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Hyperglycemia-induced endothelial inflammation participates in the pathogenesis of cardiovascular complications in diabetics. Previous studies showed that protein tyrosine phosphatase 1B (PTP1B) and ETS proto-oncogene 1 (ets1) are involved in hyperglycemia-induced endothelial inflammation. In this study, we hypothesized that ets1 modulates PTP1B expression, thus playing a crucial role in hyperglycemia-induced vascular endothelial inflammation. Our results indicated that high glucose increases monocyte/endothelial adhesion, vascular cell adhesion molecule-1 (VCAM-1) expression and p65 phosphorylation in human umbilical vein endothelial cells (HUVECs). Moreover, high glucose-mediated endothelial inflammation is reversed by PTP1B silencing. In addition, high glucose increases ets1 expression in HUVECs. Ets1 silencing reverses high glucose-mediated endothelial inflammation. Furthermore, the effect of ets1 overexpression is similar to that of high glucose treatment, which is counteracted by si-PTP1B. The results from ChIP assays indicated that ets1 occupies the PTP1B promoter region. Ets1 overexpression enhances PTP1B promoter activity, which is disappeared after specific binding site mutation. In vivo experiments demonstrated that the expressions of VCAM-1, PTP1B, and ets1, as well as the phosphorylation of p65 are augmented in the aorta of diabetic rats. In conclusion, ets1 contributes to hyperglycemia-mediated endothelial inflammation via upregulation of PTP1B expression.

Reliable obstacle detection is of great significance to the navigation technology of unmanned agricultural machinery. Currently, most of the previous works have achieved significant performance with the help of visual prior information of obstacles, where visual prior information refers to the visual features learned by models in the training stage. However, collecting enough annotated images for the training stage can be challenging. In the absence of annotated images, the current methods cannot perform optimally. To address the above problem, this paper presents a zero‐shot obstacle detection model based on the You Only Look Once X backbone, introducing the concept of zero‐shot learning into real‐time obstacle detection systems. Specifically, the cascade of encoder and decoder modules is appended to the presented model, and the integration of semantic space‐based classification and anchor‐free localization modules is used for zero‐shot obstacle detection. The feasibility of the proposed method was verified on the actual farmland test data set. The experimental results show that the F1 scores of the seen obstacle (e.g., people) and the unseen obstacle (e.g., agricultural machinery) are 96.22% and 94.66%, respectively. The average detection time for each panoramic image is 52.52 ms (equivalent to 19.04 FPS). The proposed obstacle detection method exhibits superior performance in the situation where training samples of the target category are not available. Notably, the proposed model not only performs the correct classification of unseen obstacles, but also improves the detection performance of both seen and unseen obstacles. The proposed method achieves a balance between accuracy and detection speed. [ABSTRACT FROM AUTHOR]

