Availability of timber housing construction techniques in Brazil

Se analiza la representatividad de las viviendas hechas en madera, en Brasil, indicando el porcentaje de cada técnica constructiva según la oferta de las empresas evaluadas. Los porcentajes que evidencian la frecuencia de utilización de las técnicas de construcción en madera fueron medidos por medio de dos metodologías aplicadas en las empresas: encuesta por entrevistas personales a sus propietarios y búsqueda de datos en sus sitios web. El método de encuestas por entrevistas evaluó 107 empresas brasileñas, y el de búsqueda en los sitios web alcanzó 207 empresas; se consiguió 50,95 y 98,57 %, respectivamente, de la población estimada. A pesar de esta diferencia, ambos métodos demostraron un escenario similar. Las entrevistas presentaron mayores costos de aplicación. Las técnicas contemporáneas están disponibles en más del 90 % de los productores brasileros. Las casas de tablas horizontales clavadas y las casas de tablas horizontales entre pilares fueron las que tuvieron mayores ofertas.This paper analyzes the representativeness of timber housing in Brazil, identifying the percentage of construction techniques offered by each evaluated company. Percentages that evidence the frequency of use of wooden building techniques were measured using two methods applied in the companies: survey through face-to-face interviews with owners and data search on their websites. The survey through interviews evaluated 107 Brazilian companies, while the data search included 207 companies, obtaining 50.95% and 98.57% of the estimated population, respectively. In spite of this difference, both methods showed a similar scenario. Interviews evidenced higher application costs. Contemporary techniques are available in more than 90% of Brazilian constructors. Houses with nailed horizontal boards and houses with horizontal wooden boards between columns were offered the most

Contribución del anillamiento al conocimiento y conservación de las aves en España: pasado, presente y futuro

El anillamiento científico de aves es una técnica de estudio con más de un siglo de historia que, probablemente, ha contribuido como ninguna otra metodología al conocimiento de la biología de este grupo faunístico. A pesar del desarrollo de nuevas tecnologías, el marcaje individual de aves mediante anillamiento sigue siendo una técnica plenamente vigente y necesaria. Aunque la evidencia científica sobre los beneficios de la aplicación del anillamiento en la Ornitología moderna es abrumadora, hoy vivimos un proceso de creciente desinformación que cuestiona el anillamiento de aves y su utilidad. Este dosier se ha elaborado con el fin de ofrecer una visión actualizada de la utilidad del anillamiento científico de aves en España. Ha sido elaborado por un nutrido grupo de expertos asociados a universidades y centros de investigación que abarcan buena parte de las áreas del conocimiento implicadas en el estudio y conservación de las aves. El dosier se divide en cuatro grandes apartados. (1) En primer lugar se hace una introducción sobre el anillamiento como metodología y se resumen las grandes cifras del anillamiento en España donde, hasta la fecha, se han anillado algo más de 10.000.000 de aves y se han registrado 700.000 recuperaciones (en la actualidad se anillan unas 380.000 aves y se obtienen unas 30.000 recuperaciones anualmente). (2) En un segundo bloque se resume la aplicación del anillamiento en diferentes aproximaciones al estudio científico de las aves, que van apoyadas por numerosas referencias bibliográficas sobre trabajos llevados a cabo en España. Gracias al anillamiento se han podido abordar múltiples estudios sobre movimientos y migraciones, reproducción, demografía, enfermedades, morfología, muda e identificación y taxonomía. (3) Un tercer bloque se centra en la utilidad del anillamiento más allá de la investigación básica. Es el caso de la conservación, la gestión de especies cinegéticas y el estudio de los impactos del cambio global sobre las aves, por un lado, y la educación ambiental, formación y ciencia ciudadana, por otro. (4) Finalmente, se abordan algunas ideas sobre los retos actuales y perspectivas de futuro del anillamiento en España

Kisspeptina en becerras prepúberes: I. Influencia de la edad en la respuesta de LH, FSH y GH a kisspeptina-10 y su asociación con IGF-I, leptina y estradiol

