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Placental mediated fetal growth restriction (FGR) is a leading cause of perinatal morbidity and mortality. Heparan sulphate proteoglycans (HSPG) are highly expressed in placentae and regulate haemostasis. We hypothesise that altered expression of HSPGs, glypicans (GPC) may contribute to the development of FGR and small-for-gestational-age (SGA). GPC expression was determined in first-trimester chorionic villous samples collected from women with later SGA pregnancies and in placentae from third-trimester FGR and gestation-matched uncomplicated pregnancies. The expression of both GPC1 and GPC3 were significantly reduced in first-trimester SGA as well as in the third-trimester FGR placentae compared to controls. This is the first study to report a relationship between altered placental GPC expression and subsequent development of SGA/FGR.
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Retardo del Crecimiento Fetal/metabolismo , Glipicanos/metabolismo , Placenta/metabolismo , Adulto , Estudios de Casos y Controles , Femenino , Humanos , Recién Nacido , Recién Nacido Pequeño para la Edad Gestacional , Embarazo , Primer Trimestre del Embarazo/metabolismo , Tercer Trimestre del Embarazo/metabolismoRESUMEN
Fetal growth restriction (FGR) the leading cause of perinatal mortality and morbidity is highly related to abnormal placental development, and placentas from FGR pregnancies are often characterized by increased inflammation. However, the mechanisms of FGR-associated inflammation are far from being understood. NLRP7, a member of a family of receptors involved in the innate immune responses, has been shown to be associated with gestational trophoblastic diseases. Here, we characterized the expression and the functional role of NLRP7 in the placenta and investigated its involvement in the pathogenesis of FGR. We used primary trophoblasts and placental explants that were collected during early pregnancy, and established trophoblast-derived cell lines, human placental villi, and serum samples from early pregnancy (n = 38) and from FGR (n = 40) and age-matched controls (n = 32). Our results show that NLRP7 (i) is predominantly expressed in the trophoblasts during the hypoxic period of placental development and its expression is upregulated by hypoxia and (ii) increases trophoblast proliferation ([3H]-thymidine) and controls the precocious differentiation of trophoblasts towards syncytium (syncytin 1 and 2 and ß-hCG production and xCELLigence analysis) and towards invasive extravillous trophoblast (2D and 3D cultures). We have also demonstrated that NLRP7 inflammasome activation in trophoblast cells increases IL-1ß, but not IL-18 secretion. In relation to the FGR, we demonstrated that major components of NLRP7 inflammasome machinery are increased and that IL-1ß but not IL-18 circulating levels are increased in FGR. Altogether, our results identified NLRP7 as a critical placental factor and provided evidence for its deregulation in FGR. NLRP7 inflammasome is abundantly expressed by trophoblast cells. It is regulated by a key parameter of placental development, hypoxia. It controls trophoblast proliferation, migration, and invasion and exhibits anti-apoptotic role. NLRP7 machinery is deregulated in FGR pregnancies. KEY MESSAGES: NLRP7 inflammasome is abundantly expressed by trophoblast cells. It is regulated by a key parameter of placental development, hypoxia. It controls trophoblast proliferation, migration, and invasion and exhibits anti-apoptotic role. NLRP7 machinery is deregulated in FGR pregnancies.
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Proteínas Adaptadoras Transductoras de Señales/metabolismo , Retardo del Crecimiento Fetal/metabolismo , Placenta/metabolismo , Trofoblastos/fisiología , Adulto , Diferenciación Celular , Línea Celular , Femenino , Humanos , Hipoxia/metabolismo , Interleucina-18/sangre , Interleucina-1beta/sangre , Embarazo , Primer Trimestre del Embarazo/metabolismoRESUMEN
Preparing an anatase TiO2(101) surface with a high density of oxygen vacancies and associated reduced Ti species in the near-surface region results in drastic changes in the water adsorption chemistry compared to adsorption on a highly stoichiometric surface. Using synchrotron radiation excited photoelectron spectroscopy, we observe a change in the water growth mode, from layer-by-layer growth on the highly stoichiometric surface to bilayer growth on the reduced surface. Furthermore, we have been able to observe Ti3+ enrichment at the surface upon water adsorption. The Ti3+ enrichment occurs concomitant with effective water dissociation into hydroxyls with a very high thermal stability. The water bilayer on the reduced surface is thermally more stable than that on the stoichiometric surface, and it is more efficient in promoting further water dissociation upon heating. The results thus show how the presence of subsurface defects can alter the wetting mechanism of an oxide surface.
