Optimization of laser wavelength, power and pulse duration for eye-safe Raman spectroscopy

Abstract Raising the interest in remote chemical analysis, in particular through Raman and fluorescence spectroscopy, the opportunity of increasing the exposure represents an important step for an easier and more reliable spectrum analysis. However, the European directive 2006/25/EC defines the maximum permitted exposure (MPE) to artificial radiations according to exposure duration, wavelength, coherence of the radiation and beam divergence. Though the Raman cross section scales in general according to the fourth power of the excitation wavelength, promoting the use of deep UV radiation, a synergy between wavelength and exposure time can raise the Raman signal in the near UV or in the near IR if compliance to eye-safety directives is requested. In this work we will analyze the possibilities offered by commercially available components for enhancing the Raman scattering under eye-safe conditions

The cardiovascular risk of young women with polycystic ovary syndrome: an observational, analytical, prospective case-control study

To evaluate the cardiovascular risk of polycystic ovary syndrome (PCOS), we investigated lipid profile, metabolic pattern, and echocardiography in 30 young women with PCOS and 30 healthy age- and body mass index (BMI)-matched women. PCOS women had higher fasting glucose and insulin levels, homeostasis model assessment score of insulin sensitivity, total cholesterol (TC) and low density lipoprotein cholesterol (LDL-C) levels, and TC/high density lipoprotein cholesterol (HDL-C) ratio and lower HDL-C levels than controls. Additionally, PCOS women had higher left atrium size (32.0 +/- 4.9 vs. 27.4 +/- 2.1 mm; P < 0.0001) and left ventricular mass index (80.5 +/- 18.1 vs. 56.1 +/- 5.4 g/m(2); P < 0.0001) and lower left ventricular ejection fraction (64.4 +/- 4.1 vs. 67.1 +/- 2.6%; P = 0.003) and early to late mitral flow velocity ratio (1.6 +/- 0.4 vs. 2.1 +/- 0.2; P < 0.0001) than controls. When patients and controls were grouped according to BMI [normal weight (BMI, >18 and <25 kg/m(2)), overweight (BMI, 25.1-30 kg/m(2)), and obese (BMI, >30 kg/m(2))], the differences between PCOS women and controls were maintained in overweight and obese women. In normal weight PCOS women, a significant increase in left ventricular mass index and a decrease in diastolic filling were observed, notwithstanding no change in TC, LDL-C, HDL-C, TC/HDL-C ratio, and TG compared with controls. In conclusion, our data show the detrimental effect of PCOS on the cardiovascular system even in young women asymptomatic for cardiac disease

Relationship between heart rate recovery and inflammatory markers in patients with polycystic ovary syndrome: a cross-sectional study

<p>Abstract</p> <p>Background</p> <p>Polycystic ovary syndrome (PCOS) is an endocrine disease closely related to several risk factors for cardiovascular disease. An abnormal heart rate recovery (HRR), an easily-obtained measure derived from exercise stress test and closely related to an increased risk for cardiovascular mortality, has been recently described in PCOS women. A subclinical increase of the inflammation markers has been also observed in the PCOS. This study was designed to study the relationships between HRR and inflammatory markers in PCOS women.</p> <p>Methods</p> <p>Two-hundred forty-three young PCOS patients without known risk factors for cardiovascular risk were enrolled. All patients underwent hormonal and metabolic profile, white blood cells (WBCs) count and C-reactive protein (CRP). HRR was calculated as the difference between heart rate at peak exercise and heart rate at first minute of the cool-down period. Abnormal HRR was defined as ≤18 beats/min for standard exercise testing.</p> <p>Results</p> <p>Eighty-nine out of 243 patients presented abnormal HRR. Serum CRP (1.8 ± 0.7 vs. 1.1 ± 0.4 mg/dl, <it>p </it>< 0.001) and WBCs (7.3 ± 1.8 vs. 6.6 ± 1.5 10⁹cells/l, <it>p </it>< 0.001) concentrations were significantly higher in PCOS patients with abnormal <it>versus </it>normal HRR. HRR was significantly associated with both CRP (r = -0.33, <it>p </it>< 0.001) and WBCs (r = -0.29, <it>p </it>< 0.001), although in a stepwise multiple regression HRR resulted independently associated with CRP (beta = -0.151, p = 0.001) alone. In a logistic multivariate model, the group within the highest quartile of CRP (odds ratio 1.59, 95% CI 1.07–2.33) was more likely to have abnormal HRR than those within the lowest quartile.</p> <p>Conclusion</p> <p>Abnormal HRR and inflammatory markers are closely associated in PCOS women acting probably in concert to increase the cardiovascular risk profile of these patients.</p

Early impairment of endothelial structure and function in young normal-weight women with polycystic ovary syndrome

