Preoperative ultra-hypofractionation radiotherapy in extremity/trunk wall soft tissue sarcoma - A meta-analysis of prospective studies.

PURPOSE: The neoadjuvant radiotherapy is now standard treatment in soft tissue sarcoma. Using ultra-hypofractionation radiotherapy shorten the treatment time. In the era of COVID pandemic, using less fraction to treat patient is an urgent need. Thus, we aim to use meta-analysis to investigate the clinical efficacy of preoperative stereotactic body radiotherapy. MATERIAL AND METHODS: PRISMA guideline was used in this study. PubMed, Cochrane and Embase were used. We include only prospective study. The main endpoint was set as wound complication rate. Other endpoints include R0 resection rate, overall survival, local control, and distant metastasis free survival. RESULTS: Seven studies were included. The pooled wound complication rate is 0.30 (95% CI=0.26-0.35). The pooled R0 resection rate is 0.87(95%CI: 0.74-0.94). The pooled 2-year overall survival is 0.86 (95%CI: 0.72-0.94). The pooled 2-year local control rate is 0.96(95%CI: 0.89-0.99). The pooled 2-year distant metastasis free survival is 0.60 (95%CI=0.50-0.70). CONCLUSION: Neoadjuvant ultra-hypofractionation radiotherapy in soft tissue sarcoma is a feasible and well tolerable treatment.

Using social media for smoking cessation interventions: a systematic review.

BACKGROUND: Previous studies have shown that smoking tobacco significantly increases both incidence and mortality rates for many diseases. Social media has become one of the most influential platforms for various smoking cessation interventions. However, results from smoking cessation interventions have differed from study to study. Limited studies have summarised cessation outcomes from social media-based interventions. Therefore, the objective of this review is to explore the effectiveness of using social media for smoking cessation. METHODS: We searched PubMed, MEDLINE, PsycINFO, and CINAHL for articles between June 2008 and June 2018, and also assessed the references of selected articles. We included studies that used social media as intervention platforms, provided a baseline assessment before the intervention, and provided smoking cessation outcomes after the intervention. RESULTS: We identified 13 original studies that enrolled between 16 and 1698 participants; 7-day Point Prevalence Abstinence (PPA) rate was the most frequently used measure of abstinence, with a range of 7%-75%, regardless of the measurement time, study design, and analysis methods. Social media-based smoking cessation interventions were effective, because (1) smokers reported higher 7-day PPA rates after intervention compared to baseline and (2) smokers reported higher 7-day PPA rates in intervention groups than in control groups. Moreover, at each time point, approximately half of all smokers in studies reporting abstinence were found to be biochemically abstinent. There were no significant differences in the effectiveness of smoking cessation outcomes between those that used existing popular social networking platforms (e.g. Pechmann et al's studies) and those that used individually designed interactive platforms (e.g. MyLastDip, iQuit system, Quitxt system). CONCLUSIONS: This review highlights the effectiveness of social media-based smoking cessation intervention studies. Due to the widespread use of social media, as well as its low cost, we suggest embedding smoking cessation interventions within existing popular social media platforms.

Behavioral and Structural Effects of Single and Repeat Closed-Head Injury.

BACKGROUND AND PURPOSE: The effects of multiple head impacts, even without detectable primary injury, on subsequent behavioral impairment and structural abnormality is yet well explored. Our aim was to uncover the dynamic changes and long-term effects of single and repetitive head injury without focal contusion on tissue microstructure and macrostructure. MATERIALS AND METHODS: We introduced a repetitive closed-head injury rodent model (n = 70) without parenchymal lesions. We performed a longitudinal MR imaging study during a 50-day study period (T2-weighted imaging, susceptibility-weighted imaging, and diffusion tensor imaging) as well as sequential behavioral assessment. Immunohistochemical staining for astrogliosis was examined in a subgroup of animals. Paired and independent t tests were used to evaluate the outcome change after injury and the cumulative effects of impact load, respectively. RESULTS: There was no gross morphologic evidence for head injury such as skull fracture, contusion, or hemorrhage on micro-CT and MR imaging. A significant decrease of white matter fractional anisotropy from day 21 on and an increase of gray matter fractional anisotropy from day 35 on were observed. Smaller mean cortical volume in the double-injury group was shown at day 50 compared with sham and single injury (P < .05). Behavioral deficits (P < .05) in neurologic outcome, balance, and locomotor activity were also aggravated after double injury. Histologic analysis showed astrogliosis 24 hours after injury, which persisted throughout the study period. CONCLUSIONS: There are measurable and dynamic changes in microstructure, cortical volume, behavior, and histopathology after both single and double injury, with more severe effects seen after double injury. This work bridges cross-sectional evidence from human subject and pathologic studies using animal models with a multi-time point, longitudinal research paradigm.

