Miracle-dz/UniFAR-FTUs huggingface dataset:
Image blur classification and blur usefulness assessment

Blur classification is an important and widely-studied problem in computer vision. State-of-the-art blur classification methods are designed and verified using man-made blur images of known blur types and blur kernels. In reality, natural blur occurs under wild-conditions, and thus cannot be simply simulated by several hand-crafted blur kernels. Hence, conventional blur classification methods cannot deal with complex real-world blur classification tasks. In this paper, we propose a new blur classification model, which learns from real-world images by convolutional neural network. On the basis of the blur classification network result, we further propose an interesting and useful problem, called blur usefulness assessment, which assesses the usefulness of blur image. To support blur classification and blur usefulness assessment, we establish a useful blur image classification dataset, UBICD, which contains 1; 000 sharp images and 1; 000 blur images (500 useful and 500 useless images). Compared with state-of-the-art blur classification methods, our method have achieved the highest blur classification accuracy of 98.1%. Our blur usefulness assessment also achieves an accuracy of 89.1%.
STAT1β Is Not Dominant Negative and Is Capable of Contributing to Gamma Interferon-Dependent Innate Immunity

ABSTRACT The transcription factor STAT1 is essential for interferon (IFN)-mediated immunity in humans and mice. STAT1 function is tightly regulated, and both loss- and gain-of-function mutations result in severe immune diseases. The two alternatively spliced isoforms, STAT1α and STAT1β, differ with regard to a C-terminal transactivation domain, which is absent in STAT1β. STAT1β is considered to be transcriptionally inactive and to be a competitive inhibitor of STAT1α. To investigate the functions of the STAT1 isoforms in vivo, we generated mice deficient for either STAT1α or STAT1β. As expected, the functions of STAT1α and STAT1β in IFN-α/β- and IFN-λ-dependent antiviral activity are largely redundant. In contrast to the current dogma, however, we found that STAT1β is transcriptionally active in response to IFN-γ. In the absence of STAT1α, STAT1β shows more prolonged IFN-γ-induced phosphorylation and promoter binding. Both isoforms mediate protective, IFN-γ-dependent immunity against the bacterium Listeria monocytogenes, although with remarkably different efficiencies. Our data shed new light on the potential contributions of the individual STAT1 isoforms to STAT1-dependent immune responses. Knowledge of STAT1β's function will help fine-tune diagnostic approaches and help design more specific strategies to interfere with STAT1 activity.
Effects of Pharmacologic Agents on the Clearance of Airway Secretions

As we have seen, clearance of secretions from the tracheobronchial tree is achieved by mucociliary transport and cough. An index of mucociliary function can be obtained by monitoring the distance travelled by a marker placed on the mucosa of the trachea or main bronchi over a given time. The division of distance with time yields the velocity of mucus (transporting the marker) in the particular airway. An alternative way of measuring overall efficiency of the mucociliary escalator is by monitoring (with external gamma counters) the rate of removal of deposited insoluble radiotracer particles (such as polystyrene or Teflon) after inhalation. These particles, labeled unleachably with a gamma-emitting radionuclide, are inhaled by volunteer subjects under strictly controlled conditions. Their rate of removal from the lungs is a function of the transportability of airway secretions carrying them. The radiation dose delivered to the lungs from such procedures is usually a fraction of that received from a standard posteroanterior chest radiograph. The rate of removal of airway secretions is a function of their transportability and can be affected by various physiologic factors and pharmacologic agents as well as environmental pollutants and disease. This section reviews the effect of various pharmacologic agents on the clearance of airway secretions via the mucociliary escalator. The information is based predominantly on studies carried out in humans. MUCOLYTICS AND EXPECTORANTS
Effects of cyclosporine on adriamycin induced nephropathy

