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In order to improve the recognition accuracy of parking space change, a new fusion model is proposed. The image-aware hash technique and image structure similarity algorithm are combined to construct a new parking space state combination discriminating index due to the accuracy of the recognition. Time is used to define the discriminating threshold of the parking space occupancy condition, so as to construct a vehicle position state discriminating fusion model. Based on the model, the parking lot recognition software was developed, and the parking space recognition of three environmental states, such as uniform illumination, uneven illumination and snowfall, was carried out and the validity of the model was verified. [ABSTRACT FROM AUTHOR]

It has been reported that BCL2L10 is abundantly and specifically expressed in adult human and mouse oocytes and played a very important role in oocytes maturation and early embryonic development. This study is to investigate the expression pattern of BCL2L10 in buffalo ovaries and its effect on the in vitro maturation of buffalo oocytes, so as to dissect mechanism of oocytes maturation and provide theoretical guidance for improvement of the in vitro maturation of buffalo oocytes. The results showed that BCL2L10 gene was enriched in ovary and the expression of BCL2L10 was oocyte specific and up-regulated during oocyte maturation. BCL2L10 protein and mRNA were detectable in buffalo early embryos, upregulated at 2-cell to 8-cell stages and down-regulated in the later stages. Knockdown of BCL2L10 by RNA interference resulted in a significant decrease in the maturation rate (33.5%) and cleavage rate (37.52%) of buffalo oocytes coupled with up-regulation of apoptosis-related gene Caspase-9 . We concluded that BCL2L10 is a candidate associated with buffalo oocyte maturation. [ABSTRACT FROM AUTHOR]

Angiogenesis is disrupted in age-related and postmenopausal osteoporosis. However, the mechanisms of the disorder remain elusive. We confirmed in this study that, in accordance with the decrease of H-type vessels, the proangiogenic potential of bone marrow-derived mesenchymal stem cells (BMSCs) declined during osteoporosis. Screening of the histone acetyltransferase family revealed that GCN5 decreased in BMSCs derived from osteoporotic femur. Further analysis identified that GCN5 plays important roles in regulating the proangiogenic potential of BMSCs. GCN5 promoted BMSC-mediated angiogenesis by enhancing H3K9ac levels on the promoter of Vegf. The decrease of GCN5 in osteoporotic BMSCs led to the decline of proangiogenic capacity. Accordingly, overexpression of GCN5 enhanced the proangiogenic potency of osteoporotic BMSCs. Furthermore, recovering GCN5 expression in vivo by lentiviral expression vector significantly attenuated the loss of angiogenesis in ovariectomized mouse femurs. Our study results revealed an epigenetic mechanism controlling BMSC-mediated angiogenesis and provided a novel therapeutic target for osteoporosis treatment. [ABSTRACT FROM AUTHOR]

Nanoindentation produced plastic deformation of arc-evaporated AlCrSiN and AlCrSiON nanocomposite films deposited on cemented-carbide substrates was investigated. The nanoindentation tests have the maximum penetration depth of 250 nm. Microstructure evolution in the indents was indicated by focused-ion-beam cutting and transmission-electron-microscopy observation. The results indicate that both the AlCrSiN and the AlCrSiON nanocomposite films exhibit excellent plasticity without the occurrence of microcrack initiation and propagation in the indents and grain boundaries. The prominent pile-up phenomenon produced by plastic flow was observed in the indent of the AlCrSiON film. Incorporating O into the AlCrSiN reduces both hardness and toughness of the film. This produces the pile-up in the AlCrSiON film when exposed to a nanoindenter. Rotation of the (Cr, Al)N nanograins and deflection of self-organized multilayer interface contribute to the plastic deformation of the AlCrSiN. However, shear band, interface deflection, and grain rotation contribute to the nanoindentation-induced plastic deformation of the AlCrSiON film. • Incorporating O into the AlCrSiN reduces both hardness and toughness of the film. • Pile-up was only observed in the indentation impression of the AlCrSiON. • Grain rotation and interface deflection contribute to the deformation of the AlCrSiN. • Shear band, interface deflection, and grain rotation contribute to the deformation of the AlCrSiON. [ABSTRACT FROM AUTHOR]

