76 resultados para obligation to individually identify documents in bundles
Resumo:
Pinnawala Elephant Orphanage (PEO) is a unique captive elephant-based recreation facility in Sri Lanka. Over 35,000 visitors (both local and foreign) visit the PEO per month on average for a variety of reasons. However, little or no attempt has been made to examine their reaction to its activities. This paper reports preliminary findings from two visitor surveys (one local and one foreign) conducted at the PEO to examine the characteristics of visitors, the satisfaction they gained from the visit, their attitudes towards conservation of the elephant, their reactions to the current facilities available at the orphanage, and their opinions and maximum willingness to pay (WTP) to enter the PEO. It is found that, although some variations occurred between the samples, the majority of all respondents showed a similar reaction to the activities and facilities at the Orphanage. However, some differences are evident between these two samples in relation to satisfaction received, responses to the WTP elicitation and attitudes towards the information and interpretive facilities. Overall, the majority of the respondents indicated that their support for the conservation of the Asian elephant had increased considerably with their visit to the Orphanage. This indicates that considerable unrecorded and as yet unutilised support could be generated both financially and otherwise to conserve this endangered species through wildlife based recreation facilities such as PEO in Sri Lanka.
Resumo:
Use of specific histone deacetylase inhibitors has revealed critical roles for the histone deacetylases (HDAC) in controlling proliferation. Although many studies have correlated the function of HDAC inhibitors with the hyperacetylation of histones, few studies have specifically addressed whether the accumulation of acetylated histones, caused by HDAC inhibitor treatment, is responsible for growth inhibition. In the present study we show that HDAC inhibitors cause growth inhibition in normal and transformed keratinocytes but not in normal dermal fibroblasts, This was despite the observation that the HDAC inhibitor, suberic bishydroxamate (SBHA), caused a kinetically similar accumulation of hyperacetylated histones, This cell type-specific response to SBHA was not due to the inactivation of SBHA by fibroblasts, nor was it due to differences in the expression of specific HDAC family members. Remarkably, overexpression of HDACs 1, 4, and 6 in normal human fibroblasts resulted in cells that could be growth-inhibited by SBHA. These data suggest that, although histone acetylation is a major target for HDAC inhibitors, the accumulation of hyperacetylated histones is not sufficient to cause growth inhibition in all cell types, This suggests that growth inhibition, caused by HDAC inhibitors, may be the culmination of histone hyperacetylation acting in concert with other growth regulatory pathways.
Resumo:
Objectives. To compare immunohistochemical scoring with clinical scoring and radiology for the assessment of rheumatoid arthritis (RA) disease activity, synovial tissue (ST) biopsied arthroscopically was assessed from 18 patients before and after commencement of disease-modifying anti-rheumatic drug (DMARD) therapy. Methods. Lymphocytes, macrophages, differentiated dendritic cells (DC), vascularity, tumour necrosis factor (TNF)alpha and interleukin-1 beta levels were scored. Clinical status was scored using the American College of Rheumatology (ACR) core set and serial radiographs were scored using the Larsen and Sharp methods. Histopathological evidence of activity included infiltration by lymphocytes, DC, macrophages. tissue vascularity, and expression of lining and sublining TNF alpha. These indices co-varied across the set of ST biopsies and were combined as a synovial activity score for each biopsy. Results. The change in synovial activity with treatment correlated with the ACR clinical response and with decreased radiological progression by the Larsen score, The ACR response to DMARD therapy. the change in synovial activity score and the slowing of radiological progression were each greatest in patients with high initial synovial vascularity. Conclusions. The data demonstrate an association between clinical, radiological and synovial immunopathological responses to anti-rheumatic treatment in RA. High ST vascularity may predict favourable clinical and radiological responses to treatment.
Resumo:
We compared changes in muscle fibre composition and muscle strength indices following a 10 week isokinetic resistance training programme consisting of fast (3.14 rad(.)s(-1)) or slow (0.52 rad(.)s(-1)) velocity eccentric muscle contractions. A group of 20 non-resistance trained subjects were assigned to a FAST (n = 7), SLOW (n = 6) or non-training CONTROL (n = 7) group. A unilateral training protocol targeted the elbow flexor muscle group and consisted of 24 maximal eccentric isokinetic contractions (four sets of six repetitions) performed three times a week for 10 weeks. Muscle biopsy samples were obtained from the belly of the biceps brachii. Isometric torque and concentric and eccentric torque at 0.52 and 3.14 rad(.)s(-1) were examined at 0, 5 and 10 weeks. After 10 weeks, the FAST group demonstrated significant [mean (SEM)] increases in eccentric [29.6 (6.4)%] and concentric torque [27.4 (7.3) %] at 3.14 rad(.)s(-1), isometric torque [21.3 (4.3)%] and eccentric torque [25.2 (7.2) %] at 0.52 rad(.)s(-1). The percentage of type I fibres in the FAST group decreased from [53.8 (6.6)% to 39.1 (4.4)%] while type lib fibre percentage increased from [5.8 (1.9)% to 12.9 (3.3)%; P < 0.05]. In contrast. the SLOW group did not experience significant changes in muscle fibre type or muscle torque. We conclude that neuromuscular adaptations to eccentric training stimuli may be influenced by differences in the ability to cope with chronic exposure to relatively fast and slow eccentric contraction velocities. Possible mechanisms include greater cumulative damage to contractile tissues or stress induced by slow eccentric muscle contractions.