Hyperglycemia mediates oxidative stress, thus inducing transcription factor nuclear factor kappa B (NF-[kappa]B) activation, increasing endothelial adhesion molecule expression and monocyte/endothelial interaction, and resulting in endothelial injury. Ketamine was reported to attenuate oxidative stress in many cases. In this research, we determined whether and how ketamine protects against high-glucose-mediated augmentation of monocyte/endothelial interaction and endothelial adhesion molecule expression in human umbilical vein endothelial cells. High glucose augmented monocyte/endothelial adhesion and endothelial adhesion molecule expression. High glucose induced reactive oxygen species (ROS) production and augmented phospho-protein kinase C (p-PKC) [beta]II expression and PKC activity. Moreover, high glucose inhibited the inhibitory subunit of nuclear factor-[kappa]B[alpha] (I[kappa]B[alpha]) expression in the cytoplasm and induced NF-[kappa]B nuclear translocation. Importantly, the effects induced by high glucose were counteracted by ketamine treatment. Further, CGP53353, a PKC [beta]II inhibitor, inhibited high-glucose- mediated NF-[kappa]B nuclear translocation, attenuated adhesion molecule expression, and reduced monocyte/endothelial interaction. Further, these effects of ketamine against high-glucose-induced endothelial injury were inhibited by phorbol 12-myristate 13- acetate, a PKC [beta]II activator. In conclusion, ketamine, via reducing ROS accumulation, inhibited PKC [beta]II Ser660 phosphorylation and PKC and NF-[kappa]B activation and reduced high-glucose-induced expression of endothelial adhesion molecules and monocyte/endothelial interaction. Key words: ketamine, high glucose, endothelial, inflammation. L'hyperglycemie participe a la mediation du stress oxydatif, ce qui comprend de fait l'activation du facteur de transcription du facteur nucleaire kappa B (NF-[kappa]B), l'augmentation de l'expression des molecules d'adherence endotheliale, ainsi que l'interaction entre les monocytes et l'endothelium, avec des lesions endotheliales resultantes. On a rapporte que la ketamine permet d'attenuer le stress oxydatif dans bien des cas. Dans cette etude, nous avons cherche a etablir si la participation de la ketamine a la protection contre l'augmentation de l'interaction entre les monocytes et l'endothelium et a l'expression des molecules d'adherence endotheliale mediees par l'hyperglycemie dans les cellules endotheliales de veine ombilicale humaine, ainsi que les modes d'action, le cas echeant. L'hyperglycemie entramait une augmentation de l'adherence entre les monocytes et l'endothelium, ainsi que de l'expression des molecules d'adherence de l'endothelium. L'hyperglycemie entramait la production de derives reactifs de l'oxygene et une augmentation de l'expression de la phospho-proteine kinase C (p-PKC) [beta]II et de l'activite de la PKC. En outre, l'hyperglycemie entramait une inhibition de l'expression de la sous-unite inhibitrice du facteur nucleaire [kappa]B[alpha] (I[kappa]B[alpha]) dans le cytoplasme, ainsi que la stimulation de la translocation nucleaire du NF-[kappa]B. Il est important de noter que l'administration de ketamine contrait les effets engendres par l'hyperglycemie. De plus, le CGP53353, un inhibiteur de la PKC [beta]II, permettait d'inhiber la translocation nucleaire du NF-[kappa]B mediee par l'hyperglycemie, d'attenuer l'expression des molecules d'adherence et d'inhiber l'interaction entre les monocytes et l'endothelium. Enfin, ces effets de la ketamine contre les lesions endotheliales engendrees par l'hyperglycemie etaient inhibes par le phorbol 12-myristate 13-acetate, un activateur de la PKC [beta]II. En conclusion, la ketamine, par l'intermediaire de la diminution de l'accumulation des derives reactifs de l'oxygene, de l'inhibition de la phosphorylation de la PKC [beta]II en Ser660, de l'activation de la PKC et du NF-[kappa]B entramait une diminution de l'expression des molecules d'adherence endotheliale et de l'interaction entre les monocytes et l'endothelium engendrees par l'hyperglycemie. [Traduit par la Redaction] Mots-cles: ketamine, hyperglycemie, endothelial, inflammation., Introduction Perioperative hyperglycemia is often seen in both nondiabetic patients (Werb et al. 1989) and diabetic patients (Walts et al. 1981). Hyperglycemia increases the expression of endothelial adhesion molecules, including [...]

This study focused on Middle Permian Lucaogou Formation saline lake source rocks, utilizing a combination of biomarkers and hydrocarbon generation thermal simulation to analyze their biological compositions, depositional environments, and hydrocarbon generation potential. The Pr/Ph ratio, Ph/nC18 ratio, and Pr/nC17 ratio indicate that the Lucaogou Formation was in a reducing environment during the deposition period, and the lower part of the Lucaogou Formation (P2l1) is more anoxic than the upper part of the Lucaogou Formation (P2l2). The maturity index 20S (%) and ββ (%) reflect that the maturity of organic matter in the P2l1 is slightly higher than that in the P2l2. The G/H index and the ETR index indicate that the stratification of the water column is better during the sedimentary period of Lucaogou Formation and the salinity of the P2l1 is higher than that of the P2l2. The biomarker parameters of nC21−/nC22+, CPI, S/H, and C22T/C21T reflect that the organic matter of the source rocks have a higher abundance of bacteria and algae than higher plants, and the contents of bacteria are more than that of algae. The (7- + 8-MMAs)/Cmax and (C28 + C29 − St)/St parameters indicate that cyanobacteria accounted for a certain proportion of bacteria, and the algae are mainly green algae. The co-evolution of the sedimentary environment and the biological composition reflects the control of the sedimentary paleoenvironment on biological composition. According to the relative content of cyanobacteria, green algae, and Rhodophyta, the source rocks of the upper and lower Lucaogou Formation correspond to the low-salinity type (LS-type) and the high-salinity type (HS-type), respectively. Compared with LS-type source rocks, HS-type source rocks have greater generation potential of oil and weaker gas generation potential. This study is valuable for the accurate assessment of source rocks and holds significant practical implications for the exploration of oil and gas resources. [ABSTRACT FROM AUTHOR]