SUMMARY: The effect of cyclosporine on adriamycin nephropathy was studied over both short (6 weeks) and long (26 weeks) periods. In the short‐term study, cyclosporine was introduced 2 weeks after nephritis induction and in the long‐term study, 14 weeks after the first adriamycin injection. the animals with adriamycin nephropathy treated with cyclosporine, studied for 6 weeks, developed proteinuria with increasd renal size and glomerular area. the nephrotic animals treated with cyclosporine showed less proteinuria than the nephrotic control animals. There were no differences in glomerular area, creatinine clearance or serum creatinine and kidney weight between the treated nephrotic group and the health control group. the nephrotic animals, studied for the longer period, developed intense proteinuria, decreased creatinine clearance, glomerular necrosis and sclerosis, severe tubulointerstitial nephritis, increased hydroxyproline concentration and tubulointerstitial area. No difference was observed between the nephrotic animals treated with cyclosporine and those not treated. In conclusion, Cyclosporine A reduced proteinuria, glomerular hypertrophy and kidney weight in rats with short‐term nephropathy but had no effect on the established nephropathy.
Excess mortality and guideline-indicated care following non-ST-elevation myocardial infarction

Background: Adherence to guideline-indicated care for the treatment of non-ST-elevation myocardial infarction (NSTEMI) is associated with improved outcomes. We investigated the extent and consequences of non-adherence to guideline-indicated care across a national health system. Methods: A cohort study (ClinicalTrials.gov identifier: NCT02436187) was conducted using data from the Myocardial Ischaemia National Audit Project (n = 389,057 NSTEMI, n = 247 hospitals, England and Wales, 2003–2013). Accelerated failure time models were used to quantify the impact of non-adherence on survival according to dates of guideline publication. Results: Over a period of 1,079,044 person-years (median 2.2 years of follow-up), 113,586 (29.2%) NSTEMI patients died. Of those eligible to receive care, 337,881 (86.9%) did not receive one or more guideline-indicated intervention; the most frequently missed were dietary advice (n = 254,869, 68.1%), smoking cessation advice (n = 245,357, 87.9%), P2Y12 inhibitors (n = 192,906, 66.3%) and coronary angiography (n = 161,853, 43.4%). Missed interventions with the strongest impact on reduced survival were coronary angiography (time ratio: 0.18, 95% confidence interval (CI): 0.17–0.18), cardiac rehabilitation (time ratio: 0.49, 95% CI: 0.48–0.50), smoking cessation advice (time ratio: 0.53, 95% CI: 0.51–0.57) and statins (time ratio: 0.56, 95% CI: 0.55–0.58). If all eligible patients in the study had received optimal care at the time of guideline publication, then 32,765 (28.9%) deaths (95% CI: 30,531–33,509) may have been prevented. Conclusion: The majority of patients hospitalised with NSTEMI missed at least one guideline-indicated intervention for which they were eligible. This was significantly associated with excess mortality. Greater attention to the provision of guideline-indicated care for the management of NSTEMI will reduce premature cardiovascular deaths.
CREB Binding Protein (CBP) Activation Is Required for Luteinizing Hormone Beta Expression and Normal Fertility in Mice

ABSTRACT Normal function of the hypothalamic-pituitary-gonadal axis is dependent on gonadotropin-releasing hormone (GNRH)-stimulated synthesis and secretion of luteinizing hormone (LH) from the pituitary gonadotroph. While the transcriptional coactivator CREB binding protein (CBP) is known to interact with Egr-1, the major mediator of GNRH action on the Lhb gene, the role of CBP in Lhb gene expression has yet to be characterized. We show that in the LβT2 gonadotroph cell line, overexpression of CBP augmented the response to GNRH and that knockdown of CBP eliminated GNRH responsiveness. While GNRH-mediated phosphorylation of CBP at Ser436 increased the interaction with Egr-1 on the Lhb promoter, loss of this phosphorylation site eliminated GNRH-mediated Lhb expression in LβT2 cells. In vivo, loss of CBP phosphorylation at Ser436 rendered female mice subfertile. S436A knock-in mice had disrupted estrous cyclicity and reduced responsiveness to GNRH. Our results show that GNRH-mediated phosphorylation of CBP at Ser436 is required for Egr-1 to activate Lhb expression and is a requirement for normal fertility in female mice. As CBP can be phosphorylated by other factors, such as insulin, our studies suggest that CBP may act as a key regulator of Lhb expression in the gonadotroph by integrating homeostatic information with GNRH signaling.
The Actin-Binding Protein PPP1r18 Regulates Maturation, Actin Organization, and Bone Resorption Activity of Osteoclasts

