Engineered Core-Shell SiC@SiO2 Nanofibers for Enhanced Electromagnetic Wave Absorption Performance.

To enable SiC material to achieve high electromagnetic wave (EMW) absorption performance, solving its impedance mismatch with EMW is necessary. Therefore, a novel approach is proposed for the precise control of impedance matching by adjusting the shell thickness of SiO2 nanolayers on the surface of SiC nanofibers (NFs). High-angle annular dark field-scanning transmission electron microscopy (HAADF-STEM) reveals the atomic scale oxidation process of SiC, providing fresh insights into the oxidation mechanism. By oxidizing to construct a heterogeneous core-shell structure nanofiber (NF) can effectively lock the incident EMW inside the NF through the generated charges gathered at the interface, forming an electronic barrier that prevents the outward propagation of EMWs. The produced SiC@SiO2 NFs-3 exhibits exceptional EMW absorption properties, including an impressive minimum reflection loss (RLmin) of -53.09 dB and a broad maximum effective absorption bandwidth (EABmax) of 8.85 GHz. These findings not only deepen understanding of the oxidation mechanism of SiC but also offer valuable insights for further enhancing the EMW absorption capabilities of SiC materials, paving the way for their application in advanced EMW technologies.

Construction of Cyclodextrin-Based Covalent Organic Frameworks for Efficient Encapsulation of Menthol.

The application of flavoring ingredients like menthol in the food industry is hindered by their high volatility and poor thermal stability, which lead to significant losses during processing and storage. Encapsulation of flavors into porous materials to obtain inclusion complexes (ICs) has proved to be an efficient strategy. In the present study, we synthesized a series of relatively food-safe three-dimensional anionic cyclodextrin-based covalent organic frameworks (CD-COFs) with spiroborate linkages using a facile microwave-assisted method. The high surface area and newly formed cavitied of COFs significantly enhanced the encapsulation efficiency of menthol compared to native CD materials. Our findings revealed that γ-CD-COF-Li, with Li+ as the counterion, achieved superior encapsulation efficiency of 25.9%, outperforming γ-CD-COF-Na, γ-CD-COF-K and α-CD-COF-Li under the same conditions. Thermal stability measurements show that the menthol/γ-CD-COF-Li-ICs effectively stabilize menthol against heat evaporation at elevated temperatures due to the strengthened interaction between menthol and γ-CD-COF-Li. The promising results of this research suggest that rapid advancements in COF technology will provide new opportunities for enhancing the stability of flavoring ingredients in the food industry.

Effects of CuSO4 on hepatic mitochondrial function, biogenesis and dynamics in mice.

Copper is an essential trace element for animal. Excessive intake of copper will cause a large accumulation of copper in the body, especially in the liver, and induce hepatotoxicity, however, there are few studies on the effects of copper on hepatic mitochondrial biogenesis and mitochondrial dynamics. In this study, mice were treated with different doses of CuSO4 (0, 10, 20, and 40 mg/kg) for 21 and 42 days by gavage. The results verified that CuSO4 decreased the content of mitochondrial respiratory chain complexes I-IV in mouse liver. CuSO4 treatment resulted the decrease in the protein and mRNA expression levels of PGC-1α, TFAM, and NRF1, which were the mitochondrial biogenesis regulator proteins. Meanwhile, the proteins involved in mitochondrial fusion were reduced by CuSO4 , such as Mfn1 and Mfn2, however, mitochondrial fission proteins Drip1 and Fis1 were significantly increased. Abovementioned results show that CuSO4 could induce mitochondria damage in the liver of mice, and mitochondrial biogenesis and mitochondrial dynamics are involved in the molecular mechanism of CuSO4 -induced hepatotoxicity.

Sequential Oxidation/Cyclization of Readily Available Imine Linkages to Access Benzoxazole-Linked Covalent Organic Frameworks.

