Miracle-dz/UniFAR-FTUs huggingface dataset:
A New Deep Learning Algorithm for SAR Scene Classification Based on Spatial Statistical Modeling and Features Re-Calibration

Synthetic Aperture Radar (SAR) scene classification is challenging but widely applied, in which deep learning can play a pivotal role because of its hierarchical feature learning ability. In the paper, we propose a new scene classification framework, named Feature Recalibration Network with Multi-scale Spatial Features (FRN-MSF), to achieve high accuracy in SAR-based scene classification. First, a Multi-Scale Omnidirectional Gaussian Derivative Filter (MSOGDF) is constructed. Then, Multi-scale Spatial Features (MSF) of SAR scenes are generated by weighting MSOGDF, a Gray Level Gradient Co-occurrence Matrix (GLGCM) and Gabor transformation. These features were processed by the Feature Recalibration Network (FRN) to learn high-level features. In the network, the Depthwise Separable Convolution (DSC), Squeeze-and-Excitation (SE) Block and Convolution Neural Network (CNN) are integrated. Finally, these learned features will be classified by the Softmax function. Eleven types of SAR scenes obtained from four systems combining different bands and resolutions were trained and tested, and a mean accuracy of 98.18% was obtained. To validate the generality of FRN-MSF, five types of SAR scenes sampled from two additional large-scale Gaofen-3 and TerraSAR-X images were evaluated for classification. The mean accuracy of the five types reached 94.56%; while the mean accuracy for the same five types of the former tested 11 types of scene was 96%. The high accuracy indicates that the FRN-MSF is promising for SAR scene classification without losing generality.
Effect of nicotinic acid on exogenous myocardial glucose utilization.

UNLABELLED Clinical assessment of myocardial glucose uptake with 18F-fluorodeoxyglucose (18F-FDG) and PET requires the control of circulating substrates to achieve acceptable image quality. METHODS To determine the efficacy of the hypolipemic effect of oral niacin upon myocardial 18F-FDG uptake, five volunteers were studied with 18F-FDG and PET in the fasting state, with and without treatment with niacin. Levels of glucose, fatty acids, insulin and catecholamines were measured at baseline and before and after 18F-FDG administration by programmed infusion. RESULTS No significant changes in glucose or insulin levels occurred with niacin. A significant decrease in fatty acid levels with niacin treatment was associated with a two- to three-fold increase in myocardial glucose utilization rates relative to the fasting state. Furthermore, regional variation in tracer distribution with greater uptake in the lateral wall than the septum or anterior wall in the fasting studies was not present after niacin treatment. CONCLUSION As determined by programmed infusion of 18F-FDG and PET imaging, niacin treatment in normal volunteers was associated with an increase in exogenous glucose utilization by the heart and a decrease in the cardiac regional variation of 18F-FDG. Further studies are needed to compare the relative value of niacin therapy and oral glucose loading for determination of myocardial exogenous glucose utilization rates.
Determinants of intramyocellular lipid concentrations in rat hindleg muscle

The investigation of intramyocellular lipids (IMCLs) with proton MR spectroscopy (1H‐MRS) in humans has recently received increasing attention. IMCL levels correlate with insulin resistance and are affected by diet and exercise, making IMCL an interesting marker for metabolic investigations. In the present in vivo study, the feasibility of using 1H MRS for the detection of IMCL in rats is demonstrated, and the influence of various factors, such as age, gender, muscle type, and rat strain, on IMCL levels is systematically analyzed. In healthy Wistar and Sprague Dawley (SD) rats, the highest ratios of IMCL/tCr were found in young rats, and IMCL/tCr decreased with increasing age. In addition, IMCL concentration was clearly influenced by gender and muscle type. Insulin‐resistant, male, obese, Zucker diabetic fatty (ZDF) rats showed significantly higher IMCL levels than Wistar or SD rats. In conclusion, although IMCL levels are clearly influenced by insulin resistance, several other factors influence IMCL levels, such as age, gender, muscle type, and rat strain. Therefore, when using IMCL as a surrogate marker for insulin resistance, it is necessary to carefully compare results with age‐ and gender‐matched controls, and to use identical conditions. Magn Reson Med 50:242–248, 2003. © 2003 Wiley‐Liss, Inc.
The ParB homologs, Spo0J and Noc, together prevent premature midcell Z ring assembly when the early stages of replication are blocked in Bacillus subtilis