Since its discovery in the 1940s, retinal photocoagulation has evolved immensely. Although the first photocoagulators used incandescent light, it was the invention of the laser that instigated the widespread use of photocoagulation for treatment of retinal diseases. Laser permits selection of electromagnetic wavelength, energy levels, spot size and pulse duration. These variables are crucial for accurate targeting of retinal tissue and prevention of detrimental side-effects such as central blind spots. There is ongoing clinical research dedicated to optimising such parameters and many innovative modes of laser delivery are now being offered. Laser photocoagulation is the mainstay of treatment for various retinal and macular diseases. Considering the escalating prevalence of such conditions and widespread use of photocoagulation, it is important for optometrists to grasp the basic principles and be aware of new developments in retinal laser therapy. [ABSTRACT FROM AUTHOR]

Background: One of the main reasons for the failure of prostate cancer (PCa) treatment is the generation of chemoresistance. Circular RNA hsa_circ_0000735 (hsa_circ_0000735) is connected with the progression of cancer. Nevertheless, the role and regulatory mechanism of hsa_circ_0000735 in the resistance of PCa to docetaxel (DTX) are unclear. Methods: Expression levels of hsa_circ_0000735 and miR-7-5p (miR-7) in tissue samples and cells were examined via quantitative real-time polymerase chain reaction (qRT-PCR). The DTX sensitivity, viability, colony formation, cell cycle progression, and apoptosis of DTX-resistant PCa cells were determined via Cell Counting Kit-8 (CCK-8), cell colony formation, or flow cytometry assays. The levels of multidrug resistance protein 1 (MDR1) protein, cyclinD1, and B cell lymphoma 2 (bcl-2) were detected by western blotting. The interaction between hsa_circ_0000735 and miR-7 was verified via dual-luciferase reporter, RNA immunoprecipitation (RIP), and RNA pull-down assays. The role of hsa_circ_0000735 in vivo was validated through tumor formation experiments. Results: Hsa_circ_0000735 was upregulated and miR-7 was downregulated in DTX-resistant PCa tissues and cells. High hsa_circ_0000735 expression had a shorter overall survival. Both hsa_circ_0000735 knockdown and miR-7 mimic boosted DTX sensitivity, constrained viability, colony formation, cell cycle progression, and fostered apoptosis of DTX-resistant PCa cells. Also, hsa_circ_0000735 silencing elevated DTX sensitivity and repressed tumor growth in PCa in vivo. Mechanistically, hsa_circ_0000735 served as a sponge for miR-7. MiR-7 inhibition overturned hsa_circ_0000735 silencing-mediated impacts on DTX sensitivity and the malignant behaviors of DTX-resistant PCa cells. Conclusion: Hsa_circ_0000735 downregulation boosted PCa sensitivity to DTX and reduced tumor growth via sponging miR-7, providing a promising prognostic biomarker and therapeutic target for PCa. [ABSTRACT FROM AUTHOR]

Sepsis often causes organ dysfunction and is manifested in increased endothelial cell permeability in blood vessels. Early-stage inflammation is accompanied by metabolic changes, but it is unclear how the metabolic alterations in the endothelial cells following lipopolysaccharide (LPS) stimulation affect endothelial cell function. In this study, the effects of 1 μg/ml of LPS on the metabolism of human umbilical vein endothelial cells (HUVECs) were investigated, and the metabolic changes after LPS stimulation were explained from the perspective of mRNA expression, chromatin openness and metabolic flux. We found changes in the central metabolism of endothelial cells after LPS stimulation, such as enhanced glycolysis function, decreased mitochondrial membrane potential, and increased production of reactive oxygen species (ROS). Sphingolipid metabolic pathways change at the transcriptome level, and sphingosine-1-phosphatase 2 (SGPP2) was upregulated in LPS-stimulated endothelial cells and zebrafish models. Overexpression of SGPP2 improved cell barrier function, enhanced mitochondrial respiration capacity, but also produced oxidative respiration chain uncoupling. In addition, SGPP2 overexpression inhibited the degradation of HIF-1α protein. The molecular and biochemical processes identified in this study are not only beneficial for understanding the metabolic-related mechanisms of LPS-induced endothelial injury, but also for the discovery of general therapeutic targets for inflammation and inflammation-related diseases. [Display omitted] • Warburg effect was produced in endothelial cells after LPS stimulation. • SGPP2 was up regulated in LPS induced HUVECs. • Overexpression of SGPP2 regulated mitochondrial respiration, reduced ROS, promoted cell proliferation and reduced cell permeability. • SGPP2 overexpression inhibited the degradation of HIF-1α. [ABSTRACT FROM AUTHOR]

