Miracle-dz/UniFAR-FTUs huggingface dataset:
Role of serum S100B as an early predictor of high intracranial pressure and mortality in brain injury: A pilot study

ObjectiveTo investigate whether serum S100B is suitable as a sensitive biomarker for early prediction of increased intracranial pressure and mortality rates after brain injury. DesignA prospective, longitudinal study. SettingNeurosurgical intensive care unit. PatientsTwenty-one patients with acute brain injury and 13 healthy controls. InterventionsNone. Measurements and Main ResultsWe assessed Glasgow Coma Scale score and pupil reaction on admission and quantified serum S100B (in-house enzyme-linked immunosorbent assay) and intracranial pressure on admission and the subsequent 6 days. Serum S100B concentrations on admission and day 1 were significantly higher in patients with fatal outcome (p < .05, p < .01, respectively), with a sensitivity of 100% and a specificity of 75–83%. Patients with high serum S100B on admission had an eight-fold and on day 1 a 12-fold increased relative risk of a fatal outcome. Subsequent serum S100B values predicted the development of high intracranial pressure in patients with traumatic brain injury (p < .01). Patients with high intracranial pressure on day 5 had an 11-fold and on day 6 a nine-fold increased risk of fatal outcome. ConclusionsSerum S100B is a sensitive biomarker for early prediction of the development of high intracranial pressure and fatal outcome following acute brain injury. Monitoring S100B concentrations could contribute to early detection of patients at risk of secondary increases in intracranial pressure and subsequent mortality. This would allow earlier targeting of therapy in selected patients.
Genetic analysis of the psychomotor stimulant effect of ethanol

Genetic influences on the psychomotor stimulant effect of ethanol may be a key feature of abuse liability. While earlier work has shown the activational effects of ethanol to be under the influence of a relatively uncomplicated additive genetic system, preliminary data from our laboratory suggested the possibility of nonadditive genetic variance. In the present study, a full Mendelian cross was conducted to further characterize gene action and search for quantitative trait loci (QTL) influencing the psychomotor stimulant properties of ethanol. We tested 3062 mice of the six Mendelian cross genotypes (P1, P2, F1, F2, BC1 and BC2) derived from a cross between the C57BL/6J (B6) and C3H/HeJ (C3H) inbred strains of mice. On day 1, mice were injected with saline, put in a holding cage for 5 min, then placed in an activity monitor for 5 min. On day 2, mice were injected with 1.5 g/kg ethanol, and activity again monitored for 5 min. Analysis showed the expected activation in the C3H strain and little activation in the B6 strain, with no effect of sex. Biometrical genetic analysis showed a best‐fit model that included the mean (m), additive effect (a), and an epistatic parameter (i = homozygote by homozygote interaction). Analysis showed good evidence for QTL on chromosomes 1 (logarithm of odds (LOD) 3.4–7.5, 88–100 cM), 6 (LOD 9.1–10.4, 46–50 cM) and 15 (LOD 7.3–8.8, 28–32 cM). While the regions on chromosomes 1 and 6 have previously been implicated in several different ethanol‐related phenotypes, this is the first report of a QTL influencing the psychomotor stimulant properties of ethanol on chromosome 15. Other studies have identified QTL in this region of chromosome 15 mediating locomotor activation caused by other psychostimulants, including cocaine, amphetamine and phencyclidine.
The Brachyury gene encodes a novel DNA binding protein.

Brachyury (T) mutant embryos are deficient in mesoderm formation and do not complete axial development. The notochord is most strongly affected. The T gene is expressed transiently in primitive streak‐derived nascent and migrating mesoderm cells and continuously in the notochord. Ectopic expression of T protein in the animal cap of Xenopus embryos results in ectopic mesoderm formation. The T protein is located in the nucleus. These and other data suggested that the T gene might be involved in the control of transcriptional regulation. In an attempt to demonstrate specific DNA binding of the T protein we have identified a consensus sequence among DNA fragments selected from a mixture of random oligomers. Under our experimental conditions T protein binds as a monomer to DNA. This property resides in the N‐terminal domain of 229 amino acid residues which is strongly conserved between the mouse protein, and its Xenopus and zebrafish homologues. The latter proteins also recognize the consensus DNA binding site. We suggest that the T protein is involved in the control of genes required for mesoderm formation, and for the differentiation and function of chorda mesoderm.
Review: Dietary Flavonoids and Cancer Risk: Evidence From Human Population Studies

