REDUCED FREQUENCY MOTOR STARTING FOR THIRD WORLD POWER SYSTEMS

People in modern industrialized societies live a blessed life relative to those who do not when it comes to some modern conveniences. While many think nothing of flipping on a light switch or running electric appliances, there are people in third world countries could not imagine such things. As service projects are being undertaken to bring such conveniences to those less fortunate, there often is the harsh reality of a strict budget. An item that commands a large portion of said budget is often the diesel generator used to provide the facility with electricity. Generators serving motor loads are typically oversized due to a large kVA starting requirement. This paper addresses an approach to this problem by temporarily restricting the generator fuel supply by pulling back the rack of the mechanical governor reducing the frequency and voltage output as a motor load is switched onto the system. By reducing the voltage and frequency output of the generator, the motor is switched on at a time when its typically poor power factor and resulting kVA requirement is mitigated by the lower voltage and frequency allowing for a smaller generator to be used

Brain natriuretic peptide and NT-proBNP levels reflect pulmonary artery systolic pressure in trekkers at high altitude.

Our objective was to evaluate the utility of the natriuretic peptides BNP (brain natriuretic peptide) and NT-proBNP as markers of pulmonary artery systolic pressure (PASP) in trekkers ascending to high altitude (HA). 20 participants had BNP and NT-proBNP assayed and simultaneous echocardiographic assessment of PASP performed during a trek to 5150 m. PASP increased significantly (p=0.006) with ascent from 24+/-4 to 39+/-11 mm Hg at 5150 m. At 5150 m those with a PASP>/=40 mm Hg (n=8) (versus those with PASP/=400 pg/ml) rise in NT-proBNP at 5150 m (n=4) PASP was significantly higher: 45.9+/-7.5 vs. 32.2+/-6.2 mm Hg (p=0.015). BNP and NT-proBNP may reflect elevated PASP, a central feature of high altitude pulmonary oedema, at HA

Cancer Biology Data Curation at the Mouse Tumor Biology Database (MTB)

Many advances in the field of cancer biology have been made using mouse models of human cancer. The Mouse Tumor Biology (MTB, "http://tumor.informatics.jax.org":http://tumor.informatics.jax.org) database provides web-based access to data on spontaneous and induced tumors from genetically defined mice (inbred, hybrid, mutant, and genetically engineered strains of mice). These data include standardized tumor names and classifications, pathology reports and images, mouse genetics, genomic and cytogenetic changes occurring in the tumor, strain names, tumor frequency and latency, and literature citations.

Although primary source for the data represented in MTB is peer-reviewed scientific literature an increasing amount of data is derived from disparate sources. MTB includes annotated histopathology images and cytogenetic assay images for mouse tumors where these data are available from The Jackson Laboratory’s mouse colonies and from outside contributors. MTB encourages direct submission of mouse tumor data and images from the cancer research community and provides investigators with a web-accessible tool for image submission and annotation. 

Integrated searches of the data in MTB are facilitated by the use of several controlled vocabularies and by adherence to standard nomenclature. MTB also provides links to other related online resources such as the Mouse Genome Database, Mouse Phenome Database, the Biology of the Mammary Gland Web Site, Festing's Listing of Inbred Strains of Mice, the JAX® Mice Web Site, and the Mouse Models of Human Cancers Consortium's Mouse Repository. 

MTB provides access to data on mouse models of cancer via the internet and has been designed to facilitate the selection of experimental models for cancer research, the evaluation of mouse genetic models of human cancer, the review of patterns of mutations in specific cancers, and the identification of genes that are commonly mutated across a spectrum of cancers.

MTB is supported by NCI grant CA089713

Regulation of Androgen Receptor Co-Regulators by Activation of the CXCL12/CXCR4 Axis: A Microarray and Proteomics Approach

Background: Activation of the CXCL12/CXCR4 axis is known to stimulate androgen-independent activation of the androgen receptor (AR) in the LNCaP prostate cancer cell line. In the present study, the CXCL12-stimulated expression profile of androgen responsive genes (ARGs) and AR:co-regulator protein:protein interactions has been identified by microarray and proteomic analysis, respectively. Methods: To directly identify proteins that interacted with the AR in response to CXCL12 stimulation, LNCaP cells treated with CXCL12 were subjected to a total proteomics analysis after co-immunoprecipitation (co-IP) with anti-AR antibody. AR- interacting proteins from co-IP were pre-fractionated by SDS-PAGE, in-gel trypsin digested, and analyzed by liquid chromatography coupled to MS (nanoLC-MS/MS). Acquired MS2 data was searched using MASCOT against a SWISSProt human database. Detected proteins were analyzed by spectral counting to qualitatively determine significant changes in protein expression. Results: Gene expression profiling and proteomics analysis of CXCL12-treated LNCaP cells indicated a robust regulation of ARGs, including known AR co-regulators and/or AR-interacting proteins. All known AR co-regulators were extracted and segregated according to their molecular function. GTF2 (Transcription factor), ARID1A (Chromatin Remodeling complex component) and PRDX1 (other function) are the AR co-regulators which showed greater than two fold more interaction with AR in response to CXCL12 treatment, and HNRNPD (Splicing and RNA metabolism) is the protein which is commonly differentially regulated in both microarray and proteomic analysis in response to CXCL12 treatment. The potential role of the above AR co-regulators in promoting the CXCL12- mediated and androgen-independent AR activation and hence the prostate cancer is yet to be elucidated. Conclusions: These data shed new light into the role of ARGs and/or AR Co-regulators in CXCL12- mediated androgen independent activation of AR and suggests new therapeutic targets for the treatment of castration-resistant prostate cancers

