Emergency control of Spartina alterniflora re-invasion with a chemical method in Chongming Dongtan,China

The exotic species Spartina alterniflora(S.alterniflora)seriously threatens the stability and functioning of saltmarsh ecosystems in the Yangtze Estuary.Ambitious efforts have been undertaken to control this species,but subsequent re-invasion is frequent,presenting a significant barrier to restoration.The complexity and high cost of integrated physical control programs has necessitated a shift in focus,leading to considerable attention being paid to the potential of herbicides to control S.alterniflora.To find a strategy for emergency control of small and scattered patches of re-invading S.alterniflora,an in situ field experiment using Gallant(Haloxyfop-R-methyl)herbicide was conducted.The growth parameters of plant density and height were used to evaluate the control efficiency of different treatment dosages and times and sediment samples were taken for environmental toxicity analysis.The results show the following:(1)the control efficacy of the maximum proposed application dose(2.70 g/m2)was 92%for continuous swards and 100%for small patches,while those of other dosages(0.45 g/m2,0.90 g/m2,and 1.35 g/m2)were lower than 40%;(2)the appropriate implementation time was July to August with 100%mortality resulting from a single application,while S.alterniflora was shown to be capable of recovering rapidly after treatment in May;and(3)there were no significant differences in the community structure of meiofauna among the herbicide treatments and the control,and no herbicide residues were detected in sediment samples collected from treatment areas.This chemical control method was implemented in the Shanghai Chongming Dongtan National Bird Nature Reserve(CDNR).The results of this study indicate that Gallant is an environmentally friendly herbicide with high efficiency,which can be adopted for emergency control of re-invading S.alterniflora.

TMEM181:a key mediator of cytolethal distending toxin required for Wnt signaling activity

Wnt signaling pathway plays critical roles in a variety of embryonic developmental processes and also controls homeostatic selfrenewal in a number of adult tissues(Flaherty and Dawn,2008;Nusse and Clevers,2017).At the cell membrane,Wnt ligands bind to the seven transmembrane receptors of Frizzled family and the co-receptors to activate intracellular signaling pathway,including theβ-catenin-dependent canonical Wnt signaling pathway,the noncanonical planar cell polarity(PCP)pathway and the Wnt/calcium pathway(Flaherty and Dawn,2008).In mammals,WNT4,WNT5A.

Essential role of Msx1 in regulating anterior-posterior patterning of the secondary palate in mice

Development of the secondary palate displays molecular heterogeneity along the anterior-posterior axis;however, the underlying molecular mechanism remains largely unknown. MSX1 is an anteriorly expressed transcription repressor required for palate development. Here, we investigate the role of Msx1 in regional patterning of the secondary palate. The Wnt1-Cre-mediated expression of Msx1(Rosa Msx1^(Wnt1-Cre))throughout the palatal mesenchyme leads to cleft palate in mice, associated with aberrant cell proliferation and cell death. Osteogenic patterning of the hard palate in Rosa Msx1^(Wnt1-Cre)mice is severely impaired, as revealed by a marked reduction in palatine bone formation and decreased expression of the osteogenic regulator Sp7. Overexpression and knockout of Msx1 in mice show that the transcription repressor promotes the expression of the anterior palate-specific Alx1 but represses the expression of the medialposterior palate genes Barx1, Meox2, and Tbx22. Furthermore, Tbx22 constitutes a direct Msx1 target gene in the secondary palate, suggesting that Msx1 can directly repress the expression of medial-posterior specific genes. Finally, we determine that Sp7 is downstream of Tbx22 in palatal mesenchymal cells,suggesting that a Msx1/Tbx22/Sp7 axis participates in the regulation of palate development. Our findings unveil a novel role for Msx1 in regulating the anterior-posterior growth and patterning of the secondary palate.

IMPULP:A Hardware Approach for In-Process Memory Protection via User-Level Partitioning

In recent years many security attacks occur when malicious codes abuse in-process memory resources.Due to the increasing complexity,an application program may call third-party code which cannot be controlled by programmers but may contain security vulnerabilities.As a result,the users have the risk of suffering information leakage and control flow hijacking.However,current solutions like Intel memory protection extensions(MPX)severely degrade performance,while other approaches like Intel memory protection keys(MPK)lack flexibility in dividing security domains.In this paper,we propose IMPULP,an effective and efficient hardware approach for in-process memory protection.The rationale of IMPULP is user-level partitioning that user code segments are divided into different security domains according to their instruction addresses,and accessible memory spaces are specified dynamically for each domain via a set of boundary registers.Each instruction related to memory access will be checked according to its security domain and the corresponding boundaries,and illegal in-process memory access of untrusted code segments will be prevented.IMPULP can be leveraged to prevent a wide range of in-process memory abuse attacks,such as buffer overflows and memory leakages.For verification,an FPGA prototype based on RISC-V instruction set architecture has been developed.We present eight tests to verify the effectiveness of IMPULP,including five memory protection function tests,a test to defense typical buffer overflow,a test to defense famous memory leakage attack named Heartbleed,and a test for security benchmark.We execute the SPEC CPU2006 benchmark programs to evaluate the efficiency of IMPULP.The performance overhead of IMPULP is less than 0.2%runtime on average,which is negligible.Moreover,the resource overhead is less than 5.5%for hardware modification of IMPULP.