Reflectivity and photoluminescence measurements in ZnS epilayers grown by metal-organic chemical-vapor deposition.
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Biomedical subjects
Publications and source records attributed to B Gil.
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Six flavonoid derivatives were tested for their influence on Naja naja and human recombinant synovial phospholipase A2. They showed a selectivity for the last enzyme with IC50 = 14.3, 17.6, 12.2 and 28.2 microM for quercetagetin, kaempferol-3-O-galactoside, scutellarein and scutellarein-7-O-glucuronide, respectively, while reduced effects were observed for hispidulin and hibifolin. After topical application all the flavonoids inhibited 12-O-tetradecanoylphorbol-13-acetate-induced ear oedema in mice with a potency comparable to that of indomethacin and they were also able to inhibit carrageenan-induced mouse paw oedema at a dose of 150 mg/kg p.o. The blockade of the free hydroxyl at C-7 or C-6 reduced the anti-inflammatory activity and also the inhibitory effect on human recombinant synovial phospholipase A2. These results are in accordance with the notion that group II phospholipases A2 may play a role in experimental inflammation, although several mechanisms seems to be involved in the anti-inflammatory effect of this group of flavonoids.
1. A series of flavonoids isolated from Indian medicinal plants: kaempferol-3-O-galactoside, hispidulin, nepetin, scutellarein, scutellarein-7-O-glucuronide, hibifolin and morelloflavone were studied for their activity as inhibitors of microsomal lipid peroxidation and scavengers of oxygen free radicals in vitro as well as in a model of xenobiotic toxicity in mouse. 2. All compounds inhibited lipid peroxidation in vitro. The most potent compounds were nepetin (non-enzymic lipid peroxidation) and morelloflavone (enzymic lipid peroxidation) with IC50's in the micromolar range. Some of the compounds behaved as scavengers of hydroxyl radical in the deoxyribose degradation assay, with a calculated rate constant for kaempferol-3-O-galactoside of 1.55 x 10(10) M-1 s-1. 3. Scutellarein and nepetin were found to be inhibitors of xanthine oxidase activity, whereas morelloflavone acted as a scavenger of superoxide generated by hypoxanthine/xanthine oxidase. 4. Treatment of mice with scutellarein, hispidulin, nepetin and kaempferol-3-O-galactoside after bromobenzene intoxication decreased serum glumate-pyruvate transaminase activity, although only the last flavonoid was able to significantly reduce hepatic lipid peroxidation products and to increase the reduced glutathione level. In contrast, morelloflavone increased bromobenzene toxicity.
Dermatomyositis is an inflammatory disease of unknown etiology whose association to pregnancy is uncommon. The impact of dermatomyositis with uncomplicated pregnancy while active is very high for the fetus without major maternal consequences. The monitoring of cases with pregnancy associated hypertension and dermatomyositis, must be performed independently for the mother and the fetus, since fetal prognosis is usually bad and does not modify with treatment. The case presented herein is to our knowledge the first with eclampsia and dermatomyositis which ended in a normal product delivered and the mother decreased.
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Hepatitis C virus (HCV) is an RNA virus that replicates in both the liver and lymphoid cells. Interferon-alpha (IFN-alpha) is a useful treatment of chronic hepatitis C (CHC) although resistance to this drug occurs frequently. The mechanisms underlying resistance to IFN remain unknown. In this work, we have measured the levels of glutathione in plasma and peripheral lymphoid cells from 15 healthy controls and 24 CHC patients, 10 of whom were without treatment and 14 showed high serum alanine aminotransferase (ALT) values despite therapy with lymphoblastoid IFN for more than 4 months. In all patients, glutathione levels in plasma and in mononuclear cells were depressed in comparison to controls. In IFN-unresponsive patients, the addition of 600 mg tid of oral N-acetyl cysteine (NAC), a glutathione precursor, resulted in a steady decrease of ALT values in all patients, with complete normalization in 41% of cases after 5-6 months of combined therapy. Administration of NAC alone for 1 month was without effect in the 10 patients that were not receiving IFN. Supplementation of IFN with NAC induced a near normalization of intralymphocytic glutathione, but plasma levels were only moderately increased. HCV replication was markedly inhibited in lymphocytes and viremia was cleared in one of the 8 patients tested. In conclusion, NAC enhances the response to IFN in CHC. Controlled studies are needed to ascertain whether antioxidant therapy might act in synergy with IFN in chronic viral hepatitis.
We investigated the presence of positive (genomic) and negative (replicative intermediate) hepatitis C virus RNA strands in liver, peripheral mononuclear cells and serum from patients with chronic hepatitis C using a selective and semiquantitative polymerase chain reaction procedure. Negative and positive hepatitis C virus RNA strands were present in liver, serum and lymphoid cells in all untreated patients and in all those who did not respond to interferon therapy. In the latter group of patients, the titers of RNA strands in the liver and peripheral mononuclear cells at the end of the treatment were similar to those encountered in untreated patients, but the serum titers were about 100 times lower than pretreatment values. In patients who responded to interferon with normalization of serum aminotransferase levels (n = 10), the rate of detection and the titer of the two viral strands in liver, serum and mononuclear cells were markedly decreased at the end of the therapy. In the six responders who did not relapse after interferon withdrawal, both hepatitis C virus RNA strands were absent from the liver, serum and lymphoid cells. By contrast, the positive RNA strand was present in liver cells, mononuclear cells or both at the end of therapy in all patients who experienced posttherapy relapse. In conclusion, our results indicate that interferon can clear hepatitis C virus from hepatic and extrahepatic sites only in responder patients. Disappearance of genomic hepatitis C virus RNA from the liver and from mononuclear cells may predict complete response without posttherapy relapse.
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