Comparative Transcriptome Analysis Explores the Mechanism of Angiosperm and Gymnosperm Deadwood Degradation by Fomes fomentarius.

In forest ecosystems, most of the soil organic matter is derived from trees, as deadwood lignocellulose and wood-decaying basidiomycetes are the most important decomposers of lignin and cellulose. Fomes fomentarius is one of the most common white-rot fungi colonizing angiosperm trees and is often found in birch deadwood but seldom in pine deadwood. To reveal the mechanism through which F. fomentarius selects angiosperms as its preferred host trees, birch and pinewood sticks were selected for culturing for two months. The weight loss, cellulose and lignin degradation rates, activities of degrading enzymes, and transcriptome analyses of two degradation models were compared and analyzed. The results showed that F. fomentarius-degraded birchwood with higher efficiency than pinewood. A GO enrichment analysis found that more upregulated genes related to the top 30 terms showed a molecular function related to degradation, and most genes belonged to the CAZymes family in F. fomentarius-degraded birchwood. However, pinewood degradation did not show these phenomena. A KEGG pathway analysis also indicated that, for the same pathway, more upregulated genes were involved in birchwood degradation caused by F. fomentarius than in pinewood degradation.

Heart failure in mice induces a dysfunction of the sinus node associated with reduced CaMKII signaling.

Dysfunction of the sinoatrial node (SAN), the natural heart pacemaker, is common in heart failure (HF) patients. SAN spontaneous activity relies on various ion currents in the plasma membrane (voltage clock), but intracellular Ca2+ ([Ca2+]i) release via ryanodine receptor 2 (RYR2; Ca2+ clock) plays an important synergetic role. Whereas remodeling of voltage-clock components has been revealed in HF, less is known about possible alterations to the Ca2+ clock. Here, we analyzed [Ca2+]i handling in SAN from a mouse HF model after transverse aortic constriction (TAC) and compared it with sham-operated animals. ECG data from awake animals showed slower heart rate in HF mice upon autonomic nervous system blockade, indicating intrinsic sinus node dysfunction. Confocal microscopy analyses of SAN cells within whole tissue showed slower and less frequent [Ca2+]i transients in HF. This correlated with fewer and smaller spontaneous Ca2+ sparks in HF SAN cells, which associated with lower RYR2 protein expression level and reduced phosphorylation at the CaMKII site. Moreover, PLB phosphorylation at the CaMKII site was also decreased in HF, which could lead to reduced sarco/endoplasmic reticulum Ca2+-ATPase (SERCA) function and lower sarcoplasmic reticulum Ca2+ content, further depressing the Ca2+ clock. The inhibition of CaMKII with KN93 slowed [Ca2+]i transient rate in both groups, but this effect was smaller in HF SAN, consistent with less CaMKII activation. In conclusion, our data uncover that the mechanism of intrinsic pacemaker dysfunction in HF involves reduced CaMKII activation.

Simultaneous Tuning Band Gaps of Cu2 O and TiO2 to Form S-Scheme Hetero-Photocatalyst.

Photocatalytic Z or S scheme merits higher redox potentials and faster charge separation. However, heterostructure photocatalysts with band gaps of bulk materials often have a type I band structure leading to poor photocatalytic activity. In view of this, we report simultaneous tuning of band gaps of Cu2 O and TiO2 , where quantum dot Cu2 O nanoparticles were formed on doped TiO2 with Ti3+ . The reduced size of Cu2 O made its conduction band more negative, whereas the introduction of Ti3+ made the absorption edge red shift to the visible light region. The as-formed heterostructure enabled an S-Scheme mechanism with remarkable activity and stability for visible light photodegradation of 4-chlorophenol (4-CP). The as-obtained photocatalysts' activity demonstrated ca. 510-fold increase as compared to individual ones and a mechanical blend. The as-obtained photocatalysts maintained over 80 % for 5 cycles and 2 months exposure to O2 did not decrease the degradation rate. ESR characterization and scavenger experiments proved the S-Scheme mechanism.

The Sirtuin-1 relied antioxidant and antiaging activity of 5,5'-diferulic acid glucoside esters derived from corn bran by enzymatic method.

