It has been demonstrated that the level of cross-reactivity and cross-protection among PspAs correlates learn more with sequence similarity, being low between PspAs of different families and higher within each family. Furthermore, it has been suggested that the level of cross-reactivity and cross-protection varies depending on the PspA clade

[21]. In that study, a PspA from clade 3 elicited antibodies with the lowest cross-reaction, while PspAs 4 and 5 (belonging to family 2) were highly cross-reactive. For family 1 molecules, neither PspA clade 1 nor clade 2 were able to induce antibodies cross-reactive to all family 1 strains tested. Therefore, further research was needed to better understand cross-reactivity within family 1. In the present study, the N-terminal regions of five clade 1 and five clade 2 PspAs were produced, antibodies generated and screened for their cross-reactivity against a panel of Brazilian strains containing clade 1 and 2 PspAs. The immunoblot analysis revealed a high heterogeneity in the level of cross-reactivity of the different antisera; while most cross-reacted mainly within the homologous clade, four PspAs – 245/00, M12, 94/01 and P339 – generated antibodies able to recognize most of the isolates tested. There was FK228 cost no predominance between the PspA clade and the level of cross-reaction;

clades 1 and 2 were equally cross-reactive. The hybridization of the reverse primers in distinct regions within the proline-rich moiety generated fragments with different sizes; all fragments included the entire alfa-helical domain plus the beginning of the proline-rich region, and some were longer, containing most of the proline block, several including the nonproline block. Although there was no clear correlation between the size of the fragment and the level of cross-reactivity by immunoblot – the most cross-reactive fragments included

both long and short proteins – in the more stringent assays – complement deposition and OPA – the two best candidates included the proline-rich region with the nonproline block. This result suggests a possible role for the proline-rich region with the nonproline block in the induction of functional antibodies. This data is in agreement with a recent study demonstrating that immunization of mice with the proline-rich TCL region including the nonproline block was able to protect mice against fatal challenge [28]. Complement mediated antibody-dependent phagocytosis is considered to be an important mechanism of pneumococcal clearance [29]. The ability of anti-PspA antibodies to promote complement deposition on the bacterial surface greatly contributes to their protective effect [11]. It has been demonstrated, however, that the level of complement deposited depends on the similarity between the PspA used to induce the antibodies and that expressed by the pneumococcus [21] and [30].

Since physical activity is a complex behaviour (van Sluijs et al 2007), insight into the patient’s unique viewpoint is warranted in order to enhance understanding of how people with COPD might maintain benefits of pulmonary rehabilitation and continue with an active lifestyle. Qualitative research conducted in the field of pulmonary rehabilitation has focused on patients’ immediate experiences and perspectives of undergoing a course of pulmonary rehabilitation; specifically the education component (Wilson et al Thiazovivin molecular weight 2007), the impact of pulmonary rehabilitation on the experience of living with COPD (Toms and Harrison 2002), and on perceptions of breathlessness and activity

(Williams et al 2010). Across these small studies pulmonary rehabilitation was universally perceived to be Adriamycin price highly valuable for improving coping abilities and physical and psychosocial function. Follow-up activities were seen to be important (Toms and Harrison 2002, Wilson et al 2007) but

exploration of attitudes and experiences following a course of pulmonary rehabilitation was not the primary concern of this research. At the outset of this study, the authors were unaware of any published work focusing on the views of people with COPD towards physical activity after pulmonary rehabilitation. Consideration of this subject from the patient perspective reflected key drivers of UK and worldwide health policy to consider patient opinion in evaluation and evolution of health and wellbeing services (Department of Health

2004b, IAPO 2009). The following research question was formulated: What are the views and perceptions of people with COPD towards maintaining an active lifestyle following a course of pulmonary rehabilitation? A qualitative focus group design was selected because group interaction can prompt responses that might not be elicited during interviews, leading to a deeper level of inquiry. The group setting offers a supportive environment in which participants can express their views and is familiar to people who have completed a course of pulmonary rehabilitation. Two focus groups were held Florfenicol at a community hospital. The principal researcher (LH), a respiratory physiotherapist, took the role of moderator. An independent physiotherapist (AG) observed and took notes on participants’ non-verbal communication, group interaction and key ideas (Holloway and Wheeler 2002). Focus groups were digitally audiorecorded and transcribed verbatim. Group discussion was facilitated using a topic guide of eight open-ended questions that had been developed with an experienced researcher (HF) (Box 1). All questions were piloted with a group of physiotherapists and standardised in order to enable comparability across both groups. All participants provided written, informed consent. Introductory Question: Tell me about your experience of the pulmonary rehabilitation course. 1.

