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One of the important monitoring indicators of the air pollution is atmospheric fine particulate matter (PM2.5), which can induce lung inflammation after inhalation. Coelonin can alleviate PM2.5‐induced macrophage damage through anti‐inflammation. However, its molecular mechanism remains unclear. We hypothesized that macrophage damage may involve the release of inflammatory cytokines, activation of inflammatory pathways, and pyrosis induced by inflammasome. In this study, we evaluated the anti‐inflammation activity of coelonin in PM2.5‐induced macrophage and its mechanism of action. Nitric oxide (NO) and reactive oxygen species (ROS) production were measured by NO Assay kit and dichlorofluorescein‐diacetate (DCFH‐DA), and apoptosis were measured by Flow cytometry and TUNEL staining. The concentration of inflammatory cytokines production was measured with cytometric bead arrays and ELISA kits. The activation of NF‐κB signaling pathway and NLRP3 inflammasome were measured by immunofluorescence, quantitative reverse transcription‐polymerase chain reaction and western blot. As expected, coelonin pretreatment reduced NO production significantly as well as alleviated cell damage by decreasing ROS and apoptosis. It decreased generation of interleukin (IL)‐6 and tumor necrosis factor (TNF)‐α in PM2.5‐induced RAW264.7 and J774A.1 cells. Moreover, coelonin markedly inhibited upregulating the expression of toll‐like receptor (TLR)4 and cyclo‐oxygenase (COX)‐2, blocked activation of p‐nuclear factor‐kappa B (NF‐κB) signaling pathway, and suppressed expression of NLRP3 inflammasome, ASC, GSDMD, IL‐18 and IL‐1β. In conclusion, the results showed that coelonin could protect against PM2.5‐induced macrophage damage via suppressing TLR4/NF‐κB/COX‐2 signaling pathway and NLRP3 inflammasome activation in vitro. [ABSTRACT FROM AUTHOR]

Root rot is an important disease of the medicinal plant Atractylodes macrocephala (bai zhu) in China. This study evaluates an antagonistic fungal agent, Trichoderma brevicompactum, as an alternative to chemical pesticides for control of root rot caused by Fusarium oxysporum. The inhibitory effect of T. brevicompactum on F. oxysporum was examined in dual-culture experiments, with mycelial growth of the pathogen found to be reduced by 74.4%. The results of an enzyme-linked immunosorbent assayindicated that T. brevicompactum produced enzymes such as cellulase and chitinase, suggesting that the fungal agent may inhibit F. oxysporum growth by producing cell wall hydrolases. Under greenhouse conditions, the efficacy of T. brevicompactum was evaluated based on its effects on root rot severity, plant height, root dry weight, and root fresh weight. When used as a soil treatment, T. brevicompactum reduced root rot severity by 48% to 58% and increased plant growth and biomass significantly when compared with the control (healthy) group. The plant growth-promoting effect of T. brevicompactum seems related to its production of secondary metabolites that contain an auxin (indoleacetic acid), and to the disease resistance induced in the host by the fungal agent. The results of this study suggest that T. brevicompactum not only controls root rot in A. macrocephala but may also promote growth of the plant. [ABSTRACT FROM AUTHOR]