Precise cell division in coordination with DNA replication and segregation is of utmost importance for all organisms. The earliest stage of cell division is the assembly of a division protein FtsZ into a ring, known as the Z ring, at midcell. What still eludes us, however, is how bacteria precisely position the Z ring at midcell. Work in B. subtilis over the last two decades has identified a link between the early stages of DNA replication and cell division. A recent model proposed that the progression of the early stages of DNA replication leads to an increased ability for the Z ring to form at midcell. This model arose through studies examining Z ring position in mutants blocked at different steps of the early stages of DNA replication. Here, we show that this model is unlikely to be correct and the mutants previously studied generate nucleoids with different capacity for blocking midcell Z ring assembly. Importantly, our data suggest that two proteins of the widespread ParB family, Noc and Spo0J are required to prevent Z ring assembly over the bacterial nucleoid and help fine tune the assembly of the Z ring at midcell during the cell cycle.
Cytomegalovirus Infections after Hematopoietic Stem Cell Transplantation: Current Status and Future Immunotherapy

Cytomegalovirus (CMV) infection after hematopoietic stem cell transplantation (HSCT) is one of the critical infectious complications related to host immune recovery. The spectrum of CMV infection is quite extensive, from asymptomatic CMV reactivation presenting mainly as CMV DNAemia to fatal CMV diseases involving gut, liver, lungs, or brain. In addition to organ involvement, CMV reactivation can exert indirect effects such as immunosuppression or graft failure that may result in the development of concurrent infectious complications. Currently, preemptive therapy, which is based on PCR-based monitoring of CMV from blood, is a mainstay enabling improvement in CMV-related outcomes. During the past decades, new antiviral drugs, clinical trials for prophylaxis in high-risk groups, and vaccines for preventing CMV infection have been introduced. In addition, data for immunologic monitoring and adoptive immunotherapy have also been accumulated. Here, we review the current status and recent updates in this field, with future perspectives including immunotherapy in HSCT recipients.
Method for Estimating the Eigenvectors of a Scaled Laplacian Matrix Using the Resonance of Oscillation Dynamics on Networks

Spectral graph theory gives a useful approach to analyzing network structure based on the adjacency matrix or the Laplacian matrix that represents the network topology and link weights. However, in large scale and complex social networks, since it is difficult to know the network topology and link weights, we cannot determine the components of these matrices directly. To solve this problem, we consider a method for indirectly determining a Laplacian matrix from its eigenvalues and eigenvectors. As the first step, our prior study proposed a method for estimating eigenvalues of a Laplacian matrix by using the resonance of oscillation dynamics on networks with no a priori information about the network structure, and showed the effectiveness of this method. In this paper, we propose a method for estimating the eigenvectors of a Laplacian matrix by once again using the resonance of oscillation dynamics on networks.
Irinotecan therapy in adults with recurrent or progressive malignant glioma.

PURPOSE To determine the activity, toxicity, and pharmacokinetics of irinotecan (CPT-11, Camptosar; Pharmacia & Upjohn, Kalamazoo, MI) in the treatment of adults with progressive, persistent, or recurrent malignant glioma. PATIENTS AND METHODS Patients with progressive or recurrent malignant gliomas were enrolled onto this study between October 1996 and August 1997. CPT-11 was given as a 90-minute intravenous (i.v.) infusion at a dose of 125 mg/m2 once weekly for 4 weeks followed by a 2-week rest, which comprised one course. Plasma concentrations of CPT-11 and its metabolites, SN-38 and SN-38 glucuronide (SN-38G), were determined in a subset of patients. RESULTS All 60 patients who enrolled (36 males and 24 females) were treated with CPT-11 and all were assessable for toxicity, response, and survival. Pharmacokinetic data were available in 32 patients. Nine patients (15%; 95% confidence interval, 6% to 24%) had a confirmed partial response, and 33 patients (55%) achieved stable disease lasting more than two courses (12 weeks). Toxicity observed during the study was limited to infrequent neutropenia, nausea, vomiting, and diarrhea. CPT-11, SN-38, and SN-38G area under the plasma concentration-time curves through infinite time values in these patients were approximately 40%, 25%, and 25%, respectively, of those determined previously in patients with metastatic colorectal cancer not receiving antiepileptics or chronic dexamethasone treatment. CONCLUSION Response results document that CPT-11, given with a standard starting dose and treatment schedule, has activity in patients with recurrent malignant glioma. However, the low incidence of severe toxicity and low plasma concentrations of CPT-11 and SN-38 achieved in this patient population suggest that concurrent treatment with anticonvulsants and dexamethasone enhances drug clearance.
Burst Spinal Cord Stimulation: A Clinical Review

