Miracle-dz/UniFAR-FTUs huggingface dataset:
Cirrus cloud seeding: a climate engineering mechanism with reduced side effects?

Climate engineering, the intentional alteration of Earth's climate, is a multifaceted and controversial topic. Numerous climate engineering mechanisms (CEMs) have been proposed, and the efficacies and potential undesired consequences of some of them have been studied in the safe environments of numerical models. Here, we present a global modelling study of a so far understudied CEM, namely the seeding of cirrus clouds to reduce their lifetimes in the upper troposphere, and hence their greenhouse effect. Different from most CEMs, the intention of cirrus seeding is not to reduce the amount of solar radiation reaching Earth's surface. This particular CEM rather targets the greenhouse effect, by reducing the trapping of infrared radiation by high clouds. This avoids some of the caveats that have been identified for solar radiation management, for example, the delayed recovery of stratospheric ozone or drastic changes to Earth's hydrological cycle. We find that seeding of mid- and high-latitude cirrus clouds has the potential to cool the planet by about 1.4 K, and that this cooling is accompanied by only a modest reduction in rainfall. Intriguingly, seeding of the 15% of the globe with the highest solar noon zenith angles at any given time yields the same global mean cooling as a seeding strategy that involves 45% of the globe. In either case, the cooling is strongest at high latitudes, and could therefore serve to prevent Arctic sea ice loss. With the caveat that there are still significant uncertainties associated with ice nucleation in cirrus clouds and its representation in climate models, cirrus seeding appears to represent a powerful CEM with reduced side effects.
On the geometric nature of characteristic classes of surface bundles

Each Morita–Mumford–Miller (MMM) class en assigns to each genus g⩾2 surface bundle Σg→E2n+2→M2n an integer en# (E→M):=〈 en, [M]〉∈ℤ. We prove that when n is odd the number en# (E→M) depends only on the diffeomorphism type of E, not on g, M or the map E→M. More generally, we prove that en# (E→M) depends only on the cobordism class of E. Recent work of Hatcher implies that this stronger statement is false when n is even. If E→M is a holomorphic fibering of complex manifolds, we show, that for every n, the number en# (E→M) only depends on the complex cobordism type of E.
Dilated and failing cardiomyopathy in bradykinin B(2) receptor knockout mice.

BACKGROUND The activation of B(2) receptors by kinins could exert cardioprotective effects in myocardial ischemia and heart failure. METHODS AND RESULTS To test whether the absence of bradykinin B(2) receptors may affect cardiac structure and function, we examined the developmental changes in blood pressure (BP), heart rate, and heart morphology of bradykinin B(2) receptor gene knockout (B(2)(-/-)), heterozygous (B(2)(+/-)), and wild-type (B(2)(+/+)) mice. The BP of B(2)(-/-) mice, which was still normal at 50 days of age, gradually increased, reaching a plateau at 6 months (136+/-3 versus 109+/-1 mm Hg in B(2)(+/+), P<0.01). In B(2)(+/-) mice, BP elevation was delayed. At 40 days, the heart rate was higher (P<0.01) in B(2)(-/-) and B(2)(+/-) than in B(2)(+/+) mice, whereas the left ventricular (LV) weight and chamber volume were similar among groups. Thereafter, the LV growth rate of B(2)(-/-) and B(2)(+/-) mice was accelerated, leading at 360 days to a LV weight-to-body weight ratio that was 9% and 17% higher, respectively, than that of B(2)(+/+) mice. In B(2)(-/-) mice, hypertrophy was associated with a marked chamber dilatation (42% larger than that of B(2)(+/+) mice), an elevation in LV end-diastolic pressure (25+/-3 versus 5+/-1 mm Hg in B(2)(+/+) mice, P<0.01), and reparative fibrosis. CONCLUSIONS The disruption of the bradykinin B(2) receptor leads to hypertension, LV remodeling, and functional impairment, implying that kinins are essential for the functional and structural preservation of the heart.
Robust Kernel Dictionary Learning Using a Whole Sequence Convergent Algorithm

