Publications by authors named "Fred Allen"

A deficiency of thiamine (vitamin B1), an essential cofactor for enzymes involved in metabolic processes, can be caused by the enzyme thiaminase. Thiaminase in food stocks has been linked to morbidity and mortality due to thiamine depletion in many ecologically and economically important species. Thiaminase activity has been detected in certain bacteria, plants, and fish species, including carp.

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Switchgrass can be used as an alternative source for bioenergy production. Many breeding programs focus on the genetic improvement of switchgrass for increasing biomass yield. Quantitative trait loci (QTL) mapping can help to discover marker-trait associations and accelerate the breeding process through marker-assisted selection.

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Ecological research suggests increased diversity may improve ecosystem services, as well as yield stability; however, such theories are sometimes disproven by agronomic research, particularly at higher diversity levels. We conducted a meta-analysis on 2,753 studies in 48 articles published over the last 53 years to test: if biological N2 fixation (BNF) supplies adequate nitrogen (N) for plant growth relative to synthetic fertilizers; how crop physiological traits affect legume-grass symbiosis; and, how cultural practices affect BNF over a range of soils and climates overtime (in polycultures versus sole grasslands). Globally, net primary productivity (NPP; total aboveground production response of grass and legume in higher-diversity treatments) increased 44% via legume associations relative to sole grass controls (including both with and without N fertilizer).

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Vibrio tubiashii has been linked to disease outbreaks in molluscan species, including oysters, geoducks, and clams, and shellfish hatcheries in the Pacific Northwest have been plagued by intermittent vibriosis outbreaks since 2006. Like V. tubiashii, Vibrio coralliilyticus has recently been described as an oyster pathogen in addition to its role in coral disease.

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A combined effect of protein coating and plasma modification on the quality of the osteoblast-scaffold interaction was investigated. Three-dimensional polycaprolactone (PCL) scaffolds were manufactured by the precision extrusion deposition (PED) system. The structural, physical, chemical and biological cues were introduced to the surface through providing 3D structure, coating with adhesive protein fibronectin and modifying the surface with oxygen-based plasma.

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Mary E H Mandels, who spearheaded the US Army's national bioconversion studies for four decades and was an early proponent of conversion of waste biomass to readily bioconvertible sugars for the production of chemicals and transportation fuels such as ethanol, died 17 February 2008 at Natick, MA, USA. She was 90.

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Background: In a previous report, enhanced resource commitment at a Level I trauma center was associated with improved outcomes for most major categories of injured patients, except those with gunshot wounds, which disproportionately affected the young (ages 15 to 24 years). We hypothesized that a primary violence-prevention initiative geared toward changing attitudes about interpersonal conflict among at-risk youths can be effective.

Study Design: Between May 2002 and November 2003, 97 youths (mean age 12.

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Purpose: This study evaluated the stability of implants in 51 patients following a clinical protocol of immediate functional loading. The stability during the first 3 months following implant placement was assessed according to bone type, implant location, and patient gender.

Materials And Methods: Twenty-two male and 29 female patients were treated with 344 Brånemark System implants placed in edentulous bone or extraction sites and put into functional loading using the Teeth in a Day protocol.

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Twelve isoflavones were detected by high-performance liquid chromatography in seeds of 17 soybean [Glycine max (L.) Merrill] cultivars grown at three locations. 6' '-O-Malonyldaidzin and 6' '-O-malonylgenistin together constituted 71-81% of total isoflavones, which ranged in concentration from 2038 to 9514 microg/g and averaged 5644 microg/g across locations and cultivars.

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Nerve growth factor (NGF) is a well known neurotropic and neurotrophic agonist in the nervous system, which recently was shown to also induce angiogenic effects in endothelial cells (ECs). To measure NGF effects on the migration of cultured ECs, an important step in neoangiogenesis, we optimized an omnidirectional migration assay using human aortic endothelial cells (HAECs) and validated the assay with human recombinant basic fibroblast growth factor (rhbFGF) and human recombinant vascular endothelial growth factor (rhVEGF). The potencies of nerve growth factor purified from various species (viper, mouse, and recombinant human) to stimulate HAEC migration was similar to that of VEGF and basic fibroblast growth factor (bFGF) (EC50 of approximately 0.

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Endothelialization of artificial vascular grafts is rapid and complete in numerous animal models, including dogs and rats, but not in human patients. One possible explanation for this well-known, yet puzzling observation might be that monolayer formation of human endothelial cells (ECs), and of canine or rodent ECs, is affected differently by flow-induced shear stress. To begin testing this hypothesis, the authors wounded confluent monolayers of cultured rat and human ECs and exposed these cultures for 20 h to unidirectional steady laminar shear stress of 10 dyn/cm(2) induced by fluid flow perpendicular to the wound boundaries.

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Myosin-based cell contractile force is considered to be a critical process in cell motility. However, for epidermal growth factor (EGF)-induced fibroblast migration, molecular links between EGF receptor (EGFR) activation and force generation have not been clarified. Herein, we demonstrate that EGF stimulation increases myosin light chain (MLC) phosphorylation, a marker for contractile force, concomitant with protein kinase C (PKC) activity in mouse fibroblasts expressing human EGFR constructs.

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Background: Previously, we detected linkage of idiopathic Parkinson disease (PD) to the region on chromosome 6 that contains the Parkin gene (D6S305; logarithm of odds score, 5.47) in families with at least one individual with age at onset younger than 40 years (families with early-onset disease). Further study demonstrated the presence of Parkin mutations in this data set.

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Parkin, an E2-dependent ubiquitin protein ligase, carries pathogenic mutations in patients with autosomal recessive juvenile parkinsonism, but its role in the late-onset form of Parkinson's disease (PD) is not firmly established. Previously, we detected linkage of idiopathic PD to the region on chromosome 6 containing the Parkin gene (D6S305, logarithm of odds score, 5.47) in families with at least one subject with age at onset (AAO) younger than 40 years.

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Mitochondrial (mt) impairment, particularly within complex I of the electron transport system, has been implicated in the pathogenesis of Parkinson disease (PD). More than half of mitochondrially encoded polypeptides form part of the reduced nicotinamide adenine dinucleotide dehydrogenase (NADH) complex I enzyme. To test the hypothesis that mtDNA variation contributes to PD expression, we genotyped 10 single-nucleotide polymorphisms (SNPs) that define the European mtDNA haplogroups in 609 white patients with PD and 340 unaffected white control subjects.

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During wound healing, dermal fibroblasts switch from a migratory, repopulating phenotype to a contractile, matrix-reassembling phenotype. The mechanisms controlling this switch are unknown. A possible explanation is suggested by the finding that chemokines that appear late in wound repair prevent growth factor-induced cell-substratum de-adhesion by blocking calpain activation.

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To identify genes influencing age at onset (AAO) in two common neurodegenerative diseases, a genomic screen was performed for AAO in families with Alzheimer disease (AD; n=449) and Parkinson disease (PD; n=174). Heritabilities between 40%--60% were found in both the AD and PD data sets. For PD, significant evidence for linkage to AAO was found on chromosome 1p (LOD = 3.

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