Climbing Technique Evaluation by Means of Skeleton Video Stream Analysis.

Due to the growing interest in climbing, increasing importance has been given to research in the field of non-invasive, camera-based motion analysis. While existing work uses invasive technologies such as wearables or modified walls and holds, or focuses on competitive sports, we for the first time present a system that uses video analysis to automatically recognize six movement errors that are typical for novices with limited climbing experience. Climbing a complete route consists of three repetitive climbing phases. Therefore, a characteristic joint arrangement may be detected as an error in a specific climbing phase, while this exact arrangement may not considered to be an error in another climbing phase. That is why we introduced a finite state machine to determine the current phase and to check for errors that commonly occur in the current phase. The transition between the phases depends on which joints are being used. To capture joint movements, we use a fourth-generation iPad Pro with LiDAR to record climbing sequences in which we convert the climber's 2-D skeleton provided by the Vision framework from Apple into 3-D joints using the LiDAR depth information. Thereupon, we introduced a method that derives whether a joint moves or not, determining the current phase. Finally, the 3-D joints are analyzed with respect to defined characteristic joint arrangements to identify possible motion errors. To present the feedback to the climber, we imitate a virtual mentor by realizing an application on the iPad that creates an analysis immediately after the climber has finished the route by pointing out the detected errors and by giving suggestions for improvement. Quantitative tests with three experienced climbers that were able to climb reference routes without any errors and intentionally with errors resulted in precision-recall curves evaluating the error detection performance. The results demonstrate that while the number of false positives is still in an acceptable range, the number of detected errors is sufficient to provide climbing novices with adequate suggestions for improvement. Moreover, our study reveals limitations that mainly originate from incorrect joint localizations caused by the LiDAR sensor range. With human pose estimation becoming increasingly reliable and with the advance of sensor capabilities, these limitations will have a decreasing impact on our system performance.

Paraoxonase-1 gene haplotypes are associated with metabolic disturbances, atherosclerosis, and immunologic outcome in HIV-infected patients.

BACKGROUND: Oxidative stress is associated with human immunodeficiency virus (HIV) infection. Paraoxonase-1 (PON1) is an antioxidant enzyme that is bound to high-density lipoproteins (HDLs). We evaluated whether PON1 gene haplotypes influence the metabolic disturbances, presence of subclinical atherosclerosis, and virologic outcome associated with the infection. METHODS: DNA from blood samples collected from 234 HIV-infected patients and 633 healthy control subjects had single-nucleotide polymorphisms of PON1(192), PON1(55), PON1(-162), PON1(-832), PON1(-909), PON1(-1076), and PON1(-1741) analyzed using the Iplex Gold MassArray method. Subsequently, the influence of these single-nucleotide polymorphisms on measured biochemical and clinical variables was assessed. RESULTS: We observed significant differences in the haplotype distribution between the control subjects and the HIV-infected patients. Haplotype H10 (GTCCGTC) was more prevalent in the HIV-infected patients (6.41% vs 0.64%; P < .001), and haplotype H5 (GACCGTC) was less prevalent in HIV-infected patients (27.7% vs 42.9%; P = .001). In HIV-infected patients, haplotype H7 (AATTCCT) was associated with better CD4(+) cell count recovery, higher levels of HDL cholesterol (P = .048) and apolipoprotein A-I (P = .019), lower levels of triglycerides (P = .004), and lower rates of subclinical arteriosclerosis (P < .001). CONCLUSIONS: PON1 haplotypes segregate with HIV infection, HDL metabolism, the presence of subclinical atherosclerosis, and CD4(+) cell recovery after treatment.

Metabolomic assessment of the effect of dietary cholesterol in the progressive development of fatty liver disease.

