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Purpose: A gluten-free diet (GFD) has been reported to negatively impact the quality of life (QoL) of coeliac disease (CD) patients. The gut-brain axis hormones ghrelin and leptin, with the brain-derived neurotrophic factor (BDNF), may affect QoL of CD patients undergoing GFD. Our aims were to evaluate whether: (a) the circulating concentrations of leptin, ghrelin and BDNF in CD patients were different from those in healthy subjects; (b) GFD might induce changes in their levels; (c) BDNF Val66Met polymorphism variability might affect BDNF levels; and (d) serum BDNF levels were related to dietary docosahexaenoic acid (DHA) as a neurotrophin modulator. Methods: Nineteen adult coeliac patients and 21 healthy controls were included. A QoL questionnaire was administered, and serum concentrations of ghrelin, leptin, BDNF and red blood cell membrane DHA levels were determined at the enrolment and after 1 year of GFD. BDNF Val66Met polymorphism was analysed. Results: Results from the questionnaire indicated a decline in QoL after GFD. Ghrelin and leptin levels were not significantly different between groups. BDNF levels were significantly ( p = 0.0213) lower in patients after GFD (22.0 ± 2.4 ng/ml) compared to controls (31.2 ± 2.2 ng/ml) and patients at diagnosis (25.0 ± 2.5 ng/ml). BDNF levels correlated with DHA levels ( p = 0.008, r = 0.341) and the questionnaire total score ( p = 0.041, r = 0.334). Conclusions: Ghrelin and leptin seem to not be associated with changes in QoL of patients undergoing dietetic treatment. In contrast, a link between BDNF reduction and the vulnerability of CD patients to psychological distress could be proposed, with DHA representing a possible intermediate. [ABSTRACT FROM AUTHOR]

Aim of this work was to assess the role of polymorphisms belonging to genes involved in the regulation of ionic homeostasis in Caucasian patients with Ménière Disease (MD). We recruited 155 patients with definite Ménière Disease and 186 controls (Control Group 1) without a lifetime history of vertigo, overlapping with patients for age and rate of hypertension. We validated the positive results on 413 Caucasian subjects selected from a European general population (Control Group 2). The clinical history for migraine and hypertension was collected; genomic DNA was characterized for a panel of 33 SNPs encoding proteins involved in ionic transport. We found a higher rate of migraineurs in MD subjects compared to Group 1 (46.8 vs 15.5%, p = 0.00005). Four SNPs displayed differences in MD patients compared to Group 1 controls: rs3746951 and rs2838301 in SIK1 gene, rs434082 and rs487119 in SLC8A1; the p values of Chi-squared test for genotype frequencies are 0.009, 0.023, 0.009 and 0.048, respectively. SLC8A1 gene encodes for Na-Ca exchanger, while SIK1 gene encodes for Salt Inducible Kinase 1, an enzyme associated with Na-K ATPase function. The validation with Control Group 2 displayed that only rs3746951 and rs487119 are strongly associated to MD ( p = 0.001 and p = 0.0004, respectively). These data support the hypothesis that a genetically induced dysfunction of ionic transport may act as a predisposing factors to develop MD. [ABSTRACT FROM AUTHOR]

An autonomous fire suppression system was developed for localized fire suppression in high and low visibility environments. The system contains a multispectral sensor suite, including UV sensors and infrared stereovision, to detect and target a fire for suppression. The UV sensor provides an alert to the system to begin fire detection. IR imagery is used to segment fire from the field of view and target the base of the fire and IR stereovision to determine the 3D coordinates of the fire. IR tracking provides continuously updated information on the size and intensity of the fire before and during suppression and alerts the system when to cease suppression activity. Visual servoing is used to correctly position a nozzle based on feedback of changes in the fire location and size. The autonomous system was used to suppress wood crib fires (40 kW to 50 kW) in high and low visibility environments and at varying distances (2.8 m to 5.5 m) and elevations (0.4 m to 1.3 m). The suppression time in clear conditions was 3.72 s ± 1.51 s and 4.49 s ± 1.62 s in low visibility conditions. To simulate wind effects and inaccurate initial target coordinates, forced offsets were input to the system to show effectiveness of the feedback control algorithm when an initial estimate of spray trajectory does not accurately spray the center base of the fire. System performance with a forced offset resulted in suppression times of 4.11 s ± 0.84 s. [ABSTRACT FROM AUTHOR]

The ability of countless representatives of the Kingdom Fungi to adapt to and proliferate in diverse environments is facilitated by regulation of their secretomes to respond to changes in environmental conditions and to mediate interactions with other organisms. Secretome changes often fulfill common functions of nutrient acquisition, facilitation of host/symbiont interactions, cell wall modification, and optimization of the enzyme suite to adapt to new environmental resources. In this review, we expand on our recent work on signaling and the secretome in the pathogenic fungus Cryptococcus neoformans to consider a range of selected examples of regulation of fungal secretomes. These examples include the impact of carbon source and aspects of the response to plant and animal hosts. Additionally, the influence of key protein kinases (e.g., Pka1, Snf1) and transcription factors (e.g., Rim101/PacC) is highlighted to illustrate some underlying regulatory factors influencing the secretome. Although there is a wealth of information about fungal secretomes from both experimentation and genome sequence mining, there are also major gaps in our knowledge about the complete composition of fungal secretomes and mechanisms of dynamic change. For example, a more comprehensive understanding of the composition and regulation of the secretome will require consideration of the emerging roles of unconventional secretion and extracellular vesicles in delivering proteins outside the cell. Overall, changes in the secretome are well documented in diverse fungi and the underlying mechanisms are currently under investigation; however, there remain unknown steps in the regulation of secretory pathways and gaps in understanding the regulation of unconventional secretion, which warrant further research. [ABSTRACT FROM AUTHOR]

We propose a novel ultrasound approach with the primary aim of establishing the temporal relationship of structure and function in athletes of varying sporting demographics. 92 male athletes were studied [Group IA, (low static-low dynamic) (n = 20); Group IC, (low static-high dynamic) (n = 25); Group IIIA, (high static-low dynamic) (n = 21); Group IIIC, (high static-high dynamic) (n = 26)]. Conventional echocardiography of both the left ventricles (LV) and right ventricles (RV) was undertaken. An assessment of simultaneous longitudinal strain and LV volume/RV area was provided. Data was presented as derived strain for % end diastolic volume/area. Athletes in group IC and IIIC had larger LV end diastolic volumes compared to athletes in groups IA and IIIA (50 ± 6 and 54 ± 8 ml/(m(2))(1.5) versus 42 ± 7 and 43 ± 2 ml/(m(2))(1.5) respectively). Group IIIC also had significantly larger mean wall thickness (MWT) compared to all groups. Athletes from group IIIC required greater longitudinal strain for any given % volume which correlated to MWT (r = 0.4, p < 0.0001). Findings were similar in the RV with the exception that group IIIC athletes required lower strain for any given % area. There are physiological differences between athletes with the largest LV and RV in athletes from group IIIC. These athletes also have greater resting longitudinal contribution to volume change in the LV which, in part, is related to an increased wall thickness. A lower longitudinal contribution to area change in the RV is also apparent in these athletes. [ABSTRACT FROM AUTHOR]

