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Biomedical subjects

C Y Lu

Publications and source records attributed to C Y Lu.

At least 91 records · Page 5Linked to original sources
PubMed1996

Pancreas transplantation for diabetes mellitus.

Pancreas transplantation has become a viable option for the patient wi th insulin-dependent diabetes mellitus with progressive renal failure. The most common type of pancreas transplantation is a simultaneous pancreas and kidney transplantation performed from a single cadaver donor (SPK). The next most common is pancreas transplantation after successful kidney transplantation (PAK). A few centers are performing pancreas transplantation alone (PTA) in diabetic recipients without renal disease but who have significant complications from their diabetes. Pancreas transplantation is associated with a higher morbidity than kidney transplantation alone. Most pancreas transplantation centers report a significant increase in acute rejection, which can lead to increased hospitalization and risk of opportunistic infection. In addition, the early era of pancreas transplantation was associated with significant surgical complications. However, with bladder drainage of the pancreas exocrine secretions, the surgical complication rate has decreased significantly. Despite medical and surgical complications, the overall results for pancreas transplantation are excellent, with 1 -year graft survival of 75% for SPK transplantations and 48% for PAK and PTA transplant recipients. The effects of a pancreas transplantation on the secondary complications of diabetes have been studied extensively. Most studies have shown a modest improvement in secondary complications with the exception of diabetic retinopathy. The major benefit of pancreas transplantation appears to be enhanced quality of life for patients successfully transplanted. For these reasons, the Kidney-Pancreas Committee of the American Society of Transplant Physicians believes the current results of pancreas-kidney transplantation justify its use as a valid option for insulin-dependent diabetic transplant recipients.

Costs and Cost Analysis↗
PubMed1996

Inhibition of macrophage nitric-oxide production and Ia-expression by docosahexaenoic acid, a constituent of fetal and neonatal serum.

PROBLEM: We previously demonstrated profound inhibition of macrophage activation in the murine placenta in vivo. Given the importance of macrophages both in initiating cellular immunity by presenting antigen in the context of Ia to CD4+ T cells, and in killing cellular targets by producing nitric oxide (NO), inhibition of macrophage functions in the placenta may account for the increased susceptibility of the placenta to infection. We have also showed that docosahexaenoic acid (DHA), at concentrations present in the fetal circulation, has a major role in inhibiting macrophage Ia-expression and NO production in the placenta. The concentration of DHA in fetal serum perfusing the placenta is 50x higher than in the adult. DHA has previously been reported to profoundly affect prostanoid production, to be metabolized by lipoxygenases, and to affect lipoxygenases. We now determine if these activities of DHA account for its inhibition of macrophage NO production and Ia-expression. METHODS: Murine macrophages were cultured in vitro, exposed to IFN gamma endotoxin, DHA, and various eicosanoids, and their ability to produce NO or express Ia determined. RESULTS: Although the cyclooxygenase inhibitor, indomethacin, did inhibit NO production, DHA inhibited by a different mechanism. DHA further inhibited NO production by macrophages exposed to doses of indomethacin known to maximally inhibit prostanoid production. Stable, biologically active prostanoids did not reverse the inhibitory effect of DHA. Although DHA is metabolized by lipoxygenases, the lipoxygenase inhibitor NDGA did not reverse the inhibition of either NO production nor Ia expression. This indicates that lipoxygenase products of DHA did not mediate inhibition. NDGA itself inhibited NO production and Ia expression. However, DHA did not inhibit by inhibiting lipoxygenase activity because DHA further inhibited macrophages exposed to doses of DHA known to maximally inhibit lipoxygenases. Furthermore, stable biologically active analogs of lipoxygenase products did not reverse DHA inhibition. DHA also did not inhibit by preventing PAF production because PAF did not reverse inhibition of NO production. CONCLUSION: DHA did not inhibit Ia-expression or NO production via its known effects on eicosanoid or PAF metabolism, nor by being metabolized by lipoxygenases.

Animals↗
PubMed1995

Augmentation or inhibition of IFN-gamma-induced MHC class II expression by lipopolysaccharides. The roles of TNF-alpha and nitric oxide, and the importance of the sequence of signaling.