Kernel sparse coding is an effective strategy to capture the non-linear structure of data samples. However, how to learn a robust kernel dictionary remains an open problem. In this paper, we propose a new optimization model to learn the robust kernel dictionary while isolating outliers in the training samples. This model is essentially based on the decomposition of the reconstruction error into small dense noises and large sparse outliers. The outlier error term is formulated as the product of the sample matrix in the feature space and a diagonal coefficient matrix. This facilitates the kernelized dictionary learning. To solve the non-convex optimization problem, we develop a whole sequence convergent algorithm which guarantees the obtained solution sequence is a Cauchy sequence. The experimental results show that the proposed robust kernel dictionary learning method provides significant performance improvement.
Separating centrosomes interact in the absence of associated chromosomes during mitosis in cultured vertebrate cells.

We detail here how "free" centrosomes, lacking associated chromosomes, behave during mitosis in PtK(2) homokaryons stably expressing GFP-alpha-tubulin. As free centrosomes separate during prometaphase, their associated astral microtubules (Mts) interact to form a spindle-shaped array that is enriched for cytoplasmic dynein and Eg5. Over the next 30 min, these arrays become progressively depleted of Mts until the two centrosomes are linked by a single bundle, containing 10-20 Mts, that persists for > 60 min. The overlapping astral Mts within this bundle are loosely organized, and their plus ends terminate near its midzone, which is enriched for an ill-defined matrix material. At this time, the distance between the centrosomes is not defined by external forces because these organelles remain stationary when the bundle connecting them is severed by laser microsurgery. However, since the centrosomes move towards one another in response to monastrol treatment, the kinesin-like motor protein Eg5 is involved. From these results, we conclude that separating asters interact during prometaphase of mitosis to form a spindle-shaped Mt array, but that in the absence of chromosomes this array is unstable. An analysis of the existing data suggests that the stabilization of spindle Mts during mitosis in vertebrates does not involve the chromatin (i.e., the RCC1/RanGTP pathway), but instead some other chromosomal component, e.g., kinetochores.
Differing requirements for Augmin in male meiotic and mitotic spindle formation in Drosophila

Animal cells divide using a microtubule-based, bipolar spindle. Both somatic, mitotic cells and sperm-producing male meiotic spermatocytes use centrosome-dependent and acentrosomal spindle-forming mechanisms. Here, we characterize the largely undefined, centrosome-independent spindle formation pathway used during male meiosis. Our live and fixed cell analyses of Drosophila spermatocytes reveal that acentrosomal microtubules are nucleated at kinetochores and in the vicinity of chromatin and that together these assemble into functional spindles. Mutational studies indicate that γ-tubulin and its extra-centrosomal targeting complex, Augmin, are vital for this process. In addition, Augmin facilitates efficient spindle assembly in the presence of centrosomes. In contrast to the pronounced recruitment of Augmin on spindles in other cell types, the complex is absent from those of spermatocytes but does accumulate on kinetochores. Polo kinase facilitates this kinetochore recruitment while inhibiting Augmin's spindle association, and this in turn dictates γ-tubulin distribution and spindle density. Polo's negative regulation of Augmin in male meiosis contrasts with its requirement in loading Augmin along mitotic spindles in somatic Drosophila cells. Together our data identify a novel mechanism of acentrosomal spindle formation in spermatocytes and reveal its divergence from that used in mitotic cells.
Synthetic aperture inversion

This paper considers synthetic aperture radar and other synthetic aperture imaging systems in which a backscattered wave is measured from a variety of locations. The paper begins with a (linearized) mathematical model, based on the wave equation, that includes the effects of limited bandwidth and the antenna beam pattern. The model includes antennas with poor directionality, such as are needed in the problem of foliage-penetrating radar, and can also accommodate other effects such as antenna motion and steering. For this mathematical model, we use the tools of microlocal analysis to develop and analyse a three-dimensional imaging algorithm that applies to measurements made on a two-dimensional surface. The analysis shows that simple backprojection should result in an image of the singularities in the scattering region. This image can be improved by following the backprojection with a spatially variable filter that includes not only the antenna beam pattern and source waveform but also a certain geometrical scaling factor called the Beylkin determinant. Moreover, we show how to combine the backprojection and filtering in one step. The resulting algorithm places singularities in the correct locations, with the correct orientations and strengths. The algorithm is analysed to determine which information about the scattering region is reconstructed and to determine the resolution. We introduce a notion of directional resolution to treat the reconstruction of walls and other directional elements. We also determine the fineness with which the data must be sampled in order for the theoretical analysis to apply. Finally, we relate the present analysis to previous work and discuss briefly implications for the case of a single flight track.
Intramuscular injection of a plasmid vector expressing human apolipoprotein E limits progression of xanthoma and aortic atheroma in apoE-deficient mice.

