Low fat adiponectin expression is associated with oxidative stress in nondiabetic humans with chronic kidney disease--impact on plasma adiponectin concentration

In spite of association between high plasma adiponectin and high metabolic and cardiovascular (CV) risk, highest adiponectin increments retain CV and metabolic protective effects in advanced chronic kidney disease (CKD). Passive accumulation can favor CKD-associated hyperadiponectinemia but potential additional regulation by adipose tissue remains undefined. Oxidative stress (OS) is associated with metabolic and CV disease and with CKD [increasing from conservative treatment (CT) to maintenance hemodialysis (MHD)], and OS can reduce adiponectin expression in experimental models. OS (in the form of plasma thiobarbituric acid-reactive substances: TBARS), subcutaneous adipose adiponectin mRNA, and plasma adiponectin were studied in CKD patients (stages 4 and 5) on CT (n = 7) or MHD (n = 11). Compared with CT and controls (C: n = 6) MHD had highest TBARS and lowest adiponectin mRNA (P < 0.05) with lower adipose adiponectin protein (P < 0.05 vs. CT). MHD also had lower plasma adiponectin than CT, although both had higher adiponectin than C (P < 0.05). In renal transplant recipients (RT: CKD stage 3; n = 5) normal TBARS were, in turn, associated with normal adiponectin mRNA (P < 0.05 vs. MHD). In all CKD (n = 23), adiponectin mRNA was associated positively with adiponectin plasma concentration (P < 0.01). In all subjects (n = 29), adiponectin mRNA was related (P < 0.05) negatively with TBARS after adjusting for plasma C-reactive protein (CRP) or CRP and creatinine. Thus altered OS, adiponectin expression, and plasma concentration represent a novel cluster of metabolic and CV risk factors in MHD that are normalized in RT. The data suggest novel roles of 1) MHD-associated OS in modulating adiponectin expression and 2) adipose tissue in contributing to circulating adiponectin in advanced CKD.     

Genetic mapping in the presence of genotyping errors

Genetic maps are built using the genotypes of many related individuals. Genotyping errors in these data sets can distort genetic maps, especially by inflating the distances. We have extended the traditional likelihood model used for genetic mapping to include the possibility of genotyping errors. Each individual marker is assigned an error rate, which is inferred from the data, just as the genetic distances are. We have developed a software package, called TMAP, which uses this model to find maximum-likelihood maps for phase-known pedigrees. We have tested our methods using a data set in Vitis and on simulated data and confirmed that our method dramatically reduces the inflationary effect caused by increasing the number of markers and leads to more accurate orders.     

Spatial scale and sampling size affect the concordance between remotely sensed information and plant community discrimination in restoration monitoring

Remote sensing cartography and GIS are part of ordinary practice in restoration ecology in discriminating patches of habitats, defining objectives, and planning the monitoring phase, but derived information is not always consistent with field survey. We assessed the mapping process efficiency in discriminating different communities, relying on plant composition data, and considering the effect of sample size and plot dimension (grain), in a heterogeneous environment in Tuscany (central Italy). We identified four land cover classes on a land cover map produced with object-oriented technique; hence we conducted a sampling of 64 plots (4 zones × 4 classes × 4 plots), estimating vascular plant cover using a point-quadrant method. Plots were nested squares with side lengths of 0.50 m, 1 m and, limited to a sub-sample, 2 m. We evaluated the effect of sample size and grain using permutational multivariate analysis of variance (PERMANOVA), testing the simultaneous response of species composition compared to land cover classes. Results demonstrated that for a sample size of 64 plots, grain does not influence the ability of discriminating among the habitat types investigated, while for a smaller sub-sample the effect of grain is significant and communities cannot be distinguished at all plot dimensions. Outcomes corroborate the hypothesis that sampling at a series of scales of observations and an adequate sample size can improve monitoring efficiency in restoration ecology. Nomenclature: Pignatti (1982) and Conti et al (2005) for Festuca.     

Association of GSTT1 null,XPD 751 CC and XPC 939 CC genotypes with increased levels of genomic damage among hospital pathologists

Context: Hospital workers are at risk for genotoxic damage following occupationally exposure to xenobiotics. Pathologists are exposed to chemicals during their use in health care environments, particularly throughout inhalation of airborne agents, absorption through skin or contact with the patient’s body fluids.

Objective: We evaluated the level of genomic damage in a sample of 61 hospital pathologists (occupationally exposed to antineoplastic drugs and sterilizing agents) and 60 control subjects.

Materials and methods: Lymphocytes were analyzed by SCEs and CAs assays and genotyped for GSTT1, GSTM1, CYP1A1 Ile/Val, XPD (A751C) and XPC (A939C) gene polymorphisms.

Results: Pathologists showed significantly higher frequencies of SCEs and CAs with respect to control subjects. GSTT1 null genotype was found to be associated with higher SCEs and CAs frequencies, whereas XPD 751?CC and XPC 939?CC genotypes only with a higher level of SCEs.

