158 research outputs found

    Examining morphological differences in Heschl's gyrus between neurotypical and dyslexic brains

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    Current methods of diagnosis for developmental dyslexia rely on family history report and cognitive and language behavioral testing. However, relying on these measures alone to predict dyslexia in at-risk children can result in low sensitivity and specificity, with dyslexic individuals either being missed or over-identified. Prediction accuracy could be increased by considering structural differences in the dyslexic brain along with behavioral measures. Reduplication of Heschl’s gyrus, where the primary auditory cortex resides, has been suggested as a risk factor for developing dyslexia. The current investigation explored if differences in interhemispheric duplication patterns and gray matter volume of Heschl’s gyrus could distinguish between dyslexic and neurotypical (control) brains. A detailed labeling protocol based on macroanatomical landmarks and explicitly defined reduplication morphotypes: single Heschl’s gyrus (SH), common stem duplication (CSD), complete posterior duplication (CPD), and multiple duplication (MD) was developed. Overall, there was no significant difference in the incidence of morphotypes between control and dyslexic brains. Duplication of Heschl’s gyrus was a common occurrence in both groups. However, results suggest that the MD morphotype may occur more often in dyslexic brains. Gray matter volume of anterior Heschl’s gyrus was larger in the left hemisphere in both groups but tended to be larger overall in dyslexic brain. Results of this investigation confirmed the presence of high morphological variability between and within brains and suggest that reduplications in Heschl’s gyrus alone are not enough to designate between neurotypical and dyslexic brains. It is likely that developmental dyslexia has heterogeneous origins, and it is possible that increased gyrification combined with other structural differences is one possible origin

    Effects of mavoglurant on visual attention and pupil reactivity while viewing photographs of faces in Fragile X Syndrome.

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    BackgroundNumerous preclinical studies have supported the theory that enhanced activation of mGluR5 signaling, due to the absence or reduction of the FMR1 protein, contributes to cognitive and behavioral deficits in patients with fragile X syndrome (FXS). However multiple phase 2 controlled trials in patients with FXS have failed to demonstrate efficacy of compounds that negatively modulate mGluR5, including two phase 2b randomized controlled trials (RCT) of mavoglurant (AFQ056, Novartis Pharma AG), when the primary measures of interest were behavioral ratings. This has cast some doubt onto the translation of the mGluR5 theory from animal models to humans with the disorder.MethodsWe evaluated social gaze behavior-a key phenotypic feature of the disorder-and sympathetic nervous system influence on pupil size using a previously-validated eye tracking paradigm as a biobehavioral probe, in 57 adolescent or adult patients with FXS at baseline and following three months of blinded treatment with one of three doses of mavoglurant or placebo, within the context of the AFQ056 RCTs.ResultsPatients with FXS treated with mavoglurant demonstrated increased total absolute looking time and number of fixations to the eye region while viewing human faces relative to baseline, and compared to those treated with placebo. In addition, patients had greater pupil reactivity to faces relative to baseline following mavoglurant treatment compared to placebo.DiscussionThe study shows that negative modulation of mGluR5 activity improves eye gaze behavior and alters sympathetically-driven reactivity to faces in patients with FXS, providing preliminary evidence of this drug's impact on behavior in humans with the disorder

    Laparoscopic totally extraperitoneal inguinal hernia repair with and without urethral catheterization a prospective randomized study in Hospital Raja Permaisuri Bainun, Ipoh

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    Background Urethral catheterization during laparoscopic inguinal hernia repair remains a common surgical practice in spite of the insufficient evidence supporting its routine use. The aim of this study was to prospectively evaluate the utility of urethral catheterization during laparoscopic totally extraperitoneal inguinal hernia repair (TEP). Methods Patients undergoing elective laparoscopic totally extraperitoneal inguinal hernia repair were randomized into two groups: catheter and non-catheter groups. The main outcome of the study was to assess the feasibility and safety of performing elective laparoscopic hernia repair (TEP) without urethral catheterization. Results A total of 162 patients consented to randomization and 148 patients underwent surgery. The other 14 patients defaulted surgery. The catheter group had 72 patients while the non-catheter group had 76 patients (p = 0.818). Patient characteristics and operative parameters were comparable in both groups. There were no major operative complications in both groups and only 3 patients required conversion to open hernia repair. Two patients required postoperative catheterization, 1 patient from each group (p = 0.738). No patients from the non-catheter group required intraoperativecatheterization. A total of 19 patients (12.8%) from the catheter group had urinary symptoms compared to 7 patients (4.7%) in the non-catheter group and the difference was statistically significant (p = 0.006). However, there were no patients who had bacteriuria or urinary tract infection. Conclusion Laparoscopic totally extraperitoneal inguinal hernia repair without the routine use of urethral catheter does not compromise the safety or ease of the surgery. Keywords: Laparoscopic totally extraperitoneal inguinal hernia repair, TEP, urethral catheterizatio

    Digital Initiatives Newsletter, Issue 2

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    Digital Initiatives is the newsletter of FIU Libraries’ Digital Collections and Institutional Repository (IR). This biannual newsletter serves as a resource for FIU students and faculty to keep up-to-date with the latest projects, collections, and services available from the FIU Libraries.https://digitalcommons.fiu.edu/digital_initiatives/1001/thumbnail.jp

