Miracle-dz/UniFAR-FTUs huggingface dataset:
The Impact of Exercise on Short-term Memory Fading of Cardiac Rehabilitation Patients in Rural Eastern Kentucky

About 60% of cardiac patients experience some cognitive impairment and may develop negative cognitive functioning after revascularization procedures. Cognitive impairment can be a major impediment of teaching cardiac patients lifestyle behavior changes, such as the importance of starting an exercise program. Impaired short-term memory could limit understanding of the facts, or their immediate importance. However, there is evidence that exercise may improve short-term memory. Thus, the purpose of this study was to determine the impact of exercise on the acute fading effect of short-term memory for cardiac patients. The conceptual framework is supported by human information processing theories and the Brown Peterson paradigm. This quantitative, quasi-experimental study tested cardiac patients’ short-term memory fading, using a short-term memory test, pre and post 60 minutes of exercise. A repeated measures ANOVA was used to analyze the mean scores for each memory test. The target population was from a rural southeastern US State, where one sample of 40 cardiac patients that experienced revascularization procedures was studied. An immediate increase in scores was observed after exercise, which persisted for 15 minutes, and then began to fade. Thus, an ideal window of delivery of cardiac patient educational information was identified immediately, following exercise. A fading of scores was identified throughout the duration of the study, which means participant effort level decreased with continued testing. The positive social change implications include understanding the optimal delivery timing of educational counseling for cardiac patients, in a clinical setting that can result in improvements in short-term memory. Structured Abstract Purpose: The purpose of this study was to determine the impact of exercise on the acute fading effect of short-term memory for cardiac patients. Methods: This quantitative, quasi-experimental study tested cardiac patients’ short-term memory fading, using a short-term memory test, pre and post 60 minutes of exercise. A repeated measures ANOVA was used to analyze the mean scores for each memory test. Results: An immediate increase in scores was observed after exercise, which persisted for 15 minutes, and then began to fade. The interaction of time and day was used to best analyze effects and report results. The time effect (relationship of exercise on short-term memory over time) is reported using Wilks’ Lambda results from the multivariate tests. Wilks’s Λ=. 19, F(3, 38)=55.52, p<. 001, multivariate η2=. 81. The day effect results are Wilks’s Λ=. 88, F(2, 39)=2.71, p=. 081, multivariate η 2 =. 12. Thus, an ideal window of delivery of cardiac patient educational information
Clinical Performance Of An Automated Systemic Inflammatory Response Syndrome (SIRS) / Organ Dysfunction Alert: A System-Based Patient Safety Project

Objective: We have employed our electronic medical record (EMR) in an effort to identify patients at the onset of severe sepsis through an automated analysis that identifies simultaneous occurrence of systemic inflammatory response syndrome (SIRS) and organ dysfunction. The purpose of this study was to determine the positive predictive value of this alert for severe sepsis and other important outcomes in hospitalized adults. Design: Prospective cohort. Setting: Banner Good Samaritan Medical Center, Phoenix AZ Patients: Forty adult inpatients who triggered alert logic within our EMR indicating simultaneous occurrence of SIRS and organ dysfunction. Interventions: Interview of bedside nurse and chart review within six hours of alert firing to determine the clinical event that triggered each alert. Results: Eleven of 40 patients (28%) had a major clinical event (immediately lifethreatening illness) associated with the alert firing. Severe sepsis or septic shock accounted for four of these – yielding a positive predictive value of 0.10 (95%CI: 0.040.23) of the alert for detection of severe sepsis. The positive predictive value of the alert for detection of major clinical events was 0.28 (95%CI: 0.16-0.43), and for detecting either a major or minor clinical event was 0.45 (95%CI: 0.31-0.60). Twenty-two of 40 patients (55%) experienced a false alert. Conclusions: Our first-generation SIRS/organ dysfunction alert has a low positive predictive value for severe sepsis, and generates many false alerts, but shows promise for the detection of acute clinical events that require immediate attention. We are currently investigating refinements of our automated alert system which we believe have potential to enhance patient safety.
Invariant NKT Cell Reconstitution in Pediatric Leukemia Patients Given HLA-Haploidentical Stem Cell Transplantation Defines Distinct CD4+ and CD4− Subset Dynamics and Correlates with Remission State

