the State of Utah v. Brent Jay Sessions and Louis R. Dabbs : Brief of Appellant

Defendant, Brent Jay Sessions, Appeals from a Judgement of Guilty of Burglary In The Third Judicial District, In and For Salt Lake County, State of Utah, The Honorable Hal G, Taylor, Presiding

The invasion of Doñana National Park (SW Spain) by the mosquito fern (Azolla filiculoides Lam)

In 2001, Azolla filiculoides Lam., a floating pteridophyte native to the New World, was found in Doñana National Park (SW Spain), an European protected area well known for its high value from a conservation point of view and for its ecological vulnerability. Until that time, there had been no exotic aquatic macrophyte observations in the National Park. Since then, surfaces covered by Azolla filiculoides have increased explosively forming thick floating mats which eliminate submersed plants, and seriously threaten the aquatic ecosystems in this important protected area.En 2001, Azolla filiculoides Lam., una pteridófita acuática nativa del Nuevo Mundo, fue encontrada en el Parque Nacional de Doñana (SW España), un espacio protegido europeo bien conocido por su alto valor desde el punto de vista de la conservación y por su vulnerabilidad ecológica. Hasta ese momento, no se había observado ningún macrófito acuático exótico en el Parque Nacional; desde entonces, las superficies cubiertas por Azolla filiculoides se han incrementado de manera explosiva originando gruesas capas flotantes que eliminan las plantas acuáticas sumergidas y amenazan gravemente los ecosistemas acuáticos de este importante espacio protegido

ATXN1 N-terminal region explains the binding differences of wild-type and expanded forms

BACKGROUND: Wild-type (wt) polyglutamine (polyQ) regions are implicated in stabilization of protein-protein interactions (PPI). Pathological polyQ expansion, such as that in human Ataxin-1 (ATXN1), that causes spinocerebellar ataxia type 1 (SCA1), results in abnormal PPI. For ATXN1 a larger number of interactors has been reported for the expanded (82Q) than the wt (29Q) protein. METHODS: To understand how the expanded polyQ affects PPI, protein structures were predicted for wt and expanded ATXN1, as well as, for 71 ATXN1 interactors. Then, the binding surfaces of wt and expanded ATXN1 with the reported interactors were inferred. RESULTS: Our data supports that the polyQ expansion alters the ATXN1 conformation and that it enhances the strength of interaction with ATXN1 partners. For both ATXN1 variants, the number of residues at the predicted binding interface are greater after the polyQ, mainly due to the AXH domain. Moreover, the difference in the interaction strength of the ATXN1 variants was due to an increase in the number of interactions at the N-terminal region, before the polyQ, for the expanded form. CONCLUSIONS: There are three regions at the AXH domain that are essential for ATXN1 PPI. The N-terminal region is responsible for the strength of the PPI with the ATXN1 variants. How the predicted motifs in this region affect PPI is discussed, in the context of ATXN1 post-transcriptional modifications.This work was financed by the project Norte-01-0145-FEDER-000008 -Porto Neurosciences and Neurologic Disease Research Initiative at I3S, supported by Norte Portugal Regional Operational Programme (NORTE 2020), under the PORTUGAL 2020 Partnership Agreement, through the European Regional Development Fund (FEDER). Sara Rocha is supported by a post-doctoral fellowship under this project. Hugo López-Fernández is supported by a postdoctoral fellowship from Xunta de Galicia (ED481B 2016/068–0). SING group thanks Consellería de Educación, Universidades e Formación Profesional (Xunta de Galicia) for the ED431C2018/55-GRC grant and CITI (Centro de Investigación, Transferencia e Innovación) from University of Vigo for hosting its IT infrastructure. The funding bodies played no role in the design of the study and collection, analysis, and interpretation of data and in writing the manuscript

Myofascial Trigger Points, Pain, Disability, and Sleep Quality in Patients with Chronic Nonspecific Low Back Pain