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BACKGROUND: Selection of systemic therapy for primary breast cancer is currently based on clinical biomarkers along with stage. Novel genomic tests are continuously being introduced as more precise tools for guidance of therapy, although they are often developed for specific patient subgroups. The Sweden Cancerome Analysis Network - Breast (SCAN-B) initiative aims to include all patients with breast cancer for tumour genomic analysis, and to deliver molecular subtype and mutational data back to the treating physician. METHODS: An infrastructure for collection of blood and fresh tumour tissue from all patients newly diagnosed with breast cancer was set up in 2010, initially including seven hospitals within the southern Sweden regional catchment area, which has 1.8 million inhabitants. Inclusion of patients was implemented into routine clinical care, with collection of tumour tissue at local pathology departments for transport to the central laboratory, where routines for rapid sample processing, RNA sequencing and biomarker reporting were developed. RESULTS: More than 10 000 patients from nine hospitals have currently consented to inclusion in SCAN-B with high (90 per cent) inclusion rates from both university and secondary hospitals. Tumour samples and successful RNA sequencing are being obtained from more than 70 per cent of patients, showing excellent representation compared with the national quality registry as a truly population-based cohort. Molecular biomarker reports can be delivered to multidisciplinary conferences within 1 week. CONCLUSION: Population-based collection of fresh tumour tissue is feasible given a decisive joint effort between academia and collaborative healthcare groups, and with governmental support. An infrastructure for genomic analysis and prompt data output paves the way for novel systemic therapy for patients from all hospitals, irrespective of size and location.
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Biomarcadores de Tumor/análisis , Neoplasias de la Mama/genética , Medicina de Precisión/métodos , Neoplasias de la Mama/terapia , Disparidades en Atención de Salud , Secuenciación de Nucleótidos de Alto Rendimiento/métodos , Humanos , Mutación , Aceptación de la Atención de Salud , SueciaRESUMEN
Thin films of TiOx on Pd(100) and Pd(111) have been investigated with respect to their properties after oxidation and reduction cycles. High-resolution photoemission spectroscopy (HRPES) and low energy electron diffraction (LEED) have been applied to characterize the thin film oxidation states and structure before and after oxidation and reduction under ultrahigh vacuum conditions. Fully oxidized TiO2 films were formed on both surfaces. These structures display Moiré patterns in LEED, in one dimension for Pd(100) and in two dimensions for Pd(111), and they have previously not been reported for TiO2/Pd. The oxidation process causes strong reduction in the interaction between the oxide thin film and the Pd substrate, most significantly for Pd(111). Reversible oxidation/reduction cycling of TiOx thin films on Pd(111) and Pd(100) was possible.
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Gene-panel sequencing allows comprehensive analysis of multiple genes simultaneously and is now routinely used in clinical mutation testing of high-risk breast and ovarian cancer patients. However, only BRCA1 and BRCA2 are often analyzed also for large genomic changes. Here, we have analyzed 10 clinically relevant susceptibility genes in 95 breast or ovarian cancer patients with gene-panel sequencing including also copy number variants (CNV) analysis for genomic changes. We identified 12 different pathogenic BRCA1, BRCA2, TP53, PTEN, CHEK2, or RAD51C mutations in 18 of 95 patients (19%). BRCA1/2 mutations were observed in 8 patients (8.4%) and CHEK2 protein-truncating mutations in 7 patients (7.4%). In addition, we identified a novel duplication encompassing most of the RAD51C gene. We further genotyped the duplication in breast or ovarian cancer families (n = 1149), in unselected breast (n = 1729) and ovarian cancer cohorts (n = 553), and in population controls (n = 1273). Seven additional duplication carries were observed among cases but none among controls. The duplication associated with ovarian cancer risk (3/590 of all ovarian cancer patients, 0.5%, P = .032 compared with controls) and was found to represent a large fraction of all identified RAD51C mutations in the Finnish population. Our data emphasizes the importance of comprehensive mutation analysis including CNV detection in all the relevant genes.
