Comparative analysis of complete plastid genome reveals powerful barcode regions for identifying wood of Dalbergia odorifera and D. tonkinensis (Leguminosae)

Dalbergia odorifera T. C. Chen (Leguminosae), a rare and endangered tree species endemic to Hainan Island of China, produces the most expensive and rarest wood in China. The wood characteristics of D. odorifera are remarkably similar to those of D. tonkinensis (a much less sought-after species from Vietnam), and the DNA from wood is often highly degraded, making it very difficult to identify the two species using anatomical features or DNA barcoding based on regular DNA markers. To solve the confusion of identifying wood reliably from the two species, we built and analyzed the plastome library of 26 samples from 18 Dalbergia species, of which 12 samples from eight closely related species of D. odorifera are newly sequenced in this study. Phylogenomic analysis suggested that the relationships among the 26 samples are mostly well resolved, and conspecific individuals from different populations of D. odorifera and D. tonkinensis clustered together. Between the plastid genomes of the two species, we identified 129 indels and 114 single nucleotide polymorphisms. By assessing a subset of 20 nucleotide polymorphisms and 10 indels using 37 population-level samples (20 samples of D. odorifera and 17 samples of D. tonkinensis), we recovered eight species-specific barcode regions that could be suitable for identifying the wood D. odorifera and D. tonkinensis. To examine their utility in wood identification, we amplified the eight DNA barcodes using six wood samples and recovered an amplification success rate of 83.3%, demonstrating a reliable method for precise wood identification of the two species.     

Characterization of the P protein-binding domain on the 10-kilodalton protein of Borna disease virus

The Borna disease virus (BDV) is the prototype member of the Bornaviridae, and it replicates in the cell nucleus. The BDV p24P and p40N proteins carry nuclear localization signals (NLS) and are found in the nuclei of infected cells. The BDV p10 protein does not have an NLS, but it binds with P and/or N and is translocated to the nucleus. Hence, p10 may play a role in the replication of BDV in the cell nucleus. Here, we show that the P-binding domain is located in the N terminus of p10 and that S(3) and L(16) are important for the interaction.     

Pyroptosis in glioblastoma: A crucial regulator of the tumour immune microenvironment and a predictor of prognosis

Recent studies have shown that pyroptosis, an inflammatory form of cell death, has a dual role in tumorigenesis and tumour progression and affects the prognosis of patients; however, the role of pyroptosis in glioblastoma (GBM) is still unclear. In this study, based on GBM patients'' data from two independent cohorts, we performed a comprehensive analysis of the expression and prognostic value of 33 pyroptosis‐associated genes (PAGs) in GBM, as well as their role in the tumour immune microenvironment (TIME) of GBM. We identified 29 PAGs that were differentially expressed between GBM and normal brain tissue, 18 of which were upregulated in GBM tissue. Most of the 33 PAGs were strongly correlated with the levels of immune cell infiltration. Based on the 33 PAGs, the GBM samples can be divided into two clusters (C1‐C2), with C1 having a ‘hot’ but immunosuppressive TIME and C2 having a ‘cold’ TIME, suggesting different immunotherapeutic responses in the two clusters. In addition, we identified four PAGs that were strongly associated with GBM prognosis and constructed a risk model based on these four PAGs. This risk model is an independent prognostic factor for GBM patients, and there is a different immune status between high‐ and low‐risk groups. In conclusion, this study demonstrates that pyroptosis is closely associated with the prognosis and TIME of GBM and provides an important basis for further studies on the relationship between pyroptosis and GBM.     

Dynamic ejection behaviour of water molecules passing through a nano-aperture nozzle

This study used molecular dynamics (MD) simulation to investigate the passage of water molecules through a composite graphene/Au nano-nozzle. Our focus was on the degree to which system temperature, extrusion speed, and nozzle diameter affect jet dynamics and the associated transient phenomena. Our findings show that high pressure and spatial confinement cause the nanojet from a small nozzle diameter (1.0?nm) to bend and twist, whereas the jets from a nozzle with a diameter of 1.5?nm present columns of greater stability. At 100?K, the H₂O nanojet froze at the outlet of the nozzle in the form of condensed icicles. At 500?K, the H₂O nanojet formed a loose spray and gaseous clusters. High extrusion speed of 55.824?m/s produced recirculating flow downstream from the nanojet with the appearance of an erupting volcano, which further prompted the jet column to thicken. Lower extrusion speeds produced jets with flow velocity insufficient to overcome the capillary force at the outlet of the nozzle, which subsequently manifests as unstable fluctuations in the flow rate.

