Biochar as a Biocompatible Mild Anti-Inflammatory Supplement for Animal Feed and Agricultural Fields

Biochar is an organic material and high in carbon content, besides its use for energy purposes, it is also a material that serves the purpose of improving soil fertility, organic matter content of soils and removing heavy metals from water and soil. This study aims to investigate the antimicrobial effects of biochar whose beneficial effects on agricultural productivity has been proven by different studies. Scientific literature concerning the antibacterial, antifungal, and antiviral effects of the apricot seed and olive seed biochar is limited. Biochar applications may help to alter the microbial diversity by modifying biological environment either in agriculture or in animal husbandry. Moreover, biochar has been used in animal husbandry to improve animal health especially by regulating the intestinal flora and inflammation in the intestines. Hence, in our study, we investigated the effect of biochar on the growth of Aspergillus niger, Cryphonectria parasitica, Phytophthora cinnamomi, Plenodomus tracheiphilus, Enterococcus casseliflavus, Staphylococcus aureus, Pseudomonas aeruginosa, Escherichia coli and two different bacteriophage strains. Biochar did not have any direct effect on the growth of either Gram-positive or Gram-negative bacteria, bacteriophages, and fungi. In order to test their direct effects on the immune cells, mammalian macrophages were used and biochar directly reduced the inflammatory cytokine levels produced by the in vitro activated macrophages.     

The effects of cell recycling on the production of 1,3-propanediol by Klebsiella pneumoniae

The effects of both biomass age and cell recycling on the 1,3-propanediol (1,3-PDO) production by Klebsiella pneumoniae were investigated in a membrane-supported bioreactor using hollow-fiber ultrafiltration membrane module in two separate experiments. It was determined that older cells have a negative effect on 1,3-PDO production. The concentrations of by-products, such as acetic acid and ethanol, increased in cultures with older cells, whereas the concentrations of succinic acid, lactic acid and 2,3-butanediol decreased. The effect of cell recycling was comparatively studied at a cell recycling ratio of 100 %. The results showed that cell recycling had also negative effects on 1,3-PDO fermentation. It was hypothesized that both cell recycling and biomass age caused metabolic shifts to undesired by-products which then inhibited the 1,3-PDO production. On the other hand, the use of hollow-fiber ultrafiltration membrane module was found to be very effective in terms of removal of cells from the fermentation broth.     

Mice fed a lipogenic methionine-choline-deficient diet develop hypermetabolism coincident with hepatic suppression of SCD-1

Lipogenic diets that are completely devoid of methionine and choline (MCD) induce hepatic steatosis. MCD feeding also provokes systemic weight loss, for unclear reasons. In this study, we found that MCD feeding causes profound hepatic suppression of the gene encoding stearoyl-coenzyme A desaturase-1 (SCD-1), an enzyme whose regulation has significant effects on metabolic rate. Within 7 days of MCD exposure, hepatic SCD-1 mRNA decreased to nearly undetectable levels. By day 21, SCD-1 protein was absent from hepatic microsomes and fatty acids showed a decrease in monounsaturated species. These changes in hepatic SCD-1 were accompanied by signs of hypermetabolism. Calorimetry revealed that MCD-fed mice consumed 37% more energy than control mice (P = 0.0003). MCD feeding also stimulated fatty acid oxidation, although fatty oxidation genes were not significantly upregulated. Interestingly, despite their increased metabolic rate, MCD-fed mice did not increase their food consumption, and as a result, they lost 26% of their body weight in 21 days. In summary, MCD feeding suppresses SCD-1 in the liver, which likely contributes to hypermetabolism and weight loss. MCD feeding also induces hepatic steatosis, by an independent mechanism. Viewed together, these two disparate consequences of MCD feeding (weight loss and hepatic steatosis) give the appearance of an unusual form of lipodystrophy.     

Reactivity of nitroxyl-derived sulfinamides

Sulfinamide [RS(O)NH(2)] formation is known to occur upon exposure of cysteine residues to nitroxyl (HNO), which has received recent attention as a potential heart failure therapeutic. Because this modification can alter protein structure and function, we have examined the reactivity of sulfinamides in several systems, including a small organic molecule, peptides, and a protein. Although it has generally been assumed that this thiol to sulfinamide modification is irreversible, we show that sulfinamides can be reduced back to the free thiol in the presence of excess thiol at physiological pH and temperature. We have examined this sulfinamide reduction both in peptides, where a cyclic intermediate analogous to that proposed for asparagine deamidation reactions potentially can contribute, and in a small organic molecule, where the mechanism is restricted to a direct thiolysis. These studies suggest that the contribution from the cyclic intermediate becomes more important in environments with lower dielectric constants. In addition, although sulfinic acid [RS(O)OH] formation is observed upon prolonged incubations in water, reduction of sulfinamides is found to dominate in the presence of thiols. Finally, studies with the cysteine protease, papain, suggest that the reduction of sulfinamide to the free thiol is viable in a protein environment.     

