How to ask sensitive questions in conservation: A review of specialized questioning techniques

Tools for social research are critical for developing an understanding of conservation problems and assessing the feasibility of conservation actions. Social surveys are an essential tool frequently applied in conservation to assess both people’s behaviour and to understand its drivers. However, little attention has been given to the weaknesses and strengths of different survey tools. When topics of conservation concern are illegal or otherwise sensitive, data collected using direct questions are likely to be affected by non-response and social desirability biases, reducing their validity. These sources of bias associated with using direct questions on sensitive topics have long been recognised in the social sciences but have been poorly considered in conservation and natural resource management. We reviewed specialized questioning techniques developed in a number of disciplines specifically for investigating sensitive topics. These methods ensure respondent anonymity, increase willingness to answer, and critically, make it impossible to directly link incriminating data to an individual. We describe each method and report their main characteristics, such as data requirements, possible data outputs, availability of evidence that they can be adapted for use in illiterate communities, and summarize their main advantages and disadvantages. Recommendations for their application in conservation are given. We suggest that the conservation toolbox should be expanded by incorporating specialized questioning techniques, developed specifically to increase response accuracy. By considering the limitations of each survey technique, we will ultimately contribute to more effective evaluations of conservation interventions and more robust policy decisions

Both common variations and rare non-synonymous substitutions and small insertion/deletions in CLU are associated with increased Alzheimer risk.

BACKGROUND: We have followed-up on the recent genome-wide association (GWA) of the clusterin gene (CLU) with increased risk for Alzheimer disease (AD), by performing an unbiased resequencing of all CLU coding exons and regulatory regions in an extended Flanders-Belgian cohort of Caucasian AD patients and control individuals (n = 1930). Moreover, we have replicated genetic findings by targeted resequencing in independent Caucasian cohorts of French (n = 2182) and Canadian (n = 573) origin and by performing meta-analysis combining our data with previous genetic CLU screenings. RESULTS: In the Flanders-Belgian cohort, we identified significant clustering in exons 5-8 of rare genetic variations leading to non-synonymous substitutions and a 9-bp insertion/deletion affecting the CLU β-chain (p = 0.02). Replicating this observation by targeted resequencing of CLU exons 5-8 in 2 independent Caucasian cohorts of French and Canadian origin identified identical as well as novel non-synonymous substitutions and small insertion/deletions. A meta-analysis, combining the datasets of the 3 cohorts with published CLU sequencing data, confirmed that rare coding variations in the CLU β-chain were significantly enriched in AD patients (OR(MH) = 1.96 [95% CI = 1.18-3.25]; p = 0.009). Single nucleotide polymorphisms (SNPs) association analysis indicated the common AD risk association (GWA SNP rs11136000, p = 0.013) in the 3 combined datasets could not be explained by the presence of the rare coding variations we identified. Further, high-density SNP mapping in the CLU locus mapped the common association signal to a more 5' CLU region. CONCLUSIONS: We identified a new genetic risk association of AD with rare coding CLU variations that is independent of the 5' common association signal identified in the GWA studies. At this stage the role of these coding variations and their likely effect on the β-chain domain and CLU protein functioning remains unclear and requires further studies.RIGHTS : This article is licensed under the BioMed Central licence at http://www.biomedcentral.com/about/license which is similar to the 'Creative Commons Attribution Licence'. In brief you may : copy, distribute, and display the work; make derivative works; or make commercial use of the work - under the following conditions: the original author must be given credit; for any reuse or distribution, it must be made clear to others what the license terms of this work are

The influence of personality and ability on undergraduate teamwork and team performance