ABSTRACT Osteoclasts resorb bone by attaching on the bone matrix and forming a sealing zone. In Src-deficient mice, osteoclasts cannot form the actin ring, a characteristic actin structure that seals the resorbed area, and resorb hardly any bone as a result. However, the molecular mechanism underlying the role of Src in the regulation and organization of the actin ring is still unclear. We identified an actin-regulatory protein, protein phosphatase 1 regulatory subunit 18 (PPP1r18), as an Src-binding protein in an Src-, Yes-, and Fyn-deficient fibroblast (SYF) cell line overexpressing a constitutively active form of Src. PPP1r18 was localized in the nucleus and actin ring. PPP1r18 overexpression in osteoclasts inhibited terminal differentiation, actin ring formation, and bone-resorbing activity. A mutation of the protein phosphatase 1 (PP1)-binding domain of PPP1r18 rescued these phenotypes. In contrast, PPP1r18 knockdown promoted terminal differentiation and actin ring formation. In summary, we showed that PPP1r18 likely plays a role in podosome organization and bone resorption.
Optimization of cooperative spectrum sensing with energy detection in cognitive radio networks

We consider cooperative spectrum sensing in which multiple cognitive radios collaboratively detect the spectrum holes through energy detection and investigate the optimality of cooperative spectrum sensing with an aim to optimize the detection performance in an efficient and implementable way. We derive the optimal voting rule for any detector applied to cooperative spectrum sensing. We also optimize the detection threshold when energy detection is employed. Finally, we propose a fast spectrum sensing algorithm for a large network which requires fewer than the total number of cognitive radios in cooperative spectrum sensing while satisfying a given error bound.
Outage analysis and diversity-multiplexing tradeoff bounds for opportunistic relaying coded cooperation and distributed space-time coding coded cooperation

In this paper, we analyze the outage probability of coded cooperation in opportunistic relaying (OR-CC) and distributed space-time coding (DSTC-CC) cooperative communication systems at arbitrary signal to noise ratios (SNRs) and number of available relays assuming Rayleigh fading channels. Furthermore, we obtain lower and upaper bounds for the diversity multiplexing tradeoff (DMT) for OR-CC and DSTC-CC schemes in the cases where the source node is/is not included in the cooperation. Simulation results confirm our analysis.
Differential Feedback of MIMO Channel Gram Matrices Based on Geodesic Curves

This paper proposes a differential quantization strategy to be used in the feedback link of a multiple-input multiple-output (MIMO) communication system. This algorithm is applied to the channel Gram matrix using geodesic curves and exploiting the intrinsic geometry of positive definite Hermitian matrices. It also exploits the temporal correlation of the channel, and follows on average the gradient of the cost function associated to the transmitter design criterion. A full description of the algorithm, including the computational cost and a numerical analysis of the effect of delays and errors in the feedback link is presented. Simulation results show that the proposed algorithm improves other techniques based on the direct quantization of the channel response matrix or the quantization of the subspace spanned by the strongest eigenmodes of the MIMO channel, i.e., Grassmannian based techniques. The main drawback of Grassmannian based algorithms is that the transmitter is constrained to apply a uniform power allocation among spatial transmission modes, which is not forced in the algorithm proposed in this paper.
Performance Analysis in the Downlink of Asynchronous OFDM/FBMC Based Multi-Cellular Networks

This paper provides a theoretical performance evaluation of the downlink of asynchronous orthogonal frequency division multiplexing (OFDM) and filter bank based multicarrier (FBMC) cellular radio communication systems. An accurate derivation, for the interference caused by the timing synchronization errors in the neighboring cells, is developed. The multipath effects on the interfering and desired signal are also considered. Based on computing the moment generating functions of the interference power, exact expressions are derived for average error rates of OFDM and FBMC systems considering the frequency correlation fading in the case of block subcarrier assignment scheme.
MCL-1 Depletion Impairs DNA Double-Strand Break Repair and Reinitiation of Stalled DNA Replication Forks

