Miracle-dz/UniFAR-FTUs huggingface dataset:
Low Complexity Antenna Selection for Low Target Rate Users in Dense Cloud Radio Access Networks

We propose a low complexity antenna selection algorithm for low target rate users in cloud radio access networks. The algorithm consists of two phases. In the first phase, each remote radio head (RRH) determines whether to be included in a candidate set by using a predefined selection threshold. In the second phase, RRHs are randomly selected within the candidate set made in the first phase. To analyze the performance of the proposed algorithm, we model RRHs' and users' locations by a homogeneous Poisson point process, whereby the signal-to-interference ratio (SIR) complementary cumulative distribution function is derived. By approximating the derived expression, an approximate optimum selection threshold that maximizes the SIR coverage probability is obtained. Using the obtained threshold, we characterize the performance of the algorithm in an asymptotic regime, where the RRH density goes to infinity. The obtained threshold is then modified depending on various algorithm options. A distinguishable feature of the proposed algorithm is that the algorithm complexity keeps constant independent to the RRH density, so that a user is able to connect to a network without heavy computation at baseband units.
SR Proteins Induce Alternative Exon Skipping through Their Activities on the Flanking Constitutive Exons

ABSTRACT SR proteins are well known to promote exon inclusion in regulated splicing through exonic splicing enhancers. SR proteins have also been reported to cause exon skipping, but little is known about the mechanism. We previously characterized SRSF1 (SF2/ASF)-dependent exon skipping of the CaMKIIδ gene during heart remodeling. By using mouse embryo fibroblasts derived from conditional SR protein knockout mice, we now show that SR protein-induced exon skipping depends on their prevalent actions on a flanking constitutive exon and requires collaboration of more than one SR protein. These findings, coupled with other established rules for SR proteins, provide a theoretical framework to understand the complex effect of SR protein-regulated splicing in mammalian cells. We further demonstrate that heart-specific CaMKIIδ splicing can be reconstituted in fibroblasts by downregulating SR proteins and upregulating a RBFOX protein and that SR protein overexpression impairs regulated CaMKIIδ splicing and neuronal differentiation in P19 cells, illustrating that SR protein-dependent exon skipping may constitute a key strategy for synergism with other splicing regulators in establishing tissue-specific alternative splicing critical for cell differentiation programs.
Spatiotemporal-MIMO Channel Estimator and Beamformer for 5G

With requirements of spiraling data rates and limited spectrum availability, there is an increased interest in mm-wave beamformer-based communications for 5G. For upcoming cellular networks, the critical point is to exploit the increased number of employable antennas at both Tx and Rx to: 1) combat increased path loss; 2) tackle higher interference due to higher user density; and 3) handle multipath effects in frequency selective channels. Toward this, a multi-beam spatiotemporal superresolution beamforming framework is proposed in this paper as a promising candidate to design beampatterns that mitigate/suppress co-channel interference and deliver massive gain in the desired directions. Initially, channel and signal models suitable for the mm-wave MIMO system are presented using the manifold vectors of both Tx and Rx antenna arrays. Based on these models, a novel subspace-based channel estimator is employed, which estimates delays, directions, velocities, and fading coefficients of the desired signal paths. This information is then exploited by the proposed spatiotemporal beamformer to provide a massive array gain that combats path loss without increasing the number of antenna array elements and to be tolerant to the near-far problem in a high interference environment. The performance of the proposed channel estimator and beamformer is examined using computer simulation studies.
JAK2 Tyrosine Kinase Phosphorylates and Is Negatively Regulated by Centrosomal Protein Ninein

