Real-time frequency determination of acoustic emission for different fracture mechanisms in carbon/epoxy composites

Carbon/epoxy material in the form of a unidirectional composite was loaded under different conditions to determine the frequency content of acoustic emission signals. Special specimens, designed to fail under well-defined modes such as matrix cracking, debonding, fibre pull-out and fibre failure, were tested from zero load to failure. Real-time analysis of the acoustic signals was performed with a Dantec burst spectrum analyser permitting the detection of frequencies in a wide band around a certain central frequency. The signals analyzed ranged from 50 to 600 kHz and were distinguished as being released from four special types of failure. By using different types of specimen it was concluded that matrix cracking released frequencies between 90 and 180 kHz, fibre failure frequencies above 300 kHz, debonding frequencies between 240 and 310 kHz and pull-out frequencies between 180 and 240 kHz. A comparison with published values shows agreement with the frequency bands determined for matrix and fibre failure, while for the debonding and pull-out mechanisms the frequency bands turned out to be interchanged. It can still be concluded that these failure mechanisms generate frequencies between those of matrix failure and fibre fraction.     

Nitrogen fertilizer recommendations for arable crops as based on soil analysis

The present paper is a review of previous work by the senior author [5, 6, 7, 8].As demonstrated by experimental results for winter wheat, potatoes and sugar beet, soil tests for mineral nitrogen in early spring may be looked upon as a means of better assessing optimum fertilizer nitrogen requirements in commercial farming. A second soil test, at the onset of growth in potatoes and sugar beet, may be useful in considering nitrogen topdressings. It is recognized, however, that soil mineral nitrogen data do not provide a full explanation for the variation in optimum nitrogen dressings and other soil or climatic factors may be involved.     

Long-term personal exposure to traffic-related air pollution among school children, a validation study

Several recent studies suggest an association between long-term exposure to traffic-related air pollution and health. Most studies use indicators of exposure such as outdoor air pollution or traffic density on the street of residence. Little information is available about the validity of these measurements as an estimate of long-term personal exposure to traffic-related air pollution. In this pilot study, we assessed outdoor and personal exposure to traffic-related air pollution in children living in homes on streets with different degree of traffic intensity. The personal exposure of 14 children aged 9-12 years to 'soot', NO(x) (NO and NO(2)) was assessed in Amsterdam between March and June 2003. Each child's personal exposure was monitored during four repeated 48-h periods. Concurrently, in- and outdoor NO(x) measurements were carried out at the school and at the home of each participating child. Measurements were supplemented by a questionnaire on time activity patterns and possible indoor sources. Flow-controlled battery operated pumps in a made-to-fit backpack were used to sample personal exposure to 'soot', determined from the reflectance of PM(2.5) filters. Exposure to NO(x) was assessed using Ogawa passive samplers. Children living near busy roads were found to have a 35% higher personal exposure to 'soot' than children living at an urban background location, despite that all children attended the same school that was located away from busy roads. Smaller contrasts in personal exposure were found for NO (14%), NO(2) (15%) and NO(x) (14%). This finding supports the use of 'living near a busy road' as a measure of exposure in epidemiological studies on the effects of traffic-related air pollution in children.     

Sensory Neuron-Specific Deletion of Tropomyosin Receptor Kinase A (TrkA) in Mice Abolishes Osteoarthritis (OA) Pain via NGF/TrkA Intervention of Peripheral Sensitization

Tropomyosin receptor kinase A (TrkA/NTRK1) is a high-affinity receptor for nerve growth factor (NGF), a potent pain mediator. NGF/TrkA signaling elevates synovial sensory neuronal distributions in the joints and causes osteoarthritis (OA) pain. We investigated the mechanisms of pain transmission as to whether peripheral sensory neurons are linked to the cellular plasticity in the dorsal root ganglia (DRG) and are critical for OA hyperalgesia. Sensory neuron-specific deletion of TrkA was achieved by tamoxifen injection in 4-week-old TrkA^fl/fl;Na_V1.8^CreERT2 (Ntrk1 ^fl/fl;Scn10a^CreERT2) mice. OA was induced by partial medial meniscectomy (PMM) in 12-week-old mice, and OA-pain-related behavior was analyzed for 12 weeks followed by comprehensive histopathological examinations. OA-associated joint pain was markedly improved without cartilage protection in sensory-neuron-specific conditional TrkA knock-out (cKO) mice. Alleviated hyperalgesia was associated with suppression of the NGF/TrkA pathway and reduced angiogenesis in fibroblast-like synovial cells. Elevated pain transmitters in the DRG of OA-induced mice were significantly diminished in sensory-neuron-specific TrkA cKO and global TrkA cKO mice. Spinal glial activity and brain-derived neurotropic factor (BDNF) were significantly increased in OA-induced mice but were substantially eliminated by sensory-neuron-specific deletion. Our results suggest that augmentation of NGF/TrkA signaling in the joint synovium and the peripheral sensory neurons facilitate pro-nociception and centralized pain sensitization.     