• HIGHLIGHTS

• Water molecules through a composite graphene/Au nano-nozzle forming a nanojet is investigated.

• High pressure and spatial confinement cause the nanojet from a small nozzle diameter (≤1.0?nm) to bend and twist.

• High extrusion speed (≧55.824?m/s) produced recirculating flow downstream from the nanojet.

• Figure abstract: Schematic of the H₂O nano-jet through a nano-nozzle of graphene/Au

     

Pathogenesis of renal ischemia/reperfusion injury: lessons from knockout mice

Ischemia/reperfusion-induced acute renal failure is a common clinical problem associated with a high morbidity and mortality. Upon hypoxic injury, the depletion of ATP causes mitochondrial dysfunction, and accumulation of intracellular sodium, calcium and reactive oxygen species. Subsequently, multiple enzyme systems including proteases, nitric oxide synthases, phospholipases and endonuclease are activated and responsible for cytoskeleton disruption, membrane damage, and DNA degradation, and eventually cell death. Ischemia/reperfusion injury also activates complement, cytokines, and chemokines, which are cytotoxic themselves, but also attract leukocytes into the ischemic area to cause further damage. The vascular endothelial cell injury and dysfunction prolong ischemia and induce vascular congestion, edema, and further infiltration of inflammatory cells. Many players in renal ischemia/reperfusion injury and their mechanisms have been investigated using genetically manipulated mouse models. In this review, we focus on the information gathered from these studies. Deficiency of the Na/Ca exchanger, inducible nitric oxide synthase, Caspase-1, A3 adenosine receptor, C3, C5, C6, Factor B, or midkine protects the kidney against I/R injury. Conversely, deficiency of the interleukin-1 receptor, osteopontin, C4, or recombination activation gene-1 is not protective, while the absence of adrenomedullin or endothelin receptor B delays the recovery of ischemia/reperfusion injury. The knowledge obtained from these studies provides new direction for designing potential therapeutic agents for treating ischemia/reperfusion injury.     

Unveiling the Microscopic Origin of Irreversible Capacity Loss of Hard Carbon for Sodium-Ion Batteries

The primary bottleneck hindering the application of hard carbon in sodium-ion batteries (SIBs) anodes lies in its inadequate initial Coulombic efficiency (ICE). Unclear causes of capacity loss at the microscopic level restrict the improvement of hard carbon anodes. Here, two pivotal stages that influence the structure and composition of hard carbon, namely synthesis, and storage are evaluated; subsequently identifying crucial determinants contributing to irreversible capacity loss. The results suggest that undergrown carbon layers allowing the intrusion of solvent molecules into the interior of the hard carbon is a key factor during the synthesis stage, while the gradual formation of oxygen-containing functional groups on the surface of the hard carbon is another factor leading to irreversible loss of capacity during storage stage. This research microscopically clarifies the irreversible capacity loss mechanism on hard carbon and provides guidelines for designing and applying high ICE hard carbon for SIBs.     

Association between S100B Levels and Long-Term Outcome after Aneurysmal Subarachnoid Hemorrhage: Systematic Review and Pooled Analysis

S100 calcium binding protein B (S100B), a well-studied marker for neurologic injury, has been suggested as a candidate for predicting outcome after subarachnoid hemorrhage. We performed a pooled analysis summarizing the associations between S100B protein in serum and cerebrospinal fluid (CSF) with radiographic vasospasm, delayed ischemic neurologic deficit (DIND), delayed cerebral infarction, and Glasgow Outcome Scale (GOS) outcome. A literature search using PubMed, the Cochrane Library, and the EMBASE databases was performed to identify relevant studies published up to May 2015. The weighted Stouffer’s Z method was used to perform a pooled analysis of outcome measures with greater than three studies. A total of 13 studies were included in this review. Higher serum S100B level was found to be associated with cerebral infarction as diagnosed by CT (p_adj = 3.1 x 10⁻⁴) and worse GOS outcome (p_adj = 5.5 x 10⁻¹¹). There was no association found between serum and CSF S100B with radiographic vasospasm or DIND. S100B is a potential prognostic marker for aSAH outcome.