used for these studies. Calcium-free perfusion promptly (less than 5 min) decreased the levels of polyamines and the activity of their rate-regulating synthetic enzyme, ornithine decarboxylase (ODC), and calcium reperfusion abruptly (less than 15-180 s) increased these components. alpha-Difluoromethylornithine (DFMO), a specific suicide inhibitor of ODC, suppressed the calcium reperfusion-induced increase in polyamines and the concomitant increase in myocardial cellular 45Ca influx, loss of contractility, release of cytosolic enzymes, myoglobin, and protein, and structural lesions. Putrescine, the product of ODC activity, nullified DFMO inhibition and restored the calcium reperfusion-induced increment in polyamines and the full expression of the calcium paradox. Putrescine itself enhanced the reperfusion-evoked release of myoglobin and protein in the absence of DFMO. Hypothermia blocked the changes in heart ODC and polyamines induced by calcium-free perfusion and calcium reperfusion and prevented the calcium paradox. These results indicate that rapid Ca2+-directed changes in ODC activity and polyamine levels are essential for triggering excessive transsarcolemmal transport of Ca2+ and explosive myocardial cell injury in the calcium paradox.

Animals↗
PubMed1986

Blood-brain barrier breakdown by cold injury. Polyamine signals mediate acute stimulation of endocytosis, vesicular transport, and microvillus formation in rat cerebral capillaries.

Polyamines have been previously implicated in the mediation of blood-brain barrier breakdown induced by cryogenic injury (H Koenig, AD Goldstone, CY Lu, Biochem Biophys Res Commun 116:1039, 1983). We studied acute (less than 5 minute) changes in capillary ultrastructure, microvascular permeability, and the levels of polyamines and their rate regulating synthetic enzyme ornithine decarboxylase (ODC) in rat cerebral cortex after focal cold injury. Microvascular permeability was measured by relative transport of intravenously administered fluorescein. Capillary ultrastructure was studied by quantitative stereology and morphometry after intravenous administration of horseradish peroxidase. Focal cold injury induced a 2.5-, 3.8-, 1.7-, and 1.4-fold increase in the levels of ODC, putrescine, spermidine and spermine, and a 46-fold increase in fluorescein uptake in perilesional cortex. Few capillaries in control cortex contained endocytic pits or horseradish peroxidase-positive vesicles, whereas most capillaries near lesions showed these structures. Cryoinjury induced a 5-fold increase in the relative volume of microvilli and horseradish peroxidase vesicles, a 2.3-fold increase in area of luminal endocytic pits, and a 6.3-fold increase in area of abluminal exocytic pits. The ODC inhibitor alpha-difluoromethylornithine blocked the cryoinjury-induced changes in ODC, polyamines, fluorescein uptake, and capillary ultrastructure. Putrescine negated the effect of alpha-difluoromethylornithine or capillary ultrastructure, and was previously shown to nullify the alpha-difluoromethylornithine effects on polyamines and fluorescein permeability (cited above). These data link rapid changes in ODC and polyamines to blood-brain barrier breakdown, and suggest that the abnormal permeability is associated with an acute, polyamine-mediated stimulation of microvillus formation, endocytosis, and vesicular transport in capillary endothelium.

Animals↗
PubMed1985

Effect of ochratoxin A on rat liver mitochondrial respiration and oxidative phosphorylation.

The in vitro effects of ochratoxin A on the membrane structure and bioenergetic functions of rat liver mitochondria were studied. It was found that when the toxin was added to the assay medium the respiratory control of the isolated mitochondria was decreased as the concentration of the toxin increased. The mitochondrial respiration was gradually uncoupled by the toxin when its concentration was raised above 1.2 X 10(-6) M, and became fully uncoupled at 6.2 X 10(-4) M. The oxidative phosphorylation was not damaged until the toxin concentration was higher than 9.3 X 10(-5) M. On the other hand, ochratoxin A inhibited the electron transfer functions of the mitochondria. At the concentration above 1.0 X 10(-4) M, ochratoxin A inhibited the succinate dehydrogenase, succinate-cytochrome c reductase, and succinate oxidase activities of the respiratory chain. Fifty percent of succinate-cytochrome c reductase and succinate oxidase activity was lost in the presence of 8.0 X 10(-4) and 6.2 X 10(-4) M ochratoxin A, respectively. The inhibition kinetic studies revealed that ochratoxin A is an uncompetitive inhibitor of both succinate-cytochrome c reductase and succinate dehydrogenase, and the inhibition constants for the 2 enzyme activities were estimated to be 4.4 X 10(-4) and 2.2 X 10(-4) M, respectively. However, the toxin did not inhibit either cytochrome oxidase or NADH dehydrogenase activity of the mitochondrial respiratory chain. It is thus concluded that ochratoxin A exerts its effect on the mitochondrial respiration and oxidative phosphorylation through the impairment of the mitochondrial membrane and inhibition of the succinate-supported electron transfer activities of the respiratory chain.

Adenosine Diphosphate↗
PubMed1984

Comparison of antigen-specific T cell responses in autoimmune MRL/Mp-lpr/lpr and MRL/Mp-+/+ mice.

