Harvester-Forwarder and Harvester-Yarder Systems for Fuel Reduction Treatments

Two harvesting systems were compared for reducing fuel loadings in overstocked conifer stands in eastern Oregon; forest managers also set a high priority on minimizing soil disturbance. Both employed cut-to-length (CTL) harvesters; one used a forwarder and the other a small skyline yarder. Both systems produced very similar and acceptable results in terms of fuels reduction and soil disturbance, but at different stump-to-mill costs: $46/green ton for the forwarder system versus$80/green ton for the yarder system

Real-time Alpine Measurement System Using Wireless Sensor Networks

International audienceMonitoring the snow pack is crucial for many stakeholders, whether for hydro-poweroptimization, water management or flood control. Traditional forecasting relies on regressionmethods, which often results in snow melt runoff predictions of low accuracy in non-averageyears. Existing ground-based real-time measurement systems do not cover enough physiographicvariability and are mostly installed at low elevations. We present the hardware and software designof a state-of-the-art distributedWireless Sensor Network (WSN)-based autonomous measurementsystem with real-time remote data transmission that gathers data of snow depth, air temperature,air relative humidity, soil moisture, soil temperature, and solar radiation in physiographicallyrepresentative locations. Elevation, aspect, slope and vegetation are used to select networklocations, and distribute sensors throughout a given network location, since they govern snowpack variability at various scales. Three WSNs were installed in the Sierra Nevada of NorthernCalifornia throughout the North Fork of the Feather River, upstream of the Oroville dam and multiplepowerhouses along the river. The WSNs gathered hydrologic variables and network health statisticsthroughout the 2017 water year, one of northern Sierra’s wettest years on record. These networksleverage an ultra-low-power wireless technology to interconnect their components and offer recoveryfeatures, resilience to data loss due to weather and wildlife disturbances and real-time topologicalvisualizations of the network health. Data show considerable spatial variability of snow depth, evenwithin a 1 km2 network location. Combined with existing systems, these WSNs can better detectprecipitation timing and phase in, monitor sub-daily dynamics of infiltration and surface runoffduring precipitation or snow melt, and inform hydro power managers about actual ablation andend-of-season date across the landscape

The Effects of Forest Fuel-Reduction Treatments in the United States

The current conditions of many seasonally dry forests in the western and southern United States, especially those that once experienced low- to moderate-intensity fire regimes, leave them uncharacteristically susceptible to high-severity wildfire. Both prescribed fire and its mechanical surrogates are generally successful in meeting short-term fuel-reduction objectives such that treated stands are more resilient to high-intensity wildfire. Most available evidence suggests that these objectives are typically accomplished with few unintended consequences, since most ecosystem components (vegetation, soils, wildlife, bark beetles, carbon sequestration) exhibit very subtle effects or no measurable effects at all. Although mechanical treatments do not serve as complete surrogates for fire, their application can help mitigate costs and liability in some areas. Desired treatment effects on fire hazards are transient, which indicates that after fuel-reduction management starts, managers need to be persistent with repeated treatment, especially in the faster-growing forests in the southern United States.Keywords: wildfire, forest conservation, forest management, fire surrogates, fire ecolog

MAPK ERK Signaling Regulates the TGF-β1-Dependent Mosquito Response to Plasmodium falciparum

Malaria is caused by infection with intraerythrocytic protozoa of the genus Plasmodium that are transmitted by Anopheles mosquitoes. Although a variety of anti-parasite effector genes have been identified in anopheline mosquitoes, little is known about the signaling pathways that regulate these responses during parasite development. Here we demonstrate that the MEK-ERK signaling pathway in Anopheles is controlled by ingested human TGF-β1 and finely tunes mosquito innate immunity to parasite infection. Specifically, MEK-ERK signaling was dose-dependently induced in response to TGF-β1 in immortalized cells in vitro and in the A. stephensi midgut epithelium in vivo. At the highest treatment dose of TGF-β1, inhibition of ERK phosphorylation increased TGF-β1-induced expression of the anti-parasite effector gene nitric oxide synthase (NOS), suggesting that increasing levels of ERK activation negatively feed back on induced NOS expression. At infection levels similar to those found in nature, inhibition of ERK activation reduced P. falciparum oocyst loads and infection prevalence in A. stephensi and enhanced TGF-β1-mediated control of P. falciparum development. Taken together, our data demonstrate that malaria parasite development in the mosquito is regulated by a conserved MAPK signaling pathway that mediates the effects of an ingested cytokine

Immunohistochemical analysis of oxidative stress and DNA repair proteins in normal mammary and breast cancer tissues