MHC class II expression on macrophages is one determinant of Ag presentation and the vigor of CD4+ T cell immunity. We show that LPS may either inhibit or augment IFN-gamma-induced MHC class II on macrophages depending on the sequence of the IFN-gamma and LPS signals. LPS inhibited MHC class II when added simultaneously with IFN-gamma, but augmented class II expression when added after IFN-gamma. Inhibition was due to nitric oxide (NO), which was only produced if LPS was given simultaneously with IFN-gamma. However, even when NO production was inhibited, LPS given simultaneously with IFN-gamma did not augment MHC class II expression. This suggests that LPS delivers different signals when given simultaneously vs after IFN-gamma. LPS augmentation of class II expression was functionally important because it correlated with increased Ag presentation. Augmentation by LPS of IFN-gamma-induced class II expression by macrophages has not been previously reported. We found that TNF-alpha, like LPS, inhibited IFN-gamma-induced class II expression if NO was produced, but augmented it in the absence of NO formation. Studies with a neutralizing anti-TNF-alpha Ab, however, indicate that LPS augmentation of MHC class II did not require TNF-alpha. LPS augmentation involved a different mechanism than IFN-gamma induction of MHC class II. LPS augmentation occurred at a post-transcriptional level, whereas IFN-gamma-induction occurred at the level of gene transcription. LPS augmentation was apparent after 2 h of stimulation by LPS, while IFN-gamma induction of class II expression required more than 8 h.

Animals↗
PubMed1995

Docosahexaenoic acid, a major constituent of fetal serum and fish oil diets, inhibits IFN gamma-induced Ia-expression by murine macrophages in vitro.

Decreased Ia expression by macrophages may account for the increased susceptibility of fetuses and neonates to infection. We chose to investigate the role of docosahexaenoic acid (DHA), an omega-3 fatty acid, on Ia expression in vitro, because neonatal serum concentrations of DHA (100-150 microM) are approximately 50 times higher than in the adult. In addition, DHA is a major component of fish-oil diets that ameliorate some autoimmune diseases and prevent renal allograft rejection. DHA inhibited IFN-gamma-induced Ia expression with a half-maximal inhibitory concentration of 25 microM. The inhibition was not caused by nonspecific damage, because oxidative metabolism via the mitochondrial electron-transport chain was not inhibited. There were strict biochemical requirements for inhibition of Ia expression. Polyenoic fatty acids with 22 carbons were more inhibitory than those with 20 carbons. Among 22-carbon fatty acids, those with more double bonds, and, in particular, with a double bond in the omega-3 position, were more inhibitory. Although DHA is known to inhibit cyclooxygenase and thus the production of eicosanoids, indomethacin did not inhibit Ia expression. This indicated that inhibition of cyclooxygenase was not responsible for inhibition of Ia expression. We divided induction of Ia expression by IFN-gamma into four phases, with IFN-gamma being present only during the second phase. DHA was most inhibitory when given before or with the IFN-gamma. This indicated that DHA inhibited early steps in IFN-gamma-induced Ia expression. Consistent with this idea, we found that DHA inhibited the increase in mRNA transcripts for Ia beta b, as assayed by Northern blotting. In summary, we found that DHA, a major component of fetal and neonatal sera as well as fish-oil diets, inhibited IFN-gamma-induced macrophage Ia expression in vitro by preventing increases in Ia mRNA transcripts.

Animals↗
PubMed1995

Differential regulation of TNF-alpha production by listeriolysin-producing versus nonproducing strains of Listeria monocytogenes.

Only Listeria monocytogenes that produce listeriolysin O (LLO) elicit protective immunity. Given the importance of tumor necrosis factor alpha (TNF-alpha) in anti-Listeria immunity, we have investigated TNF-alpha production by macrophages after they ingested live LLO-producing compared to LLO-non-producing bacteria. We used two genetically engineered strains of Listeria that differed only in their ability (Ly+) or inability (Ly-) to produce LLO. Ly+ and Ly- caused the same kinetics of increased mRNA abundance for TNF-alpha during the first 90 min after phagocytosis. However, only Ly+ caused sustained transcription of TNF-alpha mRNA, and this may account for the increased release of TNF-alpha. The transcriptional inhibitor 5,6-dichloro-1-beta-D-ribofuranosylbenzimidazole (DRB) prevented the sustained abundance of cytokine mRNA 20 h after ingestion of Ly+. In addition, nuclear run-on assays indicated sustained transcription of TNF-alpha genes only after ingestion of Ly+. LLO itself was not responsible for the ability of Ly+ to stimulate the sustained transcription of the TNF-alpha genes. Instead, LLO may allow Listeria to survive within macrophages so that other bacterial products cause sustained TNF-alpha gene transcription. Both Ly+ and Ly- produced molecules, isolated by 50% ammonium sulfate, that induced cytokine production. In conclusion, we now report that Ly+ causes sustained transcription of the TNF-alpha gene and production of TNF-alpha by macrophages in vitro. We speculate that the TNF-alpha may activate endothelium and thus allow the recruitment of T cells to sites of infection. This may contribute to the ability of only LLO-producing Listeria to induce protective immunity.