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Neoplasias de la Mama/diagnóstico , Neoplasias de la Mama/genética , Proteínas de Unión al ADN/genética , Duplicación de Gen , Estudios de Asociación Genética , Predisposición Genética a la Enfermedad , Neoplasias Ováricas/diagnóstico , Neoplasias Ováricas/genética , Adulto , Anciano , Alelos , Biomarcadores de Tumor , Exones , Femenino , Finlandia , Frecuencia de los Genes , Estudios de Asociación Genética/métodos , Pruebas Genéticas , Mutación de Línea Germinal , Síndrome de Cáncer de Mama y Ovario Hereditario/diagnóstico , Síndrome de Cáncer de Mama y Ovario Hereditario/genética , Secuenciación de Nucleótidos de Alto Rendimiento , Humanos , Persona de Mediana EdadRESUMEN
We present a rare case of isolated right subclavian artery arising from a right-sided patent arterial duct in a patient with DiGeorge syndrome, diagnosed on cardiac CT, along with potential complications and management approaches.
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We present two cases of severe aortic coarctation detected in adulthood and who underwent successful relief by transcatheter stent deployment using a new covered stent, Optimus® stent (AndraTec GmbH Koblenz, Germany). One patient is a 46-year old female with resistant arterial hypertension, in whom coarctation was suspected on a follow-up transthoracic echocardiogram for bicuspid aortic valve disease and subsequently confirmed on magnetic resonance imaging. The second patient is a 68-year old male whose coarctation was diagnosed incidentally at coronary angiography being performed as part of the preoperative work-up for severe aortic stenosis. Suprasternal views to assess aortic arch and flows in the proximal descending aorta should be a standard part of every transthoracic echocardiogram. Treatment of aortic coarctation should be considered irrespective of patient's age.
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We present a dedicated synchrotron radiation photoelectron spectroscopy (SR-PES) study of a photochemical reaction on the surface of rutile TiO2(110). The photoreaction kinetics of carboxylate species (trimethyl acetate, TMA) upon irradiation by UV and soft X-rays were monitored, and we show that it is possible to control the reaction rates from UV light and soft X-rays independently. We directly observe Ti4+ â Ti3+ conversion upon irradiation, attributed to electron trapping at Ti sites close to surface OH groups formed by deprotonation of the parent molecule, trimethylacetic acid (TMAA). TMA photolysis on two surface preparations with different oxygen vacancy densities shows that the vacancy-related charge quenches the amount of charge that can be trapped at hydroxyls upon irradiation. During the initial stages of reaction the correlation between the amount of photodepleted TMA and the amount of charge trapped in the Ti 3d band gap state is nearly 1:1. A first-order kinetics analysis reveals that the reaction rate decreases with decreasing TMA coverage. There is also a coverage-dependent difference in the electronic structure of TMA moieties, primarily involving the carboxyl anchor group. These changes are consistent with a decreased hole affinity of the adsorbed TMA and hence a decreased reaction rate. This discovery adds to the previously presented picture of a reactivity that is inversely proportional to the number of surface hydroxyls, suggesting that the balance between the amounts of TMA, OH, and trapped charge needs to be considered.