Effect of benign prostatic hyperplasia on the development of spine, hip, and wrist fractures.

Benign prostatic hyperplasia is one of the most common diseases in the elderly male population. The urinary tract symptoms may increase the risk of falls and fractures. The results indicated that patients with benign prostatic hyperplasia could increase the risk of vertebral compression fractures in both the thoracic and lumbar spine and also hip fractures, but did not increase the risk of wrist fracture. INTRODUCTION: The relationship between benign prostatic hyperplasia and the development of fall-related fractures, especially vertebral compression fractures, has been seldom mentioned in the literature. This study aimed to evaluate the risk of developing vertebral compression fracture, hip fracture, and wrist fracture in patients with benign prostatic hyperplasia. METHODS: This study obtained claims data retrospectively from the National Health Insurance Research Database of Taiwan and identified 48,114 patients who were diagnosed as having benign prostatic hyperplasia. Subjects of the control cohort were individually matched at a ratio of 4:1 with those in the benign prostatic hyperplasia cohort according to age and the index day. Comorbidities were classified as those existing before the index day and included a previous fracture history, osteoporosis, myocardial infarction, congestive heart failure, diabetes mellitus, hypertension, cerebrovascular accident, etc. The end of the follow-up period of the analyses was the day when the patient developed new vertebral compression fractures, hip fractures, or wrist fractures, terminated enrollment from the National Health Insurance, or died or until the end of 2012. The study used the Cox proportion hazard model to determine the hazard ratio for developing new hip fractures. RESULTS: Patients with benign prostatic hyperplasia were significantly more likely than those in the control cohort to develop new vertebral compression fractures in the thoracic spine (0.43% vs. 0.40%, adjusted hazard ratio 3.03, confidence interval 2.12-4.31) and lumbar spine (1.26% vs. 1.23%, adjusted hazard ratio 4.12, confidence interval 3.39-5.01), and hip fracture (1.47% vs. 2.09%, adjusted hazard ratio 1.22, confidence interval 1.10-1.36), but does not increase the risk of wrist fracture (0.61% vs. 0.67%, adjusted hazard ratio 1.07, confidence interval 0.85-1.34). CONCLUSIONS: Patients with benign prostatic hyperplasia exhibited an increased risk of developing vertebral compression fractures in both the thoracic and lumbar spine and also hip fractures, but did not increase the risk of wrist fracture. However, more research is needed to confirm this trend in the clinical setting.

Validating the Automatic Independent Component Analysis of DSA.

Time-density curve analysis of DSA provides useful blood flow information. However, manually selecting the ROI is time-consuming. We developed an automatic technique to provide arterial, capillary, and venous vasculatures with corresponding time-density curves. This study retrospectively analyzed the data of 36 patients with unilateral carotid stenosis. We found that the full width at half maximum of the time-density curve for the automatically segmented capillary vasculature is a suitable representation of the cerebral circulation time.

Insight, self-stigma and psychosocial outcomes in Schizophrenia: a structural equation modelling approach.

AIMS: Poor insight is prevalent in patients with schizophrenia and has been associated with acute illness severity, medication non-adherence and poor treatment outcomes. Paradoxically, high insight has been associated with various undesirable outcomes, including low self-esteem, depression and low subjective quality of life (QoL) in patients with schizophrenia. Despite the growing body of studies conducted in Western countries supporting the pernicious effects of improved insight in psychosis, which bases on the level of self-stigma, the effects are unclear in non-Western societies. The current study examined the role of self-stigma in the relationship between insight and psychosocial outcomes in a Chinese population. METHODS: A total of 170 outpatients with schizophrenia spectrum disorders were recruited from two general university hospitals. Sociodemographic data and clinical variables were recorded and self-report scales were employed to measure self-stigma, depression, insight, self-esteem and subjective QoL. Structural equation modelling (SEM) was used to analyse the cross-sectional data. RESULTS: High levels of self-stigma were reported by 39% of the participants (n = 67). The influences of insight, self-stigma, self-esteem and depression on subjective QoL were confirmed by the SEM results. Our model with the closest fit to the data (χ 2 = 33.28; df = 20; p = 0.03; χ 2/df = 1.66; CFI = 0.98; TLI = 0.97; RMSEA = 0.06) demonstrated that self-stigma might fully mediate the association of insight with low self-esteem, depression and poor subjective QoL. High insight into illness contributed to self-stigma, which caused low self-esteem and depression and, consequently, low QoL. Notably, insight did not directly affect self-esteem, depression or QoL. Furthermore, the association of insight with poor psychosocial outcomes was not moderated by self-stigma. CONCLUSIONS: Our findings support the mediating model of insight relevant to the poor psychosocial outcomes of individuals diagnosed with schizophrenia in non-Western societies, in which self-stigma plays a pivotal role. These findings elucidate the direct and indirect effects of insight on psychosocial outcomes and imply that identifying and correcting self-stigma in people with schizophrenia could be beneficial. Additional studies are required to identify whether several other neurocognitive or psychosocial variables mediate or moderate the association of insight with self-esteem, depression and QoL in patients with schizophrenia. Studies with detailed longitudinal assessments are necessary to confirm our findings.