ABSTRACT JAK2 is a cytoplasmic tyrosine kinase critical for cytokine signaling. In this study, we have identified a novel centrosome-associated complex containing ninein and JAK2. We have found that active JAK2 localizes around the mother centrioles, where it partly colocalizes with ninein, a protein involved in microtubule (MT) nucleation and anchoring. We demonstrated that JAK2 is an important regulator of centrosome function. Depletion of JAK2 or use of JAK2-null cells causes defects in MT anchoring and increased numbers of cells with mitotic defects; however, MT nucleation is unaffected. We showed that JAK2 directly phosphorylates the N terminus of ninein while the C terminus of ninein inhibits JAK2 kinase activity in vitro. Overexpressed wild-type (WT) or C-terminal (amino acids 1179 to 1931) ninein inhibits JAK2. This ninein-dependent inhibition of JAK2 significantly decreases prolactin- and interferon gamma (IFN-γ)-induced tyrosyl phosphorylation of STAT1 and STAT5. Downregulation of ninein enhances JAK2 activation. These results indicate that JAK2 is a novel member of centrosome-associated complex and that this localization regulates both centrosomal function and JAK2 kinase activity, thus controlling cytokine-activated molecular pathways.
Phosphoinositide 3-Kinase Beta Protects Nuclear Envelope Integrity by Controlling RCC1 Localization and Ran Activity

ABSTRACT The nuclear envelope (NE) forms a barrier between the nucleus and the cytosol that preserves genomic integrity. The nuclear lamina and nuclear pore complexes (NPCs) are NE components that regulate nuclear events through interaction with other proteins and DNA. Defects in the nuclear lamina are associated with the development of laminopathies. As cells depleted of phosphoinositide 3-kinase beta (PI3Kβ) showed an aberrant nuclear morphology, we studied the contribution of PI3Kβ to maintenance of NE integrity. pik3cb depletion reduced the nuclear membrane tension, triggered formation of areas of lipid bilayer/lamina discontinuity, and impaired NPC assembly. We show that one mechanism for PI3Kβ regulation of NE/NPC integrity is its association with RCC1 (regulator of chromosome condensation 1), the activator of nuclear Ran GTPase. PI3Kβ controls RCC1 binding to chromatin and, in turn, Ran activation. These findings suggest that PI3Kβ regulates the nuclear envelope through upstream regulation of RCC1 and Ran.
Different Functional Modes of p300 in Activation of RNA Polymerase III Transcription from Chromatin Templates

ABSTRACT Transcriptional coactivators that regulate the activity of human RNA polymerase III (Pol III) in the context of chromatin have not been reported. Here, we describe a completely defined in vitro system for transcription of a human tRNA gene assembled into a chromatin template. Transcriptional activation and histone acetylation in this system depend on recruitment of p300 by general initiation factor TFIIIC, thus providing a new paradigm for recruitment of histone-modifying coactivators. Beyond its role as a chromatin-modifying factor, p300 displays an acetyltransferase-independent function at the level of preinitiation complex assembly. Thus, direct interaction of p300 with TFIIIC stabilizes binding of TFIIIC to core promoter elements and results in enhanced transcriptional activity on histone-free templates. Additional studies show that p300 is recruited to the promoters of actively transcribed tRNA and U6 snRNA genes in vivo. These studies identify TFIIIC as a recruitment factor for p300 and thus may have important implications for the emerging concept that tRNA genes or TFIIIC binding sites act as chromatin barriers to prohibit spreading of silenced heterochromatin domains.
Gastric Dysplasia: Diagnosis and Significance

An elderly man complaining of vague abdominal cramping eventually underwent an upper endoscopy that revealed a slightly raised nodular antral lesion. The microscopic evaluation determined a diagnosis of high grade dysplasia. Following the diagnosis he was re-endoscoped and multiple biopsies failed to reveal any additional significant mucosal abnormalities. Another endoscopy at 6 month was also negative. However, a scheduled endoscopy the following year diagnosed a well-differentiated adenocarcinoma. A distal gastrectomy revealed an early gastric adenocarcinoma. The patient is alive and well 3 years after the initial diagnosis. This report emphasizes the diagnostic features of gastric epithelial dysplasia and the clinical significance of this diagnosis. Gastric epithelial dysplasia (GED) is believed to be the penultimate stage of gastric carcinogenesis. Its clinical importance has been underscored since the demonstration of its close association with gastric cancer was established. On this background we review the definition and classification of GED as well as its grading and natural history.
A heuristic method for sensor scheduling in infrared LEO constellation