[EN] Objective: To investigate the difference in the presence of trigger points (TrPs) between patients with chronic nonspecific low back pain (LBP) and healthy people, and to determine the relationship of TrPs with the intensity of ongoing pain, disability, and sleep quality. Design: A cross-sectional study. Setting: The role of TrPs in LBP has not been determined. Patients: Forty-two patients with nonspecific LBP (50% women), aged 23-55 years old, and 42 age- and sex-matched controls participated. Outcome measures: TrPs were bilaterally explored within the quadratus lumborum, iliocostalis lumborum, psoas, piriformis, gluteus minimus, and gluteus medius muscles in a blinded design. TrPs were considered active if the subject recognized the local and referred pain as familiar symptoms, and TrPs were considered latent if the pain was not recognized as a familiar symptom. Pain measures were collected with a numerical pain rate scale, disability was assessed with the Roland-Morris questionnaire, and sleep quality was determined with the Pittsburgh Sleep Quality Index. Results: Patients with nonspecific LBP exhibited a greater disability and worse sleep quality than healthy controls (P < 0.001). Patients with nonspecific LBP exhibited a mean of 3.5 ± 2.3 active TrPs. Further, patients with nonspecific LBP showed a greater (P < 0.001) number of latent TrPs (mean: 2.0 ± 1.5) than healthy controls (mean: 1.0 ± 1.5). Active TrPs in the quadratus lumborum, iliocostalis lumborum, and gluteus medius muscles were the most prevalent in patients with nonspecific LBP. A greater number of active TrPs was associated with higher pain intensity (rs = 0.602; P < 0.001) and worse sleep quality (rs = 0.338; P = 0.03). Conclusions: The local and referred pain elicited by active TrPs in the back and hip muscles contributes to pain symptoms in nonspecific LBP. Patients had higher disability and worse sleep quality than controls. The number of active TrPs was associated with pain intensity and sleep quality. It is possible that a complex interaction among these factors is present in patients with nonspecific LBP

Methodology for phytoplankton taxonomic group identification towards the development of a lab-on-a-chip

This paper presents the absorbance and fluorescence optical properties of various phytoplankton species, looking to achieve an accurate method to detect and identify a number of phytoplankton taxonomic groups. The methodology to select the excitation and detection wavelengths that results in superior identification of phytoplankton is reported. The macroscopic analyses and the implemented methodology are the base for designing a lab-on-a-chip device for a phytoplankton group identification, based on cell analysis with multi-wavelength lighting excitation, aiming for a cheap and portable platform. With such methodology in a lab-on-a-chip device, the analysis of the phytoplankton cells’ optical properties, e.g., fluorescence, diffraction, absorption and reflection, will be possible. This device will offer, in the future, a platform for continuous, autonomous and in situ underwater measurements, in opposition to the conventional methodology. A proof-of-concept device with LED light excitation at 450 nm and a detection photodiode at 680 nm was fabricated. This device was able to quantify the concentration of the phytoplankton chlorophyll a. A lock-in amplifier electronic circuit was developed and integrated in a portable and low-cost sensor, featuring continuous, autonomous and in situ underwater measurements. This device has a detection limit of 0.01 µ/L of chlorophyll a, in a range up to 300 µg/L, with a linear voltage output with chlorophyll concentration.Fundação para a Ciência e a Tecnologia | Ref. UIDB/04436/2020Fundação para a Ciência e a Tecnologia | Ref. UIDP/04436/2020Fundação para a Ciência e a Tecnologia | Ref. PD/BD/150581/2020Fundação para a Ciência e a Tecnologia | Ref. 2021.01087.CEECINDFundação para a Ciência e a Tecnologia | Ref. 2021.01086.CEECIN

Hormonal and Inflammatory Responses to Hypertrophy-Oriented Resistance Training at Acute Moderate Altitude

