Plant invasions differentially affected by diversity and dominant species in native‐ and exotic‐dominated grasslands

Plant invasions are an increasingly serious global concern, especially as the climate changes. Here, we explored how plant invasions differed between native‐ and novel exotic‐dominated grasslands with experimental addition of summer precipitation in Texas in 2009. Exotic species greened up earlier than natives by an average of 18 days. This was associated with a lower invasion rate early in the growing season compared to native communities. However, invasion rate did not differ significantly between native and exotic communities across all sampling times. The predictors of invasion rate differed between native and exotic communities, with invasion being negatively influenced by species richness in natives and by dominant species in exotics. Interestingly, plant invasions matched the bimodal pattern of precipitation in Temple, Texas, and did not respond to the pulse of precipitation during the summer. Our results suggest that we will need to take different approaches in understanding of invasion between native and exotic grasslands. Moreover, with anticipated increasing variability in precipitation under global climate change, plant invasions may be constrained in their response if the precipitation pulses fall outside the normal growing period of invaders.     

16,16-dimethyl prostaglandin E2 modulation of endothelial monolayer paracellular barrier function

Prostaglandins prevent gastrointestinal mucosal injury and promote healing following mucosal injury by various noxious agents. Preservation or repair of microvascular function appears to be crucial in these processes. The processes involved in prostaglandin-mediated repair and preservation of endothelial function are unclear. In the present study, we investigated the role of prostaglandins on endothelial paracellular barrier function using the filter-grown bovine aortic endothelial cell monolayers. Endothelial paracellular barrier function was assessed using a paracellular marker, mannitol. Prostaglandin analogs 16,16-dimethyl prostaglandin E₂ (DMPGE₂) and prostaglandin I₂ (PGI₂) caused an enhancement of endothelial monolayer paracellular barrier function as evidenced by a dose-dependent decrease in endothelial paracellular permeability. DMPGE₂ induced enhancement of endothelial paracellular barrier function correlated directly with increasing intracellular cAMP levels. Agents which increase intracellular cAMP levels at different stages of cAMP amplification cascade including phosphodiesterase inhibitor (3-isobutyl-1 methylxanthine [IBMX]), membrane permeable cAMP (8-bromo cAMP), and adenylate cyclase activators (isoproterenol and forskolin) also produced enhancement in endothelial paracellular barrier function. DMPGE₂ enhancement of paracellular barrier function correlated with dense accumulation of actin microfilaments near the intercellular junctions. IBMX, isoproterenol, forskolin, and 8-bromo cAMP also produced similar changes in endothelial actin microfilaments. Cytochalasin B prevented the DMPGE₂ enhancement of paracellular barrier function. Indomethacin (INDO), a cyclooxygenase inhibitor, caused a dose-dependent increase in endothelial paracellular permeability. Pharmacologic doses of INDO resulted in condensation and disruption of actin microfilaments with formation of large paracellular openings or gaps between the adjacent cells. Pretreatment of endothelial monolayers with DMPGE₂ prevented INDO-induced disturbance of actin microfilaments and paracellular barrier function. IBMX, isoproterenol, forskolin, and 8-bromo cAMP also prevented INDO-induced changes in actin microfilaments and paracellular barrier function. These findings indicate that DMPGE₂ has a paracellular barrier enhancing effect on filter-grown endothelial monolayers. This effect appears to be mediated through intracellular cAMP and actin microfilaments. © 1996 Wiley-Liss, Inc.     

mAtNOS1 induces apoptosis of human mammary adenocarcinoma cells

mAtNOS1 is a novel gene recently reported in mammalian genome with functions that are not fully understood. The present study shows that in human mammary adenocarcinoma MCF-7 cells, mAtNOS1 expression increases mitochondrial nitric oxide and calcium. Our study further shows that overexpression of mAtNOS1 induces apoptosis in MCF-7 cells by increasing mitochondrial protein tyrosine nitration and cytochrome c release. The present study suggests a novel function for mAtNOS1 in regulating mitochondrial nitric oxide and calcium and inducing apoptosis of MCF-7 cells.     

Highly Efficient Solar‐Driven Carbon Dioxide Reduction on Molybdenum Disulfide Catalyst Using Choline Chloride‐Based Electrolyte

Conversion of CO₂ to energy‐rich chemicals using renewable energy is of much interest to close the anthropogenic carbon cycle. However, the current photoelectrochemical systems are still far from being practically feasible. Here the successful demonstration of a continuous, energy efficient, and scalable solar‐driven CO₂ reduction process based on earth‐abundant molybdenum disulfide (MoS₂) catalyst, which works in synergy with an inexpensive hybrid electrolyte of choline chloride (a common food additive for livestock) and potassium hydroxide (KOH) is reported. The CO₂ saturated hybrid electrolyte utilized in this study also acts as a buffer solution (pH ≈ 7.6) to adjust pH during the reactions. This study reveals that this system can efficiently convert CO₂ to CO with solar‐to‐fuel and catalytic conversion efficiencies of 23% and 83%, respectively. Using density functional theory calculations, a new reaction mechanism in which the water molecules near the MoS₂ cathode act as proton donors to facilitate the CO₂ reduction process by MoS₂ catalyst is proposed. This demonstration of a continuous, cost‐effective, and energy efficient solar driven CO₂ conversion process is a key step toward the industrialization of this technology.     

