619 research outputs found

    Quantification of tectonic controls on the distribution and architecture of deep-water facies during the growth of the toe-thrusts region of the Niger Delta

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    Using 3D seismic data, the deep-water fold and thrust belt of the southern lobe of the Niger Delta has been investigated over an area of 4500 km2 to document, for the first time, the detailed growth history of a thrust array and how it controlled the distribution and architecture, through time, of the coeval deep-water sedimentary systems. Quantification of the growth of each structure has been achieved using line-length balancing and yielded measures of cumulative shortening and strain, and their evolving rates, along and across strike and through time. This has enabled a new model for thrust growth to be proposed and linked to the observed change in stratigraphic architecture. The results show that all thrusts nucleated coevally in the study area as small segments, deforming at low strain rates, which caused the deflection of early leveed channels. The progressive lateral propagation and linkage of the segments, along with an increase in strain rates, caused the spatial restriction of the slope channels, until it induced the deposition of ponded lobes and the alteration of the channel architectures into erosional forms. The later decrease in strain rates and smoothing of the topography linked to the deposition of channelized sheets within shallow-ponded basins. These observations lead to the development of a predictive facies model where the occurrence of a specific facies (the architecture) is explained depending on when and where (along strike) a channel (or flow) interacts with a given fold. The specific location where channels cross structures, in turn, is dictated by how deformation is partitioned between structures across-strike, and by the particular distribution of strain rates along-strike. Distribution and architecture are effectively two linked variables which depend on a set of evolving parameters during the growth of a thrust array; the cumulative strain, strain rates and degree of fault linkage.Open Acces

    A Lucky Mistake: The Splenic Glands of Marcello Malpighi

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    PURPOSE OF THE REVIEW: More than 50% of all gynaecological cancers can be classified as rare tumours (defined as an annual incidence of <6 per 100,000) and such tumours represent an important challenge for clinicians. RECENT FINDINGS: Rare cancers account for more than one fifth of all new cancer diagnoses, more than any of the single common cancers alone. Reviewing the RARECAREnet database, some of the tumours occur infrequently, whilst others because of their natural history have a high prevalence, and therefore appear to be more common, although their incidence is also rare. Harmonization of medical practice, guidelines and novel trials are needed to identify rare tumours and facilitate the development of new treatments. Ovarian tumours are the focus of this review, but we comment on other rare gynaecological tumours, as the diagnosis and treatment challenges faced are similar. FUTURE: This requires European collaboration, international partnerships, harmonization of treatment and collaboration to overcome the regulatory barriers to conduct international trials. Whilst randomized trials can be done in many tumour types, there are some for which conducting even single arm studies may be challenging. For these tumours alternative study designs, robust collection of data through national registries and audits could lead to improvements in the treatment of rare tumours. In addition, concentring the care of patients with rare tumours into a limited number of centres will help to build expertise, facilitate trials and improve outcomes

    BoltzWann: A code for the evaluation of thermoelectric and electronic transport properties with a maximally-localized Wannier functions basis

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    We present a new code to evaluate thermoelectric and electronic transport properties of extended systems with a maximally-localized Wannier function basis set. The semiclassical Boltzmann transport equations for the homogeneous infinite system are solved in the constant relaxation-time approximation and band energies and band derivatives are obtained via Wannier interpolations. Thanks to the exponential localization of the Wannier functions obtained, very high accuracy in the Brillouin zone integrals can be achieved with very moderate computational costs. Moreover, the analytical expression for the band derivatives in the Wannier basis resolves any issues that may occur when evaluating derivatives near band crossings. The code is tested on binary and ternary skutterudites CoSb_3 and CoGe_{3/2}S_{3/2}.Comment: 19 pages, 7 figure

    Engineering polar discontinuities in honeycomb lattices

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    Unprecedented and fascinating phenomena have been recently observed at oxide interfaces between centrosymmetric cubic materials, such as LaAlO3_3 and SrTiO3_3, where a polar discontinuity across the boundary gives rise to polarization charges and electric fields that drive a metal-insulator transition, with the appearance of free carriers at the interface. Two-dimensional analogues of these systems are possible, and honeycomb lattices could offer a fertile playground, thanks to their versatility and the extensive on-going experimental efforts in graphene and related materials. Here we suggest different realistic pathways to engineer polar discontinuities across interfaces between honeycomb lattices, and support these suggestions with extensive first-principles calculations. Two broad approaches are discussed, that are based on (i) nanoribbons, where a polar discontinuity against the vacuum emerges, and (ii) selective functionalizations, where covalent ligands are used to engineer polar discontinuities by selective or total functionalization of the parent system. All the cases considered have the potential to deliver innovative applications in ultra-thin and flexible solar-energy devices and in micro- and nano-electronics.Comment: 12+epsilon pages, 6 figure