Benzoxazole-linked covalent organic frameworks (BO-COFs), despite their exceptional chemical stability, are still in their infancy. This is primarily because the current prevalent methods require the use of special ortho-hydroxyl-substituted aromatic amines as monomers. Herein, we report an innovative strategy to access BO-COFs directly from imine-linked COFs (Im-COFs) without pre-embedded OH groups, using a two-step sequential oxidation/cyclization process. The two-step process included the oxidation of Im-COFs into amide-linked COFs, followed by a copper-catalyzed oxidative cyclization. Five representative BO-COFs were synthesized with retained crystallinity and high oxidization efficiency, offering the potential to convert a significant portion of Im-COFs into BO-COFs. The structural advantages of the newly designed BO-COFs were demonstrated through their application to photocatalytic organic transformations.

Covalent Organic Frameworks Based Photoenzymatic Nano-reactor for Asymmetric Dynamic Kinetic Resolution of Secondary Amines.

Bio-catalysis represents a highly efficient and stereoselective method for the synthesis of valuable chiral compounds, however, the poor stability and limited reaction types of free enzymes restrict their wide application in industrial production. In this work, to overcome these problems, a multifunctional photoenzymatic nanoreactor CALB@COF-Ir was developed through the encapsulation of Candida antarctica lipase B (CALB) in a photosensitive covalent organic framework COF-Ir. This bio-nanocluster serves as efficient catalysts in asymmetric dynamic kinetic resolution (DKR) of secondary amines to give a series of chiral amines in high yields (up to 99 %) and enantioselectivities (up to 99 % ee). The well-designed COF-Ir not only acts as safety cover to prevent CALB from deactivation but promotes racemization of secondary amines via photo-induced hydrogen atom transfer (HAT) process. Photoelectric characterization and TDDFT calculation revealed that (ppy)2Ir units in COF-Ir play crucial role in this photocatalytic system which enhance its photo-redox properties through facilitating the separation between photoelectrons (e-) and holes (h+). Furthermore, the heterogeneous photoenzymatic nanoreactor could be recycled for five rounds with slight decline of catalytic reactivity.

Stone-Wales Defect in Graphene.

2D graphene the most investigated structures from nanocarbon family studied in the last three decades. It is projected as an excellent material useful for quantum computing, artificial intelligence, and next generation advanced technologies. Graphene exists in several forms and its extraordinary thermal, mechanical, and electronic properties, principally depend on the kind of perfection of the hexagonal atomic lattice. Defects are always considered as undesired components but certain defects in graphene could be an asset for electrochemistry and quantum electronics due to the engineered electronclouds and quantum tunnelling. The authors carefully discuss the Stone-Wales imperfections in graphene and its derivatives comprehensively. A specific emphasis is focused on the experimental and theoretical aspects of the Stone-Wales defects in graphene with respect to structure-property relationships. The corroboration of extrinsic defects like external atomic doping, functionalization, edge distortion in the graphene consisting of Stone-Wales imperfections, which are very significant in designing graphene-based electronic devices, are summarized.

Evaluation of blood-based PRO-C3 testing as a diagnostic marker for staging liver fibrosis: A systematic review and meta-analysis.

