194 publications from this institution
鲍曼不动杆菌是近年来检出率较高的一种条件致病菌,广泛存在于自然界和人体表面,粘附力强,易粘附在各类医用器械上,引起一系列医院感染,如菌血症、尿路感染、继发性脑膜炎、手术部位感染及呼吸机相关性肺炎等,严重威胁患者的生命[1-2].鲍曼不动杆菌对许多抗菌药物,如β-内酰胺类、氨基糖苷类、氟喹诺酮类等均有一定的耐药性.碳青霉烯类抗菌药物是治疗鲍曼不动杆菌感染的首选药物,但随着此类抗菌药物的广泛应用,耐碳青霉烯类抗菌药物的鲍曼不动杆菌逐渐增多[3-4],使得临床治疗越来越困难.本研究对苏州大学附属第二医院临床分离的35株对美罗培南和亚胺培南均耐药的鲍曼不动杆菌进行碳青霉烯酶基因检测与分析.
Quinoa is a highly nutritious and novel crop that is resistant to various abiotic stresses. However, its growth and development is restricted due to its limited utilization of soil phosphorus. Studies on the levels of phosphorus in quinoa seedlings are limited; therefore, we analyzed transcriptome data from quinoa seedlings treated with different concentrations of phosphorus.To identify core genes involved in responding to various phosphorus levels, the weighted gene co-expression network analysis method was applied. From the 12,085 expressed genes, an analysis of the gene co-expression network was done. dividing the expressed genes into a total of twenty-five different modules out of which two modules were strongly correlated with phosphorus levels. Subsequently we identified five core genes that correlated strongly either positively or negatively with the phosphorus levels. Gene ontology and assessments of the Kyoto Encyclopedia of Genes and Genomes have uncovered important biological processes and metabolic pathways that are involved in the phosphorus level response.We discovered crucial new core genes that encode proteins from various transcription factor families, such as MYB, WRKY, and ERF, which are crucial for abiotic stress resistance. This new library of candidate genes associated with the phosphorus level responses in quinoa seedlings will help in breeding varieties that are tolerant to phosphorus levels.
The enzyme 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase isoform 3 (PFKFB3) is a critical regulator of glycolysis and plays a key role in modulating the inflammatory response, thereby contributing to the development of inflammatory diseases such as sepsis. Despite its importance, the development of strategies to target PFKFB3 in the context of sepsis remains challenging. In this study, we employed a miRNA-based approach to decrease PFKFB3 expression. Through multiple meta-analyses, we observed a downregulation of miR-106a-5p expression and an upregulation of PFKFB3 expression in clinical sepsis samples. These changes were also confirmed in blood monocytes from patients with early sepsis and from a mouse model of lipopolysaccharide (LPS)-induced sepsis. Overexpression of miR-106a-5p significantly decreased the LPS-induced increase in glycolytic capacity, inflammatory response, and pyroptosis in macrophages. Mechanistically, we identified PFKFB3 as a direct target protein of miR-106a-5p and demonstrated its essential role in LPS-induced pyroptosis and inflammatory response in macrophages. Furthermore, treatment with agomir-miR-106a-5p conferred a protective effect in an LPS mouse model of sepsis, but this effect was attenuated in myeloid-specific Pfkfb3 KO mice. These findings indicate that miR-106a-5p inhibits macrophage pyroptosis and inflammatory response in sepsis by regulating PFKFB3-mediated glucose metabolism, representing a potential therapeutic option for the treatment of sepsis.
在细菌进化过程中,非致病菌向致病菌进化的一个主要策略是由携带毒力基因的噬菌体进入宿主菌,并在宿主细菌中进行基因交流,改变宿主菌的表型或增加宿主菌的毒力,使无致病力的菌株转变为致病菌.本文就致病性霍乱弧菌的分子进化、CTXΦ和VPI基因家族的结构、功能和基因组的多样性,以及CTXΦ基因组整合的分子生物学机制进行综述. 关键词:霍乱弧菌;产毒株;毒力相关基因
In order to detect the products of car seat, propose a new car seat detection method in this paper.First, the car seat image is normalized to 256 pixels *256 pixels image.Then extract SIFT (scale invariant feature transform) feature points and match the points.According to the position of two matched points, the matching results are divided into two categories.One is vertical match point; the other is tilt matching point.Compare the number of the two categories.When the vertical match points are more than the tilt matching points, the answer is correct.Otherwise the answer is wrong.Experimental results show that for the detection of three different types of car seats, the detection accuracy is higher than 98%.
