The relationship between elastase and lactoferrin in healthy, gingivitis and periodontitis sites

OBJECTIVES: To compare the relative amounts of elastase (primary polymorphonuclear leucocyte granule constituent) and lactoferrin (secondary PMN granule constituent) in the gingival crevicular fluid (GCF) of healthy, gingivitis and periodontitis sites.
DESIGN: This cross-sectional study looked at the two GCF constituents in three categories of disease status within the same subject.
MATERIALS AND METHODS: Patients with chronic adult periodontitis were screened and those exhibiting all three types of sites ie periodontally healthy, gingivitis and periodontitis sites were recruited (n = 10) and had GCF collected from the three sites. Lactoferrin and elastase were measured in eluates of GCF by enzyme-linked immunosorbent assay.
RESULTS: The absolute amount of lactoferrin measured in ng per 30 s samples was significantly lower in healthy and gingivitis sites as compared to periodontitis sites however this difference failed to reach significance when the concentration of lactoferrin in GCF was used as the analytical unit. No significant differences were found for elastase levels at any sites when expressed as either absolute amounts or concentrations. Secondary granule release, as evidenced by lactoferrin levels, occurs during cell migration and the process is independent of primary granule release, which is thought to correlate with PMN activation. The relationship between granule constituents in the samples showed significant differences, the highest lactoferrinlelastase ratio being at periodontitis sites (P < 0.001).
CONCLUSIONS These findings imply a change in the relative amounts of elastase and lactoferrin released at different disease level sites, with an almost 10-fold increase in the proportion of lactoferrin to elastase in periodontitis sites over healthy and gingivitis sites. This variation in the release by PMNs of primary and secondary granule constituents may indicate alterations in PMN function in different disease environments.     

Ras-driven proliferation and apoptosis signaling during rat liver carcinogenesis is under genetic control

Fast growth and deregulation of G1 and S phases characterize preneoplastic and neoplastic liver lesions of genetically susceptible F344 rats, whereas a G1-S block in lesions of resistant BN rats explains their low progression capacity. However, signal transduction pathways responsible for the different propensity of lesions from the 2 rat strains to evolve to malignancy remain unknown. Here, we comparatively investigated the role of Ras/Erk pathway inhibitors, involved in growth restraint and cell death, in the acquisition of a phenotype resistant or susceptible to hepatocarcinogenesis. Moderate activation of Ras, Raf-1 and Mek proteins was paralleled in both rat models by strong induction of Dab2 and Rkip inhibitors. Levels of Dusp1, a specific ERK inhibitor, increased only in BN rat lesions, leading to modest ERK activation, whereas a progressive Dusp1 decline occurred in corresponding lesions from F344 rats and was accompanied by elevated ERK activation. Furthermore, a gradual increase of Rassf1A/Nore1A/Mst1-driven apoptosis was detected in both rat strains, with highest levels in BN hepatocellular carcinoma (HCC), whereas loss of Dab2IP, a protein implicated in ASK1-dependent cell death, occurred only in F344 rat HCC, resulting in significantly higher apoptosis in BN than F344 HCC. Taken together, our results indicate a control of the Ras/Erk pathway and the pro-apoptotic Rassf1A/Nore1A and Dab2IP/Ask1 pathways by HCC susceptibility genes. Dusp1 possesses a prominent role in the acquisition of the phenotype resistant to HCC by BN rats, whereas late activation of RassF1A/Nore1A and Dab2IP/Ask1 axes is implicated in the highest apoptosis characteristic of BN HCC.     

回春液补肾助阳药效学的实验研究

回春液由人参、鹿茸、貂鞭等名贵中药组成。有补肾助阳,填精益气等功效。药效学研究证实,该药有促进幼鼠发育及增加去势大鼠前列腺——精液囊的重量,亦显著增加小鼠血红蛋白的含量,表明回春液有雄性激素样作用。     

Interleukin-5 is at 5q31 and is deleted in the 5q- syndrome

Human interleukin-5 (IL-5) is a selective eosinophilopoietic and eosinophil-activating growth hormone. By in situ hybridization this gene is mapped to chromosome 5q23.3 to 5q32. It is shown to be deleted in two patients with the 5q-syndrome and in one patient previously diagnosed with myelodysplasia whose condition had progressed to acute myeloblastic leukemia. The clustering of other genes involved in hematopoiesis (IL-3, granulocyte-macrophage colony-stimulating factor, feline sarcoma viral oncogene homolog, colony-stimulating factor 1) to the same region as IL-5 suggests a nonrandom localization and raises interesting questions concerning the evolution and regulation of these genes.