BACKGROUND AND AIM: With the global increase in chronic liver disease and cirrhosis, there is an increasing need to identify non-invasive biomarkers to measure the severity of disease progression while reducing reliance on pathological biopsies. This study aimed to comprehensively evaluate the diagnostic value of PRO-C3 as a biomarker for staging liver fibrosis in patients with viral hepatitis or fatty liver disease. METHODS: Articles published until January 6, 2023, were searched in the PubMed, Embase, MEDLINE, Web of Science, and Cochrane Library databases. The Quality Assessment of Diagnostic Accuracy Studies-2 tool was used to evaluate the quality of the included studies. Pooled sensitivity, specificity, diagnostic odds ratio, and likelihood ratios were integrated using a random-effects model, and a summary receiver operating characteristic curve was constructed. Publication bias was also detected. Subgroup and meta-regression analyses, as well as sensitivity analysis, were also performed. RESULTS: Fourteen studies with 4315 patients were included. Summary area under the curve of PRO-C3 for the identification of significant fibrosis (≥ F2) and advanced fibrosis (≥ F3) was 0.80 (95% confidence interval: 0.76-0.83). Subgroup and meta-regression analyses suggested that disease type and sample size may be the primary factors of heterogeneity in PRO-C3 diagnosis of ≥ F2, while study design, study sample type, and enzyme-linked immunosorbent assay kit brand may be the primary sources of heterogeneity in PRO-C3 diagnosis of ≥ F3. CONCLUSIONS: PRO-C3 demonstrated clinically meaningful diagnostic accuracy when used alone as a non-invasive biomarker for diagnosing the liver fibrosis stage in individuals with viral hepatitis or fatty liver disease.

Apoptosis and DNA damage mediated by ROS involved in male reproductive toxicity in mice induced by Nickel.

Nickel (Ni) is the most important environmental pollution in the world. Ni has been confirmed to have multi-organ toxicology and carcinogenicity. Recently, Ni also can impair the male reproductive system, however, its precious mechanism still has not been clarified. The current work found that nickel chloride (NiCl2) induced histopathological lesions in testis. And, the Johnsen's score, seminiferous tubule diameter, and spermatogenic epithelium thickness were decreased in NiCl2-treated mice. The number of spermatogonium, primary spermatocyte, and round spermatid also were significantly reduced after Ni treatment. Next the potential molecular mechanism was measured. NiCl2 treatment elevated ROS production in the testis. Additionally, NiCl2 was found to induce apoptosis with features including up-regulation of Bax, cleaved-caspase-3, cleaved-caspase-8, caspase-9, and caspase-12, while down-regulation of Bcl-2 expression. In the meantime, the marker protein of DNA damage γ-H2AX was significantly increased in NiCl2-primed mice testis. To clarify effects of reactive oxygen species (ROS) in apoptosis and DNA damage induced by NiCl2, NiCl2 was used to co-treat antioxidant NAC (N-Acetyl-L-cysteine). NAC weakened ROS production induced by NiCl2, and played an inhibition role in apoptosis and DNA damage. Moreover, co-treatment using NiCl2 and NAC group also eliminated spermatogenesis disorders. In summary, research results reveal the relations of spermatogenesis disorder induced by NiCl2 with apoptosis and DNA damage mediated by ROS and apoptosis in the testis.

Autophagy-mediated ferroptosis involved in nickel-induced nephrotoxicity in the mice.

Nickel, as a widely polluted metal, has been shown nephrotoxicity. Ferroptosis is a new type of cell death driven by iron-dependent lipid peroxidation. Our study found that nickel chloride (NiCl2) induced ferroptosis in mouse kidney and TCMK-1 cells. The iron content was significantly increased in the kidney and TCMK-1 cells after NiCl2 treatment. Lipid peroxidation and MDA content were significantly increased, and GSH content and T-SOD activity were significantly decreased after exposure to NiCl2. Moreover, NiCl2 increased COX-2 protein levels, decreased SLC7A11 and GPX4 protein levels, and elevated Ptgs2 mRNA levels. Next, the mechanism of Ni-induced ferroptosis was investigated. The results showed that NiCl2 induced autophagy in TCMK-1 cells, which promoted ferroptosis induced by NiCl2. Furthermore, the data of autophagy activation or inhibition experiment showed that autophagy facilitated ferroptosis through the degradation of the iron regulation protein NCOA4 and FTH1. Otherwise, iron chelator DFOM treatment inhibited ferroptosis induced by NiCl2. Finally, ferroptosis inhibitor Fer-1 treatment significantly alleviated cytotoxicity induced by NiCl2. To sum up, our above results showed that ferroptosis is involved in NiCl2-induced nephrotoxicity, and NiCl2 induces autophagy-dependent ferritin degradation, releases iron ions, leads to iron overload, and induces ferroptosis. This study supplies a new theoretical foundation for the study of nickel and renal toxicity.

