Repeated mechanical damage enhanced Aquilaria sinensis resistance to Heortia vitessoides through jasmonic acid.

Introduction: The leaf-chewing pest Heortia vitessoides severely threatens the growth and development of Aquilaria sinensis. In our previous study, we found that mechanical damage (MD) to stem enhanced A. sinensis sapling resistance to H. vitessoides larvae. Methods: To reveal the defense mechanisms underlying this observation, we analyzed the types and contents of volatile organic compounds (VOCs), phytohormone contents, and expression of phytohormone-related genes in response to MD and herbivory wounding(HW). Results: Here, we identified several VOCs, such as the pesticides fenobucarb and 2,4-di-tert-butylphenol, in mature leaf (ML) of MD-treated plants. Compared with salicylic acid (SA) or the ethylene (ET) pathway, jasmonic acid (JA) content and JA-related genes were more strongly upregulated. Interestingly, we found a dramatic difference between JA-related upstream and downstream genes expression in YL and ML, which confirmed that JA-Ile accumulation in MD-ML and HW-ML could be derived from local damaged site. Discussion: Taken together, we provide evidence that the JA pathway plays a dominant role in the A. sinensis response to MD and HW.

Stabilizing Metal Halide Perovskites for Solar Fuel Production: Challenges, Solutions, and Future Prospects.

Metal halide perovskites (MHPs) are emerging photocatalyst materials that can enable sustainable solar-to-chemical energy conversion by virtue of their broad absorption spectra, effective separation/transport of photogenerated carriers, and solution processability. Although preliminary studies show the excellent photocatalytic activities of MHPs, their intrinsic structural instability due to the low formation energy and soft ionic nature is an open challenge for their practical applications. This review discusses the latest understanding of the stability issue and strategies to overcome this issue for MHP-based photocatalysis. First, the origin of the instability issue at atomic levels and the design rules for robust structures are analyzed and elucidated. This is then followed by presenting several different material design strategies for stability enhancement, including reaction medium modification, material surface protection, structural dimensionality engineering, and chemical composition engineering. Emphases are placed on understanding the effects of these strategies on photocatalytic stability as well as the possible structure-performance correlation. Finally, the possible future research directions for pursuing stable and efficient MHP photocatalysts in order to accelerate their technological maturity on a practical scale are outlined. With that, it is hoped to provide readers a valuable snapshot of this rapidly developing and exciting field.

The muscle-enriched myokine Musclin impairs beige fat thermogenesis and systemic energy homeostasis via Tfr1/PKA signaling in male mice.

Skeletal muscle and thermogenic adipose tissue are both critical for the maintenance of body temperature in mammals. However, whether these two tissues are interconnected to modulate thermogenesis and metabolic homeostasis in response to thermal stress remains inconclusive. Here, we report that human and mouse obesity is associated with elevated Musclin levels in both muscle and circulation. Intriguingly, muscle expression of Musclin is markedly increased or decreased when the male mice are housed in thermoneutral or chronic cool conditions, respectively. Beige fat is then identified as the primary site of Musclin action. Muscle-transgenic or AAV-mediated overexpression of Musclin attenuates beige fat thermogenesis, thereby exacerbating diet-induced obesity and metabolic disorders in male mice. Conversely, Musclin inactivation by muscle-specific ablation or neutralizing antibody treatment promotes beige fat thermogenesis and improves metabolic homeostasis in male mice. Mechanistically, Musclin binds to transferrin receptor 1 (Tfr1) and antagonizes Tfr1-mediated cAMP/PKA-dependent thermogenic induction in beige adipocytes. This work defines the temperature-sensitive myokine Musclin as a negative regulator of adipose thermogenesis that exacerbates the deterioration of metabolic health in obese male mice and thus provides a framework for the therapeutic targeting of this endocrine pathway.

Myofiber Baf60c controls muscle regeneration by modulating Dkk3-mediated paracrine signaling.

Obesity and type 2 diabetes (T2D) are the leading causes of the progressive decline in muscle regeneration and fitness in adults. The muscle microenvironment is known to play a key role in controlling muscle stem cell regenerative capacity, yet the underlying mechanism remains elusive. Here, we found that Baf60c expression in skeletal muscle is significantly downregulated in obese and T2D mice and humans. Myofiber-specific ablation of Baf60c in mice impairs muscle regeneration and contraction, accompanied by a robust upregulation of Dkk3, a muscle-enriched secreted protein. Dkk3 inhibits muscle stem cell differentiation and attenuates muscle regeneration in vivo. Conversely, Dkk3 blockade by myofiber-specific Baf60c transgene promotes muscle regeneration and contraction. Baf60c interacts with Six4 to synergistically suppress myocyte Dkk3 expression. While muscle expression and circulation levels of Dkk3 are markedly elevated in obese mice and humans, Dkk3 knockdown improves muscle regeneration in obese mice. This work defines Baf60c in myofiber as a critical regulator of muscle regeneration through Dkk3-mediated paracrine signaling.

Preparation of Hydrated TiO2 Particles by Hydrothermal Hydrolysis of Mg/Al-Bearing TiOSO4 Solution.

As the byproduct in the smelting process of vanadium titano-magnetite, titanium-bearing blast furnace slag (TBFS) can be converted to a titanyl sulfate (TiOSO4) solution containing MgSO4 and Al2(SO4)3 impurities via dissociation by concentrated H2SO4 (80-95%) at 80-200 °C, followed by leaching with H2O at 60-85 °C. In this study, hydrated TiO2 was prepared by hydrothermal hydrolysis of a Mg/Al-bearing TiOSO4 solution at 120 °C and the hydrolysis law was investigated. The experimental results indicate that MgSO4 and Al2(SO4)3 accelerated the hydrolysis and significantly affected the particle size (increasing the primary agglomerate size from 40 to 140 nm) and dispersion (reducing the aggregate size from 12.4 to 1.5 µm) of hydrated TiO2. A thermodynamic equilibrium calculation showed TiOSO4 existed as TiO2+ and SO42- in the solution, and MgSO4 and Al2(SO4)3 led to little change of [TiO2+], but an obvious decrease of [H+], which favored the hydrolysis process. At the same time, the coordination-dissociation mechanism of SO42- and Al(SO4)2- facilitated the lap bonding of Ti-O-Ti, promoting the growth of hydrated TiO2 synergistically.

The KATP channel opener, nicorandil, ameliorates brain damage by modulating synaptogenesis after ischemic stroke.

With population growth and aging, more and more patients with cerebral infarction have varying degrees of disability. ATP-sensitive potassium (KATP) channels regulate many cellular functions by coupling metabolic status with cell membrane electrical activity. Nicorandil (N-(2-hydroxyethyl)-nicotinamide nitrate) is the first KATP channel opener approved for clinical use. It has been reported that it might exert protective effects on the cerebral infarction by increasing cerebral blood flow and reducing inflammation. However, only a few studies explored its role in synaptogenesis. We made the rat model of middle cerebral artery occlusion (MCAO). Nicorandil was administered to rats via oral administration immediately after the surgery at a dose of 7.5 mg/kg and then daily for the next days. Infarct volume, cerebral edema, neurological deficits, cognitive impairment, and the level of Synaptophysin (SYP)、Growth associated protein-43 (GAP43) and neuronal nuclear antigen (NeuN) levels were measured to evaluate the effect of nicorandil. Our data showed that nicorandil treatment could decrease brain damage, improve learning and memory, and increase SYP、GAP43 and NeuN level. Taken together, we propose that nicorandil, as an opener of the KATP channel, provides a neuroprotective role in MCAO by promoting synaptic connections.