Background/objectives: Cardiovascular (CV) disease is the leading cause of death after renal transplantation. Marine n-3 polyunsaturated fatty acids (PUFAs) exert potential cardio-protective metabolic effects and might reduce CV morbidity and mortality in renal transplant recipients (RTRs).Subjects/methods: In this cross-sectional study of 1990 Norwegian RTRs, transplanted between 1999 and 2011, associations between plasma phospholipid marine n-3 PUFA levels and various CV risk markers at 10 weeks after transplant were evaluated.Results: Higher plasma marine n-3 PUFA levels were associated with lower resting heart rate (rHR), lower fasting plasma glucose (fPG) levels, lower plasma triglyceride levels and higher plasma high-density lipoprotein (HDL) cholesterol levels. Plasma levels of eicosapentaenoic acid, but not docosahexaenoic acid, showed a positive association with plasma HDL cholesterol levels. Plasma marine n-3 PUFA levels were not associated with plasma low-density lipoprotein cholesterol levels, pulse wave velocity or systolic and diastolic blood pressure. A negative association between plasma marine n-3 PUFA levels and CV mortality was weakened by additional adjustment for plasma triglyceride levels and rHR. The ratio of n-6 to n-3 PUFAs showed similar associations with CV risk markers as absolute plasma marine n-3 PUFA levels.Conclusions: This is the first study in RTRs showing that marine n-3 PUFAs are negatively associated with rHR and fPG in addition to beneficial effects on plasma HDL cholesterol and triglyceride levels. Especially, effects on autonomic nervous function and triglyceride metabolism might contribute to explain the lower CV mortality risk with higher plasma marine n-3 PUFA levels previously shown in this cohort. [ABSTRACT FROM AUTHOR]

Hepatocyte growth factor (HGF) is a pleiotropic cytokine which exerts a variety of effects on several cells, being involved in the regulation of many biological processes, such as inflammation, tissue repair, morphogenesis, angiogenesis, tumour propagation, immunomodulation of viral infections and cardio-metabolic activities. Patients undergoing regular hemodialysis (HD) present elevated levels of HGF, mainly due to the leukocyte activation associated with HD treatment. High HGF levels might account for specific clinical features of HD patients, i.e. mild liver damage in course of HCV-infection and high cardiovascular risk profile. Moreover, in patients with acute kidney injury, the induction of HGF may represent a crucial step to promote renal recovery, which can have important prognostic consequences in the short and long-term. In this review we discuss the mechanisms underlying HGF production in HD patients, the role of HGF in this particular patient population and the potential clinical implications derived from the study of HGF in HD patients. [ABSTRACT FROM AUTHOR]

Purpose: The aim of this study was to determine if omega-3 (n-3) supplementation combined with acute aerobic exercise would improve glucose and insulin responses in normoglycemic, inactive, overweight men.Methods: In a random order, ten inactive and normoglycemic men (30.6 ± 10 years, 85.4 ± 11 kg, 26.7 ± 4 BMI) completed a rest (R) and exercise trial (EX) without n-3 supplementation. Following 42 days of n-3 supplementation, participants again completed a rest (R + n-3) and exercise trial (EX + n-3) with continued n-3 supplementation. The exercise trial consisted of 3 days of ~70 % VO2peak for 60 min/session. N-3 supplementation entailed 4.55 g/day of n-3 (EPA 2.45 g, DHA 1.61 g). A 75 g oral glucose tolerance (OGTT) test was administered 14-16 h after each trial.Results: Relative to R (35,278 ± 9169 pmol/L), EX without n-3 reduced the incremental area under the curve for insulin (iAUCinsulin) during an OGTT by 21.3 % (27765 ± 4925 pmol/L, p = 0.018) and 20.6 % after the EX + n-3 trial (27,999 ± 8370 pmol/L; p = 0.007). In addition, EX (96 ± 21 pmol/L; p = 0.006) reduced C-peptide by 13.5 % when compared to R (111 ± 26 pmol/L). No difference was observed between R and n-3 trials for iAUCinsulin and iAUCC-peptide. Only EX improved insulin sensitivity index by 5.6 % (p = 0.02) when compared to R.Conclusions: These data suggest that n-3 supplementation does not add any additional benefit beyond the exercise induced insulin responses in inactive men. Furthermore, n-3 supplementation alone does not appear to impair insulin action in normoglycemic, inactive, overweight men. [ABSTRACT FROM AUTHOR]

Purpose: Studies suggest that long-chain ω-3 polyunsaturated fatty acid (LCω3PUFA) intake and its primary food source-fish-may have beneficial effects on the individual components of metabolic syndrome (MetS). We examined the longitudinal association between fish or LCω3PUFA intake and MetS incidence. Methods: We prospectively followed 4356 American young adults, free from MetS and diabetes at baseline, for incident MetS and its components in relation to fish and LCω3PUFA intake. MetS was defined by the National Cholesterol Education Program/Adult Treatment Panel III criteria. Cox proportional hazards model was used for analyses, controlling for socio-demographic, behavioral, and dietary factors. Results: During the 25-year follow-up, a total of 1069 incident cases of MetS were identified. LCω3PUFA intake was inversely associated with the incidence of MetS in a dose-response manner. The multivariable adjusted hazards ratio (HR) [95 % confidence interval (CI)] of incident MetS was 0.54 (95 % CI 0.44, 0.67; P for linear trend < 0.01) as compared the highest to the lowest quintile of LCω3PUFA intake. A threshold inverse association was found between non-fried fish consumption and the incidence of MetS. The multivariable adjusted HRs (95 % CIs) from the lowest to the highest quintile were 1.00, 0.70 (0.51, 0.95), 0.68 (0.52, 0.91), 0.67 (0.53, 0.86), and 0.71 (0.56, 0.89) ( P for linear trend = 0.49). The observed inverse associations were independent of the status of baseline individual components of MetS. Conclusions: Our findings suggest that intakes of LCω3PUFAs and non-fried fish in young adulthood are inversely associated with the incidence of MetS later in life. [ABSTRACT FROM AUTHOR]

Early detection of pulmonary hypertension (PH) is essential to ensure that patients receive timely and appropriate treatment for this progressive disease. Rest and exercise echocardiography has been used to screen patients in an attempt to identify early stage PH. However, current PH guidelines recommend against exercise tests because of the lack of evidence. We reviewed previous studies to discuss the current standpoint concerning rest and exercise echocardiography in PH. Around 20 exercise echocardiography studies were included to assess the cutoff value for exercise-induced pulmonary hypertension (EIPH). Approximately 40 exercise echocardiography studies were also included to evaluate the pulmonary artery pressure-flow relationship as assessed by the slope of the mean pulmonary artery pressure and cardiac output (ΔmPAP/ΔQ). There were several EIPH and ΔmPAP/ΔQ reference values in individuals with pulmonary vascular disease. We believed that assessing the ΔmPAP/ΔQ makes sense from a physiological standpoint, and the clinical value should be confirmed in future studies. Exercise echocardiography is an appealing alternative in PH. Further studies are needed to assess the prognostic value of the pulmonary artery pressure-flow relationship in high-risk subjects. [ABSTRACT FROM AUTHOR]