Nickel induces hepatotoxicity by mitochondrial biogenesis, mitochondrial dynamics, and mitophagy dysfunction.

Nickel (Ni) is an important and widely hazardous chemical industrial waste. Excessive Ni exposure could cause multi-organs toxicity in human and animals. Liver is the major target organ of Ni accumulation and toxicity, however, the precise mechanism is still unclear. In this study, nickel chloride (NiCl2 )-treatment induced hepatic histopathological changes in the mice, and, transmission electron microscopy results showed mitochondrial swollen and deformed of hepatocyte. Next, the mitochondrial damages including mitochondrial biogenesis, mitochondrial dynamics, and mitophagy were measured after NiCl2 administration. The results showed that NiCl2 suppressed mitochondrial biogenesis by decreasing PGC-1α, TFAM, and NRF1 protein and mRNA expression levels. Meanwhile, the proteins involved in mitochondrial fusion were reduced by NiCl2 , such as Mfn1 and Mfn2, however, mitochondrial fission proteins Drip1 and Fis1 were significantly increased. The up-regulation of mitochondrial p62 and LC3II expression indicated that NiCl2 increased mitophagy in the liver. Moreover, the receptor-mediated mitophagy and ubiquitin (Ub)-dependent mitophagy were detected. NiCl2 promoted PINK1 accumulation and Parkin recruitment on mitochondria. And, the receptor proteins of mitophagy Bnip3 and FUNDC1 were increased in the NiCl2 -treated mice liver. Overall, these results show that NiCl2 could induce mitochondria damage in the liver of mice, and, dysfunction of mitochondrial biogenesis, mitochondrial dynamics and mitophagy involved in the molecular mechanism of NiCl2 -induced hepatotoxicity.

Three-dimension titanium phosphate aerogel for selective removal of radioactive strontium(II) from contaminated waters.

The effective removal of radioactive strontium (especially 90Sr) from nuclear wastewater is crucial to environmental safety. Nevertheless, materials with excellent selectivity in Sr removal remain a challenge since the similarity with alkaline earth metal ions in the liquid phase. In this work, a novel titanium phosphate (TiP) aerogel was investigated for Sr(II) removal from the radioactive wastewater based on the sol-gel method and supercritical drying technique. The TiP aerogel has amorphous, three-dimensional and mesoporous structures with abundant phosphate groups, which was confirmed by X-ray diffraction (XRD), energy dispersive spectroscopy (EDS), atomic force microscope (AFM) and Fourier transform infrared spectroscopy (FT-IR). The adsorbent exhibited high efficiency and selectivity for the removal of Sr(II) with an extensive distribution coefficient up to 4740.03 mL/g. The adsorption equilibrium reached within 10 min and the maximum adsorption capacity was 373.6 mg/g at pH 5. And the kinetics and thermodynamics data fitted well with the pseudo-second-order model and Langmuir model respectively. It can be attributed to the rapid trapping and slow intraparticle diffusion of Sr(II) inside the mesoporous channels of the TiP aerogel. Furthermore, TiP aerogel exhibited over 80% removal for 50 mg/L Sr2+ in real water systems (seawater, lake water and tap water). X-ray photoelectron spectroscopy (XPS) and Raman spectroscopy revealed that strong ionic bonding formed during Sr(II) adsorption with the phosphate group on TiP aerogel. These results indicated that TiP aerogel is a promising high-capacity adsorbent for the effective and selective capture of Sr(II) from radioactive wastewater.

Embedding Hydrogen Atom Transfer Moieties in Covalent Organic Frameworks for Efficient Photocatalytic C-H Functionalization.

