Mapping the structure of Borneo's tropical forests across a degradation gradient

South East Asia has the highest rate of lowland forest loss of any tropical region, with logging and deforestation for conversion to plantation agriculture being flagged as the most urgent threats. Detecting and mapping logging impacts on forest structure is a primary conservation concern, as these impacts feed through to changes in biodiversity and ecosystem functions. Here, we test whether high-spatial resolution satellite remote sensing can be used to map the responses of aboveground live tree biomass (AGB), canopy leaf area index (LAI) and fractional vegetation cover (FCover) to selective logging and deforestation in Malaysian Borneo. We measured these attributes in permanent vegetation plots in rainforest and oil palm plantations across the degradation landscape of the Stability of Altered Forest Ecosystems project. We found significant mathematical relationships between field-measured structure and satellite-derived spectral and texture information, explaining up to 62% of variation in biophysical structure across forest and oil palm plots. These relationships held at different aggregation levels from plots to forest disturbance types and oil palms allowing us to map aboveground biomass and canopy structure across the degradation landscape. The maps reveal considerable spatial variation in the impacts of previous logging, a pattern that was less clear when considering field data alone. Up-scaled maps revealed a pronounced decline in aboveground live tree biomass with increasing disturbance, impacts which are also clearly visible in the field data even a decade after logging. Field data demonstrate a rapid recovery in forest canopy structure with the canopy recovering to pre-disturbance levels a decade after logging. Yet, up-scaled maps show that both LAI and FCover are still reduced in logged compared to primary forest stands and markedly lower in oil palm stands. While uncertainties remain, these maps can now be utilised to identify conservation win–wins, especially when combining them with ongoing biodiversity surveys and measurements of carbon sequestration, hydrological cycles and microclimate

Structural Characteristics and Stellar Composition of Low Surface Brightness Disk Galaxies

We present UBVI surface photometry of a sample of low surface brightness (LSB) disk galaxies. LSB disk galaxies are fairly well described as exponential disks with no preferred value for either scale length, central surface brightness, or rotational velocity. Indeed, the distribution of scale lengths is indistinguishable from that of high surface brightness spirals, indicating that dynamically similar galaxies (e.g., those with comparable Rv^2) exist over a large range in surface density. These LSB galaxies are strikingly blue. The complete lack of correlation between central surface brightness and color rules out any fading scenario. Similarly, the oxygen abundances inferred from HII region spectra are uncorrelated with color so the low metallicities are not the primary cause of the blue colors. While these are difficult to interpret in the absence of significant star formation, the most plausible scenario is a stellar population with a young mean age stemming from late formation and subsequent slow evolution. These properties suggest that LSB disks formed from low initial overdensities with correspondingly late collapse times.Comment: Astronomical Journal, in press 45 pages uuencoded postscript (368K) including 9 multipart figures also available by anonymous ftp @ ftp.ast.cam.ac.uk /pub/ssm/phot.uu CAP-30-210442962983742937

Platelet Serotonin Level Predicts Survival in Amyotrophic Lateral Sclerosis

International audienceBACKGROUND: Amyotrophic lateral sclerosis (ALS) is a life-threatening neurodegenerative disease involving upper and lower motor neurons loss. Clinical features are highly variable among patients and there are currently few known disease-modifying factors underlying this heterogeneity. Serotonin is involved in a range of functions altered in ALS, including motor neuron excitability and energy metabolism. However, whether serotoninergic activity represents a disease modifier of ALS natural history remains unknown. METHODOLOGY: Platelet and plasma unconjugated concentrations of serotonin and plasma 5-HIAA, the major serotonin metabolite, levels were measured using HPLC with coulometric detection in a cohort of 85 patients with ALS all followed-up until death and compared to a control group of 29 subjects. PRINCIPAL FINDINGS: Platelet serotonin levels were significantly decreased in ALS patients. Platelet serotonin levels did not correlate with disease duration but were positively correlated with survival of the patients. Univariate Cox model analysis showed a 57% decreased risk of death for patients with platelet serotonin levels in the normal range relative to patients with abnormally low platelet serotonin (p = 0.0195). This protective effect remained significant after adjustment with age, gender or site of onset in multivariate analysis. Plasma unconjugated serotonin and 5-HIAA levels were unchanged in ALS patients compared to controls and did not correlate with clinical parameters. CONCLUSIONS/SIGNIFICANCE: The positive correlation between platelet serotonin levels and survival strongly suggests that serotonin influences the course of ALS disease

