35 research outputs found
Australian health care providers' views on opt-out HIV testing
Background: Opt-out HIV testing is a novel concept in Australia. In the opt-out approach, health care providers (HCPs) routinely test patients for HIV unless they explicitly decline or defer. Opt-out HIV testing is only performed with the patients' consent, but pre-test counselling is abbreviated. Australian national testing guidelines do not currently recommend opt-out HIV testing for the general population. Non-traditional approaches to HIV testing (such as opt-out) could identify HIV infections and facilitate earlier treatment, which is particularly important now that HIV is a chronic, manageable disease. Our aim was to explore HCPs' attitudes toward opt-out HIV testing in an Australian context, to further understanding of its acceptability and feasibility. Methods: In this qualitative study, we used purposeful sampling to recruit HCPs who were likely to have experience with HIV testing in Western Australia. We interviewed them using a semi-structured guide and used content analysis as per Graneheim to code the data. Codes were then merged into subcategories and finally themes that unified the underlying concepts. We refined these themes through discussion among the research team. Results: Twenty four HCPs participated. Eleven participants had a questioning attitude toward opt-out HIV testing, while eleven favoured the approach. The remaining two participants had more nuanced perspectives that incorporated some characteristics of the questioning and favouring attitudes. Participants' views about opt-out HIV testing largely fell into two contrasting themes: normalisation and routinisation versus exceptionalism; and a need for proof versus openness to new approaches. Conclusion: Most HCPs in this study had dichotomous attitudes toward opt-out HIV testing, reflecting contrasting analytical styles. While some HCPs viewed it favourably, with the perceived benefits outweighing the perceived costs, others preferred to have evidence of efficacy and cost-effectiveness
Galaxy And Mass Assembly (GAMA): end of survey report and data release 2
The Galaxy And Mass Assembly (GAMA) survey is one of the largest contemporary spectroscopic surveys of low-redshift galaxies. Covering an area of ~286 deg^2 (split among five survey regions) down to a limiting magnitude of r < 19.8 mag, we have collected spectra and reliable redshifts for 238,000 objects using the AAOmega spectrograph on the Anglo-Australian Telescope. In addition, we have assembled imaging data from a number of independent surveys in order to generate photometry spanning the wavelength range 1 nm - 1 m. Here we report on the recently completed spectroscopic survey and present a series of diagnostics to assess its final state and the quality of the redshift data. We also describe a number of survey aspects and procedures, or updates thereof, including changes to the input catalogue, redshifting and re-redshifting, and the derivation of ultraviolet, optical and near-infrared photometry. Finally, we present the second public release of GAMA data. In this release we provide input catalogue and targeting information, spectra, redshifts, ultraviolet, optical and near-infrared photometry, single-component S\'ersic fits, stellar masses, H-derived star formation rates, environment information, and group properties for all galaxies with r < 19.0 mag in two of our survey regions, and for all galaxies with r < 19.4 mag in a third region (72,225 objects in total). The database serving these data is available at http://www.gama-survey.org/
Effects of sardine-enriched diet on metabolic control, inflammation and gut microbiota in drug-naïve patients with type 2 diabetes: a pilot randomized trial
Direct-trauma model of posttraumatic syringomyelia with a computer-controlled motorized spinal cord impactor
OBJECTIVE: The pathogenesis of posttraumatic syringomyelia remains enigmatic and is not adequately explained by current theories. Experimental investigations require a reproducible animal model that replicates the human condition. Current animal models are imperfect because of their low reliability, severe neurological deficits, or dissimilar mechanism of injury. The objective of this study was to develop a reproducible rodent model of posttraumatic syringomyelia using a spinal cord impactor that produces an injury that more closely mimics the human condition and does not produce severe neurological deficits. METHODS: The study consisted of 2 parts. Seventy animals were studied overall: 20 in Experiment 