Miracle-dz/UniFAR-FTUs huggingface dataset:
Carbonaceous molecules in the oxygen-rich circumstellar environment of binary post-AGB stars: ⋆

Context. The circumstellar environment of evolved stars is generally rich in molecular gas and dust. Typically, the entire environment is either oxygen-rich or carbon-rich, depending on the evolution of the central star. Aims. In this paper we discuss three evolved disc sources with evidence of atypical emission lines in their infrared spectra. The stars were taken from a larger sample of post-AGB binaries for which we have Spitzer infrared spectra, characterised by the presence of a stable oxygen-rich circumbinary disc. Our previous studies have shown that the infrared spectra of post-AGB disc sources are dominated by silicate dust emission, often with an extremely high crystallinity fraction. However, the three sources described here are selected because they show a peculiar molecular chemistry. Methods. Using Spitzer infrared spectroscopy, we study in detail the peculiar mineralogy of the three sample stars. Using the observed emission features, we identify the different observed dust, molecular and gas species. Results. The infrared spectra show emission features due to various oxygen-rich dust components, as well as CO2 gas. All three sources show the strong infrared bands generally ascribed to polycyclic aromatic hydrocarbons. Furthermore, two sample sources show C60 fullerene bands. Conclusions. Even though the majority of post-AGB disc sources are dominated by silicate dust in their circumstellar environment, we do find evidence that, for some sources at least, additional processing must occur to explain the presence of large carbonaceous molecules. There is evidence that some of these sources are still oxygen-rich, which makes the detection of these molecules even more surprising.
Distinctive features of CD4+ T cell dysfunction in chronic viral infections

Purpose of reviewTo describe recent advances in the understanding of virus-specific CD4+ T cell dysfunction in chronic viral infections, with an emphasis on HIV disease. We highlight features that are distinctive for CD4+ T cells, as opposed to their CD8+ T cell counterparts. Recent findingsCD4+ T cell activation and differentiation are tightly controlled. Regulation of these processes depends on the context of initial encounter of the naïve CD4+ T cell with the cognate antigen and on ongoing external cues to the antigen-experienced CD4+ T cell, in particular the inflammatory environment, which is prominent in HIV infection. Virus-specific CD4+ T cell dysfunction results from a combination of an exhaustion program and skewing in T helper lineage differentiation which impact function. The CD4+ and CD8+ T cell exhaustion programs present similarities and distinct features. The sets of inhibitory coreceptors expression differ, although programmed-death 1 (PD-1) and T cell immunoglobulin mucin-3 (Tim-3) are upregulated on both HIV-specific CD4+ and CD8+ T cells, cytotoxic T-lymphocyte antigen 4 (CTLA-4) is largely specific to CD4+ T cells, whereas 2B4 and CD160 are biased toward CD8+ T cells. SummaryUnderstanding the molecular basis of HIV-specific CD4+ T cell exhaustion and identifying key differences with CD8+ T cell impairment will be critical to design effective therapeutic and preventive immunotherapies against HIV.
Line graphs for directed and undirected networks: An structural and analytical comparison

The centrality and e-ciency measures of a network G are strongly related to the respective measures on the associated line graph L(G) and bipartite graph B(G) as was shown in (8). In this note we consider difierent ways to obtain a line graph from a given directed or undirected network and we obtain some interesting relations.
Oligomerization and Pore Formation by Equinatoxin II Inhibit Endocytosis and Lead to Plasma Membrane Reorganization*

Pore-forming toxins have evolved to induce membrane injury by formation of pores in the target cell that alter ion homeostasis and lead to cell death. Many pore-forming toxins use cholesterol, sphingolipids, or other raft components as receptors. However, the role of plasma membrane organization for toxin action is not well understood. In this study, we have investigated cellular dynamics during the attack of equinatoxin II, a pore-forming toxin from the sea anemone Actinia equina, by combining time lapse three-dimensional live cell imaging, fluorescence recovery after photobleaching, FRET, and fluorescence cross-correlation spectroscopy. Our results show that membrane binding by equinatoxin II is accompanied by extensive plasma membrane reorganization into microscopic domains that resemble coalesced lipid rafts. Pore formation by the toxin induces Ca2+ entry into the cytosol, which is accompanied by hydrolysis of phosphatidylinositol 4,5-bisphosphate, plasma membrane blebbing, actin cytoskeleton reorganization, and inhibition of endocytosis. We propose that plasma membrane reorganization into stabilized raft domains is part of the killing strategy of equinatoxin II.
Afa/Dr Diffusely Adhering Escherichia coli Infection in T84 Cell Monolayers Induces Increased Neutrophil Transepithelial Migration, Which in Turn Promotes Cytokine-Dependent Upregulation of Decay-Accelerating Factor (CD55), the Receptor for Afa/Dr Adhesins

