Search

In fruit production, the application of the plant growth regulator 1-(2-chloro-4-pyridyl)-3-phenylurea (CPPU) dulls the fruit aroma. Gas chromatography–mass spectrometry and transcriptome analyses were performed on CPPU-treated and pollinated fruits to determine how CPPU affects the production of aroma in melon fruit. The results showed that the contents of two important esters (benzyl acetate and phenethyl acetate) in the CPPU-treated fruits were significantly lower than those in the pollinated fruits. Transcriptome sequencing data revealed that most differentially expressed genes were involved in “phenylalanine metabolism” pathway, and their expression was significantly decreased in the CPPU-treated fruits. Further analysis showed that the phenylalanine content in the CPPU-treated fruits was significantly higher than that in the pollinated fruits. In summary, CPPU application interferes with phenylalanine metabolism in melon fruits and affects the production of aromatic esters.

Abstract Background Pelgipeptin, a potent antibacterial and antifungal agent, is a non-ribosomally synthesised lipopeptide antibiotic. This compound consists of a β-hydroxy fatty acid and nine amino acids. To date, there is no information about its biosynthetic pathway. Results A potential pelgipeptin synthetase gene cluster (plp) was identified from Paenibacillus elgii B69 through genome analysis. The gene cluster spans 40.8 kb with eight open reading frames. Among the genes in this cluster, three large genes, plpD, plpE, and plpF, were shown to encode non-ribosomal peptide synthetases (NRPSs), with one, seven, and one module(s), respectively. Bioinformatic analysis of the substrate specificity of all nine adenylation domains indicated that the sequence of the NRPS modules is well collinear with the order of amino acids in pelgipeptin. Additional biochemical analysis of four recombinant adenylation domains (PlpD A1, PlpE A1, PlpE A3, and PlpF A1) provided further evidence that the plp gene cluster involved in pelgipeptin biosynthesis. Conclusions In this study, a gene cluster (plp) responsible for the biosynthesis of pelgipeptin was identified from the genome sequence of Paenibacillus elgii B69. The identification of the plp gene cluster provides an opportunity to develop novel lipopeptide antibiotics by genetic engineering.

A series of pyrazolylimine ligated Co(II) and Fe(II) complexes with general formula of (PhC=N(C6H3(R1)2-2,6)(C3HN2 (R2)2-3,5)MtCl2 (R1 = Me, R2 = H, Mt = Co (1a), Fe (2a); R1 = Me, R2 = Me, Mt = Co (1b), Fe (2b); R1 = iPr, R2 = H, Mt = Co (1c), Fe (2c); R1 = iPr, R2 = Me, Mt = Co (1d), Fe (2d); R1 = iPr, R2 = Ph, Mt = Co (1e), Fe (2e)) were synthesized and thoroughly characterized. Determined by single crystal X-ray diffraction, complexes 1b and 2b revealed dimeric structures, in which distorted trigonal bipyramid geometries were adopted for each metal centers. In the presence of ethylaluminum sesquichloride (EASC), all the cobalt complexes displayed high activities in 1,3-butadiene polymerization, affording polybutadienes with predominant cis-1,4 contents (up to 97.0%). Influences of ligand structure and polymerization parameters on catalytic performance were investigated systematically. For pyrazolylimine iron(II) dichloride complexes, the catalytic activities and microstructures of the resultant polybutadienes were highly dependent on ligand structures and polymerization conditions. For complex 2a, changing cocatalyst from trialkyl aluminums to methyl aluminoxane (MAO) led to an shift of selectivity from high cis-1,4- to trans-1,4-/1,2- manner. Being activated by MAO, complexes 2a and 2b gave trans-1,4-/1,2- binary polybutadienes, while complexes 2c, 2d, and 2e afforded cis-1,4- enriched polymers. [ABSTRACT FROM AUTHOR]

This study was designed to investigate the effects of excessive fluoride on spleen toxicity. Twenty-four healthy female rats were randomly divided into two groups, each of 12 rats. Each group of female rats was given a control diet and either F− = 0 mg/L or an excessive F− = 150 mg/L in the drinking water for 120 days. The histomorphological and ultrastructural changes in their splenic tissues were observed under light and transmission electron microscopes. DNA damage and splenocyte apoptosis were examined using the micronucleus (MN) assay, single-cell gel electrophoresis (SCGE), and flow cytometry. The expression levels of cytokines, including interleukin (IL)-1β, IL-2, IL-6, and tumor necrosis factor (TNF)-α, were determined through immunohistochemistry and Western-blot analysis. Results demonstrated that the histomorphological characteristics and ultrastructure of the splenic tissues were affected by excessive fluoride. Nuclear dying, nuclear membrane dissolution, mitochondrial vacuolation, and endoplasmic reticulum dilation were observed. SCGE and MN assays showed that the nuclear DNA of splenocytes was damaged by fluoride treatment, and splenocyte apoptosis was exacerbated in the fluoride group. With damage to the splenocyte structure and DNA, the protein expression levels of IL-1β, IL-2, IL-6, and TNF-α were significantly downregulated by exposure to fluoride. Excessive fluoride ingestion caused splenic pathological damage and abnormal cytokine expression in female rats. [ABSTRACT FROM AUTHOR]