Recently, the Na/Ca exchanger NCX1 and the calcium binding protein calretinin have emerged as new molecular effectors of delayed preconditioning in the brain. In the present study, we investigated whether NCX1 and calretinin cooperate within the preconditioned striatum to confer neurons greater resistance to degeneration. Confocal microscopy analysis revealed that NCX1 expression was upregulated in calretinin-positive interneurons in the rat striatum after tolerance induction. Consistently, coimmunoprecipitation assays performed on human SHSY-5Y cells, a neuronal cell line which constitutively expresses calretinin, revealed a binding between NCX1 and calretinin. Finally, silencing of calretinin expression, both in vitro and in vivo, significantly prevented preconditioning-induced neuroprotection. Interestingly, our biochemical and functional studies showed that the selective silencing of calretinin in brain cells significantly prevented not only the preconditioning-induced upregulation of NCX1 expression and activity but also the activation of the prosurvival protein kinase Akt, which is involved in calretinin and NCX1 protective actions. Collectively, our results indicate that the Na/Ca exchanger NCX1 and the calcium binding protein calretinin cooperate within the striatum to confer tolerance against cerebral ischemia. [ABSTRACT FROM AUTHOR]

Left atrial (LA) strain and strain rate, determined by speckle-tracking echocardiography (STE), are reproducible indices to assess LA function. Different normal ranges for LA phasic functions have been reported. We investigated the role of the reference point (P- and R-wave), gain, and region of interest (ROI), as the major sources of variation when assessing LA function. 52 subjects were evaluated for LA conventional and STE analysis. 45 of them (46 ± 14 years, 26 men) were feasible for concomitant LA deformation, and LA phasic volumes and ejection fractions (LAEF) evaluation. First, we compared the P- and R-wave methods, for the evaluation of the LA functions. We used diastolic mitral profile to clearly delineate the time intervals for each LA function. For the P-wave method, active function was assessed from negative global strain as a difference between the strain at pre-atrial contraction and strain just before mitral valve closure (GSA-), and late diastolic strain rate (GSRL); passive function from positive strain at MVO (GSA+), and from early negative diastolic strain rate (GSRE); reservoir function from the sum of GSA− and GSA+ (TGSA), and positive strain rate at the beginning of LV systole (GSR+). For the R-wave method we used the same SR parameters. The active function was evaluated by late positive global strain (GSAC), the reservoir by positive peak before the opening of the mitral valve (TGSA), and conduit function by the difference between TGSA and GSAC (GSA+). Then, by using P-wave method, we measured all previously described parameters for different gains-minimum (G0), medium (G12), and maximum (G24), and for different ROIs-minimum (ROI0), step 1 (ROI1), and 2 (ROI2). Feasibility of the LA strain measurements was 87 %. Active LA function was similar in the absolute value (GSAC and GSA−), whereas passive and reservoir functions were significantly higher (GSA+, TGSA) with the R-wave method. Active LAEF correlated with GSA− measured by the P-wave ( r = −0.44, p = 0.002), but not with the GSAC measured by the R-wave method. Similar correlations were found for passive and reservoir LAEF with correspondent strain parameters, only with P-wave method. There were no differences between methods regarding SR indices and their correlations with correspondent LAEFs. Increase of gain from minimum to maximum overestimated all measured LA functions (all p < 0.05). Intermediary changes did not have a significant impact on the measurement of active and conduit function, but they do have on the measurement of the reservoir function. Increase of ROI from minimum to ROI2 was associated with an overestimation of all measurements of atrial functions (all p < 0.05). For all parameters, except GSR+, a decrease of atrial S and SR values from minimum ROI to step 1 was recorded. For GSA+, TGSA, GSRE a decrease of S and SR values with each ROI step was recorded. The two methods used to assess LA functions by STE do not provide similar results. The R-wave method essentially ignores negative peak, creating a positive strain for atrial contraction, and also provides higher values for the reservoir and conduit functions, by comparison with the P-wave method. Increase of gain overestimates, whereas increase of ROI underestimates all parameters of LA functions. Therefore, we suggest that P-wave as a reference point, a medium gain, and a minimum ROI should be used as the best choice for a correct assessment. [ABSTRACT FROM AUTHOR]

In a number of dimorphic and hemibiotrophic pathogens, cell cycle regulation has been shown to be important for morphological changes related to infectious growth or infection-related morphogenesis. However, the role of mitotic CDK kinase Cdc2, the key regulator of cell cycle, in pathogenic growth is not clear, because most fungal pathogens have a single CDC2 gene that is essential for cell cycle progression and viability. Interestingly, the wheat scab fungus Fusarium graminearum has two CDC2 genes. Although CDC2A and CDC2B have redundant functions in vegetative growth and asexual production, only CDC2A is required for invasive growth and plant infection. In this study, we showed that Cdc2A and Cdc2B interacted with each other and may form homo- and heterodimers in vegetative hyphae. We also identified sequence and structural differences between Cdc2A and Cdc2B that may be related to their functional divergence. These results, together with earlier studies with cyclins, important for differentiation and infection in Candida albicans and Ustilago maydis, indicated that dimorphic and hemibiotrophic fungal pathogens may have stage-specific cyclin-CDK combinations or CDK targets during saprophytic and pathogenic growth. [ABSTRACT FROM AUTHOR]

In order to obtain accurate diagnosis, treatment and prognostication in many cardiac conditions, there is a need for assessment of left ventricular (LV) filling pressure. While systole depends on ejection function of LV, diastole and its disturbances influence filling function and pressures. The commonest condition that represents the latter is heart failure with preserved ejection fraction in which LV ejection is maintained, but diastole is disturbed and hence filling pressures are raised. Significant diastolic dysfunction results in raised LV end-diastolic pressure, mean left atrial (LA) pressure and pulmonary capillary wedge pressure, all referred to as LV filling pressures. Left and right heart catheterization has traditionally been used as the gold standard investigation for assessing these pressures. More recently, Doppler echocardiography has taken over such application because of its noninvasive nature and for being patient friendly. A number of indices are used to achieve accurate assessment of filling pressures including: LV pulsed-wave filling velocities (E/A ratio, E wave deceleration time), pulmonary venous flow (S wave and D wave), tissue Doppler imaging (E' wave and E/E' ratio) and LA volume index. LA longitudinal strain derived from speckle tracking echocardiography (STE) is also sensitive in estimating intracavitary pressures. It is angle-independent, thus overcomes Doppler limitations and provides highly reproducible measures of LA deformation. This review examines the application of various Doppler echocardiographic techniques in assessing LV filling pressures, in particular the emerging role of STE in assessing LA pressures in various conditions, e.g., HF, arterial hypertension and atrial fibrillation. [ABSTRACT FROM AUTHOR]

