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The gulf of Annaba, the most important touristic and economic coastal zone located in Northeast Algeria, is contaminated by several pollutants from urban, agricultural, harbor and industrial activities. Elevated levels of heavy metals were detected in a locally prevalent edible mollusk Donax trunculus (Bivalvia, Donacidae) widely used as a sentinel species for the assessment of marine pollution. The present work aims to measure the difference between two localities, one being full of different pollutants (Sidi Salem) and the other being relatively clean (El Battah) and to evaluate the ability of D. trunculus to overcome the environmental stress during a transplantation experiment by a determination of fatty acid profile, the enzymes activities and the level of metallothioneins (MTs), a biomarker of metallic contamination. Adults of D. trunculus were collected at Sidi Salem (contaminated site) and transplanted into El Battah (reference site) for 21 days in cages (60 × 60 × 60 cm with a 2 mm mesh). Biochemical analyzes were conducted at different times (0, 7, 14 and 21 days). At 0-day experiment: the rate of the fatty acids, the enzymes activities and MT levels at the site of Sidi Salem (polluted site) were significantly different from those of El Battah. During the transplantation a gradual restoration of fatty acids rates, enzymes activities and MT levels was observed. At the end of the period of transplantation, the values are comparable to those of El Battah. A two-way ANOVA (time, site) on data revealed significant effects of time and site. Overally, D. trunculus is able to induce its detoxification system and to restore relatively rapidly the status of individuals from the reference site (El Battah). [ABSTRACT FROM AUTHOR]

Abstract: The regulation of alkaline phosphatase activity by dissolved inorganic (DIP) and organic phosphorus (DOP) and the contribution of DOP as phosphorus source were studied monthly in Toulon Bay (NW Mediterranean, France) in 2005–2006. The concentrations of DIP and DOP varied respectively from 0 to 0.185μM and from 0 to 0.329μM. The bulk activities (Vm, Km, Vm/Km) were measured using MUFP as substrate. Its high affinity component (Km: 0.05–1.00μM) was negatively correlated with the sum of the concentrations of DIP and DOP but not with these compounds taken independently. A negative correlation with DIP was found when the concentrations of DOP were lower than 0.08μM. A negative correlation with DOP was shown when the concentrations of DIP were lower than 0.05μM. This high affinity component can be considered as a valuable indicator for the potential utilization of the compounds which contribute to the intracellular phosphorus pool. [Copyright &y& Elsevier]

Somatic hypermutation of immunoglobulin genes is a highly mutagenic process that is B cell-specific and occurs during antigen-driven responses leading to antigen specificity and antibody affinity maturation. Mutations at the Ig locus are initiated by Activation-Induced cytidine Deaminase and are equally distributed at G/C and A/T bases. This requires the establishment of error-prone repair pathways involving the activity of several low fidelity DNA polymerases. In the physiological context, the G/C base pair mutations involve multiple error-prone DNA polymerases, while the generation of mutations at A/T base pairs depends exclusively on the activity of DNA polymerase η. Using two large cohorts of individuals with xeroderma pigmentosum variant (XP-V), we report that the pattern of mutations at Ig genes becomes highly enriched with large deletions. This observation is more striking for patients older than 50 years. We propose that the absence of Pol η allows the recruitment of other DNA polymerases that profoundly affect the Ig genomic landscape.

The endothelial protein C receptor (EPCR) facilitates protein C activation and plays a protective role in the response to Escherichia coli-mediated sepsis in primates. Previously, a soluble form of EPCR (sEPCR) in human plasma was characterized, and several studies indicated that generation of sEPCR is regulated by inflammatory mediators, including thrombin-mediated up-regulation of surface metalloproteolytic activity in vitro. This study addressed the question of whether plasma sEPCR levels reflect changes in thrombin generation in patients undergoing anticoagulant treatment. The sEPCR levels in patients treated with coumarin-type oral anticoagulants were significantly lower than those in healthy asymptomatic adult volunteers (105.3 +/- 70.8 ng/mL [n = 55] versus 165.8 +/- 115.8 ng/mL [n = 200]; P <.0001). A similar decline in plasma sEPCR levels was found in patients treated with unfractionated heparin. In healthy volunteers, sEPCR levels declined to about 100 ng/mL within 3 days after initiation of an 8-day period of warfarin administration and increased within 2 days after its cessation. Plasma sEPCR levels returned to pretreatment values within 1 week, and the changes in plasma sEPCR levels mirrored changes in values for international normalized ratios. A similar decline in sEPCR levels with time was observed in 7 patients beginning treatment with warfarin for a thrombotic disorder. Prothrombin fragment 1 + 2 levels also decreased in volunteers and patients given warfarin. These results show that plasma sEPCR levels decline in response to treatment with anticoagulants whose mechanism of action is known to decrease in vivo thrombin production.

The thyrotropin receptor (TSHR), a member of the large family of G protein-coupled receptors, controls both the function and growth of thyroid cells via stimulation of adenylyl cyclase. We report two different mutations in the TSHR gene of affected members of two large pedigrees with non-autoimmune autosomal dominant hyperthyroidism (toxic thyroid hyperplasia), that involve residues in the third (Val509Ala) and seventh (Cys672Tyr) transmembrane segments. When expressed by transfection in COS-7 cells, the mutated receptors display a higher constitutive activation of adenylyl cyclase than wild type. This new disease entity is the germline counterpart of hyperfunctioning thyroid adenomas, in which different somatic mutations with similar functional characteristics have been demonstrated.