Influence of Indentation on the Fatigue Strength of Carbonitrided Plain Steel

To study the influence of indentation on the fatigue strength of untreated and carbonitrided specimens of S38C steel, the fatigue limit of specimens with and without indentations was tested. Fracture surfaces were observed using scanning electron microscopy (SEM). The results show that the fatigue strength of the untreated specimen decreases with increasing dimension of indentation, without significant difference compared to the predicted results. Compared to the fatigue limit of the untreated specimen, those of the carbonitrided specimen and the carbonitrided specimen whose compound layer was polished were improved by 12% and 40%, respectively. The fatigue strength of the carbonitrided specimen decreased sharply with increasing indentation size because of the presence of microcracks in the compound layer. When the compound layer was removed, the fatigue limit was observed to be less sensitive to indentation than that of the carbonitrided specimen

Direct and indirect effects of climate on richness drive the latitudinal diversity gradient in forest trees

Data accessibility statement: Full census data are available upon reasonable request from the ForestGEO data portal, http://ctfs.si.edu/datarequest/ We thank Margie Mayfield, three anonymous reviewers and Jacob Weiner for constructive comments on the manuscript. This study was financially supported by the National Key R&D Program of China (2017YFC0506100), the National Natural Science Foundation of China (31622014 and 31570426), and the Fundamental Research Funds for the Central Universities (17lgzd24) to CC. XW was supported by the Strategic Priority Research Program of the Chinese Academy of Sciences (XDB3103). DS was supported by the Czech Science Foundation (grant no. 16-26369S). Yves Rosseel provided us valuable suggestions on using the lavaan package conducting SEM analyses. Funding and citation information for each forest plot is available in the Supplementary Information Text 1.Peer reviewedPostprin

Advances in DNA Barcoding of Toxic Marine Organisms

There are more than 200,000 marine species worldwide. These include many important economic species, such as large yellow croaker, ribbonfish, tuna, and salmon, but also many potentially toxic species, such as blue-green algae, diatoms, cnidarians, ctenophores, Nassarius spp., and pufferfish. However, some edible and toxic species may look similar, and the correct identification of marine species is thus a major issue. The failure of traditional classification methods in certain species has promoted the use of DNA barcoding, which uses short, standard DNA fragments to assist with species identification. In this review, we summarize recent advances in DNA barcoding of toxic marine species such as jellyfish and pufferfish, using genes including cytochrome oxidase I gene (COI), cytochrome b gene (cytb), 16S rDNA, internal transcribed spacer (ITS), and Ribulose-1,5-bisphosphate carboxylase oxygenase gene (rbcL). We also discuss the application of this technique for improving the identification of marine species. The use of DNA barcoding can benefit the studies of biological diversity, biogeography, food safety, and the detection of both invasive and new species. However, the technique has limitations, particularly for the analysis of complex objects and the selection of standard DNA barcodes. The development of high-throughput methods may offer solutions to some of these issues

Metalorganic Chemical Vapor Deposition of GaNAs Alloy Using Dimethylhydrazine as Nitrogen Precursor

GaNAs alloy is grown by metalorganic chemical vapor deposition (MOCVD) using dimethylhydrazine (DMHy) as the nitrogen precursor. High-resolution X-ray diffraction (HRXRD) and secondary ion mass spectrometry (SIMS) are combined in determining the nitrogen contents in the samples. Room temperature photoluminescence (RTPL) measurement is also used in characterizing. The influence of different Ga precursors on GaNAs quality is investigated. Samples grown with triethylgallium (TEGa) have better qualities and less impurity contamination than those with trimethylgallium (TMGa). Nitrogen content of 5.688% is achieved with TEGa. The peak wavelength in RTPL measurement is measured to be 1278.5nm

Interaction between Fungal Communities, Soil Properties, and the Survival of Invading E. coli O157:H7 in Soils