A palladium-catalyzed two-component coupling of allenylphosphine oxides with conjugated N-tosylhydrazones is revealed. For the first time, the cleavage of α-allenylic aryl ether toward pyrazolemethylene-substituted phosphinyl allenes enabled facile synthesis of combined motifs with pyrazole and allene. Moreover, the obtained adducts could be easily transformed to potential bioactive multifunctionalized phosphinates via a novel alkenyl C-P(O) cleavage. [ABSTRACT FROM AUTHOR]

FOXF2 (forkhead box F2) is a mesenchyme-specific transcription factor that plays a critical role in tissue homeostasis through the maintenance of epithelial polarity. In a previous study, we demonstrated that FOXF2 is specifically expressed in basal-like breast cancer (BLBC) cells and functions as an epithelial-mesenchymal transition suppressor. FOXF2 deficiency enhances the metastatic ability of BLBC cells through activation of the epithelial-mesenchymal transition program, but reduces cell proliferation. In this study, we demonstrate that CpG island methylation of the FOXF2 proximal promoter region is involved in the regulatory mechanism of the subtype-specific expression of FOXF2 in breast cancer cells. DNMT1, DNMT3A, and DNMT3B commonly or individually contributed to this DNA methylation in different breast cancer cells. SP1 regulated the transcriptional activity of FOXF2 through direct binding to the proximal promoter region, whereas this binding was abrogated through DNA methylation. FOXF2 mediated the SP1-regulated suppression of progression and promotion of proliferation of non-methylated BLBC cells. Thus, we conclude that the subtype-specific expression and function of FOXF2 in breast cancer cells are regulated through the combined effects of DNA methylation and SP1 transcriptional regulation. [ABSTRACT FROM AUTHOR]

Vehicle platooning can improve traffic efficiency with access to better fuel economy and environmental benefits. The work selected the car model of DrivAer closer to the actual passenger car and used the new generation of CFD (Computational Fluid Dynamics) simulation software XFlow to simulate the energy efficiency of passenger car platoon. The vehicle fuel efficiency model based on the aerodynamic drag coefficient CD was deduced by using the vehicle driving equation. Three body types of car model, which are fast back, step back, and straight back, were selected to form a platoon separately; the number of car is two and the distance between two cars is 1 L (L is the vehicle body length) in the platoon. The fuel economy of vehicle platoon was obtained through simulation combed with the fuel efficiency model, and sorting results are fast back < step back < straight back. Besides, step back car model and 11 kinds of vehicle distance between 0 and 3 L were selected, 3 cars were made up of a platoon, and those of the platoon analyzed the relationship between vehicle distance and aerodynamic drag, the relationship between vehicle distance and fuel saving rate. The average fuel saving rate of cars in the platoon was about 4–8%, and it was dramatic decline as vehicle distance changes from 0 to 0.5 L; but when the distance is bigger than 0.5 L, it was almost not changed. Setting the distance between two vehicles to 1 L, the authors studied the fuel economy of two-vehicle platoon running at seven kinds of speed. With the increase of speed, the fuel saving rate of each car has increased and it is bigger for rear car than that of front car. The work can provide a technical basis for the control strategy of vehicle platooning in intelligent and networked traffic system. [ABSTRACT FROM AUTHOR]

