Enhanced nighttime fog and low stratus occurrence over the Landes forest, France

Understanding the drivers of fog and low stratus (FLS) cloud occurrence is important for traffic, ecosystems and climate models, but challenging to analyze due to the complex interactions between meteorological factors and land cover. Here, we use active and passive satellite data, as well as reanalysis data to investigate nighttime FLS occurrence over the expansive Landes forest in France from 2006-2015. We find significant FLS enhancement over the forest compared to surrounding areas, especially in summer and fall. Lower wind speed and lower temperatures are found over the forest at night, which can enhance FLS development over the forest. Still, other drivers, such as biovolatile organic compounds acting as cloud condensation nuclei, are most likely important as well. The results show that the influence of forests on boundary layer clouds is not limited to convective daytime conditions

Aggregates and Disrupted Dynein-Dependent Trafficking in ALS

Amyotrophic Lateral Sclerosis (ALS) is an adult-onset neuro-degenerative disease. The death of motor neurons leads to progressive paralysis of voluntary muscles, making patients unable to control their movements, and ultimately leads to paralysis of respiratory muscles and death. So far there is no effective treatment available. It is not clear how motor neurons die in ALS-patients. 10% of the ALS-cases are familial, and so far mutations in 6 genes have been identified in ALS-families. Mutations in the gene for SOD1 were the first to be discovered and account for up to 20% of familial ALS-cases. Most likely, mutant SOD1-protein is misfolded and accumulates in insoluble aggregates, that are toxic to motor neurons. In the studies described in this thesis, we use transgenic mice that express human mutant SOD1, and that develop paralysis and other pathological changes resembling ALS. We have studied changes in motor neurons in the spinal cord of these SOD1-ALS mice in great detail, and show that the appearance of aggregates is a very early phenomenon in these cells. In addition, motor neurons develop accumulations resembling a traffic jam, and a fragmented Golgi apparatus, an indication for disrupted cellular transport. Supporting cell-types, as astrocytes and microglia, are also affected in the spinal cord of SOD1-ALS mice. To study which cell-types are primarily responsible for the death of motor neurons, we developed transgenic mice with a restricted expression of mutant SOD1 in neurons. These mice develop similar pathological changes as SOD1-ALS mice, indicating that mutant SOD1 acting solely in neurons is sufficient to induce an ALS-like disease. Several studies have indicated that disruptions of axonal transport could cause motor neuron death. We have generated transgenic mice with a disruption of the retrograde microtubule motor dynein/dynactin, by expressing the dominant-negative linker protein BICD2-N in neurons. These mice have impaired retrograde axonal transport and develop cellular changes that resemble those found in SOD1-ALS-mice, like a disrupted Golgi apparatus and neurofilament accumulations. However, up to two years the mice are healthy and do not show any forms of paralysis. Moreover, if we cross these BICD2-N mice with SOD1-ALS mice, animals develop paralysis at a later age and survive longer, indicating that a disruption of retrograde transport could be beneficial for SOD1-linked ALS. Mutations in the gene for VAPB were most recently discovered in ALS-patients. We show that this relatively unknown protein is expressed at high levels in motor neurons in humans and mice and localizes to the Endoplasmic Reticulum. The ALS-linked mutation mislocalize

Time- and dose-dependent effects of curcumin on gene expression in human colon cancer cells

BACKGROUND: Curcumin is a spice and a coloring food compound with a promising role in colon cancer prevention. Curcumin protects against development of colon tumors in rats treated with a colon carcinogen, in colon cancer cells curcumin can inhibit cell proliferation and induce apoptosis, it is an anti-oxidant and it can act as an anti-inflammatory agent. The aim of this study was to elucidate mechanisms and effect of curcumin in colon cancer cells using gene expression profiling. METHODS: Gene expression changes in response to curcumin exposure were studied in two human colon cancer cell lines, using cDNA microarrays with four thousand human genes. HT29 cells were exposed to two different concentrations of curcumin and gene expression changes were followed in time (3, 6, 12, 24 and 48 hours). Gene expression changes after short-term exposure (3 or 6 hours) to curcumin were also studied in a second cell type, Caco-2 cells. RESULTS: Gene expression changes (>1.5-fold) were found at all time points. HT29 cells were more sensitive to curcumin than Caco-2 cells. Early response genes were involved in cell cycle, signal transduction, DNA repair, gene transcription, cell adhesion and xenobiotic metabolism. In HT29 cells curcumin modulated a number of cell cycle genes of which several have a role in transition through the G2/M phase. This corresponded to a cell cycle arrest in the G2/M phase as was observed by flow cytometry. Functional groups with a similar expression profile included genes involved in phase-II metabolism that were induced by curcumin after 12 and 24 hours. Expression of some cytochrome P450 genes was downregulated by curcumin in HT29 and Caco-2 cells. In addition, curcumin affected expression of metallothionein genes, tubulin genes, p53 and other genes involved in colon carcinogenesis. CONCLUSIONS: This study has extended knowledge on pathways or processes already reported to be affected by curcumin (cell cycle arrest, phase-II genes). Moreover, potential new leads to genes and pathways that could play a role in colon cancer prevention by curcumin were identified