The Impact of Dreissenid Mussels on Growth of the Fragile Papershell (Leptodea fragilis), the Most Abundant Unionid Species in Lake Erie

The arrival of zebra mussels (Dreissena polymorpha (Pallas, 1771)) and subsequently quagga mussels (Dreissena bugensis Andrusov, 1897) (Dreissenidae) in the Great Lakes in the 1980s induced many changes, most notably the devastation of native freshwater mussel species. Recently, empty shells of the fragile papershell (Leptodea fragilis (Rafinesque, 1820)) have become common, particularly in the western basin of Lake Erie, suggesting that this fast-growing species may be increasing in numbers in the lake. To examine continued competition with dreissenids, shell age and length of L. fragilis were used to contrast lifespan and growth rate, estimated as the slope of age on shell length, for shells from two beach localities where byssal threads were present on most shells and two sites where dreissenids were rare or absent. Few recent shells from Lake Erie beaches exceeded 5 years of age, and byssal thread counts were more numerous on older shells. Growth and lifespan were estimated to be significantly lower where dreissenid mussels remained numerous than when measured either from historic collections along Lake Erie or from protected populations. Therefore, even for this early-reproducing species, competition from dreissenids may continue to interfere with growth and shorten lifespan, which are effects few other unionid species can likely tolerate sufficiently to sustain population growt

Mechanistic determination of tear film thinning via fitting simplified models to tear breakup

Purpose: To determine whether evaporation, tangential flow, or a combination of the two cause tear film breakup in a variety of instances; to estimate related breakup parameters that cannot be measured in breakup during subject trials; and to validate our procedure against previous work. Methods: Five ordinary differential equation models for tear film thinning were designed that model evaporation, osmosis, and various types of flow. Eight tear film breakup instances of five healthy subjects that were identified in fluorescence images in previous work were fit with these five models. The fitting procedure used a nonlinear least squares optimization that minimized the difference of the computed theoretical fluorescent intensity from the models and the experimental fluorescent intensity from the images. The optimization was conducted over the evaporation rate and up to three flow rate parameters. The smallest norm of the difference was determined to correspond to the model that best explained the tear film dynamics. Results: All of the breakup instances were best fit by models with time-dependent flow. Our optimal parameter values and thinning rate and fluid flow profiles compare well with previous partial differential equation model results in most instances. Conclusion: Our fitting procedure suggests that the combination of the Marangoni effect and evaporation cause most of the breakup instances. Comparison with results from previous work suggests that the simplified models can capture the essential tear film dynamics in most cases, thereby validating this procedure as one that could be used on many other instances.Comment: 28 pages, 11 figures, 6 table

Neutrophil gelatinase-associated lipocalin: its response to hypoxia and association with acute mountain sickness.

Acute Mountain Sickness (AMS) is a common clinical challenge at high altitude (HA). A point-of-care biochemical marker for AMS could have widespread utility. Neutrophil gelatinase-associated lipocalin (NGAL) rises in response to renal injury, inflammation and oxidative stress. We investigated whether NGAL rises with HA and if this rise was related to AMS, hypoxia or exercise. NGAL was assayed in a cohort (n = 22) undertaking 6 hours exercise at near sea-level (SL); a cohort (n = 14) during 3 hours of normobaric hypoxia (FiO2 11.6%) and on two trekking expeditions (n = 52) to over 5000 m. NGAL did not change with exercise at SL or following normobaric hypoxia. During the trekking expeditions NGAL levels (ng/ml, mean ± sd, range) rose significantly (P < 0.001) from 68 ± 14 (60-102) at 1300 m to 183 ± 107 (65-519); 143 ± 66 (60-315) and 150 ± 71 (60-357) at 3400 m, 4270 m and 5150 m respectively. At 5150 m there was a significant difference in NGAL between those with severe AMS (n = 7), mild AMS (n = 16) or no AMS (n = 23): 201 ± 34 versus 171 ± 19 versus 124 ± 12 respectively (P = 0.009 for severe versus no AMS; P = 0.026 for mild versus no AMS). In summary, NGAL rises in response to prolonged hypobaric hypoxia and demonstrates a relationship to the presence and severity of AMS

Risks associated with obesity in pregnancy, for the mother and baby: a systematic review of reviews

Maternal obesity is linked with adverse outcomes for mothers and babies. To get an overview of risks related to obesity in pregnant women, a systematic review of reviews was conducted. For inclusion, reviews had to compare pregnant women of healthy weight with women with obesity, and measure a health outcome for mother and/or baby. Authors conducted full-text screening, quality assurance using the AMSTAR tool and data extraction steps in pairs. Narrative analysis of the 22 reviews included show gestational diabetes, pre-eclampsia, gestational hypertension, depression, instrumental and caesarean birth, and surgical site infection to be more likely to occur in pregnant women with obesity compared with women with a healthy weight. Maternal obesity is also linked to greater risk of preterm birth, large-for-gestational-age babies, foetal defects, congenital anomalies and perinatal death. Furthermore, breastfeeding initiation rates are lower and there is greater risk of early breastfeeding cessation in women with obesity compared with healthy weight women. These adverse outcomes may result in longer duration of hospital stay, with concomitant resource implications. It is crucial to reduce the burden of adverse maternal and foetal/child outcomes caused by maternal obesity. Women with obesity need support to lose weight before they conceive, and to minimize their weight gain in pregnancy