This research was funded by the Spanish Ministry of Science, Innovation and Universities, grant number PGC2018-097388-B-I00, by the Andalusian FEDER Operational Program, grant number A-SEJ-246-UGR18 and FPU pre-doctoral, grant number FPU18/00686 awarded to one of the authors.The authors thank the High Performance Center of Sierra Nevada, Spain and all the participants who volunteered for this investigation. The authors also thank Dymatize Europe for supplying the meal replacement supplements used in this study.This study investigated the effect of a traditional hypertrophy-oriented resistance training (R-T) session at acute terrestrial hypoxia on inflammatory, hormonal, and the expression of miR-378 responses associated with muscular gains. In a counterbalanced fashion, 13 resistance trained males completed a hypertrophic R-T session at both moderate-altitude (H; 2320 m asl) and under normoxic conditions (N; <700 m asl). Venous blood samples were taken before and throughout the 30 min post-exercise period for determination of cytokines (IL6, IL10, TNF alpha), hormones (growth hormone [GH], cortisol [C], testosterone), and miR-378. Both exercise conditions stimulated GH and C release, while miR-378, testosterone, and inflammatory responses remained near basal conditions. At H, the R-T session produced a moderate to large but nonsignificant increase in the absolute peak values of the studied cytokines. miR-378 revealed a moderate association with GH (r = 0.65; p = 0.026 and r = -0.59; p = 0.051 in N and H, respectively) and C (r = 0.61; p = 0.035 and r = 0.75; p = 0.005 in N and H, respectively). The results suggest that a R-T session at H does not differentially affect the hormonal, inflammatory, and miR-378 responses compared to N. However, the standardized mean difference detected values in the cytokines suggest an intensification of the inflammatory response in H that should be further investigated.Spanish Ministry of Science, Innovation and Universities PGC2018-097388-B-I00Andalusian FEDER Operational Program A-SEJ-246-UGR18FPU pre-doctoral FPU18/0068

Photocatalytic activity of nanostructured anatase coatings obtained by cold gas spray

This article describes a photocatalytic nanostructured anatase coating deposited by cold gas spray (CGS)supported on titanium sub-oxide (TiO22x) coatings obtained by atmospheric plasma spray (APS) onto stainless steel cylinders. The photocatalytic coating was homogeneous and preserved the composition and nanostructure of the starting powder. The inner titanium sub-oxide coating favored the deposition of anatase particles in the solid state. Agglomerated nano-TiO2 particles fragmented when impacting onto the hard surface of the APS TiO22x bond coat. The rough surface provided by APS provided an ideal scenario for entrapping the nanostructured particles, which may be adhered onto the bond coat due to chemical bonding; a possible bonding mechanism is described. Photocatalytic experiments showed that CGS nano-TiO2 coating was active for photodegrading phenol and formic acid under aqueous conditions. The results were similar to the performance obtained by competitor technologies and materials such as dip-coating P25 photocatalysts. Disparity in the final performance of the photoactive materials may have been caused by differences in grain size and the crystalline composition of titanium dioxide

A genome-wide association study follow-up suggests a possible role for PPARG in systemic sclerosis susceptibility

Introduction: A recent genome-wide association study (GWAS) comprising a French cohort of systemic sclerosis (SSc) reported several non-HLA single-nucleotide polymorphisms (SNPs) showing a nominal association in the discovery phase. We aimed to identify previously overlooked susceptibility variants by using a follow-up strategy.&lt;p&gt;&lt;/p&gt; Methods: Sixty-six non-HLA SNPs showing a P value &#60;10-4 in the discovery phase of the French SSc GWAS were analyzed in the first step of this study, performing a meta-analysis that combined data from the two published SSc GWASs. A total of 2,921 SSc patients and 6,963 healthy controls were included in this first phase. Two SNPs, PPARG rs310746 and CHRNA9 rs6832151, were selected for genotyping in the replication cohort (1,068 SSc patients and 6,762 healthy controls) based on the results of the first step. Genotyping was performed by using TaqMan SNP genotyping assays. Results: We observed nominal associations for both PPARG rs310746 (PMH = 1.90 × 10-6, OR, 1.28) and CHRNA9 rs6832151 (PMH = 4.30 × 10-6, OR, 1.17) genetic variants with SSc in the first step of our study. In the replication phase, we observed a trend of association for PPARG rs310746 (P value = 0.066; OR, 1.17). The combined overall Mantel-Haenszel meta-analysis of all the cohorts included in the present study revealed that PPARG rs310746 remained associated with SSc with a nominal non-genome-wide significant P value (PMH = 5.00 × 10-7; OR, 1.25). No evidence of association was observed for CHRNA9 rs6832151 either in the replication phase or in the overall pooled analysis.&lt;p&gt;&lt;/p&gt; Conclusion: Our results suggest a role of PPARG gene in the development of SSc