Targeting of Aberrant αvß6 Integrin Expression in Solid Tumors Using Chimeric Antigen Receptor-Engineered T Cells.

Expression of the αvß6 integrin is upregulated in several solid tumors. In contrast, physiologic expression of this epithelial-specific integrin is restricted to development and epithelial re-modeling. Here, we describe, for the first time, the development of a chimeric antigen receptor (CAR) that couples the recognition of this integrin to the delivery of potent therapeutic activity in a diverse repertoire of solid tumor models. Highly selective targeting αvß6 was achieved using a foot and mouth disease virus-derived A20 peptide, coupled to a fused CD28+CD3 endodomain. To achieve selective expansion of CAR T cells ex vivo, an IL-4-responsive fusion gene (4αß) was co-expressed, which delivers a selective mitogenic signal to engineered T cells only. In vivo efficacy was demonstrated in mice with established ovarian, breast, and pancreatic tumor xenografts, all of which express αvß6 at intermediate to high levels. SCID beige mice were used for these studies because they are susceptible to cytokine release syndrome, unlike more immune-compromised strains. Nonetheless, although the CAR also engages mouse αvß6, mild and reversible toxicity was only observed when supra-therapeutic doses of CAR T cells were administered parenterally. These data support the clinical evaluation of αvß6 re-targeted CAR T cell immunotherapy in solid tumors that express this integrin.

Elevated hydrostatic pressure enhances the motility and enlarges the size of the lung cancer cells through aquaporin upregulation mediated by caveolin-1 and ERK1/2 signaling.

The mechanical characteristics presented in cancer microenvironment are known to have pivotal roles in cancer metastasis, which accounts for the leading cause of death from malignant tumors. However, while a uniformly distributed high interstitial fluid pressure (IFP) is a common feature in solid tumors, the effects of high IFP on the motility and invasiveness of cancer cells remain obscure. Using cell-culture devices that simulated increased IFP conditions by applying hydrostatic pressure (HP) ranging from 0 to 20 mm Hg to the cells, we found that the elevated HPs increased the migration speeds, invasiveness, cell volume, filopodial number and aquaporin-1 (AQP1), Snail and vinculin expression levels, as well as phosphorylation of caveolin-1 and extracellular signal-regulated kinase1/2 (ERK1/2), in the lung cancer cells CL1-5 and A549. The increases of migration speed and cell volume correlated temporally with the increase of AQP1 expression. The elevated HP-induced migration acceleration was hindered by AQP1 knockdown using small interfering RNA (siRNA) transfection. Inhibition of ERK1/2 phosphorylation using the mitogen-activated protein kinase kinase inhibitor PD98059 abrogated the elevated HP-induced AQP1 upregulation and migration acceleration in the cancer cells. Caveolin-1 knockdown by siRNA transfection attenuated the HP-induced, ERK1/2-depedent AQP1 upregulation and migration acceleration. Further biochemical studies revealed that the caveolin-1 activation-driven ERK1/2 signaling is mediated by Akt1/2 phosphorylation. By contrast, the elevated HPs had negligible effects on the migration speed and volume of normal bronchial epithelial cells. These results disclose a novel mechanism relating high IFP to the invasiveness of cancer cells and highlight potential targets to impede cancer spreading.

A comparison of left and right atrial fibroblasts reveals different collagen production activity and stress-induced mitogen-activated protein kinase signalling in rats.