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Fetal growth restriction (FGR) is a leading cause of perinatal morbidity and mortality. FGR pregnancies are often associated with histological evidence of placental vascular thrombosis. The proteoglycans are important components and regulators of vascular homeostasis. Previous studies from our laboratory highlighted mRNA and protein expression differences in placental proteoglycan decorin (DCN), within a clinically well-characterised cohort of third-trimester idiopathic FGR compared with gestation-matched uncomplicated control pregnancies. We also showed that decorin contributes to abnormal angiogenesis and increased thrombin generation in vitro. These observations suggest that DCN gene expression may contribute to the etiology of FGR. Small for gestational age (SGA) is frequently used as a proxy for FGR and is defined as a birth weight below the 10th percentile of a birth weight curve. We therefore made use of a unique resource of first trimester tissues obtained via chorionic villus sampling during the first trimester to investigate the temporal relationship between altered DCN expression and any subsequent development of SGA. We hypothesized that placental DCN expression is decreased early in gestation in SGA pregnancies. Surplus chorionic villus specimens from 15 women subsequently diagnosed with FGR and 50 from women with uncomplicated pregnancies were collected. DCN mRNA and DCN protein were determined using real-time PCR and immunoblotting, respectively. Both DCN mRNA and protein were significantly decreased in placentae from first-trimester SGA-pregnancies compared with controls (p < 0.05). This is the first study to report a temporal relationship between altered placental DCN expression and subsequent development of SGA.
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Decorina/metabolismo , Regulación hacia Abajo , Placenta/metabolismo , Adulto , Femenino , Humanos , Recién Nacido Pequeño para la Edad Gestacional , Edad Materna , Embarazo , Primer Trimestre del Embarazo/metabolismoRESUMEN
BACKGROUND: A mutation found in the BRCA1 or BRCA2 gene of a breast tumor could be either germline or somatically acquired. The prevalence of somatic BRCA1/2 mutations and the ratio between somatic and germline BRCA1/2 mutations in unselected breast cancer patients are currently unclear. PATIENTS AND METHODS: Paired normal and tumor DNA was analyzed for BRCA1/2 mutations by massively parallel sequencing in an unselected cohort of 273 breast cancer patients from south Sweden. RESULTS: Deleterious germline mutations in BRCA1 (n = 10) or BRCA2 (n = 10) were detected in 20 patients (7%). Deleterious somatic mutations in BRCA1 (n = 4) or BRCA2 (n = 5) were detected in 9 patients (3%). Accordingly, about 1 in 9 breast carcinomas (11%) in our cohort harbor a BRCA1/2 mutation. For each gene, the tumor phenotypes were very similar regardless of the mutation being germline or somatically acquired, whereas the tumor phenotypes differed significantly between wild-type and mutated cases. For age at diagnosis, the patients with somatic BRCA1/2 mutations resembled the wild-type patients (median age at diagnosis, germline BRCA1: 41.5 years; germline BRCA2: 49.5 years; somatic BRCA1/2: 65 years; wild-type BRCA1/2: 62.5 years). CONCLUSIONS: In a population without strong germline founder mutations, the likelihood of a BRCA1/2 mutation found in a breast carcinoma being somatic was â¼1/3 and germline 2/3. This may have implications for treatment and genetic counseling.
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Proteína BRCA1/genética , Proteína BRCA2/genética , Neoplasias de la Mama/genética , Adulto , Anciano , Neoplasias de la Mama/epidemiología , Neoplasias de la Mama/patología , Femenino , Predisposición Genética a la Enfermedad , Mutación de Línea Germinal , Humanos , Persona de Mediana Edad , Mutación , Suecia/epidemiologíaRESUMEN
Therapy directed against oncogenic FLT3 has been shown to induce response in patients with acute myeloid leukemia (AML), but these responses are almost always transient. To address the mechanism of FLT3 inhibitor resistance, we generated two resistant AML cell lines by sustained treatment with the FLT3 inhibitor sorafenib. Parental cell lines carry the FLT3-ITD (tandem duplication) mutation and are highly responsive to FLT3 inhibitors, whereas resistant cell lines display resistance to multiple FLT3 inhibitors. Sanger sequencing and protein mass-spectrometry did not identify any acquired mutations in FLT3 in the resistant cells. Moreover, sorafenib treatment effectively blocked FLT3 activation in resistant cells, whereas it was unable to block colony formation or cell survival, suggesting that the resistant cells are no longer FLT3 dependent. Gene expression analysis of sensitive and resistant cell lines, as well as of blasts from patients with sorafenib-resistant AML, suggested an enrichment of the PI3K/mTOR pathway in the resistant phenotype, which was further supported by next-generation sequencing and phospho-specific-antibody array analysis. Furthermore, a selective PI3K/mTOR inhibitor, gedatolisib, efficiently blocked proliferation, colony and tumor formation, and induced apoptosis in resistant cell lines. Gedatolisib significantly extended survival of mice in a sorafenib-resistant AML patient-derived xenograft model. Taken together, our data suggest that aberrant activation of the PI3K/mTOR pathway in FLT3-ITD-dependent AML results in resistance to drugs targeting FLT3.