Abstract: High dietary intake of fruits and vegetables is consistently associated with a reduced risk of common human cancers, including cancers of the lung, breast, prostate, and colon. It is unknown which bioactive compound or compounds in plant foods provide the chemoprotective effects. One class of compounds currently under investigation is flavonoids, a large group of compounds with similar structure, consisting of two phenolic benzene rings linked to a heterocyclic pyran or pyrone. Although there are numerous in vitro and animal model data suggesting that flavonoids influence important cellular and molecular mechanisms related to carcinogenesis, such as cell cycle control and apoptosis, there are limited data from human population studies. This article reviews data from four cohort studies and six case-control studies, which have examined associations of flavonoid intake with cancer risk. There is consistent evidence from these studies that flavonoids, especially quercetin, may reduce the risk of lung cancer. Further research using new dietary databases for food flavonoid content is needed to confirm these findings before specific public health recommendations about flavonoids can be formulated.
Human population studies with cytogenetic biomarkers: Review of the literature and future prospectives

Cytogenetic biomarkers are by far the most frequently used endpoints in human population studies. Their sensitivity for measuring exposure to genotoxic agents and their role as early predictors of cancer risk have contributed to this success. In this article, we present an overview of the last 25 years of population studies with cytogenetic biomarkers, describing the evolution of this research and addressing the most promising innovations for the future. The evaluation has been restricted to the most popular assays, i.e., chromosomal aberrations (CAs) and micronucleus (MN), which are considered to be causally related to early stages of chronic diseases, especially cancer, and may therefore play a major role in prevention. An extensive literature search covering the period 1 January 1980 to 31 December 2003 was performed using the Medline/PubMed database. A total of 833 population studies using CAs and 434 using matched MN inclusion criteria were included in the analysis. We report the distribution of selected papers by year of publication, country, language, agents investigated, and methods employed. The state of the art and future prospects regarding cytogenetic techniques and epidemiologic and statistical methods are discussed. The role of susceptibility and its potential impact on genotoxic damage are discussed with special attention to the effect of major genetic polymorphisms on the baseline frequency of CAs and micronuclei. Environ. Mol. Mutagen. , 2005. © 2005 Wiley‐Liss, Inc.
Modeling SCMA in D2D underlaid cellular network

Sparse code multiple access (SCMA) has been recently proposed as an efficient multiple access scheme, which allows non-orthogonal spectrum resource sharing and enables system overloading. In this paper, we apply SCMA into device-to-device (D2D) communication underlaid cellular network, targeting at using the overload feature of SCMA to increase device connectivity and expand network capacity. In particular, we develop a stochastic geometry based framework to analyze the influence of SCMA on the signal-to-interference ratio (SIR) statistics of a typical cellular uplink and a typical D2D link. Based on the results, we analytically compare SCMA with orthogonal frequency-division multiple access (OFDMA) using area spectral efficiency (ASE) and quantify the closed-form ASE gain of SCMA over OFDMA. Notably, it is numerically shown that system ASE can be significantly improved using SCMA, asymptotically 38% increase over OFDMA under typical system settings. In addition, we enable interference management by allowing D2D users to use slotted ALOHA and derive the optimal multiple access probability (MAP) in order to maximize the proportional fairness utility function. The results are helpful in the implementation of SCMA in D2D underlaid cellular network.
Autophagy genes function in apoptotic cell corpse clearance during C. elegans embryonic development