The isolated endophytic

fungi was inoculated in Malt Glucose Yeast Peptone (MGYP) broth13 containing yeast Dinaciclib mouse extract and malt extract – 0.3% each, glucose – 1%, peptone – 0.5%, at 28 °C in static position. After 72 h of incubation the biomass was filtered and then extensively washed with distilled water to remove the medium components. This biomass was taken into flasks containing 100 ml distilled water and incubated at same position for 48 h. The biomass was filtered with Whatman filter paper no.1, the filtrate was used further. The fungal filtrate was mixed with aqueous solution of silver nitrate (AgNO3) of 1 mM concentration for reduction. The formation of silver nanoparticles was monitored by visual observation of color change from pale white to reddish brown and was further confirmed by sharp peaks given by Ibrutinib cell line silver nanoparticles in the visible region from UV-vis spectrum of the reaction solution using double beam UV visible spectrophotometer. The characterization of silver nanoparticles was done by TEM (Hitachi-H-7500) to know the size and shape of nanoparticles. The samples were prepared by drop coating the silver

nanoparticle solution into carbon coated copper grid and subjected to vacuum desiccation before loading onto a specimen holder. TEM micrographs were taken by analyzing the prepared grids. Silver nanoparticle solution was purified by centrifugation at 10,000 rpm for 15 min, and then the pellets were resuspended in sterile distilled water and again centrifuged at 10,000 rpm for 10 min. The collected pellets were air dried at room temperature for IR analysis. The probable biomolecules involved in the synthesis and stabilization of nanoparticles was recorded by FTIR spectrum. Biosynthesis of silver nanoparticles was studied for antibacterial activity against pathogenic bacteria (clinical isolates) using agar well diffusion assay method.14 and 15 The test organisms used were Escherichia coli, Pseudomonas

aeruginosa, Klebsiella pneumoniae, Salmonella typhimurium, and Enterobacter aerogenes. The bacterial test organisms were grown in nutrient broth for 12 h. Lawns of pathogenic bacteria were prepared on nutrient agar many plates using swabs. Agar wells were made on nutrient plates using gel puncture and each well was loaded with-20 μl, 40 μl, 60 μl, and 80 μl of silver nanoparticle solution. The plates containing bacterial and silver nanoparticles were incubated at 37 °C. The plates were examined for the zone of inhibition, which appeared as clear area around the wells. Inhibition zone diameter was measured. From the surface sterilized leaf segment of C. longa (turmeric), the endophytic fungi was grown from the cut ends of the leaves after 48 h and luxuriant growth after 72 h. Subculturing was done on PDA. The microscopic images and morphological characteristic features study revealed that the fungal isolate is Pencillium sp. ( Fig. 1).

Quercetin was used as standard. IC50 values express the concentration selleck chemicals llc of antioxidant samples necessary to quench 50% radicals in the reaction mixture. IC50 values were calculated using nonlinear regression and expressed in μg dried material equivalents/ml

for sample extracts. The nonlinear regression analysis was performed using GraphPad Prism 4.01 (GraphPad Software, San Diego, CA, USA). All the antioxidant measurements were performed in triplicate, and the data were expressed as average ± standard deviations (SD). The α-amylase inhibitory potential of each extract was carried out as per the established procedures based on spectrophotometric assay. Briefly, starch solution (0.5% w/v) was prepared by stirring 0.125 g of potato starch in 25 ml selleck chemicals of 20 mM sodium phosphate buffer with 6.7 mM sodium chloride, pH 6.9 at 65 °C for 15 min. The enzyme solution (amylase) was prepared by mixing 0.0253 g of the enzyme in 100 ml of cold distilled water. The colorimetric reagent was prepared by mixing sodium potassium tartrate solution (12.0 g of sodium potassium tartrate tetrahydrate in 8.0 ml of 2 M NaOH) and 96 mM of 3,5 dinitrosalycylic acid solution (0.88 g of 3,5 dinitrosalycylic acid in 46 ml of deionized water) 1:1 (v/v). The crude

hydroalcoholic extract and its various fractions were dissolved in suitable solvents to give concentrations ranging from 10 to 100 μg/ml (10, 20, 40, 60, 80, 100 μg/ml). The plant extract Rebamipide (1 ml) and 1 ml enzyme solution were incubated with 1 ml starch solution at 25 °C for 30 min. Then,

