Miracle-dz/UniFAR-FTUs huggingface dataset:
Assessment of Left Ventricular Enlargement at Multidetector Computed Tomography

Purpose Because left ventricular (LV) enlargement (LVE) is indicative of an array of cardiac pathologies, including cardiomyopathic, ischemic, and valvular heart diseases, it is important to recognize it early in the course of these diseases. The recognition of LVE on nongated contrast-enhanced computed tomography (CT) scans should be facilitated by the availability of a dimensional index. To our knowledge, no CT index of LVE has been proposed. Therefore, the study aimed to define whether the maximum LV diameter (LVd) measured on nongated multidetector computed tomography can identify LVE when referencing echocardiography as the diagnostic standard. Materials and Methods The patient population consisted of 438 consecutive patients who had a contrast-enhanced, nongated 16- or 64-detector CT of the chest for evaluation of pulmonary embolism or aortic dissection between January 2006 and March 2008. One hundred fifty-five patients in this group also had an echocardiogram within 2 months of the CT study. The maximum LV cavity size, septal to lateral wall dimension, was measured perpendicularly to the long axis of the left ventricle on the axial CT scans by 2 observers blinded to the echocardiography data. An receiver operating characteristic analysis was performed to identify a highly specific cutoff for the diagnosis of LVE on CT, using echocardiogram as the standard of reference. Interobserver agreement was assessed using Bland-Altman analysis. Results A total of 84 females and 71 males were evaluated (female to male ratio of 1.09). The mean age for the 155 patients was 58 years. Six percent of these patients had a diagnosis of LVE on 2-dimensional echocardiography. The mean (SEM) LV internal diameter at nongated multidetector computed tomography between the group with normal LV and the group with LVE by echocardiography was 4.4 (0.7) cm for the normal LV and 5.9 (1.2) cm for the dilated LVs (P < 0.0001). With the use of threshold value of LVd of 5.6 cm, a sensitivity of 78%, specificity of 100%, positive likelihood ratio of 113.5, and negative likelihood ratio of 0.22 were calculated. The LVd measurements had an excellent agreement between observers on the Bland-Altman analysis. Conclusions Left ventricular enlargement can be reliably identified on nongated contrast-enhanced multidetector CT when the maximum luminal diameter of the LV is greater than 5.6 cm. Nongated contrast-enhanced CT scan can be used to recognize LVE.
Epithelial Sodium Channels in Pulmonary Epithelial Progenitor and Stem Cells

Regeneration of the epithelium of mammalian lungs is essential for restoring normal function following injury, and various cells and mechanisms contribute to this regeneration and repair. Club cells, bronchioalveolar stem cells (BASCs), and alveolar type II epithelial cells (ATII) are dominant stem/progenitor cells for maintaining epithelial turnover and repair. Epithelial Na+ channels (ENaC), a critical pathway for transapical salt and fluid transport, are expressed in lung epithelial progenitors, including club and ATII cells. Since ENaC activity and expression are development- and differentiation-dependent, apically located ENaC activity has therefore been used as a functional biomarker of lung injury repair. ENaC activity may be involved in the migration and differentiation of local and circulating stem/progenitor cells with diverse functions, eventually benefiting stem cells spreading to re-epithelialize injured lungs. This review summarizes the potential roles of ENaC expressed in native progenitor and stem cells in the development and regeneration of the respiratory epithelium.
Influence of epithelio‐mesenchymal interactions on tumor induction by polyoma virus

Submandibular salivary glands (strain C3H/Bi mice), at stages of development ranging from prerudimentary condition through full development, were tested for their capacity to give rise to tumors after infection with polyoma virus (PV). Responsiveness was judged on the basis of (1) morphologic transformation in organotypic culture, and (2) the development of tumors within PV‐infected transplants to syngeneic newborn hosts.
Ki-67 immunostaining and stereologic estimation of nuclear volume in melanocytic skin tumors.