Discussion and conclusions: The SCEs and CAs results are consistent with other published data, placing hospital workers as a category at risk for genotoxic damage caused by chronic exposure to xenobiotics. The higher levels of cytogenetic damage observed among GSTT1 null, XPD 751 and XPC 939?CC homozygote subjects confirm the importance of the genetic polymorphisms analysis associated to genotoxicological studies.     

High potential for temperate viruses to drive carbon cycling in chemoautotrophy‐dominated shallow‐water hydrothermal vents

Viruses are the most abundant life forms in the world's oceans and they are key drivers of biogeochemical cycles, but their impact on the microbial assemblages inhabiting hydrothermal vent ecosystems is still largely unknown. Here, we analysed the viral life strategies and virus‐host interactions in the sediments of a newly discovered shallow‐water hydrothermal field of the Mediterranean Sea. Our study reveals that temperate viruses, once experimentally induced to replicate, can cause large mortality of vent microbes, significantly reducing the chemoautotrophic carbon production, while enhancing the metabolism of microbial heterotrophs and the re‐cycling of the organic matter. These results provide new insights on the factors controlling primary and secondary production processes in hydrothermal vents, suggesting that the inducible provirus‐host interactions occurring in these systems can profoundly influence the functioning of the microbial food web and the efficiency in the energy transfer to the higher trophic levels.     

A Real‐World Multicentre Retrospective Study of Paclitaxel‐Bevacizumab and Maintenance Therapy as First‐Line for HER2‐Negative Metastatic Breast Cancer

Bevacizumab in combination with taxanes in HER2‐negative metastatic breast cancer (MBC) patients has shown improved progression‐free survival (PFS), despite the lack of clear overall survival (OS) benefit. We performed a retrospective analysis to evaluate the impact of paclitaxel‐bevacizumab and of maintenance therapy with bevacizumab (BM) and endocrine therapy (ET) in the real‐world practice. We identified 314 HER2‐negative MBC patients treated in 12 cancer centers. Overall, the median PFS and OS were 14 and 40 months, respectively. Among the 254 patients potentially eligible for BM, 183 received BM after paclitaxel discontinuation until progression/toxicity. PFS and OS were improved in patients who had received BM in comparison with those potentially eligible but who did not receive BM (P< 0.0001 and P = 0.001, respectively). Results were confirmed when adjusting for propensity score. Among the 216 hormone‐receptor positive patients eligible for BM, a more favorable PFS and OS were observed when maintenance ET was administered (P < 0.0001). Multivariate analysis showed that PS, BM, number of disease sites and maintenance ET were related to PFS, while response and maintenance ET were related to OS. In hormone‐receptor positive patients, BM produced a significant PFS and a trend towards OS benefit only in absence of maintenance ET (P = 0.0007 and P = 0.06, respectively). In the triple‐negative subgroup, we observed a trend towards a better OS for patients who received BM (P = 0.06), without differences in PFS (P = 0.21). Our results confirmed the efficacy of first‐line paclitaxel‐bevacizumab in real‐world practice; both BM and maintenance ET significantly improved PFS and OS compared to no maintenance therapies. J. Cell. Physiol. 232: 1571–1578, 2017. © 2016 Wiley Periodicals, Inc.     

Effect of Some Growth Factors on Tissue Transglutaminase Overexpression Induced by β-Amyloid in Olfactory Ensheathing Cells

Herein, we assessed in a particular glial cell type, called olfactory ensheathing cells (OECs), the effect of some growth factors (GFs) on tissue transglutaminase (TG2) overexpression induced by amyloid-beta (Aβ) with native full-length peptide 1–42 or by fragments, 25–35 or 35–25, as control. Previously, we demonstrated that TG2 overexpression induced by some stressors was down-regulated by GFs exposure in OECs. To monitor cell viability, an MTT test was used, while TG2 expression was examined using immunocytochemical and Western blot analysis. We also considered the involvement of the TG2-mediated apoptotic pathway. Vimentin expression was evaluated as well. Reactive oxygen species and reduced glutathione levels were utilized to test the oxidative intracellular status. Lactate dehydrogenase released into the medium, as a marker of necrotic cell death, was evaluated. We found that in OECs exposed to Aβ(1–42) or Aβ(25–35) for 24 h, TG2 expression increased, and we observed that the protein appeared prevalently localized in the cytosol. The pre-treatment with GFs, basic fibroblast growth factor (bFGF) or glial-derived neurotrophic factor (GDNF), down-regulated the TG2 level, which was prevalently limited to the nuclear compartment. Vimentin expression and caspase cleavage showed a significant enhancement in Aβ(1–42) and Aβ(25–35) exposed cells. The pre-treatment with bFGF or GDNF was able to restore the levels of the proteins to control values, and the intracellular oxidative status modified by the exposure to Aβ(1–42) or Aβ(25–35). Our data suggest that both bFGF or GDNF could be an innovative mechanism to contrast TG2 expression, which plays a key role in Alzheimer’s disease.     

Integrin Beta 3 Regulates Cellular Senescence by Activating the TGF-β Pathway

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