Probabilistic modeling of future electricity systems with high renewable energy penetration using machine learning

The increasing penetration of weather-dependent renewable energy generation calls for high-resolution modeling of the possible future energy mixes to support the energy strategy and policy decisions. Simulations relying on the data of only a few years, however, are not only unreliable but also unable to quantify the uncertainty resulting from the year-to-year variability of the weather conditions. This paper presents a new method based on artificial neural networks that map the relationship between the weather data from atmospheric reanalysis and the photovoltaic and wind power generation and the electric load. The regression models are trained based on the data of the last 3 to 6 years, and then they are used to generate synthetic hourly renewable power production and load profiles for 42 years as an ensemble representation of possible outcomes in the future. The modeled profiles are post-processed by a novel variance-correction method that ensures the statistical similarity of the modeled and real data and thus the reliability of the simulation based on these profiles. The probabilistic modeling enabled by the proposed approach is demonstrated in two practical applications for the Hungarian electricity system. First, the so-called Dunkelflaute (dark doldrum) events, are analyzed and categorized. The results reveal that Dunkelflaute events most frequently happen on summer nights, and their typical duration is less than 12 h, even though events ranging through multiple days are also possible. Second, the renewable energy supply is modeled for different photovoltaic and wind turbine installed capacities. Based on our calculations, the share of the annual power consumption that weather-dependent renewable generation can directly cover is up to 60% in Hungary, even with very high installed capacities and overproduction, and higher carbon-free electricity share targets can only be achieved with an energy mix containing nuclear power and renewable sources. The proposed method can easily be extended to other countries and used in more detailed electricity market simulations in the future

β1 Integrin Deficiency Results in Multiple Abnormalities of the Knee Joint*

The lack of β1 integrins on chondrocytes leads to severe chondrodysplasia associated with high mortality rate around birth. To assess the impact of β1 integrin-mediated cell-matrix interactions on the function of adult knee joints, we conditionally deleted the β1 integrin gene in early limb mesenchyme using the Prx1-cre transgene. Mutant mice developed short limbed dwarfism and had joint defects due to β1 integrin deficiency in articular regions. The articular cartilage (AC) was structurally disorganized, accompanied by accelerated terminal differentiation, altered shape, and disrupted actin cytoskeleton of the chondrocytes. Defects in chondrocyte proliferation, cytokinesis, and survival resulted in hypocellularity. However, no significant differences in cartilage erosion, in the expression of matrix-degrading proteases, or in the exposure of aggrecan and collagen II cleavage neoepitopes were observed between control and mutant AC. We found no evidence for disturbed activation of MAPKs (ERK1/2, p38, and JNK) in vivo. Furthermore, fibronectin fragment-stimulated ERK activation and MMP-13 expression were indistinguishable in control and mutant femoral head explants. The mutant synovium was hyperplastic and frequently underwent chondrogenic differentiation. β1-null synoviocytes showed increased proliferation and phospho-focal adhesion kinase expression. Taken together, deletion of β1 integrins in the limb bud results in multiple abnormalities of the knee joints; however, it does not accelerate AC destruction, perturb cartilage metabolism, or influence intracellular MAPK signaling pathways

Chondromodulin I Is Dispensable during Enchondral Ossification and Eye Development

Chondromodulin I (chm-I), a type II transmembrane protein, is highly expressed in the avascular zones of cartilage but is downregulated in the hypertrophic region, which is invaded by blood vessels during enchondral ossification. In vitro and in vivo assays with the purified protein have shown chondrocyte-modulating and angiogenesis-inhibiting functions. To investigate chm-I function in vivo, we generated transgenic mice lacking chm-I mRNA and protein. Null mice are viable and fertile and show no morphological changes. No abnormalities in vascular invasion and cartilage development were detectable. No evidence was found for a compensating function of tendin, a recently published homologue highly expressed in tendons and also, at low levels, in cartilage. Furthermore, no differences in the expression of other angiogenic or antiangiogenic factors such as transforming growth factor β1 (TGF-β1), TGF-β2, TGF-β3, fibroblast growth factor 2, and vascular endothelial growth factor were found. The surprising lack of phenotype in the chm-I-deficient mice suggests either a different function for chm-I in vivo than has been proposed or compensatory changes in uninvestigated angiogenic or angiogenesis-inhibiting factors. Further analysis using double-knockout technology will be necessary to analyze the function of chm-I in the complex process of enchondral ossification

Adhesive Properties of the Hyaluronan Pericellular Coat in Hyaluronan Synthases Overexpressing Mesenchymal Stem Cells

Hyaluronan (HA), a natural component of the extracellular matrix, is supposed to have a regulatory function in the stem cell niche. Bone marrow-derived human mesenchymal stem cells (hMSCs) are known to express all three hyaluronan synthases (HASes), which are responsible for HA production. HA is extruded into the extracellular matrix, but also stays bound to the plasma membrane forming a pericellular coat, which plays a key role during early cell adhesion. Since HAS isoenzymes, HAS1, HAS2 and HAS3, produce HA with different molecular weights, a difference in their role for cell adhesion is expected. Here, we transduced the immortalized hMSC cell line SCP1 to constitutively express eGFP-tagged HASes (SCP1-HAS-eGFP) by lentiviral gene transfer. The overexpression of the HAS-eGFP was shown on RNA and protein levels, HA was determined by ELISA and the stained HA-coat was analyzed using confocal microscopy. Time-lapse microscopy, spreading assay and single cell force spectroscopy using atomic force microscopy were applied to characterize adhesion of the different HAS transduced SCP1 cells. We showed in this study that HAS3 overexpressing cells formed the thickest pericellular coat compared with control or HAS1 and HAS2 transduced cells. Furthermore, SCP1-HAS3-eGFP displayed faster and stronger adhesion compared to cells overexpressing the other synthases or control cells. We conclude that overexpression of HASes in hMSCs differentially modulates their initial adhesive interactions with the substrate. This observation might be helpful in regenerative medicine goals