The impact of weapons and unusual objects on the construction of facial composites

The presence of a weapon in the perpetration of a crime can impede an observer’s ability to describe and/or recognise the person responsible. In the current experiment, we explore whether weapons when present at encoding of a target identity interfere with the construction of a facial composite. Participants encoded an unfamiliar target face seen either on its own or paired with a knife. Encoding duration (10 or 30 s) was also manipulated. The following day, participants recalled the face and constructed a composite of it using a holistic system (EvoFIT). Correct naming of the participants’ composites was found to reduce reliably when target faces were paired with the weapon at 10 s but not at 30 s. These data suggest that the presence of a weapon reduces the effectiveness of facial composites following a short encoding duration. Implications for theory and police practice are discussed

The Impact of HAART on the Respiratory Complications of HIV Infection: Longitudinal Trends in the MACS and WIHS Cohorts

Objective: To review the incidence of respiratory conditions and their effect on mortality in HIV-infected and uninfected individuals prior to and during the era of highly active antiretroviral therapy (HAART). Design: Two large observational cohorts of HIV-infected and HIV-uninfected men (Multicenter AIDS Cohort Study [MACS]) and women (Women's Interagency HIV Study [WIHS]), followed since 1984 and 1994, respectively. Methods: Adjusted odds or hazards ratios for incident respiratory infections or non-infectious respiratory diagnoses, respectively, in HIV-infected compared to HIV-uninfected individuals in both the pre-HAART (MACS only) and HAART eras; and adjusted Cox proportional hazard ratios for mortality in HIV-infected persons with lung disease during the HAART era. Results: Compared to HIV-uninfected participants, HIV-infected individuals had more incident respiratory infections both pre-HAART (MACS, odds ratio [adjusted-OR], 2.4; 95% confidence interval [CI], 2.2-2.7; p<0.001) and after HAART availability (MACS, adjusted-OR, 1.5; 95%CI 1.3-1.7; p<0.001; WIHS adjusted-OR, 2.2; 95%CI 1.8-2.7; p<0.001). Chronic obstructive pulmonary disease was more common in MACS HIV-infected vs. HIV-uninfected participants pre-HAART (hazard ratio [adjusted-HR] 2.9; 95%CI, 1.02-8.4; p = 0.046). After HAART availability, non-infectious lung diseases were not significantly more common in HIV-infected participants in either MACS or WIHS participants. HIV-infected participants in the HAART era with respiratory infections had an increased risk of death compared to those without infections (MACS adjusted-HR, 1.5; 95%CI, 1.3-1.7; p<0.001; WIHS adjusted-HR, 1.9; 95%CI, 1.5-2.4; p<0.001). Conclusion: HIV infection remained a significant risk for infectious respiratory diseases after the introduction of HAART, and infectious respiratory diseases were associated with an increased risk of mortality. © 2013 Gingo et al

Neither loss of Bik alone, nor combined loss of Bik and Noxa, accelerate murine lymphoma development or render lymphoma cells resistant to DNA damaging drugs

The pro-apoptotic BH3-only protein, BIK, is widely expressed and although many critical functions in developmental or stress-induced death have been ascribed to this protein, mice lacking Bik display no overt abnormalities. It has been postulated that Bik can serve as a tumour suppressor, on the basis that its deficiency and loss of apoptotic function have been reported in many human cancers, including lymphoid malignancies. Evasion of apoptosis is a major factor contributing to c-Myc-induced tumour development, but despite this, we found that Bik deficiency did not accelerate Eμ-Myc-induced lymphomagenesis. Co-operation between BIK and NOXA, another BH3-only protein, has been previously described, and was attributed to their complementary binding specificities to distinct subsets of pro-survival BCL-2 family proteins. Nevertheless, combined deficiency of Bik and Noxa did not alter the onset of Eμ-Myc transgene induced lymphoma development. Moreover, although p53-mediated induction of Bik has been reported, neither Eμ-Myc/Bik−/− nor Eμ-Myc/Bik−/−Noxa−/− lymphomas were more resistant than control Eμ-Myc lymphomas to killing by DNA damaging drugs, either in vitro or in vivo. These results suggest that Bik, even in combination with Noxa, is not a potent suppressor of c-Myc-driven tumourigenesis or critical for chemotherapeutic drug-induced killing of Myc-driven tumours