To evaluate effects of age on the response of LH, FSH and GH to kisspeptin-10 (KISS) in prepubertal heifers and its association with circulating levels of IGF-I, estradiol (E2) and leptin, 21 heifer calves that were 4, 7 or 11 mo old, received an iv injection of KISS (5 μg/kg). LH, FSH and GH were quantified in blood serum taken every 15 min (4 h pre- and 4 h post-KISS-10). In three pre- and six post-KISS samples, IGF-I, leptin and E2 were determined. All heifers responded to KISS with an LH increment but the response magnitude differed among groups since maximum value was higher (P<0.05) in 11 mo (11.6+1.3 ng/ml) than in 7 mo (7.2±1.3 ng/ml) and 4 mo (6.1±1.3 ng/ml) old calves. Duration of response differed (P<0.05) among ages (11 mo=132.9+20 mina; 7 mo=92±20 mina,b; 4 mo=64.3±20 minb). For FSH, all and 11 mo calves responded to KISS but only 71.4 % of 4 mo did. In GH, 71.4 % of 4 mo and 85.7 % of 7 mo calves responded to KISS whereas 100 % of 11 mo animals responded. FSH and GH did not differ among age groups. The 11 mo heifers had the highest IGF-I and E2 but the lowest leptin levels. In conclusion, KISS evokes LH increments in all calves 4 to 11 mo old, but the response increases with age in association with high circulating IGF-I and E2 and low leptin. The response of FSH and GH to KISS is not influenced by age or variations in circulating IGF-I, E2 or leptin. El objetivo fue evaluar la respuesta de LH, FSH y GH a kisspeptina-10 (KISS) en becerras prepúberes de distintas edades, y su asociación con IGF-I, E2 y leptina circulantes. A 21 becerras de 4, 7 y 11 meses de edad se les aplicó una inyección i.v. de 5 µg de KISS/kg de peso. En suero obtenido de la yugular (cada 15 min, 4 h pre hasta 4 h post-KISS) se cuantificó LH, FSH y GH. En nueve muestras (tres pre y seis post-KISS) se determinó IGF-I, leptina y estradiol (E2). En todas las becerras aumentó la LH post-KISS, con un valor máximo (6.1±1.3a, 7.2±1.3a, 11.6+1.3b ng/ml) y duración de respuesta (64.3±20a, 92±20b, 132.9+20c min) que aumentó (P<0.05) con la edad. Para FSH, 71.4, 100 y 100 % de las becerras de 4, 7 y 11 meses respondieron a KISS-10; situación que para GH fue 71.4, 85.7 y 100 %, respectivamente. La magnitud de la respuesta de FSH y GH a KISS fue similar entre edades. Las becerras de 11 meses tuvieron las máximas concentraciones de IGF-I y E2 y las menores de leptina. Se concluye que KISS-10 evoca un aumento de LH en becerras de 4 a 11 meses, cuya magnitud de respuesta se asocia con la edad, con el incremento en sangre periférica de IGF-I y E2 y con la disminución de leptina sérica; en contraste, la respuesta de GH y FSH a KISS-10 no es afectada por la edad ni por las variaciones en IGF-I, E2 y leptina

Autoantibody screening in Guillain-Barré syndrome

Background: Guillain?Barré syndrome (GBS) is an acute inflammatory neuropathy with a heterogeneous presentation. Although some evidences support the role of autoantibodies in its pathogenesis, the target antigens remain unknown in a substantial proportion of GBS patients. The objective of this study is to screen for autoantibodies targeting peripheral nerve components in Guillain-Barré syndrome. Methods: Autoantibody screening was performed in serum samples from all GBS patients included in the International GBS Outcome study by 11 different Spanish centres. The screening included testing for anti-ganglioside antibodies, anti-nodo/paranodal antibodies, immunocytochemistry on neuroblastoma-derived human motor neurons and murine dorsal root ganglia (DRG) neurons, and immunohistochemistry on monkey peripheral nerve sections. We analysed the staining patterns of patients and controls. The prognostic value of anti-ganglioside antibodies was also analysed. Results: None of the GBS patients (n = 100) reacted against the nodo/paranodal proteins tested, and 61 (61%) were positive for, at least, one anti-ganglioside antibody. GBS sera reacted strongly against DRG neurons more frequently than controls both with IgG (6% vs 0%; p = 0.03) and IgM (11% vs 2.2%; p = 0.02) immunodetection. No differences were observed in the proportion of patients reacting against neuroblastoma-derived human motor neurons. Reactivity against monkey nerve tissue was frequently detected both in patients and controls, but specific patterns were only detected in GBS patients: IgG from 13 (13%) patients reacted strongly against Schwann cells. Finally, we confirmed that IgG anti-GM1 antibodies are associated with poorer outcomes independently of other known prognostic factor

