272. Poziom białka S-100 u chorych na czerniaka złośliwego w III i IV stopniu zaawansowania klinicznego

Cel pracyBiałko S-100 występuje fizjologicznie w komórkach układu nerwowego, mięśniach prążkowanych, makrofagach i melanocytach. Obecność tego białka stwierdzono również w komórkach czerniaka złośliwego. S-100 jest rutynowo stosowane do identyfikacji komórek czerniaka w diagnostyce histopatologicznej. W ostatnich latach stwierdzono podwyższony poziom białka S-100 we krwi obwodowej u chorych na czerniaka złośliwego. Celem pracy było porównanie poziomu białka S-100 w surowicy chorych na czerniaka w III i IV stopniu zaawansowania klinicznego.Materiał i metodyBadania przeprowadzono w grupie pacjentów, leczonych z powodu czerniaka w Wielkopolskim Centrum Onkologii. Diagnoza i stopień zaawansowania choroby były potwierdzone badaniami histopatologicznymi, klinicznymi i technikami obrazowymi (RTG, USG, TK). Oznaczenie poziomu białka S-100 wykonano w surowicy krwi chorych (44 pacjentów w III stopniu i 41 pacjentów w IV stopniu zaawansowania klinicznego) metodą immunoluminometryczną przy użyciu zestawu Liaison Sangtec S100. Równocześnie przeprowadzono badania kontrolne w surowicy krwi osób zdrowych (n=16). Jako punkt odcięcia (cut-off) przyjęto wartość zalecaną przez producenta 0.15 μg/1.WynikiPodwyższony poziom białka S-100 powyżej wartości cut-off (0,15 μg/l) stwierdzono u 15 z 44 (34%) pacjentów w III stopniu i u 32 z 41 (78%) pacjentów w IV stopniu zaawansowania klinicznego. Analiza statystyczna potwierdziła znamienną statystycznie różnicę między stężeniem białka S-100 w surowicach pochodzących od pacjentów w III i IV stopniu. Czułość stosowanej metody wyniosła 55%, swoistość 100%, dodatnia wartość predykcyjna 100%, ujemna wartość predykcyjna 30%.WnioskiWyniki badań wskazują, że oznaczanie poziomu białka S-100 w surowicy może być dodatkowym wskaźnikiem laboratoryjnym w ocenie stopnia zaawansowania klinicznego chorych na czerniaka złośliwego

Evanescent wave optical trapping and transport of micro- and nanoparticles on tapered optical fibers

We investigate the manipulation of microscopic and nanoscopic particles using the evanescent optical field surrounding an optical fiber that is tapered to a micron-scale diameter, and propose that this scheme could be used to discriminate between, and thereby sort, metallic nanoparticles. First we show experimentally the concept of the transport of micron-sized spheres along a tapered fiber and measure the particle velocity. Having demonstrated the principle we then consider theoretically the application to the optical trapping and guiding of metallic nanoparticles, where the presence of a plasmon resonance is used to enhance optical forces. We show that the dynamics of the nanoparticles trapped by the evanescent field can be controlled by the state of polarization of the fiber mode, and by using more than one wavelength differently detuned from the nanoparticle plasmon resonance. Such a scheme could potentially be used for selectively trapping and transporting nano- or microscopic material from a polydisperse suspension

Host microenvironment in breast cancer development: Inflammatory cells, cytokines and chemokines in breast cancer progression: reciprocal tumor–microenvironment interactions

A comprehensive overview of breast cancer development and progression suggests that the process is influenced by intrinsic properties of the tumor cells, as well as by microenvironmental factors. Indeed, in breast carcinoma, an intensive interplay exists between the tumor cells on one hand, and inflammatory cells/cytokines/chemokines on the other. The purpose of the present review is to outline the reciprocal interactions that exist between these different elements, and to shed light on their potential involvement in breast cancer development and progression

Macrophage Inhibitory Cytokine 1 (MIC-1/GDF15) Decreases Food Intake, Body Weight and Improves Glucose Tolerance in Mice on Normal & Obesogenic Diets

Food intake and body weight are controlled by a variety of central and peripheral factors, but the exact mechanisms behind these processes are still not fully understood. Here we show that that macrophage inhibitory cytokine-1 (MIC-1/GDF15), known to have anorexigenic effects particularly in cancer, provides protection against the development of obesity. Both under a normal chow diet and an obesogenic diet, the transgenic overexpression of MIC-1/GDF15 in mice leads to decreased body weight and fat mass. This lean phenotype was associated with decreased spontaneous but not fasting-induced food intake, on a background of unaltered energy expenditure and reduced physical activity. Importantly, the overexpression of MIC-1/GDF15 improved glucose tolerance, both under normal and high fat-fed conditions. Altogether, this work shows that the molecule MIC-1/GDF15 might be beneficial for the treatment of obesity as well as perturbations in glucose homeostasis

Relationships between serum adiponectin and soluble TNF-α receptors and glucose and lipid oxidation in lean and obese subjects

Insulin resistance might be associated with an impaired ability of insulin to stimulate glucose oxidation and inhibit lipid oxidation. Insulin action is also inversely associated with TNF-α system and positively related to adiponectin. The aim of the present study was to analyze the associations between serum adiponectin, soluble TNF-α receptors concentrations and the whole-body insulin sensitivity, lipid and glucose oxidation, non-oxidative glucose metabolism (NOGM) and metabolic flexibility in lean and obese subjects. We examined 53 subjects: 25 lean (BMI < 25 kg × m−2) and 28 with overweight or obesity (BMI > 25 kg × m−2) with normal glucose tolerance. Hyperinsulinemic euglycemic clamp and indirect calorimetry were performed. An increase in respiratory exchange ratio in response to insulin was used as a measure of metabolic flexibility. Obese subjects had lower insulin sensitivity, adiponectin and higher sTNFR1 (all P < 0.001) and sTNFR2 (P = 0.001). Insulin sensitivity was positively related to adiponectin (r = 0.49, P < 0.001) and negatively related to sTNFR1 (r = −0.40, P = 0.004) and sTNFR2 (r = −0.52, P < 0.001). Adiponectin was related to the rate of glucose (r = 0.47, P < 0.001) and lipid (r = −0.40, P = 0.003) oxidation during the clamp, NOGM (r = 0.41, P = 0.002) and metabolic flexibility (r = 0.36, P = 0.007). Serum sTNFR1 and sTNFR2 were associated with the rate of glucose (r = −0.45, P = 0.001; r = −0.51, P < 0.001, respectively) and lipid (r = 0.52, P < 0.001; r = 0.46, P = 0.001, respectively) oxidation during hyperinsulinemia, NOGM (r = −0.31, P = 0.02; r = −0.43, P = 0.002, respectively) and metabolic flexibility (r = −0.47 and r = −0.51, respectively, both P < 0.001) in an opposite manner than adiponectin. Our data suggest that soluble TNF-α receptors and adiponectin have multiple effects on glucose and lipid metabolism in obesity