Two NHX-type transporters from Helianthus tuberosus improve the tolerance of rice to salinity and nutrient deficiency stress.

The NHX-type cation/H+ transporters in plants have been shown to mediate Na+ (K+ )/H+ exchange for salinity tolerance and K+ homoeostasis. In this study, we identified and characterized two NHX homologues, HtNHX1 and HtNHX2 from an infertile and salinity tolerant species Helianthus tuberosus (cv. Nanyu No. 1). HtNHX1 and HtNHX2 share identical 5'- and 3'-UTR and coding regions, except for a 342-bp segment encoding 114 amino acids (L272 to Q385 ) which is absent in HtNHX2. Both hydroponics and soil culture experiments showed that the expression of HtNHX1 or HtNHX2 improved the rice tolerance to salinity. Expression of HtNHX2, but not HtNHX1, increased rice grain yield, harvest index, total nutrient uptake under K+ -limited salt-stress or general nutrient deficiency conditions. The results provide a novel insight into NHX function in plant mineral nutrition

Exploring the optimal impact force for chronic skeletal muscle injury induced by drop-mass technique in rats

Introduction: Skeletal muscle injuries are widespread in sports, traffic accidents and natural disasters and some of them with poor prognoses can lead to chronic skeletal muscle damage in the clinic. We induced a chronic skeletal muscle injury by controlling time and contusion force using an acute blunt trauma model that will help us better comprehend the pathological features of chronic skeletal muscle injury.Methods: Several levels of injury were induced by repeatedly striking in 5, 10, and 15 times the gastrocnemius muscle from the same height with 200 g weights. After injury, the markers of muscle injury were assessed at 2 and 4 weeks by serum elisa. Electron microscopy, histologic and immunohistochemical staining, and mRNA analysis were used to evaluate the ultrastructure, inflammation, extracellular matrix decomposition, and anabolism of injured muscle in 2 and 4 weeks.Results: All three different kinetic energies can result in skeletal muscle injuries. However, the injured skeletal muscles of rats in each group could not recover within 2 weeks. After 4 weeks, tissue self-repair and reconstruction caused the damage induced by 5 J kinetic energy to almost return to normal. In contrast, damage induced by 10 J kinetic energy displayed slight improvement compared to that at 2 weeks. Despite this, collagen fibers on the surface of the tissue were disorganized, directionally ambiguous, and intertwined with each other. Myofilaments within the tissue were also arranged disorderly, with blurry and broken Z-lines. Damage caused by 15 J kinetic energy was the most severe and displayed no improvements at 4 weeks compared to 2 weeks. At 4 weeks, IL-1β, IL-6, Collagen I, and Collagen III, MMP2 expressions in the 10 J group were lower than those at 2 weeks, showing a tendency towards injury stabilization.Conclusion: After 4 weeks of remodeling and repair, the acute skeletal muscle injury model induced by 10 J kinetic energy can stabilize pathological manifestations, inflammatory expression, and extracellular matrix synthesis and catabolism, making it an appropriate model for studying chronic skeletal muscle injuries caused by acute injury

Design of a Semi-confocal Fluorescence Microscope for Observing Excitation Spectrum of Soluble Molecules Adsorbed at the Air/water Interface

A semi-confocal fluorescence microscope is designed and constructed aiming to observe fluorescence excitation spectrum of soluble molecules adsorbed at the air/water interface. With a conventional confocal fluorescence microscope, the target molecules of pyrene arises some difficulties: excitation wavelength in deep ultraviolet forces low transmission performance of microscopic objectives and low wavelength-tunable performance of an excitation laser. A total internal reflection illumination with a light-guide coupled monochromated-xenon lamp is combined with the confocal fluorescence microscope. Theoretical feasibility and performance of the microscope are discussed with preliminary results obtained

Important role of platelets in modulating endotoxin-induced lung inflammation in CFTR-deficient mice.

