928 resultados para Defect centers
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Background Centers for Disease Control Guidelines recommend replacement of peripheral intravenous (IV) catheters every 72 to 96 hours. Routine replacement is thought to reduce the risk of phlebitis and bacteraemia. Catheter insertion is an unpleasant experience for patients and replacement may be unnecessary if the catheter remains functional and there are no signs of inflammation. Costs associated with routine replacement may be considerable. Objectives To assess the effects of removing peripheral IV catheters when clinically indicated compared with removing and re-siting the catheter routinely.
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Two recent and related social developments of note for libraries are an upsurge in cultural participation enabled by Web 2.0 media and calls in government policy for enhanced innovation through education. Ironically, these have occurred at the same time that increasingly stringent copyright laws have restricted access to cultural content. Concepts of governmentality are used here to examine these tensions and contradictions. In particular, Foucault’s critique of the author figure and of freedom as part of the will to govern within liberal democratic societies is used to argue for better quality copyright education programs in school libraries and library information science education programs. For purposes of teaching and research, copyrights are defined as agglomerations of legal, economic, and educational discourses that enable and constrain what can and cannot be done with text in homes, schools, and library media centers. The article presents some possibilities for renewal of school libraries around copyright education and Creative Commons licensing.
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The use of polycaprolactone (PCL) as a biomaterial, especially in the fields of drug delivery and tissue engineering, has enjoyed significant growth. Understanding how such a device or scaffold eventually degrades in vivo is paramount as the defect site regenerates and remodels. Degradation studies of three-dimensional PCL and PCL-based composite scaffolds were conducted in vitro (in phosphate buffered saline) and in vivo (rabbit model). Results up to 6 months are reported. All samples recorded virtually no molecular weight changes after 6 months, with a maximum mass loss of only about 7% from the PCL-composite scaffolds degraded in vivo, and a minimum of 1% from PCL scaffolds. Overall, crystallinity increased slightly because of the effects of polymer recrystallization. This was also a contributory factor for the observed stiffness increment in some of the samples, while only the PCL-composite scaffold registered a decrease. Histological examination of the in vivo samples revealed good biocompatibility, with no adverse host tissue reactions up to 6 months. Preliminary results of medical-grade PCL scaffolds, which were implanted for 2 years in a critical-sized rabbit calvarial defect site, are also reported here and support our scaffold design goal for gradual and late molecular weight decreases combined with excellent long-term biocompatibility and bone regeneration. (C) 2008 Wiley Periodicals, Inc. J Biomed Mater Res 90A: 906-919, 2009
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This project report presents the results of a study on wireless communication data transfer rates for a mobile device running a custombuilt construction defect reporting application. The study measured the time taken to transmit data about a construction defect, which included digital imagery and text, in order to assess the feasibility of transferring various types and sizes of data and the ICT-supported construction management applications that could be developed as a consequence. Data transfer rates over GPRS through the Telstra network and WiFi over a private network were compared. Based on the data size and data transfer time, the rate of transfer was calculated to determine the actual data transmission speeds at which the information was being sent using the wireless mobile communication protocols. The report finds that the transmission speeds vary considerably when using GPRS and can be significantly slower than what is advertised by mobile network providers. While WiFi is much faster than GPRS, the limited range of WiFi limits the protocol to residential-scale construction sites.
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A cross-sectional study was performed to investigate the prevalence and predictors of suicidal ideation and past suicide attempt in an Australian sample of human imumunodeficiency virus (HIV)-positive and HIV-negative homosexual and bisexual men. Sixty-five HIV-negative and 164 HIV-positive men participated. A suicidal ideation score was derived from using five items selected from the Beck Depression Inventory and the General Health Questionnaire (28-item version). Lifetime and current prevalence rates of psychiatric disorder were evaluated with the Diagnostic Interview Schedule Version-III-R. The HIV-positive (Centers for Disease Control and Prevention [CDC] Stage IV) men (n=85) had significantly higher total suicidal ideation scores than the asymptomatic HIV-positive men (CDC Stage II/III) (n=79) and the HIV-negative men. High rates of past suicide attempt were detected in the HIV-negative (29%) and HIV-positive men (21%). Factors associated with suicidal ideation included being HIV-positive, the presence of current psychiatric disorder, higher neuroticism scores, external locus of control, and current unemployment. In the HIV-positive group analyzed separately, higher suicidal ideation was discriminated by the adjustment to HIV diagnosis (greater hopelessness and lower fighting spirit), disease factors (greater number of current acquired immunodeficiency syndrome [AIDS]-related conditions), and background variables (neuroticism). Significant predictors of a past attempted suicide were a positive lifetime history of psychiatric disorder (particularly depression diagnoses), a lifetime history of injection drug use, and a family history of suicide attempts. The findings indicate increased levels of suicidal ideation in symptomatic HIV-positive men and highlight the role that multiple psychosocial factors associated with suicidal ideation and attempted suicide play in this population.