1 ml of coloring reagent (3,5 dinitrosalycylic acid) was added and the reaction mixture was incubated into water bath at 85 °C for 15 min. The absorbance was recorded at 540 nm spectrophotometrically. Plant extracts were replaced in control tubes with distilled water or DMSO.1 Acarbose was used as positive control. In presence of an α-amylase inhibitor, less maltose would be produced and the absorbance value will increase less rapidly. Percent inhibition was calculated as follows: Percent inhibition = A540 control − (A540 test/A540 control) × 100 The results are expressed as mean ± standard error of the mean (SEM). Statistical analysis and linear regression analysis were performed using GraphPad Instat, software, version 4.01. The values were analyzed by one way Analysis of variance followed by Tukey multiple comparison test at a significant level of p < 0.05. The DPPH free radical is a stable free radical, which has been widely accepted as a tool for estimating free radical scavenging activities of antioxidants.

All patients gave written consent prior to coronary intervention. Coronary angiography was reviewed by two interventional cardiologists. All frames were calibrated with the tip of the catheter as a reference guide before contrast injection. Two orthogonal

projections were used before and after stent implantation. Whenever a patient had two or more atrial branches arising from the same coronary artery, we selected for this study the largest branch. In each coronary segment, we measured the luminal diameters and the Cell Cycle inhibitor percentage of stenosis using the QCA. The coronary artery flow was qualitatively evaluated using the TIMI score [15]. Patients were divided into two groups according to the loss or preservation of the AB flow at the end of angioplasty. ABO group were those patients in whom the AB flow fell from TIMI grades 2–3 to 0–1 after the procedure. Non-ABO group were those patients in whom the baseline TIMI was normal and did not change after PTCA. We also evaluated the length of the coronary lesion and the plaque composition characteristics according to the American College of Cardiology/American Heart Association (ACC/AHA) classification [16]. In each

AB, we specifically analyzed the presence of atherosclerotic plaques, maximal luminal diameter, and TIMI flow before and after the PTCA. To assess the spatial relationship between the location Romidepsin mw of the target atherosclerotic plaques for PTCA and the output of the AB, we followed the Medina’s classification [17]. Due to the variety of stent models implanted in this series of patients, the influence of a given model on ABO could not be specifically analyzed and therefore we created the variable “Bare-metal Thiamine-diphosphate kinase stent (BMS) versus drug-eluting stent (DES)” to asses statistical differences.

Descriptive analyses were performed at the first step. Categorical variables were described by frequencies and percentages and statistical differences were analyzed using a 2 × 2 table test and the χ2 test. Continuous variables were described by the mean ± standard deviation and statistical differences were analyzed using the Student’s t test in the case of a normal distribution. A multivariable logistic regression model was performed, adjusting for the covariates statistically significant at the univariable analysis (p value less than 0.20 as a criterion of entry into multivariate analysis), to identify independent predictors of ABO. A forward step method was used to define the final model and the independent predictors of ABO. Additionally, the final model was adjusted for those variables categorized as clinically relevant. Significant predictors of ABO were expressed in terms of odds ratio and 95% confidence intervals (CIs). To assess the model’s predictive ability of our data, we calculated the area under the receiver operating characteristics following a nonparametric distribution assumption. A p value less than 0.

Microvessel counts were performed at ×400 (×40 objective lens and ×10 ocular lens; 0.74 mm2 per field). Tumors with <200 microvessels/mm−2 were assigned a low microvessel density, whereas those with >200 microvessels/mm−2 were assigned a high microvessel density (Couvelard et al., 2005). One-way ANOVA followed by Dunnett’s and Tukey’s Multiple Comparison Selisistat Tests were performed to determine the significance of differences between control and all treatment groups and among groups

respectively using GraphPad PRISM version 5.0. Differences were considered significant in all experiments at p < 0.05 (*, significantly different from untreated controls; **, significantly different from C-DIM-5 and C-DIM-8 and doc single treatments unless otherwise stated). C-DIM-5 and C-DIM-8 were significantly cytotoxic (p < 0.05) to A549 cells with 24 h IC50 values of 14.29 ± 2.30 μM and 16.18 ± 1.59 μM respectively ( Fig. 1A and B). The broad spectrum of cytotoxic activities of the C-DIM compounds was also evident in LnCap, PC3, and H460 cell lines ( Fig. 1C and D). Interaction of C-DIM-5 and C-DIM-8 with doc inhibited A549 cell growth exponentially with