ABSTRACT Myeloid cell leukemia 1 (MCL-1) is a prosurvival BCL-2 protein family member highly expressed in hematopoietic stem cells (HSCs) and regulated by growth factor signals that manifest antiapoptotic activity. Here we report that depletion of MCL-1 but not its isoform MCL-1S increases genomic instability and cell sensitivity to ionizing radiation (IR)-induced death. MCL-1 association with genomic DNA increased postirradiation, and the protein colocalized with 53BP1 foci. Postirradiation, MCL-1-depleted cells exhibited decreased γ-H2AX foci, decreased phosphorylation of ATR, and higher levels of residual 53BP1 and RIF1 foci, suggesting that DNA double-strand break (DSB) repair by homologous recombination (HR) was compromised. Consistent with this model, MCL-1-depleted cells had a reduced frequency of IR-induced BRCA1, RPA, and Rad51 focus formation, decreased DNA end resection, and decreased HR repair in the DR-GFP DSB repair model. Similarly, after HU induction of stalled replication forks in MCL-1-depleted cells, there was a decreased ability to subsequently restart DNA synthesis, which is normally dependent upon HR-mediated resolution of collapsed forks. Therefore, the present data support a model whereby MCL-1 depletion increases 53BP1 and RIF1 colocalization at DSBs, which inhibits BRCA1 recruitment, and sensitizes cells to DSBs from IR or stalled replication forks that require HR for repair.
P2Y4 Receptor-Mediated Pinocytosis Contributes to Amyloid Beta-Induced Self-Uptake by Microglia

ABSTRACT Brain disturbances, like injuries or aberrant protein deposits, evoke nucleotide release or leakage from cells, leading to microglial chemotaxis and ingestion. Recent studies have identified P2Y12 purinergic receptors as triggers for microglial chemotaxis and P2Y6 receptors as mediators for phagocytosis. However, pinocytosis, known as the internalization of fluid-phase materials, has received much less attention. We found that ATP efficiently triggered pinocytosis in microglia. Pharmacological analysis and knockdown experiments demonstrated the involvement of P2Y4 receptors and the phosphatidylinositol 3-kinase/Akt cascade in the nucleotide-induced pinocytosis. Further evidence indicated that soluble amyloid beta peptide 1-42 induced self-uptake in microglia through pinocytosis, a process involving activation of P2Y4 receptors by autocrine ATP signaling. Our results demonstrate a previously unknown function of ATP as a “drink me” signal for microglia and P2Y4 receptors as a potential therapeutic target for the treatment of Alzheimer's disease.
Design of OMC-MAC: An Opportunistic Multi-Channel MAC with QoS Provisioning for Distributed Cognitive Radio Networks

Dynamic resource availability and lack of central control unit offer many challenges while designing medium access control (MAC) protocol for a distributed cognitive radio network (DCRN). In this paper, we propose a novel MAC design for DCRN which provides an efficient approach to address quality of service (QoS) requirements of delay sensitive applications by defining higher priority to such applications during channel reservation. It also combats other major challenges such as efficient spectrum utilization, multi-channel hidden terminal problem (MHTP) and collision with primary user (PU) due to sensing error at SU. We develop an analytical framework to study the performance of the proposed protocol. We then compare the performance of proposed protocol with those of two existing protocols. Comparison results show that proposed MAC outperforms the existing protocols by providing better throughput and reducing DCRN users' collision probability with PUs in presence of sensing error. The results achieved from the analytical model and validated by simulations show that our simple yet efficient design identifies and fulfils the QoS requirements of delay sensitive applications, achieves excellent spectrum utilization, shows superb robustness in presence of sensing errors and handles MHTP effectively.
Mild Glucose Starvation Induces KDM2A-Mediated H3K36me2 Demethylation through AMPK To Reduce rRNA Transcription and Cell Proliferation

