Non-Invasive Monitoring of Microvascular Oxygenation and Reactive Hyperemia using Hybrid, Near-Infrared Diffuse Optical Spectroscopy for Critical Care.

The detection of levels of impairment in microvascular oxygen consumption and reactive hyperemia is vital in critical care. However, there are no practical means for a robust and quantitative evaluation. This paper describes a protocol to evaluate these impairments using a hybrid near-infrared diffuse optical device. The device contains modules for near-infrared time-resolved and diffuse correlation spectroscopies and pulse-oximetry. These modules allow the non-invasive, continuous, and real-time measurement of the absolute, microvascular blood/tissue oxygen saturation (StO2) and the blood flow index (BFI) along with the peripheral arterial oxygen saturation (SpO2). This device uses an integrated, computer-controlled tourniquet system to execute a standardized protocol with optical data acquisition from the brachioradialis muscle. The standardized vascular occlusion test (VOT) takes care of the variations in the occlusion duration and pressure reported in the literature, while the automation minimizes inter-operator differences. The protocol we describe focuses on a 3-min occlusion period but the details described in this paper can readily be adapted to other durations and cuff pressures, as well as other muscles. The inclusion of an extended baseline and post-occlusion recovery period measurement allows the quantification of the baseline values for all the parameters and the blood/tissue deoxygenation rate that corresponds to the metabolic rate of oxygen consumption. Once the cuff is released, we characterize the tissue reoxygenation rate, magnitude, and duration of the hyperemic response in BFI and StO2. These latter parameters correspond to the quantification of the reactive hyperemia, which provides information about the endothelial function. Furthermore, the above-mentioned measurements of the absolute concentration of oxygenated and deoxygenated hemoglobin, BFI, the derived metabolic rate of oxygen consumption, StO2, and SpO2 provide a yet-to-be-explored rich data set that can exhibit disease severity, personalized therapeutics, and management interventions.

Role of adropin in arterial stiffening associated with obesity and type 2 diabetes.

Adropin is a peptide largely secreted by the liver and known to regulate energy homeostasis; however, it also exerts cardiovascular effects. Herein, we tested the hypothesis that low circulating levels of adropin in obesity and type 2 diabetes (T2D) contribute to arterial stiffening. In support of this hypothesis, we report that obesity and T2D are associated with reduced levels of adropin (in liver and plasma) and increased arterial stiffness in mice and humans. Establishing causation, we show that mesenteric arteries from adropin knockout mice are also stiffer, relative to arteries from wild-type counterparts, thus recapitulating the stiffening phenotype observed in T2D db/db mice. Given the above, we performed a set of follow-up experiments, in which we found that 1) exposure of endothelial cells or isolated mesenteric arteries from db/db mice to adropin reduces filamentous actin (F-actin) stress fibers and stiffness, 2) adropin-induced reduction of F-actin and stiffness in endothelial cells and db/db mesenteric arteries is abrogated by inhibition of nitric oxide (NO) synthase, and 3) stimulation of smooth muscle cells or db/db mesenteric arteries with a NO mimetic reduces stiffness. Lastly, we demonstrated that in vivo treatment of db/db mice with adropin for 4 wk reduces stiffness in mesenteric arteries. Collectively, these findings indicate that adropin can regulate arterial stiffness, likely via endothelium-derived NO, and thus support the notion that "hypoadropinemia" should be considered as a putative target for the prevention and treatment of arterial stiffening in obesity and T2D.NEW & NOTEWORTHY Arterial stiffening, a characteristic feature of obesity and type 2 diabetes (T2D), contributes to the development and progression of cardiovascular diseases. Herein we establish that adropin is decreased in obese and T2D models and furthermore provide evidence that reduced adropin may directly contribute to arterial stiffening. Collectively, findings from this work support the notion that "hypoadropinemia" should be considered as a putative target for the prevention and treatment of arterial stiffening in obesity and T2D.

Impact of Lymphocyte and Neutrophil Counts on Mortality Risk in Severe Community-Acquired Pneumonia with or without Septic Shock.

