The impacts of precipitation increase and nitrogen addition on soil respiration in a semiarid temperate steppe

Soil respiration, Rs, is strongly controlled by water availability in semiarid grasslands. However, how Rs is affected by precipitation change (either as rainfall or as snowfall) especially under increasing nitrogen (N) deposition has been uncertain. A manipulative experiment to investigate the responses of growing season Rs to changes in spring snowfall or summer rainfall with or without N addition was conducted in the semiarid temperate steppe of China during three hydrologically contrasting years. Our results showed that both spring snow addition and summer water addition significantly increased Rs by increasing soil moisture. The effect of spring snow addition only occurred in years with both relatively lower natural snowfall and later snowmelt time. Summer water addition showed a much stronger effect on Rs by increasing plant root growth and microbial activities, but the magnitude also largely depended on the possible legacy effect of previous year precipitation. Our results indicated that precipitation increase in the form of snowfall had weaker effects than that in the form of rainfall as the former only accounted for less than 30% of total precipitation. Compared with other ecosystem processes, Rs was less responsible for increase in N deposition as it did not increase root productivity and microbial activities in the soils. Our results provided field data constraints for modeling the ecosystem carbon balance under the future global change scenarios in semiarid grasslands

High-dimensional orbital angular momentum entanglement concentration based on Laguerre-Gaussian mode selection

Twisted photons enable the definition of a Hilbert space beyond two dimensions by orbital angular momentum (OAM) eigenstates. Here we propose a feasible entanglement concentration experiment, to enhance the quality of high-dimensional entanglement shared by twisted photon pairs. Our approach is started from the full characterization of entangled spiral bandwidth, and is then based on the careful selection of the Laguerre–Gaussian (LG) modes with specific radial and azimuthal indices p and `. In particular, we demonstrate the possibility of high-dimensional entanglement concentration residing in the OAM subspace of up to 21 dimensions. By means of LabVIEW simulations with spatial light modulators, we show that the Shannon dimensionality could be employed to quantify the quality of the present concentration. Our scheme holds promise in quantum information applications defined in high-dimensional Hilbert space

The Molecular Mechanisms of OPA1-Mediated Optic Atrophy in Drosophila Model and Prospects for Antioxidant Treatment

Mutations in optic atrophy 1 (OPA1), a nuclear gene encoding a mitochondrial protein, is the most common cause for autosomal dominant optic atrophy (DOA). The condition is characterized by gradual loss of vision, color vision defects, and temporal optic pallor. To understand the molecular mechanism by which OPA1 mutations cause optic atrophy and to facilitate the development of an effective therapeutic agent for optic atrophies, we analyzed phenotypes in the developing and adult Drosophila eyes produced by mutant dOpa1 (CG8479), a Drosophila ortholog of human OPA1. Heterozygous mutation of dOpa1 by a P-element or transposon insertions causes no discernable eye phenotype, whereas the homozygous mutation results in embryonic lethality. Using powerful Drosophila genetic techniques, we created eye-specific somatic clones. The somatic homozygous mutation of dOpa1 in the eyes caused rough (mispatterning) and glossy (decreased lens and pigment deposition) eye phenotypes in adult flies; this phenotype was reversible by precise excision of the inserted P-element. Furthermore, we show the rough eye phenotype is caused by the loss of hexagonal lattice cells in developing eyes, suggesting an increase in lattice cell apoptosis. In adult flies, the dOpa1 mutation caused an increase in reactive oxygen species (ROS) production as well as mitochondrial fragmentation associated with loss and damage of the cone and pigment cells. We show that superoxide dismutase 1 (SOD1), Vitamin E, and genetically overexpressed human SOD1 (hSOD1) is able to reverse the glossy eye phenotype of dOPA1 mutant large clones, further suggesting that ROS play an important role in cone and pigment cell death. Our results show dOpa1 mutations cause cell loss by two distinct pathogenic pathways. This study provides novel insights into the pathogenesis of optic atrophy and demonstrates the promise of antioxidants as therapeutic agents for this condition

CD151-α3β1 Integrin Complexes are Prognostic Markers of Glioblastoma and Cooperate with EGFR to Drive Tumor Cell Motility and Invasion