Our previous study showed that excessive fluoride (F) intake can induce liver dysfunction. The aim of this study was to investigate the mechanisms of F-induced mitochondrial damage resulting in liver dysfunction. Damaged mitochondrial ultrastructure and state of liver cells were estimated by TEM, TUNEL staining and BrdU measurement. The ROS level and ATP content in the liver tissue were measured by ELISA kit. Meanwhile, optic atrophy (OPA1), mitofusin-1 (Mfn1), NDUFV2, SDHA, CYC1, and COX Ⅳ expression levels were measured through real-time PCR and Western-blot. Results showed that the ROS level increased, thereby resulting in mitochondrial ultrastructure damage and abundant liver cells presented evident apoptotic characteristics after F treatment. Decreased ATP content and the abnormal expression of OPA1, Mfn1, NDUFV2, SDHA, CYC1, and COX Ⅳ of the liver tissue were observed. In conclusion, excessive F-induced mitochondrial respiratory chain damaged and mitochondrial fusion disorder resulted in liver dysfunction. • Excessive fluoride intake resulted in liver dysfunction. • Fluoride increased ROS production and decreased ATP content in the liver tissue. • Fluoride damaged the liver tissue ultrastructure. • Fluoride induced mitochondrial respiratory chain damaged. • Fluoride induced mitochondrial fusion disorder. [ABSTRACT FROM AUTHOR]

This study was based on the observation of volatile organic compounds (VOCs), conventional gaseous air pollutants, and meteorological parameters observed at the Xinxiang Municipal Party School site from June to August 2021. The ozone (O 3 ) characteristics and sensitivity of O 3 pollution days and the control strategy of its precursors were studied using an observation-based model (OBM). It was found that the meteorological conditions were characterized by high temperature, low humidity, and low pressure in O 3 -pollution days. The concentrations of O 3 and its precursors all increased in the O 3 pollution days. Oxygenated volatile organic compounds (OVOCs) and alkanes were the highest-concentration components of VOCs on O 3 pollution days in Xinxiang, and OVOCs had the highest ozone formation potential (OFP) and hydroxyl (·OH) reactivity. According to the relative incremental reactivity (RIR) analysis, during the O 3 pollution days in Xinxiang, O 3 sensitivity was in the VOCs-limited regime in June and in the transitional regime in July and August. Ozone production was more sensitive to alkenes and OVOCs. The RIR values of the precursors in June changed throughout the day, but O 3 sensitivity remained the VOCs-limited regime. In July and August, O 3 sensitivity was the VOCs-limited regime in the morning, transitional regime at noon, transitional and NO x -limited regime, respectively in the afternoon. By simulating different precursor-reduction scenarios, the results showed that the reduction of VOCs was always beneficial to the control of O 3 , whereas the reduction of NO x had little effect on the control of O 3 and a risk of increasing O 3 .

Objectives: Regulatory T (Treg) cells are crucial players in the prevention of autoimmunity. Mechanistic target of rapamycin (mTOR) signalling negatively controls the development and function of Treg cells. The aim of the present study was to evaluate the effects of rapamycin, under the generic name sirolimus, on CD4+CD25+FoxP3+ Treg cells in rheumatoid arthritis (RA) patients with low disease activity or in DAS28 remission., Methods: Fifty-five RA patients and 60 healthy controls were enrolled in this study. All patients had previously received conventional disease-modifying anti-rheumatic drugs (DMARDs) and were considered to have a low DAS28 score (≤3.2). Peripheral blood samples and clinical information were obtained at baseline and following 6 and 12 weeks of sirolimus treatment, or after 12 weeks of conventional treatment. Peripheral blood samples were also obtained from the healthy controls. The circulating levels of lymphocyte subpopulations were assessed by flow cytometry., Results: Thirty-five patients received sirolimus and 20 patients continued treatment with conventional DMARDs. The absolute counts and proportions of CD4+CD25+FoxP3+ Treg cells were significantly lower in all RA patients with DAS28 ≤ 3.2 as compared with those in healthy controls. By contrast, the difference in circulating Th17 cell numbers was not significant. Sirolimus administration resulted in elevations in circulating Treg cell numbers and significant reductions in the Th17/Treg cell ratio, whereas the circulating level of Treg cells and the Th17/Treg cell ratio in patients under conventional treatment both showed a tendency of reduction. Furthermore, a greater proportion of patients under sirolimus treatment achieved DAS28-based remission at 12 weeks., Conclusions: Sirolimus can favourably expand Treg cells in RA patients with DAS28 ≤3.2, consequently restoring a healthy balance of Th17/Treg cells, which might improve the likelihood of long-term and sustained clinical remission and reduce the probability of disease flare-ups in RA.

