The identification of specific cells involved in the pathogenesis of these diseases could provide unique diagnostic and therapeutic opportunities to prevent disease progression by preventing EMT and specific pro-fibrotic signals.Data are the fundamental building blocks to conduct scientific studies that seek to understand natural phenomena in space and time. The notion of data processing is ubiquitous and nearly operates in any project that requires gaining insight from the data. The increasing availability of information sources, data formats and download services offered to the users, makes it difficult to reuse or exploit the potential of those new resources in multiple scientific fields. In this paper, we present a spatial extract-transform-load (spatial-ETL) approach for downloading atmospheric datasets in order to produce new biometeorological indices and expose them publicly for reuse in research studies. The technologies and processes involved in our work are clearly defined in a context where the GDAL library and the Python programming language are key elements for the development and implementation of the geoprocessing tools. Since the National Oceanic and Atmospheric Administration (NOAA) is the source of information, the ETL process is executed each time this service publishes an updated atmospheric prediction model, thus obtaining different forecasts for spatial and temporal analyses. As a result, we present a web application intended for downloading these newly created datasets after processing, and visualising interactive web maps with the outcomes resulting from a number of geoprocessing tasks. We also elaborate on all functions and technologies used for the design of those processes, with emphasis on the optimisation of the resources as implemented in cloud services.The aim of study was to characterize patterns of interception and distribution of photosynthetically active radiation (PAR) in an apple orchard and to examine its relationship with morphophysiological characteristics of “Royal Gala” and “Fuji Suprema” apple trees. The experiments were conducted during three production cycles in two distinct orchard areas, one covered by black anti-hail netting and another uncovered (control). We analyzed PAR characteristics with data from meteorological sensors installed on the canopy, as well as growth, anatomical, and physiological variables of apple trees. The reduction of PAR by netting influenced the components of radiation balance. PAR intercepted, absorbed, transmitted, and reflected by the canopy under netting decreased by 33%, 31%, 32%, and 46%, respectively, in comparison to uncovered canopy. When leaf area index (LAI) was 1.5 (under netting) and 2.5 (uncovered), maximum PAR interception efficiency was reached. During the three production cycles, a light extinction coefficient of 1.09 and 0.76 was found under netting and in the control, respectively. Inhibitor Library price Plant height was greater under netting in all three cycles for both cultivars. Number of leaves, LAI, and shape index did not differ between treatments. At stage 85, leaves of “Royal Gala” under netting showed lower chlorophyll content and thinner parenchymas in comparison to the control. However, physiological and anatomical characteristics of Fuji “Suprema” did not change under anti-hail netting.Local joint inflammation plays an important role in the pathogenesis of temporomandibular joint (TMJ) osteoarthrosis (TMJOA). Yohimbine, an alpha-2 adrenergic receptor antagonist, possesses anti-inflammatory properties; however, the ability of Yohimbine to protect against TMJOA-associated chondrocyte inflammation remains unclear. We conducted in vitro and in vivo analyses to investigate whether Yohimbine could ameliorate TMJOA-induced chondrocyte inflammation and to elucidate the mechanisms involved. Chondrocytes of TMJOA mice were stimulated with interleukin (IL)-1β or noradrenaline (NE), and the resulting production of inflammation-related factors was evaluated in the presence or absence of Yohimbine. Furthermore, two TMJOA mouse models were treated with Yohimbine and the therapeutic effect was quantified. NE (10-6 M) triggered inflammatory cytokine secretion by TMJ chondrocytes, and Yohimbine suppressed IL-1β- or NE-induced IL-6 upregulation in TMJ chondrocytes with the nuclear factor (NF)-κB pathway inhibition. Yohimbine also ameliorated cartilage destruction in the TMJOA models. Interestingly, αmpT, a tyrosine hydroxylase inhibitor, reversed the effects of Yohimbine by activating the NF-κB pathway. Collectively, these findings show that Yohimbine ameliorated TMJ chondrocyte inflammation and the suppression of NF-κB pathway contributes to this effect.Activating transcription factor 2(ATF2), a transcription factor belonging to the AP-1 family, plays an important role in inflammation. However, its biological functions and underlying molecular mechanisms in rheumatoid arthritis (RA) remain unclear. Western blot and immunohistochemistry were used to identify the expression of ATF2 and Sprouty2(SPRY2) in RA synovial tissues. SW982 cells were stimulated by TNF-α to establish an in vitro RA fibroblast-like synoviocyte (RA-FLS) model. Transwell and monolayer wound-healing were used to detect cell migration and invasion. RNA interference (si-ATF2) and adenovirus vector (Ad-SPRY2) methods were employed to manipulate ATF2 or SPRY2 expression in SW982 cells. The protein expression and phosphorylation levels in SW982 cells were evaluated by western blot. ATF2 expression and phosphorylation were upregulated in the RA synovial tissues. In RA-FLS model, ATF2 expression and phosphorylation were increased in a time-dependent manner. ATF2 knockdown inhibited the migration and invasion of RA-FLS model, reducing the inflammatory factors, which was consistent with the influence on cell behaviors caused by SPRY2 overexpression. Moreover, SPRY2 overexpression inhibited the TNF-α-induced phosphorylation of ERK and ATF2 in SW982 cells. The high expression and phosphorylation of ATF2 promoted migration and invasion of RA-FLSs. SPRY2 might inhibited the inflammatory responses of RA-FLSs via suppressing ERK-ATF2 pathway.