Intrinsic plasticity complements long-term potentiation in parallel fiber input gain control in cerebellar Purkinje cells

Synaptic gain control and information storage in neural networks are mediated by alterations in synaptic transmission, such as in long-term potentiation (LTP). Here,weshowusingboth in vitroandin vivo recordingsfromthe rat cerebellum that tetanization protocols for the induction of LTP at parallel fiber (PF)-to-Purkinje cell synapsescanalsoevokeincreases in intrinsic excitability. Thisformof intrinsic plasticity shares with LTP a requirement for the activation of protein phosphatases 1, 2A, and 2B for induction. Purkinje cell intrinsic plasticity resembles CA1 hippocampal pyramidal cell intrinsic plasticity in that it requires activity of protein kinase A(PKA) and casein kinase 2 (CK2) and is mediated by a downregulation of SK-type calcium-sensitive K conductances. In addition, Purkinje cell intrinsic plasticity similarly results in enhanced spine calcium signaling. However, there are fundamental differences: first, while in the hippocampus increases in excitability result in a higher probability for LTP induction, intrinsic plasticity in Purkinj

Enhanced Nighttime Fog and Low Stratus Occurrence Over the Landes Forest, France

Understanding the drivers of fog and low stratus (FLS) cloud occurrence is important for traffic, ecosystems, and climate models, but it is challenging to analyze due to the complex interactions between meteorological factors and land cover. Here, we use active and passive satellite data, as well as reanalysis data to investigate nighttime FLS occurrence over the expansive Landes forest in France from 2006 to 2015. We find significant FLS enhancement over the forest compared to surrounding areas, especially in summer and fall. Lower wind speed and lower temperatures are found over the forest at night, which can enhance FLS development over the forest. Still, other drivers, such as biovolatile organic compounds acting as cloud condensation nuclei, are most likely important as well. The results show that the influence of forests on boundary layer clouds is not limited to convective daytime conditions

SK2 channel expression and function in cerebellar Purkinje cells

Small-conductance calcium-activated K(+) channels (SK channels) regulate the excitability of neurons and their responsiveness to synaptic input patterns. SK channels contribute to the afterhyperpolarization (AHP) following action potential bursts, and curtail excitatory postsynaptic potentials (EPSPs) in neuronal dendrites. Here we review evidence that SK2 channels are expressed in rat cerebellar Purkinje cells during development and throughout adulthood, and play a key role in diverse cellular processes such as the regulation of the spike firing frequency and the modulation of calcium transients in dendritic spines. In Purkinje cells as well as in other types of neurons, SK2 channel plasticity seems to provide an important mechanism allowing these cells to adjust their intrinsic excitability and to alter the probabilities for the induction of synaptic learning correlates, such as long-term potentiation (LTP)

Atmospheric Aridity and Apparent Soil Moisture Drought in European Forest During Heat Waves

Land-atmosphere feedbacks, in particular the response of land evaporation to vapor pressure deficit (VPD) or the dryness of the air, remain poorly understood. Here we investigate the VPD response by analysis of a large database of eddy covariance flux observations and simulations using a conceptual model of the atmospheric boundary layer. Data analysis reveals that under high VPD and corresponding high temperatures, forest in particular reduces evaporation and emits more sensible heat. In contrast, grass increases evaporation and emits less sensible heat. Simulations show that this VPD feedback can induce significant temperature increases over forest of up to 2 K during heat wave conditions. It is inferred from the simulations that the effect of the VPD feedback corresponds to an apparent soil moisture depletion of more than 50%. This suggests that previous studies may have incorrectly attributed the effects of atmospheric aridity on temperature to soil dryness.</p