Publications by authors named "Juan Carlos-Romero"

5 Publications

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Clinical and cost-effectiveness analysis of early detection of patients at nutrition risk during their hospital stay through the new screening method CIPA: a study protocol.

BMC Health Serv Res 2017 04 20;17(1):292. Epub 2017 Apr 20.

General and digestive surgery Department, Hospital Universitario Nuestra Señora de Candelaria, Santa Cruz de Tenerife, Spain.

Background: Malnutrition is highly prevalent in hospitalized patients and results in a worsened clinical course as well as an increased length of stay, mortality, and costs. Therefore, simple nutrition screening systems, such as CIPA (control of food intake, protein, anthropometry), may be implemented to facilitate the patient's recovery process. The aim of this study is to evaluate the effectiveness and cost-effectiveness of implementing such screening tool in a tertiary hospital, consistent with the lack of similar, published studies on any hospital nutrition screening system.

Methods: The present study is carried out as an open, controlled, randomized study on patients that were admitted to the Internal Medicine and the General and Digestive Surgery ward; the patients were randomized to either a control or an intervention group (n = 824, thereof 412 patients in each of the two study arms). The control group underwent usual inpatient clinical care, while the intervention group was evaluated with the CIPA screening tool for early detection of malnutrition and treated accordingly. CIPA nutrition screening was performed upon hospital admission and classified positive when at least one of the following parameters was met: 72 h food intake control < 50%, serum albumin < 3 g/dL, body mass index < 18.5 kg/m (or mid-upper arm circumference ≤ 22.5 cm). In this case, the doctor decided on whether or not providing nutrition support. The following variables will be evaluated: hospital length of stay (primary endpoint), mortality, 3-month readmission, and in-hospital complications. Likewise, the quality of life questionnaires EQ-5D-5 L are being collected for all patients at hospital admission, discharge, and 3 months post-discharge. Analysis of cost-effectiveness will be performed by measuring effectiveness in terms of quality-adjusted life years (QALYs). The cost per patient will be established by identifying health care resource utilization; cost-effectiveness will be determined through the incremental cost-effectiveness ratio (ICER). We will calculate the incremental cost per QALY gained with respect to the intervention.

Discussion: This ongoing trial aims to evaluate the cost-effectiveness of implementing the malnutrition screening tool CIPA in a tertiary hospital.

Trial Registration: Clinical ( NCT02721706 ). First receivevd: March 1, 2016 Last updated: April 8, 2017 Last verified: April 2017.
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April 2017

Synthesis, anti-inflammatory activity and modeling studies of cycloartane-type terpenes derivatives isolated from Parthenium argentatum.

Bioorg Med Chem 2014 Dec 25;22(24):6893-8. Epub 2014 Oct 25.

Instituto de Química, Universidad Nacional Autónoma de México, Ciudad Universitaria, Circuito Exterior, Coyoacán, C. P. 04510 México, D.F., Mexico. Electronic address:

The 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced edema model in mice determined the anti-inflammatory activities in vivo of argentatins A, B and D, the main cycloartenol-type triterpenes present in Parthenium argentatum. Our results showed that argentatin B (ED50=1.5×10(-4)mmol/ear) and argentatin A (ED50=2.8×10(-4)mmol/ear) were more potent anti-inflammatory agents than indomethacin (ED50=4.5×10(-4)mmol/ear), the reference drug. Based on these findings, we decided to evaluate 13 derivatives of argentatins A and B. All the derivatives showed anti-inflammatory activity in the TPA-induced edema model in mice. The most active compound was 25-nor-cycloart-3, 16-dione-17-en-24-oic acid, obtained from argentatin A (ED50=1.4×10(-4)mmol/ear). Argentatin B was assayed as inhibitor of COX-2 activity one of the key enzymes involved in the TPA assay. The results showed that argentatin B at 15μM doses inhibited 77% COX-2 activity. Docking studies suggest that argentatin B interacts with Arg 120, a key residue for COX-2 activity.
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December 2014

Determinations of renal cortical and medullary oxygenation using blood oxygen level-dependent magnetic resonance imaging and selective diuretics.

Invest Radiol 2011 Jan;46(1):41-7

Department of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, MN 55905, USA.

Objective: This study was undertaken to test the hypothesis that blood O2 level-dependent magnetic resonance imaging (BOLD MRI) can detect changes in cortical proximal tubule (PT) and medullary thick ascending limb of Henle (TAL) oxygenation consequent to successive administration of furosemide and acetazolamide (Az). Assessment of PT and TAL function could be useful to monitor renal disease states in vivo. Therefore, the adjunct use of diuretics that inhibit Na reabsorption selectively in PT and TAL, Az and furosemide, respectively, may help discern tubular function by using BOLD MRI to detect changes in tissue oxygenation.

Material And Methods: BOLD MRI signal R2* (inversely related to oxygenation) and tissue oxygenation with intrarenal O2 probes were measured in pigs that received either furosemide (0.05 mg/kg) or Az (15 mg/kg) alone, Az sequentially after furosemide (n = 6 each, 15-minute intervals), or only saline vehicle (n = 3).