<p>Abstract</p> <p>Background</p> <p>During the course of normal cellular metabolism, oxygen is consumed and reactive oxygen species (ROS) are produced. If not effectively dissipated, ROS can accumulate and damage resident proteins, lipids, and DNA. Enzymes involved in redox regulation and DNA repair dissipate ROS and repair the resulting damage in order to preserve a functional cellular environment. Because increased ROS accumulation and/or unrepaired DNA damage can lead to initiation and progression of cancer and we had identified a number of oxidative stress and DNA repair proteins that influence estrogen responsiveness of MCF-7 breast cancer cells, it seemed possible that these proteins might be differentially expressed in normal mammary tissue, benign hyperplasia (BH), ductal carcinoma in situ (DCIS) and invasive breast cancer (IBC).</p> <p>Methods</p> <p>Immunohistochemistry was used to examine the expression of a number of oxidative stress proteins, DNA repair proteins, and damage markers in 60 human mammary tissues which were classified as BH, DCIS or IBC. The relative mean intensity was determined for each tissue section and ANOVA was used to detect statistical differences in the relative expression of BH, DCIS and IBC compared to normal mammary tissue.</p> <p>Results</p> <p>We found that a number of these proteins were overexpressed and that the cellular localization was altered in human breast cancer tissue.</p> <p>Conclusions</p> <p>Our studies suggest that oxidative stress and DNA repair proteins not only protect normal cells from the damaging effects of ROS, but may also promote survival of mammary tumor cells.</p

Sponge non-metastatic Group I Nme gene/protein - structure and function is conserved from sponges to humans

<p>Abstract</p> <p>Background</p> <p>Nucleoside diphosphate kinases NDPK are evolutionarily conserved enzymes present in Bacteria, Archaea and Eukarya, with human Nme1 the most studied representative of the family and the first identified metastasis suppressor. Sponges (Porifera) are simple metazoans without tissues, closest to the common ancestor of all animals. They changed little during evolution and probably provide the best insight into the metazoan ancestor's genomic features. Recent studies show that sponges have a wide repertoire of genes many of which are involved in diseases in more complex metazoans. The original function of those genes and the way it has evolved in the animal lineage is largely unknown. Here we report new results on the metastasis suppressor gene/protein homolog from the marine sponge <it>Suberites domuncula</it>, NmeGp1Sd. The purpose of this study was to investigate the properties of the sponge Group I Nme gene and protein, and compare it to its human homolog in order to elucidate the evolution of the structure and function of Nme.</p> <p>Results</p> <p>We found that sponge genes coding for Group I Nme protein are intron-rich. Furthermore, we discovered that the sponge NmeGp1Sd protein has a similar level of kinase activity as its human homolog Nme1, does not cleave negatively supercoiled DNA and shows nonspecific DNA-binding activity. The sponge NmeGp1Sd forms a hexamer, like human Nme1, and all other eukaryotic Nme proteins. NmeGp1Sd interacts with human Nme1 in human cells and exhibits the same subcellular localization. Stable clones expressing sponge NmeGp1Sd inhibited the migratory potential of CAL 27 cells, as already reported for human Nme1, which suggests that Nme's function in migratory processes was engaged long before the composition of true tissues.</p> <p>Conclusions</p> <p>This study suggests that the ancestor of all animals possessed a NmeGp1 protein with properties and functions similar to evolutionarily recent versions of the protein, even before the appearance of true tissues and the origin of tumors and metastasis.</p

Rosiglitazone Inhibits Transforming Growth Factor-β1 Mediated Fibrogenesis in ADPKD Cyst-Lining Epithelial Cells

BACKGROUND: Interstitial fibrosis plays an important role in progressive renal dysfunction in autosomal dominant polycystic kidney disease (ADPKD). In our previous studies, we confirmed that PPAR-γ agonist, rosiglitazone could protect renal function and prolong the survival of a slowly progressive ADPKD animal model by reducing renal fibrosis. However, the mechanism remains unknown. METHODS: Primary culture epithelial cells pretreated with TGF-β1 were incubated with rosiglitazone. Extracellular matrix proteins were detected using real-time PCR and Western blotting. MAPK and Smad2 phosphorylation were measured with western blot. ERK1/2 pathway and P38 pathway were inhibited with the specific inhibitors PD98059 and SB203580. The Smad2 pathway was blocked with the siRNA. To address whether PPAR-γ agonist-mediated inhibition of TGF-β1-induced collagen type I expression was mediated through a PPAR-γ dependent mechanism, genetic and pharmaceutical approaches were used to block the activity of endogenous PPARγ. RESULTS: TGF-β1-stimulated collagen type I and fibronectin expression of ADPKD cyst-lining epithelia were inhibited by rosiglitazone in a dosage-dependent manner. Smad2, ERK1/2 and P38 pathways were activated in response to TGF-β1; however, TGF-β1 had little effect on JNK pathway. Rosiglitazone suppressed TGF-β1 induced Smad2 activation, while ERK1/2 and P38MAPK signals remained unaffected. Rosiglitazone could also attenuate TGF-β1-stimulated collagen type I and fibronectin expression in primary renal tubular epithelial cells, but had no effect on TGF-β1-induced activation of Smad2, ERK1/2 and P38 pathways. There was no crosstalk between the Smad2 and MAPK pathways in ADPKD cyst-lining epithelial cells. These inhibitory effects of rosiglitazone were reversed by the PPARγ specific antagonist GW9662 and PPARγ siRNA. CONCLUSION: ADPKD cyst-lining epithelial cells participate in TGF-β1 mediated fibrogenesis. Rosiglitazone could suppress TGF-β1-induced collagen type I and fibronectin expression in ADPKD cyst-lining epithelia through modulation of the Smad2 pathway. Our study may provide therapeutic basis for clinical applications of rosiglitazone in retarding the progression of ADPKD