Biology and management of Japanese beetle

Abstract supplied by cataloger."This publication is partially funded by a USDA NIFA grant in the Crop Protection and Pest Management Program."An informational article about how to identify and manage Japanese beetles.Written by: Kelsey J. Benthall (GRA, Division of Plant Sciences, University of Missouri), Emily R. Althoff (GRA, Division of Plant Sciences, University of Missouri), Kevin B. Rice (Assistant Professor, Division of Plant Sciences, University of Missouri)New 7/2

Intraspecific and Diffuse Competition: The Response of Nassella pulchra in a California Grassland

In inland California grasslands, the high densities of alien annual species have altered the growing environment for native perennial grasses. Using variable-density plots, we measured the influence of intraspecific competition (conspecifics only) and diffuse competition (mixed-composition neighborhoods that include conspecifics) on growth and survival of Nassella pulchra, purple needlegrass. We assessed the effects of intraspecific and diffuse competition in weeded plots and unweeded plots, respectively, across a density gradient of N. pulchra plants (16–356 plants/m2). We used summer fire and spring sheep grazing to reduce diffuse competition in unweeded plots. The potential effect of rooting volume on competitive interactions was explored by establishing plots on two sites of different soil depth. Diffuse competition had an overriding influence on N. pulchra growth in all treatments. Intraspecific competitive effects were apparent only in the absence of diffuse competition. The effects of grazing and soil depth on growth were only short-lived interactions with the burning treatment. Burning was a longer-lived interaction, but only in weeded plots. Plant mortality was significantly increased by diffuse competition. Overall, N. pulchra survival was greatest in weeded plots, in grazed plots, and in deeper soil plots. The growth of N. pulchra individuals was negatively affected by alien annual species in all treatment combinations. Our data indicate that recruitment of N. pulchra within inland California grasslands is reduced by the adverse environment created by high densities of alien annual species. Successful attempts to increase populations of N. pulchra through management of the grassland community must involve significant modification of the biotic environment

Effect of aging on cellular mechanotransduction

Aging is becoming a critical heath care issue and a burgeoning economic burden on society. Mechanotransduction is the ability of the cell to sense, process, and respond to mechanical stimuli and is an important regulator of physiologic function that has been found to play a role in regulating gene expression, protein synthesis, cell differentiation, tissue growth, and most recently, the pathophysiology of disease. Here we will review some of the recent findings of this field and attempt, where possible, to present changes in mechanotransduction that are associated with the aging process in several selected physiological systems, including musculoskeletal, cardiovascular, neuronal, respiratory systems and skin

LOWER LEG MORPHOLOGY AND STRETCH-SHORTENING CYCLE PERFORMANCE IN YOUNG AND ELDERLY MALES

The purpose of this investigation was to examine bone and muscle characteristics of the lower leg and stretch-shortening cycle capabilities of the ankle in young (22.3 ± 1.3 yrs) and elderly (67.5 ± 3.3 yrs) males. Peripheral quantitiative computed tomography (pQCT) was utilized to assess bone stress-strain index, bone ultimate fracture load, muscle density, muscle cross-sectional area (CSA), fat CSA and muscle+bone CSA. Maximal voluntary isometric plantarflexion (MVIP) force and force-velocity measurments during a countermovement hop (CMH) and drop hops from 20, 30 and 40 cm (DH20, DH30, DH40) were also measured. Bone stress-strain index was significantly higher in young males as well as muscle density, muscle CSA and muscle+bone CSA in comparison to elderly males. MVIP peak force and rate of force development was significantly higher in young males in comparsion to elderly males as well. An analysis of the force-velocity curves indicated that young males had significanlty higher levels of force and velocity in both the eccentric and concentric phase during the CMH, DH20, DH30 and DH40 in comparsion to elderly males. The data from this investigation indicate that aging potentially negatively influences lower leg bone and muscle strength and this may be reflected in lower stretch-shortening cycle capabilities of the ankle

Uniaxial stretch-induced regulation of mitogen-activated protein kinase, Akt and p70S6 kinase in the ageing Fischer 344 × Brown Norway rat aorta

The effects of ageing on the cardiovascular system contribute to substantial alterations in cellular morphology and function. The variables regulating these changes are unknown; however, one set of signalling molecules that may be of particular importance in mediating numerous cellular responses, including control of cell growth, differentiation and adaptation, are the proteins associated with the mitogen-activated protein kinase (MAPK) signalling systems. The MAPKs, in conjunction with the p70 S6k signalling cascade, have emerged as critical components for regulating numerous mechanotransduction-related cellular responses. Here we investigate the ability of uniaxial stretch to activate the MAPK and p70 S6k pathways in adult (6-month-old), aged (30-month-old) and very aged (36-month-old) Fischer 344/NNiaHSd × Brown Norway/BiNia (FBN) rats. Western blotting of the MAPK family proteins extracellular signal-regulated kinase (Erk) 1/2, p38- and c-Jun NH2-terminal kinase (Jnk)-MAPKs showed differential expression and activation between these proteins with age. An acute 15 min interval of 20% uniaxial stretch using an ex vivo aortic preparation demonstrated similar regulation of Erk1/2, p38- and Jnk-MAPK. However, ageing altered uniaxial induced p70 S6k pathway signalling. These observations confirm previous data demonstrating that MAPK proteins are mechanically regulated and also suggest that p70 S6k signalling expression and activation are controlled differently with ageing. Taken together, these data may help to explain, in part, the age-related changes in vascular morphology, function and response to injury