Abstract Objective Clinical review on outcomes using burst spinal cord stimulation (SCS) in the treatment of chronic, intractable pain. Design Narrative clinical literature review conducted utilizing a priori search terms including key words for burst spinal cord stimulation. Synthesis and reporting of data from publications including an overview of comparative SCS outcomes. Results Burst SCS demonstrated greater pain relief over tonic stimulation in multiple studies, which included blinded, sham-controlled, randomized trials. Additionally, burst stimulation impacts multiple dimensions of pain, including somatic pain as well as emotional and psychological elements. Patient preference is weighted toward burst over tonic due to increased pain relief, a lack of paresthesias, and impression of change in condition. Conclusion Burst SCS has been shown to be both statistically and clinically superior to tonic stimulation and may provide additional benefits through different mechanisms of action. Further high-quality controlled studies are warranted to not only elucidate the basic mechanisms of burst SCS but also address how this unique stimulation signature/pattern may more adequately handle the multiple affective dimensions of pain in varying patient populations.
Reiterative Mechanisms of Retinoic Acid Signaling during Vertebrate Heart Development

Tightly-regulated levels of retinoic acid (RA) are critical for promoting normal vertebrate development. The extensive history of research on RA has shown that its proper regulation is essential for cardiac progenitor specification and organogenesis. Here, we discuss the roles of RA signaling and its establishment of networks that drive both early and later steps of normal vertebrate heart development. We focus on studies that highlight the drastic effects alternative levels of RA have on early cardiomyocyte (CM) specification and cardiac chamber morphogenesis, consequences of improper RA synthesis and degradation, and known effectors downstream of RA. We conclude with the implications of these findings to our understanding of cardiac regeneration and the etiologies of congenital heart defects.
The reaction of heart and other organ extracts with the sera of animals immunized with group A streptococci.

Extracts of guinea-pig skeletal muscle, heart, kidney and liver tissues contain soluble antigens which react in gel precipitation and immunoelectrophoresis with sera of animals immunized with group A streptococci, and with γ-globulin preparations obtained from these sera. These are specific immunological reactions. The antigens in extracts of heart tissue and other organs are proteins. They are cross-reactive antigens since absorption of sera with homologous strains of streptococci abolishes these reactions.
DeepDSC: A Deep Learning Method to Predict Drug Sensitivity of Cancer Cell Lines