Maize is the food crop with the highest total output in the world. However, corn bran is only a by-product with low price. The 5,5'-diferulic acid glucoside esters (DFG) were obtained from corn bran using the enzymatic method. DFG showed obvious antioxidant capacity in cell, Caenorhabditis elegans (C. elegans) and in mouse. DFG decreased ROS and MDA content in 500 µM H2 O2 stimulated ARPE-19 cells to 48.6% and 32.2%, respectively. DFG decreased ROS content in C. elegans to 49.1% and MDA content in acute ethanol (50%, 12 ml/kg) stimulated mouse to 30.4%. DFG also increased SOD protein content significantly in cell, C. elegans and mouse to 175.5%, 120.1%, and 126.2%, respectively. DFG significantly extended the lifespan of C. elegans both under heat stress and natural situation. The median survival time was prolonged to 133.3% and 116.7%, respectively. This capacity relied on the SIR-2.1 activity. SIR-2.1 is an ortholog of human Sirtuin-1 (SIRT-1). DFG also upregulated SIRT-1 and PCG-1α expression level obviously in H2 O2 -stimulated ARPE-19 cells (to 134.4% and 127.1%, respectively) and in acute ethanol stimulated mouse eyes (to 135.1% and 111.5%, respectively) and liver (to 123.3% and 113.6%, respectively). These results indicate that DFG has multiple bioactivities. Our research provides a new application prospect of corn bran. And to our best knowledge, this is the first time, the sirtuins-relied lifespan extension activity of the 5,5'-diferulic acid extracted from corn bran was reported. PRACTICAL APPLICATIONS: The traditional method for extracting diferulic acid from corn bran is to use the strong alkali. Obviously, this is not welcomed by the food industry. We employed the biological enzyme method in a relatively mild pH range during the extraction process. It is more environmentally friendly and more economical. DFG can be added as a raw material for functional foods like yogurt, fruit juice, and cereals. As well, the solid precipitate obtained after extraction can also be used as high-quality dietary fiber to produce functional food. Meanwhile, concerning for the 5,5'-diferulic acid derived from corn bran, the relevant research is still not abundant. And to our best knowledge, we have reported for the first time about the effect of this kinds of diferulic acid on prolonging life span and its SIRT-1-dependent activity. It also provides a new perspective for the study of diferulic acid.

Aberrant sinus node firing during ß-adrenergic stimulation leads to cardiac arrhythmias in diabetic mice.

AIM: Cardiovascular complications, including cardiac arrhythmias, result in high morbidity and mortality in patients with type-2 diabetes mellitus (T2DM). Clinical and experimental data suggest electrophysiological impairment of the natural pacemaker of the diabetic heart. The present study examined sinoatrial node (SAN) arrhythmias in a mouse model of T2DM and physiologically probed their underlying cause. METHODS: Electrocardiograms were obtained from conscious diabetic db/db and lean control db/+ mice. In vivo SAN function was probed through pharmacological autonomic modulation with isoprenaline, atropine and carbachol. Blood pressure stability and heart rate variability (HRV) were evaluated. Intrinsic SAN function was evaluated through ex vivo imaging of spontaneous Ca2+ transients in isolated SAN preparations. RESULTS: While lean control mice showed constant RR intervals during isoprenaline challenge, the diabetic mice experienced SAN arrhythmias with large RR fluctuations in a dose-dependent manner. These arrhythmias were completely abolished by atropine pre-treatment, while carbachol pretreatment significantly increased SAN arrhythmia frequency in the diabetic mice. Blood pressure and HRV were comparable in db/db and db/+ mice, suggesting that neither augmented baroreceptor feedback nor autonomic neuropathy is a likely arrhythmia mechanism. Cycle length response to isoprenaline was comparable in isolated SAN preparations from db/db and db/+ mice; however, Ca2+ spark frequency was significantly increased in db/db mice compared to db/+ at baseline and after isoprenaline. CONCLUSION: Our results demonstrate a dysfunction of cardiac pacemaking in an animal model of T2DM upon challenge with a ß-adrenergic agonist. Ex vivo, higher Ca2+ spark frequency is present in diabetic mice, which may be directly linked to in vivo arrhythmias.

Effects of hereditary moderate high fat diet on metabolic performance and physical endurance capacity in C57BL/6 offspring.

Obesity in pregnant women presents a risk to fetal health, leading to numerous metabolic syndromes and chronic inflammation risks. Previously, physical exercise was considered to be one of the primary treatments for obesity. However, the effect of fat consumption throughout the life cycle on physical endurance capacity remains unknown. A total of two groups of female mice (age, 6 weeks; C57BL/6J) were fed with a normal chow diet and a moderate high fat diet (MHFD), during pregnancy and lactation (8 weeks), with the offspring receiving the same diet as the mother. When filial mice were 8, 16 and 24 weeks old, they were tested for endurance, blood pressure (BP) and glucose tolerance, as well as adipose tissue infiltration and macrophage subtype. Compared with the control group, filial mice in MHFD groups exhibited increased BP and glucose levels and larger adipose cells (~4­fold). During adolescence, the obese filial mice demonstrated increased endurance compared with controls. Endurance declines in middle and old age; the endurance of aged obese mice was 29% that of lean ones. In addition, body coordination and movement memory did not notably change. The expression of cluster of differentiation 68, one of the most reliable markers of macrophages, increased by 2.48­fold, demonstrating that macrophages were recruited and underwent infiltration. In addition, increased tumor necrosis factor­α and decreased interleukin­10 expression demonstrated that infiltrated macrophages are polarized to the M1 state, which weakens physical endurance and resists type M2 macrophages, which exhibit repairing functions. In conclusion, hereditary MHFD weakens physical endurance and alters the metabolic characteristics of C57BL/6 offspring.