Sensor scheduling problem in infrared LEO constellation by bearing-only location is studied to ensure its continuous tracking and parallel processing multitask. Firstly, the problem is defined in detail, and a mathematical model is presented. Secondly, an adaptive multitask programming on probabilistic selection algorithm(AMPPSA) is proposed, which utilizes trend catching, random selection and clone variation to keep from sub optimizing and applies heuristic rules to avoid blind searching. Finally, simulations show that the algorithm fits to sensor management of multi-objective optimization in infrared LEO constellation.
An Experimental Evaluation of Switched Combining Based Macro-Diversity for Wearable Communications Operating in an Outdoor Environment

This paper investigates the potential improvement in signal reliability for outdoor wearable communications channels operating at 868 MHz using switched combining based macro-diversity. In this paper, a number of different macro-diversity configurations consisting of two and four base stations were considered to help mitigate the impact of body shadowing upon a wearable node, which was located on the central chest region of an adult male. During the field measurements, five different walking movements were performed, and then analyzed to investigate the efficacy of using macro-diversity. It was found that all of the considered switched combining schemes, including switch-and-stay combining, switch-and-examine combining (SEC) and SEC with post-examining selection (SECps) provided a worthwhile signal improvement when an appropriate switching threshold was adopted. The maximum diversity gain obtained in this paper was found to be 19.5 dB when using four-base station SECps. The diversity gain, the number of path examinations, and the number of path switches between base stations for the switched combiner output varied according to the determined switching threshold, highlighting the importance of the selection of an appropriate threshold level. Furthermore, the performance/complexity tradeoff is demonstrated. Finally, the fading behavior at the output of the switched diversity combiners was then characterized using the diversity specific equations developed under the assumption of independent and non-identically distributed Nakagami- $m$ fading channels. Over all of the measurement scenarios considered in this paper, the theoretical models provided an adequate fit to the fading observed at the output of the virtual switched combiner.
Design of Contract-Based Trading Mechanism for a Small-Cell Caching System

Recently, content-aware-enabled distributed cach- ing relying on local small-cell base stations (SBSs), namely, small-cell caching, has been intensively studied for reducing transmission latency as well as alleviating the traffic load over backhaul channels. In this paper, we consider a commercialized small-cell caching system consisting of a network service provider (NSP), several content providers (CPs), and multiple mobile users (MUs). The NSP, as a network facility monopolist in charge of the SBSs, leases its resources to the CPs for gaining profits. At the same time, the CPs are intended to rent the SBSs for providing better downloading services to the MUs. We focus on solving the profit maximization problem for the NSP within the framework of contract theory. To be specific, we first formulate the utility functions of the NSP and the CPs by modeling the MUs and SBSs as two independent Poisson point processes. Then, we develop the optimal contract problem for an information asymmetric scenario, where the NSP only knows the distribution of CPs’ popularity among the MUs. Also, we derive the necessary and sufficient conditions of feasible contracts. Lastly, the optimal contract solutions are proposed with different CPs’ popularity parameter $\gamma $ . Numerical results are provided to show the optimal quality and the optimal price designed for each CP. In addition, we find that the proposed contract-based mechanism is superior to the benchmarks from the perspective of maximizing the NSP’s profit.
Approximation of continuous functions defined on a curve by feed-forward neural networks

It's an important problem in computer aided geometry design to approximate continuous functions defined on a smooth curve, which is widely applied in industry and engineering. In this paper, we approximate continuous functions defined on a smooth single-value curve by means of a new and popular tool- single-hidden layer feed-forward neural networks. It's checked that the approximation is simple, quick and can be easily realized by the Matlab.
Analysis of crack stability in concrete dams with chaos optimized neural network

Because calculation of stress intensity factors using the finite element method of the linear elastic fracture mechanics cannot satisfy the need for the real-time monitoring and the real-time analysis of cracks in concrete dams, a four-layer neural network for calculating stress intensity factors is proposed. The neural network is improved by chaos optimization algorithm. An example is given to validate the improvement. The example shows that the optimized neural network can yield-good results.
Categorization of infliximab dose changes and healthcare utilization and expenditures for patients with rheumatoid arthritis in commercially insured and Medicare-eligible populations*

