NDVI With Artificial Neural Networks For SRTM Elevation Model Improvement – Hydrological Model Application

Digital elevation model (DEM) plays a substantial role in hydrological study, from understanding the catchment characteristics, setting up a hydrological model to mapping the flood risk in the region. Depending on the nature of study and its objectives, high resolution and reliable DEM is often desired to set up a sound hydrological model. However, such source of good DEM is not always available and it is generally high-priced. Obtained through radar based remote sensing, Shuttle Radar Topography Mission (SRTM) is a publicly available DEM with resolution of 92m outside US. It is a great source of DEM where no surveyed DEM is available. However, apart from the coarse resolution, SRTM suffers from inaccuracy especially on area with dense vegetation coverage due to the limitation of radar signals not penetrating through canopy. This will lead to the improper setup of the model as well as the erroneous mapping of flood risk. This paper attempts on improving SRTM dataset, using Normalised Difference Vegetation Index (NDVI), derived from Visible Red and Near Infra-Red band obtained from Landsat with resolution of 30m, and Artificial Neural Networks (ANN). The assessment of the improvement and the applicability of this method in hydrology would be highlighted and discussed

Finishing the euchromatic sequence of the human genome

The sequence of the human genome encodes the genetic instructions for human physiology, as well as rich information about human evolution. In 2001, the International Human Genome Sequencing Consortium reported a draft sequence of the euchromatic portion of the human genome. Since then, the international collaboration has worked to convert this draft into a genome sequence with high accuracy and nearly complete coverage. Here, we report the result of this finishing process. The current genome sequence (Build 35) contains 2.85 billion nucleotides interrupted by only 341 gaps. It covers ∼99% of the euchromatic genome and is accurate to an error rate of ∼1 event per 100,000 bases. Many of the remaining euchromatic gaps are associated with segmental duplications and will require focused work with new methods. The near-complete sequence, the first for a vertebrate, greatly improves the precision of biological analyses of the human genome including studies of gene number, birth and death. Notably, the human enome seems to encode only 20,000-25,000 protein-coding genes. The genome sequence reported here should serve as a firm foundation for biomedical research in the decades ahead

Antecedent Hindbrain Glucoprivation Does Not Impair the Counterregulatory Response to Hypoglycemia

Recurrent hypoglycemia impairs hormonal counterregulatory responses (CRRs) to further bouts of hypoglycemia. The hypothalamus and hindbrain are both critical for sensing hypoglycemia and triggering CRRs. Hypothalamic glucose sensing sites are implicated in the pathogenesis of defective CRRs; however, the contribution of hindbrain glucose sensing has not been elucidated. Using a rat model, we compared the effect of antecedent glucoprivation targeting hindbrain or hypothalamic glucose sensing sites with the effect of antecedent recurrent hypoglycemia on CRR to hypoglycemia induced 24 h later. Recurrent hypoglycemia decreased sympathoadrenal (1,470 ± 325 vs. 3,811 ± 540 pg/ml in controls [t = 60 min], P = 0.001) and glucagon secretion (222 ± 43 vs. 494 ± 56 pg/ml in controls [t = 60]), P = 0.003) in response to hypoglycemia. Antecedent 5-thio-glucose (5TG) injected into the hindbrain did not impair sympathoadrenal (3,806 ± 344 pg/ml [t = 60]) or glucagon (513 ± 56 pg/ml [t = 60]) responses to subsequent hypoglycemia. However, antecedent 5TG delivered into the third ventricle was sufficient to blunt CRRs to hypoglycemia. These results show that hindbrain glucose sensing is not involved in the development of defective CRRs. However, neural substrates surrounding the third ventricle are particularly sensitive to glucoprivic stimulation and may contribute importantly to the development of defective CRRs.There is a long history of anatomical and pharmacological evidence supporting the role of both the hypothalamus (6–14) and hindbrain (15–18) in glucose sensing and in the initiation of hormonal CRRs. Although there is evidence supporting the role of the hypothalamus, in particular the ventromedial nucleus, in the development of defective hypoglycemic CRRs (10,19–21), the contribution of hindbrain glucose sensing mechanisms is unknown. Given their anatomical differences and the fact that hindbrain glucoreceptors can function independently from the hypothalamus (16), recurrent hypoglycemic stimulation may differentially affect these two distinct glucose sensing brain regions. In the present study, we adapted our recurrent hypoglycemia rat model, which results in significant deficits in hormonal CRRs (22), to identify the contribution of a hindbrain glucose sensing site (17) in defective CRRs. We compared the effect of antecedent 5-thio-glucose (5TG), delivered into the hindbrain or third ventricle, with the effect of antecedent recurrent hypoglycemia on hormonal CRRs to subsequent hypoglycemia. We hypothesized that either antecedent hindbrain or third ventricular glucoprivation would impair CRRs to subsequent hypoglycemia. As expected, antecedent third ventricular glucoprivation, similar to recurrent hypoglycemia, blunted hormonal CRRs to subsequent hypoglycemia. In marked contrast, antecedent glucoprivation localized to a caudal hindbrain glucose sensing site did not impair hypoglycemia CRRs. Therefore, the hindbrain does not appear to be vulnerable to the central nervous system's adaptive mechanisms that impair CRRs under conditions of recurren