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This paper describes a work-in-progress on developing design environments that combine wireless and mobile technologies with augmented reality to facilitate bringing context from the physical environment to the virtual models for design work. One of the challenges for designers in a variety of end-user-oriented design disciplines such as architecture and industrial design has been capturing and replaying the contextual information of the intended domain of the artifact being designed. Either the technology is decidedly low-tech, such as charcoal drawings in a sketchbook, out-of-reach, such as immersive virtual reality CAVEs, or a “make-do” with existing technologies, such as a collage of digital photos. This paper describes a novel combination of “off-the-shelf” technologies that may allow designers more capability to create models using standard computer-aided design applications and augmented reality to combine the current, physical context with the projected, digital context. We demonstrate this approach in the building design domain to address a common problem in building construction, construction defect resolution.
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This paper presents findings from an Australian study examining the behavioral correlates and stability of social status for preschool-aged children. The social status of an initial sample of 187 (94 boys and 93 girls) preschool children (mean age 62.4 months, SD = 4.22) was determined through sociometric assessment. Children classified as rejected, neglected and popular (n = 70) were selected for observation. Children were observed for a total of 25 minutes over a three-month period engaging in free play within their preschool centers. Results indicated that children classified as popular were more likely than rejected or neglected children to engage in cooperative play, ongoing connected conversation and to display positive affect. Popular children were less likely than rejected or neglected children to engage in parallel play, onlooker behavior or alone directed behavior. Six months after initial sociometric classification, sociometric interviews were repeated to test for stability and change. Results indicated that preschool-aged children’s social status classifications showed a moderate to high rate of stability for those children classified as popular, rejected and neglected.
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The purpose of this study was to examine the impact of pain on functioning across multiple quality of life (QOL) domains among individuals with multiple sclerosis (MS). A total of 219 people were recruited from a regional MS society membership database to serve as the community-based study sample. All participants completed a questionnaire containing items about their demographic and clinical characteristics, validated measures of QOL and MS-related disability, and a question on whether or not they had experienced clinically significant pain in the preceding 2 weeks. Respondents who reported pain then completed an in-person structured pain interview assessing pain characteristics (intensity, quality, location, extent, and duration). Comparisons between participants with and without MS-related pain demonstrated that pain prevalence and intensity were strongly correlated with QOL: physical health, psychological health, level of independence, and global QOL were more likely to be impaired among people with MS when pain was present, and the extent of impairment was associated with the intensity of pain. Moreover, these relationships remained significant even after statistically controlling for multiple demographic and clinical covariates associated with self-reported QOL. These findings suggest that for people with MS, pain is an important source of distress and disability beyond that caused by neurologic impairments.