ABSTRACT Ulcerative colitis and Crohn's disease are inflammatory bowel diseases thought to involve strains of Escherichia coli. We report here that two wild-type Afa/Dr diffusely adhering E. coli (DAEC) strains, C1845 and IH11128, which harbor the fimbrial F1845 adhesin and the Dr hemagglutinin, respectively, and the E. coli laboratory strain HB101, transformed with the pSSS1 plasmid to produce Afa/Dr F1845 adhesin, all induced interleukin-8 (IL-8) production and transepithelial migration of polymorphonuclear leukocytes (PMNL) in polarized monolayers of the human intestinal cell line T84 grown on semipermeable filters. We observed that after PMNL migration, expression of decay-accelerating factor (DAF, or CD55), the brush border-associated receptor for Afa/Dr adhesins, was strongly enhanced, increasing the adhesion of Afa/Dr DAEC bacteria. When examining the mechanism by which DAF expression was enhanced, we observed that the PMNL transepithelial migration induced epithelial synthesis of tumor necrosis factor alpha and IL-1β, which in turn promoted the upregulation of DAF.
Callosal Bisection and Transcallosal Secondary Antiepileptogenesis

Summary: More than 28,000 neuroscientists and 3,000 epileptologists gathered at their respective 2001 meetings of the Society for Neuroscience and the American Epilepsy Society. Yet only six articles, one directly and five indirectly, discussed the corpus callosum (CC). Is not this in itself a remarkable finding? Are there no mysteries left? The reality is that considerable uncertainties exist regarding the rationale for callosal bisection (CCB) that causes contrasting effects (i.e., amelioration of generalized seizure, at times leading to freedom from seizure, and intensification of postoperatively fragmented seizure, at times leading to status epilepticus). Similarly, the clinical relevance of EEG mirror focus formation, an experimentally well‐established transcallosal consequence of partial cortical epileptogenesis, continues to be debated. This presentation revisits these unresolved issues (a) to gain insight into the dynamic role played by the CC in medically refractory epilepsy, and (b) to promote the development of antiepileptogenic tools that are currently unavailable.
Hypoxia Induces Cyclooxygenase-2 via the NF-κB p65 Transcription Factor in Human Vascular Endothelial Cells*

The inducible cyclooxygenase, COX-2, has been associated with vascular inflammation and cellular proliferation. We have discovered that hypoxia increases expression of the COX-2 gene in human vascular endothelial cells in culture independent of other stimuli. Western analysis of human umbilical vein endothelial cells (HUVEC) revealed a greater than 4-fold induction of protein by hypoxia (1% O2). The steady-state level of COX-2 mRNA was correspondingly elevated by both Northern blot and reverse transcriptase-polymerase chain reaction analysis. Using electrophoretic mobility shift assays with antibody supershifting, we also found that hypoxia causes increased binding of NF-κB p65 (Rel A) to the one out of the two NF-κB consensus elements in the COX-2 promoter which is closest to the transcription start site of the COX-2 gene. Transfection of an immortalized human microvascular endothelial cell line (HMEC-1) with mutation reporter gene constructs and HUVEC with both mutation and deletion reporter gene constructs suggested that transcription of the COX-2 gene was enhanced by hypoxia. In transcription factor decoy experiments, hypoxic HUVEC were exposed in culture to 20 μM of the same NF-κB element found to bind NF-κB protein. The wild type transcription factor decoy prevented hypoxic induction of COX-2, presumably by binding with cytoplasmic p65; however, mutated or scrambled oligonucleotides did not prevent the increase in COX-2 protein expression by hypoxia. Thus, the intracellular signaling mechanism that leads to induction of COX-2 by hypoxia includes binding of p65 to the relatively 3′ NF-κB consensus element in the COX-2 upstream promoter region in human vascular endothelial cells.
PTSD and the War of Words