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Resistencia a Antineoplásicos/genética , Leucemia Mieloide Aguda/tratamiento farmacológico , Morfolinas/administración & dosificación , Niacinamida/análogos & derivados , Compuestos de Fenilurea/administración & dosificación , Triazinas/administración & dosificación , Tirosina Quinasa 3 Similar a fms/genética , Animales , Antineoplásicos/administración & dosificación , Apoptosis/efectos de los fármacos , Línea Celular Tumoral , Proliferación Celular/efectos de los fármacos , Humanos , Leucemia Mieloide Aguda/genética , Leucemia Mieloide Aguda/patología , Ratones , Mutación , Niacinamida/administración & dosificación , Fosfatidilinositol 3-Quinasas/genética , Inhibidores de las Quinasa Fosfoinosítidos-3 , Inhibidores de Proteínas Quinasas/administración & dosificación , Transducción de Señal/efectos de los fármacos , Sorafenib , Serina-Treonina Quinasas TOR/antagonistas & inhibidores , Serina-Treonina Quinasas TOR/genética , Ensayos Antitumor por Modelo de XenoinjertoRESUMEN
BACKGROUND: Obesity is a global epidemic with the Mediterranean island of Malta being no exception. The World Health Organization (WHO) has identified Malta as one of the European countries with the highest obesity prevalence. METHOD: A cross-sectional study was conducted (2014-2016) under the auspices of the University of Malta. The prevalence of overweight-obesity in Malta was calculated and then age stratified for comparisons with previous studies. RESULTS: The study identified 69.75% (95% CI: 68.32-71.18) of the Maltese population to be either overweight or obese. The men overweight/obese prevalence (76.28% 95% CI: 74.41-78.14) was statistically higher than that for women (63.06% 95% CI: 60.92-65.20) (p = 0.0001). Age stratification revealed that both genders had the highest overweight prevalence rates between 55 and 64 years (Men = 23.25% 95% CI: 20.43-26.33; Women = 24.68% 95% CI: 21.44-28.22). Men obesity prevalence rates were highest in the 35 to 44 years group (22.52% 95% CI: 19.65-25.68) while for women it was highest in the 55 to 64 years group (28.90%, 95% CI: 25.44-30.63). CONCLUSION: Over a 35-year period, an overall decrease in the normal and overweight BMI categories occurred with an increase in the prevalence of obesity. An exception was observed in the women, where the prevalence of normal BMI increased over this time period. Also, it appears that while the total population obesity prevalence increased (for 2016), a percentage of the women have shifted from an obese to an overweight status.