The MRL-1 mouse develops severe autoimmune disease characterized by high titers of autoantibodies at an early age (3 to 5 mo). The congeneic MRL-n mouse, which differs only in the lymphoproliferative (lpr) gene, exhibits no such pathologic or serologic abnormalities at the same age. We examined antigen-specific T cell responses in the MRL-1 mouse and compared them to age- and sex-matched MRL-n controls. We found broad defects in these responses in the MRL-1 mouse; an inability to generate primary allospecific and hapten-specific cytolytic T lymphocytes (CTL), secondary hapten- and virus-specific CTL, as well as a deficient proliferative response to hapten and natural antigens and a weak delayed-type hypersensitivity response were demonstrated. Our data furthermore suggest a lack of interleukin 2 (IL 2) acceptor sites in the proliferating T cell, while suggesting no such lack on CTL precursors. In fact, the deficient CTL responses in MRL-1 mice can be restored to levels seen in MRL-n by the in vitro addition of IL 2. The implications of these findings and the possible explanations for the relative deficit in helper function in the MRL-1 mouse are discussed.

Aging↗
PubMed1984

Alpha-fetoprotein inhibits macrophage expression of Ia antigens.

Murine alpha-fetoprotein (AFP) is a major protein in amnionic fluid and perinatal sera. AFP has been postulated to contribute to the immunologic hyporesponsiveness of the fetus and neonate, as well as protecting the fetus from rejection by the mother. We now report that AFP acts in vitro to inhibit macrophage expression of cell surface Ia antigens, the class II glycoproteins of the major histocompatibility gene complex. In culture, macrophages incubated with a T cell lymphokine developed Ia as detected by either immunofluorescence or a cell radioimmunoassay. Both mouse amnionic fluid and AFP inhibited the expression of Ia in a dose-dependent manner. Five preparations of AFP derived from three sources--day-old neonates, amnionic fluid, and a hepatoma cell line--were effective. The concentration of AFP that inhibited by 50% the expression of Ia was about 10(-6) M. Mouse amnionic fluid and AFP did not affect the viability of the macrophage nor was the surface expression of H-2K and C3 receptors affected. The inhibitory effect of AFP did not depend on the presence of T cells in the culture. AFP did not appear to inhibit the direct interaction of lymphokine with macrophages; AFP did inhibit if given days after a pulse of lymphokine. The concentrations of prostaglandins carried by AFP were insignificant and could not explain the inhibitory effects.

Amniotic Fluid↗
PubMed1984

The delayed ontogenesis of Ia-positive macrophages: implications for host defense and self-tolerance in the neonate.

We have recently compared a number of macrophage functions in new-born and adult mice. In the adult, the most efficient resistance against Listeria infection requires a number of macrophage-T lymphocyte interactions which ultimately result in activated macrophages which eliminate the bacteria. A subpopulation of adult macrophages are distinguished by the presence of cell-surface; immune-response-gene-associated (Ia) antigens. These macrophages ingest and then "present" antigen to and thus activate T lymphocytes. Extensive in vitro experiments have shown that T lymphocyte activation requires both antigen and Ia-bearing macrophages. Ia-negative macrophages are not involved in this process. The T lymphocyte thus stimulated secretes lymphokines which then activate macrophages to acquire bactericidal and tumoricidal activity. In contrast to the adult mouse, essentially no Ia-bearing antigen presenting macrophages can be found in the neonatal spleen and peritoneal cavity. Neonatal and adult macrophages were similar in all other examined aspects--phagocytic activity, cytocidal function after lymphokine stimulation, and interleukin-1 secretion after exposure to endotoxin. The absence of Ia-bearing macrophages in neonates would be expected to contribute to their increased susceptibility to Listeria. The absence of Ia-bearing macrophages in the neonate is not the result of any intrinsic defects in these cells, as they can be made to express Ia in vitro. Nor is the deficit in Ia-bearing macrophages due to the hyporeactivity of neonatal helper T lymphocytes as adult athymic mice have significant numbers of Ia-bearing macrophages. Neonatal splenocytes or their conditioned media inhibit macrophage Ia expression when transferred into adult mice.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1983

Blood brain barrier breakdown in brain edema following cold injury is mediated by microvascular polyamines.

A focal freeze injury to rat cerebral cortex induces an early (less than 5 min) increase in brain ornithine decarboxylase activity and an accumulation of polyamines involving cerebral microvessels. This polyamine synthesis correlates with the abnormal increase in microvascular permeability, monitored by uptake of Evans Blue and sod. fluorescein. The ornithine decarboxylase inhibitor alpha-difluoromethylornithine suppressed the injury-induced increment in spermidine and spermine and microvascular permeability. Putrescine nullified alpha-difluoromethylornithine inhibition and restored microvessel spermidine and spermine and the pathological increase in microvascular permeability. These results indicate that polyamine synthesis is obligatory for blood-brain barrier breakdown. alpha-Difluoromethylornithine may be useful in the treatment of vasogenic brain edema.

Animals↗