Apolipoprotein-E (apoE) protects against coronary artery disease via hepatic removal of atherogenic remnant lipoproteins, sequestration of cholesterol from vessel walls and local anti-oxidant, anti-platelet and anti-inflammatory actions. ApoE gene transfer may thus ameliorate a hyperlipidaemic profile and have beneficial effects at lesion sites to prevent or regress atherosclerosis, a concept endorsed by adenoviral-mediated hepatic expression studies. Here, using plasmid vectors expressing allelic human apoE2 or apoE3 isoforms, skeletal muscle was evaluated as an effective secretory platform for apoE gene augmentation. Transfected myoblasts and myotubes were found to efficiently secrete recombinant apoE in vitro as spherical 10-16 nm lipoprotein particles with pre-beta mobility. Intramuscular plasmid injection in apoE(-/-) mice, which develop spontaneous atherosclerotic plaque and xanthoma resulted in expression and secretion of apoE. Human apoE mRNA was detected by RT-PCR in injected muscles and, although concentrations of apoE3, which is rapidly cleared from plasma, were near ELISA detection limits, levels of plasma apoE2 were measurable (17.5 +/- 4.3 ng/ml). To assess whether muscle-based expression of apoE2 could inhibit atherogenesis, long-term follow-up studies were conducted. Although hyperlipidaemia was not reduced in treated animals, end-point pathology showed clear retardation of atherosclerotic and xanthomatous lesions. Up to 9 months following a single apoE2 plasmid administration, atherosclerotic lesion coverage in proximal aorta was significantly reduced by 20-30% (P < 0.01), whereas development of gross dorsal xanthoma (>5 mm diameter) was effectively reduced to zero. We conclude that expression of apoE from ectopic muscle sites has therapeutic potential to limit progression of atherosclerosis.
Ligand-induced assembly and activation of the gamma interferon receptor in intact cells

Functionally active gamma interferon (IFN-gamma) receptors consist of an alpha subunit required for ligand binding and signal transduction and a beta subunit required primarily for signaling. Although the receptor alpha chain has been well characterized, little is known about the specific role of the receptor beta chain in IFN-gamma signaling. Expression of the wild-type human IFN-gamma receptor beta chain in murine L cells that stably express the human IFN-gamma receptor alpha chain (L.hgR) produced a murine cell line (L.hgR.myc beta) that responded to human IFN-gamma. Mutagenesis of the receptor beta-chain intracellular domain revealed that only two closely spaced, membrane-proximal sequences (P263PSIP267 and I270EEYL274) are required for function. Coprecipitation studies showed that these sequences are necessary for the specific and constitutive association of the receptor beta chain with the JAK-2 tyrosine kinase. These experiments also revealed that the IFN-gamma receptor alpha and beta chains are not preassociated on the surface of unstimulated cells but rather are induced to associate in an IFN-gamma-dependent fashion. A chimeric protein in which the intracellular domain of the beta chain was replaced by JAK-2 complemented human IFN-gamma signaling and biologic responsiveness in L.hgR. In contrast, a c-src-containing beta-chain chimera did not. These results indicate that the sole obligate role of the IFN-gamma receptor beta chain in signaling is to recruit JAK-2 into the ligand-assembled receptor complex.
Fucosylation Is a Promising Target for Cancer Diagnosis and Therapy

