A decomposition of the Jacobian of a Humbert-Edge curve

A \textit{Humbert-Edge curve of type} $n$ is a non-degenerate smooth complete intersection of $n-1$ diagonal quadrics. Such a curve has an interesting geometry since it has a natural action of the group $(\mathbb{Z}/2\mathbb{Z})^n$. We present here a decomposition of its Jacobian variety as a product of Prym-Tyurin varieties, and we compute the kernel of the corresponding isogeny.Comment: 9 pages, comments welcome! To appear in Contemporary Mathematic

On families of Riemann surfaces with automorphisms

In this article we determine the maximal possible order of the automorphism group of the form $ag + b$, where $a$ and $b$ are integers, of a complex three and four-dimensional family of compact Riemann surfaces of genus $g$, appearing for all genus. In addition, we construct and describe explicit complex three and four-dimensional families possessing these maximal number of automorphisms.Comment: 19 pages, To appear in Journal of Pure and Applied Algebr

On the Jacobian variety of the Accola-Maclachlan curve of genus four

In this short note, we study the Jacobian variety of the Accola-Maclachlan curve of genus four and obtain explicitly its Poincar\'e isogeny decomposition. More precisely, we show that its Jacobian variety is isomorphic to the product of two abelian surfaces that are simple, and provide explicitly a Riemann matrix for each one of the involved abelian surfacesComment: 11 page

Oxic and Anoxic Organic Polymer Degradation Potential of Endophytic Fungi From the Marine Macroalga, Ecklonia radiata

Cellulose and chitin are the most abundant polymeric, organic carbon source globally. Thus, microbes degrading these polymers significantly influence global carbon cycling and greenhouse gas production. Fungi are recognized as important for cellulose decomposition in terrestrial environments, but are far less studied in marine environments, where bacterial organic matter degradation pathways tend to receive more attention. In this study, we investigated the potential of fungi to degrade kelp detritus, which is a major source of cellulose in marine systems. Given that kelp detritus can be transported considerable distances in the marine environment, we were specifically interested in the capability of endophytic fungi, which are transported with detritus, to ultimately contribute to kelp detritus degradation. We isolated 10 species and two strains of endophytic fungi from the kelp Ecklonia radiata. We then used a dye decolorization assay to assess their ability to degrade organic polymers (lignin, cellulose, and hemicellulose) under both oxic and anoxic conditions and compared their degradation ability with common terrestrial fungi. Under oxic conditions, there was evidence that Ascomycota isolates produced cellulose-degrading extracellular enzymes (associated with manganese peroxidase and sulfur-containing lignin peroxidase), while Mucoromycota isolates appeared to produce both lignin and cellulose-degrading extracellular enzymes, and all Basidiomycota isolates produced lignin-degrading enzymes (associated with laccase and lignin peroxidase). Under anoxic conditions, only three kelp endophytes degraded cellulose. We concluded that kelp fungal endophytes can contribute to cellulose degradation in both oxic and anoxic environments. Thus, endophytic kelp fungi may play a significant role in marine carbon cycling via polymeric organic matter degradation.German Research Foundation/[GR1540/30-1]/DFG/AlemaniaUCR::Vicerrectoría de Docencia::Ciencias Básicas::Facultad de Ciencias::Escuela de Biologí

Assessment of Factors Involved in Non-Adherence to Infant Hearing Diagnostic Testing

Abstract Introduction: Delayed diagnosis of pediatric hearing loss can cause delays in cognitive and social development. This study described the sociodemographic factors associated with delayed timing of a final hearing diagnosis after an abnormal newborn hearing screening (NBHS). Methods: Parent-infant dyads were recruited after being referred for further audiologic testing on an abnormal result from the NBHS. Results: Of the 53 participants, 55% (n=29) did not receive a final diagnosis by the recommended 3 months of age. Of those with a delayed diagnosis, 45% (n=13) had their first appointment within 3 months, but a delay was caused by an inconclusive or abnormal auditory brainstem response (ABR), middle ear pathology, or the presence of risk factors requiring additional testing. In a univariate analysis, older parental age (OR: 0.90, 95% CI: [0.82, 0.99]) and more total children in the household ([OR: 0.66, 95% CI: {0.18, 2.49}] for 1 child vs. 2 and [OR: 0.14, 95% CI: {0.03, 0.69}] for 1 children vs. 3 or more) were shown to were shown to significantly increase the odds of a delayed diagnosis, whereas younger infant age at first appointment (OR: 0.95, 95% CI: [0.92, 0.99]) was shown to significantly decrease the odds of a delayed diagnosis. In multivariate analyses, delayed diagnosis was also decreased by younger infant age at the initial appointment (OR=0.94, 95% CI: [0.90, 0.99]). Conclusions: Parental age, number of total children in the household, and timing of first appointment may predict delayed diagnosis. Because many patients with a delayed diagnosis attended an appointment within 3 months, further standardization of the process and targeted interventions for families could improve chances of achieving a diagnosis within the first appointment