Dendritic cell deficiencies persist seven months after SARS-CoV-2 infection

Severe Acute Respiratory Syndrome Coronavirus (SARS-CoV)-2 infection induces an exacerbated inflammation driven by innate immunity components. Dendritic cells (DCs) play a key role in the defense against viral infections, for instance plasmacytoid DCs (pDCs), have the capacity to produce vast amounts of interferon-alpha (IFN-α). In COVID-19 there is a deficit in DC numbers and IFN-α production, which has been associated with disease severity. In this work, we described that in addition to the DC deficiency, several DC activation and homing markers were altered in acute COVID-19 patients, which were associated with multiple inflammatory markers. Remarkably, previously hospitalized and nonhospitalized patients remained with decreased numbers of CD1c+ myeloid DCs and pDCs seven months after SARS-CoV-2 infection. Moreover, the expression of DC markers such as CD86 and CD4 were only restored in previously nonhospitalized patients, while no restoration of integrin β7 and indoleamine 2,3-dyoxigenase (IDO) levels were observed. These findings contribute to a better understanding of the immunological sequelae of COVID-19

SARS-CoV-2 viral load in nasopharyngeal swabs is not an independent predictor of unfavorable outcome

The aim was to assess the ability of nasopharyngeal SARS-CoV-2 viral load at first patient’s hospital evaluation to predict unfavorable outcomes. We conducted a prospective cohort study including 321 adult patients with confirmed COVID-19 through RT-PCR in nasopharyngeal swabs. Quantitative Synthetic SARS-CoV-2 RNA cycle threshold values were used to calculate the viral load in log10 copies/mL. Disease severity at the end of follow up was categorized into mild, moderate, and severe. Primary endpoint was a composite of intensive care unit (ICU) admission and/or death (n = 85, 26.4%). Univariable and multivariable logistic regression analyses were performed. Nasopharyngeal SARS-CoV-2 viral load over the second quartile (≥ 7.35 log10 copies/mL, p = 0.003) and second tertile (≥ 8.27 log10 copies/mL, p = 0.01) were associated to unfavorable outcome in the unadjusted logistic regression analysis. However, in the final multivariable analysis, viral load was not independently associated with an unfavorable outcome. Five predictors were independently associated with increased odds of ICU admission and/or death: age ≥ 70 years, SpO2, neutrophils > 7.5 × 103/µL, lactate dehydrogenase ≥ 300 U/L, and C-reactive protein ≥ 100 mg/L. In summary, nasopharyngeal SARS-CoV-2 viral load on admission is generally high in patients with COVID-19, regardless of illness severity, but it cannot be used as an independent predictor of unfavorable clinical outcome

Effect of TNF-α genetic variants and CCR5Δ32 on the vulnerability to HIV-1 infection and disease progression in Caucasian Spaniards

<p>Abstract</p> <p>Background</p> <p>Tumor necrosis factor alpha (TNF-α) is thought to be involved in the various immunogenetic events that influence HIV-1 infection.</p> <p>Methods</p> <p>We aimed to determine whether carriage of the <it>TNF-α-238G>A, -308G>A </it>and <it>-863 C>A </it>gene promoter single nucleotide polymorphisms (SNP) and the <it>CCR5Δ32 </it>variant allele influence the risk of HIV-1 infection and disease progression in Caucasian Spaniards. The study group consisted of 423 individuals. Of these, 239 were uninfected (36 heavily exposed but uninfected [EU] and 203 healthy controls [HC]) and 184 were HIV-1-infected (109 typical progressors [TP] and 75 long-term nonprogressors [LTNP] of over 16 years' duration). <it>TNF-α </it>SNP and the <it>CCR5Δ32 </it>allele were assessed using PCR-RFLP and automatic sequencing analysis methods on white blood cell DNA. Genotype and allele frequencies were compared using the χ 2 test and the Fisher exact test. Haplotypes were compared by logistic regression analysis.</p> <p>Results</p> <p>The distribution of <it>TNF-α-238G>A, -308G>A </it>and <it>-863 C>A </it>genetic variants was non-significantly different in HIV-1-infected patients compared with uninfected individuals: <it>-238G>A</it>, p = 0.7 and p = 0.3; <it>-308G>A</it>, p = 0.05 and p = 0.07; <it>-863 C>A</it>, p = 0.7 and p = 0.4, for genotype and allele comparisons, respectively. Haplotype analyses, however, indicated that carriers of the haplotype H3 were significantly more common among uninfected subjects (p = 0.04). Among the infected patients, the distribution of the three <it>TNF-α </it>genetic variants assessed was non-significantly different between TP and LTNP: <it>-238G>A</it>, p = 0.35 and p = 0.7; <it>-308G>A</it>, p = 0.7 and p = 0.6: <it>-863 C>A</it>, p = 0.2 and p = 0.2, for genotype and allele comparisons, respectively. Haplotype analyses also indicated non-significant associations. Subanalyses in the LTNP subset indicated that the <it>TNF-α-238A </it>variant allele was significantly overrepresented in patients who spontaneously controlled plasma viremia compared with those who had a detectable plasma viral load (genotype comparisons, p = 0.02; allele comparisons, p = 0.03). The <it>CCR5Δ32 </it>distribution was non-significantly different in HIV-1-infected patients with respect to the uninfected population (p = 0.15 and p = 0.2 for genotype and allele comparisons, respectively) and in LTNP vs TP (p = 0.4 and p = 0.5 for genotype and allele comparisons, respectively).</p> <p>Conclusions</p> <p>In our cohort of Caucasian Spaniards, <it>TNF-α </it>genetic variants could be involved in the vulnerability to HIV-1 infection. <it>TNF-α </it>genetic variants were unrelated to disease progression in infected subjects. The <it>-238G>A </it>SNP may modulate the control of viremia in LTNP. Carriage of the <it>CCR5Δ32 </it>variant allele had no effect on the risk of infection and disease progression.</p