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Abnormal trophoblast function is associated with fetal growth restriction (FGR). The JAK-STAT pathway is one of the principal signalling mechanisms by which cytokines and growth factors modulate cell proliferation, differentiation, cell migration and apoptosis. The expression of placental JAK-STAT genes in human idiopathic FGR is unknown. In this study, we propose the hypothesis that JAK-STAT pathway genes are differentially expressed in idiopathic FGR-affected pregnancies and contribute to abnormal feto-placental growth by modulating the expression of the amino acid transporter SNAT2, differentiation marker CGB/human chorionic gonadotrophin beta-subunit (ß-hCG) and apoptosis markers caspases 3 and 8, and TP53. Expression profiling of FGR-affected placentae revealed that mRNA levels of STAT3, STAT2 and STAT5B decreased by 69, 52 and 50%, respectively, compared with gestational-age-matched controls. Further validation by real-time PCR and immunoblotting confirmed significantly lower STAT3 mRNA and STAT3 protein (total and phosphorylated) levels in FGR placentae. STAT3 protein was localised to the syncytiotrophoblast (ST) in both FGR and control placentae. ST differentiation was modelled by in vitro differentiation of primary villous trophoblast cells from first-trimester and term placentae, and by treating choriocarcinoma-derived BeWo cells with forskolin in cell culture. Differentiation in these models was associated with increased STAT3 mRNA and protein levels. In BeWo cells treated with siRNA targeting STAT3, the mRNA and protein levels of CGB/ß-hCG, caspases 3 and 8, and TP53 were significantly increased, while that of SNAT2 was significantly decreased compared with the negative control siRNA. In conclusion, we report that decreased STAT3 expression in placentae may contribute to abnormal trophoblast function in idiopathic FGR-affected pregnancies.
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Apoptosis , Retardo del Crecimiento Fetal/patología , Placenta/citología , Factor de Transcripción STAT3/metabolismo , Trofoblastos/patología , Adulto , Western Blotting , Estudios de Casos y Controles , Diferenciación Celular , Proliferación Celular , Células Cultivadas , Estudios de Cohortes , Femenino , Retardo del Crecimiento Fetal/genética , Retardo del Crecimiento Fetal/metabolismo , Técnica del Anticuerpo Fluorescente , Humanos , Técnicas para Inmunoenzimas , Recién Nacido de Bajo Peso , Masculino , Placenta/metabolismo , Embarazo , Primer Trimestre del Embarazo , Tercer Trimestre del Embarazo , ARN Mensajero/genética , Reacción en Cadena en Tiempo Real de la Polimerasa , Reacción en Cadena de la Polimerasa de Transcriptasa Inversa , Factor de Transcripción STAT3/genética , Trofoblastos/metabolismoRESUMEN
UNLABELLED: Fetal growth restriction (FGR) affects up to 5 % of pregnancies worldwide, and trophoblast function plays a significant role on the outcome. An epidemiological study has linked vitamin D deficiency to adverse perinatal outcomes, which include decreased birth weight. The placenta as an important source of vitamin D regulates its metabolism through the vitamin D receptor (VDR), but the mechanism by which VDR regulates trophoblast function is poorly understood. Our study aimed at determining placental VDR expression in FGR and gestation-matched control (GMC) pregnancies and identifying the actions of VDR in trophoblast differentiation and apoptosis. Placentae were collected from a well-defined cohort of idiopathic FGR and GMC pregnancies. VDR mRNA and protein expressions were determined by PCR, immunohistochemistry and immunoblotting, while functional consequences of VDR inactivation in vitro were determined on BeWo cells by determining changes in differentiation, attachment and apoptosis. Significant decreases in VDR mRNA expression (p = 0.0005) and protein expression (p = 0.0003) were observed in the FGR samples, while VDR inactivation, which showed markers for differentiation, cell attachment and apoptosis, was significantly increased. Thus, decreased placental VDR may contribute to uncontrolled premature differentiation and apoptosis of trophoblasts that are characteristics of idiopathic FGR pregnancies. KEY MESSAGE: Fetal growth restriction (FGR) affects up to 5 % of all pregnancies worldwide. FGR is the second highest cause of perinatal mortality and morbidity. The placenta plays a pivotal role in vitamin D metabolism during pregnancy. Vitamin D deficiency is associated with adverse pregnancy outcomes. Placental vitamin D receptor expression is decreased in FGR.