Nuclear matrix proteins distinguish normal diploid osteoblasts from osteosarcoma cells

We have recently discovered in Torino (Italy) a new pedigree with early-onset Alzheimer's disease. The index patient is a woman who, at the age of 43 years, showed progressive memory impairment and ideomotor apraxia. Several relatives of the patient have had a history of dementia. The ancestors of the patient were from Calabria (southern Italy) and members of the family emigrated to the north of Italy, to France, and to the United States. Up to now, the new kindred comprises 1950 members, distributed in eight generations. Thirty members affected with Alzheimer's disease have been identified. Neuropathologic confirmation of antemortem clinically diagnosed Alzheimer's disease has been achieved for one patient. The pedigree is consistent with autosomal dominant inheritance. The clinical course of the disease is fairly uniform: the first symptom is memory loss, beginning around age 40 years. Psychiatric symptoms like hallucinations and delusions follow. At a later stage of the disease, several patients developed myoclonus and generalized epileptic seizures and eventually died with profound dementia. The "Torino family" shows several genealogic and clinical similarities with other large multigenerational familial Alzheimer's disease pedigrees originating from the Calabria region.     

Saxs study of silica gel formation from aqueous silicate solutions

In situ SAXS measurements of silica gel formation in the presence of different cations are presented as a function of reaction time. Conditions used are similar to those applied to prepare catalyst supports. The data can be interpreted in terms of aggregation of elementary silica particles with sizes of approximately 1 nm, thus finally forming a continuous silica gel network. The aggregates are fractal with respect to their masses, in the range 2–10 nm. The dimensionality of the fractals can be determined from the SAXS curves; it increases from 1.8 to 2.5 during gelformation, corresponding with a diffusion limited aggregation process (DLA) of gel formation followed by densification of the silica gel network. The finding that the rate of change in fractal dimensionality does not change as a function of cation, indicates strongly that gelformation is a diffusion limited aggregation process.Beatrixlaan 12, 6165 CX Geleen, The Netherlands     

In situ preservation of kidneys from non-heart-beating donors--a proposal for a standardized protocol

The growing success in renal transplantation has resulted in an increase in the need for donor organs. Procurement of kidneys from heart-beating (HB) donors is unlikely ever to meet this demand. Non-heart-beating (NHB) donors offer a yet untapped source of renal grafts. Cadaver kidneys from patients who have sustained cardiac standstill are often considered unsuitable for transplantation due to prolonged warm ischemia time. Using an emergency in situ perfusion technique it is possible to limit warm ischemic damage and to salvage these kidneys for transplantation. The procedure requires prompt action and cooperation of emergency service personnel. This report presents a protocol for the emergency in situ preservation procedure that can be practiced in most hospitals. At the University Hospital of Maastricht, The Netherlands, implementation of this procedure resulted in 20% more kidneys available for transplantation. Although NHB donor kidneys showed a higher rate of delayed function compared with a matched HB donor kidney population, there was no significant difference in long-term graft survival between the two groups.     

von Willebrand factor as a regulator of intrinsic factor X activation

Factor VIII is an important cofactor in the intrinsic activation of factor X. To function effectively as a cofactor, factor VIII must be activated. In plasma, factor VIII circulates in a complex with von Willebrand factor, and although thrombin can activate complexed factor VIII, the activation by activated factor X is inhibited by von Willebrand factor. In this study, the effect of von Willebrand factor on the generation of factor Xa by the factor IXa-VIII complex was investigated. Purified human factors VIII, IXa, and X were incubated on human umbilical vein endothelial cells or phospholipid vesicles in the presence of calcium ions, and the generation of factor Xa was followed. In the presence of von Willebrand factor, a prolonged lag-phase and a dose-dependent inhibition of factor X activation was observed. These effects were not observed when von Willebrand factor was preincubated with a monoclonal antibody directed against von Willebrand factor that blocks factor VIII binding. When factor VIII was activated with thrombin before the incubation, neither the monoclonal antibody nor von Willebrand factor had an effect on the rate of factor X activation. Preincubation of endothelial cells with the monoclonal antibody resulted in a somewhat higher rate of factor X activation. When endothelial cells from a patient with von Willebrand's disease type I were used, preincubation of the monoclonal antibody had no effect on the rate of factor X activation. We conclude that von Willebrand factor on the surface of endothelial cells can modulate the intrinsic factor X activation. This effect is greatly enhanced, however, by the addition of exogenous von Willebrand factor.(ABSTRACT TRUNCATED AT 250 WORDS)