Nonalcoholic fatty liver disease is considered to be the hepatic manifestation of metabolic syndrome and is usually related to high-fat, high-cholesterol diets. With the rationale that the identification and quantification of metabolites in different metabolic pathways may facilitate the discovery of clinically accessible biomarkers, we report the use of (1)H NMR metabolomics for quantitative profiling of liver extracts from LDLr(-/-) mice, a well-documented mouse model of fatty liver disease. A total of 55 metabolites were identified, and multivariate analyses in a diet- and time-comparative strategy were performed. Dietary cholesterol increased the hepatic concentrations of cholesterol, triglycerides, and oleic acid but also decreased the [PUFA/MUFA] ratio as well as the relative amount of long-chain polyunsaturated fatty acids in the liver. This was also accompanied by variations of the hepatic concentration of taurine, glutathione, methionine, and carnitine. Heat-map correlation analyses demonstrated that hepatic inflammation and development of steatosis correlated with cholesterol and triglyceride NMR derived signals, respectively. We conclude that dietary cholesterol is a causal factor in the development of both liver steatosis and hepatic inflammation.

Hepatic monocyte chemoattractant protein-1 is upregulated by dietary cholesterol and contributes to liver steatosis.

To assess the role of monocyte chemoattractant protein-1 (MCP-1/CCL2) in the development of fatty liver, we have used LDLr(-/-) mice as an animal model of high-fat, high-cholesterol diet-induced liver steatosis. The rapid dietary induction of hepatic mRNA MCP-1 expression was paralleled by a concomitant increase in plasma MCP-1 that was strongly associated with the degree of liver steatosis. Hepatocytes showed an intense immunoreactivity for MCP-1 that was mainly located surrounding the hepatic lipid droplets. The intake of cholesterol also increased the concentration of MCP-1 in liver homogenates. This was accompanied by a differential expression of members of the PPAR family. Additionally, complete MCP-1 deficiency prevents the development of liver steatosis in LDLr(-/-) mice and partial deficiency is accompanied by a certain protective effect. Our data also suggest that MCP-1 may be important in the regulation of hepatic insulin resistance and may represent a link between inflammation and metabolic diseases. We conclude that dietary cholesterol upregulation of hepatic MCP-1 may help to understand the role of circulating MCP-1 in conditions where liver derangements are clinically important and in the association of liver steatosis with the metabolic syndrome.

Paraoxonase-1 is related to inflammation, fibrosis and PPAR delta in experimental liver disease.

BACKGROUND: Paraoxonase-1 (PON1) is an antioxidant enzyme synthesized by the liver. It protects against liver impairment and attenuates the production of the pro-inflammatory monocyte chemoattractant protein-1 (MCP-1). We investigated the relationships between hepatic PON1 and MCP-1 expression in rats with liver disease and explored the possible molecular mechanisms involved. METHODS: CCl4 was administered for up to 12 weeks to induce liver damage. Serum and hepatic levels of PON1 and MCP-1, their gene and protein expression, nuclear transcription factors, and histological and biochemical markers of liver impairment were measured. RESULTS: High levels of PON1 and MCP-1 expression were observed at 12th week in the hepatocytes surrounding the fibrous septa and inflammatory areas. CCl4-administered rats had an increased hepatic PON1 concentration that was related to decreased gene transcription and inhibited protein degradation. Decreased PON1 gene transcription was associated with PPARdelta expression. These changes were accompanied by increased hepatic MCP-1 concentration and gene expression. There were significant direct relationships between hepatic PON1 and MCP-1 concentrations (P = 0.005) and between PON1 and the amount of activated stellate cells (P = 0.001). CONCLUSION: Our results from this experimental model suggest a hepato-protective role for PON1 against inflammation, fibrosis and liver disease mediated by MCP-1.

Serum concentrations of extracellular fatty acid synthase in patients with steatohepatitis.

BACKGROUND: Fatty acid synthase (FASN) is an enzyme synthesized by the liver and plays an important role in lipogenesis. The present study aimed to assess whether serum FASN concentrations are altered in patients with chronic liver disease, and to investigate whether its measurement may be a useful tool in the clinical evaluation of this derangement. METHODS: We investigated 93 patients with chronic liver disease (14 minimal change disease, 79 steatohepatitis) and 100 control subjects. Serum FASN concentrations were measured using ELISA. RESULTS: Patients had a significant increase in serum FASN concentration (p<0.001), which was specifically associated with the hepatic Knodell sub-index III of portal inflammation (p=0.019). In addition, serum FASN concentrations were significantly correlated with the circulating levels of the monocyte chemoattractant protein-1 (MCP-1) (Spearman rho=0.375; p<0.001) and type III procollagen-N-peptide (P-III-P) (Spearman rho=0.297; p<0.001). CONCLUSIONS: Serum FASN concentrations are increased in patients with chronic liver impairment, and are associated with specific histological alterations and biochemical markers of portal inflammation. These data suggest that FASN measurement may contribute significantly to the evaluation of these patients.