AIM: Atrial fibrosis plays a pivotal role in the pathophysiology of heart failure (HF). The left atrium (LA) experiences greater fibrosis than the right atrium (RA) during HF. It is not clear whether LA cardiac fibroblasts contain distinctive activities that predispose LA to fibrosis. METHODS: LA and RA fibrosis were evaluated in healthy and isoproterenol-induced HF Sprague Dawley rats. Rat LA and RA primary isolated fibroblasts were subjected to proliferation assay, oxidative stress assay, cell migration analysis, collagen measurement, cytokine array and Western blot. RESULTS: Healthy rat LA and RA had a similar extent of collagen deposition. HF significantly increased fibrosis to a greater severity in LA than in RA. Compared to isolated RA fibroblasts, the in vitro experiments showed that isolated LA fibroblasts had higher oxidative stress and exhibited higher collagen, transforming growth factor-ß1, connective tissue growth factor production and less vascular endothelial growth factor (VEGF) production, but had similar migration, myofibroblast differentiation and proliferation activities. VEGF significantly increased the collagen production ability of LA fibroblasts, but not RA fibroblasts. LA fibroblasts had more phosphorylated ERK1/2 and P38 expression. ERK inhibitor (PD98059, 50 µmol L-1 ) significantly attenuated collagen production and increased VEGF production in RA fibroblasts but not in LA fibroblasts. P38 inhibitor (SB203580, 30 µmol L-1 ) significantly attenuated collagen production in LA fibroblasts but not in RA fibroblasts. P38 inhibitor also significantly increased VEGF production in RA and LA fibroblasts. CONCLUSIONS: Differences in profibrotic activity between LA and RA fibroblasts may be caused by different responses to mitogen-activated protein kinase signalling.

Identification of the chitinase genes from the diamondback moth, Plutella xylostella.

Chitinases have an indispensable function in chitin metabolism and are well characterized in numerous insect species. Although the diamondback moth (DBM) Plutella xylostella, which has a high reproductive potential, short generation time, and characteristic adaptation to adverse environments, has become one of the most serious pests of cruciferous plants worldwide, the information on the chitinases of the moth is presently limited. In the present study, using degenerated polymerase chain reaction (PCR) and rapid amplification of cDNA ends-PCR strategies, four chitinase genes of P. xylostella were cloned, and an exhaustive search was conducted for chitinase-like sequences from the P. xylostella genome and transcriptomic database. Based on the domain analysis of the deduced amino acid sequences and the phylogenetic analysis of the catalytic domain sequences, we identified 15 chitinase genes from P. xylostella. Two of the gut-specific chitinases did not cluster with any of the known phylogenetic groups of chitinases and might be in a new group of the chitinase family. Moreover, in our study, group VIII chitinase was not identified. The structures, classifications and expression patterns of the chitinases of P. xylostella were further delineated, and with this information, further investigations on the functions of chitinase genes in DBM could be facilitated.

Peritherapeutic Hemodynamic Changes of Carotid Stenting Evaluated with Quantitative DSA in Patients with Carotid Stenosis.

BACKGROUND AND PURPOSE: Quantitative data from DSA have become important tools for understanding hemodynamic changes of intracranial lesions. In this study, we evaluated 8 hemodynamic parameters in patients before and after carotid artery angioplasty. MATERIALS AND METHODS: DSA images of 34 patients with carotid stenosis who underwent angioplasty and stent placement were retrospectively analyzed. Eleven ROIs (M1, M2, A1, A2, the parietal vein, superior sagittal sinus, internal jugular vein, and 4 in the ICA) were selected on color-coded DSA. Eight hemodynamic parameters (bolus arrival time, TTP, relative TTP, full width at half maximum, wash-in slope, washout slope, maximum enhancement, and area under the curve) were measured from the time-concentration curves of these ROIs. The dependent t test for paired samples was applied to these parameters before and after stent placement. RESULTS: We found that the treatment significantly reduced TTP, relative TTP, bolus arrival time, and washout slope at all arterial ROIs and full width at half maximum and area under the curve at some arterial ROIs. Bolus arrival time was significantly reduced after treatment for all arterial ROIs, the parietal vein, and the superior sagittal sinus. The maximum enhancement and wash-in slope did not show significant changes after treatment. After treatment, the relative TTP from the ICA to M1, M2, and the parietal vein returned to normal values. CONCLUSIONS: In addition to TTP and relative TTP, other parameters can be used to evaluate peritherapeutic cerebral hemodynamic changes. Bolus arrival time has the potential to evaluate brain circulation at arterial and venous sites, especially when TTP cannot be measured because of an incomplete time-concentration curve.