Systemic sclerosis patients with COVID-19 pose a serious challenge for monitoring of oxygen saturation through finger probe pulse oximetry due to sclerodactyly, microvascular damage and digital ulceration. However, ear lobe, forehead or oesophageal oximetry may be utilized for oxygen saturation measurements in systemic sclerosis patients with COVID-19 where diffuse involvement of all fingers is present. Keywords: Pulse oximetry; Systemic sclerosis; COVID-19; Accuracy EN Pulse oximetry Systemic sclerosis COVID-19 Accuracy 2243 2244 2 10/28/21 20211201 NES 211201 Dear Editor, The ongoing corona virus disease 2019 (COVID-19) pandemic has posed a serious threat to everybody. [Extracted from the article]

Optic neuritis associated with multiple sclerosis and its animal model, experimental autoimmune optic neuritis (EAON), is characterized by inflammation, T cell activation, demyelination, and neuronal damage, which might induce permanent vision loss. Elucidating the chronological relationship among the features is critical for treatment of demyelinating optic neuritis. EAON was induced in C57BL/6 mice immunized with myelin oligodendrocyte glycoprotein subcutaneously, and visual function was assessed by flash-visual evoked potential (F-VEP) at days 7, 11, 14, 19, 23, 28 post-immunization. Retinal ganglion cell (RGC) apoptosis was measured by terminal-deoxynucleotidyl transferase-mediated nick-end labeling. Demyelination and axonal damage were verified with myelin basic protein (MBP) and β-amyloid precursor protein staining, respectively. Real-time polymerase chain reaction quantified IL-17, IL-1β, TGF-β, FoxP3, IL-6, and IL-10 mRNA expression in the optic nerve, as well as FoxP3 and IL-17 staining. Systemic changes of Th17 and Treg cells were tested by flow cytometry in spleen. F-VEP latency was prolonged at 11 days and peaked at 23 days commensurate with demyelination. However, F-VEP amplitude was reduced at 11 days, preceding axon damage, and was exacerbated at 23 days when a peak in RGC apoptosis was detected. Th17 cells up-regulated as early as 7 days and peaked at 11 days, while Treg cells down-regulated inversely compared to Th17 cells change as verified by IL-17 and FoxP3 expression; spleen cell samples were slightly different, demonstrating marked changed at 14 days. Treg/Th17 cell imbalance in the optic nerve precedes and may initiate neuronal damage of axons and RGCs. These changes are commensurate with the appearances of visual dysfunction reflected in F-VEP and hence may offer a novel therapeutic avenue for vision preservation. [ABSTRACT FROM AUTHOR]

The mission of the Italian Society of Colorectal Surgery (SICCR) is to optimize patient care. Providing evidence-based practice guidelines is therefore of key importance. About the present report it concernes the SICCR practice guidelines for the diagnosis and treatment of diverticular disease of the colon. The guidelines are not intended to define the sole standard of care but to provide evidence-based recommendations regarding the available therapeutic options. [ABSTRACT FROM AUTHOR]

Over the past decades, extensive studies have addressed the therapeutic effects of omega-3 polyunsaturated fatty acids (omega-3 FAs) against different human diseases such as cardiovascular and neurodegenerative diseases, cancer, etc. A growing body of scientific research shows the pharmacokinetic information and safety of these natural occurring substances. Moreover, during recent years, a plethora of studies has demonstrated that omega-3 FAs possess therapeutic role against certain types of cancer. It is also known that omega-3 FAs can improve efficacy and tolerability of chemotherapy. Previous reports showed that suppression of nuclear factor-κB, activation of AMPK/SIRT1, modulation of cyclooxygenase (COX) activity, and up-regulation of novel anti-inflammatory lipid mediators such as protectins, maresins, and resolvins, are the main mechanisms of antineoplastic effect of omega-3 FAs. In this review, we have collected the available clinical data on the therapeutic role of omega-3 FAs against breast cancer, colorectal cancer, leukemia, gastric cancer, pancreatic cancer, esophageal cancer, prostate cancer, lung cancer, head and neck cancer, as well as cancer cachexia. We also discussed the chemistry, dietary source, and bioavailability of omega-3 FAs, and the potential molecular mechanisms of anticancer and adverse effects. [ABSTRACT FROM AUTHOR]

Objectives: The traditional view of differential left ventricular adaptation to training type has been questioned. Right ventricular (RV) data in athletes are emerging but whether training type mediates this is not clear. The primary aim of this study was to evaluate the RV phenotype in endurance- vs. resistance-trained male athletes. Secondary aims included comparison of RV function in all groups using myocardial speckle tracking, and the impact of allometric scaling on RV data interpretation. Methods: A prospective cross-sectional design assessed RV structure and function in 19 endurance-trained (ET), 21 resistance-trained (RT) and 21 sedentary control subjects (CT). Standard 2D tissue Doppler imaging and speckle tracking echocardiography assessed RV structure and function. Indexing of RV structural parameters to body surface area (BSA) was undertaken using allometric scaling. Results: A higher absolute RV diastolic area was observed in ET (mean ± SD: 27 ± 4 cm) compared to CT (22 ± 4 cm; P < 0.05) that was maintained after scaling. Whilst absolute RV longitudinal dimension was greater in ET (88 ± 9 mm) than CT (81 ± 10 mm; P < 0.05), this difference was removed after scaling. Wall thickness was not different between ET and RT and there were no between group differences in global or regional RV function. Conclusion: We present some evidence of RV adaptation to chronic ET in male athletes but limited structural characteristics of an athletic heart were observed in RT. Global and regional RV functions were comparable between groups. Allometric scaling altered data interpretation in some variables. [ABSTRACT FROM AUTHOR]

Lipid mediators influence immunity in myriad ways. For example, circulating sphingosine-1-phosphate (S1P) is a key regulator of lymphocyte egress. Although the majority of plasma S1P is bound to apolipoprotein M (ApoM) in the high-density lipoprotein (HDL) particle, the immunological functions of the ApoM-S1P complex are unknown. Here we show that ApoM-S1P is dispensable for lymphocyte trafficking yet restrains lymphopoiesis by activating the S1P1 receptor on bone marrow lymphocyte progenitors. Mice that lacked ApoM (Apom−/−) had increased proliferation of Lin− Sca-1+ cKit+ haematopoietic progenitor cells (LSKs) and common lymphoid progenitors (CLPs) in bone marrow. Pharmacological activation or genetic overexpression of S1P1 suppressed LSK and CLP cell proliferation in vivo. ApoM was stably associated with bone marrow CLPs, which showed active S1P1 signalling in vivo. Moreover, ApoM-bound S1P, but not albumin-bound S1P, inhibited lymphopoiesis in vitro. Upon immune stimulation, Apom−/− mice developed more severe experimental autoimmune encephalomyelitis, characterized by increased lymphocytes in the central nervous system and breakdown of the blood-brain barrier. Thus, the ApoM-S1P-S1P1 signalling axis restrains the lymphocyte compartment and, subsequently, adaptive immune responses. Unique biological functions imparted by specific S1P chaperones could be exploited for novel therapeutic opportunities. [ABSTRACT FROM AUTHOR]