    The role of histology in the study of tumor cell metabolism: the TRAP1 paradigm

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    Background. Metabolic reprogramming is a key feature of neoplastic transformation and mitochondria are the most important organelles in such oncogenic process. Recent evidence suggests that TRAP1 is a key player in tumor-related metabolic rewiring. Most studies have addressed TRAP1- related oncogenesis by in vitro and in vivo analyses. Little is however known on the possible contribution of histology to such studies. Study aims. This study assessed the role of histology in the study of TRAP1-related metabolic reprogramming. Specifically, it aimed: (i) to integrate the results of in vitro and in vivo studies with the histological analysis of tumor samples; (ii) to verify the correspondence between primary human neoplasms and animal tumor models; (iv) to identify novel fields for the study of TRAP1-related oncogenic cascades. Materials and methods. This project considered the following neoplastic settings: (i) neurofibromatosis type 1 (NF1)-related benign and malignant nerve sheath tumors; and (ii) germinal center (GC)-derived lymphoproliferative disorders. For the NF1-related tumors, morphological analysis and phenotypic characterization (TRAP1, HIF1a and related metabolic markers) were performed on: (i) human samples of plexiform neurofibroma (PN) and malignant nerve sheath tumors (MPNST); (ii) engineered mouse models of NF1-related neoplasms; and (iii) xenografts of MPNST. For GC-derived lymphomas, TRAP1 expression was assessed in non-neoplastic lymphoid tissues and in Burkitt lymphoma (BL), diffuse large B-cell lymphoma (DLBCL) and Hodgkin lymphoma (HL) samples. The immunohistochemical results were integrated with the results of in silico gene expression studies (Oncomine database). Results. Histological analysis of human PNs and MPNSTs documented the expression of TRAP1, HIF1a and downstream metabolic markers in both benign and malignant samples. A progressive increase in the positivity for such proteins was noted along the oncogenic cascade from nonneoplastic nerves to benign (PN) and malignant (MPNST) tumors. Similar expression patterns were observed in the animal tumor models. In this context, histological evaluation also proved instrumental: (i) to confirm the correspondence between human and animal tumors; (ii) to investigate the metastatic potential of MPNST xenografts; (iii) to detect the effects of TRAP1 knock-down on tumor cell growth and metabolic reprograming; and (iv) to highlight strongly versus minimally activated metabolic pathways in NF1-related oncogenic cascades. The histological characterization of reactive lymphoid tissues highlighted TRAP1 expression in subsets of GC blasts (i.e. differentiating immunoblasts and re-cycling centroblasts). The joint expression of TRAP1 and HIF1a in GC blasts confirmed the presence and activation of the TRAP1/HIF1a axis in GC physiology. In silico studies of GC-derived lymphomas showed very high TRAP1 mRNA levels in BL and (to a lesser extent) DLBCL and HL. Immunohistochemical analysis of primary tumor samples confirmed the in silico results. Conclusions. Histological analysis contributes to the understanding of tumor metabolism and integrates the results of in vitro and in vivo biochemical studies. In particular, it confirms the relevance of TRAP1 activation in NF1-related peripheral nerve sheath tumors and discloses a tight correspondence between primary human samples and animal tumor models. Immunohistochemical characterization of reactive lymphoid tissues and primary lymphoma samples also identifies specific TRAP1 expression profiles, possibly subtending tumor-related metabolic networks

    The effects of hematopoietic stem cell transplant on splenic extramedullary hematopoiesis in patients with myeloproliferative neoplasm-associated myelofibrosis

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    Background/objective: Hematopoietic stem cell transplant (HSCT) is the only curative treatment for myeloproliferative neoplasm-associated myelofibrosis (MPN-MF). The main clinical manifestation of MPN-MF is splenomegaly secondary to extramedullary hematopoiesis (EMH). The effects of HSCT on splenic EMH and associated vascular and stromal changes are unknown. This study compares the findings seen in spleens following HSCT with those of nontransplanted patients, normal controls, and matched bone marrow (BM) samples. Methods: This study included three transplanted MPN-MF spleens, three nontransplanted MPN-MF spleens, and three normal controls. Spleens were assessed for: (a) presence/extent of EMH; (b) presence of Gamna–Gandy bodies; (c) splenic fibrosis; (d) CD34-positive microvessel density; (e) CD8-positive sinusoids; (f) frequency of smooth muscle actin-positive myoid cells; and (g) nerve growth factor receptor-positive adventitial reticulum cells. In two cases, matched BM samples were assessed for cellularity, presence of atypical megakaryocytes, and fibrosis. Results: Compared with normal controls, all MPN-MF spleens were larger in size, had EMH, red pulp fibrosis, higher CD34-positive microvessel density, and decreased CD8-positive sinusoids. Compared with nontransplanted cases, post-HSCT spleens showed disappearance or reduction of EMH. Gamna–Gandy bodies were increased; no differences in the remaining parameters were found. A reduction of splenic EMH was associated with normalization of BM cellularity and megakaryopoiesis. Conclusion: HSCT reduces/abrogates splenic EMH and is associated with an increased number of Gamna–Gandy bodies, which may suggest vascular damage. The lack of stromal changes in spleens removed shortly after transplant is in line with similar observations in the BM, where a longer interval is often necessary for resolution of fibrosis. Keywords: Hematopoietic stem cell transplant, Myelofibrosis, Myeloproliferative neoplasms, Splee