A novel inhibitor of fatty acid synthase shows activity against HER2+ breast cancer xenografts and is active in anti-HER2 drug-resistant cell lines

Introduction: Inhibiting the enzyme Fatty Acid Synthase (FASN) leads to apoptosis of breast carcinoma cells, and this is linked to human epidermal growth factor receptor 2 (HER2) signaling pathways in models of simultaneous expression of FASN and HER2. Methods: In a xenograft model of breast carcinoma cells that are FASN+ and HER2+, we have characterised the anticancer activity and the toxicity profile of G28UCM, the lead compound of a novel family of synthetic FASN inhibitors. In vitro, we analysed the cellular and molecular interactions of combining G28UCM with anti-HER drugs. Finally, we tested the cytotoxic ability of G28UCM on breast cancer cells resistant to trastuzumab or lapatinib, that we developed in our laboratory. Results: In vivo, G28UCM reduced the size of 5 out of 14 established xenografts. In the responding tumours, we observed inhibition of FASN activity, cleavage of poly-ADPribose polymerase (PARP) and a decrease of p-HER2, p- protein kinase B (AKT) and p-ERK1/2, which were not observed in the nonresponding tumours. In the G28UCM-treated animals, no significant toxicities occurred, and weight loss was not observed. In vitro, G28UCM showed marked synergistic interactions with trastuzumab, lapatinib, erlotinib or gefitinib (but not with cetuximab), which correlated with increases in apoptosis and with decreases in the activation of HER2, extracellular signal-regulated kinase (ERK)1/2 and AKT. In trastuzumab-resistant and in lapatinib-resistant breast cancer cells, in which trastuzumab and lapatinib were not effective, G28UCM retained the anticancer activity observed in the parental cells. Conclusions: G28UCM inhibits fatty acid synthase (FASN) activity and the growth of breast carcinoma xenografts in vivo, and is active in cells with acquired resistance to anti-HER2 drugs, which make it a candidate for further pre-clinical development

Clonal chromosomal mosaicism and loss of chromosome Y in elderly men increase vulnerability for SARS-CoV-2

The pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2, COVID-19) had an estimated overall case fatality ratio of 1.38% (pre-vaccination), being 53% higher in males and increasing exponentially with age. Among 9578 individuals diagnosed with COVID-19 in the SCOURGE study, we found 133 cases (1.42%) with detectable clonal mosaicism for chromosome alterations (mCA) and 226 males (5.08%) with acquired loss of chromosome Y (LOY). Individuals with clonal mosaic events (mCA and/or LOY) showed a 54% increase in the risk of COVID-19 lethality. LOY is associated with transcriptomic biomarkers of immune dysfunction, pro-coagulation activity and cardiovascular risk. Interferon-induced genes involved in the initial immune response to SARS-CoV-2 are also down-regulated in LOY. Thus, mCA and LOY underlie at least part of the sex-biased severity and mortality of COVID-19 in aging patients. Given its potential therapeutic and prognostic relevance, evaluation of clonal mosaicism should be implemented as biomarker of COVID-19 severity in elderly people. Among 9578 individuals diagnosed with COVID-19 in the SCOURGE study, individuals with clonal mosaic events (clonal mosaicism for chromosome alterations and/or loss of chromosome Y) showed an increased risk of COVID-19 lethality