Climate data system supports FIRE

The NASA Climate Data System (NCDS) at Goddard Space Flight Center is serving as the FIRE Central Archive, providing a centralized data holding and data cataloging service for the FIRE project. NCDS members are carrying out their responsibilities by holding all reduced observations and data analysis products submitted by individual principal investigators in the agreed upon format, by holding all satellite data sets required for FIRE, by providing copies of any of these data sets to FIRE investigators, and by producing and updating a catalog with information about the FIRE holdings. FIRE researchers were requested to provide their reduced data sets in the Standard Data Format (SDF) to the FIRE Central Archive. This standard format is proving to be of value. An improved SDF document is now available. The document provides an example from an actual FIRE SDF data set and clearly states the guidelines for formatting data in SDF. NCDS has received SDF tapes from a number of investigators. These tapes were analyzed and comments provided to the producers. One product which is now available is William J. Syrett's sodar data product from the Stratocumulus Intensive Field Observation. Sample plots from all SDF tapes submitted to the archive will be available to FSET members. Related cloud products are also available through NCDS. Entries describing the FIRE data sets are being provided for the NCDS on-line catalog. Detailed information for the Extended Time Observations is available in the general FIRE catalog entry. Separate catalog entries are being written for the Cirrus Intensive Field Observation (IFO) and for the Marine Stratocumulus IFO. Short descriptions of each FIRE data set will be installed into the NCDS Summary Catalog

Medicolegal Alcohol Determination: Variability of the Blood- to Breath-Alcohol Ratio and Its Effect on Reported Breath-Alcohol Concentrations

Peer Reviewe

The recoverability of fingerprints on paper exposed to elevated temperatures - Part 2: natural fluorescence

Previous work by the authors [1] investigated the recoverability of fingerprints on paper which had been exposed to elevated temperatures by comparing various chemical enhancement techniques (ninhydrin, 1,8-diazafluoren-9-one (DFO), and physical developer (PD)). During that study, it became apparent, as a consequence of observations made in operational work [2], that fingerprints on paper subjected to 150˚C fluoresced under examination with green light of waveband 473-548nm with a 549nm viewing filter. This work examined the three types of prints (eccrine, sebaceous, and ungroomed) after 20 min exposure to the temperature range 110˚C to 190˚C (in 10˚C increments) and found that the eccrine fingerprints fluoresced more brightly. This indicated that it was a component of the eccrine deposit which was causing the fluorescence. Luminance measurements found that the maximum fluorescence was experienced at 170˚C on both types of paper. As a consequence, eccrine heat-treated fingerprints were viewed under violet-blue (350-469nm), blue (352-509nm), and green light (473-548nm) which indicated that the greatest luminance intensities were obtained under blue light and the smallest under green light. In order to determine what component of the eccrine fingerprint was causing this fluorescence, five of the most prevalent amino acids (alanine, aspartic acid, glycine, lysine, and serine) [3-4] were exposed to this temperature range. The luminance measurements were taken under exposure to the green light in order for the minimum fluorescence to be observed, with an assumption that blue-violet or blue illumination will provide brighter fluorescence in practice. The results indicated that four of the amino acids are behaving similarly across the temperature range, but with slightly different luminance measurements, but all are exhibiting some level of fluorescence. Thermal degradation products of alanine and aspartic acid have been suggested by Richmond-Aylor et al. [5]. The structure of these thermal degradation products is cyclic in nature, and as such, there is a possibility that two of these products would fluorescence. Sodium chloride and urea were also exposed to the temperature range and they also fluoresced to some extent. This work shows that eccrine fingerprints that have been exposed to temperatures of between 130˚C to 180˚C will fluoresce under violet-blue, blue, and green light. This level of fluorescence for ungroomed fingerprints is much less but this will be dependent on the individual, the more eccrine the deposit, the stronger the fluorescence. This work shows that the amino acids, sodium chloride, and urea present in fingerprint deposits are all contributing to the fluorescence of the print, but may not be the sole contributor as other eccrine components have not yet been tested

Obesity and type-2 diabetes as inducers of premature cellular senescence and ageing

Cellular senescence is now considered as a major mechanism in the development and progression of various diseases and this may include metabolic diseases such as obesity and type-2 diabetes. The presence of obesity and diabetes is a major risk factor in the development of additional health conditions, such as cardiovascular disease, kidney disease and cancer. Since senescent cells can drive disease development, obesity and diabetes can potentially create an environment that accelerates cell senescence within other tissues of the body. This can consequently manifest as age-related biological impairments and secondary diseases. Cell senescence in cell types linked with obesity and diabetes, namely adipocytes and pancreatic beta cells will be explored, followed by a discussion on the role of obesity and diabetes in accelerating ageing through induction of premature cell senescence mediated by high glucose levels and oxidised low-density lipoproteins. Particular emphasis will be placed on accelerated cell senescence in endothelial progenitor cells, endothelial cells and vascular smooth muscle cells with relation to cardiovascular disease and proximal tubular cells with relation to kidney disease. A summary of the potential strategies for therapeutically targeting senescent cells for improving health is also presented

mTOR regulates the expression of DNA damage response enzymes in long‐lived Snell dwarf, GHRKO, and PAPPA‐KO mice