Animals↗
PubMed1995

Polyamines and NMDA receptors modulate pericapillary astrocyte swelling following cerebral cryo-injury in the rat.

Four hours following cryo-injury rat cerebral pericapillary astrocytes from the perilesional area were markedly swollen occupying 17% of the pericapillary space as compared to 11% in sham operated controls. Ornithine decarboxylase activity and polyamine levels were increased over sham controls. The astrocytic swelling, the percentage of the pericapillary space occupied by astrocytic processes, and polyamine levels were reduced to near control levels by the following: (1) alpha-difluoromethylornithine; (2) Ifenprodil; and (3) MK-801. alpha-Difluoromethylornithine is a specific inhibitor of ornithine decarboxylase, Ifenprodil is an inhibitor of the polyamine binding site on the n-methyl-d-aspartate receptor, and MK-801 is an antagonist to n-methyl-d-aspartate binding to the n-methyl-d-aspartate receptor. Addition of putrescine, the product of ornithine decarboxylase activity, reversed the effect of alpha-difluoromethylornithine and restored the pericapillary swelling. Putrescine did not affect the MK-801-induced reduction in pericapillary astrocytic swelling. Therefore, polyamines and the n-methyl-d-aspartate receptor modulate excitotoxic responses to cryo-injury in pericapillary cerebral astrocytes.

Animals↗
PubMed1995

Delayed thromboxane or tumor necrosis factor-alpha, but not leukotriene inhibition, attenuates prolonged pulmonary hypertension in endotoxemia.

The early phase of endotoxin-induced acute hemodynamic disturbances and hypoxemia is mediated by various factors, including eicosanoids and tumor necrosis factor-alpha (TNF alpha). Thromboxane A2 is the major mediator of the early pulmonary hypertension associated with endotoxemia, but the mechanisms underlying the prolonged hemodynamic disturbances observed in ongoing endotoxemia are not well understood. The authors used a chronically instrumental young piglet model to determine the roles of several eicosanoids and of TNF alpha in the prolonged endotoxin-induced pulmonary hypertension and other cardiovascular derangements. Animals were given 40 micrograms/kg endotoxin intravenously per hour for 30 minutes, followed by 20 micrograms/kg per hour. In all animals, persistent pulmonary hypertension, lowered cardiac output, any hypoxemia developed during endotoxin infusion. After 3 hours of endotoxin infusion, randomly ordered infusions of 1 mg/kg dazmegrel (a thromboxane A2 synthesis inhibitor), 5mg/kg nordihydroguaiaretic acid (a 5-lipoxygenase inhibitor), and 20 mg/kg pentoxifylline (A TNF alpha inhibitor) were given intravenously at 30-to-60-minute intervals. Dazmegrel and pentoxifylline lowered pulmonary arterial pressure and resistance and raised arterial oxygen tension. Cardiac output increased significantly after pentoxifylline. These hemodynamic effects persisted for 30-60 minutes, despite continued endotoxin infusion. The elevated plasma concentrations of thromboxane B2 and TNF alpha returned toward preendotoxin baseline values after dazmegrel and pentoxifylline treatment, respectively. No beneficial effects were noted after administration of nordihydroguaiaretic acid. Based on these results, both thromboxane A2 and TNF alpha, but not 5-lipoxygenase products, play active roles in prolonged endotoxin-induced pulmonary hypertension and hypoxemia in young piglets. Combined thromboxane A2 and TNF alpha blockade may be clinically useful in treatment of advanced sepsis in neonates.

6-Ketoprostaglandin F1 alpha↗
PubMed1995

Lymphoproliferative disease presenting as obstructive uropathy after renal transplantation.

Lymphoproliferative disorders occur with a greater frequency in recipients of solid organ transplants. Unlike in the general population, these tumors tend to arise in extranodal sites and are often confined to a single organ. We report on a patient with lymphoproliferative disease confined to the hilum of the renal allograft. The only clinical clue to the presence of the tumor was an increase in the serum creatinine secondary to ureteral obstruction by the mass.