Pathogens that invade into the soil cancontaminate food and water, andinfect animals and human beings. It is well documented that individual bacterial phyla are well correlated with the survival of E. coliO157 (EcO157), while the interaction betweenthe fungal communities and EcO157 survival remains largely unknown. In this study, soil samples from Tongliao, Siping, and Yanji in northeast China were collected and characterized. Total DNA was extracted for fungal and bacterial community characterization. EcO157 cells were spiked into the soils, and their survival behavior was investigated. Results showed that both fungal and bacterial communities were significantly correlated (p < 0.01) with the survival of EcO157 in soils, and the relative abundances of fungal groups (Dothideomycetes and Sordariomycetes) and some bacterial phyla (Acidobacteria, Firmicutes, gamma- and delta-Proteobacteria)weresignificantly correlated with ttds (p < 0.01). Soil pH, EC (electric conductance) salinity, and water-soluble nitrate nitrogen were significantly correlated with survival time (time to reach the detection limit, ttd) (p < 0.05). The structural equation model indicated that fungal communities could directly influence ttds, and soil properties could indirectly influence the ttds through fungal communities. The first log reduction time (δ) was mainly correlated with soil properties, while the shape parameter (p) was largely correlated with fungal communities. Our data indicated that both fungal and bacterial communities were closely correlated (p < 0.05)with the survival of EcO157 in soils, and different fungal and bacterial groups might play different roles. Fungal communities and bacterial communities explained 5.87% and 17.32% of the overall variation of survival parameters, respectively. Soil properties explained about one-third of the overall variation of survival parameters. These findings expand our current understanding of the environmental behavior of human pathogens in soils

Activation of the ACE2/Ang-(1–7)/Mas Pathway Reduces Oxygen–Glucose Deprivation-Induced Tissue Swelling, ROS Production, and Cell Death in Mouse Brain with Angiotensin II Overproduction

We previously demonstrated that mice which overexpress human renin and angiotensinogen (R+A+) show enhanced cerebral damage in both in vivo and in vitro experimental ischemia models. Angiotensin-converting enzyme 2 (ACE2) counteracts the effects of angiotensin (Ang-II) by transforming it into Ang-(1–7), thus reducing the ligand for the AT1 receptor and increasing stimulation of the Mas receptor. Triple transgenic mice, SARA, which specifically overexpress ACE2 in neurons of R+A+ mice were used to study the role of ACE2 in ischemic stroke using oxygen and glucose deprivation (OGD) of brain slices as an in vitro model. We examined tissue swelling, the production of reactive oxygen species (ROS), and cell death in the cerebral cortex (CX) and the hippocampal CA1 region during OGD. Expression levels of NADPH oxidase (Nox) isoforms, Nox2 and Nox4 were measured using western blots. Results show that SARA mice and R+A+ mice treated with the Mas receptor agonist Ang-(1–7) had less swelling, cell death, and ROS production in CX and CA1 areas compared to those in R+A+ animals. Treatment of slices from SARA mice with the Mas antagonist A779 eliminated this protection. Finally, western blots revealed less Nox2 and Nox4 expression in SARA mice compared with R+A+ mice both before and after OGD. We suggest that reduced brain swelling and cell death observed in SARA animals exposed to OGD result from diminished ROS production coupled with lower expression of Nox isoforms. Thus, the ACE2/Ang-(1–7)/Mas receptor pathway plays a protective role in brain ischemic damage by counteracting the detrimental effects of Ang-II-induced ROS production

Activation of the ACE2/Ang-(1–7)/Mas Pathway Reduces Oxygen–Glucose Deprivation-Induced Tissue Swelling, ROS Production, and Cell Death in Mouse Brain with Angiotensin II Overproduction

We previously demonstrated that mice which overexpress human renin and angiotensinogen (R+A+) show enhanced cerebral damage in both in vivo and in vitro experimental ischemia models. Angiotensin-converting enzyme 2 (ACE2) counteracts the effects of angiotensin (Ang-II) by transforming it into Ang-(1–7), thus reducing the ligand for the AT1 receptor and increasing stimulation of the Mas receptor. Triple transgenic mice, SARA, which specifically overexpress ACE2 in neurons of R+A+ mice were used to study the role of ACE2 in ischemic stroke using oxygen and glucose deprivation (OGD) of brain slices as an in vitro model. We examined tissue swelling, the production of reactive oxygen species (ROS), and cell death in the cerebral cortex (CX) and the hippocampal CA1 region during OGD. Expression levels of NADPH oxidase (Nox) isoforms, Nox2 and Nox4 were measured using western blots. Results show that SARA mice and R+A+ mice treated with the Mas receptor agonist Ang-(1–7) had less swelling, cell death, and ROS production in CX and CA1 areas compared to those in R+A+ animals. Treatment of slices from SARA mice with the Mas antagonist A779 eliminated this protection. Finally, western blots revealed less Nox2 and Nox4 expression in SARA mice compared with R+A+ mice both before and after OGD. We suggest that reduced brain swelling and cell death observed in SARA animals exposed to OGD result from diminished ROS production coupled with lower expression of Nox isoforms. Thus, the ACE2/Ang-(1–7)/Mas receptor pathway plays a protective role in brain ischemic damage by counteracting the detrimental effects of Ang-II-induced ROS production