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Desarrollo Fetal/fisiología , Retardo del Crecimiento Fetal/patología , Placenta/fisiopatología , Receptores de Calcitriol/biosíntesis , Vitamina D/metabolismo , Apoptosis , Diferenciación Celular/genética , Línea Celular Tumoral , Femenino , Desarrollo Fetal/genética , Retardo del Crecimiento Fetal/genética , Humanos , Masculino , Embarazo , Interferencia de ARN , ARN Mensajero/biosíntesis , ARN Interferente Pequeño/genética , Receptores de Calcitriol/genética , Trofoblastos/citologíaRESUMEN
INTRODUCTION: Pre-eclampsia (PE) has a familial association, with daughters of women who had PE during pregnancy having more than twice the risk of developing PE themselves. Through genome-wide linkage and genetic association studies in PE-affected families and large population samples, we previously identified the following as positional candidate maternal susceptibility genes for PE; ACVR1, INHA, INHBB, ERAP1, ERAP2, LNPEP, COL4A1 and COL4A2. The aims of this study were to determine mRNA expression levels of previously identified candidate maternal pre-eclampsia susceptibility genes from normotensive and severe PE (SPE) pregnancies and correlate mRNA expression levels with the clinical severity of SPE. METHODS: Third trimester decidual tissues were collected from both normotensive (n = 21) and SPE pregnancies (n = 24) and mRNA expression levels were determined by real-time PCR. Gene expression was then correlated with several parameters of clinical severity in SPE. Statistical significance was determined by Mann-Whitney U test and Spearman's Correlation. RESULTS: The data demonstrate significantly increased decidual mRNA expression levels of ACVR1, INHBB, ERAP1, ERAP2, LNPEP, COL4A1 and COL4A2 in SPE (p < 0.05). Increased mRNA expression levels of several genes - INHA, INHBB, COL4A1 and COL4A2 were correlated with earlier onset of PE and earlier delivery of the fetus (p < 0.05). CONCLUSION: These results suggest altered expression of maternal susceptibility genes may play roles in PE development and the course of disease severity.
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Decidua/metabolismo , Predisposición Genética a la Enfermedad/genética , Subunidades beta de Inhibinas/biosíntesis , Preeclampsia/genética , Preeclampsia/metabolismo , ARN Mensajero/metabolismo , Receptores de Activinas Tipo I/biosíntesis , Adulto , Colágeno Tipo IV/biosíntesis , Femenino , Humanos , Inhibinas/biosíntesis , Embarazo , Tercer Trimestre del EmbarazoRESUMEN
We have studied the oxidation of CO over Rh(100) using high pressure x-ray photoelectron spectroscopy under CO and O2 pressures ranging from 0.01 to 1 mbar. The results show a very low or no conversion for the CO covered surface found at low temperatures, while the activity rises slightly when the temperature is high enough for some CO to desorb, exposing surface sites for dissociative O2 adsorption. As the temperature is increased further, more CO desorbs and oxygen replaces CO as the dominating species at the surface. At the same time we find a sudden increase in the reactivity, such that all CO that reaches the surface is instantly transformed into CO2. We find that the O coverage in the active state is highly dependent on the total pressure and, although we do not detect any presence of a surface oxide as in previous surface x-ray diffraction studies, the highest O coverage indicates that the surface is close to being oxidized.
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We demonstrate heterogeneous chemistry between Li and anatase TiO2 nanoparticles under UHV. The reduction of TiO2 upon formation of lithium oxide proceeds via two different schemes: one that reduces Ti(4+) to Ti(3+) and one that reduces Ti(4+) directly to Ti(2+). The second scheme sets in only after a critical degree of reduction (i.e. Li amount) has been reached (Li/Ti = 0.28) and is associated with restructuring of the film. Two films with different morphologies were compared and the results demonstrate that the reaction between Li and larger TiO2 structures (30-50 nm) is kinetically restricted while such effects were significantly less prominent for small particles (10 nm).
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The partition of energy flux in magnetic reconnection is examined experimentally using Cluster satellite observations of collisionless reconnection in Earth's magnetotail. In this plasma regime, the dominant component of the energy flux is ion enthalpy flux, with smaller contributions from the electron enthalpy and heat flux and the ion kinetic energy flux. However, the Poynting flux is not negligible, and in certain parts of the ion diffusion region the Poynting flux in fact dominates. Evidence for earthward-tailward asymmetry is ascribed to the presence of Earth's dipole fields.