Humans↗
PubMed1995

Point mutation in the pribnow box, the molecular basis of beta-lactamase overproduction in Klebsiella oxytoca.

Klebsiella oxytoca mutants resistant to a variety of beta-lactams were obtained in vitro on aztreonam. Constitutive beta-lactamase production was much higher in the mutants than in the susceptible strains (75-fold). The only difference observed in these mutants compared with the susceptible strains were point mutations in the Pribnow box: a transversion (G-->T) in the first base for one mutant or a transition (G-->A) in the fifth base of the -10 consensus sequence for the other three mutants. The transcriptional output of the beta-lactamase gene (blaOXY) from the mutants was significantly higher than that of the blaOXY gene from the susceptible strains.

Anti-Bacterial Agents↗
PubMed1995

[Study of toxicity of iodophor,glutaradehyde and chlorhexidine to L929 Cells.].

We comparatively studied the toxicity of iodophor,glutaradehyde and chlorhexidine in different concentration and time.The result shows that the toxicity of iodophor to L929 cells is the lowest in all kinds of drug concentration and action time is much lower than that of glutaradehyde and chlorhexidine(P<0.05) with prolonging time.It indicates that iodophor can be used to oral diseases therapy with lower concentration.

English Abstract↗
PubMed1995

[The Chinese traditional treatment with "ShengYang" prescription as a post-operative auxiliary method using on the oral squamous cells carcinoma patients.].

This paper observed the clinic investigation.Which prove the relationship among the Chinese dialectical fur condition pulse condition,dialectical divided into types and survival time,immunity function before and after therapy,which will provide scientific basis and new train of thinking for recovery of stomatological carcinoma patient following operation.These patients according to dialectical type.were divided into type of feeble kidney and type of mixed excess and deficiency syndrome that the survive time compare with control group through treat by statistics,were P<0.05.The positive cases of immunity response of administration group were more increased than control group, the rate was 22.2%,maintenance and decrease rate were 7.5% and 14.6% compare with control group,with multiple factor computer analysis in two groups.There is some evidence that the traditional Chinese prescription of "ShengYang" treat in tumor patients with the type of feeble kidney and type of mixed excess an deficiency syndrome were remarkably regulate the immunity function and promote the action of anti tumor.For recovery therapy after tumor operation which reach a fairly action.

English Abstract↗
PubMed1995

[Effect of Chinese traditional prescription "Shen Yang" on the immune function of oral squamous cells carcinoma patients.].

This report tries to compare the immunologic function of being take the Chinese medicine "Fu-Fang Shen Yang" or placebo C which is based on randomized clinical trials after operation for 238 cases of oral squamous cancer.DNCB test is for observable index.The results as follows:DNCB position rate of 1 "Shen Yang" group is significantly increased to compare with the placebo C group,after 3m(P<0.01) 6m (P<0.001).Two groups are significantly increased after one year.This suggestion that "Fu-Fang Shen Yang" can enhance immunologic function after operation fro oral squamous cells carcinoma patients.

English Abstract↗
PubMed1994

Inhibition of macrophage Ia expression by nitric oxide.

Bacterial LPS inhibits the expression of Ia by macrophages stimulated by IFN-gamma. We now present the following observations that suggest a causal relationship between nitric oxide (NO) and this inhibition of Ia expression: 1) NO production precedes inhibition of Ia, 2) the ability of LPS to inhibit Ia expression by IFN-gamma stimulated macrophages is correlated in a dose-dependent fashion with NO production, 3) Ia expression is restored if NO production is inhibited by NG-monomethyl-L-arginine or culturing the macrophages in L-arginine-free medium, and 4) exogenous NO inhibits IFN-gamma-stimulated Ia expression. Taken together these experiments indicate that NO inhibits macrophage expression of Ia. Furthermore, the following studies showed that inhibition of Ia by NO was not due to macrophage death: trypan blue exclusion, macrophage adhesion, conversion of the tetrazolium dye (MTT) to its formazan by a functioning electron transport system, and phagocytosis of IgG opsonized SRBCs. By inhibiting Ia expression, NO may inhibit Ag-presentation to T cells, secretion of IFN-gamma by these T cells, and ultimately inhibit the IFN-gamma-dependent production of NO synthetase. This inhibitory mechanism may prevent excessive NO formation and tissue injury.

Animals↗