Longitudinal outcomes of obeticholic acid therapy in ursodiol-nonresponsive primary biliary cholangitis: Stratifying the impact of add-on fibrates in real-world practice

Background Suboptimal response to ursodeoxycholic acid occurs in 40% of primary biliary cholangitis (PBC) patients, affecting survival. Achieving a deep response (normalisation of alkaline phosphatase [ALP] and bilirubin ≤0.6 upper limit of normal) improves survival. Yet, the long-term effectiveness of second-line treatments remains uncertain. Aims To evaluate the long-term effectiveness of obeticholic acid (OCA) ± fibrates. Focusing on biochemical response (ALP ≤1.67 times the upper limit of normal, with a decrease of at least 15% from baseline and normal bilirubin levels), normalisation of ALP, deep response and biochemical remission (deep response plus aminotransferase normalisation). Methods We conducted a longitudinal, observational, multicentre study involving ursodeoxyccholic acid non-responsive PBC patients (Paris-II criteria) from Spain and Portugal who received OCA ± fibrates. Results Of 255 patients, median follow-up was 35.1 months (IQR: 20.2–53). The biochemical response in the whole cohort was 47.2%, 61.4% and 68.6% at 12, 24 and 36 months. GLOBE-PBC and 5-year UK-PBC scores improved (p < 0.001). Triple therapy (ursodeoxycholic acid plus OCA plus fibrates) had significantly higher response rates than dual therapy (p = 0.001), including ALP normalisation, deep response and biochemical remission (p < 0.001). In multivariate analysis, triple therapy remained independently associated with biochemical response (p = 0.024), alkaline phosphatase normalisation, deep response and biochemical remission (p < 0.001). Adverse effects occurred in 41.2% of cases, leading to 18.8% discontinuing OCA. Out of 55 patients with cirrhosis, 12 developed decompensation. All with baseline portal hypertension. Conclusion Triple therapy was superior in achieving therapeutic goals in UDCA-nonresponsive PBC. Decompensation was linked to pre-existing portal hypertension

Congenital Hyperinsulinism in Two Siblings with ABCC8 Mutation: Same Genotype, Different Phenotypes

Congenital hyperinsulinism (CHI) is a heterogenous disease caused by insulin secretion regulatory defects, being ABCC8/KCNJ11 the most commonly affected genes. Therapeutic options include diazoxide, somatostatin analogues and surgery, which is curative in focal CHI. We report the case of two siblings (born two years apart) that presented themselves with hypoketotic hyperinsulinemic persistent hypoglycemias during neonatal period. The diagnosis of diffuse CHI due to an ABCC8 compound mutation (c.3576delG and c.742C>T) was concluded. They did not benefit from diazoxide therapy (or pancreatectomy performed in patient number 1) yet responded to somatostatin analogues. Patient number 1 developed various neurological deficits (including epilepsy), however patient number 2 experienced an entirely normal neurodevelopment. We believe this case shows how previous knowledge of the firstborn sibling's disease contributed to a better and timelier medical care in patient number 2, which could potentially explain her better neurological outcome despite their same genotype.info:eu-repo/semantics/publishedVersio