1 and 48 in Experiment 2 after two rats with severe deficits were killed early. Experiment 1 aimed to determine the optimal force setting for inducing a cystic cavity without neurological deficits using a computer-controlled motorized spinal cord impactor. Twenty animals received an impact that ranged from 50 to 150 kDyn. Using the optimal force for producing an initial cyst determined from Experiment 1, Experiment 2 aimed to compare the progression of cavities in animals with and those without arachnoiditis induced by kaolin. Forty-eight animals were killed at 1, 3, 6, or 12 weeks after syrinx induction. Measurements of cavity size and maximum anteroposterior and lateral diameters were evaluated using light microscopy. RESULTS: In Experiment 1, cavities were present in 95% of the animals. The duration of limb weakness and spinal cord cavity size correlated with the delivered force. The optimal force chosen for Experiment 2 was 75 kDyn. In Experiment 2, cavities occurred in 92% of the animals. Animals in the kaolin groups developed larger cavities and more vacuolations and enlarged perivascular spaces than those in the nonkaolin groups. CONCLUSIONS This impact model reliably produces cavities that resemble human posttraumatic syringomyelia and is suitable for further study of posttraumatic syringomyelia pathophysiology
Roles of peroxisome proliferator-activated receptor-α and -γ in the development of non-small cell lung cancer
Peroxisome proliferator-activated receptor Peroxisome proliferator- activated receptor (PPAR)-α and PPARδ participate in cell proliferation and apoptosis. Few studies have simultaneously investigated both PPARα and PPARγ in lung cancers in vivo. The roles of PPARα and -γ were investigated in the development of pulmonary tumors induced in the adult A/J mouse by treatment with 4-(methylnitrosamino)-l-(3-pyridyl)- lbutanone (NNK). Compared with the normal lung tissues, PPARγ expression was much higher in the NNK-induced lung tumor tissues. However, PPARγ transcriptional activity, and the levels of two major endogenous PPARγ ligands, 13-hydroxyoctadecadienoic acid and 15-hydroxyeicosatetraenoic acid, were significantly lower in the NNK-treated lung tissues. The ligand changes in mice were confirmed in human lung cancer tissues. Along with the alteration of PPARγ and its endogenous ligands, the level of PPARα and its activity were increased in the NNK-induced mouse lung tumors. Treatment of mice with the synthetic PPARγ ligand, pioglitazone, significantly inhibited the formation of mouse lung tumors induced by NNK. Our study demonstrated that the reduction of endogenous PPARγ ligands and increased PPARα occurred before the formation of lung tumors, indicating that the molecular changes play a role in lung carcinogenesis. The results suggest that the enhancement of PPARγ activity with its ligands, and the suppression of PPARα with its inhibitors, may prevent the formation of lung tumors, as well as accelerate the therapy of lung cancer. Our findings may also reveal the possibility of using the level of endogenous PPARγ ligands and the activities of PPARγ or PPARα as tumor markers for lung cancer.link_to_subscribed_fulltex
Syntheses, structures and adsorption properties of two-dimensional Cd(II) coordination polymers
Racial/Ethnic Differences in the Use of Primary Care Providers and Preventive Health Services at a Midwestern University
Directing the Self-assembly of Tumour Spheroids by Bioprinting Cellular Heterogeneous Models within Alginate/Gelatin Hydrogels
"Human tumour progression is a dynamic process involving diverse biological and biochemical events such as genetic mutation and selection in addition to physical, chemical, and mechanical events occurring between cells and the tumour microenvironment. Using 3D bioprinting we have developed a method to embed MDA-MB-231 triple negative breast cancer cells, and IMR-90 fibroblast cells, within a cross-linked alginate/gelatin matrix at specific initial locations relative to each other. After 7 days of co-culture the MDA-MB-231 cells begin to form multicellular tumour spheroids (MCTS) that increase in size and frequency over time. After similar to 15 days the IMR-90 stromal fibroblast cells migrate through a non-cellularized region of the hydrogel matrix and infiltrate the MDA-MB-231 spheroids creating mixed MDA-MB-231/IMR-90 MCTS. This study provides a proof-of-concept that biomimetic in vitro tissue coculture models bioprinted with both breast cancer cells and fibroblasts will result in MCTS that can be maintained for durations of several weeks.