Evaluation of Current Knowledge, Awareness and Practice of Spirometry among Hospital -based Nigerian Doctors

<p>Abstract</p> <p>Background</p> <p>Spirometry is a cost-effective diagnostic tool for evaluation of lung function and for case-finding in a resource-limited setting. The acceptance of this test depends on the awareness of its indications and the ability to interpret the results. No studies have assessed the knowledge of spirometry among Nigerian doctors. The aim of this study was to evaluate the current knowledge, awareness and practice of spirometry among hospital-based Nigerian doctors.</p> <p>Methods</p> <p>We carried out a cross-sectional survey among 321 doctors working in Nigerian hospitals between March 2008 and June 2008. Information on knowledge, awareness, practice of and barriers to spirometry were obtained using a pre-tested, self-administered structured questionnaire and the data were then analysed.</p> <p>Results</p> <p>Of the 321 doctors that participated, 108 (33.6%) reported that they have good knowledge of spirometry. One hundred and ninety-five (60.7%) were aware of the importance of spirometry in aiding the diagnosis of respiratory diseases; 213(66.4%) were aware of the importance of spirometry in determining the severity of diseases. Medical school was the most common source of knowledge on spirometry (64.5%). Eighty-one (25.2%) doctors reported having a spirometer in their hospitals. Doctors having access to a spirometer used it more frequently for aiding the diagnosis of COPD (40.7% vs.27.5%) and for monitoring of asthma (18.5% vs.11.3%) than those without access to a spirometer. The doctors working in University Teaching Hospitals and Federal Medical Centres (FMC) (22.4% vs. 4.5%) and those having access to a spirometer (40.7 vs.11.3%) were very confident of interpreting spirometry results compared to those working in District and General Hospitals and without access to a spirometer. Irrespective of access to a spirometer or the type of hospital they were employed in, doctors reported that unavailability of a spirometer was the greatest barrier to its use (62.5%) followed by lack of awareness about its usefulness (17.2%).</p> <p>Conclusion</p> <p>The knowledge and practice of spirometry were poor among hospital-based Nigerian doctors because of unavailability of spirometers in most hospitals. These findings have implications for further evaluation, planning and management of patient care in respiratory disease. Spirometers should be made available in all hospitals, and the knowledge of spirometry should be improved among doctors.</p

Model for estimating the population prevalence of chronic obstructive pulmonary disease: cross sectional data from the Health Survey for England

BACKGROUND: Chronic obstructive pulmonary disease (COPD) is a major but neglected public health problem. Currently 1.4% of the England population has a clinical diagnosis of COPD, but the true burden of the disease has not been known with certainty, as many cases remain undiagnosed. METHODS: A mathematical model based on cross sectional data from a representative sample of the population in England (the Heath Survey for England 2001, n = 10,750) was developed allowing estimates on the prevalence of COPD (defined based on the presence of airflow obstruction) to be obtained. Logistic regression analysis was used to investigate and choose risk factors for inclusion in the model and to derive the prevalence estimates based on the strength of association between selected risk factors and the outcome COPD. The model allows the prevalence to be estimated in populations at national level and also at regional and large local areas, based on their compositions according to age, sex, smoking and ethnicity, and on area degrees of urbanisation and deprivation. We applied the model to measure the prevalence of COPD in England and in some sub-groups of the population within the country. RESULTS: The prevalence of COPD in England is estimated as 3.1% (3.9% in men and 2.4% in women) in the population over 15 years of age, and 5.3% (6.8% in men and 3.9% in women) in 45 year-olds and over. There was a 7-fold variation in the prevalence across subgroups of the population, with lowest values in Asian women from wealthy rural areas (1.7%), and highest in black men from deprived urban areas (12.5%). CONCLUSION: The model can be used to estimate population prevalence of COPD from large general practices to national level, and as a tool to identify areas of high levels of unmet needs for COPD priority health actions. The results from the model highlight the importance of including variables other than age, sex and smoking, i.e. levels of deprivation, urbanisation and ethnicity, when estimating population prevalence of COPD. The model should be validated at local level and incorporated into case-finding strategies