Results: R2* decreased in the cortex of Az-treated and medulla of furosemide-treated kidneys, corresponding to an increase in their tissue O2 assessed with probes. However, BOLD MRI also showed decreased cortical R2* following furosemide that was additive to the Az-induced decrease. Az administration, both alone and after furosemide, also decreased renal blood flow (-26% ± 3.5% and -29.2% ± 3%, respectively, P < 0.01).

Conclusion: These results suggest that an increase in medullary and cortical tissue O2 elicited by selective diuretics is detectable by BOLD MRI, but may be complicated by hemodynamic effects of the drugs. Therefore, the BOLD MRI signal may reflect functional changes additional to oxygenation, and needs to be interpreted cautiously.
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January 2011

Increased hypoxia and reduced renal tubular response to furosemide detected by BOLD magnetic resonance imaging in swine renovascular hypertension.

Am J Physiol Renal Physiol 2009 Oct 29;297(4):F981-6. Epub 2009 Jul 29.

Department of Physiology and Biomedical Engineering, Rochester, MN 55905, USA.

Oxygen consumption beyond the proximal tubule is mainly determined by active solute reabsorption, especially in the thick ascending limb of the Loop of Henle. Furosemide-induced suppression of oxygen consumption (FSOC) involves inhibition of sodium transport in this segment, which is normally accompanied by a marked decrease in the intrarenal deoxyhemoglobin detectable by blood oxygen level-dependent (BOLD)-magnetic resonance imaging (MRI). This study tested the hypothesis that the magnitude of BOLD-MRI signal change after furosemide is related to impaired renal function in renovascular hypertension. In 16 pigs with unilateral renal artery stenosis, renal hemodynamics, function, and tubular function (FSOC and fluid concentration capacity) were evaluated in both kidneys using MR and multidetector computerized tomography (MDCT) imaging. Animals with adequate FSOC (23.6 +/- 2.2%, P > 0.05 vs. baseline) exhibited a mean arterial pressure (MAP) of 113 +/- 7 mmHg, and relatively preserved glomerular filtration rate (GFR) of 60 +/- 4.5 ml/min, comparable to their contralateral kidney (66 +/- 4 ml/min, P > 0.05). In contrast, animals with low FSOC (3.1 +/- 2.1%, P = NS vs. baseline) had MAP of 124 +/- 9 mmHg and GFR (22 +/- 6 ml/min) significantly lower than the contralateral kidneys (66 +/- 4 ml/min, P < 0.05). The group with preserved GFR and FSOC showed an increase in intratubular fluid concentration as assessed by MDCT that was greater than that observed in the low GFR group, suggesting better preservation of tubular function in the former group. These results suggest that changes in BOLD-MRI after furosemide can differentiate between underperfused kidneys with preserved tubular function and those with tubular dysfunction. This approach may allow more detailed physiologic evaluation of poststenotic kidneys in renovascular hypertension than previously possible.
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October 2009

Effect of salt on isoprostanes in salt-sensitive essential hypertension.

Hypertension 2006 Mar 23;47(3):434-40. Epub 2006 Jan 23.

Department of Pharmacology, New York Medical College, Valhalla, NY 10595, USA.

The controversy over beneficial versus harmful effects of salt on cardiovascular outcomes may be caused by different effects of salt on intermediate phenotypes of hypertension not characterized in epidemiological studies. Hence, we investigated acute effects of salt on oxidative stress in hypertensive subjects classified as salt sensitive (SS, n=14) or salt resistant (SR, n=13) by an inpatient protocol of salt loading (460 mmol NaCl) and salt depletion (10 mmol NaCl and furosemide). Oxidative stress was assessed by measuring the plasma isoprostane 8-iso-PGF2alpha. SS had lower plasma renin activity, higher aldosterone/renin ratios, and exaggerated endothelin and catecholamine responses to salt depletion compared with SR. Baseline lipid-bound isoprostanes (749+/-70 pmol/L) were 83% of the total and were slightly but not significantly higher in SS than SR. Baseline free isoprostanes did not differ between groups. After salt loading, lipid-bound isoprostanes were higher in SS (945+/-106) than SR (579+/-57; P<0.01). Salt depletion significantly decreased them in SS (-174+/-84) and increased them in SR (+129+/-58), equalizing their levels (771+/-61 versus 708+/-91; P value not significant). Free isoprostanes were decreased by salt depletion only if data in all of the patients were analyzed together. Total isoprostanes followed the pattern of the lipid-bound fraction. Correlations between salt depletion-induced changes in lipid-bound isoprostanes, plasma renin activity (r=0.45; P<0.02), and aldosterone/renin ratios (r=-0.41; P<0.04) suggested that the more SS the patient, the greater the reduction of oxidative stress by salt depletion. Our research is the first to show that salt affects oxidative stress acutely in humans, particularly in SS hypertension, which may explain the controversial results of epidemiological studies on salt and morbidity and may have implications for therapy.
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March 2006