High-throughput screening technologies have provided a large amount of drug sensitivity data for a panel of cancer cell lines and hundreds of compounds. Computational approaches to analyzing these data can benefit anticancer therapeutics by identifying molecular genomic determinants of drug sensitivity and developing new anticancer drugs. In this study, we have developed a deep learning architecture to improve the performance of drug sensitivity prediction based on these data. We integrated both genomic features of cell lines and chemical information of compounds to predict the half maximal inhibitory concentrations <inline-formula><tex-math notation="LaTeX">$(\text{IC}_{50})$</tex-math><alternatives><mml:math><mml:mrow><mml:mo>(</mml:mo><mml:msub><mml:mtext>IC</mml:mtext><mml:mn>50</mml:mn></mml:msub><mml:mo>)</mml:mo></mml:mrow></mml:math><inline-graphic xlink:href="li-ieq1-2919581.gif"/></alternatives></inline-formula> on the Cancer Cell Line Encyclopedia (CCLE) and the Genomics of Drug Sensitivity in Cancer (GDSC) datasets using a deep neural network, which we called DeepDSC. Specifically, we first applied a stacked deep autoencoder to extract genomic features of cell lines from gene expression data, and then combined the compounds’ chemical features to these genomic features to produce final response data. We conducted 10-fold cross-validation to demonstrate the performance of our deep model in terms of root-mean-square error (RMSE) and coefficient of determination <inline-formula><tex-math notation="LaTeX">$\text{R}^{2}$</tex-math><alternatives><mml:math><mml:msup><mml:mtext>R</mml:mtext><mml:mn>2</mml:mn></mml:msup></mml:math><inline-graphic xlink:href="li-ieq2-2919581.gif"/></alternatives></inline-formula>. We show that our model outperforms the previous approaches with RMSE of 0.23 and <inline-formula><tex-math notation="LaTeX">$\text{R}^{2}$</tex-math><alternatives><mml:math><mml:msup><mml:mtext>R</mml:mtext><mml:mn>2</mml:mn></mml:msup></mml:math><inline-graphic xlink:href="li-ieq3-2919581.gif"/></alternatives></inline-formula> of 0.78 on CCLE dataset, and RMSE of 0.52 and <inline-formula><tex-math notation="LaTeX">$\text{R}^{2}$</tex-math><alternatives><mml:math><mml:msup><mml:mtext>R</mml:mtext><mml:mn>2</mml:mn></mml:msup></mml:math><inline-graphic xlink:href="li-ieq4-2919581.gif"/></alternatives></inline-formula> of 0.78 on GDSC dataset, respectively. Moreover, to demonstrate the prediction ability of our models on novel cell lines or novel compounds, we left cell lines originating from the same tissue and each compound out as the test sets, respectively, and the rest as training sets. The performance was comparable to other methods.
Impact and Relevance of the Unfolded Protein Response in HNSCC

Head and neck squamous cell carcinomas (HNSCC) encompass a heterogeneous group of solid tumors that arise from the upper aerodigestive tract. The tumor cells face multiple challenges including an acute demand of protein synthesis often driven by oncogene activation, limited nutrient and oxygen supply and exposure to chemo/radiotherapy, which forces them to develop adaptive mechanisms such as the Unfolded Protein Response (UPR). It is now well documented that the UPR, a homeostatic mechanism, is induced at different stages of cancer progression in response to intrinsic (oncogenic activation) or extrinsic (microenvironment) perturbations. This review will discuss the role of the UPR in HNSCC as well as in the key processes that characterize the physiology of HNSCC. The role of the UPR in the clinical context of HNSCC will also be addressed.
Does smoking marijuana contribute to the risk of developing lung cancer?

Different concentrations of THC stimulate formation of reactive oxygen species in cells that are exposed to smoke from the distal end of the “joint,” indicating that cell damage is caused by toxic gas in the smoke. Lung cancer has emerged as the most common cause of cancer-related death in men and women in the United States (Edmondson, 2008; Swaney, 2002). Marijuana, a product of the Cannabis sativa plant, is the most frequently used illegal substance in the United States (Mehra, Moore, Crothers, Tetrauld, & Fiellin, 2006). The question explored here is whether evidence links marijuana use to lung cancer development. Tobacco use was known to Native Americans, but the first recorded harvest of a tobacco crop in North America was in 1611 in the Jamestown colony (Cruz et al., 1998). Marijuana has a world history that dates back to 4000 BC, when it was grown in China for the hemp fibers. Oral traditions from China list medical uses for marijuana as far back as 2700 BC (Zuardi, 2005). Marijuana use in the United States dates to the early 1900s, when it was used as a cure for morphine addiction (Cruz et al., 1998). Marijuana primarily is obtained from the leaves and flower heads of the female Cannabis sativa plant. The active ingredient is delta-9 tetrahydrocannabinol (THC), with the highest content found in the flower heads and decreasing in concentration from the stems down to the seeds (Campbell, 1999; Hall & Solowij, 1998).
Romantic relationship breakup: An experimental model to study effects of stress on depression (-like) symptoms

