Biochemistry of hydrogen metabolism in Chlamydomonas reinhardtii wild type and a Rubisco-less mutant

Sulfate nutrient-deprivation in Chlamydomonas reinhardtii   brings about prompt degradation of Rubisco and a concomitant substantial accumulation of starch. These changes precede hydrogen (_H2${\mathrm{H}}_2$) photoevolution by the cells. The cause-and-effect relationship between Rubisco loss, starch accumulation and subsequent _H2${\mathrm{H}}_2$-photoevolution in C. reinhardtii, and the role of illumination for these changes to occur, was investigated in this work. A Rubisco-less and acetate-requiring mutant of C. reinhardtii   (CC2653) was employed as a tool in this investigation and compared to the wild type (WT) in terms of protein and starch metabolic flux and _H2${\mathrm{H}}_2$-evolution upon sulfur deprivation. Results showed a prompt Rubisco degradation and concomitant 10-fold starch accumulation in the WT in the light, which was completed within 48 h of S-deprivation. This was followed by a regulated starch degradation and concomitant _H2${\mathrm{H}}_2$-photoevolution, which lasted for up to 120 h in S-deprivation. This massive flux of primary metabolites (protein and starch) did not occur in the dark in the WT, suggesting a strictly light-dependent and integrated process in metabolite rearrangement and _H2${\mathrm{H}}_2$-photoevolution in C. reinhardtii  . The Rubisco-less CC2653 mutant failed to accumulate starch upon S-deprivation in the light or dark and also failed to evolve _H2${\mathrm{H}}_2$ gas. These results suggested a temporal cause-and-effect relationship between the light-dependent catabolism of Rubisco and starch accumulation, and the subsequent ability of the cell to perform a light-dependent starch degradation and _H2${\mathrm{H}}_2$-photoevolution. The regulated starch breakdown in the light apparently provides the endogenous substrate that supports _H2${\mathrm{H}}_2$-evolution, both by feeding electrons into the plastoquinone pool in chloroplasts, and indirectly by sustaining mitochondrial respiration for the maintenance of anaerobiosis in the cell.     

Greenhouse effect reduction and energy recovery from waste landfill

Waste management systems are a non-negligible source of greenhouse gases. In particular, methane and carbon dioxide emissions occur in landfills due to the breakdown of biodegradable carbon compounds operated on by anaerobic bacteria. The conventional possibilities of reducing the greenhouse effect (GHE) from waste landfilling consists in landfill gas (LFG) flaring or combustion with energy recovery in reciprocating engines. These conventional treatments are compared with three innovative possibilities: the direct LFG feeding to a fuel cell (FC); the production of a hydrogen-rich gas, by means of steam reforming and CO₂ capture, to feed a stationary FC; the production of a hydrogen-rich gas, by means of steam reforming and CO₂ capture, to feed a vehicle FC. The comparison is carried out from an environmental point of view, calculating the specific production of GHE per unit mass of waste disposed in landfill equipped with the different considered technologies.     

Galectins in Early Pregnancy and Pregnancy-Associated Pathologies

Galectins are a family of conserved soluble proteins defined by an affinity for β-galactoside structures present on various glycoconjugates. Over the past few decades, galectins have been recognized as important factors for successful implantation and maintenance of pregnancy. An increasing number of studies have demonstrated their involvement in trophoblast cell function and placental development. In addition, several lines of evidence suggest their important roles in feto-maternal immune tolerance regulation and angiogenesis. Changed or dysregulated galectin expression is also described in pregnancy-related disorders. Although the data regarding galectins’ clinical relevance are still at an early stage, evidence suggests that some galectin family members are promising candidates for better understanding pregnancy-related pathologies, as well as predicting biomarkers. In this review, we aim to summarize current knowledge of galectins in early pregnancy as well as in pregnancy-related pathologies.     