OBJECTIVE To investigate the proliferative activity and mean nuclear volume (MNV) of melanocytic skin tumors. STUDY DESIGN Proliferative activity, assessed by immunostaining for the Ki-67 monoclonal antibody (reactive with all actively cycling cells), and MNV, estimated by means of a stereologic method, were determined in 60 cutaneous melanocytic tumors, including 28 primary malignant melanomas (PMM), 13 compound nevi (CN), 11 dysplastic nevi and 8 metastatic malignant melanomas. RESULTS Both MNV and Ki-67 expression differed significantly between CN and other melanocytic tumors and showed a good correlation with Clark's level (a well-established prognostic parameter in PMM). CONCLUSION The association of proliferative activity and quantitative nuclear features may be helpful in the interpretation of the degree of malignancy in melanocytic skin tumors.
Theory of the perpendicular magnetoresistance in magnetic multilayers.

In the talk presented by one of us (AF) at Cargese, the mechanisms of the giant magnetoresistance (MR) in magnetic multilayers were discussed very generally for both the CIP (current in plane) and CPP (current perpendicular to the planes) geometries. A so general discussion would be too long for these proceedings and the present paper will be restricted to the CPP case. We present the theoretical model that we have recently worked out [1,2] and discuss its application to experimental data obtained for the Ag/Co and Cu/Co systems at Michigan State University [3,4,5] and presented at Cargese by Pr. P.A. Schroeder [6]. We describe the specific fundamental problems related to the spin accumulation effects occuring in the CPP geometry and we calculate the magnetoresistance. The expressions of the MR become relatively simple in the limit where the layer thicknesses are much smaller than the spin diffusion length and we justify the analysis of experimental results developed at Michigan State University [3–6]. We also relate our theory to those of Johnson et al [7,8], van Son et al [9] and Zhang and Levy [10]. Of course, it is not in the scope of the present paper to develop calculations presented elsewhere in detail [1] and we will focus on the presentation of the basis of the model and the discussion of our results.
S-nitrosothiol chemistry at the single-molecule level.

Nitric oxide (NO) and its relatives (notably RSNO and HNO) perform important roles as regulatory molecules in health and disease. NO activates guanylate cyclase by binding to its ferrous heme (see the Supporting Information, Figure S1). The lifetime of NO is short, being milliseconds to seconds, and therefore it is unlikely that NO diffuses more than approximately 100 mm, which is in the range of a few cells, from the site at which it is generated. Through poorly understood mechanisms, 2] NO is also converted in vivo into small molecule and protein S-nitrosothiols (RSNOs). RSNOs modulate cellular activity in ways that differ from the direct action of NO. Furthermore, RSNO derivatives of albumin and hemoglobin are sufficiently long-lived to be transported in the circulation. In addition, NO is passed from one thiol to another by transnitrosation, which can be facilitated by specific protein–protein interactions, and protein function can be modulated by S nitrosation. Protein SNOs are also converted into other derivatives, such as S-glutathionylated proteins, thus generating a complex signaling web (Figure S1). RSNO also act as a source of HNO (nitroxyl), which is also a locally acting regulatory molecule with biological effects that differ from and even oppose those of NO. Although the actual effectors (NO, RSNO, HNO etc.) are not always clearly distinguished, NO has been implicated in numerous medical disorders beyond its well-known role in erectile function. Examples include disorders involving the cardiovascular system, neuronal cell death in trauma and disease, the immune system, and cancer. RSNOs and several agents that generate either NO or HNO are under development as therapeutic agents. 9, 12] Here, we have used the protein nanoreactor approach to examine RSNO chemistry at the single-molecule level. Reactant molecules are tethered within the lumen of a protein pore, staphylococcal a-hemolysin (aHL), and a non-perturbing current carried through the pore by aqueous ions registers changes in molecular structure that occur during bondmaking and bond-breaking events, thus revealing the kinetics of the steps involved in a series or cycle of reactions (Figure 1a). The technique is sufficiently sensitive to distinguish enantiomers or determine a deuterium isotope effect, and herein we show that the two atoms, -NO, in RSNO are readily detected. Clearly, it would not be possible to examine the single-molecule chemistry of RSNO in a meaningful way with bulky fluorescent reagents, the main alternative to our approach. We have investigated the lifetime of the proposed nitroxyl disulfide intermediate, RSN(O)SR , in transnitrosation, examined the competition between transnitrosation and S thiolation by S-nitrosoglutathione, and studied the reaction between RSNO and sulfite. The latter is especially relevant to the exacerbating effect in asthma of sulfite acting through the NO pathway. S-Nitrosoglutathione (GSNO) mediates cell signaling through transnitrosation, 18] which is the transfer of the
Diagnostic de systèmes complexes par comparaison de listes d’alarmes : application aux systèmes de contrôle du LHC