Objective To develop a national level cost model of both the direct and indirect costs of hospitalisations for impacted teeth in Australia. This model will then be used to compare a watchful monitoring strategy for impacted third molars versus prophylactic removal under GA, and calculate possible cost savings in the scenario where Australia would adopt guidelines comparable to the UK.Methods Western Australian real hospitalisation data for impacted/embedded teeth removal for 2008/2009 were extrapolated into a national, Australian-wide cost-distribution model for removal strategy. The components of a watchful monitoring strategy were calculated over a one-year, and 20-year period. Cost estimates for both strategies were then compared.Results The estimated number of hospitalisations for impacted teeth in Australia in 2008/2009 for the age group 15-34 years was 97,949. The estimated average annual direct cost was $350 million, the indirect cost was $181 million and total cost was $531 million. Individual cost of the watchful monitoring strategy over 20 years was $1,077, with an annual estimated cost of $53. The proposed guidelines would lead to an annual figure of 83,850 individuals avoiding hospitalisation and shifting to watchful monitoring strategy, and an annual reduction of costs ranging between $420-513 million.Conclusion With no evidence to support the prophylactic removal of asymptomatic wisdom teeth, a proposed watchful monitoring strategy is a more cost-effective alternative in the Australian context. [ABSTRACT FROM AUTHOR]

Aim/hypothesis: Dietary polyphenols and long chain n-3 polyunsaturated fatty acids (LCn3) are associated with lower cardiovascular risk. This may relate to their influence on glucose metabolism and diabetes risk. We evaluated the effects of diets naturally rich in polyphenols and/or LCn3 of marine origin on glucose metabolism in people at high cardiometabolic risk. Methods: According to a 2 × 2 factorial design, individuals with high waist circumference and at least one more component of the metabolic syndrome were recruited at the obesity outpatient clinic. Eighty-six participants were randomly assigned by MINIM software to an isoenergetic diet: (1) control, low in LCn3 and polyphenol (analysed n = 20); (2) rich in LCn3 ( n = 19); (3) rich in polyphenols ( n = 19); or (4) rich in LCn3 and polyphenols ( n = 19). The assigned diets were known for the participants and blinded for people doing measurements. Before and after the 8 week intervention, participants underwent a 3 h OGTT and a test meal with a similar composition as the assigned diet for the evaluation of plasma glucose, insulin and glucagon-like peptide 1 (GLP-1) concentrations, and indices of insulin sensitivity and beta cell function. Results: During OGTT, polyphenols significantly reduced plasma glucose total AUC ( p = 0.038) and increased early insulin secretion ( p = 0.048), while LCn3 significantly reduced beta cell function ( p = 0.031) (two-factor ANOVA). Moreover, polyphenols improved post-challenge oral glucose insulin sensitivity (OGIS; p = 0.05 vs control diet by post hoc ANOVA). At test meal, LCn3 significantly reduced GLP-1 total postprandial AUC ( p < 0.001; two-factor ANOVA). Conclusion/interpretation: Diets naturally rich in polyphenols reduce blood glucose response, likely by increasing early insulin secretion and insulin sensitivity. These effects may favourably influence diabetes and cardiovascular risk. The implications of the decrease in insulin secretion and postprandial GLP-1 observed with diets rich in marine LCn3 need further clarification. Trial registration: ClinicalTrials.gov NCT01154478 Funding: The trial was funded by European Community's Seventh Framework Programme FP7/2009-2012 under grant agreement FP7-KBBE-222639, Etherpaths Project and 'Ministero Istruzione Università e Ricerca' PRIN 2010-2011 - 2010JCWWKM. [ABSTRACT FROM AUTHOR]

The purpose of this pictorial review is to demonstrate gastric pathology seen on magnetic resonance imaging (MRI) and discuss the essential MRI sequences for the evaluation of benign and malignant gastric pathologies. Common tumors of the stomach, polyposis syndromes, iatrogenic conditions, as well as other conditions of the stomach will be reviewed. The utility of MRI in the evaluation of patients with gastric malignancies and disorders of gastric motility will also be discussed. [ABSTRACT FROM AUTHOR]

Several studies have evidenced high prevalence of myocardial systolic and diastolic dysfunction among patients with systemic sclerosis (SSc). Exercise echocardiography has shown a diagnostic and prognostic role in identifying early left ventricular (LV) dysfunction in several myocardial pathological settings. The aim of our study was to evaluate early signs of LV impairment under exercise and their correlation to patient's exercise tolerance. Forty-five patients (age 60.4 ± 10.3 years) with SSc and 20 age and sex comparable controls were enrolled in the study. All patients underwent clinical evaluation, 2D echocardiography associated with Tissue Doppler and speckle tracking to evaluate LV deformation indexes, and an exercise echocardiography to evaluate left ventricle contractile reserve (LVCR) and exercise pulmonary pressures. Finally, a 6-minute walking test (6MWT) to evaluate exercise tolerance was also performed. Compared to controls, SSc patients showed an impaired diastolic function (E/E′ 10.9 ± 3.7 vs 8.36 ± 2.01; p < 0.01) associated with larger left atrial dimensions (LAVI 28.4 ± 8.7 vs 19.3 ± 4.6 mL/m; p < 0.01). During exercise echocardiography, a reduced global longitudinal strain at peak exercise (S-GLS) was highlighted compared to controls (15.7 ± 3.6 vs 18.2 ± 2.2; p = 0.001). A S-GLS cutoff <18 %, identified by ROC analysis, identified SSc patients with a reduced diastolic function, exercise tolerance at the 6MWT and higher pulmonary pressures. Our data show that in SSc patients a reduced LVCR characterizes the patients with a more extensive cardiovascular impairment in terms of LV diastolic function, pulmonary pressures and exercise tolerance. These data underline the importance of exercise echocardiography for the preclinical screening of the LV impairment in this population. [ABSTRACT FROM AUTHOR]

Purpose: To explore the optimal timing for hCG triggering by investigating the impact of different proportion of dominant follicles on the oocyte developmental competence. Methods: One hundred ninety-eight infertile women were divided into three groups according to the proportion of dominant follicles on hCG day: (1) low: <15 % ( n = 66); (2) middle: 15-27 % ( n = 66); (3) high: >27 % ( n = 66). The grouping criteria were the bottom and top tertiles of the proportion of dominant follicles. Results: The gonadotropin dosage, duration and maximum follicle diameter in the low proportion group were lower than those in the middle and high proportion groups. Oocyte maturation and the abnormal fertilization rate in the low proportion group were lower than those in the middle and high proportion groups. The normal fertilization rate did not differ among the three groups. The cleavage rate and number of transferable embryos in the low proportion group were significantly higher than those in the high proportion group. The high-quality embryo rate, implantation rate, and pregnancy rate in the low proportion group were significantly higher than those in the middle and high proportion groups. Conclusions: A high proportion of dominant follicles are closely associated with impaired oocyte developmental competence and low pregnancy rate. These findings suggest that follicular overgrowth induced by delayed hCG triggering may undermine oocyte developmental competence and the proportion of dominant follicles may be a potential parameters for hCG triggering. [ABSTRACT FROM AUTHOR]