Evaluation of internet access and utilization by medical students in Lahore, Pakistan

<p>Abstract</p> <p>Background</p> <p>The internet is increasingly being used worldwide in imparting medical education and improving its delivery. It has become an important tool for healthcare professionals training but the data on its use by medical students in developing countries is lacking with no study on the subject from Pakistan. This study was, therefore, carried out with an aim to evaluate the pattern of internet access and utilization by medical students in Pakistan.</p> <p>Methods</p> <p>A structured pre-tested questionnaire was administered to a group of 750 medical students in clinical years studying at various public and private medical colleges in Lahore. The questions were related to patterns of internet access, purpose of use and self reported confidence in performing various internet related tasks, use of health related websites to supplement learning and the problems faced by students in using internet at the institution.</p> <p>Results</p> <p>A total of 532 medical students (70.9%) returned the questionnaire. The mean age of study participants was 21.04 years (SD 1.96 years). Majority of the respondents (84.0%) reported experience with internet use. About half of the students (42.1%) were using internet occasionally with 23.1%, 20.9% and 13.9% doing so frequently, regularly and rarely respectively. About two third of the students (61.0%) stated that they use internet for both academic and professional activities. Most of the participants preferred to use internet at home (70.5%). Self reported ability to search for required article from PubMed and PakMedinet was reported by only 34.0% of the entire sample. Students were moderately confident in performing various internet related tasks including downloading medical books from internet, searching internet for classification of diseases and downloading full text article. Health related websites were being accessed by 55.1% students to supplement their learning process. Lack of time, inadequate number of available computers and lack of support from staff were cited as the most common problems faced by students while accessing internet in the institution premises. There were significant differences among male and female students with respect to the place of internet use (p = 0.001) and the ability to search online databases for required articles (p = 0.014).</p> <p>Conclusions</p> <p>Majority of the medical students in this study had access to internet and were using it for both academic and personal reasons. Nevertheless, it was seen that there is under utilization of the potential of internet resources to augment learning. Increase in awareness, availability of requisite facilities and training in computing skills are required to enable better utilization of digital resources of digital resources by medical students.</p

Common Inherited Variation in Mitochondrial Genes Is Not Enriched for Associations with Type 2 Diabetes or Related Glycemic Traits

Mitochondrial dysfunction has been observed in skeletal muscle of people with diabetes and insulin-resistant individuals. Furthermore, inherited mutations in mitochondrial DNA can cause a rare form of diabetes. However, it is unclear whether mitochondrial dysfunction is a primary cause of the common form of diabetes. To date, common genetic variants robustly associated with type 2 diabetes (T2D) are not known to affect mitochondrial function. One possibility is that multiple mitochondrial genes contain modest genetic effects that collectively influence T2D risk. To test this hypothesis we developed a method named Meta-Analysis Gene-set Enrichment of variaNT Associations (MAGENTA; http://www.broadinstitute.org/mpg/magenta). MAGENTA, in analogy to Gene Set Enrichment Analysis, tests whether sets of functionally related genes are enriched for associations with a polygenic disease or trait. MAGENTA was specifically designed to exploit the statistical power of large genome-wide association (GWA) study meta-analyses whose individual genotypes are not available. This is achieved by combining variant association p-values into gene scores and then correcting for confounders, such as gene size, variant number, and linkage disequilibrium properties. Using simulations, we determined the range of parameters for which MAGENTA can detect associations likely missed by single-marker analysis. We verified MAGENTA's performance on empirical data by identifying known relevant pathways in lipid and lipoprotein GWA meta-analyses. We then tested our mitochondrial hypothesis by applying MAGENTA to three gene sets: nuclear regulators of mitochondrial genes, oxidative phosphorylation genes, and ∼1,000 nuclear-encoded mitochondrial genes. The analysis was performed using the most recent T2D GWA meta-analysis of 47,117 people and meta-analyses of seven diabetes-related glycemic traits (up to 46,186 non-diabetic individuals). This well-powered analysis found no significant enrichment of associations to T2D or any of the glycemic traits in any of the gene sets tested. These results suggest that common variants affecting nuclear-encoded mitochondrial genes have at most a small genetic contribution to T2D susceptibility