Certain mutations in mitochondrial DNA (mtDNA) are associated with Leber's hereditary optic neuropathy (LHON). In particular, the well-known NADH dehydrogenase 4 (ND4) m.11778G>A mutation is one of the most common LHON-associated primary mutations worldwide. However, how specific mtDNA mutations, or variants, affect LHON penetrance is not fully understood. The aim of the current study was to explore the relationship between mtDNA mutations and LHON, and to provide useful information for early detection and prevention of this disease. Following the molecular characterization of a Han Chinese family with maternally inherited LHON, four out of eight matrilineal relatives demonstrated varying degrees of both visual impairment and age of onset. Through PCR amplification of mitochondrial genomes and direct Sanger sequencing analysis, a homoplasmic mitochondrial-encoded ND4 m.11778G>A mutation, alongside a set of genetic variations belonging to human mtDNA haplogroup B5b1 were identified. Among these sequence variants, alanine transfer RNA (tRNA)Ala m.5601C>T was of particular interest. This variant occurred at position 59 in the TψC loop and altered the base pairing, which led to mitochondrial RNA (mt-RNA) metabolism failure and defects in mitochondrial protein synthesis. Bioinformatics analysis suggested that the m.5601C>T variant altered tRNAAla structure. Therefore, impaired mitochondrial functions caused by the ND4 m.11778G>A mutation may be enhanced by the mt-tRNAAla m.5601C>T variant. These findings suggested that the tRNAAla m.5601C>T variant might modulate the clinical manifestation of the LHON-associated primary mutation. [ABSTRACT FROM AUTHOR]

Highly uniformed barium-strontium titanate nanotube arrays were fabricated using a porous anodic aluminum oxide template from a barium-strontium titanate sol-gel solution. Electron microscope results showed that nanotubes with uniform length and diameter were obtained. The diameters and lengths of these nanotubes were dependent on the pore diameter and the thickness of the applied anodic aluminum oxide template. High resolution transmission electron microscopy and the selected-area electron diffraction pattern investigations demonstrated the perovskite structure and the polycrystalline of the fabricated barium-strontium titanate nanotubes. The characterization of the electrical and dielectric properties had also been made. Compared to thin film material, the intrinsic leakage current density is almost the same. Besides, at 30 °C, the dielectric constant and dielectric loss of the fabricated nanotube is 80 and 0.027 at 1 MHz respectively. [ABSTRACT FROM AUTHOR]

Bi1.5Zn1.0Nb1.5O7/Ba0.6Sr0.4TiO3/Bi1.5Zn1.0Nb1.5O7 (BZN/BST/BZN) sandwich films were deposited by radio frequency magnetron sputtering. The relative permittivity and dielectric loss of the sandwich films were measured using planar Pt/BZN/BST/BZN/Pt/Ti/SiO2/Si capacitor structures. The sandwich films with thickness of about 280 nm exhibited relative permittivity around 206–247 and dielectric loss tangent (tan δ) less than 0.008 at 1 MHz. Films annealed at 750 °C had an ∼11% relative tunability of the permittivity at a maximum applied bias field of 0.77 MV/cm. The sandwich films are not ferroelectric at room temperature. [ABSTRACT FROM AUTHOR]

La3+ and V5+ co-doped BiFeO3 ceramics are synthesized by rapid liquid sintering technique. The modulated structure in Bi0.85La0.15Fe0.97V0.03O3 is investigated by using transmission electron microscopy (TEM). Two kinds of superstructures are observed in the samples. One is the component modulated superstructure and twin-domain, which is generated by La3+ ordered substitution for Bi3+ and frequently appears. The chemical composition of the superstructure is explored by x-ray energy dispersive spectroscopy (EDS). The model of the ordered structure is proposed. Simulation based on the model is conducted. The second is the fluorite-type δ-Bi2O3 related superstructure. The relation between the ferroelectric property and the microstructure of the sample is also discussed. [ABSTRACT FROM AUTHOR]

We have investigated the preparation and properties of Bi4Zr0.5Ti2.5O12 thin films on the LaNiO3 bottom electrode. The Bi4Zr0.5Ti2.5O12 thin films were fabricated on the LaNiO3 bottom electrode using the sol–gel method. The structure and morphology of the films were characterized using x-ray diffraction and scanning electron microscopy. The results show that the films are a perovskite phase with a dense microstructure. The 2Pr and 2Vc of the Pt/BZT/LaNiO3 capacitor are 28.2 µC cm−2 and 14.7 V respectively under the applied voltage of 25 V. After the switching of 1 × 1010 cycles, the Pr value decreases to 87% of its pre-fatigue values. The dielectric constant and the dielectric loss are about 204 and 0.024 at 1 kHz, respectively. The films show good insulating behaviour according to the test of leakage current. [ABSTRACT FROM AUTHOR]