Glioblastoma, one of the most aggressive forms of brain cancer, is featured by high tumor cell motility and invasiveness, which not only fuel tumor infiltration, but also enable escape from surgical or other clinical interventions. Thus, better understanding of how these malignant traits are controlled will be key to the discovery of novel biomarkers and therapies against this deadly disease. Tetraspanin CD151 and its associated α3β1 integrin have been implicated in facilitating tumor progression across multiple cancer types. How these adhesion molecules are involved in the progression of glioblastoma, however, remains largely unclear. Here, we examined an in-house tissue microarray-based cohort of 96 patient biopsies and TCGA dataset to evaluate the clinical significance of CD151 and α3β1 integrin. Functional and signaling analyses were also conducted to understand how these molecules promote the aggressiveness of glioblastoma at molecular and cellular levels. Results from our analyses showed that CD151 and α3 integrin were significantly elevated in glioblastomas at both protein and mRNA levels, and exhibited strong inverse correlation with patient survival (p \u3c 0.006). These adhesion molecules also formed tight protein complexes and synergized with EGF/EGFR to accelerate tumor cell motility and invasion. Furthermore, disruption of such complexes enhanced the survival of tumor-bearing mice in a xenograft model, and impaired activation of FAK and small GTPases. Also, knockdown- or pharmacological agent-based attenuation of EGFR, FAK or Graf (ARHGAP26)/small GTPase-mediated pathways markedly mitigated the aggressiveness of glioblastoma cells. Collectively, our findings provide clinical, molecular and cellular evidence of CD151-α3β1 integrin complexes as promising prognostic biomarkers and therapeutic targets for glioblastoma

Drosophila IAP1-Mediated Ubiquitylation Controls Activation of the Initiator Caspase DRONC Independent of Protein Degradation

Ubiquitylation targets proteins for proteasome-mediated degradation and plays important roles in many biological processes including apoptosis. However, non-proteolytic functions of ubiquitylation are also known. In Drosophila, the inhibitor of apoptosis protein 1 (DIAP1) is known to ubiquitylate the initiator caspase DRONC in vitro. Because DRONC protein accumulates in diap1 mutant cells that are kept alive by caspase inhibition (“undead” cells), it is thought that DIAP1-mediated ubiquitylation causes proteasomal degradation of DRONC, protecting cells from apoptosis. However, contrary to this model, we show here that DIAP1-mediated ubiquitylation does not trigger proteasomal degradation of full-length DRONC, but serves a non-proteolytic function. Our data suggest that DIAP1-mediated ubiquitylation blocks processing and activation of DRONC. Interestingly, while full-length DRONC is not subject to DIAP1-induced degradation, once it is processed and activated it has reduced protein stability. Finally, we show that DRONC protein accumulates in “undead” cells due to increased transcription of dronc in these cells. These data refine current models of caspase regulation by IAPs

RIVER CONSERVANCY AND AGRICULTURAL DEVELOPMENT OF THE NORTH CHINA PLAIN AND LOESS HIGHLANDS STRATEGIES AND RESEARCH

The North China Plain is the Chinese counterpart to the North American Great Plains. This largest plain in China suffers frequently from drought. Although agricultural production has been significantly increased in recent years, it is still far too low and too unstable to compensate for population growth and the demands of a rising standard of living. One of the major factors limiting agricultural development on the North China Plain is drought. A complication is that not only have surface and underground water resources been utilized almost to their limits for agrarian needs but also water shortages due to rapidly mounting urban and industrial demands have become more and more acute. At the same time, perhaps ironically, too much water is also a menace to the North China Plain. Poor drainage and soil salinization are characteristic of extensive areas, and the potential hazard of inundations from the Yellow River is a historic and worsening problem

A brief review on anterior urethral strictures

The treatment of urethral strictures remains a challenging field in urology even though there are a variety of procedures to treat it at present, as no one approach is superior over another. This paper reviewed the surgical options for the management of different sites and types of anterior urethral stricture, providing a brief discussion of the controversies regarding this issue and suggesting possible future advancements. Among the existing procedures, simple dilation and direct vision internal urethrotomy are more commonly used for short urethral strictures ( <1 cm, soft and no previous intervention). Currently, urethroplasty using buccal mucosa or penile skin is the most widely adopted clinical techniques and have proved successful. Nonetheless, complications such as donor site morbidity remain problem. Tissue engineering techniques are considered as a promising solution for urethral reconstruction, but require further investigation, as does stem cell therapy. Keywords: Anterior urethral strictures, Urethral reconstruction, Tissue engineering, Urethral stricture

Zinc Binding Directly Regulates Tau Toxicity Independent of Tau Hyperphosphorylation

Tau hyperphosphorylation is thought to underlie tauopathy. Working in a Drosophila tauopathy model expressing a human Tau mutant (hTauR406W, or Tau∗), we show that zinc contributes to the development of Tau toxicity through two independent actions: by increasing Tau phosphorylation and, more significantly, by directly binding to Tau. Elimination of zinc binding through amino acid substitution of Cys residues has a minimal effect on phosphorylation levels yet essentially eliminates Tau toxicity. The toxicity of the zinc-binding-deficient mutant Tau∗ (Tau∗C2A) and overexpression of native Drosophila Tau, also lacking the corresponding zinc-binding Cys residues, are largely impervious to zinc concentration. Importantly, restoration of zinc-binding ability to Tau∗ by introduction of a zinc-binding residue (His) into the original Cys positions restores zinc-responsive toxicities in proportion to zinc-binding affinities. These results indicate zinc binding is a substantial contributor to tauopathy and have implications for therapy development