Liquid Galaxy POIs Controller

Per tal de contextualitzar la proposta del TFG, al llarg d'aquesta memòria, presentarem el programa Google Summer of Code (durant la memòria també referenciat com a “GSoC”). Així doncs, introduirem els conceptes de GSoC, algunes dades històricament significatives, l’estructura que el composa, la seva organització, el procediment per a escollir els membres que en formaran part i la meva relació amb el programa. També explicarem breument què és el projecte Open Source Liquid Galaxy (d’aquí en endavant anomenat també com “LG”), en què consisteix, la relació amb els dos projectes que vam presentar al GSoC 2015 (Liquid Galaxy POIs Controller, el qual va ser finalment escollit, i Wikipedia Liquid Galaxy Mashup) i algunes de les seves característiques. Posteriorment, essent el nucli d’informació més rellevant d’aquesta memòria, expliquem les tasques realitzades prèviament a l’inici del projecte com són l’aprenentatge de tecnologies i llenguatges nous, la presa de requeriments i riscs, l’establiment dels objectius del projecte i el càlcul de la línia de temps que guia aquest. Definim l’estructura de la base de dades de l’aplicació i exposem exemples del seu funcionament, expliquem el disseny i l’estructura de l’aplicació, tant en aspectes a nivell d’usuari com a nivell d’implementació, detallem l’evolució de l’aplicació juntament amb els problemes sorgits i les corresponents solucions i finalment determinem les tasques que s’han de realitzar per finalitzar la implementació de l’aplicació juntament amb una avaluació del treball realitzat

Baseline characteristics of the participants in different quartiles of uric acid levels.

*<p>To convert to SI unit multiply by 59.48.</p>**<p>P-value adjusted for age and sex for continuous measure of uric acid.</p>†<p>Standard Deviation.</p

The association between serum uric acid (mg/dL) and decline in estimated glomerular filtration rate (ml/min per 1.73 m²).

*<p>CI: confidence interval.</p>**<p>Adjusted for age, sex, and baseline eGFR.</p>†<p>Adjusted for age, sex, systolic blood pressure, body mass index, alcohol consumption, smoking, high density lipoprotein, diabetes mellitus, coronary heart disease, total cholesterol, and the use of diuretics, beta blockers, calcium channel blockers, ACE inhibitors, and baseline eGFR.</p

The association between serum uric acid (mg/dL) and incidence of chronic kidney disease.

*<p>HR: hazard ratio.</p>**<p>CI: confidence interval.</p>†<p>Adjusted for age, sex, and baseline eGFR.</p>††<p>Adjusted for age, sex, systolic blood pressure, body mass index, alcohol consumption, smoking, high density lipoprotein, diabetes mellitus, coronary heart disease, total cholesterol, diuretics, beta blockers, calcium channel blockers, ACE inhibitors, and baseline eGFR.</p

Population for analysis.

<p>Population for analysis.</p

Forest plot of multivariate adjusted relative risk for CKD incidence associated with continuous values of serum uric acid (mg/dL).

<p>Forest plot of multivariate adjusted relative risk for CKD incidence associated with continuous values of serum uric acid (mg/dL).</p

Flow diagram of studies through the different phases of the meta-analysis.

<p>Flow diagram of studies through the different phases of the meta-analysis.</p

Association of serum uric acid with kidney function in normotensive and hypertensive subjects (A) Annual decline in eGFR in relation to serum uric acid quartiles in hypertensive and normotensive participants.

<p>Analyses are adjusted for age, sex and baseline eGFR. Quartiles are compared with participants in the first quartile of serum uric acid (<4.5 mg/dL) (<b>B</b>) Risk of incident CKD in relation to quartiles of serum uric acid level in hypertensive and normotensive participants. Analyses are adjusted for sex, age and baseline eGFR. All odds ratios are compared with participants in the first quartile of serum uric acid (<4.5 mg/dL).</p

NaCl cotransporter abundance in urinary vesicles is increased by calcineurin inhibitors and predicts thiazide sensitivity

<div><p>Animal studies have shown that the calcineurin inhibitors (CNIs) cyclosporine and tacrolimus can activate the thiazide-sensitive NaCl cotransporter (NCC). A common side effect of CNIs is hypertension. Renal salt transporters such as NCC are excreted in urinary extracellular vesicles (uEVs) after internalization into multivesicular bodies. Human studies indicate that CNIs also increase NCC abundance in uEVs, but results are conflicting and no relationship with NCC function has been shown. Therefore, we investigated the effects of CsA and Tac on the abundance of both total NCC (tNCC) and phosphorylated NCC at Thr60 phosphorylation site (pNCC) in uEVs, and assessed whether NCC abundance in uEVs predicts the blood pressure response to thiazide diuretics. Our results show that in kidney transplant recipients treated with cyclosporine (n = 9) or tacrolimus (n = 23), the abundance of both tNCC and pNCC in uEVs is 4–5 fold higher than in CNI-free kidney transplant recipients (n = 13) or healthy volunteers (n = 6). In hypertensive kidney transplant recipients, higher abundances of tNCC and pNCC prior to treatment with thiazides predicted the blood pressure response to thiazides. During thiazide treatment, the abundance of pNCC in uEVs increased in responders (n = 10), but markedly decreased in non-responders (n = 8). Thus, our results show that CNIs increase the abundance of both tNCC and pNCC in uEVs, and these increases correlate with the blood pressure response to thiazides. This implies that assessment of NCC in uEVs could represent an alternate method to guide anti-hypertensive therapy in kidney transplant recipients.</p></div

pNCC and tNCC abundances in uEVs before and after treatment with chlorthalidone.

<p>Panel A shows pNCC and tNCC abundances in uEVs before (B) and after (A) the 8-week treatment period with chlorthalidone in both responders (n = 10) and non-responders (n = 8). The fold-changes in the before-after abundances of pNCC and tNCC in uEVs (as measured by densitometry) of both responders and non-responders are shown in panel B (Fold-change of 1 means no change, *<i>P</i><0.05). The scatter plots represent the fold change in tNCC, pNCC or their ratio after treatment with chlorthalidone (densitometry values before treatment with chlorthalidone were set to 1). <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0176220#pone.0176220.s010" target="_blank">S5</a> and <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0176220#pone.0176220.s011" target="_blank">S6</a> Figs, show the original immunoblots from which the individual panels in Fig 4A were derived.</p