Efficient apoptotic corpse clearance is essential for metazoan development and adult tissue homeostasis. Several autophagy proteins have been previously shown to function in apoptotic cell clearance; however, it remains unknown whether autophagy genes are essential for efficient apoptotic corpse clearance in the developing embryo. Here we show that, in Caenorhabditis elegans embryos, loss-of-function mutations in several autophagy genes that act at distinct steps in the autophagy pathway resulted in increased numbers of cell corpses and delayed cell corpse clearance. Further analysis of embryos with a null mutation in bec-1, the C. elegans ortholog of yeast VPS30/ATG6/mammalian beclin 1 (BECN1), revealed normal phosphatidylserine exposure on dying cells. Moreover, the corpse clearance defects of bec-1(ok691) embryos were rescued by BEC-1 expression in engulfing cells, and bec-1(ok691) enhanced corpse clearance defects in nematodes with simultaneous mutations in the engulfment genes, ced-1, ced-6 or ced-12. Together, these data demonstrate that autophagy proteins play an important role in cell corpse clearance during nematode embryonic development, and likely function in parallel to known pathways involved in corpse removal.
Sclerosing Epithelioid Fibrosarcoma: A Study of 16 Cases and Confirmation of a Clinicopathologically Distinct Tumor

Sclerosing epithelioid fibrosarcoma (SEF) is an uncommon tumor of deep soft tissues, originally described in 1995 by Meis–Kindblom et al. In the current study, the authors identified 16 cases of SEF in the pathology files of their institutions and studied their pathologic features and disease course. The group consisted of six male and 10 female patients (age range, 14–55 years; mean age, 40 years), and the tumors were located in a limb or limb girdle (n = 7), base of the penis (n = 1), back or chest wall (n = 3), and head and neck (n = 5). Tumor size ranged from 3.7 to 22 cm (mean, 8.9 cm). Histologically, the SEFs were composed predominantly of small to moderate-size round to ovoid, relatively uniform cells, often with clear cytoplasm, embedded in a hyalinized fibrous stroma. The only consistent immunohistochemical finding was a strong, diffuse reactivity of tumor cells for vimentin. Ultrastructural analysis performed in eight cases confirmed their fibroblastic nature. Bone invasion and tumor necrosis, features not reported before, were found in six cases each. Treatment consisted of intralesional excision (n = 2), attempted wide local excision (n = 11), and amputation (n = 3), with either adjuvant radiation therapy (n = 9) or chemotherapy (n = 3). Follow-up of at least 1 year in 14 cases revealed persistent disease or local recurrence in seven patients (50%), and distant metastasis in 12 patients (86%). Eight patients (57%) died of disease 16 to 86 months after diagnosis. Five patients were alive with disease as of last follow-up. SEF shares some pathologic features with two other fibrosing fibrosarcomas, low-grade fibromyxoid sarcoma and hyalinizing spindle cell tumor with giant rosettes, but in the authors' experience behaves clinically as a fully malignant sarcoma.
Magnétisme, activité et interactions magnétosphériques dans les systèmes étoile/planète géante proche

Les planetes extrasolaires en orbite proche (Jupiter chauds ou Pegasides) sont soumises a de fortes interactions avec leur etoile: rayonnement, effets gravitationnels, flot de particules, champ magnetique. La planete, baignee dans le champ magnetique de son etoile tout au long de son orbite, peut declencher des reactions en retour sur son etoile, qui se manifesteraient par exemple par une activite photospherique induite ou une influence sur le champ magnetique stellaire par interactions de maree. Au cours de cette these, le suivi en spectropolarimetrie d'un echantillon d'etoiles hotes de Jupiter chaud m'a permis d'etudier la structure et l'evolution de leur champ magnetique par imagerie Zeeman-Doppler. Les etoiles etudiees montrent des caracteristiques magnetiques similaires celles des etoiles froides sans Jupiter chaud. Mais pour la premiere fois, un cycle magnetique a ete observe pour une autre etoile que le Soleil. Compare au cycle magnetique solaire, ce cycle est accelere, suggerant que la planete pourrait influencer l'etoile. J'ai egalement explore un deuxieme moyen d'etude de l'influence planetaire sur l'etoile: l'activite stellaire. En plus de ce travail observationnel, j'ai etudie le champ magnetique dans la couronne stellaire, par extrapolation des magnetogrammes de surface. J'ai pu calculer ainsi le budget energetique au niveau de la planete, un ingredient essentiel dans la prediction de l'emission radio exoplanetaire effectue pendant cette these.
Synthetic recombinant bat SARS-like coronavirus is infectious in cultured cells and in mice