Trauma-related symptoms among veterans of military engagement have been documented at least since the time of the ancient Greeks.1 Since the third edition of the Diagnostic and Statistical Manual in 1980, this condition has been known as posttraumatic stress disorder, but the name has changed repeatedly over the past century, including shell shock, war neurosis, and soldier’s heart. Using over 14 million articles in the digital archives of the New York Times, Associated Press, and Reuters, we quantify historical changes in trauma-related terminology over the past century. These data suggest that posttraumatic stress disorder has historically peaked in public awareness after the end of US military engagements, but denoted by a different name each time—a phenomenon that could impede clinical and scientific progress.
Hypothalamic proopiomelanocortin promoter methylation becomes altered by early overfeeding: an epigenetic model of obesity and the metabolic syndrome

Pre‐ and neonatal overfeeding programmes a permanent obesity disposition and accompanying diabetic and cardiovascular disorders, by unknown mechanisms. We proposed that early overfeeding may alter DNA methylation patterns of hypothalamic promoter regions of genes critically involved in the lifelong regulation of food intake and body weight. We induced neonatal overfeeding by rearing Wistar rats in small litters (SL) and thereafter mapped the DNA methylation status of CpG dinucleotides of gene promoters from hypothalamic tissue, using bisulfite sequencing. Neonatal overfeeding led to rapid early weight gain, resulting in a metabolic syndrome phenotype, i.e. obesity, hyperleptinaemia, hyperglycaemia, hyperinsulinaemia, and an increased insulin/glucose ratio. Accompanying, without group difference to controls, the promoter of the main orexigenic neurohormone, neuropeptide Y, was methylated at low levels (i.e. < 5%). In contrast, in SL rats the hypothalamic gene promoter of the main anorexigenic neurohormone, proopiomelanocortin (POMC), showed hypermethylation (P < 0.05) of CpG dinucleotides within the two Sp1‐related binding sequences (Sp1, NF‐κB) which are essential for the mediation of leptin and insulin effects on POMC expression. Consequently, POMC expression lacked upregulation, despite hyperleptinaemia and hyperinsulinaemia. Accordingly, the extent of DNA methylation within Sp1‐related binding sequences was inversely correlated to the quotients of POMC expression/leptin (P= 0.02) and POMC expression/insulin (P < 0.001), indicating functionality of acquired epigenomic alterations. These data for the first time demonstrate a nutritionally acquired alteration of the methylation pattern and, consequently, the regulatory ‘set point’ of a gene promoter that is critical for body weight regulation. Our findings reveal overfeeding as an epigenetic risk factor of obesity programming and consecutive diabetic and cardiovascular disorders and diseases, in terms of the metabolic syndrome.
Prevention and Early Diagnosis of Lung Cancer

Received June 19, 2000; accepted June 19, 2000. S ince the turn of the 20th century, lung carcinoma rapidly has become a major health issue in the U.S. and around the world. Over the past 100 years, lung carcinoma has gone from being a rare condition to becoming the world’s most pervasive cancer killer. Why such a dramatic turn for the worse in such a short period of time? In 1900, Americans consumed approximately 2.5 billion cigarettes annually. By 1981, that number had increased over 250-fold to 640 billion cigarettes consumed each year (Fig. 1). Clearly, much of the exponential rise in lung carcinoma rates throughout the 20th century can be attributed to the marked increase in cigarette consumption. But is the rise in cigarette consumption the only factor to consider when asking why lung carcinoma rates have skyrocketed over the past century? Aside from the introduction of the mass production of cigarettes in the late 1800s, the onslaught of the industrial revolution and the concomitant explosion in environmental carcinogens also are likely to have played a part in the precipitation of the current lung carcinoma epidemic. Beginning in the 19th century through the first half of the 20th century, the world experienced two phases of the industrial revolution. The first phase was an agricultural and mechanical revolution that led to more efficient tools and the advent of machinery to perform work previously performed manually. Increased efficiency in raw material production and the proliferation of the steam engine were a few hallmarks of the first half of the greater revolution. The second phase of the revolution was defined by a sharp increase in manufacturing and industrialization with the birth of the railroad industry, electrical and chemical production, as well as coal, iron, and steel production. Ship building and later aircraft construction also played roles in the changing national and global landscape. Unfortunately, a natural consequence to the numerous benefits of the industrial revolution was an increase in environmental pollution on an unprecedented scale. In addition to the water and noise pollution that became commonplace at the turn of the century, problems relating to air quality were just beginning. While appraising the recent successes of smoking cessation and avoidance programs and the recent declines in the numbers of smokers, consider the well studied natural selection case of Biston betularia, more commonly referred to as peppered moths. Prior to the industrial revolution in Manchester, England, the predominant color of peppered moths was white. A few of the species were darkly colored, appearing nearly black-gray. White color predominated because the color closely resembled that of neighboring trees, thereby making it difficult for birds, the moths’ natural predators, to see them at rest. During the 2377
Weaving a Tapestry from Threads Spun by Geneticists: The Series Perspectives on Genetics, 1987–2008