Oligosaccharides, sequences of carbohydrates conjugated to proteins and lipids, are arguably the most abundant and structurally diverse class of molecules. Fucosylation is one of the most important oligosaccharide modifications involved in cancer and inflammation. Recent advances in glycomics have identified several types of glyco-biomarkers containing fucosylation that are linked to certain types of cancer. Fucosylated alpha-fetoprotein (AFP) is widely used in the diagnosis of hepatocellular carcinoma because it is more specific than alpha-fetoprotein. High levels of fucosylated haptoglobin have also been found in sera of patients with various carcinomas. We have recently established a simple lectin-antibody ELISA to measure fucosylated haptoglobin and to investigate its clinical use. Cellular fucosylation is dependent upon fucosyltransferase activity and the level of its donor substrate, guanosine diphosphate (GDP)-fucose. GDP-mannose-4,6-dehydratase (GMDS) is a key enzyme involved in the synthesis of GDP-fucose. Mutations of GMDS found in colon cancer cells induced a malignant phenotype, leading to rapid growth in athymic mice resistant to natural killer cells. This review describes the role of fucosylated haptoglobin as a cancer biomarker, and discusses the possible biological role of fucosylation in cancer development.
Musical Experience and the Aging Auditory System: Implications for Cognitive Abilities and Hearing Speech in Noise

Much of our daily communication occurs in the presence of background noise, compromising our ability to hear. While understanding speech in noise is a challenge for everyone, it becomes increasingly difficult as we age. Although aging is generally accompanied by hearing loss, this perceptual decline cannot fully account for the difficulties experienced by older adults for hearing in noise. Decreased cognitive skills concurrent with reduced perceptual acuity are thought to contribute to the difficulty older adults experience understanding speech in noise. Given that musical experience positively impacts speech perception in noise in young adults (ages 18–30), we asked whether musical experience benefits an older cohort of musicians (ages 45–65), potentially offsetting the age-related decline in speech-in-noise perceptual abilities and associated cognitive function (i.e., working memory). Consistent with performance in young adults, older musicians demonstrated enhanced speech-in-noise perception relative to nonmusicians along with greater auditory, but not visual, working memory capacity. By demonstrating that speech-in-noise perception and related cognitive function are enhanced in older musicians, our results imply that musical training may reduce the impact of age-related auditory decline.
The Signaling Cascades of Ginkgolide B-Induced Apoptosis in MCF-7 Breast Cancer Cells

Ginkgolide B, the major active component of Ginkgo biloba extracts, can both stimulate and inhibit apoptotic signaling. Here, we demonstrate that ginkgolide B can induce the production of reactive oxygen species in MCF-7 breast cancer cells, leading to an increase in the intracellular concentrations of cytoplasmic free Ca2+ and nitric oxide (NO), loss of mitochondrial membrane potential (MMP), activation of caspase-9 and -3, and increase the mRNA expression levels of p53 and p21, which are known to be involved in apoptotic signaling. In addition, prevention of ROS generation by pretreatment with N-acetyl cysteine (NAC) could effectively block intracellular Ca2+ concentrations increases and apoptosis in ginkgolide B-treated MCF-7 cells. Moreover, pretreatment with nitric oxide (NO) scavengers could inhibit ginkgolide B-induced MMP change and sequent apoptotic processes. Overall, our results signify that both ROS and NO played important roles in ginkgolide B-induced apoptosis of MCF-7 cells. Based on these study results, we propose a model for ginkgolide B-induced cell apoptosis signaling cascades in MCF-7 cells.
Bullous pemphigoid antigen II (BP180) and its soluble extracellular domains are major autoantigens in mucous membrane pemphigoid: the pathogenic relevance to HLA class II alleles and disease severity

Background Mucous membrane pemphigoid (MMP), a chronic autoimmune subepithelial blistering disease, is associated with circulating IgG and/or IgA autoantibodies against several basement membrane zone antigens. The heterogeneity of clinical presentation and diversity of target autoantigens have contributed to difficulties in characterizing this condition immunologically.
A Fuzzy Reputation-based Trust Management Scheme for Cloud Computing