Covalent organic frameworks (COFs) have emerged as efficient heterogeneous photocatalysts for a wide range of relatively simple organic reactions, whereas their application in complex organic transformations, like site-selective functionalization of unactivated C-H bonds, is underexplored, which can be mainly attributed to the lack of highly active organophotocatalytic cores. Herein through bonding oxygen atoms at the N-terminus of quinolines in nonsubstituted quinoline-linked COFs (NQ-COFs), we successfully realized the embedding of active hydrogen atom transfer (HAT) moieties into the skeleton of COFs. This novel designed COF (NQ-COFE5 -O), serving as both an excellent photosensitizer and HAT catalyst, exhibited much higher efficiency in C-H functionalization than the corresponding NQ-COFE5 . Specially, we evaluated the photocatalytic performance of NQ-COFE5 -O on ten different substrates, including quinolines, benzothiazole, and benzoxazole, all of which were transferred to desired products in moderate to high yields (up to 93 %). Furthermore, the as-synthesized NQ-COFE5 -O displayed excellent photostability and could be reused with negligible loss of activity for five catalytic cycles.

Switchable and Scalable Heteroarylation of Primary Amines with 2-Chlorobenzothiazoles under Transition-Metal-Free and Solvent-Free Conditions.

2-Aminobenzothiazoles comprise a valuable structural motif, which prevails in versatile natural products and biologically active compounds. Herein, a switchable and scalable C-N coupling protocol was developed for the synthesis of these compounds from 2-chlorobenzothiazoles and primary amines. Gratifyingly, this protocol was achieved under transition-metal-free and solvent-free conditions. Moreover, introducing an appropriate amount of NaH completely switched the selectivity from mono- toward di-heteroarylation, and further investigations provided a rationale for this new finding. Furthermore, gram-scale synthesis of representative products 3a and 4a was realized by applying operationally simple and glovebox-free procedures, which revealed the practical usefulness of this work. Finally, evaluation of the quantitative green metrics provided evidence that our protocol was superior over the literature ones in terms of green chemistry and sustainability.

Nickel induces autophagy via PI3K/AKT/mTOR and AMPK pathways in mouse kidney.

Nickel (Ni), a widely distributed metal, is an important pollutant in the environment. Although kidney is a crucial target of Ni toxicity, information on autophagy and the potential mechanisms of Ni-induced renal toxicity are still poorly described. As we discovered, NiCl2 could induce renal damage including decrease in renal weight, renal histological alterations, and renal function injury. According to the obtained results, NiCl2 could obviously increase autophagy, which was characterized by increase of LC3 expression and decrease of p62 expression. Meanwhile, the result of ultrastructure observation showed increased autolysosomes numbers in the kidney of NiCl2-treated mice. In addition, NiCl2 increased mRNA and protein levels of autophagy flux proteins including Beclin1, Atg5, Atg12, Atg16L1, Atg7, and Atg3. Furthermore, NiCl2 induced autophagy through AMPK and PI3K/AKT/mTOR pathways which featured down-regulated expression levels of p-PI3K, p-AKT and p-mTOR and up-regulated expression levels of p-AMPK and p-ULK1. In summary, the above results indicate involvement of autophagy in renal injury induced by NiCl2, and NiCl2 induced autophagy via PI3K/AKT/mTOR and AMPK pathways in mouse kidney.

Copper exposure induces hepatic G0/G1 cell-cycle arrest through suppressing the Ras/PI3K/Akt signaling pathway in mice.