Bone marrow-derived mesenchymal stem cell (BMSC) cytotherapy has emerged as a promising treatment strategy for refractory immune diseases; however, the influence of the pathologic conditions of donors on the immunomodulatory properties of BMSCs is still poorly understand. Here, we found that BMSCs that were derived from donors with osteoporosis were ineffective as cytotherapy for patients with experimental colitis and graft-vs.-host disease (GVHD). In vivo and in vitro assays revealed that the capacity of osteoporotic BMSCs to induce T-cell apoptosis declined as a result of decreased Fas and FasL protein. Additional analysis revealed that let-7a, a microRNA induced by TNF-a in osteoporosis, inhibited the expression of the Fas/FasL system via post-transcriptional regulation. By knocking down let-7a expression, we successfully recovered the immunosuppressive capacity of osteoporotic BMSCs and improved their therapy for experimental colitis and GVHD. Taken together, our study demonstrates that the immunomodulatory properties of BMSCs are suppressed in osteoporosis and illustrates the molecular mechanism that underlies this suppression. These findings might have important implications for the development of targeted strategies to improve BMSC cytotherapy. [ABSTRACT FROM AUTHOR]

Myc-associated zinc finger protein (MAZ) is a transcription factor with C2H2-type zinc-finger motifs that can bind GC-rich cis-elements. MAZ activates the transcription of some cancer-related genes and represses that of others, suggesting that changes in MAZ expression may play different roles in the development and progression of different types or subtypes of cancers depending on its target genes. However, the functions and mechanisms of MAZ in regulating the carcinogenesis and progression of breast cancer have remained unclear. In the current study, we show that MAZ performs dual function in basal-like breast cancer (BLBC): suppression of aggressiveness and promotion of proliferation. Forkhead box F2 (FOXF2) is a novel transcription target of MAZ and mediates the functions of MAZ. The MAZ mRNA level, particularly in combination with the FOXF2 mRNA level, may serve as a prognostic marker for BLBC patients. Our results indicate that the dual function of the MAZ-FOXF2 axis reflect the pleiotropic nature of multifunctional transcription factors in regulating the different stages of cancer development and progression, which could lead to the complexity of cancer diagnosis and treatment. [ABSTRACT FROM AUTHOR]

Mineralocorticoid receptor (MR) has been considered as a potential target for treating atherosclerosis. However, the cellular and molecular mechanisms are not completely understood. We aim to explore the functions and mechanisms of macrophage MR in atherosclerosis. Atherosclerosis-susceptible LDLRKO chimeric mice with bone marrow cells from floxed control mice or from myeloid MR knock-out (MRKO) mice were generated and fed with high cholesterol diet. Oil red O staining showed that MRKO decreased atherosclerotic lesion area in LDLRKO mice. In another mouse model of atherosclerosis, MRKO/APOEKO mice and floxed control/APOEKO mice were generated and treated with angiotensin II. Similarly, MRKO inhibited the atherosclerotic lesion area in APOEKO mice. Histological analysis showed that MRKO increased collagen coverage and decreased necrosis and macrophage accumulation in the lesions. In vitro results demonstrated that MRKO suppressed macrophage foam cell formation and up-regulated the expression of genes involved in cholesterol efflux. Furthermore, MRKOdecreased accumulation of apoptotic cells and increased effective efferocytosis in atherosclerotic lesions. In vitro study further revealed that MRKO increased the phagocytic index of macrophages without affecting their apoptosis. In conclusion, MRKOreduces high cholesterol- or angiotensin II-induced atherosclerosis and favorably changes plaque composition, likely improving plaque stability. Mechanistically, MR deficiency suppresses macrophage foam cell formation and up-regulates expression of genes related to cholesterol efflux, as well as increases effective efferocytosis and phagocytic capacity of macrophages. [ABSTRACT FROM AUTHOR]

Estrogen protects bone loss by promoting Fas ligand (FasL) transcription in osteoclasts and osteoblasts to induce apoptosis of osteoclasts. Bone marrow-derived mesenchymal stem cells (BMMSCs) express FasL protein, which is necessary for BMMSCs to induce T-cell apoptosis in cell therapy. However, the physiologic function of FasL in BMMSCs is unknown. In this study, using an in vitro coculture system and an in vivo BMMSC transplantation assay, we found that BMMSCs potently induced apoptosis of osteoclasts through the FasL/Fas pathway. Estrogen was necessary for this process as a promoter of FasL protein accumulation in BMMSCs. Furthermore, estrogen elevated FasL protein accumulation, not by increasing FasL gene transcription, but through microRNA-mediated posttranscriptional regulation. In brief, estrogen down-regulated expression of miR-181a, a negative modulator of FasL targeting the 3'-UTR of FasL mRNA. Estrogen deficiency resulted in excessive miR-181a, which decreased FasL protein levels to suppress BMMSC-induced osteoclast apoptosis. Furthermore, knockdown of miR-181a recovered the BMMSC defect to induce osteoclast apoptosis during estrogen deficiency. Taken together, our results showed that estrogen preserves FasL protein accumulation by inhibiting miR-181a expression in BMMSCs to maintain bone remodeling balance, suggesting a novel mechanism by which estrogen preserves bone mass. [ABSTRACT FROM AUTHOR]