ABSTRACT Environmental conditions control rRNA transcription. Previously, we found that serum and glucose deprivation induces KDM2A-mediated H3K36me2 demethylation in the rRNA gene (rDNA) promoter and reduces rRNA transcription in the human breast cancer cell line MCF-7. However, the molecular mechanism and biological significance are still unclear. In the present study, we found that glucose starvation alone induced the KDM2A-dependent reduction of rRNA transcription. The treatment of cells with 2-deoxy-d-glucose, an inhibitor of glycolysis, reduced rRNA transcription and H3K36me2 in the rDNA promoter, both of which were completely dependent on KDM2A in low concentrations of 2-deoxy-d-glucose, that is, mild starvation conditions. The mild starvation induced these KDM2A activities through AMP-activated kinase (AMPK) but did not affect another AMPK effector of rRNA transcription, TIF-IA. In the triple-negative breast cancer cell line MDA-MB-231, the mild starvation also reduced rRNA transcription in a KDM2A-dependent manner. We detected KDM2A in breast cancer tissues irrespective of their estrogen receptor, progesterone receptor, and HER2 status, including triple-negative cancer tissues. In both MCF-7 and MDA-MB-231 cells, mild starvation reduced cell proliferation, and KDM2A knockdown suppressed the reduction of cell proliferation. These results suggest that under mild glucose starvation AMPK induces KDM2A-dependent reduction of rRNA transcription to control cell proliferation.
Genomic Uracil Homeostasis during Normal B Cell Maturation and Loss of This Balance during B Cell Cancer Development

ABSTRACT Activation-induced deaminase (AID) converts DNA cytosines to uracils in immunoglobulin genes, creating antibody diversification. It also causes mutations and translocations that promote cancer. We examined the interplay between uracil creation by AID and its removal by UNG2 glycosylase in splenocytes undergoing maturation and in B cell cancers. The genomic uracil levels remain unchanged in normal stimulated B cells, demonstrating a balance between uracil generation and removal. In stimulated UNG−/− cells, uracil levels increase by 11- to 60-fold during the first 3 days. In wild-type B cells, UNG2 gene expression and enzymatic activity rise and fall with AID levels, suggesting that UNG2 expression is coordinated with uracil creation by AID. Remarkably, a murine lymphoma cell line, several human B cell cancer lines, and human B cell tumors expressing AID at high levels have genomic uracils comparable to those seen with stimulated UNG−/−splenocytes. However, cancer cells express UNG2 gene at levels similar to or higher than those seen with peripheral B cells and have nuclear uracil excision activity comparable to that seen with stimulated wild-type B cells. We propose that more uracils are created during B cell cancer development than are removed from the genome but that the uracil creation/excision balance is restored during establishment of cell lines, fixing the genomic uracil load at high levels.
Orthogonal Transmissions for Spectrum Underlay MISO Cognitive Radio

This work studies a cognitive radio (CR) communication system in which multiple antennas assist the secondary user to achieve transmission diversity, while the constraint of zero interference to the primary user is satisfied. We show that due to the zero interference constraint, the secondary link may occasionally suffer from low signal levels, as if it is in deep fading. Employing space time coding for diversity does not help this situation. We show that a beamformer that is mutually orthogonal in time domain across the antennas is effective in mitigating the low signal effects. Further, N antennas provide an equivalent (N-1) × 1 Rayleigh channel due to the function of this beamformer. The effect of a non-orthogonal beamformer is also analyzed and shown by simulations.
Unusual Telomeric DNAs in Human Telomerase-Negative Immortalized Cells

ABSTRACT A significant fraction of human cancer cells and immortalized cells maintain telomeres in a telomerase-independent manner called alternative lengthening of telomeres (ALT). It has been suggested that ALT involves homologous recombination that is expected to generate unique intermediate DNAs. However, the precise molecular mechanism of ALT is not known. To gain insight into how telomeric DNAs (T-DNAs) are maintained in ALT, we examined the physical structures of T-DNAs in ALT cells. We found abundant single-stranded regions in both G and C strands of T-DNAs. Moreover, two-dimensional gel electrophoreses and native in-gel hybridization analyses revealed novel ALT-specific single-stranded T-DNAs, in addition to previously reported t-circles. These newly identified ALT-specific T-DNAs include (i) the t-complex, which consists of highly branched T-DNAs with large numbers of internal single-stranded portions; (ii) ss-G, which consists of mostly linear single-G-strand T-DNAs; and (iii) ss-C, which consists of most likely circular single-C-strand T-DNAs. Cellular-DNA fractionation by the Hirt protocol revealed that t-circles and ss-G exist in ALT cells as extrachromosomal and chromatin-associated DNAs. We propose that such ALT-specific T-DNAs are produced by telomere metabolism specific to ALT, namely, homologous recombination and the rolling-circle replication mechanism.