The aim of this study was to evaluate the presence of early vascular damage in young normal-weight women with polycystic ovary syndrome (PCOS).Thirty young normal-weight women with PCOS, who had no additional metabolic or cardiovascular diseases, and 30 healthy women (controls) matched for age and body mass index were studied. A complete hormonal assay was performed in each subject. Serum insulin and glucose levels were measured at baseline and after the oral glucose tolerance test. Plasma endothelin-1 levels and serum lipid profile were also assessed. The endothelial function was studied by flow-mediated dilation on the brachial artery, and arterial structure was evaluated by intima-media thickness measurement using Doppler ultrasound of both common carotid arteries.A significant (P &lt; 0.05) difference in flow-mediated dilation (14.3 +/- 1.9% vs. 18.1 +/- 2.0% for PCOS patients and controls, respectively) and in intima-media thickness (0.53 +/- 0.09 mm vs. 0.39 +/- 0.08 mm for PCOS patients and controls, respectively) was found between PCOS and control subjects. Serum endothelin-1 levels were also significantly (P &lt; 0.05) higher in PCOS patients compared with controls (1.1 +/- 0.4 pmol/liter vs. 0.5 +/- 0.2 pmol/liter for PCOS patients and controls, respectively).In conclusion, our data show that young, normal-weight, nondyslipidemic, nonhypertensive women with PCOS have an early impairment of endothelial structure and function

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Gut: A key player in the pathogenesis of type 2 diabetes?

The gut regulates glucose and energy homeostasis; thus, the presence of ingested nutrients into the gut activates sensing mechanisms that affect both glucose homeostasis and regulate food intake. Increasing evidence suggest that gut may also play a key role in the pathogenesis of type 2 diabetes which may be related to both the intestinal microbiological profile and patterns of gut hormones secretion. Intestinal microbiota includes trillions of microorganisms but its composition and function may be adversely affected in type 2 diabetes. The intestinal microbiota may be responsible of the secretion of molecules that may impair insulin secretion/action. At the same time, intestinal milieu regulates the secretion of hormones such as GLP-1, GIP, ghrelin, gastrin, somatostatin, CCK, serotonin, peptide YY, GLP-2, all of which importantly influence metabolism in general and in particular glucose metabolism. Thus, the aim of this paper is to review the current evidence on the role of the gut in the pathogenesis of type 2 diabetes, taking into account both hormonal and microbiological aspects

Comparison of Antarctic polar stratospheric cloud observations by ground-based and space-borne lidar and relevance for chemistry–climate models

Abstract. A comparison of polar stratospheric cloud (PSC) occurrence from 2006 to 2010 is presented, as observed from the ground-based lidar station at McMurdo (Antarctica) and by the satellite-borne CALIOP lidar (Cloud-Aerosol Lidar with Orthogonal Polarization) measuring over McMurdo. McMurdo (Antarctica) is one of the primary lidar stations for aerosol measurements of the NDACC (Network for Detection of Atmospheric Climate Change). The ground-based observations have been classified with an algorithm derived from the recent v2 detection and classification scheme, used to classify PSCs observed by CALIOP. A statistical approach has been used to compare ground-based and satellite-based observations, since point-to-point comparison is often troublesome due to the intrinsic differences in the observation geometries and the imperfect overlap of the observed areas. A comparison of space-borne lidar observations and a selection of simulations obtained from chemistry–climate models (CCMs) has been made by using a series of quantitative diagnostics based on the statistical occurrence of different PSC types. The distribution of PSCs over Antarctica, calculated by several CCMVal-2 and CCMI chemistry–climate models has been compared with the PSC coverage observed by the satellite-borne CALIOP lidar. The use of several diagnostic tools, including the temperature dependence of the PSC occurrences, evidences the merits and flaws of the different models. The diagnostic methods have been defined to overcome (at least partially) the possible differences due to the resolution of the models and to identify differences due to microphysics (e.g., the dependence of PSC occurrence on T−TNAT). A significant temperature bias of most models has been observed, as well as a limited ability to reproduce the longitudinal variations in PSC occurrences observed by CALIOP. In particular, a strong temperature bias has been observed in CCMVal-2 models with a strong impact on PSC formation. The WACCM-CCMI (Whole Atmosphere Community Climate Model – Chemistry-Climate Model Initiative) model compares rather well with the CALIOP observations, although a temperature bias is still present

The GH-IGF-SST system in hepatocellular carcinoma: biological and molecular pathogenetic mechanisms and therapeutic targets