This paper presents and validates a discrete-time/frequency-domain approach to the problem of Volterra-series-based behavioral modeling for high-frequency systems. The proposed technique is based on the acquisition of samples of the input/output data, both of which are sampled at the Nyquist rate corresponding to the input signal. The method is capable of identifying the time-/frequency-domain Volterra kernels/transfer functions of arbitrary causal time-invariant weakly nonlinear circuits and systems operating at high frequencies subject to essentially a general random or multitone excitation. The validity and efficiency of the proposed modeling approach has been demonstrated by several examples in high-frequency applications and good agreement has been obtained between results calculated using the proposed model and results measured or simulated with commercial simulation tools. Index Terms--Behavioral modeling, high-frequency systems, nonlinear circuits and systems, Volterra series.

Glycogen phosphorylase B (PYGB), the rate-determining enzyme in glycogen degradation, plays a critical role in progression of various tumors. The present study focused on the potential molecular mechanism toward PYGB in non-small cell lung cancer (NSCLC) progression. Expression of PYGB in NSCLC tissues and cell lines was evaluated via quantitative real-time PCR (qRT-PCR), western blot and immunohistochemistry. Cell viability, proliferation and apoptosis were investigated using 3-(4,5-Dimethylthiazol)-2,5-diphenyltetrazolium bromide (MTT) assay, 5-bromo-2-deoxyuridine (BrdU) and flow cytometry, respectively. Cell migration and invasion ability were detected by wound healing and transwell invasion assays, respectively. The in vivo effect of PYGB on NSCLC tumor growth was determined via subcutaneous xenotransplanted tumor model. PYGB was upregulated in NSCLC tissues and cell lines, suggesting a poor prognosis in NSCLC patients. In vitro functional assays indicated that knockdown of PYGB suppressed cell viability, proliferation, migration and invasion, while promoted cell apoptosis in NSCLC. Mechanistically, we found that overexpression of PYGB could activate phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway, while these effects were effectively reversed by knockdown of PYGB. In vivo tumorigenesis and PI3K/AKT signaling pathway were also inhibited by PYGB knockdown. Knockdown of PYGB suppressed NSCLC progression, suggesting PYGB as a novel biomarker and potential molecular therapeutic target for further investigation in NSCLC. [ABSTRACT FROM AUTHOR]

Microglia inflammation induces pro‐inflammatory cytokines and pro‐inflammatory enzymes expression, thus leading to inflammation‐mediated neuronal cell death. Increased intracellular glycolysis participates in LPS‐mediated microglia inflammation. Dexmedetomidine exhibits neuroprotective effects in some situations. In this study, we mainly focused on whether and how dexmedetomidine inhibits LPS‐mediated cellular glycolysis and inflammation in BV2 cells. LPS induced pro‐inflammatory cytokines and pro‐inflammatory enzymes expression, and increased glycolysis capacity in BV2 cells. Moreover, inhibition of glycolysis by 2DG attenuated LPS‐induced pro‐inflammatory cytokines and pro‐inflammatory enzymes expression. Moreover, LPS upregulated hypoxia‐inducible factor 1α (HIF1α) expression and decreased sirt1 expression. Dexmedetomidine counteracted these effects induced by LPS. Further, 2‐methoxyestradiol, a HIF1α inhibitor, could inhibit LPS‐mediated glycolysis and inflammation in BV2 cells, which was similar to the effects of dexmedetomidine. In addition, these effects of dexmedetomidine could be reversed by EX527, a sirt1 inhibitor. The present study indicated that dexmedetomidine, via upregulation of sirt1 expression, inhibited HIF‐1α expression and glycolysis, thus reducing LPS‐mediated inflammation in BV2 cells. [ABSTRACT FROM AUTHOR]