The ability to work effectively on a team is highly valued by employers, and collaboration among students can lead to intrinsic motivation, increased persistence, and greater transferability of skills. Moreover, innovation often arises from multidisciplinary teamwork. The influence of personality and ability on undergraduate teamwork and performance is not comprehensively understood. An investigation was undertaken to explore correlations between team outcomes, personality measures and ability in an undergraduate population. Team outcomes included various self-, peer- and instructor ratings of skills, performance, and experience. Personality measures and ability involved the Five-Factor Model personality traits and GPA. Personality, GPA, and teamwork survey data, as well as instructor evaluations were collected from upper division team project courses in engineering, business, political science, and industrial design at a large public university. Characteristics of a multidisciplinary student team project were briefly examined. Personality, in terms of extraversion scores, was positively correlated with instructors’ assessment of team performance in terms of oral and written presentation scores, which is consistent with prior research. Other correlations to instructor-, students’ self- and peer-ratings were revealed and merit further study. The findings in this study can be used to understand important influences on successful teamwork, teamwork instruction and intervention and to understand the design of effective curricula in this area moving forward

Stereotactic body radiotherapy for organ-confined prostate cancer

<p>Abstract</p> <p>Background</p> <p>Improved understanding of prostate cancer radiobiology combined with advances in delivery of radiation to the moving prostate offer the potential to reduce treatment-related morbidity and maintain quality of life (QOL) following prostate cancer treatment. We present preliminary results following stereotactic body radiotherapy (SBRT) treatment for organ-confined prostate cancer.</p> <p>Methods</p> <p>SBRT was performed on 304 patients with clinically localized prostate cancer: 50 received 5 fractions of 7 Gy (total dose 35 Gy) and 254 received 5 fractions of 7.25 Gy (total dose 36.25 Gy). Acute and late toxicity was assessed using the Radiation Therapy Oncology Group scale. The Expanded Prostate Cancer Index Composite questionnaire was used to assess QOL. Prostate-specific antigen response was monitored.</p> <p>Results</p> <p>At a median 30-month (26 - 37 month, range) follow-up there were no biochemical failures for the 35-Gy dose level. Acute Grade II urinary and rectal toxicities occurred in 4% of patients with no higher Grade acute toxicities. One Grade II late urinary toxicity occurred with no other Grade II or higher late toxicities. At a median 17-month (8 - 27 month, range) follow-up the 36.25 Gy dose level had 2 low- and 2 high-risk patients fail biochemically (biopsy showed 2 low- and 1 high-risk patients were disease-free in the gland). Acute Grade II urinary and rectal toxicities occurred in 4.7% (12/253) and 3.6% (9/253) of patients, respectively. For those patients with a minimum of 12 months follow-up, 5.8% (12/206) had late Grade II urinary toxicity and 2.9% (6/206) had late Grade II rectal toxicities. One late Grade III urinary toxicity occurred; no Grade IV toxicities occurred. For both dose levels at 17 months, bowel and urinary QOL returned to baseline values; sexual QOL decreased by 10%.</p> <p>Conclusions</p> <p>The low toxicity and maintained QOL are highly encouraging. Additional follow-up is needed to determine long-term biochemical control and maintenance of low toxicity and QOL.</p

Single blind randomized Phase III trial to investigate the benefit of a focal lesion ablative microboost in prostate cancer (FLAME-trial): study protocol for a randomized controlled trial