Au CERN (Organisation europeenne pour la recherche nucleaire), le controle et la supervision du plus grand accelerateur du monde, le LHC (Large Hadron Collider), sont bases sur des solutions industrielles (SCADA). Le LHC est compose de sous-systemes disposant d’un grand nombre de capteurs et d’actionneurs qui rendent la surveillance de ces equipements un veritable defi pour les operateurs. Meme avec les solutions SCADA actuelles, l’occurrence d’un defaut declenche de veritables avalanches d’alarmes, rendant le diagnostic de ces systemes tres difficile. Cette these propose une methodologie d’aide au diagnostic a partir de donnees historiques du systeme. Les signatures des defauts deja rencontres et representes par les listes d’alarmes qu’ils ont declenches sont comparees a la liste d’alarmes du defaut a diagnostiquer. Deux approches sont considerees. Dans la premiere, l’ordre d’apparition des alarmes n’est pas pris en compte et les listes d’alarmes sont representees par un vecteur binaire. La comparaison se fait a l’aide d’une distance ponderee. Le poids de chaque alarme est evalue en fonction de son aptitude a caracteriser chaque defaut. La seconde approche prend en compte l’ordre d’apparition des alarmes, les listes d’alarmes sont alors representees sous forme de sequences symboliques. La comparaison entre ces deux sequences se fait a l’aide d’un algorithme derive de l’algorithme de Needleman et Wunsch utilise dans le domaine de la Bio-Informatique. Les deux approches sont testees sur des donnees artificielles ainsi que sur des donnees extraites d’un simulateur tres realiste d’un des systemes du LHC et montrent de bons resultats.
Figure-ground image segmentation using genetic programming and feature selection

Figure-ground segmentation is an essential but difficult preprocessing step for many computer vision and image preprocessing tasks, such as object recognition. One challenge is to separate objects from backgrounds on images with high variations (e.g. in object shapes), which requires both effective feature sets and powerful segmentors. This paper develops a GP based segmentation method, which transforms segmentation tasks into pixel classification based problems. To control the complexity of evolved solutions, parsimony pressure is introduced in GP. Tested on two datasets with high variations (the Weizmann and Pascal datasets), the proposed method achieves similar performance in F\ score with much simpler solutions, compared with a reference GP based method that does not consider solution complexity. Moreover, it is the first time that the occurrence rates of the features used by the evolved solutions are studied to conduct feature selection for figure-ground segmentation. Compared with the whole feature set using traditional classifier based segmentation methods, the selected feature subsets can improve the segmentation performance. Moreover, analyses on the evolved solutions reveal how they function and why specific features are selected.
Immunohistochemical analysis of Smac/DIABLO expression in human carcinomas and sarcomas

Second mitochondria‐derived activator of caspases (Smac/DIABLO) is released from mitochondria into the cytosol during apoptosis, promoting caspase activation by neutralizing the inhibition of inhibitor of apoptosis proteins (IAPs) on caspases. Alteration of apoptosis is essential for cancer development, and cancer cell death by radiation and chemotherapy is largely dependent upon apoptosis. In this study, archival tissues of 100 carcinomas and 50 sarcomas from various origins were analyzed by immunohistochemistry for the expression of Smac/DIABLO. Smac/DIABLO immunoreactivity was seen in 62 of 100 (62%) carcinomas, including 42 of 60 stomach carcinomas, 7 of 10 colorectal carcinomas, 4 of 10 lung carcinomas, 7 of 10 ovarian carcinomas, and 2 of 10 prostate carcinomas. Smac/DIABLO is expressed in 11 of 50 (22%) sarcomas, including 2 of 8 malignant schwannomas, 5 of 11 rhabdomyosarcomas, 2 of 7 malignant fibrous histiocytomas, 1 of 6 leiomyosarcomas, 0 of 8 angiosarcomas, 0 of 8 liposarcomas, and 1 of 2 Ewing's sarcomas. These data demonstrated that Smac/DIABLO expression levels vary depending on the individual cancer types. Furthermore, the present study showed that many human cancers do not express Smac/DIABLO, and suggest that lack of Smac/DIABLO expression in the cancer cells may inhibit apoptosis, thereby promoting their survival.
M-COPA suppresses endolysosomal Kit-Akt oncogenic signalling through inhibiting the secretory pathway in neoplastic mast cells