CI values of 0.46 ± 0.027 and 0.51 ± 0.031 (i.e. synergistic) respectively. Deposition on stages 3, 4, 5 and 6 were selected, representative of the respirable mass and used in the assessment of cytotoxicity ( Fig. 1E and F). Cell survival on stage 5 of the viable impactor significantly decreased to 17.75% and 17.10% (p < 0.05) after treatment with nebulized C-DIM-5 and C-DIM-8 respectively. Representative fluorescence micrographs Dinaciclib order of acridine orange-ethidium bromide-stained cells revealed the percentages of cells undergoing apoptosis (Fig. 2A). This was after treatment with DMSO, doc (10 nM), C-DIM-5 (10 μM),

C-DIM-5 (10 μM) + doc (5 nM), C-DIM-8 (10 μM), C-DIM-8 (10 μM) + doc (5 nM), C-DIM-5 (20 μM), C-DIM-5 (20 μM) + doc (5 nM), C-DIM-8 (20 μM), and C-DIM-8 (20 μM) + doc (5 nM) ( Fig. 2A). There was evidence of induction of early and late apoptosis by doc (10 nM) [11.5 ± 1.00%], others C-DIM-5 (10 μM) [20.5 ± 1.85%], and C-DIM-8 (10 μM) [26 ± 1.05%] ( Fig. 2B). This was augmented when C-DIM-5 and C-DIM-8 where combined with doc [C-DIM-5 (10 μM) + doc (5 nM), 30 ± 2.90%; C-DIM-8 (10 μM) + doc (5 nM), 34 ± 3.60%] ( Fig. 2B). The number of apoptotic cells significantly increased (p < 0.05) at higher concentrations (20 μM) of C-DIM-5 [24 ± 1.80%] and C-DIM-8 [25.5 ± 2.40%]. This was further enhanced when 20 μM C-DIM-5 and C-DIM-8 were co-treated with 5 nM doc [40 ± 3.45%, and 41 ± 3.60% respectively] ( Fig. 2B). Treatment of A549 cells with DMSO resulted in accumulation of 72.34 ± 0.51% of cells in G1, 3.20 ± 0.13% in G2 and 24.58 ± 0.49% of cells in S-phase (Fig. 2C). However, after treatment with 10 μM C-DIM-5, 76.98 ± 0.51% of cells accumulated in G1, 1.20 ± 0.21% in G2 and 21.82 ± 0.52% in S-phase.

The correlation

between the Tampa Scale for Kinesiophobia and its substitute question (r = 0.46) approximated the value nominated as large (r = 0.50) by Cohen (1992). The substitute question showed the same prognostic properties as the Tampa Scale for Kinesiophobia in predicting recovery at 1 year follow-up, and even better prognostic properties in predicting severity of leg pain at 1 year follow-up. Although the explained variations of the models decreased when the cut-off point of the outcome pain severity in the leg was set at 2 or 3 instead of 1, the decrease was relatively stable in the models and did not change the conclusions derived from our data. These consistent findings show that it might be feasible to replace Selumetinib mouse the Tampa Scale for Kinesiophobia by its unique substitute question in predicting outcome at 1 year follow-up in people with sciatica in primary care. Nevertheless, these results need to be further evaluated and validated in additional studies. Extensive psychometric testing of the substitute question for the Tampa Scale for Kinesiophobia was not done in this present study

as this was not our aim, but will be necessary in future studies. Especially, further testing of the reliability, validity, and responsiveness of the substitute question is needed to establish the usefulness of this question in daily clinical practice. Item Response Theory can be applied to determine whether the scales are uni-dimensional and measure the same underlying construct as the substitute questions. No study was found that reported on the prognostic properties of the Tampa Scale for Kinesiophobia and EQ-5D in people with sciatica. http://www.selleckchem.com/products/ON-01910.html On the other hand, the Roland Morris Disability Questionnaire (Edwards et al 2007, Jensen et al 2010, Peul et al 2008a) and the SF-36 Physical Component Summary (Atlas et al 2006, Edwards et al 2007) are prognostic in people with sciatica. In the present exploratory analyses, both the Tampa Scale for Kinesiophobia and the SF-36 Physical Component Rutecarpine Summary were consistently prognostic. Although this study presents novel results, its exploratory design brings inevitable limitations. First, we