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Introduction During development and regeneration, odontogenesis and osteogenesis are initiated by a cascade of signals driven by several master regulatory genes. Methods In this study, we investigated the differential expression of 84 stem cell–related genes in dental pulp cells (DPCs) and periodontal ligament cells (PDLCs) undergoing odontogenic/osteogenic differentiation. Results Our results showed that, although there was considerable overlap, certain genes had more differential expression in PDLCs than in DPCs. CCND2, DLL1, and MME were the major upregulated genes in both PDLCs and DPCs, whereas KRT15 was the only gene significantly downregulated in PDLCs and DPCs in both odontogenic and osteogenic differentiation. Interestingly, a large number of regulatory genes in odontogenic and osteogenic differentiation interact or crosstalk via Notch, Wnt, transforming growth factor β (TGF-β)/bone morphogenic protein (BMP), and cadherin signaling pathways, such as the regulation of APC, DLL1, CCND2, BMP2, and CDH1. Using a rat dental pulp and periodontal defect model, the expression and distribution of both BMP2 and CDH1 have been verified for their spatial localization in dental pulp and periodontal tissue regeneration. Conclusions This study has generated an overview of stem cell–related gene expression in DPCs and PDLCs during odontogenic/osteogenic differentiation and revealed that these genes may interact through the Notch, Wnt, TGF-β/BMP, and cadherin signalling pathways to play a crucial role in determining the fate of dental derived cell and dental tissue regeneration. These findings provided a new insight into the molecular mechanisms of the dental tissue mineralization and regeneration
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A bioactive and bioresorbable scaffold fabricated from medical grade poly (epsilon-caprolactone) and incorporating 20% beta-tricalcium phosphate (mPCL–TCP) was recently developed for bone regeneration at load bearing sites. In the present study, we aimed to evaluate bone ingrowth into mPCL–TCP in a large animal model of lumbar interbody fusion. Six pigs underwent a 2-level (L3/4; L5/6) anterior lumbar interbody fusion (ALIF) implanted with mPCL–TCP þ 0.6 mg rhBMP-2 as treatment group while four other pigs implanted with autogenous bone graft served as control. Computed tomographic scanning and histology revealed complete defect bridging in all (100%) specimen from the treatment group as early as 3 months. Histological evidence of continuing bone remodeling and maturation was observed at 6 months. In the control group, only partial bridging was observed at 3 months and only 50% of segments in this group showed complete defect bridging at 6 months. Furthermore, 25% of segments in the control group showed evidence of graft fracture, resorption and pseudoarthrosis. In contrast, no evidence of graft fractures, pseudoarthrosis or foreign body reaction was observed in the treatment group. These results reveal that mPCL–TCP scaffolds could act as bone graft substitutes by providing a suitable environment for bone regeneration in a dynamic load bearing setting such as in a porcine model of interbody spine fusion.
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Neurodegenerative disorders are heterogenous in nature and include a range of ataxias with oculomotor apraxia, which are characterised by a wide variety of neurological and ophthalmological features. This family includes recessive and dominant disorders. A subfamily of autosomal recessive cerebellar ataxias are characterised by defects in the cellular response to DNA damage. These include the well characterised disorders Ataxia-Telangiectasia (A-T) and Ataxia-Telangiectasia Like Disorder (A-TLD) as well as the recently identified diseases Spinocerebellar ataxia with axonal neuropathy Type 1 (SCAN1), Ataxia with Oculomotor Apraxia Type 2 (AOA2), as well as the subject of this thesis, Ataxia with Oculomotor Apraxia Type 1 (AOA1). AOA1 is caused by mutations in the APTX gene, which is located at chromosomal locus 9p13. This gene codes for the 342 amino acid protein Aprataxin. Mutations in APTX cause destabilization of Aprataxin, thus AOA1 is a result of Aprataxin deficiency. Aprataxin has three functional domains, an N-terminal Forkhead Associated (FHA) phosphoprotein interaction domain, a central Histidine Triad (HIT) nucleotide hydrolase domain and a C-terminal C2H2 zinc finger. Aprataxins FHA domain has homology to FHA domain of the DNA repair protein 5’ polynucleotide kinase 3’ phosphatase (PNKP). PNKP interacts with a range of DNA repair proteins via its FHA domain and plays a critical role in processing damaged DNA termini. The presence of this domain with a nucleotide hydrolase domain and a DNA binding motif implicated that Aprataxin may be involved in DNA repair and that AOA1 may be caused by a DNA repair deficit. This was substantiated by the interaction of Aprataxin with proteins involved in the repair of both single and double strand