Non-indigenous grasses impede woody succession

With the proliferation of old fields and the decline of native grasslands in North America, non-indigenous grasses, which tend to colonize and dominate North American old fields, have become progressively more abundant. These new grasses can differ from native grasses in a number of ways, including root and shoot morphology (e.g., density of root mat, height of shoots), growth phenology (e.g., cool season vs. warm season growth), and plant–soil–water relations due to differences in photosynthetic physiology (C₃ vs. C₄). Woody plants have been slow to colonize some old fields in the prairie-forest border area of North America and it is hypothesized that non-indigenous grasses may be contributing to the poor establishment success of woody plants in this region, possibly through more intense competition for resources. To test this hypothesis, a multi-factorial field experiment was conducted in which water, nitrogen, and grass functional group (non-indigenous C₃ and native C₄ species) were manipulated in a study of survival of oak seedlings. The grass type variously affected some of the different growth measurements, however, the effects of grass type on seedling growth were small compared to the effects on seedling survival. The results showed that when grown under dry conditions, seedlings growing in non-indigenous grasses experienced up to a 50% reduction in survival compared to those growing in native grasses under the same conditions. Analyses of root and shoot competition showed that the cause for the reduced survival in the non-indigenous grasses was due primarily to underground processes. The findings confirmed our initial hypothesis that non-indigenous grasses are likely contributing to the poor establishment success of woody plants in these old fields. However, the explanation for the reduced oak seedling survival in non-indigenous grasses does not appear to be due to reduced resource availability since soil water levels did not differ between non-indigenous and native grass plots and other resource levels measured (light, NO₃, and NH₄) were higher in non-indigenous grass plots under dry conditions. An alternative explanation is that the non-indigenous grasses modify the soil environment in ways that, under dry conditions, are deleterious to emerging oak seedlings. Since current climate projections for the upper Midwest are for hotter and drier summers, the results suggest that the resistance of these old fields to oak encroachment will likely increase in the future.     

Consequences of Low Dose Ionizing Radiation Exposure on the Hippocampal Microenvironment

The response of the brain to irradiation is complex, involving a multitude of stress inducible pathways that regulate neurotransmission within a dynamic microenvironment. While significant past work has detailed the consequences of CNS radiotherapy following relatively high doses (≥ 45 Gy), few studies have been conducted at much lower doses (≤ 2 Gy), where the response of the CNS (like many other tissues) may differ substantially from that expected from linear extrapolations of high dose data. Low dose exposure could elicit radioadaptive modulation of critical CNS processes such as neurogenesis, that provide cellular input into hippocampal circuits known to impact learning and memory. Here we show that mice deficient for chemokine signaling through genetic disruption of the CCR2 receptor exhibit a neuroprotective phenotype. Compared to wild type (WT) animals, CCR2 deficiency spared reductions in hippocampal neural progenitor cell survival and stabilized neurogenesis following exposure to low dose irradiation. While radiation-induced changes in microglia levels were not found in WT or CCR2 deficient animals, the number of Iba1+ cells did differ between each genotype at the higher dosing paradigms, suggesting that blockade of this signaling axis could moderate the neuroinflammatory response. Interestingly, changes in proinflammatory gene expression were limited in WT animals, while irradiation caused significant elevations in these markers that were attenuated significantly after radioadaptive dosing paradigms in CCR2 deficient mice. These data point to the importance of chemokine signaling under low dose paradigms, findings of potential significance to those exposed to ionizing radiation under a variety of occupational and/or medical scenarios.     