Copper (Cu), as a common chemical contaminant in environment, is known to be toxic at high concentrations. The current research demonstrates the effects of copper upon hepatocyte cell-cycle progression (CCP) in mice. Institute of cancer research (ICR) mice (n = 240) at an age of four weeks were divided randomly into groups treated with different doses of Cu (0, 4, 8, and 16 mg/kg) for 21 and 42 days. Results showed that high Cu exposure caused hepatocellular G0/G1 cell-cycle arrest (CCA) and reduced cell proportion in the G2/M phase. G0/G1 CCA occurred with down-regulation (p < 0.05) of Ras, p-PI3K (Tyr458), p-Akt (Thr308), p-forkhead box O3 (FOXO3A) (Ser253), p-glycogen synthase kinase 3-ß (GSK3-ß) (Ser9), murine double minute 2 (MDM2) protein, and mRNA expression levels, and up-regulation (p < 0.05) of PTEN, p-p53 (Ser15), p27, p21 protein, and mRNA expression levels, which subsequently suppressed (p < 0.05) the protein and mRNA expression levels of CDK2/4 and cyclin E/D. These results indicate that Cu exposure suppresses the Ras/PI3K/Akt signaling pathway to reduce the level of CDK2/4 and cyclin E/D, which are essential for the G1-S transition, and finally causes hepatocytes G0/G1 CCA.

Nickel chloride induces spermatogenesis disorder by testicular damage and hypothalamic-pituitary-testis axis disruption in mice.

As a common environmental pollutant, nickel chloride (NiCl2) poses serious threat to human and animals health. NiCl2 has adverse effects on reproductive function in male, however, the underlying mechanisms are not fully illuminated. In this study, 64 male ICR mice were divided into four groups (8 mice per each period/ group), in which mice orally administrated with 0, 7.5, 15 or 30 mg/kg body weight for 14 or 28 consecutive days, respectively. The results showed that the sperm concentration (12.95%, 29.78% and 37.63% -) and sperm motility (19.79%, 34.88% and 43.10%) were dose-dependent significantly reduced, and the total sperm malformation rates (110.15%, 206.84% and 292.27%) were dose-dependent significantly elevated in the 7.5, 15 and 30 mg/kg NiCl2 treatment groups (vs control at 28 days), respectively (P < 0.05). Meanwhile, NiCl2 also decreased the relative weights of testis and epididymis and caused histopathological lesions of testis and epididymis. Furthermore, serum testosterone levels were significantly decreased after NiCl2 treatment. And the findings showed that NiCl2 down-regulated the expression of LH-R, StAR, P450scc, 3ß-HSD, 17ß-HSD, ABP and INHßB in the testis, however, the relative genes in the hypothalamus (Kiss-1, GPR54 and GnRH) and pituitary (GnRH-R, LHß and FSHß) did not exhibit noticeable change. In summary, NiCl2 induced spermatogenesis disorder by testicular damage and hypothalamic-pituitary-testis axis disruption in mice, and only impaired the genes on the testis of HPT axis.

Attenuated Cardiac oxidative stress, inflammation and apoptosis in Obese Mice with nonfatal infection of Escherichia coli.

Obesity is a risk factor of many diseases, but could be beneficial to the individuals with bacterial infection. The present study was conducted to investigate the relationship between obesity and heart during nonfatal bacterial infection. Male normal (lean) and diet-induced obesity mice (DIO, fed with high-fat diet) were chosen to perform nasal instillation with E. coli to establish a nonfatal acute mouse model. The cardiac histopathology, inflammation and oxidative damage, as well as apoptosis were detected post-infection. The results revealed that the Escherichia coli (E.coli)-infected mice exhibited increased cardiac index, contents of IL-1ß, IL-6, IL-8, TNF-α, leptin and resistin, levels of apoptotic proteins (caspase-3 and caspase-9, and bax/bcl-2 ratio), cardiac pathological changes and oxidative stress. Furthermore, these parameters were more serious in the lean mice than those in the DIO mice. In summary, our findings gave a new sight that E.coli infection impaired heart via histopathological lesions, inflammation and oxidative stress and excessive apoptosis of cardiomyocytes. Interestingly, obesity exerted attenuated effects on the heart of mice with non-fatal infection of E.coli through decreased inflammation, oxidative stress and apoptosis of cardiac tissue.

Oxidative stress-mediated apoptosis and autophagy involved in Ni-induced nephrotoxicity in the mice.