Mutation of CFTR (cystic fibrosis transmembrane conductance regulator) leads to cystic fibrosis (CF). Patients with CF develop abnormalities of blood platelets and recurrent lung inflammation. However, whether CFTR-mutated platelets play a role in the development of lung inflammation is elusive. Therefore, we intratracheally challenged wildtype and F508del (a common type of CFTR mutation) mice with LPS to observe changes of F508del platelets in the peripheral blood and indexes of lung inflammation (BAL neutrophils and protein levels). Furthermore, we investigated whether or not and how F508del platelets modulate the LPS-induced acute lung inflammation by targeting anti-platelet aggregation, depletion of neutrophils, reconstitution of bone marrow or neutrophils, blockade of P-selectin glycoprotein ligand-1 (PSGL-1), platelet activating factor (PAF), and correction of mutated CFTR trafficking. We found that LPS-challenged F508del mice developed severe thrombocytopenia and had higher levels of plasma TXB2 coincided with neutrophilic lung inflammation relative to wildtype control. Inhibition of F508del platelet aggregation or depletion of F508del neutrophils diminished the LPS-induced lung inflammation in the F508del mice. Moreover, wildtype mice reconstituted with either F508del bone marrow or neutrophils developed worse thrombocytopenia. Blocking PSGL-1, platelet activating factor (PAF), or rectifying trafficking of mutated CFTR in F508del mice diminished and alveolar neutrophil transmigration in the LPS-challenged F508del mice. These findings suggest that F508del platelets and their interaction with neutrophils are requisite for the development of LPS-induced lung inflammation and injury. As such, targeting platelets might be an emerging strategy for dampening recurrent lung inflammation in cystic fibrosis patients

Tuning Photophysical Properties via Positional Isomerization of the Pyridine Ring in Donor–Acceptor-Structured Aggregation-Induced Emission Luminogens Based on Phenylmethylene Pyridineacetonitrile Derivatives

A series of aggregation-induced emission (AIE)-featured phenylmethylene pyridineacetonitrile derivatives named o-DBCNPy ((Z)-3-(4-(di-p-tolylamino)phenyl)-2-(pyridin-2-yl)acrylonitrile), m-DBCNPy ((Z)-3-(4-(di-p-tolylamino)phenyl)-2-(pyridin-3-yl)acrylonitrile), and p-DBCNPy ((Z)-3-(4-(di-p-tolylamino)phenyl)-2-(pyridin-4-yl)acrylonitrile) have been synthesized by tuning the substitution position of the pyridine ring. The linkage manner of the pyridine ring had influences on the molecular configuration and conjugation, thus leading to different photophysical properties. The absorption and fluorescence emission peak showed a bathochromic shift when the linking position of the pyridine ring changed from the meta to the ortho and para position. Meanwhile, o-DBCNPy exhibited the highest fluorescence quantum yield of 0.81 and the longest fluorescence lifetime of 7.96 ns as a neat film among all three isomers. Moreover, non-doped organic light-emitting diodes (OLEDs) were assembled in which the molecules acted as the light-emitting layer. Due to the relatively prominent emission properties, the electroluminescence (EL) performance of the o-DBCNPy-based OLED was superior to those of the devices based on the other two isomers with an external quantum efficiency (EQE) of 4.31%. The results indicate that delicate molecular modulation of AIE molecules could endow them with improved photophysical properties, making them potential candidates for organic photoelectronic devices

Differential regulation of mouse pancreatic islet insulin secretion and Smad proteins by activin ligands

International audienceGlucose-stimulated insulin secretion (GSIS) from pancreatic beta cells is regulated by paracrine factors, the identity and mechanisms of action of which are incompletely understood. Activins are expressed in pancreatic islets and have been implicated in the regulation of GSIS. Activins A and B signal through a common set of intracellular components, but it is unclear whether they display similar or distinct functions in glucose homeostasis

Transcriptome Analysis Reveals the Dynamic and Rapid Transcriptional Reprogramming Involved in Heat Stress and Identification of Heat Response Genes in Rice

High temperature is one of the most important environmental factors influencing rice growth, development, and yield. Therefore, it is important to understand how rice plants cope with high temperatures. Herein, the heat tolerances of T2 (Jinxibai) and T21 (Taizhongxianxuan2hao) were evaluated at 45 °C, and T21 was found to be sensitive to heat stress at the seedling stage. Analysis of the H2O2 and proline content revealed that the accumulation rate of H2O2 was higher in T21, whereas the accumulation rate of proline was higher in T2 after heat treatment. Meanwhile, transcriptome analysis revealed that several pathways participated in the heat response, including “protein processing in endoplasmic reticulum”, “plant hormone signal transduction”, and “carbon metabolism”. Additionally, our study also revealed that different pathways participate in heat stress responses upon prolonged stress. The pathway of “protein processing in endoplasmic reticulum” plays an important role in stress responses. We found that most genes involved in this pathway were upregulated and peaked at 0.5 or 1 h after heat treatment. Moreover, sixty transcription factors, including the members of the AP2/ERF, NAC, HSF, WRKY, and C2H2 families, were found to participate in the heat stress response. Many of them have also been reported to be involved in biotic or abiotic stresses. In addition, through PPI (protein–protein interactions) analysis, 22 genes were identified as key genes in the response to heat stress. This study improves our understanding of thermotolerance mechanisms in rice, and also lays a foundation for breeding thermotolerant cultivars via molecular breeding