Zinc (Zn) is an essential micronutrient for plant growth and development, but the soil available Zn is low in arable land worldwide. Therefore, crop Zn deficiency is a serious issue that threatens the sustainable development of agriculture. Quinoa (Chenopodium quinoa Willd.) is a high-efficiency Zn utilization crop. However, the molecular regulatory mechanisms underlying Zn uptake and Zn deficiency response in quinoa remain largely unclear. Here, using the method of Zn depletion and resupply, we investigated Zn deficiency responses in the hydroponic-grown quinoa seedlings by integrating physiol-biochemical and transcriptomic analyses. Zn depletion leads to H2O2 accumulation and lipid peroxidation in plants. Accordingly, the increased enzyme activities of superoxide dismutase and peroxidase alleviate Zn deficiency-induced oxidative damage in quinoa roots. Subsequently, a genome-wide transcriptome analysis revealed that the expression of genes encoding Zn sensors bZIP19/23 and metal transporters was upregulated in Zn-depleted plants but downregulated in Zn-resupplied plants. Interestingly, the high expression of several iron (Fe) deficiency-responsive transcription factors/transcription regulator genes may not be induced by Fe status in Zn-depleted plants, suggesting that the expression of these genes may be directly induced by Zn deficiency and subsequently regulate micronutrient homeostasis in plants. Zn depletion decreased the contents of indoacetic acid, trans-zeatin-riboside, abscisic acid and salicylic acid 2-O-β-d-glucose but increased the jasmonic acid content in quinoa roots. These results collectively indicated that Zn deficiency affects plant growth and development by modulating phytohormone pathways. Our results provide comprehensive insight into the mechanism of Zn uptake and Zn deficiency response in quinoa and provide a theoretical basis for breeding Zn-efficient crops.
SUMMARY Cytokinin is central to coordinating plant adaptation to environmental stresses. Here, we first demonstrated the involvement of cytokinin in Arabidopsis responses to arsenite [As(III)] stress. As(III) treatment reduced cytokinin contents, while cytokinin treatment repressed further primary root growth in Arabidopsis plants under As(III) stress. Subsequently, we revealed that the cytokinin signaling members ARR1 and ARR12, the type‐B ARABIDOPSIS RESPONSE REGULATORs, participate in cytokinin signaling‐mediated As(III) responses in plants as negative regulators. A comprehensive transcriptome analysis of the arr1 and arr12 single and arr1,12 double mutants was then performed to decipher the cytokinin signaling‐mediated mechanisms underlying plant As(III) stress adaptation. Results revealed important roles for ARR1 and ARR12 in ion transport, nutrient responses, and secondary metabolite accumulation. Furthermore, using hierarchical clustering and regulatory network analyses, we identified two NODULIN 26‐LIKE INTRINSIC PROTEIN (NIP)‐encoding genes, NIP1;1 and NIP6;1 , potentially involved in ARR1/12‐mediated As(III) uptake and transport in Arabidopsis . By analyzing various combinations of arr and nip mutants, including high‐order triple and quadruple mutants, we demonstrated that ARR1 and ARR12 redundantly function as negative regulators of As(III) tolerance by acting upstream of NIP1;1 and NIP6;1 to modulate their function in arsenic accumulation. ChIP–qPCR, EMSA, and transient dual‐LUC reporter assays revealed that ARR1 and ARR12 transcriptionally activate the expression of NIP1;1 and NIP6;1 by directly binding to their promoters and upregulating their expression, leading to increased arsenic accumulation under As(III) stress. These findings collectively provide insights into cytokinin signaling‐mediated plant adaptation to excessive As(III), contributing to the development of crops with low arsenic accumulation.