Resumo:
This paper reports a study in the wet tropics of Queensland on the fate of urea applied to a dry or wet soil surface under banana plants. The transformations of urea were followed in cylindrical microplots (10.3 cm diameter x 23 cm long), a nitrogen (N) balance was conducted in macroplots (3.85 m x 2.0 m) with N-15 labelled urea, and ammonia volatilization was determined with a mass balance micrometeorological method. Most of the urea was hydrolysed within 4 days irrespective of whether the urea was applied onto dry or wet soil. The nitrification rate was slow at the beginning when the soil was dry, but increased greatly after small amounts of rain; in the 9 days after rain 20% of the N applied was converted to nitrate. In the 40 days between urea application and harvesting, the macroplots the banana plants absorbed only 15% of the applied N; at harvest the largest amounts were found in the leaves (3.4%), pseudostem (3.3%) and fruit (2.8%). Only 1% of the applied N was present in the roots. Sixty percent of the applied N was recovered in the soil and 25% was lost from the plant-soil system by either ammonia volatilization, leaching or denitrification. Direct measurements of ammonia volatilization showed that when urea was applied to dry soil, and only small amounts of rain were received, little ammonia was lost (3.2% of applied N). In contrast, when urea was applied onto wet soil, urea hydrolysis occurred immediately, ammonia was volatilized on day zero, and 17.2% of the applied N was lost by the ninth day after that application. In the latter study, although rain fell every day, the extensive canopy of banana plants reduced the rainfall reaching the fertilized area under the bananas to less than half. Thus even though 90 mm of rain fell during the volatilization study, the fertilized area did not receive sufficient water to wash the urea into the soil and prevent ammonia loss. Losses by leaching and denitrification combined amounted to 5% of the applied N.
Resumo:
ISCOMs(R) are typically 40 nm cage-like structures comprising antigen, saponin, cholesterol and phospholipid. ISCOMs(R) have been shown to induce antibody responses and activate T helper cells and cyrolytic T lymphocytes in a number of animal species, including non-human primates. Recent clinical studies have demonstrated that ISCOMs(R) are also able to induce antibody and cellular immune responses in humans. This review describes the current understanding of the ability of ISCOMs(R) to induce immune responses and the mechanisms underlying this property. Recent progress in the characterisation and manufacture of ISCOMs(R) will also be discussed. (C) 2001 Elsevier Science Ltd. All rights reserved.
Resumo:
The immunoregulatory signaling (IRS) family includes several molecules, which play major roles in the regulation of the immune response. The CMRF-35A and CMRF-35H molecules are two new members of the IRS family of molecules, that are found on a wide variety of haemopoietic lineages. The extracellular functional interactions of these molecules is presently unknown, although CMRF-35H on initiate an inhibitory signal and is internalized when cross-linked. In this paper, we described the gene structure for the CMRF-35A gene and its localization to human chromosome 17. The gene consists of four exons spanning approximately 4.5 kb. Exon 1 encodes the 5' untranslated region and leader sequence, exon 2 encodes the immunoglobulin (Ig)-like domain, exon 3 encodes the membrane proximal region and exon 4 encodes the transmembrane region, the cytoplasmic tail and the 3' untranslated region. A region in the 5' flanking sequence of the CMRF-35A gene, that promoted expression of a reporter gene was identified. The genes for the CMRF-35A and CMRF-35H molecules are closely linked on chromosome 17. Similarity between the Ig-like exons and the preceding intron of the two genes suggests exon duplication was involved in their evolution. We also identified a further member of the CMRF-35 family, the CMRF-35J pseudogene. This gene appears to have arisen by gene duplication of the CMRF-35A gene. These three loci-the CMRF-35A, CMRF-35J and CMRF-35H genes-form a new complex of IRS genes on chromosome 17.