Our previous study indicated that excessive fluoride (F) induces ATP5J and ATP5H proactive expression by interfering cardiomyocyte mitochondrial dysfunction in mice. This study aimed to investigate underlying mechanisms of F ¯ induced damage to cardiomyocytes. A total of 100 mg/L F ¯ was added to distilled water to treat Kunming mice for 70 days. Pathological and morphological changes in myocardial tissues were observed under transmission electron microscope and light microscope. Content of ATP and ATP enzyme distributed in cardiomyocytes were determined by fluorescence and ATP enzyme staining. Expression levels of troponin (Tn) C, TnI, TnT and tropomyosin (TPM) were measured by immunofluorescence, western blot, and real-time polymerase chain reaction. Contents of Ca 2+ in blood, myocardial cells and faeces were also detected by confocal microscopy and ethylenediaminetetraacetic acid. Using 100 mg/L F ¯ resulted in nuclaer enrichment, the myocardial fibre breakage and mitochondrial lysis. Following mitochondrial structure damage, contents of ATP and ATP enzyme significantly decreased in the fluoride group. Expression levels of TnT and TnI were significantly down-regulated, whereas that of TPM was up-regulated. Content of Ca 2+ in cardiomyocytes of fluoride group visibly increased. Interestingly, contents of Ca 2+ in blood and faeces decreased. These findings reveal that excessive F ingestion induces Ca 2+ metabolic disorder, and an abnormal expression of cardiac Tn are involved in F-induced cardiomyocyte damage., (Copyright © 2018 Elsevier Ltd. All rights reserved.)

The aim of the present study was to investigate the efficacy of dynamic contrast-enhanced magnetic resonance imaging (MRI) in predicting the outcome of using ultrasound-guided high-intensity focused ultrasound (USgHIFU) ablation for the treatment of uterine fibroids with T2 hyperintensity under MRI. A total of 131 uterine fibroids from 131 patients that appeared hyperintense under T2-weighted MRI were analyzed. The uterine fibroids were subjectively categorized into slight, irregular or regular enhancement groups, according to pretreatment dynamic contrast-enhanced MRI in the arterial phase within 60 sec after the injection of gadolinium. The non-perfused volume (NPV), which is indicative of successful ablation, was represented as the non-perfused area inside the uterine fibroids on enhanced MRI scans following treatment. Additionally, the treatment duration, treatment efficiency, sonication duration, energy efficiency ratio and any adverse events were recorded. The results indicated that the average NPV ratio for all the treated fibroids was 68.5%, while the average NPV ratios for fibroids with slight, irregular or regular enhancement were 84.7, 70.6 and 57.1%, respectively. Fibroids with regular enhancement were associated with the lowest NPV ratio and the lowest treatment efficiency, but exhibited the highest energy effect ratio and an elevated risk of severe adverse effects. The results of the present study indicate that hyperintense uterine fibroids with slight and irregular enhancement in the arterial phase of dynamic contrast-enhanced MRI are suitable for USgHIFU treatment. By contrast, uterine fibroids with regular enhancement were associated with the lowest treatment efficacy and safety.

Focal adhesion kinase (FAK) is known to promote the proliferation, migration and survival of synovial cells and plays an important role in the occurrence, development and pathological process of rheumatoid arthritis (RA). The aim of the present study was to observe FAK changes in synovial cells of rats with collagen-induced arthritis (CIA) and after intervention with disease modifying anti-rheumatic drugs (DMARDs) alone or in combination in a CIA female SD rat model induced by collagen type II. The rats were randomized to 8 groups: normal control group, CIA model control group, methotrexate (MTX, 0.9 mg/kg/w) group, cyclophosphamide (CTX, 24 mg/kg/3 w) group, leflunomide (LEF, 1.2 mg/kg/d) group, MTX + CTX group, LEF + CTX group, and MTX + LEF group. They were intervened with DMARDs alone or in combination for six weeks. The experiment lasted a total of 9 weeks in vivo. Articular inflammation was measured during the process of drug intervention in terms of the degree of swelling degree in the right hind foot using a venire caliper. All animals were sacrificed by breaking the neck after 9 weeks. Then, the ankle was fixed, decalcified, embedded, and HE stained, and prepared into slices to observe pathological changes in the synovial tissue. FAK expression in synovial cells was assayed by immunohistochemistry and the mean optical density (OD) value was measured using the HPIAS-2000 image analysis system. It was found that FAK expression was negative in normal control group, positive in CIA model control group, and decreased in the three DMARD combination treatment groups significantly as compared with that in the three single-drug groups (P < 0.05). FAK expression in LEF + CTX group or MTX + CTX group decreased more significantly than that in MTX + LEF group (P < 0.05), and there was no statistically significant difference between LEF + CTX and MTX + CTX groups. The arthritis index and pathological change in the synovial tissue in LEF + CTX group or MTX + CTX group were improved more significantly than those in MTX + LEF group or single-drug groups. Our results showed that FAK expression was positive in CIA rats, indicating that it played an important role in the pathogenesis of RA, and that intervention with DMARDs could reduce the FAK expression in synovial cells of CIA rats. We hope these findings would contribute to the treatment of RA and other rheumatic diseases by reducing adhesion, proliferation and migration of synovial cells and inhibiting the over-expression of FAK.