Mutations in mitochondrial 12S rRNA (MT-RNR1) are the important causes of sensorineural hearing loss. Of these mutations, the homoplasmic m.1555A > G or m.1494C > T mutation in the highly conserved A-site of MT-RNR1 gene has been found to be associated with both aminoglycoside-induced and non-syndromic hearing loss in many families worldwide. Since the m.1555A > G and m.1494C > T mutations are sensitive to ototoxic drugs, therefore, screening for the presence of these mutations is important for early diagnosis and prevention of deafness. For this purpose, we recently developed a novel allele-specific PCR (AS-PCR) which is able to simultaneously detect these mutations. To assess its accuracy, in this study, we employed this method to screen the frequency of m.1555A > G and m.1494C > T mutations in 200 deafness patients and 120 healthy subjects. Consequently, four m.1555A > G and four m.1494C > T mutations were identified; among these, only one patient with the m.1494C > T mutation had an obvious family history of hearing loss. Strikingly, clinical evaluation showed that this family exhibited a high penetrance of hearing loss. In particular, the penetrances of hearing loss were 80% with the aminoglycoside included and 20% when excluded. PCR-Sanger sequencing of the mitochondrial genomes confirmed the presence of the m.1494C > T mutation and identified a set of polymorphisms belonging to mitochondrial haplogroup A. However, the lack of functional variants in mitochondrial and nuclear modified genes ( GJB2 and TRMU ) in this family indicated that mitochondrial haplogroup and nuclear genes may not play important roles in the phenotypic expression of the m.1494C > T mutation. Thus, other modification factors, such as environmental factor, aminoglycosides or epigenetic modification may have contributed to the high penetrance of hearing loss in this family. Taken together, our data showed that this assay is an effective approach that could be used for detection the deafness-associated MT-RNR1 mutations. [ABSTRACT FROM AUTHOR]

One of the important monitoring indicators of the air pollution is atmospheric fine particulate matter (PM 2.5 ), which can induce lung inflammation after inhalation. Coelonin can alleviate PM 2.5 -induced macrophage damage through anti-inflammation. However, its molecular mechanism remains unclear. We hypothesized that macrophage damage may involve the release of inflammatory cytokines, activation of inflammatory pathways, and pyrosis induced by inflammasome. In this study, we evaluated the anti-inflammation activity of coelonin in PM 2.5 -induced macrophage and its mechanism of action. Nitric oxide (NO) and reactive oxygen species (ROS) production were measured by NO Assay kit and dichlorofluorescein-diacetate (DCFH-DA), and apoptosis were measured by Flow cytometry and TUNEL staining. The concentration of inflammatory cytokines production was measured with cytometric bead arrays and ELISA kits. The activation of NF-κB signaling pathway and NLRP3 inflammasome were measured by immunofluorescence, quantitative reverse transcription-polymerase chain reaction and western blot. As expected, coelonin pretreatment reduced NO production significantly as well as alleviated cell damage by decreasing ROS and apoptosis. It decreased generation of interleukin (IL)-6 and tumor necrosis factor (TNF)-α in PM 2.5 -induced RAW264.7 and J774A.1 cells. Moreover, coelonin markedly inhibited upregulating the expression of toll-like receptor (TLR)4 and cyclo-oxygenase (COX)-2, blocked activation of p-nuclear factor-kappa B (NF-κB) signaling pathway, and suppressed expression of NLRP3 inflammasome, ASC, GSDMD, IL-18 and IL-1β. In conclusion, the results showed that coelonin could protect against PM 2.5 -induced macrophage damage via suppressing TLR4/NF-κB/COX-2 signaling pathway and NLRP3 inflammasome activation in vitro., (© 2023 Wiley Periodicals LLC.)