The Perspectives column was initiated in 1987 when Jan Drake, Editor-in-Chief of GENETICS, invited Jim Crow and William Dove to serve as coeditors of “Anecdotal, Historical, and Critical Commentaries. ” As the series evolved over 21 years, under the guidance of Crow and Dove, the input of stories told by geneticists from many countries created a panorama of 20th-century genetics. Three recurrent themes are visible: how geneticists have created the science (as solitary investigators, in pairs, or in cooperative groups); how geneticists work hard, but find ways to have fun; and how public and private institutions have sustained the science of genetics, particularly in the United States. This article ends by considering how the Perspectives series and other communication formats can carry forward the core science of genetics from the 20th into the 21st century.
CD40 Restrains In Vivo Growth of Toxoplasma gondii Independently of Gamma Interferon

ABSTRACT CD40-CD154 interaction is pivotal for resistance against numerous pathogens. However, it is not known if this pathway can also enhance in vivo resistance in gamma interferon (IFN-γ)-deficient hosts. This is an important question because patients and mice with defects in type 1 cytokine response can control a variety of pathogens. While blockade of endogenous CD154 resulted in a remarkable increase in parasite load in IFN-γ−/− mice infected with Toxoplasma gondii, in vivo administration of a stimulatory anti-CD40 monoclonal antibody markedly reduced parasite load. This latter effect took place even in T-cell-depleted mice and was accompanied by induction of macrophage toxoplasmacidal activity. CD40 stimulation restricted T. gondii replication independently of STAT1, p47 GTPases, and nitric oxide. In vivo CD40 ligation enhanced tumor necrosis factor alpha (TNF-α) production by T. gondii-infected macrophages. In addition, CD40 stimulation required the presence of TNF receptor 2 to reduce parasite load in vivo. These results suggest that CD40-CD154 interaction regulates IFN-γ-independent mechanisms of host protection through induction of macrophage antimicrobial activity and modulation of TNF-α signaling.
Effects of extended lamivudine therapy in Asian patients with chronic hepatitis B. Asia Hepatitis Lamivudine Study Group.

BACKGROUND & AIMS One-year lamivudine therapy significantly suppressed hepatitis B virus (HBV) replication, improved hepatic necroinflammatory activity, and prevented progression of fibrosis. However, the effects of prolonged therapy are unknown. METHODS A total of 334 Asian patients with chronic hepatitis B from a previously reported 1-year study were randomized to receive either lamivudine (100 or 25 mg) or placebo for another year. The effects of treatment on serum HBV-DNA suppression, alanine transaminase (ALT) normalization, and hepatitis B e antigen (HBeAg) seroconversion were measured. The presence of YMDD variant HBV and its effect were also determined. RESULTS A significantly greater proportion of patients achieved sustained HBV-DNA suppression and ALT normalization with 100 mg lamivudine daily for 2 years compared with lamivudine for 1 year followed by placebo for the second year (P<0.001). Daily lamivudine therapy for 2 years was safe and resulted in incremental HBeAg seroconversion from 17% at week 52 to 27% at week 104. HBeAg seroconversion during continued lamivudine therapy increased linearly with increasing pretherapy ALT levels (P< 0.001). Despite the emergence of YMDD mutant in 38% of the patients, they continued to clear serum HBeAg and maintain lower median serum HBV-DNA and ALT levels than baseline values. In contrast, ALT levels increased 8-12 weeks after switching from lamivudine to placebo, but returned to normal once lamivudine treatment was resumed. CONCLUSIONS Treatment with lamivudine for 2 years is both well tolerated and efficacious in patients with chronic hepatitis B.
Algebraic Formalization and Verification of PKMv3 Protocol using Maude