Epigenetic and Genetic Factors Predict Women's Salivary Cortisol following a Threat to the Social Self

10.1371/journal.pone.0048597PLoS ONE711

Multiple Cellular Responses to Serotonin Contribute to Epithelial Homeostasis

Epithelial homeostasis incorporates the paradoxical concept of internal change (epithelial turnover) enabling the maintenance of anatomical status quo. Epithelial cell differentiation and cell loss (cell shedding and apoptosis) form important components of epithelial turnover. Although the mechanisms of cell loss are being uncovered the crucial triggers that modulate epithelial turnover through regulation of cell loss remain undetermined. Serotonin is emerging as a common autocrine-paracine regulator in epithelia of multiple organs, including the breast. Here we address whether serotonin affects epithelial turnover. Specifically, serotonin's roles in regulating cell shedding, apoptosis and barrier function of the epithelium. Using in vivo studies in mouse and a robust model of differentiated human mammary duct epithelium (MCF10A), we show that serotonin induces mammary epithelial cell shedding and disrupts tight junctions in a reversible manner. However, upon sustained exposure, serotonin induces apoptosis in the replenishing cell population, causing irreversible changes to the epithelial membrane. The staggered nature of these events induced by serotonin slowly shifts the balance in the epithelium from reversible to irreversible. These finding have very important implications towards our ability to control epithelial regeneration and thus address pathologies of aberrant epithelial turnover, which range from degenerative disorders (e.g.; pancreatitis and thyrioditis) to proliferative disorders (e.g.; mastitis, ductal ectasia, cholangiopathies and epithelial cancers)

Cytokine Gene Polymorphisms across Tuberculosis Clinical Spectrum in Pakistani Patients

BACKGROUND: Pakistan ranks 7(th) globally in terms of tuberculosis (TB) disease burden (incidence 181/100000 pop./yr; prevalence of 329/pop./yr). Reports from different populations show variable associations of TB susceptibility and severity with cytokine gene polymorphisms. Tuberculosis clinical severity is multi-factorial and cytokines play a pivotal role in the modulation of disease severity. We have recently reported that the ratio of two key cytokines (IFNgamma and IL10) show significant correlation with the severity spectrum of tuberculosis. The objective of the current study was to analyze the frequency of cytokine gene polymorphisms linked to high and low responder phenotypes (IFNgamma +874 T(hi)-->A(lo) and IL10 -1082 G(lo)-->A(hi)) in tuberculosis patients. METHODS AND FINDINGS: STUDY GROUPS WERE STRATIFIED ACCORDING TO DISEASE SITE AS WELL AS DISEASE SEVERITY: Pulmonary N = 111 (Minimal, PMN = 19; Moderate, PMD = 63; Advance, PAD = 29); Extra-pulmonary N = 67 (Disseminated DTB = 20, Localized LTB = 47) and compared with healthy controls (TBNA = 188). Genotype analyses were carried out using amplification refractory mutation system-PCR (ARMS-PCR) and stimulated whole blood (WB) culture assay was used for assessing cytokine profiles. Our results suggest that the IFNgamma +874 TT genotype and T allele was overrepresented in PMN (p = 0.01) and PMD (p = 0.02). IFNgamma +874 TT in combination with IL10 GG(lo) genotypes showed the highest association (chi(2) = 6.66, OR = 6.06, 95% CI = 1.31-28.07, p = 0.01). IFNgamma AA(lo) on the other hand in combination with IL10 GG(lo) increased the risk of PAD (OR = 5.26; p = 0.005) and DTB (OR = 3.59; p = 0.045). CONCLUSION: These findings are consistent with the role of IL10 in reducing collateral tissue damage and the protective role of IFNgamma in limiting disease in the lung