ABSTRACT Objective: To evaluate how changes in infliximab dose influence resource utilization and expenditures for patients with rheumatoid arthritis (RA). Research design and methods: A retrospective analysis using claims from January 1, 1999 through March 31, 2005 in the MedStat MarketScan databases for RA patients who had an increase, decrease, or no change in infliximab dose within 1 year of initiating therapy. Eligibility criteria included at least one claim with a diagnosis of RA and no biologic treatment within 6 months before the index infliximab claim, continuous health plan enrollment (commercial or Medicare) for 6 months before and 12 months after the index date, and three consecutive infliximab infusions. The index and final infliximab doses were estimated from claims data. Results: Data were included for 1678 commercially insured patients and 616 Medicare-eligible patients; 45.4% and 39.3%, respectively, had an increase in dose, 24.7% and 43.2%, respectively, had a decrease in dose, and 29.9% and 17.5%, respectively, had no change in dose. Overall, resource utilization was higher in the increase-in-dose groups and lower in the no change-in-dose groups when compared with the decrease-in-dose groups for both cohorts. Medical costs were also highest for the increase-in-dose groups for both cohorts. Pharmacy expenditures for the no-change-in-dose groups were lower than the decrease-in-dose groups in both cohorts. Conclusions: An increase in dose was the most common dose change for the commercial cohort, while a decrease in dose was the most common dose change for the Medicare-eligible cohort. Patients with an increase in dose had the highest utilization and expenditures while those with no change in dose had the lowest levels. The nature of this utilization needs to be examined to better understand how dosing changes may influence medical utilization. Changes in dose were defined by the difference between the first and final doses and may not have captured changes in interim doses.
Tim4- and MerTK-Mediated Engulfment of Apoptotic Cells by Mouse Resident Peritoneal Macrophages

ABSTRACT Apoptotic cells are swiftly engulfed by macrophages to prevent the release of noxious materials from dying cells. Apoptotic cells expose phosphatidylserine (PtdSer) on their surface, and macrophages engulf them by recognizing PtdSer using specific receptors and opsonins. Here, we found that mouse resident peritoneal macrophages expressing Tim4 and MerTK are highly efficient at engulfing apoptotic cells. Neutralizing antibodies against either Tim4 or MerTK inhibited the macrophage engulfment of apoptotic cells. Tim4-null macrophages exhibited reduced binding and engulfment of apoptotic cells, whereas MerTK-null macrophages retained the ability to bind apoptotic cells but failed to engulf them. The incubation of wild-type peritoneal macrophages with apoptotic cells induced the rapid tyrosine phosphorylation of MerTK, which was not observed with Tim4-null macrophages. When mouse Ba/F3 cells were transformed with Tim4, apoptotic cells bound to the transformants but were not engulfed. Transformation of Ba/F3 cells with MerTK had no effect on the binding or engulfment of apoptotic cells; however, Tim4/MerTK transformants exhibited strong engulfment activity. Taken together, these results indicate that the engulfment of apoptotic cells by resident peritoneal macrophages proceeds in two steps: binding to Tim4, a PtdSer receptor, followed by MerTK-mediated cell engulfment.
A Conserved Patch near the C Terminus of Histone H4 Is Required for Genome Stability in Budding Yeast

ABSTRACT A screen of Saccharomyces cerevisiae histone alanine substitution mutants revealed that mutations in any of three adjacent residues, L97, Y98, or G99, near the C terminus of H4 led to a unique phenotype. The mutants grew slowly, became polyploid or aneuploid rapidly, and also lost chromosomes at a high rate, most likely because their kinetochores were not assembled properly. There was lower histone occupancy, not only in the centromeric region, but also throughout the genome for the H4 mutants. The mutants displayed genetic interactions with the genes encoding two different histone chaperones, Rtt106 and CAF-I. Affinity purification of Rtt106 and CAF-I from yeast showed that much more H4 and H3 were bound to these histone chaperones in the case of the H4 mutants than in the wild type. However, in vitro binding experiments showed that the H4 mutant proteins bound somewhat more weakly to Rtt106 than did wild-type H4. These data suggest that the H4 mutant proteins, along with H3, accumulate on Rtt106 and CAF-I in vivo because they cannot be deposited efficiently on DNA or passed on to the next step in the histone deposition pathway, and this contributes to the observed genome instability and growth defects.
Distinct Mechanisms of Ferritin Delivery to Lysosomes in Iron-Depleted and Iron-Replete Cells