Vibration parameters affecting vibration-induced reflex muscle activity

Purpose: To determine vibration parameters affecting the amplitude of the reflex activity of soleus muscle during low-amplitude whole-body vibration (WBV).

Materials and methods: This study was conducted on 19 participants. Vibration frequencies of 25, 30, 35, 40, 45, and 50?Hz were used. Surface electromyography, collision force between vibration platform and participant’s heel measured using a force sensor, and acceleration measured using an accelerometer fixed to the vibration platform were simultaneously recorded.

Results: The collision force was the main independent predictor of electromyographic amplitude.

Conclusion: The essential parameter of vibration affecting the amplitude of the reflex muscle activity is the collision force.     

Molybdenum-containing nitrite reductases: Spectroscopic characterization and redox mechanism

Objectives: This review summarizes the spectroscopic results, which will provide useful suggestions for future research. In addition, the fields that urgently need more information are also advised.

Background: Nitrite-NO-cGMP has been considered as an important signaling pathway of NO in human cells. To date, all the four known human molybdenum-containing enzymes, xanthine oxidase, aldehyde oxidase, sulfite oxidase, and mitochondrial amidoxime-reducing component, have been shown to function as nitrite reductases under hypoxia by biochemical, cellular, or animal studies. Various spectroscopic techniques have been applied to investigate the structure and catalytic mechanism of these enzymes for more than 20 years.

Methods: We summarize the published data on the applications of UV-vis and EPR spectroscopies, and X-ray crystallography in studying nitrite reductase activity of the four human molybdenum-containing enzymes.

Results: UV-vis has provided useful information on the redox active centers of these enzymes. The utilization of EPR spectroscopy has been critical in determining the coordination and redox status of the Mo center during catalysis. Despite the lack of substrate-bound crystal structures of these nitrite reductases, valuable structural information has been obtained by X-ray crystallography.

Conclusions: To fully understand the catalytic mechanisms of these physiologically/pathologically important nitrite reductases, structural studies on substrate-redox center interaction are needed.     

Modified nucleotides at the 5' end of human U2 snRNA are required for spliceosomal E-complex formation

U2 snRNA, a key player in nuclear pre-mRNA splicing, contains a 5'-terminal m3G cap and many internal modifications. The latter were shown in vertebrates to be generally required for U2 function in splicing, but precisely which residues are essential and their role in snRNP and/or spliceosome assembly is presently not clear. Here, we investigated the roles of individual modified nucleotides of HeLa U2 snRNA in pre-mRNA splicing, using a two-step in vitro reconstitution/complementation assay. We show that the three pseudouridines and five 2'O-methyl groups within the first 20 nucleotides of U2 snRNA, but not the m3G cap, are required for efficient pre-mRNA splicing. Individual pseudouridines were not essential, but had cumulative effects on U2 function. In contrast, four of five 2'O-methylations (at positions 1, 2, 12, and 19) were individually required for splicing. The in vitro assembly of 17S U2 snRNPs was not dependent on the presence of modified U2 residues. However, individual internal modifications were required for the formation of the ATP-independent early spliceosomal E complex. Our data strongly suggest that modifications within the first 20 nucleotides of U2 play an important role in facilitating the interaction of U2 with U1 snRNP and/or other factors within the E complex.     

JAK/STAT signaling in Drosophila muscles controls the cellular immune response against parasitoid infection

The role of JAK/STAT signaling in the cellular immune response of Drosophila is not well understood. Here, we show that parasitoid wasp infection activates JAK/STAT signaling in somatic muscles of the Drosophila larva, triggered by secretion of the cytokines Upd2 and Upd3 from circulating hemocytes. Deletion of upd2 or upd3, but not the related os (upd1) gene, reduced the cellular immune response, and suppression of the JAK/STAT pathway in muscle cells reduced the encapsulation of wasp eggs and the number of circulating lamellocyte effector cells. These results suggest that JAK/STAT signaling in muscles participates in a systemic immune defense against wasp infection.