A search for the plant ingredients that protect cells from air pollutants and benz[a]pyrene phototoxicity.

A diversity of antioxidants and plant ingredients were examined for their protective effect in cultured Balb/c 3T3 cells against ultraviolet A (UVA)-induced cytotoxicities of extracted air pollutants and benz[a]pyrene (B[a]P) in an effort to find effective protectors against the phototoxicity of air pollutants and B[a]P. As has been observed for B[a]P phototoxicity, air pollutants themselves and those previously exposed to UVA light in the absence of cells exhibited faintly weak cytotoxicity, but the toxicity was markedly elevated when they were exposed to UVA light concomitantly with cells. The B[a]P phototoxicity was not eliminated by well-known antioxidants but was markedly diminished by diversity of plant ingredients. Among the plant ingredients tested in the current study, morin, naringin, and quercetin were found to be desirable protectors against B[a]P phototoxicity.

Mutations within the tyrosine kinase domain of EGFR gene specifically occur in lung adenocarcinoma patients with a low exposure of tobacco smoking.

Somatically acquired mutations in the epidermal growth factor receptor (EGFR) gene in lung cancer are associated with significant clinical responses to gefitinib, a tyrosine kinase inhibitor that targets EGFR. We screened the EGFR in 469 resected tumours of patients with lung cancer, which included 322 adenocarcinomas, 102 squamous cell carcinomas, 27 large cell carcinomas, 13 small cell carcinomas, and five other cell types. PCR with a specific condition was performed to identify any deletion in exon 19, while mutant-allele-specific amplification was performed to identify a mutation in codon 858 of exon 21. EGFR mutations were found in 136 cases (42.2%) with adenocarcinoma, in one case with large cell carcinoma, and in one case with pleomorphic carcinoma. An in-frame deletion in exon 19 was found in 62 cases while an L858R mutation was found in 77 cases. In the 322 cases with adenocarcinoma, these mutations were more frequently found in women than in men (P=0.0004), in well differentiated tumours than in poorly differentiated tumours (P=0.0014), and in patients who were never smokers than in patients who were current/former smokers (P<0.0001). The mutation was more frequently observed in patients who smoked

[Autologous blood transfusion in surgery of urologic malignant tumor].

BACKGROUND: Autologous blood transfusion has been widely endorsed, because of the adverse effects attributed to homologous blood transfusion. So we employed autologous blood transfusion to avoid homologous blood transfusion in operation of urological malignant patients. We reviewed our experience with autologous blood transfusion in 48 patients. METHODS: A total of 48 patients underwent operation with 400 to 1,200 ml preoperative autologous blood donation, in 41 patients with administration of erythropoietin and 7 patients without erythropoietin. The details of operations are radical nephrectomy in 18 cases (2 cases were bilateral), radical nephro-ureterectomy in 2 cases, retroperitoneal lymph node dissection (RPLND) in 2 cases, radical prostatectomy in 12 cases and radical cystectomy in 14 cases. RESULTS: The volume of surgical blood loss were 381 +/- 522 ml in nephrectomy (1,158 +/- 202 ml in bilateral case), 517 +/- 5 ml in radical nephro-ureterectomy 636 +/- 574 ml in RPLND, 665 +/- 291 ml in radical prostatectomy and 1,123 +/- 417 ml in radical cystectomy. Only three cases needed homologous blood transfusion. CONCLUSION: We can avoid homologous blood transfusion in 94% of patients. Autologous blood transfusion is recommended as safe and convenient.

Prolonging discordant xenograft survival with anticomplement reagents K76COOH and FUT175.

The guinea pig heart, when transplanted into the rat heterotopically, is rejected within 30 min via activation of the alternative complement pathway. Natural antibody does not contribute to rejection. This xenotransplantation model was used to assess the effect of anti-complement reagents on discordant xenograft survival. In vivo administration of K76COOH (K76) to rats induced only slight suppression of factors B and D and a marked decrease of C3, leading to the depression of ACH50 (reflecting the potency of the alternative pathway). On the other hand, FUT175 (FUT) reduced C3 activity by about 80% and inhibited factor B activity nearly 100% < 1 hr after the administration, but inhibited factor D activity only marginally. FUT abrogated ACH50 for > 6 hr. Of note, the xenograft beating time was prolonged approximately 3 times by FUT but not by K76, suggesting that direct inhibition of plasma serine protease factor B results in the complete suppression of ACH50 and graft survival. The administration of both K76 and FUT resulted in the longest graft survival, but the effects of these reagents were abolished by additional antigraft antibody. Anticomplement reagents that block factor B and C3 are therefore effective for prolongation of discordant xenograft survival when the graft rejection is associated with the complement alternative pathway.

Effect of ingested toxic bean lectins on the gastrointestinal tract in the rat.

The present study was undertaken to provide further evidence for the mechanisms proposed for the toxicity of ingested bean lectins in animals: to show the stability of concanavalin A (Con A) in the gastrointestinal tract so that it has enough time to interact with some enzymes localized in the intestinal membrane and to find its effect on the activities of those enzymes that have been adopted as criteria for adaptive changes in response to altered diets, namely intestinal sucrase, alkaline phosphatase and leucine aminopeptidase. Significant amounts of ingested Con A were recovered unaltered (as seen from affinity chromatography and electrophoresis) from the cecal content of rats 4 h after its oral administration and from feces (90% recovery) 4 d later. This indicated that Con A is quite stable during its passage through the gastrointestinal tract. Con A, given at a level of 0.3 or 0.5% in the diet, completely prevented adaptive changes in the activities of those enzymes. These results substantiate the mechanisms proposed earlier by other investigators that the toxicity of ingested bean lectins involves their binding to the luminal surface of the small intestine, where they disturb the function of the brush border membrane.