Modelling the Warm H2 Infrared Emission of the Helix Nebula Cometary Knots

Molecular hydrogen emission is commonly observed in planetary nebulae. Images taken in infrared H2 emission lines show that at least part of the molecular emission is produced inside the ionised region. In the best-studied case, the Helix nebula, the H2 emission is produced inside cometary knots (CKs), comet-shaped structures believed to be clumps of dense neutral gas embedded within the ionised gas. Most of the H2 emission of the CKs seems to be produced in a thin layer between the ionised diffuse gas and the neutral material of the knot, in a mini photodissociation region (PDR). However, PDR models published so far cannot fully explain all the characteristics of the H2 emission of the CKs. In this work, we use the photoionisation code \textsc{Aangaba} to study the H2 emission of the CKs, particularly that produced in the interface H^+/H^0 of the knot, where a significant fraction of the H2 1-0S(1) emission seems to be produced. Our results show that the production of molecular hydrogen in such a region may explain several characteristics of the observed emission, particularly the high excitation temperature of the H2 infrared lines. We find that the temperature derived from H2 observations even of a single knot, will depend very strongly on the observed transitions, with much higher temperatures derived from excited levels. We also proposed that the separation between the H_alpha and NII peak emission observed in the images of CKs may be an effect of the distance of the knot from the star, since for knots farther from the central star the NII line is produced closer to the border of the CK than H_alpha.Comment: Accepted by MNRAS. The paper contains 12 pages, 9 figures, and 3 table

Parameters optimization for enzymatic assays using experimental design

The conditions for maximization enzymatic activity were determined using experimental design and inulinase from Kluyveromyces marxianus ATCC 16045. The effects of substrate concentration (sucrose and inulin), pH and temperature on inulinase activity were verified using four factorial design and surface response analysis. Using sucrose as substrate. It has bean shown that the effects sucrose on enzymatic activity is not statistically significant and the best condition for the highest activity (110 U/mL) was achieved with temperature between 60°C and 68°C and pH between 4.5 and 5.0. Using inulin as substrate it was verified that temperature is the only variable statistically significant and the maximum activity was 7.3 U/mL at temperature between 50°C and 51°C

Processo De Obtenção De Dextrana Clìnica Oligossacarìdeos E Frutose A Partir Da Sacarose

PROCESSO DE OBTENÇÃO DE DEXTRANA CLÍNICA, OLIGOSSACARÍDEOS E FRUTOSE A PARTIR DA SACAROSE. A presente invenção se refere a um processo de obtenção de dextrana clínica, frutose e oligossacaríeos a partir de sacarose, utilizando a enzima dextrana-sacarose de Leuconostoc mesenteroides NRRL B512 F. Os produtos citados são obtidos através de síntese enzimática, hidrólise química, fracionamento e separação de oligossacarídeos e frutose, através de colunas de adsorção, com leito de zeólita bárica, e de permeação em gel. A dextrana clínica tem diversas aplicações principalmente na indústria farmacêutica (sendo utilizada como expansor volumétrico de sangue e auxiliador da circulação sanguínea entre outros), os oligossacarídeos são muito aplicados em alimentos, como fibras solúveis e alimentos pré-biótícos, ou seja, compostos que estimulam a flora benéfica, microrganismos ditos pró-bióticos, dos intestinos de humanos e animais em geral. Também são utilizados em cosméticos, sendo cada vez maior o número de aplicações possíveis. A frutose é um produto secundário gerado durante a síntese, em que a sacarose é quebrada para a formação da dextrana, gerando a frutose livre. Devido á sua importância econômica a flutose é recuperada neste processo, obtendo-se, portanto, um aproveitamento completo do açúcar utilizado.BRPI0400893 (A)C12P19/08C12R1/01C12P19/08C12R1/01BR2004PI00893C12P19/08C12R1/01C12P19/08C12R1/0

Peak O2‐pulse predicts exercise training‐induced changes in peak V̇O2 in heart failure with preserved ejection fraction

Abstract Aims Exercise training (ET) has been consistently shown to increase peak oxygen consumption (V̇O2) in patients with heart failure with preserved ejection fraction (HFpEF); however, inter‐individual responses vary significantly. Because it is unlikely that ET‐induced improvements in peak V̇O2 are significantly mediated by an increase in peak heart rate (HR), we aimed to investigate whether baseline peak O2‐pulse (V̇O2 × HR−1, reflecting the product of stroke volume and arteriovenous oxygen difference), not baseline peak V̇O2, is inversely associated with the change in peak V̇O2 (adjusted by body weight) following ET versus guideline control (CON) in patients with HFpEF. Methods and results This was a secondary analysis of the OptimEx‐Clin (Optimizing Exercise Training in Prevention and Treatment of Diastolic Heart Failure, NCT02078947) trial, including all 158 patients with complete baseline and 3 month cardiopulmonary exercise testing measurements (106 ET, 52 CON). Change in peak V̇O2 (%) was analysed as a function of baseline peak V̇O2 and its determinants (absolute peak V̇O2, peak O2‐pulse, peak HR, weight, haemoglobin) using robust linear regression analyses. Mediating effects on change in peak V̇O2 through changes in peak O2‐pulse, peak HR and weight were analysed by a causal mediation analysis with multiple correlated mediators. Change in submaximal exercise tolerance (V̇O2 at the ventilatory threshold, VT1) was analysed as a secondary endpoint. Among 158 patients with HFpEF (66% female; mean age, 70 ± 8 years), changes in peak O2‐pulse explained approximately 72% of the difference in changes in peak V̇O2 between ET and CON [10.0% (95% CI, 4.1 to 15.9), P = 0.001]. There was a significant interaction between the groups for the influence of baseline peak O2‐pulse on change in peak V̇O2 (interaction P = 0.04). In the ET group, every 1 mL/beat higher baseline peak O2‐pulse was associated with a decreased mean change in peak V̇O2 of −1.45% (95% CI, −2.30 to −0.60, P = 0.001) compared with a mean change of −0.08% (95% CI, −1.11 to 0.96, P = 0.88) following CON. None of the other factors showed significant interactions with study groups for the change in peak V̇O2 (P > 0.05). Change in V̇O2 at VT1 was not associated with any of the investigated factors (P > 0.05). Conclusions In patients with HFpEF, the easily measurable peak O2‐pulse seems to be a good indicator of the potential for improving peak V̇O2 through exercise training. While changes in submaximal exercise tolerance were independent of baseline peak O2‐pulse, patients with high O2‐pulse may need to use additional therapies to significantly increase peak V̇O2