Background: The treatment results of external beam radiotherapy for intermediate and high risk prostate cancer patients are insufficient with five-year biochemical relapse rates of approximately 35%. Several randomized trials have shown that dose escalation to the entire prostate improves biochemical disease free survival. However, further dose escalation to the whole gland is limited due to an unacceptable high risk of acute and late toxicity. Moreover, local recurrences often originate at the location of the macroscopic tumor, so boosting the radiation dose at the macroscopic tumor within the prostate might increase local control. A reduction of distant metastases and improved survival can be expected by reducing local failure. The aim of this study is to investigate the benefit of an ablative microboost to the macroscopic tumor within the prostate in patients treated with external beam radiotherapy for prostate cancer.Methods/Design: The FLAME-trial (Focal Lesion Ablative Microboost in prostatE cancer) is a single blind randomized controlled phase III trial. We aim to include 566 patients (283 per treatment arm) with intermediate or high risk adenocarcinoma of the prostate who are scheduled for external beam radiotherapy using fiducial markers for position verification. With this number of patients, the expected increase in five-year freedom from biochemical failure rate of 10% can be detected with a power of 80%. Patients allocated to the standard arm receive a dose of 77 Gy in 35 fractions to the entire prostate and patients in the experimental arm receive 77 Gy to the entire prostate and an additional integrated microboost to the macroscopic tumor of 95 Gy in 35 fractions. The secondary outcome measures include treatment-related toxicity, quality of life and disease-specific survival. Furthermore, by localizing the recurrent tumors within the prostate during follow-up and correlating this with the delivered dose, we can obtain accurate dose-effect information for both the macroscopic tumor and subclinical disease in prostate cancer. The rationale, study design and the first 50 patients included are described.Biological, physical and clinical aspects of cancer treatment with ionising radiatio

Phosphorylation of GFAP is associated with injury in the neonatal pig hypoxic-ischemic brain

Glial fibrillary acidic protein (GFAP) is an intermediate filament protein expressed in the astrocyte cytoskeleton that plays an important role in the structure and function of the cell. GFAP can be phosphorylated at six serine (Ser) or threonine (Thr) residues but little is known about the role of GFAP phosphorylation in physiological and pathophysiological states. We have generated antibodies against two phosphorylated GFAP (pGFAP) proteins: p8GFAP, where GFAP is phosphorylated at Ser-8 and p13GFAP, where GFAP is phosphorylated at Ser-13. We examined p8GFAP and p13GFAP expression in the control neonatal pig brain and at 24 and 72 h after an hypoxic-ischemic (HI) insult. Immunohistochemistry demonstrated pGFAP expression in astrocytes with an atypical cytoskeletal morphology, even in control brains. Semi-quantitative western blotting revealed that p8GFAP expression was significantly increased at 24 h post-insult in HI animals with seizures in frontal, parietal, temporal and occipital cortices. At 72 h post-insult, p8GFAP and p13GFAP expression were significantly increased in HI animals with seizures in brain regions that are vulnerable to cellular damage (cortex and basal ganglia), but no changes were observed in brain regions that are relatively spared following an HI insult (brain stem and cerebellum). Increased pGFAP expression was associated with poor neurological outcomes such as abnormal encephalography and neurobehaviour, and increased histological brain damage. Phosphorylation of GFAP may play an important role in astrocyte remodelling during development and disease and could potentially contribute to the plasticity of the central nervous system

Primary T-lymphocytes rescue the replication of HIV-1 DIS RNA mutants in part by facilitating reverse transcription

The dimerization initiation site (DIS) stem-loop within the HIV-1 RNA genome is vital for the production of infectious virions in T-cell lines but not in primary cells. In comparison to peripheral blood mononuclear cells (PBMCs), which can support the replication of both wild type and HIV-1 DIS RNA mutants, we have found that DIS RNA mutants are up to 100 000-fold less infectious than wild-type HIV-1 in T-cell lines. We have also found that the cell-type-dependent replication of HIV-1 DIS RNA mutants is largely producer cell-dependent, with mutants displaying a greater defect in viral cDNA synthesis when viruses were not derived from PBMCs. While many examples exist of host–pathogen interplays that are mediated via proteins, analogous examples which rely on nucleic acid triggers are limited. Our data provide evidence to illustrate that primary T-lymphocytes rescue, in part, the replication of HIV-1 DIS RNA mutants through mediating the reverse transcription process in a cell-type-dependent manner. Our data also suggest the presence of a host cell factor that acts within the virus producer cells. In addition to providing an example of an RNA-mediated cell-type-dependent block to viral replication, our data also provides evidence which help to resolve the dilemma of how HIV-1 genomes with mismatched DIS sequences can recombine to generate chimeric viral RNA genomes