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/136007/1/acel12525.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/136007/2/acel12525_am.pd

Early recognition of multiple sclerosis using natural language processing of the electronic health record

Background Diagnostic accuracy might be improved by algorithms that searched patients’ clinical notes in the electronic health record (EHR) for signs and symptoms of diseases such as multiple sclerosis (MS). The focus this study was to determine if patients with MS could be identified from their clinical notes prior to the initial recognition by their healthcare providers. Methods An MS-enriched cohort of patients with well-established MS (n = 165) and controls (n = 545), was generated from the adult outpatient clinic. A random sample cohort was generated from randomly selected patients (n = 2289) from the same adult outpatient clinic, some of whom had MS (n = 16). Patients’ notes were extracted from the data warehouse and signs and symptoms mapped to UMLS terms using MedLEE. Approximately 1000 MS-related terms occurred significantly more frequently in MS patients’ notes than controls’. Synonymous terms were manually clustered into 50 buckets and used as classification features. Patients were classified as MS or not using Naïve Bayes classification. Results Classification of patients known to have MS using notes of the MS-enriched cohort entered after the initial ICD9[MS] code yielded an ROC AUC, sensitivity, and specificity of 0.90 [0.87-0.93], 0.75[0.66-0.82], and 0.91 [0.87-0.93], respectively. Similar classification accuracy was achieved using the notes from the random sample cohort. Classification of patients not yet known to have MS using notes of the MS-enriched cohort entered before the initial ICD9[MS] documentation identified 40% [23–59%] as having MS. Manual review of the EHR of 45 patients of the random sample cohort classified as having MS but lacking an ICD9[MS] code identified four who might have unrecognized MS. Conclusions Diagnostic accuracy might be improved by mining patients’ clinical notes for signs and symptoms of specific diseases using NLP. Using this approach, we identified patients with MS early in the course of their disease which could potentially shorten the time to diagnosis. This approach could also be applied to other diseases often missed by primary care providers such as cancer. Whether implementing computerized diagnostic support ultimately shortens the time from earliest symptoms to formal recognition of the disease remains to be seen

UNITED STATES-LATIN AMERICAN TRADE RELATIONS: IMPORTANCE TO U.S. AGRICULTURAL POLICY DECISIONS

International Relations/Trade,

New Molecular Mechanism for Ullrich Congenital Muscular Dystrophy: A Heterozygous In-Frame Deletion in the COL6A1 Gene Causes a Severe Phenotype

Recessive mutations in two of the three collagen VI genes, COL6A2 and COL6A3, have recently been shown to cause Ullrich congenital muscular dystrophy (UCMD), a frequently severe disorder characterized by congenital muscle weakness with joint contractures and coexisting distal joint hyperlaxity. Dominant mutations in all three collagen VI genes had previously been associated with the considerably milder Bethlem myopathy. Here we report that a de novo heterozygous deletion of the COL6A1 gene can also result in a severe phenotype of classical UCMD precluding ambulation. The internal gene deletion occurs near a minisatellite DNA sequence in intron 8 that removes 1.1 kb of genomic DNA encompassing exons 9 and 10. The resulting mutant chain contains a 33–amino acid deletion near the amino-terminus of the triple-helical domain but preserves a unique cysteine in the triple-helical domain important for dimer formation prior to secretion. Thus, dimer formation and secretion of abnormal tetramers can occur and exert a strong dominant negative effect on microfibrillar assembly, leading to a loss of normal localization of collagen VI in the basement membrane surrounding muscle fibers. Consistent with this mechanism was our analysis of a patient with a much milder phenotype, in whom we identified a previously described Bethlem myopathy heterozygous in-frame deletion of 18 amino acids somewhat downstream in the triple-helical domain, a result of exon 14 skipping in the COL6A1 gene. This deletion removes the crucial cysteine, so that dimer formation cannot occur and the abnormal molecule is not secreted, preventing the strong dominant negative effect. Our studies provide a biochemical insight into genotype-phenotype correlations in this group of disorders and establish that UCMD can be caused by dominantly acting mutations

Step 4: stick or twist? A review of asthma therapy

Many people with asthma do not achieve disease control, despite bronchodilators and inhaled corticosteroid therapy. People with uncontrolled asthma are at higher risk of an asthma attack and death, with mortality rates estimated at 1000 deaths/ year in England and Wales. The recent National Review of Asthma Deaths (NRAD) report, ‘Why asthma still kills’, recommended that patients at step 4 or 5 of the British Thoracic Society/Scottish Intercollegiate Guidelines Network (BTS/SIGN) guidance must be referred to a specialist asthma service. This article reviews the 2014 evidence base for therapy of asthma patients at BTS/SIGN step 4 of the treatment cascade, in response to key findings of the NRAD report and lack of preferred treatment option at this step