BACKGROUND: Community-acquired pneumonia (CAP) is a frequent cause of death worldwide. As recently described, CAP shows different biological endotypes. Improving characterization of these endotypes is needed to optimize individualized treatment of this disease. The potential value of the leukogram to assist prognosis in severe CAP has not been previously addressed. METHODS: A cohort of 710 patients with CAP admitted to the intensive care units (ICUs) at Hospital of Mataró and Parc Taulí Hospital of Sabadell was retrospectively analyzed. Patients were split in those with septic shock (n = 304) and those with no septic shock (n = 406). A single blood sample was drawn from all the patients at the time of admission to the emergency room. ICU mortality was the main outcome. RESULTS: Multivariate analysis demonstrated that lymphopenia <675 cells/mm3 or <501 cells/mm3 translated into 2.32- and 3.76-fold risk of mortality in patients with or without septic shock, respectively. In turn, neutrophil counts were associated with prognosis just in the group of patients with septic shock, where neutrophils <8850 cells/mm3 translated into 3.6-fold risk of mortality. CONCLUSION: lymphopenia is a preserved risk factor for mortality across the different clinical presentations of severe CAP (sCAP), while failing to expand circulating neutrophils counts beyond the upper limit of normality represents an incremental immunological failure observed just in those patients with the most severe form of CAP, septic shock.

Polysomnography-based diagnosis in Mexican adult patients with Obstructive Sleep Apnea Syndrome (OSAS) clinical suspicion.

INTRODUCTION: Obstructive sleep apnea syndrome (OSA) occurs in 2-4% of adults, increasing by 2.5 times the risk of sudden death. OBJECTIVE: Establish the concordance of the clinical diagnostic and electrical diagnosis in an adult series that underwent polysomnography. MATERIALS AND METHODS: Patients with sleep disorders that underwent consecutively polysomnography recording. RESULTS: In this study, 51 subjects from 24 to 77 years old (54.1±12.12) were included in the study; 23 males and 28 females; 78.43% were overweight or obese; 35.29% were smokers; 31.37% alcohol consumers; 47.05% hypertensive; 21% diabetics; 35.29% with airway alterations; 29.41% with depression; 13.72% dyslipidaemic and 7.84% with ischemic heart disease. Only 22 of the subjects qualified for OSA and the concordance between the clinical diagnostic and polysomnographic recording was 54% (Ko=0.60, Ke 0.50, Ka=0.20) with a 0.55 sensibility, 0.66 specificity, PPV 0.54, NPV 0.65, PLR 1.2, RVN 0.69 and PPP 0.47. The neck circumference in OSA was 40.68±5 vs. 37.7±3.5 cm. (p<0.02) and BMI was 36.48±13.16 vs 29.37±6.58 (p<0.008); male/female proportion was 1.8:1 (p<0.01), BMI was higher in OSA (p<0.002). The Epworth Sleepiness Scale did not discriminate between OSA and other sleep alteration (p<0.29). DISCUSSION AND CONCLUSIONS: We observed a poor agreement between clinical diagnosis and polysomnography. The Epworth Sleepiness Scale did not discern between OSA and other sleep disorders and finally there was no association with a systemic process.

Revisión histórica sobre la llamada ley de curación o ley de Hering / Historical review on the so-called healing law or Hering law

En el presente trabajo, se realiza una revisión no sistemática, documental e histórica de la Ley de Curación o Ley de Hering, se analizó lo escrito por Hahnemann sobre la curación, se examinó lo propuesto por Hering y finalmente se revisó lo escrito por Kent y otros autores sobre este tema. Como resultado de esta revisión se encontró que Hahnemann estableció unas indicaciones importantes para descubrir, en cada caso individual, si la mejoría sintomática observada está en el camino correcto hacia la curación de la enfermedad. Posteriormente Hering describió una guía, trazada previamente por Hahnemann, donde reafirmó que existe una dirección correcta en la evolución de la curación; esta guía con el tiempo se transformó para la comunidad homeopática en la Ley de Curación y que fue Kent quien estableció el término: "Ley de Hering", nombre que se ha venido repitiendo en las escuelas homeopáticas sin profundizar en lo establecido por Hahnemann en sus obras, por lo que es necesario tener precaución al invocar ésta, como una Ley. Por último se consideraron aportes que algunos homeópatas modernos han venido desarrollando sobre el tema. Finalmente, se documentó lo revisado recomendando utilizar el nombre de Guía para la curación con Homeopatía, por considerarlo más apropiado.