Novel 1,3,5-Triazinyl Aminobenzenesulfonamides Incorporating Aminoalcohol,Aminochalcone and Aminostilbene Structural Motifs as Potent Anti-VRE Agents,and Carbonic Anhydrases I,II, VII,IX, and XII Inhibitors

A series of 1,3,5-triazinyl aminobenzenesulfonamides substituted by aminoalcohol, aminostilbene, and aminochalcone structural motifs was synthesized as potential human carbonic anhydrase (hCA) inhibitors. The compounds were evaluated on their inhibition of tumor-associated hCA IX and hCA XII, hCA VII isoenzyme present in the brain, and physiologically important hCA I and hCA II. While the test compounds had only a negligible effect on physiologically important isoenzymes, many of the studied compounds significantly affected the hCA IX isoenzyme. Several compounds showed activity against hCA XII; (E)-4-{2-[(4-[(2,3-dihydroxypropyl)amino]-6-[(4-styrylphenyl)amino]-1,3,5-triazin-2-yl)amino]ethyl}benzenesulfonamide (31) and (E)-4-{2-[(4-[(4-hydroxyphenyl)amino]-6-[(4-styrylphenyl)amino]-1,3,5-triazin-2-yl)amino]ethyl}benzenesulfonamide (32) were the most effective inhibitors with K_Is = 4.4 and 5.9 nM, respectively. In addition, the compounds were tested against vancomycin-resistant Enterococcus faecalis (VRE) isolates. (E)-4-[2-({4-[(4-cinnamoylphenyl)amino]-6-[(4-hydroxyphenyl)amino]-1,3,5-triazin-2-yl}amino)ethyl]benzenesulfonamide (21) (MIC = 26.33 µM) and derivative 32 (MIC range 13.80–55.20 µM) demonstrated the highest activity against all tested strains. The most active compounds were evaluated for their cytotoxicity against the Human Colorectal Tumor Cell Line (HCT116 p53 +/+). Only 4,4’-[(6-chloro-1,3,5-triazin-2,4-diyl)bis(iminomethylene)]dibenzenesulfonamide (7) and compound 32 demonstrated an IC₅₀ of ca. 6.5 μM; otherwise, the other selected derivatives did not show toxicity at concentrations up to 50 µM. The molecular modeling and docking of active compounds into various hCA isoenzymes, including bacterial carbonic anhydrase, specifically α-CA present in VRE, was performed to try to outline a possible mechanism of selective anti-VRE activity.     

Characterization of a Si-SiO2 Mixture Generated from SiO(g) and CO(g)

Metallurgical and Materials Transactions B - The reaction between SiO(g) and CO(g) is a relevant intermediate reaction in the silicon production process. One of the products generated from this gas...     

PACAP-38 and PAC1 Receptor Alterations in Plasma and Cardiac Tissue Samples of Heart Failure Patients

Pituitary adenylate cyclase activating polypeptide-38 (PACAP-38) is a multifunctional neuropeptide, which may play a role in cardioprotection. However, little is known about the presence of PACAP-38 in heart failure (HF) patients. The aim of our study was to measure the alterations of PACAP-38 like immunoreactivity (LI) in acute (n = 13) and chronic HF (n = 33) and to examine potential correlations between PACAP-38 and HF predictors (cytokines, NT-proBNP). Tissue PACAP-38 LI and PAC1 receptor levels were also investigated in heart tissue samples of patients with HF. Significantly higher plasma PACAP-38 LI was detected in patients with acute HF, while in chronic HF patients, a lower level of immunoreactivity was observed compared to healthy controls (n = 13). Strong negative correlation was identified between plasma PACAP-38 and NT-proBNP levels in chronic HF, as opposed to the positive connection seen in the acute HF group. Plasma IL-1 β, IL-2 and IL-4 levels were significantly lower in chronic HF, and IL-10 was significantly higher in patients with acute HF. PACAP-38 levels of myocardial tissues were lower in all end-stage HF patients and lower PAC1 receptor levels were detected in the primary dilated cardiomyopathy group compared to the controls. We conclude that PACAP-38 and PAC1 expression correlates with some biomarkers of acute and chronic HF; therefore, further studies are necessary to explore whether PACAP could be a suitable prognostic biomarker in HF patients.