Betulinic acid enhances TGF-ß signaling by altering TGF-ß receptors partitioning between lipid-raft/caveolae and non-caveolae membrane microdomains in mink lung epithelial cells.

BACKGROUND: TGF-ß is a key modulator in the regulation of cell proliferation and migration, and is also involved in the process of cancer development and progression. Previous studies have indicated that TGF-ß responsiveness is determined by TGF-ß receptor partitioning between lipid raft/caveolae-mediated and clathrin-mediated endocytosis. Lipid raft/caveolae-mediated endocytosis facilitates TGF-ß degradation and thus suppressing TGF-ß responsiveness. By contrast, clathrin-mediated endocytosis results in Smad2/3-dependent endosomal signaling, thereby promoting TGF-ß responsiveness. Because betulinic acid shares a similar chemical structure with cholesterol and has been reported to insert into the plasma membrane, we speculate that betulinic acid changes the fluidity of the plasma membrane and modulates the signaling pathway associated with membrane microdomains. We propose that betulinic acid modulates TGF-ß responsiveness by changing the partitioning of TGF-ß receptor between lipid-raft/caveolae and non-caveolae microdomain on plasma membrane. METHODS: We employed sucrose-density gradient ultracentrifugation and confocal microscopy to determine membrane localization of TGF-ß receptors and used a luciferase assay to examine the effects of betulinic acid in TGF-ß-stimulated promoter activation. In addition, we perform western blotting to test TGF-ß-induced Smad2 phosphorylation and fibronectin production. RESULTS AND CONCLUSIONS: Betulinic acid induces translocation of TGF-ß receptors from lipid raft/caveolae to non-caveolae microdomains without changing total level of TGF-ß receptors. The betulinic acid-induced TGF-ß receptors translocation is rapid and correlate with the TGF-ß-induced PAI-1 reporter gene activation and growth inhibition in Mv1Lu cells.

Impact of lumbar instrumented circumferential fusion on the development of adjacent vertebral compression fracture.

We evaluated the impact of lumbar instrumented circumferential fusion on the development of adjacent level vertebral compression fractures (VCFs). Instrumented posterior lumbar interbody fusion (PLIF) has become a popular procedure for degenerative lumbar spine disease. The immediate rigidity produced by PLIF may cause more stress and lead to greater risk of adjacent VCFs. However, few studies have investigated the relationship between PLIF and the development of subsequent adjacent level VCFs. Between January 2005 and December 2009, a total of 1936 patients were enrolled. Of these 224 patients had a new VCF and the incidence was statistically analysed with other covariants. In total 150 (11.1%) of 1348 patients developed new VCFs with PLIF, with 108 (72%) cases at adjacent segment. Of 588 patients, 74 (12.5%) developed new subsequent VCFs with conventional posterolateral fusion (PLF), with 37 (50%) patients at an adjacent level. Short-segment fusion, female and age older than 65 years also increased the development of new adjacent VCFs in patients undergoing PLIF. In the osteoporotic patient, more rigid fusion and a higher stress gradient after PLIF will cause a higher adjacent VCF rate.

Anti-inflammatory effects of platelet biomaterials in a macrophage cellular model.

BACKGROUND AND OBJECTIVES: Recent clinical data suggested that platelet materials used in regenerative medicine exert anti-inflammatory effects. One must understand whether functionality varies among platelet preparations and also the role of the various protein compartments. MATERIALS AND METHODS: Platelet-poor-plasma (PPP), platelet lysate with cell debris (PL) or cell-free (CFPL), platelet gel releasate (PGR) and solvent/detergent-treated PL (SDPL) were prepared from four apheresis platelet donations. Protein profile was examined by SDS-PAGE, and growth factors and cytokines by ELISA, multiplexed Luminex assay and cytokine array. Anti-inflammatory activity was evaluated in RAW 264.7 mouse macrophages treated for 24 h with the blood fractions followed by 24 h of stimulation with 500 ng/ml lipopolysaccharides (LPS). Inflammatory marker nitric oxide (NO) was determined by colorimetry, tumour necrosis factor (TNF)-α by ELISA and inducible NO synthase (iNOS) and cyclooxygenase (COX)-2 by Western blotting. RESULTS: Proteins, growth factors and cytokines composition differed among preparations. Blood fractions alone did not stimulate inflammatory markers expression. Following LPS stimulus, NO and iNOS expressions were significantly inhibited (P < 0.001) by all blood fractions, but inhibition was more pronounced with SDPL. In addition, only SDPL inhibited TNF-α (P < 0.001) and COX-2 expressions. CONCLUSIONS: All the plasma and platelet fractions evaluated in this study exert an anti-inflammatory effect on macrophages, suggesting that both the plasma and platelet proteomes contribute to anti-inflammation. However, the extent and nature of the anti-inflammatory action vary among products. Further studies are needed to better understand the functionality of platelet biomaterials and optimize their clinical use.