Immunohistochemical analysis of paraoxonases-1, 2, and 3 expression in normal mouse tissues.

The paraoxonase (PON) enzyme family, comprising PON1, PON2, and PON3, are antioxidant enzymes that degrade oxidised phospholipids. We describe the immunohistochemical localisation of the PON proteins in the normal mouse. Antibodies were obtained by inoculating rabbits with peptides derived from specific sequences of mature PONs. PON1 and PON3 were detected in the skin external epithelium, acini of the sebaceous glands, tongue epithelium, acini of the submandibular gland, surface epithelia of the stomach and the intestine, hepatocytes, exocrine pancreas acini, fibre tracts of the encephalon and the spinal cord, skeletal and cardiac muscle, eye lens epithelium and retinal layers, adipocytes, chondrocytes, epithelial cells of the trachea and bronchiole, ovary follicular fluid, seminiferous tubules, spermatozoa, and kidney proximal tubules. PON2 expression was weaker than that of PON1 and PON3, and was absent in some of the tissues studied, such as submandibular gland, nerve cells, and adipocytes. In muscle cells, PON2 expression was restricted to the endomysium. Apolipoprotein A-I did not colocalise with PONs, suggesting local synthesis. This study provides an experimental model to investigate the role played by these enzymes as antioxidants and their relationship with the development of a variety of diseases.

Metabolic phenotyping of genetically modified mice: An NMR metabonomic approach.

Monocyte chemoattractant protein-1 (MCP-1) plays a relevant role in macrophage migration but recent findings suggest an additional role in lipid and glucose metabolism. We report the use of (1)H NMR spectroscopy as a useful complementary method to assess the metabolic function of this gene in a comparative strategy. This metabonomic analysis was rapid, simple, quantitative and reproducible, and revealed a suggestive relationship between the expression of the MCP-1 gene and hepatic glucose and taurine concentrations. This approach should be considered in genetically modified mice when a metabolic alteration is suspected, or in routine assessment of metabolic phenotype.

The measurement of the lactonase activity of paraoxonase-1 in the clinical evaluation of patients with chronic liver impairment.

AIMS: We investigated the analytical performance of a new assay of the lactonase activity of paraoxonase-1 and its efficacy in the assessment of liver damage. DESIGN AND METHODS: Serum lactonase activity was determined by the hydrolysis of 5-thiobutyl butyrolactone in 633 healthy individuals and 369 patients with chronic liver disease. Paraoxonase-1, 2, and 3 gene polymorphisms were analyzed by the MassArray method. RESULTS: Linearity was up to 10 U/L. Detection limit was 0.12 U/L. Imprecision was < or = 17.7%. Lactonase values in our normal population were 5.99 (3.29-13.61) U/L. Lactonase activity showed a lower influence of genetic polymorphisms than the classical assay using paraoxon. Both measurements showed a similar efficiency in testing for liver dysfunction. CONCLUSION: We report a reliable assay using a non-toxic substrate for the measurement of serum lactonase activity. The influence of genetic variability is low. The assay could be a useful addition to tests evaluating liver impairment.

Changes in the expression of genes related to apoptosis and fibrosis pathways in CCl4-treated rats.