The selective serotonin reuptake inhibitor sertraline enhances counterregulatory responses to hypoglycemia

Selective serotonin reuptake inhibitors (SSRIs) are widely prescribed for patients with comorbid diabetes and depression. Clinical case studies in diabetic patients, however, suggest that SSRI therapy may exacerbate hypoglycemia. We hypothesized that SSRIs might increase the risk of hypoglycemia by impairing hormonal counterregulatory responses (CRR). We evaluated the effect of the SSRI sertraline on hormonal CRR to single or recurrent hypoglycemia in nondiabetic rats. Since there are time-dependent effects of SSRIs on serotonin neurotransmission that correspond with therapeutic action, we evaluated the effect of 6- or 20-day sertraline treatment on hypoglycemia CRR. We found that 6-day sertraline (SERT) treatment specifically enhanced the epinephrine response to a single bout of hypoglycemia vs. vehicle (VEH)-treated rats (t = 120: VEH, 2,573 ± 448 vs. SERT, 4,202 ± 545 pg/ml, P < 0.05). In response to recurrent hypoglycemia, VEH-treated rats exhibited the expected impairment in epinephrine secretion (t = 60: 678 ± 73 pg/ml) vs. VEH-treated rats experiencing firsttime hypoglycemia (t = 60: 2,081 ± 436 pg/ml, P < 0.01). SERT treatment prevented the impaired epinephrine response in recurrent hypoglycemic rats (t = 60: 1,794 ± 276 pgl/ml). In 20-day SERTtreated rats, epinephrine, norepinephrine, and glucagon CRR were all significantly elevated above VEH-treated controls in response to hypoglycemia. Similarly to 6-day SERT treatment, 20-day SERT treatment rescued the impaired epinephrine response in recurrent hypoglycemic rats. Our data demonstrate that neither 6- nor 20-day sertraline treatment impaired hormonal CRR to hypoglycemia in nondiabetic rats. Instead, sertraline treatment resulted in an enhancement of hypoglycemia CRR and prevented the impaired adrenomedullary response normally observed in recurrent hypoglycemic rats

Activation of persons living with HIV for treatment, the great study Health behavior, health promotion and society

Background: Patient empowerment represents a potent tool for addressing racial, ethnic and socioeconomic disparities in health care, particularly for chronic conditions such as HIV infection that require active patient engagement. This multimodal intervention, developed in concert with HIV patients and clinicians, aims to provide HIV patients with the knowledge, skills, attitudes and tools to become more activated patients. Methods/design: Randomized controlled trial of a multimodal intervention designed to activate persons living with HIV. The intervention includes four components: 1) use of a web-enabled hand-held device (Apple iPod Touch) loaded with a Personal Health Record (ePHR) customized for HIV patients; 2) six 90-minute group-based training sessions in use of the device, internet and the ePHR; 3) a pre-visit coaching session; and 4) clinician education regarding how they can support activated patients. Outcome measures include pre- post changes in patient activation measure score (primary outcome), eHealth literacy, patient involvement in decision-making and care, medication adherence, preventive care, and HIV Viral Load. Discussion: We hypothesize that participants receiving the intervention will show greater improvement in empowerment and the intervention will reduce disparities in study outcomes. Disparities in these measures will be smaller than those in the usual care group. Findings have implications for activating persons living with HIV and for other marginalized groups living with chronic illness. Trial registration: ClinicalTrials.gov Identifier: NCT02165735, 6/13/2014

Strategies and performance of the CMS silicon tracker alignment during LHC Run 2

The strategies for and the performance of the CMS silicon tracking system alignment during the 2015–2018 data-taking period of the LHC are described. The alignment procedures during and after data taking are explained. Alignment scenarios are also derived for use in the simulation of the detector response. Systematic effects, related to intrinsic symmetries of the alignment task or to external constraints, are discussed and illustrated for different scenarios