PKMv3 is the third version of Privacy and Key Management protocol, which plays an important role by providing key distribution and security access control in IEEE802.16m, the standard of Worldwide Interoperability for Microwave Access. The protocol should be guaranteed safe in terms of confidentiality, authentication and integrity. In this paper, we develop an executable formal specification of PKMv3 in an algebraic language called Maude and verify safety properties of the protocol using state exploration and LTL model checking in Maude. Unlike existing approaches, we consider the behaviors of intruders and time feature in our verification and verify both safety properties and time-related properties of the protocol.
Exploring the relationship between innovativeness and the stages of knowledge management in Technology and Engineering Consultancies in Singapore

This paper aims to examine the impact of the various stages of managing knowledge - knowledge acquisition, dissemination and utilization - on the innovativeness of Technology and Engineering Consultancies (TEC) in Singapore, by drawing on results from questionnaires mailed to 446 TEC firms. According to the findings, knowledge acquisition and knowledge utilization have a positive impact on the innovativeness of TEC firms and this impact is stronger for firms operating in more volatile environments. TEC firms are typically relying on having a large portfolio of existing plans that can be reused rather than innovating. However, the clients of TEC firms are usually lead users in the industry, which may lead to the need for further development of inadequate current practices in order to remain innovative in the long run.
Reflections of an Eclectic Skeptic

Following primary and secondary education in Europe, I came to the United States for further education. After majoring in engineering, I shifted to liberal arts and social sciences. I minored in mathematics, philosophy, and education at the undergraduate level and physiology at the graduate level, ultimately obtaining a PhD in personality psychology. My interests were primarily academic, but I did not neglect the emerging field of clinical psychology. After working in hospitals for 9 years, I joined the faculty of Michigan State University where I established the psychological clinic and served as its director for 13 years. Subsequently, during 2 sabbaticals in Israel, I researched personality development in unconventional family settings (the kibbutz). I also studied such diverse issues as motivation for parenthood, time perception and time perspective, and cognition in psychopathology. After editing several textbooks on assessment techniques, I initiated the series of triennial Murray lectures that highlighted the dynamic approach to the study of personality.
A 400 MHz 4.5 nW −63.8 dBm sensitivity wake-up receiver employing an active pseudo-balun envelope detector

A 402–405 MHz MICS-band wake-up receiver is presented that achieves −63.8 dBm sensitivity at 4.5 nW. High sensitivity at 400 MHz is accomplished via an 18.5 dB passive voltage gain transformer filter loaded by a high input impedance (Rin > 30 kΩ), high scaling factor (kED > 300), 1.8 nW current re-use pseudo-balun envelope detector, while low power is achieved by operating all active circuits, including the re-generative comparator, baseband correlator, and temperature compensated relaxation oscillator in sub-threshold with a single 0.4 V supply. The chip is fabricated using 0.18 μm CMOS SOI process and achieves the highest figure of merit of all direct envelope detection-based wake-up receivers operating above 400 MHz.
Quality-aware bandwidth allocation for scalable on-demand streaming in wireless networks

In this paper, we propose a scalable transport scheme for delivering on-demand video streams over broadband wireless networks in next-generation network/IP multimedia subsystem (NGN/IMS) architecture. The proposed transport scheme makes use of fine-granular-scalability (FGS) encoded videos to accommodate high bandwidth variation of wireless networks. We formulate the bandwidth allocation to FGS-encoded streams as a resource allocation problem and develop a quality-aware bandwidth allocation scheme, called QABA. With QABA, the proposed transport scheme can dynamically adjust the bit rate allocated to different streams to maximize the overall perceptual quality when available network bandwidth varies with time. QABA is theoretically proven to be able to find the optimal bandwidth allocation for all on-demand streams. To validate the effectiveness of QABA, extensive trace-based simulations are performed.