Defining prospective pathways by which zoonoses evolve and emerge as human pathogens is critical for anticipating and controlling both natural and deliberate pandemics. However, predicting tenable pathways of animal-to-human movement has been hindered by challenges in identifying reservoir species, cultivating zoonotic organisms in culture, and isolating full-length genomes for cloning and genetic studies. The ability to design and recover pathogens reconstituted from synthesized cDNAs has the potential to overcome these obstacles by allowing studies of replication and pathogenesis without identification of reservoir species or cultivation of primary isolates. Here, we report the design, synthesis, and recovery of the largest synthetic replicating life form, a 29.7-kb bat severe acute respiratory syndrome (SARS)-like coronavirus (Bat-SCoV), a likely progenitor to the SARS-CoV epidemic. To test a possible route of emergence from the noncultivable Bat-SCoV to human SARS-CoV, we designed a consensus Bat-SCoV genome and replaced the Bat-SCoV Spike receptor-binding domain (RBD) with the SARS-CoV RBD (Bat-SRBD). Bat-SRBD was infectious in cell culture and in mice and was efficiently neutralized by antibodies specific for both bat and human CoV Spike proteins. Rational design, synthesis, and recovery of hypothetical recombinant viruses can be used to investigate mechanisms of transspecies movement of zoonoses and has great potential to aid in rapid public health responses to known or predicted emerging microbial threats.
Phosphatidylinositol system's role in serotonin-induced facilitation at the crayfish neuromuscular junction.

1. In a crustacean neuromuscular preparation, the walking leg opener muscle of the freshwater crayfish Procambarus clarkii, application of serotonin (1 microM) produces presynaptic depolarization and long-lasting facilitation of excitatory postsynaptic potentials (EPSPs). The frequency of spontaneously released transmitter quanta also increases. Facilitation of evoked EPSPs declines after serotonin application in two phases. 2. Serotonin-induced facilitation was examined using simultaneous pre- and postsynaptic intracellular microelectrode recording. A presynaptic microelectrode recorded action potentials and membrane potential of a presynaptic axonal branch, and one or more postsynaptic microelectrodes recorded EPSPs in muscle fibers innervated by the excitatory motor axon. Components of the phosphatidylinositol second messenger system and pharmacologic agents affecting this system were injected through the presynaptic electrode, and changes in synaptic transmission were measured. 3. Presynaptic injection of inositol 1,4,5-triphosphate (IP3) causes presynaptic depolarization, increases the frequency of spontaneously released transmitter quanta, and promotes a relatively short-lasting facilitation of evoked EPSPs. These actions are consistent with elevation of intracellular Ca2+ and resemble the early phase of serotonin-induced facilitation. 4. Application of a phorbol ester, 12-O-tetradecanoyl-phorbol-13-acetate (TPA), that activates protein kinase C (C-kinase), produces a long-lasting, low-level facilitation of evoked EPSPs. Application of another phorbol ester, phorbol-12-monoacetate (PTMA), which does not activate C-kinase has no effect. 5. Presynaptic injection of RA 233, a phospholipase C (PLP-C) inhibitor, blocks all aspects of serotonin-induced facilitation. This compound was found to have no general deleterious effects on synaptic transmission and does not block other forms of synaptic facilitation in this preparation. (ABSTRACT TRUNCATED AT 250 WORDS)
Rescue of Cardiomyopathy in Peroxisome Proliferator-Activated Receptor-α Transgenic Mice by Deletion of Lipoprotein Lipase Identifies Sources of Cardiac Lipids and Peroxisome Proliferator-Activated Receptor-α Activators