SNUPN deficiency causes a recessive muscular dystrophy due to RNA mis-splicing and ECM dysregulation

SNURPORTIN-1, encoded by SNUPN, plays a central role in the nuclear import of spliceosomal small nuclear ribonucleoproteins. However, its physiological function remains unexplored. In this study, we investigate 18 children from 15 unrelated families who present with atypical muscular dystrophy and neurological defects. Nine hypomorphic SNUPN biallelic variants, predominantly clustered in the last coding exon, are ascertained to segregate with the disease. We demonstrate that mutant SPN1 failed to oligomerize leading to cytoplasmic aggregation in patients’ primary fibroblasts and CRISPR/Cas9-mediated mutant cell lines. Additionally, mutant nuclei exhibit defective spliceosomal maturation and breakdown of Cajal bodies. Transcriptome analyses reveal splicing and mRNA expression dysregulation, particularly in sarcolemmal components, causing disruption of cytoskeletal organization in mutant cells and patient muscle tissues. Our findings establish SNUPN deficiency as the genetic etiology of a previously unrecognized subtype of muscular dystrophy and provide robust evidence of the role of SPN1 for muscle homeostasis

Effects of antiplatelet therapy on stroke risk by brain imaging features of intracerebral haemorrhage and cerebral small vessel diseases: subgroup analyses of the RESTART randomised, open-label trial

Background Findings from the RESTART trial suggest that starting antiplatelet therapy might reduce the risk of recurrent symptomatic intracerebral haemorrhage compared with avoiding antiplatelet therapy. Brain imaging features of intracerebral haemorrhage and cerebral small vessel diseases (such as cerebral microbleeds) are associated with greater risks of recurrent intracerebral haemorrhage. We did subgroup analyses of the RESTART trial to explore whether these brain imaging features modify the effects of antiplatelet therapy

Effects of DHA- Rich n-3 Fatty Acid Supplementation on Gene Expression in Blood Mononuclear Leukocytes: The OmegAD Study

Background: Dietary fish oil, rich in n-3 fatty acids (n-3 FAs), e. g. docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), regulate inflammatory reactions by various mechanisms, e. g. gene activation. However, the effects of long-term treatment with DHA and EPA in humans, using genome wide techniques, are poorly described. Hence, our aim was to determine the effects of 6 mo of dietary supplementation with an n-3 FA preparation rich in DHA on global gene expression in peripheral blood mononuclear cells. Methods and Findings: In the present study, blood samples were obtained from a subgroup of 16 patients originating from the randomized double-blind, placebo-controlled OmegAD study, where 174 Alzheimer disease (AD) patients received daily either 1.7 g of DHA and 0.6 g EPA or placebo for 6 months. In blood samples obtained from 11 patients receiving n-3 FA and five placebo, expressions of approximately 8000 genes were assessed by gene array. Significant changes were confirmed by real-time PCR. At 6 months, the n-3 FAs group displayed significant rises of DHA and EPA plasma concentrations, as well as up-and down-regulation of nine and ten genes, respectively, was noticed. Many of these genes are involved in inflammation regulation and neurodegeneration, e. g. CD63, MAN2A1, CASP4, LOC399491, NAIP, and SORL1 and in ubiqutination processes, e. g. ANAPC5 and UBE2V1. Down-regulations of ANAPC5 and RHOB correlated to increases of plasma DHA and EPA levels. Conclusions: We suggest that 6 months of dietary n-3 FA supplementatio