The occurrence of a stressful event is considered to increase the risk of developing depression. In the present study we explore whether the breakup of a romantic relationship can be used as an experimental model to study a depression-like state during a period of stress in individuals without a psychiatric disorder. The primary aim of our study was to investigate: 1) whether individuals with a recent romantic relationship breakup (‘‘heartbreak”) demonstrate symptoms of depression, 2) how to describe heartbreak characteristics based on data from a comprehensive questionnaire battery, and 3) whether this description can capture severity of depression symptoms. Secondary, we were interested in gender differences with regard to the above study objectives. Subjects who have experienced a relationship breakup in the preceding six months (N = 71) or are in a romantic relationship (N = 46) participated in our study. A questionnaire battery was administered to acquire information related to depression, mood, the breakup and (former) relationship. Principal Component Analysis with Procrustes bootstrapping was performed to extract components from the questionnaire data. Even though our sample of individuals who recently have experienced a relationship breakup can be on average considered non-depressed, group-level depression scores were elevated compared to individuals in a relationship (p = .001) and 26.8% reported symptoms corresponding to mild, moderate or severe depression. We described heartbreak by two principal components interpreted as ‘‘sudden loss” and ‘‘lack of positive affect”, respectively. Highly significant correlations between the component scores and depression scores were found (p < .001 and p < .001, respectively), although these correlations differed between the genders. Based on these findings, we propose that the experience of a romantic relationship breakup is a viable experimental model to examine symptoms of depression in individuals without a psychiatric disorder. This way, stress-related coping and depression vulnerability can be studied in further research.
Effects of methylphenidate on the ERP amplitude in youth with ADHD: A double-blind placebo-controlled cross-over EEG study

Methylphenidate (MPH) is a first line drug for attention-deficit/hyperactivity disorder (ADHD), yet the neuronal mechanisms underlying the condition and the treatment are still not fully understood. Previous EEG studies on the effect of MPH in ADHD found changes in evoked response potential (ERP) components that were inconsistent between studies. These inconsistencies highlight the need for a well-designed study which includes multiple baseline sessions and controls for possible fatigue, learning effects and between-days variability. To this end, we employ a double-blind placebo-controlled cross-over study and explore the effect of MPH on the ERP response of subjects with ADHD during a Go/No-Go cognitive task. Our ERP analysis revealed significant differences in ADHD subjects between the placebo and MPH conditions in the frontal-parietal region at 250ms-400ms post stimulus (P3). Additionally, a decrease in the late 650ms-800ms ERP component (LC) is observed in frontal electrodes of ADHD subjects compared to controls. The standard deviation of response time of ADHD subjects was significantly smaller in the MPH condition compared to placebo and correlated with the increased P3 ERP response in the frontoparietal electrodes. We suggest that mental fatigue plays a role in the decrease of the P3 response in the placebo condition compared to pre-placebo, a phenomenon that is significant in ADHD subjects but not in controls, and which is interestingly rectified by MPH.
Hypersensitivity Pneumonitis: Current Concepts of Pathogenesis and Potential Targets for Treatment.

Hypersensitivity pneumonitis (HP) is a disease triggered by different inducers in susceptible individuals. The inhaled inducing particles can be of both organic and less frequently inorganic origin. Environmental exposure is usually complex and exposure to monocomponent antigen is rather rare. The disease has heterogenous clinical presentation based on the interaction of individual host factors and components of inducing matter. The complex underlying pathogenetic mechanisms associated to HP contribute to the vast interindividual variation in clinical presentation of the disease. Innate immune response plays a substantial role in antigen recognition, processing and presentation. The antigens are then expressed in context with MHC molecules on surface of antigen presenting cells and initiate the humoral and cellular adaptive immune response. HP is characterized by an exaggerated T cell-mediated immunity primarily Th1 type, however, immune-complex-mediated lung injury with specific immunoglobulin G antibodies may participate as well. Persistent and/or recurrent exposure of the inducer/s leads to progressive fibrosis and manifest features of chronic HP similar to patients with idiopathic pulmonary fibrosis. Genetic factors, senescence and biochemical properties of inducer and contributing factors like smoking and air pollutants can contribute to unfavourable fibroproliferative course of HP. Aside avoidance of exposure, and corticosteroids in acute HP, there is currently no evidence- based treatment in HP. New treatment targets should be identified based on revelation of critical pathogenetic steps, Clinical trials utilizing currently available antifibrotic medications and/or newer agents targeting the innate immune and fibrotic pathway are warranted.