We present our study of four patients with occupational type I allergy to red midge larvae (group 1) who we compared with seven individuals also sensitized to red midge larvae but who had not apparently been exposed to them (group 2). All patients showed elevated specific IgE against Chironomus thummi, and positive skin prick tests (SPT) and provocation tests with red midge larvae. We carried out SPT with Dermatophagoides pteronyssinus, Acarus siro, shrimp, cockroach and common mosquito (Culex pipiens) and specific serum IgE was also determined. The red midge larvae wheal size was significantly larger in group 1 (x = 149.2 mm2) than in group 2 (x = 18 mm2). Significant differences between levels of IgE anti-C. thummi were also found in group 1 (x = 52.12 kU/l) and in group 2 (x = 1.5 kU/l). The patients in group 2 had high levels of specific IgE against other allergens (D. pteronyssinus, shrimp and/or common mosquito) and had positive SPTs with these allergens, while the patients in group 1 were only sensitized to chironomids. The IgE-immunoblotting profile was quite different in both groups. The patients in group 1 seemed to have IgE against Chi t 1, the main Chironomus allergen, while the patients in group 2 had IgE against several protein bands in Chironomus, mosquito, shrimp and D. pteronyssinus extracts, some of them with equivalent molecular weights. We believe that the patients in group 2 were sensitized to Chironomus as a result of cross-reactivity with other insect or crustacean species.

Adolescent↗

PubMedDate not supplied

Nonpigmented fixed drug eruption caused by paracetamol.

Fixed drug eruption from paracetamol is not rare but no cases of nonpigmented fixed drug eruption caused by paracetamol have been previously described. We present the case of a woman who developed a nonpigmented fixed drug eruption following administration of paracetamol. Patch tests performed on affected and unaffected skin with paracetamol were negative. The diagnosis was made by a double-blind oral challenge with paracetamol. The patient tolerated aspirin.

Acetaminophen↗

PubMedDate not supplied

Comparative effects of L-methionine, S-adenosyl-L-methionine and 5'-methylthioadenosine on the growth of preneoplastic lesions and DNA methylation in rat liver during the early stages of hepatocarcinogenesis.

Male Wistar rats, initiated with diethylnitrosamine (DENA), were subjected to a selection treatment, according to the "resistant hepatocyte" model, followed or not followed by phenobarbital (PB). Rats received, for 3 weeks after selection, 4 i.m. doses (96 mmol/kg) of L-methionine, S-adenosyl-L-methionine (SAM), or 5'-methylthioadenosine (MTA), a SAM catabolite formed during polyamine synthesis or by spontaneous splitting of SAM at physiologic temperature and pH. They were then killed. In some rats, SAM and MTA treatments were started 20 weeks after initiation. The animals were killed 3 weeks later and persistent (neoplastic) nodules (PN) were collected. Some rat groups received 1/2 and 1/4 of the above SAM and MTA doses, or 1/8 of the above MTA dose. SAM and MTA, but not methionine, caused a dose-dependent decrease in number and surface area of gamma-glutamyltranspeptidase (GGT)-positive foci, and in labeling index (LI) of focal cells, coupled with remodeling. SAM and MTA liver contents, SAM/S-adenosylhomocysteine (SAH) ratio and overall methylation of liver DNA were low during the development of GGT-positive foci. SAM, but not methionine, caused a dose-dependent recovery of SAM content and DNA methylation, and a partial reconstitution of liver MTA pool. Exogenous MTA only induced the reconstitution of MTA pool, without affecting SAM level and DNA methylation. Recovery of SAM and MTA pool and DNA methylation was found in the rats subjected to SAM plus MTA, indicating the absence of inhibition of DNA methyltransferases in vivo by MTA. MTA also inhibited liver reparative growth in partially hepatectomized rats, without modifying SAM content and DNA methylation of regenerating liver (RL). A high activity of ornithine decarboxylase (ODC) was found in the liver, during the development of preneoplastic foci, and in PN. This activity was inhibited by SAM and MTA treatments. Although MTA was more effective than SAM, the decrease in ODC activity was coupled with a larger fall in DNA synthesis in SAM-treated than in MTA-treated rats. Thus the antipromotion effect of SAM could not merely depend on its (spontaneous) transformation into MTA. Although MTA production may play a role in the SAM antipromotion effect, other mechanisms could be involved. A role of DNA methylation in the inhibition of growth by SAM is suggested. MTA is a potential chemopreventive agent for liver carcinogenesis.

Adenosine↗

PubMedDate not supplied

The influence of lipid composition on some physical and functional properties of cellular membranes in rat liver and hepatomas.

Explore the source record for details and available documents.

Animals↗

PubMedDate not supplied

[Cycles of swelling and contraction of slight degree in rat liver mitochondria and mitochondria of Yoshida ascites hepatoma].

Explore the source record for details and available documents.

Adenine Nucleotides↗

PubMedDate not supplied

Genomic abnormalities in hepatocarcinogenesis. Implications for a chemopreventive strategy.

Carcinogenesis is a complex process characterized by the cumulative activation of various oncogenes and the inactivation of suppressor genes. Epigenetic mechanisms are also involved. Mutational activation of ras family genes occurs in most spontaneous or carcinogen-induced liver tumors, in susceptible mice, and less frequently in preneoplastic lesions. This suggests a pathogenetic role of these changes in hepatic carcinogenesis, in the mouse. Overexpression of various growth-related genes occurs in preneoplastic tissue during rat liver carcinogenesis, but mutational activation of protooncogenes, notably of ras family genes, seems to be a late and rare event, while c-myc amplification is a late but frequent event in both rodent and human carcinogenesis. However, mutation of the suppressor p53 gene has been found in relatively early preneoplastic lesions in rat liver, and it may be frequently seen in human hepatocellular carcinomas. The possibility that this mutation is involved in the initiation stage of liver carcinogenesis is an attractive hypothesis which needs further evaluation. DNA hypomethylation is involved in carcinogenesis, but the mechanisms underlying this effect are still elusive. Hypomethylation of growth-related genes is associated with their overexpression and this could favor overgrowth of preneoplastic liver tissue. Decrease in S-adenosyl methionine/S-adenosylhomocysteine (SAM/SAH) ratio occurs in the liver of rats fed a methyl deficient diet, which is a carcinogenic treatment, and in preneoplastic liver tissue, developing in initiated/promoted rats fed an adequate diet. The role of low SAM/SAH ratio in carcinogenesis is substantiated by the tumor chemopreventive effect of lipotropic compounds. Treatment with exogenous SAM prevents the development of preneoplastic and neoplastic lesions in rat liver. This is associated with recovery of SAM/SAH ratio, DNA methylation and inhibition of growth-related gene expression. SAM effect on prenoplastic cell growth is abolished by 5-azacytidine, a hypomethylating agent, indicating the involvement of DNA methylation. The possibility that in SAM-treated rats, methylation and inhibition of the expression of growth-related genes is implicated in growth restraint is attractive and should be further evaluated. Modulation of rat liver carcinogenesis by influencing gene expression through DNA methylation or other epigenetic mechanisms could be a new approach to chemoprevention of these tumors.

Adenoma↗