Plasma membrane estrogen receptors signal to antiapoptosis in breast cancer

Chemotherapy or irradiation treatment induces breast cancer cell apoptosis, but this can be limited by estradiol (E2) through unknown mechanisms. To investigate this, we subjected estrogen receptor-expressing human breast cancer cells (MCF-7 and ZR-75-1) to paclitaxel (taxol) or to UV irradiation. Marked increases in cell apoptosis were induced, but these were significantly reversed by incubation with E2. Taxol or UV stimulated c-Jun N-terminal kinase (JNK) activity, which was inhibited by E2. Expression of a dominant-negative Jnk-1 protein strongly prevented taxol- or UV-induced apoptosis, whereas E2 inhibition of apoptosis was reversed by expression of constituitively active Jnk-1. As targets for participation in apoptosis, Bcl-2 and Bcl-xl were phosphorylated in response to JNK activation by taxol or UV; this was prevented by E2. Taxol or UV activated caspase activity in a JNK-dependent fashion and caused the cleavage of procaspase-9 to caspase-9, each inhibited by E2. Independently, the steroid also activated extracellular signal-regulated protein kinase activity, which contributed to the antiapoptotic effects. We report novel and rapid mechanisms by which E2 prevents chemotherapy or radiation-induced apoptosis of breast cancer, probably mediated through the plasma membrane estrogen receptor.     

A process for purifying xylosugars of pre-hydrolysis liquor from kraft-based dissolving pulp production process

Background

In the kraft-based dissolving pulp production process, pre-hydrolysis liquor (PHL) is produced, which contains hemicelluloses, lignin, furfural and acetic acid. PHL is currently burned in the recovery boiler of the kraft pulping process, but it can be utilized for the generation of high-valued products, such as xylitol and xylanase, via fermentation processes. However, some PHL constituents, e.g., furfural and lignin, are contaminants for fermentation processes and they must be eliminated for production of value-added products.

Results

In this work, a process is introduced for removing contaminants of PHL. Ca(OH)₂ treatment is the first step of this process, which removed 41.2% of lignin and negligible amount of sugars. In this step, a notable increase in the concentration of acetic acid was achieved (ranging from 6.2 to 11.7 g/L). In the second step, the implementation of adsorption using activated carbon (AC) at 1 wt% dosage led to additional 32% lignin and 5.9% xylosugar removals. In addition, laccase assisted activated carbon treatment led to further removal of lignin via accelerating lignin polymerization and adsorption on AC (i.e., removal from PHL). Overall, 90.7% of lignin, 100% of furfural, 5.7% of xylose, and 12% of xylan were removed from PHL, while the concentration of acetic acid became twofolds in the PHL.

Conclusions

This study reports an attractive process for purifying sugars and acetic acid of PHL. This process may be implemented for producing sugar-based value-added products from PHL. It also discusses the mechanism of Ca(OH)₂ treatment, AC adsorption and laccase assisted activated carbon treatment for lignin removal.

     

BRCA1 inhibits membrane estrogen and growth factor receptor signaling to cell proliferation in breast cancer

BRCA1 mutations and estrogen use are risk factors for the development of breast cancer. Recent work has identified estrogen receptors localized at the plasma membrane that signal to cell biology. We examined the impact of BRCA1 on membrane estrogen and growth factor receptor signaling to breast cancer cell proliferation. MCF-7 and ZR-75-1 cells showed a rapid and sustained activation of extracellular signal-related kinase (ERK) in response to estradiol (E2) that was substantially prevented by wild-type (wt) but not mutant BRCA1. The proliferation of MCF-7 cells induced by E2 was significantly inhibited by PD98059, a specific ERK inhibitor, or by dominant negative ERK2 expression and by expression of wt BRCA1 (but not mutant BRCA1). E2 induced the synthesis of cyclins D1 and B1, the activity of cyclin-dependent kinases Cdk4 and CDK1, and G(1)/S and G(2)/M cell cycle progression. The intact tumor suppressor inhibited all of these. wt BRCA1 also inhibited epidermal growth factor and insulin-like growth factor I-induced ERK and cell proliferation. The inhibition of ERK and cell proliferation by BRCA1 was prevented by phosphatase inhibitors and by interfering RNA knockdown of the ERK phosphatase, mitogen-activated kinase phosphatase 1. Our findings support a novel tumor suppressor function of BRCA1 that is relevant to breast cancer and identify a potential interactive risk factor for women with BRCA1 mutations.