Gain-of-function mutations in Kit receptor tyrosine kinase result in the development of a variety of cancers, such as mast cell tumours, gastrointestinal stromal tumours (GISTs), acute myeloid leukemia, and melanomas. The drug imatinib, a selective inhibitor of Kit, is used for treatment of mutant Kit-positive cancers. However, mutations in the Kit kinase domain, which are frequently found in neoplastic mast cells, confer an imatinib resistance, and cancers expressing the mutants can proliferate in the presence of imatinib. Recently, we showed that in neoplastic mast cells that endogenously express an imatinib-resistant Kit mutant, Kit causes oncogenic activation of the phosphatidylinositol 3-kinase-Akt (PI3K-Akt) pathway and the signal transducer and activator of transcription 5 (STAT5) but only on endolysosomes and on the endoplasmic reticulum (ER), respectively. Here, we show a strategy for inhibition of the Kit-PI3K-Akt pathway in neoplastic mast cells by M-COPA (2-methylcoprophilinamide), an inhibitor of this secretory pathway. In M-COPA-treated cells, Kit localization in the ER is significantly increased, whereas endolysosomal Kit disappears, indicating that M-COPA blocks the biosynthetic transport of Kit from the ER. The drug greatly inhibits oncogenic Akt activation without affecting the association of Kit with PI3K, indicating that ER-localized Kit-PI3K complex is unable to activate Akt. Importantly, M-COPA but not imatinib suppresses neoplastic mast cell proliferation through inhibiting anti-apoptotic Akt activation. Results of our M-COPA treatment assay show that Kit can activate Erk not only on the ER but also on other compartments. Furthermore, Tyr568/570, Tyr703, Tyr721, and Tyr936 in Kit are phosphorylated on the ER, indicating that these five tyrosine residues are all phosphorylated before mutant Kit reaches the plasma membrane (PM). Our study provides evidence that Kit is tyrosine-phosphorylated soon after synthesis on the ER but is unable to activate Akt and also demonstrates that M-COPA is efficacious for growth suppression of neoplastic mast cells.
Towards reversible QCA computers: Reversible gates and ALU

This work presents a novel implementation of reversible gates and reversible ALU, all based in quantum-dot cellular automata (QCA). QCA has been considered as an alternative for field-effect transistors due to its quite small size (nanometers), ultra-low power consumption and clock rate (terahertz range). On the other hand, reversible computation is a new paradigm where all logic operations can be performed in an invertible way. This feature is important to different technologies, such as quantum computing, adiabatic circuits, low power computation, etc. Regarding low power consumption, QCA has been seen as a promising technology for approaching the thermodynamic limit of computation and this work focus on designing a QCA reversible ALU in order to go beyond that limit, bridging the gap between QCA technology and reversible components. In a bottom-up approach, we first discuss QCA reversible gates and a few design choices. We also present the ALU's QCA design, demonstrate the functionality, test and validate the proposed architecture using QCADesigner simulator. Due to the importance of these new computational paradigms, this study is central in consolidating possible emerging technologies.
Estudio contrastivo inglés-español de la caracterización de sustantivos