Cloud computing requires that customers trust that a service provider’s platforms are secured and provide a sufficient level of integrity for the client’s data. However, a lack of trust between cloud customers and providers has hindered the universal acceptance of clouds as an increasingly popular approach for the processing of large data sets and computationally expensive programs. Existing techniques do not satisfactorily solve the problem, a good solution is to leverage trust management technology to build trust into utility cloud computing. Recently, trust modeling is paid more and more attention in cloud computing. Therefore, in the paper we propose a fuzzy reputation-based trust model (FRTM) based on fuzzy logic inferences. The main idea of our trust model is to use fuzzy logic inferences to handle uncertainty, fuzziness, and incomplete information in cloud trust reports. The proposed trust model will help cloud customers determine the level of trust that is to be placed on any particular cloud service provider. Experiments and results demonstrate the accuracy of the proposed trust model. Through analysis and experiments, we believe our approach is useful for cloud customers to make the decision regarding who to interact with.
From Hall's Matching Theorem to Optimal Routing on Hypercubes

We introduce a concept of so-called disjoint ordering for any collection of finite sets. It can be viewed as a generalization of a system of distinctive representatives for the sets. It is shown that disjoint ordering is useful for network routing. More precisely, we show that Hall's “marriage” condition for a collection of finite sets guarantees the existence of a disjoint ordering for the sets. We next use this result to solve a problem in optimal routing on hypercubes. We give a necessary and sufficient condition under which there are internally node-disjoint paths each shortest from a source node to any others(s? n) target nodes on ann-dimensional hypercube. When this condition is not necessarily met, we show that there are always internally node-disjoint paths each being either shortest or near shortest, and the total length is minimum. An efficient algorithm is also given for constructing disjoint orderings and thus disjoint short paths. As a consequence, Rabin's information disposal algorithm may be improved.
Is the ADHD brain wired differently? A review on structural and functional connectivity in attention deficit hyperactivity disorder

In recent years, a change in perspective in etiological models of attention deficit hyperactivity disorder (ADHD) has occurred in concordance with emerging concepts in other neuropsychiatric disorders such as schizophrenia and autism. These models shift the focus of the assumed pathology from regional brain abnormalities to dysfunction in distributed network organization. In the current contribution, we report findings from functional connectivity studies during resting and task states, as well as from studies on structural connectivity using diffusion tensor imaging, in subjects with ADHD. Although major methodological limitations in analyzing connectivity measures derived from noninvasive in vivo neuroimaging still exist, there is convergent evidence for white matter pathology and disrupted anatomical connectivity in ADHD. In addition, dysfunctional connectivity during rest and during cognitive tasks has been demonstrated. However, the causality between disturbed white matter architecture and cortical dysfunction remains to be evaluated. Both genetic and environmental factors might contribute to disruptions in interactions between different brain regions. Stimulant medication not only modulates regionally specific activation strength but also normalizes dysfunctional connectivity, pointing to a predominant network dysfunction in ADHD. By combining a longitudinal approach with a systems perspective in ADHD in the future, it might be possible to identify at which stage during development disruptions in neural networks emerge and to delineate possible new endophenotypes of ADHD. Hum Brain Mapp, 2010. © 2010 Wiley‐Liss, Inc.
Identification of a Salt-Induced Primary Transporter for Glycine Betaine in the Methanogen Methanosarcina mazei Gö1

ABSTRACT The salt adaptation of the methanogenic archaeon Methanosarcina mazei Gö1 was studied at the physiological and molecular levels. The freshwater organism M. mazei Gö1 was able to adapt to salt concentrations up to 1 M, and the addition of the compatible solute glycine betaine to the growth medium facilitated adaptation to higher salt concentrations. Transport studies with cell suspensions revealed a salt-induced glycine betaine uptake activity in M. mazei Gö1, and inhibitor studies argue for a primary transport device. Analysis of the genome of M. mazei Gö1 identified a homolog of known primary glycine betaine transporters. This gene cluster was designated Ota (osmoprotectant transporter A). Its sequence and gene organization are very similar to those of the glycine betaine transporter OpuA of Bacillus subtilis. Northern blot analysis of otaC revealed a salt-dependent transcription of this gene. Ota is the first identified salt-induced transporter for compatible solutes in Archaea.