Lifetime environmental tobacco smoke exposure and the risk of chronic obstructive pulmonary disease

BACKGROUND: Exposure to environmental tobacco smoke (ETS), which contains potent respiratory irritants, may lead to chronic airway inflammation and obstruction. Although ETS exposure appears to cause asthma in children and adults, its role in causing COPD has received limited attention in epidemiologic studies. METHODS: Using data from a population-based sample of 2,113 U.S. adults aged 55 to 75 years, we examined the association between lifetime ETS exposure and the risk of developing COPD. Participants were recruited from all 48 contiguous U.S. states by random digit dialing. Lifetime ETS exposure was ascertained by structured telephone interview. We used a standard epidemiologic approach to define COPD based on a self-reported physician diagnosis of chronic bronchitis, emphysema, or COPD. RESULTS: Higher cumulative lifetime home and work exposure were associated with a greater risk of COPD. The highest quartile of lifetime home ETS exposure was associated with a greater risk of COPD, controlling for age, sex, race, personal smoking history, educational attainment, marital status, and occupational exposure to vapors, gas, dusts, or fumes during the longest held job (OR 1.55; 95% CI 1.09 to 2.21). The highest quartile of lifetime workplace ETS exposure was also related to a greater risk of COPD (OR 1.36; 95% CI 1.002 to 1.84). The population attributable fraction was 11% for the highest quartile of home ETS exposure and 7% for work exposure. CONCLUSION: ETS exposure may be an important cause of COPD. Consequently, public policies aimed at preventing public smoking may reduce the burden of COPD-related death and disability, both by reducing direct smoking and ETS exposure

Assessing Recent Smoking Status by Measuring Exhaled Carbon Monoxide Levels

The main expectations of applying proteomics technologies to clinical questions are the discovery of disease related biomarkers. Despite technological advancement to increase proteome coverage and depth to meet these expectations the number of generated biomarkers for clinical use is small. One of the reasons is that found potential biomarkers often are false discoveries. Small sample sizes, in combination with patient sample heterogeneity increase the risk of false discoveries. To be able to extract relevant biological information from such data, high demands are put on the experimental design and the use of sensitive and quantitatively accurate technologies. The overall aim of this thesis was to apply quantitative proteomics methods for biomarker discovery in clinical samples. A method for reducing bias by controlling for individual variation in smoking habits is described in paper I. The aim of the method was objective assessment of recent smoking in clinical studies on inflammatory responses. In paper II, the proteome of alveolar macrophages obtained from smoking subjects with and without the inflammatory lung disease chronic obstructive pulmonary disease (COPD) were quantified by two-dimensional gel-electrophoresis (2-DE). A gender focused analysis showed protein level differences within the female group, with down-regulation of lysosomal pathway and up-regulation of oxidative pathway in COPD patients. Paper III, a mass spectrometry based proteomics analysis of tumour samples, contributes to the molecular understanding of vulvar squamous cell carcinoma (VSCC) and we identified a high risk patient subgroup of HPV-negative tumours based on the expression of four proteins, further suggesting that this subgroup is characterized by an altered ubiquitin-proteasome signalling pathway. Paper III describes a data analysis workflow for the extraction of biological information from quantitative mass spectrometry based proteomics data. High patient-to-patient tumour proteome variability was addressed by using pathway profiling on individual tumour data, followed by comparison of pathway association ranks in a multivariate analysis. We show that pathway data on individual tumour level can detect subpopulations of patients and identify pathways of specific importance in pre-defined clinical groups by the use of multivariate statistics. In paper IV, the potentials and limits of quantitative mass spectrometry on clinical samples was evaluated by defining the quantitative accuracy of isobaric labels and label-free quantification. Quantification by isobaric labels in combination with pI pre-fractionation showed a lower limit of quantification (LOQ) than a label-free analysis without pI pre-fractionation, and 6-plex TMT were more sensitive than 8-plex iTRAQ. Precursor mixing measured by isolation interference (MS1 interference) is more linked to the quantitative accuracy of isobaric labels than reporter ion interference (MS2 interference). Based on that we could define recommendations for how much isolation interference that can be accepted; in our data <30% isolation interference had little effect the quantitative accuracy. In conclusion, getting biological knowledge from proteomics studies requires a careful study design, control of possible confounding factors and the use of clinical data to identify disease subtypes. Further, to be able to draw conclusions from the data, the analysis requires accurate quantitative data and robust statistical tools to detect significant protein alterations. Methods around these issues are developed and discussed in this thesis