A Systematic Review of Genetic Influence on Psychological Resilience

When exposed to adversity, some individuals are at an increased risk of posttraumatic stress disorder, experiencing persistent biopsychosocial disturbances, whereas others adapt well, described as resilience. Resilience is a complex biopsychosocial phenomenon conceptualized as adaptation to adversity influenced by an individual’s genetic variants, epistasis, epigenetics, and gene-by-environment interactions. Studies on psychological resilience have focused on behavioral and psychosocial variables with far less examination of the genetic contributions. The purpose of this review is to identify specific genetic variants contributing to the biological capacity for psychological resilience. PubMed and PsycINFO were searched using the following key words: psychological resilience AND genotype(s). Additional articles were identified from the Human Genome Epidemiology Navigator using the term resilience, psychological. Ten studies met the criteria. Six genes were empirically associated with psychological resilience: serotonin-transporter-linked polymorphic region (5-HTTLPR), dopamine receptor D4, brain-derived neurotrophic factor (BDNF), corticotropin-releasing hormone receptor 1, oxytocin receptor and regulator of G-protein signaling 2. The findings of this systematic review suggest that the L/L or L′/L′ genotype of 5-HTTLPR and rs25531 in children/adolescents and the S/S or S′/S′ genotype in adults are most frequently related to resilience. Additionally, the Val/Val genotype of rs6265 in BDNF in Caucasians was also associated with resilience. There are numerous factors contributing to the complexity of determining the genetic influence on resilience including analysis of rs25531, assumptions of the mode of inheritance, operationalization of resilience, demographic and population characteristics, sample size, and other types of genetic influence including epistasis and epigenetics. While current evidence is supportive, further investigation of the genetic influence on resilience is required

Fluprostenol-Induced MAPK Signaling is Independent of Aging in Fischer 344/NNiaHSd x Brown Norway/BiNia Rat Aorta

The factors that regulate vascular mechanotransduction and how this process may be altered with aging are poorly understood and have not been widely studied. Recent data suggest that increased tissue loading can result in the release of prostaglandin F2 alpha (PGF2α) and other reports indicate that aging diminishes the ability of the aged aorta to activate mitogen activated protein kinase (MAPK) signaling in response to increased loading. Using ex vivo incubations, here we investigate whether aging affects the ability of the aorta to induce phosphorylation of extracellular signal-regulated kinase 1/2 (ERK½-MAPK), p38-MAPK, and Jun N-terminal kinase (JNK-MAPK) activation following stimulation with a PGF2α analog, fluprostenol. Compared to aortas from 6-mo animals, the amounts of ERK½- and p38-MAPK remained unchanged with aging, while the level of JNK-MAPK protein increased by 135% and 100% at 30- and 36-mo, respectively. Aging increased the basal phosphorylation of ERK½ (115% and 47%) and JNK (29% and 69%) (p \u3c0.05) in 30- and 36-mo aortas, while p38 phosphorylation levels remained unaltered. Compared to age-matched controls, fluprostenol induced phosphorylation of ERK½ (310%, 286%, and 554%), p38-MAPK (unchanged, 48%, and 148%), and JNK (78%, 88%, and 95%) in 6-, 30- and 36-mo aortas, respectively. These findings suggest that aging does not affect the ability of the rat aorta to activate ERK½-, p38-MAPK, and JNK-MAPK phosphorylation in response to PGF2α stimulation

Diabetes alters vascular mechanotransduction: pressure-induced regulation of mitogen activated protein kinases in the rat inferior vena cava

BACKGROUND: Diabetes mellitus is an important risk factor for increased vein graft failure after bypass surgery. However, the cellular and molecular mechanism(s) underlying vessel attrition in this population remain largely unexplored. Recent reports have suggested that the pathological remodeling of vein grafts may be mediated by mechanically-induced activation of the mitogen activated protein kinase (MAPK) signaling pathways and the MAPK-related induction of caspase-3 activity. On the basis of these findings, we hypothesized that diabetes may be associated with alterations in how veins "sense" and "respond" to altered mechanical loading. METHODS: Inferior venae cavae (IVC) from the non-diabetic lean (LNZ) and the diabetic obese (OSXZ) Zucker rats were isolated and incubated ex vivo under basal or pressurized conditions (120 mmHg). Protein expression, basal activation and the ability of increased pressure to activate MAPK pathways and apoptosis-related signaling was evaluated by immunoblot analysis. RESULTS: Immunoblot analyses revealed differential expression and activation of extracellular signal-regulated kinase (ERK1/2), p38 and c-Jun NH2-terminal kinase (JNK) MAPKs in the IVCs of diabetic rats as compared to non-diabetic rats. In particular, the expression and basal phosphorylation of p38β- (52.3 ± 11.8%; 45.8 ± 18.2%), JNK 1- (21.5 ± 9.3%; 19.4 ± 11.6%) and JNK3-MAPK (16.8 ± 3.3%; 29.5 ± 17.6%) were significantly higher (P < 0.05) in the diabetic vena cava. An acute increase in IVC intraluminal pressure failed to increase the phosphorylation of ERK1-, JNK-2, or any of the p38-MAPKs in the diabetic obese Zucker rats. Also, IVC loading in the LNZ led to a 276.0 ± 36.0% and 85.8 ± 25.1% (P < 0.05) increase in the cleavage of caspase-3 and caspase-9, respectively, with no effect on these molecules in the OSXZ. No differences were found in the regulation of Bax and Bcl-2 between groups. However, basal expression levels of Akt, phospho-Akt, PTEN, phospho-PTEN and phospho-Bad were higher in the diabetic venae cavae (P < 0.05). CONCLUSION: These data suggest that diabetes is associated with significant alteration in the ability of the vena cava to activate MAPK- and apoptosis-related signaling. Whether these changes are associated with the increased vein graft attrition seen in the diabetic population will require further investigation