Hepatocellular carcinoma (HCC) is the sixth most common malignancy worldwide. Different signalling pathways have been identified to be implicated in the pathogenesis of HCC; among these, GH, IGF and somatostatin (SST) pathways have emerged as some of the major pathways implicated in the development of HCC. Physiologically, GH-IGF-SST system plays a crucial role in liver growth and development since GH induces IGF1 and IGF2 secretion and the expression of their receptors, involved in hepatocytes cell proliferation, differentiation and metabolism. On the other hand, somatostatin receptors (SSTRs) are exclusively present on the biliary tract. Importantly, the GH-IGF-SST system components have been indicated as regulators of hepatocarcinogenesis. Reduction of GH binding affinity to GH receptor, decreased serum IGF1 and increased serum IGF2 production, overexpression of IGF1 receptor, loss of function of IGF2 receptor and appearance of SSTRs are frequently observed in human HCC. In particular, recently, many studies have evaluated the correlation between increased levels of IGF1 receptors and liver diseases and the oncogenic role of IGF2 and its involvement in angiogenesis, migration and, consequently, in tumour progression. SST directly or indirectly influences tumour growth and development through the inhibition of cell proliferation and secretion and induction of apoptosis, even though SST role in hepatocarcinogenesis is still opened to argument. This review addresses the present evidences suggesting a role of the GH-IGF-SST system in the development and progression of HCC, and describes the therapeutic perspectives, based on the targeting of GH-IGF-SST system, which have been hypothesised and experimented in HCC

Serum 25-Hydroxyvitamin D Levels, phosphoprotein enriched in diabetes gene product (PED/PEA-15) and leptin-to-adiponectin ratio in women with PCOS

<p>Abstract</p> <p>Background</p> <p>Polycystic ovary syndrome (PCOS) is frequently associated with hypovitaminosis D. Vitamin D is endowed with pleiotropic effects, including insulin resistance (IR) and apoptotic pathway. Disruption of the complex mechanism that regulated ovarian apoptosis has been reported in PCOS. Phosphoprotein enriched in diabetes gene product (PED/PEA-15), an anti-apoptotic protein involved in type 2 diabetes mellitus (T2DM), is overexpressed in PCOS women, independently of obesity. Leptin-to-adiponectin ratio (L/A) is a biomarker of IR and low-grade inflammation in PCOS. The aim of the study was to investigate the levels of 25-hydroxy vitamin D (25(OH)D), and L/A, in association with PED/PEA-15 protein abundance, in both lean and overweight/obese (o/o) women with PCOS.</p> <p>Patients and Methods</p> <p>PED/PEA-15 protein abundance and circulating levels of 25(OH)D, L/A, sex hormone-binding globulin, and testosterone were evaluated in 90 untreated PCOS patients (25 ± 4 yrs; range 18-34) and 40 healthy controls age and BMI comparable, from the same geographical area. FAI (free androgen index) and the homeostasis model assessment of insulin resistance (HoMA-IR) index were calculated.</p> <p>Results</p> <p>In o/o PCOS, 25(OH)D levels were significantly lower, and L/A values were significantly higher than in lean PCOS (p < 0.001), while there were no differences in PED/PEA-15 protein abundance. An inverse correlation was observed between 25(OH)D and BMI, PED/PEA-15 protein abundance, insulin, HoMA-IR, FAI (p < 0.001), and L/A (p < 0.05). At the multivariate analysis, in o/o PCOS L/A, insulin and 25(OH)D were the major determinant of PED/PEA-15 protein abundance (β = 0.45, β = 0.41, and β = -0.25, respectively).</p> <p>Conclusions</p> <p>Lower 25(OH)D and higher L/A were associated to PED/PEA-15 protein abundance in PCOS, suggesting their involvement in the ovarian imbalance between pro-and anti-apoptotic mechanisms, with high L/A and insulin and low 25(OH)D levels as the main determinants of PED/PEA-15 protein variability. Further studies, involving also different apoptotic pathways or inflammatory cytokines and granulosa cells are mandatory to better define the possible bidirectional relationships between 25(OH)D, PED/PEA-15 protein abundance, leptin and adiponectin in PCOS pathogenesis.</p

Nutrition, inflammation and liver-spleen axis

Chronic low-grade systemic inflammation represents a mechanism common to many diseases linked to atherosclerosis-related pathways. There is a growing body of evidence indicating that the combination of food quantity and quality along with genetic susceptibility are able to induce the aberrant activation of innate immune signalling, which initially contributes to chronic low-grade inflammation. Liver represents the central player to inflammatory response. Dietary/metabolic factors contribute to the pathogenesis of Non-alcoholic Fatty Liver Disease (NAFLD), the main causes of liver disease in the Western world. Enlargement of the spleen, central organ in regulating the inflammation-related immune response, is commonly seen in patients with of NAFLD, depicting the so called "liver-spleen axis." The aim of this review was to provide an at-a-glance overview of the possible bi-directional mechanisms linking nutrition and inflammation, particularly pinpointing the inflammatory effects stemmed by nutrition on "liver-spleen axis." In particular, the role of unhealthy diet, healthy dietary patterns, such as the Mediterranean diet style, dietary vitamins and micronutrients, such as vitamin D or Magnesium, and Glucagon-Like Peptide-1, a well-known incretin released in response to meal intake, will be discussed. The highly variability of the inflammatory response highlights the role of expert nutritionists in refining methodologies apt to assess nutritional epidemiology and to apply appropriate dietary intervention to counteract diet-induced inflammation mechanisms