Pulmonary Function and Incident Bronchitis and Asthma in Children: A Community-Based Prospective Cohort Study

BACKGROUND: Previous studies revealed that reduction of airway caliber in infancy might increase the risks for wheezing and asthma. However, the evidence for the predictive effects of pulmonary function on respiratory health in children was still inconsistent. METHODS: We conducted a population-based prospective cohort study among children in 14 Taiwanese communities. There were 3,160 children completed pulmonary function tests in 2007 and follow-up questionnaire in 2009. Poisson regression models were performed to estimate the effect of pulmonary function on the development of bronchitis and asthma. RESULTS: After adjustment for potential confounders, pulmonary function indices consistently showed protective effects on respiratory diseases in children. The incidence rate ratios of bronchitis and asthma were 0.86 (95% CI 0.79-0.95) and 0.91 (95% CI 0.82-0.99) for forced expiratory volume in 1 second (FEV₁). Similar adverse effects of maximal mid-expiratory flow (MMEF) were also observed on bronchitis (RR = 0.73, 95% CI 0.67-0.81) and asthma (RR = 0.85, 95% CI 0.77-0.93). We found significant decreasing trends in categorized FEV₁ (p for trend = 0.02) and categories of MMEF (p for trend = 0.01) for incident bronchitis. Significant modification effects of traffic-related air pollution were noted for FEV₁ and MMEF on bronchitis and also for MMEF on asthma. CONCLUSIONS: Children with high pulmonary function would have lower risks on the development of bronchitis and asthma. The protective effect of high pulmonary function would be modified by traffic-related air pollution exposure

Expression of the proapoptotic protein Bid is an adverse prognostic factor for radiotherapy outcome in carcinoma of the cervix

The Bcl-2 family of apoptotic regulators is thought to play an essential role in cancer development and influence the sensitivity of tumour cells to radiotherapy. Bid is an abundantly expressed Bcl-2 family protein playing a central role in various pathways of apoptosis by integrating and converging signals at the mitochondria. The relevance of apoptotic modulation by Bcl-2 and related proteins in tumour development and radiation response for human tumours remains undefined. Therefore, a study was made regarding the expression of Bid in patients with locally advanced cervix carcinoma who received radiotherapy. Bid expression was assessed using immunohistochemistry in pretreatment archival biopsies from 98 patients. The data were correlated with clinicopathologic characteristics and treatment outcome. Pretreatment tumour radiosensitivity data were available for 60 patients. Strong Bid expression was associated with a patient age less than the median of 52 years (P=0.034) and poor metastasis-free survival. In multivariate analysis, after allowing for stage, Bid expression was a significant prognostic factor for both disease-specific and metastasis-free survival (P=0.026). It is concluded that strong tumour Bid expression is associated with poor outcome following radiotherapy regardless of intrinsic tumour cell radiosensitivity, and is adverse prognostic for disease-specific and metastasis-free survival in younger patients