As an extensively environmental pollution, Nickel (Ni) represents a serious hazard to human health. The present study focused on exploring the mechanism of Ni-mediated nephrotoxicity, such as apoptosis, autophagy and oxidative stress. In the current work, NiCl2 treatment could induce kidney damage. Meanwhile, NiCl2 treatment elevated ROS production and MDA content and suppressed the antioxidant activity, which was characterized by reducing T-AOC, CAT, SOD activity and GSH content. For investigating the role of oxidative stress on NiCl2-mediated nephrotoxicity, N-acetyl cysteine (NAC, effective antioxidant and free radical scavenger) was co-treated with NiCl2. The results showed that NAC significantly suppressed the NiCl2-mediated oxidative stress and mitigated NiCl2-induced the kidney damage. Then, whether oxidative stress-induced autophagy and apoptosis were involved in NiCl2-induced nephrotoxicity was explored. The findings demonstrated that NAC relieved NiCl2-induced autophagy and reversed the activation of Akt/AMPK/mTOR pathway. Concurrently, the results indicated that NAC attenuated NiCl2-induced apoptosis, as evidenced by reduction of apoptotic cells and cleaved-caspase-3/- 8/- 9 together with cleaved-PARP protein levels. To sum up, our findings suggested that NiCl2-mediated renal injury was associated with oxidative stress-induced apoptosis and autophagy. This study provides new theoretical basis for excess Ni exposure nephrotoxic researches.

Pharmacokinetics of levofloxacin mesylate in healthy adult giant panda after single-dose administration via different routes.

The pharmacokinetics of levofloxacin mesylate in healthy adult giant panda is unknown. In this study, the pharmacokinetics of levofloxacin after intramuscular administration at a dose of 2 mg/kg and oral administration at a dose of 3 mg/kg in healthy adult giant pandas was determined. Levofloxacin concentrations in plasma were determined using liquid chromatography. In the levofloxacin intramuscular administration group, the absorption and elimination half-lives of the drug were determined to be 0.123 (range: 0.02) hr and 5.402 (range: 0.70) hr, respectively. In the levofloxacin oral administration group, the absorption and elimination half-lives were determined to be 0.325 (range: 0.02) hr and 7.143 (range: 0.63) hr, respectively. Furthermore, the blood-drug concentration of levofloxacin was found to be above 1 µg/ml after 8 hr of intramuscular administration and above 0.5 µg/ml after 12 hr of oral administration. In this study, HPLC conditions and pretreatment methods of plasma samples were optimized and a detection method was established. Our results indicated that in healthy adult giant pandas, levofloxacin was rapidly absorbed and slowly eliminated. This study will therefore provide to be a guide in veterinary research and will be helpful in the rational use of levofloxacin in giant panda.

Response of Wheat DREB Transcription Factor to Osmotic Stress Based on DNA Methylation.

Dehydration-responsive element-binding protein (DREB) plays an important role in response to osmotic stress. In this study, DREB2, DREB6 and Wdreb2 are isolated from wheat AK58, yet they belong to different types of DREB transcription factors. Under osmotic stress, the transcript expression of DREB2, DREB6 and Wdreb2 has tissue specificity and is generally higher in leaves, but their expression trends are different along with the increase of osmotic stress. Furthermore, some elements related to stresses are found in their promoters, promoters of DREB2 and Wdreb2 are slightly methylated, but DREB6's promoter is moderately methylated. Compared with the control, the level of promoter methylation in Wdreb2 is significantly lower under osmotic stress and is also lower at CG site in DREB2, yet is significantly higher at CHG and CHH sites in DREB2, which is also found at a CHG site in DREB6. The status of promoter methylation in DREB2, DREB6 and Wdreb2 also undergoes significant changes under osmotic stress; further analysis showed that promoter methylation of Wdreb2 is negatively correlated with their expression. Therefore, the results of this research suggest the different functions of DREB2, DREB6 and Wdreb2 in response to osmotic stress and demonstrate the effects of promoter methylation on the expression regulation of Wdreb2.