Flow regulation of collecting duct endothelin-1 production

Collecting duct (CD) endothelin-1 (ET-1) is an important autocrine inhibitor of CD Na(+) reabsorption. Salt loading is thought to increase CD ET-1 production; however, definitive evidence of this, as well as understanding of the mechanisms transducing this effect, is lacking. Tubule fluid flow increases in response to Na(+) loading; hence, we studied flow modulation of CD ET-1 production. Three days of a high-salt diet increased mouse and rat inner medullary CD (IMCD) ET-1 mRNA expression. Acute furosemide infusion increased urinary ET-1 excretion in anesthetized rats. Primary cultures of mouse or rat IMCD detached in response to flow using a closed perfusion chamber, consequently a CD cell line (mpkCCDcl4) was examined. Flow increased ET-1 mRNA at shear stress rates exceeding 1 dyne/cm(2), with the maximal effect seen between 2 and 10 dyne/cm(2). Induction of ET-1 mRNA was first evident after 1 h, and most apparent after 2 h, of flow. Inhibition of calmodulin or dihydropyridine-sensitive Ca(2+) channels did not alter the flow response; however, chelation of intracellular Ca(2+) or removal of extracellular Ca(2+) largely prevented flow-stimulated ET-1 mRNA accumulation. Downregulation of protein kinase C (PKC) using phorbol 12-myristate 13-acetate, or PKC inhibition with calphostin C, markedly reduced flow-stimulated ET-1 mRNA levels. Flow-stimulated ET-1 mRNA accumulation was abolished by inhibition of phospholipase C (PLC). Taken together, these data indicate that flow increases CD ET-1 production and this is dependent on extracellular and intracellular Ca(2+), PKC, and PLC. These studies suggest a novel pathway for coupling alterations in extracellular fluid volume to CD ET-1 production and ultimately control of CD Na(+) reabsorption.     

Trends in sheltering and welfare at the Hawaiian Humane Society, Oahu, Hawaii

One of the major goals of an animal welfare organization is to reduce the number of homeless, nonhuman animals in a community. In Hawaii, the Hawaiian Humane Society has provided numerous animal welfare services to work toward this goal, such as offering sterilizations and microchipping at reduced rates and facilitating animal adoptions and education. In addition, the Leash Law and the Cat Identification Program have increased animal welfare through increasing the responsibilities of companion animal caregivers (owners). The goal of this research was to assess if temporal changes in animal sheltering have occurred in Hawaii. The study assessed this by analyzing historical data on dogs (Canis familiaris) and cats (Felis catus) admitted, returned to owner, sterilized, euthanized, and adopted from the Humane Societies of Oahu, Hawaii, from 1993 to 2008. The study also analyzed dog and cat admittance and Honolulu population growth from 1975 to 2008. Sterilizations and pets returned to owners have increased significantly, whereas admittance and euthanasia rates have decreased significantly. Thus, although these data cannot conclusively state that there are fewer homeless animals in Hawaii, the results provide positive indicators of reducing homeless pets, especially when coupled with an increase in both the human population of Honolulu County and dog ownership.     

Estradiol promotes the development of a fibrotic phenotype and is increased in the serum of patients with systemic sclerosis

Introduction

Systemic sclerosis (SSc) is more prevalent in women. Our goal is to determine the effects of 17β-estradiol (E2) on the development of fibrosis and to compare circulating levels of estrogens in SSc patients and healthy controls.

Methods

Using primary human dermal fibroblasts, we evaluated the effect of E2 on fibronectin (FN) expression with and without the estrogen receptor (ER) antagonist ICI 182,780, inhibitors of signaling, propyl-pyrazole-triol, an ERα specific ligand, and genistein, an ERβ selective ligand, to identify the signaling pathways mediating E2''s effect. We confirmed the fibrotic effect of E2 in human skin using an ex vivo organ culture model. Lastly, we measured levels of E2 and estrone in serum samples from SSc patients with diffuse cutaneous involvement and healthy controls using mass spectrometry.

Results

E2 increased expression of FN in dermal fibroblasts. ICI 182,780, inositol-1,4,5-triphosphate inhibitor, and p38 mitogen-activated protein kinase inhibitor blocked the effects of E2 on FN. Propyl-pyrazole-triol, but not genistein, significantly increased FN expression. Ex vivo, E2 induced fibrosis of human skin. The effects of E2 were abrogated by ICI 182,780. Circulating levels of E2 and estrone were significantly increased in sera of patients with diffuse cutaneous SSc.