Water-soluble and stable CdTe quantum dots were synthesized in aqueous solution with thioglycolic acid as the stabilizer. A spectrofluorometric method for the determination of iron (II) has been developed based on quenching of the fluorescence of CdTe quantum dots by iron (II) in aqueous solutions. It can perform an accurate and simple determination of iron (II) concentration in water samples. Under optimum conditions, the quenched fluorescence intensity increased linearly with the concentration of iron (II) ranging from 5.0 × 10−8to 4.0 × 10−6 mol/L with a correlation coefficient R = 0.9969. The limit of detection for iron (II) was found to be 1.2 × 10−8 mol/L. As an application, the proposed method was successfully applied to the analysis of iron (II) in water samples, and the results were satisfactory. [ABSTRACT FROM PUBLISHER]

A novel CdTe quantum dots (QDs) based technology platform was established in aqueous solution. It can perform accurate and simple determination of aminophylline concentration in pharmaceutical samples with satisfactory results. Under optimum conditions, the relative fluorescence intensity of CdTe quantum dots is linearly proportional aminophylline concentration from 2.00 to 80.0 μg mL with a correlation coefficient of 0.9979 for aminophylline determination and a detection limit of 0.531 μg mL. [ABSTRACT FROM AUTHOR]

Background: The histopathological and molecular heterogeneity of normal tissue adjacent to cancerous tissue (NTAC) and normal tissue adjacent to benign tissue (NTAB), and the availability of limited specimens make deciphering the mechanisms of carcinogenesis challenging. Our goal was to identify histogenetic biomarkers that could be reliably used to define a transforming fingerprint using RNA in situ hybridization. Methods: We evaluated 15 tumor-related RNA in situ hybridization biomarkers using tumor microarray and samples of seven tumor-adjacent normal tissues from 314 patients. Biomarkers were determined using comprehensive statistical methods (significance of support vector machine-based artificial intelligence and area under curve scoring of classification distribution). Results: TP53 was found to be a most reliable index (P <10-7; area under curve >87%) for distinguishing NTAC from NTAB, according to the results of a significance panel (BCL10, BECN1, BRCA2, FITH, PTCH11 and TP53). Conclusions: The genetic alterations in TP53 between NTAC and NTAB may provide new insight into the field of cancerization and tumor transformation. [ABSTRACT FROM AUTHOR]

Epidermal regeneration is a complex process, strongly influenced by growth factors, including keratinocyte growth factor (KGF). The objective of this study was to establish immortalized HaCaT keratinocytes and KMST-6-fibroblasts stably expressing KGF. Transfection efficiency, genomic integration, and functionality of the transgene were determined by ELISA and PCR, and KGF-expressing clones were selected using an air–liquid interface test system. HaCaT cells displayed stronger transgene expression compared to transfected fibroblasts, and the most effective HaCaT clone was incubated on a membrane carrier to form a “membrane cell graft.” Twenty-one superficial second-degree burn wounds were created in each of three pigs, and wound healing capacity of the generated “polypeptide cell delivery system” after grafting was examined. Untransfected HaCaT keratinocytes and membrane-covered and untreated burn wounds served as controls. Histological and macroscopical follow-up revealed that grafting of transfected HaCaT cells resulted in complete reepithelialization within 5 days, while wounds covered with untransfected cells needed 2 days longer. At untreated sites, a thin epithelium was detectable after 10 days. The results indicate that wound healing processes can be stimulated distinctly by growth factors secreted from HaCaT cells, with a prominent role for transgenic KGF. [Copyright &y& Elsevier]