Síndrome metabólico: una mirada interdisciplinaria / Metabolic syndrome: an interdisciplinary outlook

El síndrome metabólico se caracteriza por la presencia de alteraciones como resistencia a la insulina, que se manifiestan por hiperinsulinismo y asociación con obesidad, diabetes mellitus tipo 2, hipertensión arterial y dislipidemia.Existen, entre otros, factores de riesgo como sobrepeso, obesidad, ingestión alta de carbohidratos y grasa, tabaquismo y sedentarismo. Diferentes grupos revisaron el concepto de síndrome metábólico: Organización Mundial de la Salud, Grupo Europeo para el Estudio de la Resistencia a la Insulina, Asociación Americana de Endocrinólogos Clínicos, Panel de expertos en detección, evaluación y tratamiento del colesterol alto en adultos y Federación Internacional de Diabetes. Estudios epidemiológicos reportan diversas cifras en prevalencia dependiendo de la población estudiada y del criterio diagnóstico; sin embargo, todos ellos muestran una problemática importante de salud pública.El eje de las alteraciones del síndrome está en la resistencia a la insulina que involucra un estado proinflamatorio que disminuye la capacidad de la insulina para ejercer las acciones en los órganos blanco. El tejido adiposo visceral sintetiza gran cantidad de hormonas e interleuquinas que influyen en las alternaciones metabólicas asociadas.Las medidas de prevención primaria y secundaria son necesarias para reducir la morbimortalidad y con ello lograr efectos importantes en la sociedad y en la calidad de vida de los individuos. El tratamiento contempla aspectos no farmacológicos y la prescripción de medicamentos en caso de requerirse. El tratamiento farmacológico debe considerar el control de los factores de riesgo cardiovascular.

Acute ischemic stroke in a pediatric patient.

Acute ischemic stroke in a pediatric patient is a complex disease with a variety of etiologies that differ from adults. Though rare, they are a real phenomenon with potentially devastating consequences. Some treating institutions are using anti-thrombotic drug therapy with unclear benefits. Available literature, which is limited to case reports and retrospective reviews of databases, clouds this topic with both positive and negative outcomes. Emergency department management should focus on stabilization and resuscitation with immediate involvement of a pediatric neurologist and intensivist. The decision to use anti-thrombotic drug therapy, including anti-platelet drugs and thrombolytics, should be in consult with the specialists involved until randomized controlled trials determine their safety and efficacy in the pediatric population.

Reduction of global cardiovascular risk with nutritional versus nutritional plus physical activity intervention in Colombian adults.

BACKGROUND: Cardiovascular disease is a major cause of morbidity/mortality in non-developed countries. Reports of the effects of non-pharmacological interventions on global cardiovascular risk in Latin American adults, however, are scarce. OBJECTIVE: To compare the change in global cardiovascular risk induced by a tailored, Adult Treatment Panel-III compliant nutrition program versus the same program with addition of supervised, regular physical activity in Colombian adults. DESIGN: The study was a randomized, controlled trial. METHODS: Seventy-five Colombian patients aged 40-70 years and with Framingham-estimated global cardiovascular risk of 1% or higher were randomly assigned to a nutritional intervention program or a combined nutritional intervention-physical exercise program for 16 weeks. Patients underwent medical and anthropometric evaluation, bioelectrical impedance, lipid profile and Framingham global cardiovascular risk determination at baseline and at the end of follow-up. RESULTS: The groups were comparable at baseline; 21 persons in the nutritional intervention program group and 27 in the nutritional intervention-physical exercise program group completed the follow-up. Global cardiovascular risk modification (mean+/-SE) was -2.04+/-1.1 absolute percentage points (relative reduction 19.6%) in the nutritional intervention-physical exercise program group, compared with 0.23+/-0.9 (relative increase 2.8%) in the nutritional intervention program group. Mean difference in global cardiovascular risk modification between groups reached borderline statistical significance in ANCOVA (P=0.054). Reductions in systolic and diastolic blood pressure, waist circumference and low-density lipoprotein cholesterol were similar, but the nutritional intervention-physical exercise program group achieved significantly greater improvements in body weight, body mass index, percentage body fat and high-density lipoprotein cholesterol. CONCLUSIONS: Our data suggest that a structured nutritional intervention-physical exercise program is more efficacious than a nutritional intervention program in the reduction of global cardiovascular risk and cardiovascular risk factors, in only 16 weeks.