    Hydrolysis of Chlorogenic Acid in Sunflower Flour Increases Consumer Acceptability of Sunflower Flour Cookies by Improving Cookie Color

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    Sunflower meal, a byproduct of sunflower oil pressing, is not commonly used in alkaline baking applications. This is because chlorogenic acid, the main phenolic antioxidant in sunflower seeds, reacts with protein, giving the baked product a green discoloration. Our group previously demonstrated that a chlorogenic acid esterase from Lactobacillus helveticus hydrolyzes chlorogenic acid in sunflower dough cookie formulations, resulting in cookies that were brown instead of green. This study presents a sensory analysis to determine the acceptability of enzymatically upcycled sunflower meal as an alternative protein source for those allergic to meals from legumes or tree nuts. We hypothesized that the mechanism of esterase-catalyzed chlorogenic acid breakdown does not influence the cookies’ sensory properties other than color and that consumers would prefer treated, brown cookies over non-treated cookies. Cookies made from sunflower meal were presented under green lights to mask color and tested by 153 panelists. As expected, the sensory properties (flavor, smell, texture, and overall acceptability) of the treated and non-treated cookies were not statistically different. These results corroborate proximate analysis, which demonstrated that there was no difference between enzymatically treated and non-treated cookies other than color and chlorogenic acid content. After the cookie color was revealed, panelists strongly preferred the treated cookies with 58% indicating that they “probably” or “definitely” would purchase the brown cookies, whereas only 5.9% would buy green, non-treated cookies. These data suggest that esterase-catalyzed breakdown of chlorogenic acid represents an effective strategy to upcycle sunflower meal for baking applications

    Combining microscopic and macroscopic probes to untangle the single-ion anisotropy and exchange energies in an S=1 quantum antiferromagnet

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    The magnetic ground state of the quasi-one-dimensional spin-1 antiferromagnetic chain is sensitive to the relative sizes of the single-ion anisotropy (D) and the intrachain (J) and interchain (J') exchange interactions. The ratios D/J and J'/J dictate the material's placement in one of three competing phases: a Haldane gapped phase, a quantum paramagnet and an XY-ordered state, with a quantum critical point at their junction. We have identified [Ni(HF)2(pyz)_2]SbF6, where pyz = pyrazine, as a rare candidate in which this behavior can be explored in detail. Combining neutron scattering (elastic and inelastic) in applied magnetic fields of up to 10~tesla and magnetization measurements in fields of up to 60~tesla with numerical modeling of experimental observables, we are able to obtain accurate values of all of the parameters of the Hamiltonian [D = 13.3(1)~K, J = 10.4(3)~K and J' = 1.4(2)~K], despite the polycrystalline nature of the sample. Density-functional theory calculations result in similar couplings (J = 9.2~K, J' = 1.8~K) and predict that the majority of the total spin population resides on the Ni(II) ion, while the remaining spin density is delocalized over both ligand types. The general procedures outlined in this paper permit phase boundaries and quantum-critical points to be explored in anisotropic systems for which single crystals are as yet unavailable

    Monitoring observations of SMC X-1's excursions (MOOSE)-II: A new excursion accompanies spin-up acceleration

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    SMC X-1 is a high-mass X-ray binary showing superorbital modulation with an unstable period. Previous monitoring shows three excursion events in 1996--1998, 2005--2007, and 2014--2016. The superorbital period drifts from >60 days to <40 days and then evolves back during an excursion. Here we report a new excursion event of SMC X-1 in 2020--2021, indicating that the superorbital modulation has an unpredictable, chaotic nature. We trace the spin-period evolution and find that the spin-up rate accelerated one year before the onset of this new excursion, which suggests a possible inside-out process connecting the spin-up acceleration and the superorbital excursion. This results in a deviation of the spin period residual, similar to the behaviour of the first excursion in 1996--1998. In further analysis of the pulse profile evolution, we find that the pulsed fraction shows a long-term evolution and may be connected to the superorbital excursion. These discoveries deepen the mystery of SMC X-1 because they cannot be solely interpreted by the warped disc model. Upcoming pointed observations and theoretical studies may improve our understanding of the detailed accretion mechanisms taking place.Comment: 7 pages, 3 figures, Accepted for publication in MNRA

    Pathologic gene network rewiring implicates PPP1R3A as a central regulator in pressure overload heart failure

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    Heart failure is a leading cause of mortality, yet our understanding of the genetic interactions underlying this disease remains incomplete. Here, we harvest 1352 healthy and failing human hearts directly from transplant center operating rooms, and obtain genome-wide genotyping and gene expression measurements for a subset of 313. We build failing and non-failing cardiac regulatory gene networks, revealing important regulators and cardiac expression quantitative trait loci (eQTLs). PPP1R3A emerges as a regulator whose network connectivity changes significantly between health and disease. RNA sequencing after PPP1R3A knockdown validates network-based predictions, and highlights metabolic pathway regulation associated with increased cardiomyocyte size and perturbed respiratory metabolism. Mice lacking PPP1R3A are protected against pressure-overload heart failure. We present a global gene interaction map of the human heart failure transition, identify previously unreported cardiac eQTLs, and demonstrate the discovery potential of disease-specific networks through the description of PPP1R3A as a central regulator in heart failure
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