DNA breaks (XRay Cross-Complementing 1, XRCC4 and Poly-ADP Ribose Polymerase-1) and the hypersensitivity of AOA1 patient cell lines to single and double strand break inducing agents. At the commencement of this study little was known about the in vitro and in vivo properties of Aprataxin. Initially this study focused on generation of recombinant Aprataxin proteins to facilitate examination of the in vitro properties of Aprataxin. Using recombinant Aprataxin proteins I found that Aprataxin binds to double stranded DNA. Consistent with a role for Aprataxin as a DNA repair enzyme, this binding is not sequence specific. I also report that the HIT domain of Aprataxin hydrolyses adenosine derivatives and interestingly found that this activity is competitively inhibited by DNA. This provided initial evidence that DNA binds to the HIT domain of Aprataxin. The interaction of DNA with the nucleotide hydrolase domain of Aprataxin provided initial evidence that Aprataxin may be a DNA-processing factor. Following these studies, Aprataxin was found to hydrolyse 5’adenylated DNA, which can be generated by unscheduled ligation at DNA breaks with non-standard termini. I found that cell extracts from AOA1 patients do not have DNA-adenylate hydrolase activity indicating that Aprataxin is the only DNA-adenylate hydrolase in mammalian cells. I further characterised this activity by examining the contribution of the zinc finger and FHA domains to DNA-adenylate hydrolysis by the HIT domain. I found that deletion of the zinc finger ablated the activity of the HIT domain against adenylated DNA, indicating that the zinc finger may be required for the formation of a stable enzyme-substrate complex. Deletion of the FHA domain stimulated DNA-adenylate hydrolysis, which indicated that the activity of the HIT domain may be regulated by the FHA domain. Given that the FHA domain is involved in protein-protein interactions I propose that the activity of Aprataxins HIT domain may be regulated by proteins which interact with its FHA domain. We examined this possibility by measuring the DNA-adenylate hydrolase activity of extracts from cells deficient for the Aprataxin-interacting DNA repair proteins XRCC1 and PARP-1. XRCC1 deficiency did not affect Aprataxin activity but I found that Aprataxin is destabilized in the absence of PARP-1, resulting in a deficiency of DNA-adenylate hydrolase activity in PARP-1 knockout cells. This implies a critical role for PARP-1 in the stabilization of Aprataxin. Conversely I found that PARP-1 is destabilized in the absence of Aprataxin. PARP-1 is a central player in a number of DNA repair mechanisms and this implies that not only do AOA1 cells lack Aprataxin, they may also have defects in PARP-1 dependant cellular functions. Based on this I identified a defect in a PARP-1 dependant DNA repair mechanism in AOA1 cells. Additionally, I identified elevated levels of oxidized DNA in AOA1 cells, which is indicative of a defect in Base Excision Repair (BER). I attribute this to the reduced level of the BER protein Apurinic Endonuclease 1 (APE1) I identified in Aprataxin deficient cells. This study has identified and characterised multiple DNA repair defects in AOA1 cells, indicating that Aprataxin deficiency has far-reaching cellular consequences. Consistent with the literature, I show that Aprataxin is a nuclear protein with nucleoplasmic and nucleolar distribution. Previous studies have shown that Aprataxin interacts with the nucleolar rRNA processing factor nucleolin and that AOA1 cells appear to have a mild defect in rRNA synthesis. Given the nucleolar localization of Aprataxin I examined the protein-protein interactions of Aprataxin and found that Aprataxin interacts with a number of rRNA transcription and processing factors. Based on this and the nucleolar localization of Aprataxin I proposed that Aprataxin may have an alternative role in the nucleolus. I therefore examined the transcriptional activity of Aprataxin deficient cells using nucleotide analogue incorporation. I found that AOA1 cells do not display a defect in basal levels of RNA synthesis, however they display defective transcriptional responses to DNA damage. In summary, this thesis demonstrates that Aprataxin is a DNA repair enzyme responsible for the repair of adenylated DNA termini and that it is required for stabilization of at least two other DNA repair proteins. Thus not only do AOA1 cells have no Aprataxin protein or activity, they have additional deficiencies in PolyADP Ribose Polymerase-1 and Apurinic Endonuclease 1 dependant DNA repair mechanisms. I additionally demonstrate DNA-damage inducible transcriptional defects in AOA1 cells, indicating that Aprataxin deficiency confers a broad range of cellular defects and highlighting the complexity of the cellular response to DNA damage and the multiple defects which result from Aprataxin deficiency. My detailed characterization of the cellular consequences of Aprataxin deficiency provides an important contribution to our understanding of interlinking DNA repair processes.