    Benign TdT-positive cells in pediatric and adult lymph nodes: a potential diagnostic pitfall

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    Benign TdT-positive cells have been documented in a variety of non-hematopoietic tissues. Scant data are however available on their presence in non-neoplastic lymph nodes. This study is aimed to: (i) characterize the presence/distribution of benign TdT-positive cells in pediatric and adult reactive lymph nodes; (ii) define the phenotype and nature of such elements. This retrospective study considered 141 reactive lymph nodes from pediatric and adult patients without history of neoplastic disease. TdT-positive cells were characterized by immunohistochemical and morphometric analyses and their presence was correlated with the clinical-pathological features. The nature of TdT-positive cells was investigated by: (i) double immunostaining for early lymphoid cell markers; and (ii) assessment of TdT expression in fetal lymph nodes. Sparse TdT-positive cells were documented in all pediatric cases and in most (76%) adult lymph nodes. TdT-positive cell density was higher in children than adults (15.9/mm2 versus 8.6/mm2; P<.05). TdT positivity did not correlate with any clinical and histological parameter and double immunostaining disclosed a phenotype compatible with early lymphoid precursors (positivity for CD34, CD10 and variable expression of CD7). A very high TdT-positive cell density (802.4/mm2) was reported in all fetal lymph nodes. In conclusion, TdT-positive cells are a common finding in pediatric and adult lymph nodes. The interstitial distribution and low number of such cells allows for the differential diagnosis with precursor lymphoid neoplasms. The high density in fetal lymph nodes and the phenotype of such cells suggest their belonging to an immature lymphoid subset gradually decreasing with age

    Protein kinase CK2 is widely expressed in follicular, Burkitt and diffuse large B-cell lymphomas and propels malignant B-cell growth.

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    Serine-threonine kinase CK2 is highly expressed and pivotal for survival and proliferation in multiple myeloma, chronic lymphocytic leukemia and mantle cell lymphoma. Here, we investigated the expression of \u3b1 catalytic and \u3b2 regulatory CK2 subunits by immunohistochemistry in 57 follicular (FL), 18 Burkitt (BL), 52 diffuse large B-cell (DLBCL) non-Hodgkin lymphomas (NHL) and in normal reactive follicles. In silico evaluation of available Gene Expression Profile (GEP) data sets from patients and Western blot (WB) analysis in NHL cell-lines were also performed. Moreover, the novel, clinical-grade, ATP-competitive CK2-inhibitor CX-4945 (Silmitasertib) was assayed on lymphoma cells. CK2 was detected in 98.4% of cases with a trend towards a stronger CK2\u3b1 immunostain in BL compared to FL and DLBCL. No significant differences were observed between Germinal Center B (GCB) and non-GCB DLBCL types. GEP data and WB confirmed elevated CK2 mRNA and protein levels as well as active phosphorylation of specific targets in NHL cells. CX-4945 caused a dose-dependent growth-arresting effect on GCB, non-GCB DLBCL and BL cell-lines and it efficiently shut off phosphorylation of NF-\u3baB RelA and CDC37 on CK2 target sites. Thus, CK2 is highly expressed and could represent a suitable therapeutic target in BL, FL and DLBCL NHL

    6G to Take the Digital Divide by Storm: Key Technologies and Trends to Bridge the Gap

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    The pandemic caused by COVID-19 has shed light on the urgency of bridging the digital divide to guarantee equity in the fruition of different services by all citizens. The inability to access the digital world may be due to a lack of network infrastructure, which we refer to as service-delivery divide, or to the physical conditions, handicaps, age, or digital illiteracy of the citizens, that is mentioned as service-fruition divide. In this paper, we discuss the way how future sixth-generation (6G) systems can remedy actual limitations in the realization of a truly digital world. Hence, we introduce the key technologies for bridging the digital gap and show how they can work in two use cases of particular importance, namely eHealth and education, where digital inequalities have been dramatically augmented by the pandemic. Finally, considerations about the socio-economical impacts of future 6G solutions are drawn
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