ABSTRACT Ferritin is a cytosolic protein that stores excess iron, thereby protecting cells from iron toxicity. Ferritin-stored iron is believed to be utilized when cells become iron deficient; however, the mechanisms underlying the extraction of iron from ferritin have yet to be fully elucidated. Here, we demonstrate that ferritin is degraded in the lysosome under iron-depleted conditions and that the acidic environment of the lysosome is crucial for iron extraction from ferritin and utilization by cells. Ferritin was targeted for degradation in the lysosome even under iron-replete conditions in primary cells; however, the mechanisms underlying lysosomal targeting of ferritin were distinct under depleted and replete conditions. In iron-depleted cells, ferritin was targeted to the lysosome via a mechanism that involved autophagy. In contrast, lysosomal targeting of ferritin in iron-replete cells did not involve autophagy. The autophagy-independent pathway of ferritin delivery to lysosomes was deficient in several cancer-derived cells, and cancer-derived cell lines are more resistant to iron toxicity than primary cells. Collectively, these results suggest that ferritin trafficking may be differentially regulated by cell type and that loss of ferritin delivery to the lysosome under iron-replete conditions may be related to oncogenic cellular transformation.
Lipolysis in Intraabdorninal Adipose Tissues of Obese Women and Men

Intraabdominal fat in humans is located in two major depots, the omental and mesenteric. We compared basal and stimulated lipolysis in adipose tissue from these two depots and the subcutaneous abdominal depot of obese women and men. Omental fat cells of women are smaller and have lower rates of basal lipolysis than in men. Basal Iipolysis rates are significantly higher in subcutaneous than intraabdominal adipose tissues of both genders. In men, the incremental lipolytic response to norepinephrine is significantly greater in both intraabdominal fat depots than in the subcutaneous fat, while in women tlie response of tlie mesenteric is lower than tlie omental. In women, but not men, responsiveness to tlie beta agonist isoproterenol is also increased in omental tissue. Thus, in women, omental and mesenteric adipose tissues show distinctly different metabolic properties which may moderate the impact of intraabdominal obesity.
Selective Accumulation of Aggregation-Prone Proteasome Substrates in Response to Proteotoxic Stress

ABSTRACT Conditions causing an increase in misfolded or aberrant proteins can impair the activity of the ubiquitin/proteasome system (UPS). This observation is of particular interest, given the fact that proteotoxic stress is closely associated with a large variety of disorders. Although impairment of the UPS appears to be a general consequence of proteotoxic insults, the underlying mechanisms remain enigmatic. Here, we show that heat shock-induced proteotoxic stress resulted in conjugation of ubiquitin to detergent-insoluble protein aggregates, which coincided with reduced levels of free ubiquitin and impediment of ubiquitin-dependent proteasomal degradation. Interestingly, whereas soluble proteasome substrates returned to normal levels after a transient accumulation, the levels of an aggregation-prone substrate remained high even when the free ubiquitin levels were restored. Consistently, overexpression of ubiquitin prevented accumulation of soluble but not aggregation-prone substrates in thermally stressed cells. Notably, cells were also unable to resume degradation of aggregation-prone substrates after treatment with the translation inhibitor puromycin, indicating that selective accumulation of aggregation-prone proteins is a consistent feature of proteotoxic stress. Our data suggest that the failure of the UPS to clear aggregated proteins in the aftermath of proteotoxic stress episodes may contribute to the selective deposition of aggregation-prone proteins in conformational diseases.