Esta tesis presenta un analisis contrastivo ingles-espanol basado en datos obtenidos de corpues linguisticos informatizados. El trabajo versa sobre la funcion semantica de la caracterizacion de sustantivos, y trata de dilucidar cuales son los distintos recursos empleados por los hablantes nativos de las dos lenguas para la expresion de esta funcion. Las aplicaciones de los resultados revierten en la ensenanza de lenguas extranjeras y en el campo de la traduccion ingles-espanol. Se trata de un estudio teorico-descriptivo que sigue el modelo linguistico funcional (Bondarko 1991; Halliday 1994). Las herramientas de trabajo han sido el corpus cobuild para ingles y el CREA (Corpues de Referencia del Espanol Actual) para el espanol. El trabajo esta basado en una orientacion doble: onomasiologica, del contenido a la forma, y semasiologica, de la forma al contenido. El procedimiento de trabajo siguio diversas etapas: la seleccion de los datos, la descripcion de los mismos, la yuxtaposicion, y por ultimo, el contraste propiamente dicho, cuya finalidad es establecer equivalencias semantico-funcionales entre estas dos lenguas en la caracterizacion de sustantivos. Analizando 7882 concordancias de los sustantivos mas comunes en ingles y espanol pudimos extraer un total de 24 estructuras caracterizadoras en ingles y 16 en espanol. Posteriormente, un analisis semantico mas detallado nos permitio aislar 9 funciones semanticas distintas en ingles y 10 en espanol. , practicamente todas coincidentes. El estudio se centra en comparar la distinta distribucion de los recursos gramaticales de acuerdo con las funciones semanticas encontradas para establecer los campos semantico-funcionales de cada significado en ingles y espanol.
Parlez-vous VUS?

Human genome sequencing is routine and will soon be a staple in research and clinical genetics. However, the promise of sequencing is often just that, with genome data routinely failing to reveal useful insights about disease in general or a person's health in particular. Nowhere is this chasm between promise and progress more evident than in the designation, “variant of uncertain significance” (VUS). Although it serves an important role, careful consideration of VUS reveals it to be a nebulous description of genomic information and its relationship to disease, symptomatic of our inability to make even crude quantitative assertions about the disease risks conferred by many genetic variants. In this perspective, I discuss the challenge of “variant interpretation” and the value of comparative and functional genomic information in meeting that challenge. Although already essential, genomic annotations will become even more important as our analytical focus widens beyond coding exons. Combined with more genotype and phenotype data, they will help facilitate more quantitative and insightful assessments of the contributions of genetic variants to disease.
Glucocorticoid “Programming” and PTSD Risk

Abstract: Epidemiological data have linked an adverse fetal environment with increased risks of cardiovascular, metabolic, neuroendocrine, and psychiatric disorders in adulthood. Prenatal stress and/or glucocorticoid excess might underlie this link. In animal models, prenatal stress, glucocorticoid exposure or inhibition/knockout of 11ß‐hydroxysteroid dehydrogenase type 2 (11ß‐HSD‐2), the feto‐placental barrier to maternal glucocorticoids, reduces birth weight and causes permanent hypertension, hyperglycemia, increased hypothalamic‐pituitary‐adrenal (HPA) axis activity and behavior resembling of anxiety. In humans, 11ß‐HSD‐2 gene mutations cause low birth weight and placental 11ß‐HSD‐2 activity correlates directly with birth weight and inversely with infant blood pressure. Low birth weight babies have higher plasma cortisol levels throughout adult life, indicating HPA programming. In human pregnancy, severe maternal stress affects the offspring HPA axis and associates with neuropsychiatric disorders. Posttraumatic stress disorder (PTSD) appears to be a variable in the effects. Intriguingly, some of these effects appear to be ‘inherited’ into a further generation, itself unexposed to exogenous glucocorticoids at any point in the lifespan from fertilization, implying epigenetic marks persist into subsequent generation(s). Overall, the data suggest that prenatal exposure to excess glucocorticoids programs peripheral and CNS functions in adult life, predisposing to some pathologies, perhaps protecting from others, and these may be transmitted perhaps to one or two subsequent generations.
Performance of OpenDPI to identify truncated network traffic

The identification of the nature of the traffic flowing through a TCP/IP network is a relevant target for traffic engineering and security related tasks. Traditional methods based on port assignments are no longer valid due to the use of ephemeral ports and ciphering. Despite the privacy concerns it arises, Deep Packet Inspection (DPI) is one of the most successful current techniques. Nevertheless, the performance of DPI is strongly limited by computational issues related to the huge amount of data it needs to handle, both in terms of number of packets and the length of the packets. This paper addresses the sensitivity of OpenDPI, one of the most powerful freely available DPI systems, when truncation of the payloads of the monitored traffic is applied. The results show that it is highly dependent on the protocol being monitored.