OBJECTIVES:Helicobacter pylori eradication rates with clarithromycin-based triple therapy are declining, and an alternative strategy is needed urgently. We sought to compare the efficacy of pretreatment antimicrobial susceptibility-guided vs. clarithromycin-based triple therapy for H. pylori eradication in a region with high rates of multiple drug resistance.METHODS:Consecutive H. pylori-infected patients with gastric epithelial neoplasms were randomized to receive antimicrobial susceptibility-guided therapy or clarithromycin-based triple therapy for 7 days. In patients in whom the infection was not eradicated, antibiotics were given according to an initial antimicrobial susceptibility test as a second-line therapy in both groups. Eradication rates, antibiotics resistance rates, and drug compliance owing to adverse effects were compared between the groups.RESULTS:In total, 114 patients were enrolled, and 112 completed the protocols. Drug compliance and side effects were similar between the groups. The intention-to-treat eradication rates were 94.7% (95% confidence interval (CI)=88.8-100%, 54/57) in the antimicrobial susceptibility-guided group and 71.9% (95% CI=60.2-83.5%, 41/57) in the clarithromycin-based triple therapy group after the initial treatment (P=0.002), whereas the per-protocol (PP) eradication rates were 96.4% (95% CI=91.5-100%, 54/56) in the antimicrobial susceptibility-guided group and 73.2% (95% CI=61.5-84.8%, 41/56) in the clarithromycin-based triple therapy group (P=0.001). In H. pylori with clarithromycin resistance, the eradication failure rate with first-line treatment was lower in the susceptibility-guided therapy group (0%, 0/12) compared with the clarithromycin-based triple therapy group (80.0%, 95% CI=59.7-100%, 12/15) by PP analysis (P<0.001).CONCLUSIONS:Pretreatment antimicrobial susceptibility-guided therapy is more effective than clarithromycin-based triple therapy for H. pylori eradication in a region with high rates of multiple drug resistance. [ABSTRACT FROM AUTHOR]

Background: Cancer cells show enhanced glycolysis and inhibition of oxidative phosphorylation, even in the presence of sufficient oxygen (aerobic glycolysis). Glycolysis is much less efficient for energy production than oxidative phosphorylation, and the reason why cancer cells selectively use glycolysis remains unclear. Methods: Biospecimens were collected from 45 hepatocellular carcinoma patients. Protein samples were prepared through subcellular localization or whole-cell lysis. Protein synthesis was measured by SDS-PAGE and immunoblotting. mRNA transcription was measured using quantitative RT-PCR. Statistical correlation among immunoblotting data and clinicolaboratory factors were analyzed using SPSS. Results: Enzymes for oxidative phosphorylation (SDHA and SDHB) were frequently decreased (56 and 48 % of patients, respectively) in hepatocellular carcinomas. The lowered amount of the SDH protein complex was rarely accompanied by stabilization of HIF1α and subsequent activation of the hypoxia response. On the other hand, protein synthesis of G6PD and TKT, enzymes critical for pentose phosphate pathway (PPP), was increased (in 45 and 55 % of patients, respectively), while that of ALDOA, an enzyme for mainstream glycolysis, was eliminated (in 55 % of patients). Alteration of protein synthesis was correlated with gene expression for G6PD and TKT, but not for TKTL1, ALDOA, SDHA or SDHB. Augmented transcription and synthesis of PPP enzymes were accompanied by nuclear accumulation of NRF2. Conclusion: Hepatocellular carcinomas divert glucose metabolism to the anabolic shunt by activating transcription factor NRF2. [ABSTRACT FROM AUTHOR]

The effect of polydopamine coated titanium such as surface roughness, wettability, cell growth and toxicity, and corrosion resistance. The polydopamine-coated titanium was successfully prepared from dopamine solution and bright polydopamine granules were randomly distributed on titanium surface after coating process. The surface roughness was not significantly decreased in the pure titanium (P>0.05), but significantly decreased (P<0.05) in the spark anodized titanium after the dopamine coating treatment. The contact angle of polydopamine-coated titanium surface was found to be lower than that of the untreated titanium surface. At the potentiodynamic polarization corrosion test, polydopamine-coated titanium has better corrosion-resistance than untreated titanium. The resistance of cytotoxicity is decreased by dopamine coating surface treatment (P<0.05). Findings from this research suggested that polydopamine coating offer a versatile approach for the titanium surface modification. [ABSTRACT FROM AUTHOR]

In few mammalian species including rat, post-ovulatory aging induces abortive spontaneous egg activation (SEA), which is morphologically characterized by exit from metaphase-II (M-II) arrest. A possibility exists that the RyR channel-mediated insufficient increase of cytosolic free Ca level could be one of the causes for post-ovulatory aging-induced abortive SEA. To test this possibility, eggs collected after 17 h post-hCG surge were cultured with or without various concentrations of nifedipine (NF), ruthenium red (RR), and KN-93 for 3 h in vitro. Morphological changes characteristic of abortive SEA, cytosolic free Ca level, cyclin B1 level, and meiotic status were analyzed. Data of the present study indicate that NF and RR inhibited post-ovulatory aging-induced abortive SEA in a concentration-dependent manner. Further, RR protected against RyR channel as well as caffeine-mediated increase of cytosolic free Ca level. In addition, KN-93 inhibited post-ovulatory aging-induced abortive SEA in a concentration-dependent manner. An increase of cytosolic free Ca level was associated with a reduction of cyclin B1 level during post-ovulatory aging-induced abortive SEA. These data indirectly suggest the involvement of RyR channels in the increase of cytosolic free Ca level. The increased cytosolic free Ca level triggers cyclin B1 degradation possibly through CaMK-II activity during post-ovulatory aging-induced abortive SEA in rat eggs cultured in vitro. [ABSTRACT FROM AUTHOR]