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Describes a brief intensive program of cognitive therapy for depression that was designed for 4 adult residents of country towns in Australia, who resided some distance from treatment centers. Ss were assessed prior to treatment, at posttreatment, and at 4-wk, 8-wk, and 20-mo follow-ups. Treatments took place over 3 consecutive days for a total period of 15 hrs. Effects were highly consistent with the impact of group treatments delivered on a more traditional schedule. If confirmed in a controlled group study, these results suggest that cognitive therapy may be applied more economically and more widely than was previously realized.
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PURPOSE. This study was conducted to determine the magnitude of pupil center shift between the illumination conditions provided by corneal topography measurement (photopic illuminance) and by Hartmann-Shack aberrometry (mesopic illuminance) and to investigate the importance of this shift when calculating corneal aberrations and for the success of wavefront-guided surgical procedures. METHODS. Sixty-two subjects with emmetropia underwent corneal topography and Hartmann-Shack aberrometry. Corneal limbus and pupil edges were detected, and the differences between their respective centers were determined for both procedures. Corneal aberrations were calculated using the pupil centers for corneal topography and for Hartmann-Shack aberrometry. Bland-Altmann plots and paired t-tests were used to analyze the differences between corneal aberrations referenced to the two pupil centers. RESULTS. The mean magnitude (modulus) of the displacement of the pupil with the change of the illumination conditions was 0.21 ± 0.11 mm. The effect of this pupillary shift was manifest for coma corneal aberrations for 5-mm pupils, but the two sets of aberrations calculated with the two pupil positions were not significantly different. Sixty-eight percent of the population had differences in coma smaller than 0.05 µm, and only 4% had differences larger than 0.1 µm. Pupil displacement was not large enough to significantly affect other higher-order Zernike modes. CONCLUSIONS. Estimated corneal aberrations changed slightly between photopic and mesopic illumination conditions given by corneal topography and Hartmann-Shack aberrometry. However, this systematic pupil shift, according to the published tolerances ranges, is enough to deteriorate the optical quality below the theoretically predicted diffraction limit of wavefront-guided corneal surgery.
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Several components of the metabolic syndrome, particularly diabetes and cardiovascular disease, are known to be oxidative stress-related conditions and there is research to suggest that antioxidant nutrients may play a protective role in these conditions. Carotenoids are compounds derived primarily from plants and several have been shown to be potent antioxidant nutrients. The aim of this study was to examine the associations between metabolic syndrome status and major serum carotenoids in adult Australians. Data on the presence of the metabolic syndrome, based on International Diabetes Federation 2005 criteria, were collected from 1523 adults aged 25 years and over in six randomly selected urban centers in Queensland, Australia, using a cross-sectional study design. Weight, height, BMI, waist circumference, blood pressure, fasting and 2-hour blood glucose and lipids were determined, as well as five serum carotenoids. Mean serum alpha-carotene, beta-carotene and the sum of the five carotenoid concentrations were significantly lower (p<0.05) in persons with the metabolic syndrome (after adjusting for age, sex, education, BMI status, alcohol intake, smoking, physical activity status and vitamin/mineral use) than persons without the syndrome. Alpha, beta and total carotenoids also decreased significantly (p<0.05) with increased number of components of the metabolic syndrome, after adjusting for these confounders. These differences were significant among former smokers and non-smokers, but not in current smokers. Low concentrations of serum alpha-carotene, beta-carotene and the sum of five carotenoids appear to be associated with metabolic syndrome status. Additional research, particularly longitudinal studies, may help to determine if these associations are causally related to the metabolic syndrome, or are a result of the pathologies of the syndrome.
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Reports on the reemergence of a concern with planning city centers as focal points in the 1980s. De-industrialization of older industrial areas; Revalorization of city center sites; Emergence of city-to-city competitiveness at a national and supranational level.