Background— Emerging evidence in obesity and diabetes mellitus demonstrates that excessive myocardial fatty acid uptake and oxidation contribute to cardiac dysfunction. Transgenic mice with cardiac-specific overexpression of the fatty acid–activated nuclear receptor peroxisome proliferator-activated receptor-α (myosin heavy chain [MHC]-PPARα mice) exhibit phenotypic features of the diabetic heart, which are rescued by deletion of CD36, a fatty acid transporter, despite persistent activation of PPARα gene targets involved in fatty acid oxidation. Methods and Results— To further define the source of fatty acid that leads to cardiomyopathy associated with lipid excess, we crossed MHC-PPARα mice with mice deficient for cardiac lipoprotein lipase (hsLpLko). MHC-PPARα/hsLpLko mice exhibit improved cardiac function and reduced myocardial triglyceride content compared with MHC-PPARα mice. Surprisingly, in contrast to MHC-PPARα/CD36ko mice, the activity of the cardiac PPARα gene regulatory pathway is normalized in MHC-PPARα/hsLpLko mice, suggesting that PPARα ligand activity exists in the lipoprotein particle. Indeed, LpL mediated hydrolysis of very-low-density lipoprotein activated PPARα in cardiac myocytes in culture. The rescue of cardiac function in both models was associated with improved mitochondrial ultrastructure and reactivation of transcriptional regulators of mitochondrial function. Conclusions— MHC-PPARα mouse hearts acquire excess lipoprotein-derived lipids. LpL deficiency rescues myocyte triglyceride accumulation, mitochondrial gene regulatory derangements, and contractile function in MHC-PPARα mice. Finally, LpL serves as a source of activating ligand for PPARα in the cardiomyocyte.
The concept of sporadic cerebral small vessel disease: A road map on key definitions and current concepts

Sporadic cerebral small vessel disease is considered to be among the most common known neuropathological processes and has an important role in stroke, cognitive impairment, and functional loss in elderly persons. The term is now commonly used to describe a range of neuroimaging, neuropathological, and associated clinical features, the pathogenesis of which is largely unclear but that are thought to arise from disease affecting the perforating cerebral arterioles, capillaries, and venules. Modern neuroimaging has revolutionized our understanding of the consequences of small vessels disease on the brain parenchyma, even though small arteries, arterioles, capillaries, and venules are difficult to be directly visualized with current techniques used in clinical practice. In this short review, we focus on histopathological and neuroimaging perspectives, basic definitions, and recent advances in the field.
The simplified papilla preservation flap in the regenerative treatment of deep intrabony defects: clinical outcomes and postoperative morbidity.

BACKGROUND The aims of the present multi-center, randomized, controlled clinical trial were: 1) to compare the efficacy of the simplified papilla preservation flap with and without a barrier membrane in deep intrabony defects; 2) to evaluate the postoperative morbidity and surgical complications; and 3) to preliminarily test the impact of baseline tooth mobility on clinical outcomes. METHODS This parallel group, randomized, multi-center, controlled clinical trial involved 112 patients in 8 periodontal practices in 4 countries. A deep intrabony defect in each patient was accessed with the simplified papilla preservation flap. In the test defects, a bioabsorbable membrane was positioned. Patients' experiences with the surgical procedure and postoperative period were evaluated with a questionnaire. Clinical outcomes included clinical attachment level (CAL) and probing depth (PD) changes. RESULTS Complete observations were available for 55 test and 54 control defects. CAL gains at 1 year were 3.5 +/- 2.1 mm in the guided tissue regeneration (GTR) group and 2.6 +/- 1.8 mm in the control group (P = 0.0117). CAL gains > or = 4 mm were observed in 50.9% of GTR sites and 33.3% of control sites. A significant center effect of 2.1 mm was observed (P= 0.01). Initial PD (P= 0.01) and baseline tooth mobility (P= 0.036) were significant covariates. During the procedure, 30.4% of test and 28.6% of controls reported feeling moderate pain, and subjects estimated the hardship of the procedure at 24 +/- 25 visual analog scale (VAS) units in the test group, and at 22 +/- 23 VAS in controls. In terms of the investigated outcomes, differences between test and control groups were not statistically significant. Among the postoperative complications, edema was most prevalent at week 1, and more frequently associated with the test treatment (P= 0.01). In the test group, 53.6% of membranes were exposed at week 3. CONCLUSIONS The present study further supports the added benefits of guided tissue regeneration with respect to access flap alone in the treatment of deep intrabony defects, as well as the general efficacy of GTR in different clinical settings. Furthermore, our study indicates a possible influence of baseline tooth mobility on clinical outcomes.