do not know if the substitute questions exactly cover the scope and content of the questionnaires for which they were developed. It is possible that the substitute question explains a different part of the model and that comparing the explained variations between the models may not be fully valid. Second, firm conclusions on the replacement of the Tampa Scale for Kinesiophobia by its substitute question cannot be made as further extensive psychometric testing is needed. Third, the relatively small sample size may have limited the power of the analyses. Finally, because we tested the feasibility of replacing a questionnaire by one unique substitute question in a prediction model only in people with sciatica in primary care, the generalisability of these results to other groups is limited.

Although the buy Bioactive Compound Library incidence of varicella and related morbidity have decreased dramatically in the U.S. and Canada following the introduction of routine 1-dose

varicella vaccination [11], [12], [13], [14], [15] and [16], post licensure studies have confirmed some of the above concerns. Varicella outbreaks occur within highly vaccinated populations [17], [18], [19] and [20] and one dose of vaccine has been observed to be 80–85% effective against any disease presentation [17], [18], [20], [21], [22] and [23]. It remains unclear though whether the lower efficacy estimated in post licensure studies, compared to the results from clinical trials, are due to waning over time [24] and [25]. However, breakthrough varicella is generally mild and less contagious than varicella in unvaccinated persons [20] and [24]. TSA HDAC clinical trial Finally, surveillance studies in the U.S. have shown a small increase in zoster [26], [27], [28] and [29]. However, it is too early to link these increases with varicella vaccination as many of the U.S. surveillance

systems do not have pre-program zoster incidence data and increases in age-specific zoster incidence rates have been observed in other countries prior to varicella vaccination programs [16] and [30]. A clinical trial was conducted (among healthy children followed up for 10 years) to measure the efficacy of 2 doses of varicella vaccine compared to 1-dose [5]. The efficacy for 2 doses was significantly higher than for 1-dose of varicella vaccine (98% versus 94%) [5]. Given the high number of breakthrough see more cases in vaccinees, the higher efficacy of 2 doses compared to 1-dose and continuing endemic disease, the U.S. Advisory Committee on Immunization Practices (ACIP) adopted a recommendation that children between 4 and 6 years of age receive a second dose of varicella vaccine [31]. The panel also recommended that a second catch-up dose of varicella vaccine be given to anyone who previously had received one dose [31]. In countries, such as Canada,

that have introduced a 1-dose varicella vaccination program, policymakers will be asked to make recommendations and decisions regarding the introduction of a second dose of varicella vaccination. In other countries, that have yet to introduce varicella vaccination, policy questions will be related to whether they should be introducing varicella vaccination and, if so, using how many doses. The aim of this study is to examine the potential short and long-term population-level impact of a 1-dose versus a 2-dose varicella vaccination program on the epidemiology of varicella and zoster, using Canada as an example. The modeled population is assumed to be stable and is stratified into 101 age cohorts (0, 1,., 100+). The birth rate is constant through each year and age-specific all cause mortality rates were taken from Statistics Canada [32].

05 were considered significant (* = p < 0.05). The erythroid differentiation of

K562 cells was investigated after the treatment with six this website psoralens and five angelicins, whose structures are described in Fig. 1. K652 cells were irradiated with two UV-A doses (1 and 2 J/cm2) and then erythroid differentiation was measured by benzidine test after 5, 6 and 7 days from irradiation. At the same time, cellular viability was evaluated by MTT, obtaining evidences suggesting antiproliferative effects and phototoxicity. Different concentrations of compounds were employed because of their different phototoxic effects; accordingly, concentrations were chosen to maximize the erythroid effect without extensive reduction of cell viability. Moreover, considering the fact that some angelicins were powerful γ-globin inducers without irradiation [26], the same tests were performed with higher concentration CT99021 supplier of furocumarins in the absence of irradiation. With the exception of 4,6,4′-trimethylangelicin (4,6,4′-TMA) [26], without irradiation all furocoumarins, when administered at 50 μM, showed a very low capability