Cumulative risk assessment for plasticizer-contaminated food using the hazard index approach.

Phthalates strongly and adversely affect reproduction, development and liver function. We did a cumulative risk assessment for simultaneous exposure to nine phthalates using the hazard index (HI) and the levels of nine phthalates in 1200 foodstuff samples. DEHP (di-2-ethylhexyl phthalate) present the highest level (mean: 0.443 mg/kg) in 1200 samples, and the highest average daily dose (ADD) was found in DEHP, ΣDBP(i + n) (the sum of dibutyl phthalate [DBP] isomers [DnBP + DiBP]) posed the highest risk potential of all the phthalates. In seven phthalates, the 95th percentiles of the ADDs for ΣDBP(i + n) in 0-6-yr-old children accounted for 91% (79-107%) of the tolerable daily intake, and the 95th percentiles of the HIs for the anti-androgenic effects of five phthalates in 0-3-yr-old children and 4-6-yr-old girls were >1. We conclude that the health of younger Taiwanese may be adversely affected by overexposure of phthalate-contaminated foods.

The dipeptidyl peptidase-4 inhibitor-sitagliptin modulates calcium dysregulation, inflammation, and PPARs in hypertensive cardiomyocytes.

BACKGROUND: Hypertension induces cardiac dysfunction, calcium (Ca(2+)) dysregulation, and arrhythmogenesis. Dipeptidyl peptidase (DPP)-4 inhibitors, an antidiabetic agent with anti-inflammation and anti-hypertension potential, may regulate peroxisome proliferator-activated receptors (PPARs)-α, -γ, and -δ and Ca(2+) homeostasis. OBJECTIVE: The purpose of this study was to investigate whether DPP-4 inhibitor, sitagliptin, can modulate PPARs and Ca(2+) handling proteins in hypertensive hearts. METHODS: A Western blot analysis was used to evaluate protein expressions of myocardial PPAR isoforms, tumor necrosis factor (TNF)-α, interleukin (IL)-6, sarcoplasmic reticulum ATPase (SERCA2a), Na(+)-Ca(2+) exchanger (NCX), ryanodine receptor (RyR), voltage-dependent Ca(2+) (CaV1.2), slow-voltage potassium currents (Kvs), angiotensin II type 1 receptor (AT1R), and receptor of advanced glycated end-products (RAGE) from Wistar-Kyoto (WKY) rats, spontaneously hypertensive rats (SHR), and SHR treated with sitagliptin (10mg/kg for 4weeks). Conventional microelectrodes were used to record action potentials (APs) in the ventricular myocytes from each group. RESULTS: Compared to the control group, SHR had lower cardiac PPAR-α and PPAR-δ protein expressions, but had greater cardiac PPAR-γ levels, and TNF-α, IL-6, RAGE, and AT1R protein expressions, which were ameliorated in the sitagliptin-treated SHR. SHR had prolonged QT interval and AP duration with less SERCA2a and RyR, and greater CaV1.2 expressions, which were also attenuated in sitagliptin-treated SHR. CONCLUSIONS: Sitagliptin significantly changed the cardiac electrophysiological characteristics and Ca(2+) regulation, which may have been caused by its effects on cardiac PPARs, proinflammatory cytokines, and AT1R.

School participation, supports and barriers of students with and without disabilities.

BACKGROUND: We compared school participation patterns of students ages 5-17 with and without disabilities and examined whether features of the school environment were perceived to help or hinder their participation. METHODS: Parents (n = 576) residing in the USA and Canada completed the Participation and Environment Measure for Children and Youth (PEM-CY) via the internet. RESULTS: Parents of students with disabilities reported that their children participated less frequently in school clubs and organizations and getting together with peers outside the classroom and that they were less involved in all school activities. Parents of students with disabilities also were significantly more likely to report that features of the environment hindered school participation and that resources needed to support their child's participation were not adequate. CONCLUSIONS: Parents of students with disabilities report that their children are participating less in important school-related activities. Barriers limiting school participation include features of the physical and social environment as well as limited resources.