Ischemic preconditioning (IPC), an important endogenous adaptive mechanism of the CNS, renders the brain more tolerant to lethal cerebral ischemia. The molecular mechanisms responsible for the induction and maintenance of ischemic tolerance in the brain are complex and still remain undefined. Considering the increased expression of the two sodium calcium exchanger (NCX) isoforms, NCX1 and NCX3, during cerebral ischemia and the relevance of nitric oxide (NO) in IPC modulation, we investigated whether the activation of the NO/PI3K/Akt pathway induced by IPC could regulate calcium homeostasis through changes in NCX1 and NCX3 expression and activity, thus contributing to ischemic tolerance. To this aim, we set up an in vitro model of IPC by exposing cortical neurons to a 30-min oxygen and glucose deprivation (OGD) followed by 3-h OGD plus reoxygenation. IPC was able to stimulate NCX activity, as revealed by Fura-2AM single-cell microfluorimetry. This effect was mediated by the NO/PI3K/Akt pathway since it was blocked by the following: (a) the NOS inhibitors L-NAME and 7-Nitroindazole, (b) the IP3K/Akt inhibitors LY294002, wortmannin and the Akt-negative dominant, (c) the NCX1 and NCX3 siRNA. Intriguingly, this IPC-mediated upregulation of NCX1 and NCX3 activity may control calcium level within endoplasimc reticulum (ER) and mitochondria, respectively. In fact, IPC-induced NCX1 upregulation produced an increase in ER calcium refilling since this increase was prevented by siNCX1. Moreover, by increasing NCX3 activity, IPC reduced mitochondrial calcium concentration. Accordingly, the inhibition of NCX by CGP37157 reverted this effect, thus suggesting that IPC-induced NCX3-increased activity may improve mitochondrial function during OGD/reoxygenation. Collectively, these results indicate that IPC-induced neuroprotection may occur through the modulation of calcium homeostasis in ER and mitochondria through NO/PI3K/Akt-mediated NCX1 and NCX3 upregulation. [ABSTRACT FROM AUTHOR]

In multiple sclerosis (MS), inflammation leads to damage of central nervous system myelin and axons. Previous studies have postulated impaired GABA transmission in MS, and recent postmortem analysis has shown that GABAergic parvalbumin (PV)-positive interneurons are decreased in the primary motor cortex (M1) of patients with MS. In this report, we present evidence for the loss of a specific population of GABAergic interneurons in the experimental autoimmune encephalomyelitis mouse model of MS. Using experimental autoimmune encephalomyelitis, we evaluated the distribution of both PV-positive interneurons and of the inhibitory presynaptic input in the M1 of experimental autoimmune encephalomyelitis and control mice. Our results demonstrate a specific decrease in the number of PV-positive interneurons in the M1 of mice with experimental autoimmune encephalomyelitis. We detected a significant reduction in the number of PV-positive interneurons in the layers II and III of the M1 of diseased mice, while there was no difference in the number of calretinin (CR)-positive cells between animals with experimental autoimmune encephalomyelitis and control animals. Moreover, we observed a significant reduction in the inhibitory presynaptic input in the M1 of treated mice. These changes were specific for the mice with elevated clinical score, while they were not detectable in the mice with low clinical score. Our results support the hypothesis that reinforcing the action of the GABAergic network may represent a therapeutic alternative to limit the progression of the neuronal damage in MS patients. [ABSTRACT FROM AUTHOR]

The concept of personalized medicine has led to a paradigm shift in recent years. It integrates multiple clinical and biological levels of investigation aimed at offering the best possible and patient-tailored healthcare. This holds great potential in a rare and heterogeneous disease such as systemic sclerosis (SSc). The development of validated clinical screening algorithms and the identification of predictors for disease outcomes can help in stratifying patients according to their individual risk of progression. The ongoing search for biomarkers and key pathogenic molecules has brought valuable insights into molecular networks operative in SSc. In parallel, genetic and genomic studies have revealed new SSc susceptibility loci and validated gene expression profiles that might identify patients benefiting from specific therapies. In this review, we focus on recent findings relevant for the concept of personalized medicine in patients with SSc. [ABSTRACT FROM AUTHOR]

Self-generated identification codes (SGICs) are an increasingly utilized methodological feature of longitudinal prevention research among adolescents. This study sought to test the differences between the matched and unmatched groups at baseline on a number of background, health, and well-being and risk behavior measures in a prevention study among 13- to 16-year-old Icelandic adolescents where a SGIC was constructed and used to link individual-level respondent data over two data collection points one year apart. We use pilot data from two Reykjavik city secondary schools collected as part of the population study Youth in Iceland in February 2010 and 2011 ( N = 366, SGIC matching rate 61 %). Baseline results for the matched and unmatched participants are compared. Findings indicate that the unmatched subjects are both more likely to be substance users than their matched counterparts as well as being more likely to be boys and/or from disrupted families. Five out of the seven scaled measures for risk and protective factors and personality indicators reveal no difference between the matched and unmatched subjects and the significantly different measures reveal small effect sizes between the two groups. However, the effect sizes for substance use are significantly different between the matched and unmatched groups for all seven substance use measures with effect sizes from 0.52 to 1.32. These findings therefore indicate that the measurement validity of adolescent risk behaviors such as substance use may be put in jeopardy when using SGIC and that unmatched subjects may be more likely to distrust the SGIC process. [ABSTRACT FROM AUTHOR]

Cardiotrophin-1 (CT-1) is a member of the interleukin (IL-6) family of cytokines. Plasma CT-1 levels correlate with the left ventricle mass index in patients with dilatated cardiomyopathy and congestive heart failure (CHF). The aim of this paper was to evaluate CT-1 plasma levels, before and after cardiac resynchronization therapy CRT, and to characterizeits prognostic role in patients with CHF. Fifty-two consecutive patients (M/F = 39/13; 56 ± 11 years old) underwent clinical and echocardiographic evaluation, and blood sample collection at baseline. The same evaluation was repeated 6.4 ± 0.79 months after CRT. Patients with a decreased LV end-systolic volume by at least 15% (reverse remodeling) were considered echo responders to CRT. Twenty-nine patients (56%) were responders to CRT. After CRT, only 15 patients (29%) showed increased CT-1 after CRT. They were all non responders to CRT. A multivariate, logistic modelshowed CT-1 as an independent predictor of CRT echo response ( p = 0.005; OR 0.97). During follow-up (18 ± 7 months), 21 cardiac events in 18 patients occurred. A Cox multivariable model showed plasma BNP pre-CRT ( p = 0.02; CI 1.2-5.6; OR 3.1) and CT1 post-CRT ( p = 0.01; CI 1.4-4.3; OR 2.7) as independent predictors of cardiac events. Analysis of CT-1 plasma levels deserves future consideration for larger, longitudinal studies in patients with CHF. [ABSTRACT FROM AUTHOR]

Stroke causes a rapid cell death in the core of the injured region and triggers mechanisms in surrounding penumbra area that leads to changes in concentrations of several ions like intracellular Ca, Na, H, K, and radicals such as reactive oxygen species and reactive nitrogen species. When a dysregulation of homeostasis of these messengers occurs, it can trigger cell death. In particular, it is widely accepted that a critical factor in determining neuronal death during cerebral ischemia is progressive dysregulation of Ca, Na, K, and H homeostasis that activate several death pathways, including oxidative and nitrosative stress, mitochondrial dysfunction, protease activation, and apoptosis. In the last decade, several seminal experimental works are markedly changing the scenario of research of principal players of an ischemic event. Indeed, some plasma membrane channels and transporters, involved in the control of Ca, Na, K, and H ion influx or efflux and, therefore, responsible for maintaining the homeostasis of these four cations, might function as crucial players in initiation of brain ischemic process. Indeed, these proteins, by regulating ionic homeostasis, may provide the molecular basis underlying glutamate-independent Ca and Na overload mechanisms in neuronal ischemic cell death and, most importantly, may represent more suitable molecular targets for therapeutic intervention. Recently, a great deal of interest has been devoted to clarify the role of the plasma membrane protein known as Na/Ca exchanger, a transporter able to control Na and Ca homeostasis. In this review, the pathophysiological role of NCX and its implication as a potential target in stroke intervention will be examined. [ABSTRACT FROM AUTHOR]