Chronic liver diseases are accompanied by changes in the biochemical pathways related to the regulation of apoptosis and extra-cellular matrix deposition. The present study was designed to investigate, using low density arrays, changes in the hepatic gene expression together with hepatic biochemical and histological alterations in rats that had liver impairment induced by chronic exposure to CCl(4). Further, we examined the possible recovery of genetic and pathological changes following the cessation of the hepatotoxic injury. Experimental fibrosis was induced in male Wistar rats by CCl(4) administration. Animals were subdivided into two groups. One group was given CCl(4 )and animals were killed at 8 and 12 weeks of treatment. The other group was treated with CCl(4) for 6 weeks, the CCl(4 )was then stopped and, subsequently, subgroups of animals were killed after 1 and 2 weeks of recovery. CCl(4) administration over 12 weeks was associated with significant changes in B-cell leukemia/lymphoma 2, procollagen type I alpha 2, matrix metalloproteinases 3 and 8, tissue inhibitors of metalloproteinases 1, 2, and 3 and the inhibitor of apoptosis 4 gene expressions. Recovery after CCl(4) cessation was associated with changes in procollagen type I alpha 2, matrix metalloproteinase 7, tissue inhibitors of metalloproteinases 1 and 2, inhibitor of apoptosis 4, and survivin gene expressions. This study shows an association between changes in the expression of several genes regulating hepatic cell apoptosis, the fibrosis process, and the recovery of the hepatic function after removal of the toxic injury.

Selective extraction, separation, and identification of anthocyanins from Hibiscus sabdariffa L. using solid phase extraction-capillary electrophoresis-mass spectrometry (time-of-flight /ion trap).

A method for selective extraction using SPE, electrophoretic separation at basic condition and the identification by using exact masses and fragmentation patterns has been developed in order to know the anthocyanins in dried calyces of Hibiscus sabdariffa L. A detailed and comparative study of several extraction procedures has been carried out to obtain the maximum number of anthocyanidins from the calyces and then a CE-TOF-MS method in positive mode using ESI has been developed for the separation and rapid identification of anthocyanins in H. sabdariffa L. Delphinidin-3-sambubioside, cyanidin-3-sambubioside have been detected as main components and cyanidin-3-O-rutinoside, delphinidin-3-O-glucoside and cyanidin-3,5-diglucoside, and chlorogenic acid as minor constituents. The confirmation of the anthocyanidins and chlorogenic acid was carried out using fragmentation ions with the IT-mass spectrometer (IT-MS).

Observación de los efectos del ejercicio dinámico continuo controlado en la variación de los niveles de química sanguínea, cuadro hematico, y tension arterial media, en pacientes con insuficiencia renal cronica sometidos a hemodialisis en la caja nacional de prevision de Santafé de Bogotá D.C., 1991-1992 / Analysis about the changes in the blood chemistry, blood pressure and hematologic values in patients with chronic renal failure

En el siguiente estudio se realizó un análisis del ejercicio dinámico contínuo controlado en la variación de los valores de química sanguínea, cuadro hemático y presión arterial en pacientes con insuficiencia renal crónica sometidos a hemodiálisis. En el estudio se trabajó con 8 pacientes de la Caja Nacional de Previsión, de Santafé de Bogotá D.C., durante 1991-1992 a quienes se les realizó una prueba de esfuerzo inicial para medir la capacidad de ejercicio tolerable por paciente. Esta prueba se realizó bajo supervisión médica contínua, se hizo un registro electrocardiográfico y control de la presión arterial antes, durante y después de la prueba de esfuerzo. Con los resultados de la prueba de esfuerzo se elaboró un protocolo único de ejercicios para todos los pacientes, teniendo como base que no sobrepasara los límites superiores de la carga máxima del paciente que toleró menos. Este protocolo era realizado por los pacientes antes de cada hemodiálisis. A los mismos se les tomaban exámenes paraclínicos mensualmente antes de la hemodiálisis, de los cuales se realizaron 3 cortes, tiempo considerado adecuado para observar cambios significativos. Para los análisis de los datos, se uso el Test no paramétrico de Friedman. Con los hallazgos concluímos que no se encontró una variación clínica y que estadísticamente no fué significativa excepto para la glicemia. El ejercicio no presentó efectos adversos en los pacientes, aunque el protocolo realizado era por debajo de la carga tolerada que podía soportar cada uno, lo ideal es la realización de un estudio en el cual se elabore un protocolo de ejercicios dado por las características individuales de cada paciente, basados en parámetros encontrados en la prueba de esfuerzo, para someter al paciente a una carga submáxima que pueda tolerar y que modifique su condición física