Conclusion

Our findings implicate estrogens in the fibrotic process and may explain the preponderance of SSc in women. ICI 182,780 or other ER signaling antagonists may be effective agents for the treatment of fibrosis.     

Spread of Academic Success in a High School Social Network

Application of social network analysis to education has revealed how social network positions of K-12 students correlate with their behavior and academic achievements. However, no study has been conducted on how their social network influences their academic progress over time. Here we investigated correlations between high school students’ academic progress over one year and the social environment that surrounds them in their friendship network. We found that students whose friends’ average GPA (Grade Point Average) was greater (or less) than their own had a higher tendency toward increasing (or decreasing) their academic ranking over time, indicating social contagion of academic success taking place in their social network.     

Combining Functional and Structural Genomics to Sample the Essential Burkholderia Structome

Background

The genus Burkholderia includes pathogenic gram-negative bacteria that cause melioidosis, glanders, and pulmonary infections of patients with cancer and cystic fibrosis. Drug resistance has made development of new antimicrobials critical. Many approaches to discovering new antimicrobials, such as structure-based drug design and whole cell phenotypic screens followed by lead refinement, require high-resolution structures of proteins essential to the parasite.

Methodology/Principal Findings

We experimentally identified 406 putative essential genes in B. thailandensis, a low-virulence species phylogenetically similar to B. pseudomallei, the causative agent of melioidosis, using saturation-level transposon mutagenesis and next-generation sequencing (Tn-seq). We selected 315 protein products of these genes based on structure-determination criteria, such as excluding very large and/or integral membrane proteins, and entered them into the Seattle Structural Genomics Center for Infection Disease (SSGCID) structure determination pipeline. To maximize structural coverage of these targets, we applied an “ortholog rescue” strategy for those producing insoluble or difficult to crystallize proteins, resulting in the addition of 387 orthologs (or paralogs) from seven other Burkholderia species into the SSGCID pipeline. This structural genomics approach yielded structures from 31 putative essential targets from B. thailandensis, and 25 orthologs from other Burkholderia species, yielding an overall structural coverage for 49 of the 406 essential gene families, with a total of 88 depositions into the Protein Data Bank. Of these, 25 proteins have properties of a potential antimicrobial drug target i.e., no close human homolog, part of an essential metabolic pathway, and a deep binding pocket. We describe the structures of several potential drug targets in detail.

Conclusions/Significance

This collection of structures, solubility and experimental essentiality data provides a resource for development of drugs against infections and diseases caused by Burkholderia. All expression clones and proteins created in this study are freely available by request.     

Exercise Protects against Diet-Induced Insulin Resistance through Downregulation of Protein Kinase Cβ in Mice

Physical exercise is an important and effective therapy for diabetes. However, its underlying mechanism is not fully understood. Protein kinase Cβ (PKCβ) has been suggested to be involved in the pathogenesis of obesity and insulin resistance, but the role of PKCβ in exercise-induced improvements in insulin resistance is completely unknown. In this study, we evaluated the involvement of PKCβ in exercise-attenuated insulin resistance in high-fat diet (HFD)-fed mice. PKCβ^-/- and wild-type mice were fed a HFD with or without exercise training. PKC protein expression, body and tissue weight change, glucose and insulin tolerance, metabolic rate, mitochondria size and number, adipose inflammation, and AKT activation were determined to evaluate insulin sensitivity and metabolic changes after intervention. PKCβ expression decreased in both skeletal muscle and liver tissue after exercise. Exercise and PKCβ deficiency can alleviate HFD-induced insulin resistance, as evidenced by improved insulin tolerance. In addition, fat accumulation and mitochondrial dysfunction induced by HFD were also ameliorated by both exercise and PKCβ deficiency. On the other hand, exercise had little effect on PKCβ^-/- mice. Further, our data indicated improved activation of AKT, the downstream signal molecule of insulin, in skeletal muscle and liver of exercised mice, whereas PKCβ deficiency blunted the difference between sedentary and exercised mice. These results suggest that downregulation of PKCβ contributes to exercise-induced improvement of insulin resistance in HFD-fed mice.