This is the first-time work to integrate transcriptome and metabolome sequencing data, providing a comprehensive knowledge of how the pathogen Armillaria solidipes affects the spore development, biofilm creation, and antifungal activity of Bacillus velezensis BY6. The dynamic growth of BY6 indicated that A. solidipes had a significant growth-inhibiting effect on BY6. Using scanning electron microscopy (SEM), it was discovered that the cell wall and cell membrane was compromised, resulting in the leakage of intracellular components. On the basis of gene and metabolite network analysis, several genes and metabolites are predominantly involved in the " Phosphotransferase system (PTS)", "Two-component system", and "Ubiquinone and other terpenoid-quinone biosynthesis" pathway. The mechanism by which A. solidipes inhibits the biological control ability of BY6 is influenced by numerous factors, including cell membrane damage (Folding, disintegration, disappearance), nutrient limitation (Pyruvic acid, Menadione concentration down-regulated), and spore and biofilm formation inhibition (Spo0 A, Spo0 B and Kin B ∼ D genes down-regulated). We conclude that interference of A. solidipes with the growth and development of BY6 results in a decrease in BY6 biocontrol levels. This result contributes to a complete and thorough understanding of the mechanism by which A. solidipes inhibits BY6′s biocontrol ability and identifies additional potential molecular targets. To further genetically modify the BY6 strains for tackle the problem of drug resistance.
A new type of Wireless Dynamometer for Oil-Well Measurement was developed.Microcontroller with CORTEX-M3 kernel was applied in the system.The system includes sensor nodes and remote terminal units in two parts,each of which was added with wireless module like ZigBee or GPRS module.Introduced the overall hardware structure and software development of wireless dynamometes.Experimental results show that the system has low power consumption cost,safe for the oil production,and provide a reliable guarantee for daily management.
In this article, canonical correlation analysis was used to explore the relationship between the toxicity-attenuating effect and the variation of chemical contents in rhubarb caused by processing. With quasi-acute toxicity test, the difference of hepatic and renal toxicity to mice with the processed materials of rhubarb was researched. The chemical contents of anthraquinones and tannins in rhubarb were measured by UV-vis spectrophotometry and high performance liquid chromatography. The results showed that there were toxic effects to liver and kidney in mice after repeated intragastric administration of rhubarb and its processed materials for 14 days at a dosage of 76 g x kg(-1). The toxic effect of processed materials was much lower than crude drug. With canonical correlation analysis, the sequence of the hepatic and renal toxicity of chemical contents in rhubarb were found as follows: total anthraquinone glycosides (AQGs) > tannins (Tns) > total anthraquinones (AQs); aloe-emodin (AE) > physcione (Ph) > rhein (Rn) > emodin (Ed) > chrysophanol (Ch) and AEG > PhG > ChG > EdG > RnG of glycosyl-anthraquinone. It could be concluded that processing would attenuate the toxicity of crude drug of rhubarb. The toxicity-attenuating effect might be correlated to the decline of the contents of both anthraquinone glycosides and tannins, especially the aloe-emodin glycoside and physcione glycoside. The results also suggested that the serum alanine aminotransferase (ALT) and creatine (CREA) would be useful to monitor the hepatic and renal toxicity of rhubarb.
The simulation-based testing of Autonomous Driving Systems (ADSs) has gained significant attention. However, current approaches often fall short of accurately assessing ADSs for two reasons: over-reliance on expert knowledge and the utilization of simplistic evaluation metrics. That leads to discrepancies between simulated scenarios and naturalistic driving environments. To address this, we propose the Matrix-Fuzzer, a behavior tree-based testing framework, to automatically generate realistic safety-critical test scenarios. Our approach involves the $log2BT$ method, which abstracts logged road-users' trajectories to behavior sequences. Furthermore, we vary the properties of behaviors from real-world driving distributions and then use an adaptive algorithm to explore the input space. Meanwhile, we design a general evaluation engine that guides the algorithm toward critical areas, thus reducing the generation of invalid scenarios. Our approach is demonstrated in our Matrix Simulator. The experimental results show that: (1) Our $log2BT$ achieves satisfactory trajectory reconstructions. (2) Our approach is able to find the most types of safety-critical scenarios, but only generating around 30% of the total scenarios compared with the baseline algorithm. Specifically, it improves the ratio of the critical violations to total scenarios and the ratio of the types to total scenarios by at least 10x and 5x, respectively, while reducing the ratio of the invalid scenarios to total scenarios by at least 58% in two case studies.