Ecosystem-based planning and management have stimulated the need to gather sociocultural values and human uses of land in formats accessible to diverse planners and researchers. Human Ecology Mapping (HEM) approaches offer promising spatial data gathering and analytical tools, while also addressing important questions about human-landscape connections. This article reviews and compares the characteristics of three HEM approaches that are increasingly used in natural resource management contexts, each focused on a particular aspect of human-environmental interactions. These aspects include tenure and resource use (TRU), local ecological knowledge (LEK), and sense of place (SOP). We discuss their origins, provide examples of their use, and identify challenges to their application. Our review serves as a guide for environmental managers, planners, and communities interested in gathering spatial data on aspects of human ecology important in ecosystem-based management and planning, and for scientists designing socioecological research. [ABSTRACT FROM AUTHOR]

Interleukin-25 (IL-25) is the only anti-inflammatory cytokine of the IL-17 family, and it has been shown to be efficacious in inhibiting neuroinflammation. Known for its effects on cells of the adaptive immune system, it has been more recently described to be effective also on cells of the innate immune system, namely macrophages. We used a lentiviral-mediated gene therapy approach to deliver IL-25 to the central nervous system (CNS) in two mouse models of neuroinflammation, entorhinal cortex lesion and experimental autoimmune encephalomyelitis. In both, we found that IL-25 gene therapy was able to modulate CNS myeloid cells, either infiltrating macrophages or resident microglia, towards an anti-inflammatory, tissue-protective phenotype, as testified by the increase in markers such as Arginase-1 (Arg1), Mannose receptor 1 (CD206) and Chitinase 3-like 3 (Ym1). As a consequence, neuroinflammation was partly inhibited and the CNS protected from immune-mediated damage. To our knowledge, this is the first example of M2 shift (alternative activation) induced in vivo on CNS-resident myeloid cells by gene therapy, and may constitute a promising strategy to investigate the potential role of protective microglia in neurological disorders. [ABSTRACT FROM AUTHOR]

Although many echocardiographic studies are available about the adaptation of left ventricle to intensive training, right heart function has been poorly investigated and no data are available about the right atrial (RA) function in top-level athletes. The aim of the study was to investigate RA function and dimension by standard echocardiography and 2D speckle tracking echocardiography (STE). One hundred top-levels athletes were recruited from professional sports team and were compared with 78 normal subjects. Athletes during an off-training period or during prolonged forced rest resulting from injuries were excluded. Top-level athletes had higher BSA as compared with controls and, as expected, a lower resting heart rate ( p ≤ 0.001). RA area, volume, and volume index were significantly greater in athletes than in controls ( p ≤ 0.001). This increase was associated with greater right ventricular and inferior vena cava diameters ( p ≤ 0.001). Peak atrial longitudinal strain and peak atrial contraction strain values were significantly lower in athletes in comparison with controls (40.92 ± 9.86 % vs. 48.00 ± 12.68 %, p ≤ 0.001; 13.05 ± 4.84 % vs. 15.99 ± 5.74 %, p ≤ 0.001, respectively). Interestingly, while athletes presented a higher E/A ratio ( p ≤ 0.001) and a lower peak A velocity ( p ≤ 0.001), the E/e′ ratio did not differ between the two groups. In top-level athletes the RA presents a physiological adaptation to intensive exercise conditioning which determines not only a morphological but also a functional remodeling. We reported for the first time reference values of RA strain in elite athletes, demonstrating that 2D STE is a useful tool to investigate RA longitudinal myocardial deformation dynamics in athlete's heart. [ABSTRACT FROM AUTHOR]

Purpose: Clinical features of symptomatic uncomplicated diverticular disease are poorly investigated. Abdominal symptoms may be similar to those of irritable bowel syndrome. This survey aimed to assess clinical features associated with symptomatic uncomplicated diverticular disease. Methods: This multicenter survey included consecutive outpatients with symptomatic uncomplicated diverticular disease to whom a detailed clinical questionnaire regarding demographic, lifestyle, and clinical features was administered. Diagnosis was based on the presence of diverticula and abdominal pain/discomfort. Irritable bowel syndrome and functional dyspepsia were assessed according to Rome III criteria. Results: A total of 598 patients (50 % female, age 69 years), 71 % with newly diagnosed symptomatic uncomplicated diverticular disease and 29 % with history of colonic diverticula, were recruited. Diverticula were localized in the left colon in 78 % of the patients. Recurrent short-lived abdominal pain (<24 h) was present in 70 % (relieved by evacuation in 73 %), prolonged abdominal pain (>24 h) in 27 %, and recurrent abdominal bloating in 61 % of the patients. Normal, loose, or hard stools were reported by 58, 29, and 13 % of patients, respectively. Irritable bowel syndrome (IBS)-like and functional dyspepsia-like symptoms were recorded in 59 and 7 % of patients, respectively. IBS-like symptoms (odds ratio, 4.3) were associated in patients with prolonged abdominal pain. Conclusions: Symptomatic uncomplicated diverticular disease is associated with a gender ratio of 1:1 and an unspecific clinical picture mainly characterized by normal stools, short-lived abdominal pain, abdominal bloating, IBS-like symptoms, while functional dyspepsia-like symptoms are not commonly present. These findings suggest that symptomatic uncomplicated diverticular disease often shows similar findings rather than overlaps IBS. [ABSTRACT FROM AUTHOR]

Fire behavior modeling systems are important in predicting wildfire risk, fire growth, and fire effects. However, simulation software requires a new fuel modeling to include fuel treatments, prescribed fire and the transition to crown fire. The thirteen Rothermel models are insufficient in completely representing Mediterranean ecosystems. In this sense, the new American modeling includes five fuel types, requiring the acquisition of hybrid models made up of the mixture of grass and shrub and the grass or shrub mixed with litter from forest canopy. Respecting meteorological conditions and shrub characteristics, field studies have shown significant differences between American and Mediterranean models. As a consequence, the definition of new Mediterranean models requires the adjustment of specific parameters such as fuel load by category (live and dead) and particle size class (1-, 10- and 100-h time-lag), fuelbed depth and surface area-to-volume ratio. These new parameters were obtained in situ of sample itineraries, prescribed fires, and forest fires. The availability of this new modeling, validated on a field of regional scale, will facilitate preventive planning and management as well as an efficient application of suppression techniques, both ground and aerial operations, required in defending a territory against forest fires. [ABSTRACT FROM AUTHOR]