of causing an increase of benzidine positive cells (lower than 10%) with respect to control (data not shown). On the contrary, after irradiation all tested molecules were able to induce a clear increase of benzidine positive cells, as displayed in Table 1. Table 1 reports the most percentages of benzidine positive cells and cellular viability after 6 days after irradiation at the highest concentration for each compound. In general, psoralens induced a higher proportion of erythroid differentiating cells (38.4–78.1%) in comparison to angelicins (24.3–58.7%), and these data confirmed the ones obtained with other furocoumarins [7]. Furthermore, the

induction of erythroid differentiation was dependent on the UV-A dose with the exception of some cases in which the antiproliferative effect was a major effect (see for example 5,5′-dimethylpsoralen or 4,6,4′-TMA or 4,4′,5′-trimethylangelicin). In the panel A of Fig. 2, the concentration-dependent increase of the ratio of benzidine positive cells was illustrated for some compounds as examples. Moreover, the panel B of Fig. 2 shows representative pictures of treated cells after benzidine staining: cells irradiated in the presence of 4′,5′-dimethylpsoralen (4′,5′-DMP) clearly were blue-colored1 and became larger with respect to control (this effect is not unusual within already reported inducers of erythroid differentiation, such as cytosine arabinoside [10]). Further experiments were carried out to determine whether the induced erythroid differentiation was reversible. To this aim, 6 days after irradiation (1 J/cm2), K562 cells were incubated for additional 4 days with fresh medium, and the benzidine test was performed at this point.

Dès la troisième semaine d’interruption de la substitution par androgènes de jeunes adultes atteints d’hypogonadisme hypogonadotrope a été observée une réduction de la sensibilité à l’insuline suggérant que le rôle modulateur de la testostérone passe en partie par des mécanismes indépendants des variations de la composition corporelle [37]. Bien que cela n’ait pas été observé au cours de la substitution androgénique d’hypogonadismes hypogonadotropes congénitaux [33], de nombreuses études ont montré que la substitution par androgènes d’hommes adultes hypogonadiques améliorait [4] and [38] ou faisait disparaître les stigmates de SMet [39], [40] and [41].

Un phénotype d’une similitude étroite à celui du SMet est observé

chez l’homme www.selleckchem.com/products/MDV3100.html traité par « blocage androgénique » pour carcinome de prostate ne relevant pas d’un geste chirurgical curateur [42]. La profonde hypotestostéronémie ainsi induite s’associe à une élévation significative www.selleckchem.com/TGF-beta.html de la glycémie à jeun, du taux des triglycérides et à une surcharge pondérale de type androïde, trois pièces constitutives du puzzle clinico-biologique caractéristique du SMet. Les chiffres de pression artérielle ne sont pas modifiés et le taux de LDL-cholestérol n’est que modestement accru. À l’inverse, l’élévation de la glycémie est une des principales répercussions métaboliques du « blocage androgénique ». Une glycémie à jeun > 7 mmol/L [43] a été retrouvée chez près de la moitié des hommes traités de cette manière. À glycémie égale, l’insulinémie à jeun s’élève significativement trois mois après l’initiation de la thérapeutique chez les deux tiers des hommes traités par « blocage androgénique » [44]. Une réduction de la sensibilité tissulaire à l’insuline apparaît être ainsi une des principales conséquences de l’absence d’androgènes. Parallèlement à la correction de certains paramètres du SMet grâce à la réduction

pondérale chez l’homme s’observe une élévation des taux plasmatique de testostérone et de SHBG [45] and [46]. Ceci fournit un lien de causalité inverse entre SMet et hypotestostéronémie. Les relations entre testostéronémie et SMet Casein kinase 1 sont à l’évidence bidirectionnelles, vraisemblablement composites et sous-tendues par des mécanismes partagés pour partie par ceux de la déflation androgénique accompagnatrice de l’obésité (voir supra) ou du DT2 (voir infra). Les résultats des études épidémiologiques effectuées chez les hommes et les femmes adultes apportent de plus en plus d’arguments en faveur de l’implication de la SHBG [30] and [47] dans l’émergence d’un SMet. Un abaissement du taux plasmatique de SHBG et/ou un polymorphisme particulier de la molécule pourraient intervenir comme un des facteurs physiopathologiques du SMet ou même du DT2 [48] and [49].