Immune reconstitution plays a crucial role on the outcome of patients given T cell-depleted HLA-haploidentical hematopoietic stem cell transplantation (hHSCT) for hematological malignancies. CD1d-restricted invariant NKT (iNKT) cells are innate-like, lipid-reactive T lymphocytes controlling infections, cancer, and autoimmunity. Adult mature iNKT cells are divided in two functionally distinct CD4+ and CD4− subsets that express the NK receptor CD161 and derive from thymic CD4+CD161− precursors. We investigated iNKT cell reconstitution dynamics in 33 pediatric patients given hHSCT for hematological malignancies, with a follow-up reaching 6 y posttransplantation, and correlated their emergence with disease relapse. iNKT cells fully reconstitute and rapidly convert into IFN-γ–expressing effectors in the 25 patients maintaining remission. CD4+ cells emerge earlier than the CD4− ones, both displaying CD161− immature phenotypes. CD4− cells expand more slowly than CD4+ cells, though they mature with significantly faster kinetics, reaching full maturation by 18 mo post-hHSCT. Between 4 and 6 y post-hHSCT, mature CD4− iNKT cells undergo a substantial expansion burst, resulting in a CD4+<CD4− NKT cell ratio similar to that found in healthy adults. In contrast with patients maintaining remission, iNKT cells failed to reconstitute in all eight patients experiencing disease relapse. These findings define the peripheral dynamics of human iNKT cells and suggest a contribution of these cells to maintain remission, possibly via early IFN-γ provision. Adoptive transfer of donor-derived iNKT cells into HLA-haploidentical patients failing to reconstitute these cells might represent a novel therapeutic option to prevent leukemia recurrence.
Nucleotide-Binding Oligomerization Domain 1 Mediates Recognition of Clostridium difficile and Induces Neutrophil Recruitment and Protection against the Pathogen

Clostridium difficile is a Gram-positive obligate anaerobic pathogen that causes pseudomembranous colitis in antibiotics-treated individuals. However, host immune protective mechanisms against C. difficile are largely unknown. In this study, we show that C. difficile possesses potent stimulatory activity for nucleotide-binding oligomerization domain 1 (Nod1), an intracellular pattern recognition molecule that senses bacterial peptidoglycan-related molecules. Nod1−/−, but not Nod2−/−, mice exhibited increased lethality in response to C. difficile intestinal infection despite comparable levels of intestinal damage and epithelial permeability in Nod1−/− and control mice. The enhanced lethality was accompanied by impaired C. difficile clearance, increased bacterial translocation, and elevated levels of endotoxin and IL-1β in the serum of Nod1−/− mice. Histological and flow cytometric analyses revealed that Nod1−/− mice had defective recruitment of neutrophils, but not macrophages, to the intestine after C. difficile infection. The reduced recruitment of neutrophils correlated with impaired production of CXCL1, but not CCL2, XCL1, and other cytokines/chemokines, in infected Nod1−/− mice. The influx of neutrophils also was reduced when C. difficile was administered i.p., suggesting that Nod1 directly recognizes C. difficile to induce the recruitment of neutrophils to the infected site. These results indicate that Nod1 regulates host susceptibility to C. difficile and suggest that Nod1-mediated neutrophil recruitment is an important immune response against the enteric pathogen.
NLRP3/Caspase-1–Independent IL-1β Production Mediates Diesel Exhaust Particle-Induced Pulmonary Inflammation

Inhalation of diesel exhaust particles (DEP) induces an inflammatory reaction in the lung; however, the mechanisms are largely unclear. IL-1β/IL-1RI signaling is crucial in several lung inflammatory responses. Typically, caspase-1 is activated within the NLRP3 inflammasome that recognizes several damage-associated molecular patterns, which results in cleavage of pro–IL-1β into mature IL-1β. In this study, we hypothesized that the NLRP3/caspase-1/IL-1β pathway is critical in DEP-induced lung inflammation. Upon DEP exposure, IL-1RI knockout mice had reduced pulmonary inflammation compared with wild-type mice. Similarly, treatment with rIL-1R antagonist (anakinra) and IL-1β neutralization impaired the DEP-induced lung inflammatory response. Upon DEP exposure, NLRP3 and caspase-1 knockout mice, however, showed similar IL-1β levels and comparable pulmonary inflammation compared with wild-type mice. In conclusion, these data show that the DEP-induced pulmonary inflammation acts through the IL-1β/IL-1RI axis. In addition, DEP initiates inflammation independent of the classical NLRP3/caspase-1 pathway, suggesting that other proteases might be involved.
Reproducibility and validity of a semiquantitative food frequency questionnaire to assess dietary intakes for the Korean elderly

We examined the reproducibility and validity of a semiquantitative food frequency questionnaire (SFFQ) for older Korean adults. Dietary intakes of 78 Koreans over 60 years old were measured by both a 96 item SFFQ twice during a four-month period and five or six 24-hour recalls over the same period. Correlation coefficients of nutrients for reproducibility and validity assessments ranged 0.42-0.60 (median = 0.54) and 0.24-0.62 (median = 0.51), respectively. Cereals and vegetable food groups, supplying a major proportion of nutrients, were least reproducible and valid. Milk and milk product were the most reproducible. Dietary quality measured by the SFFQ was inversely associated with nutritional risks. Reproducibility and validity of the SFFQ developed in this study were significantly similar to those reported from studies for younger Korean adults, however somewhat lower than those for Western populations partly due to culturally different eating patterns.
4-1BB Signaling Synergizes with Programmed Death Ligand 1 Blockade To Augment CD8 T Cell Responses during Chronic Viral Infection

Previous studies have identified the inhibitory role that the programmed death 1 (PD-1) pathway plays during chronic infection. Blockade of this pathway results in rescue of viral-specific CD8 T cells, as well as reduction of viral loads in mice chronically infected with lymphocytic choriomeningitis virus (LCMV). We tested the effect of combining PD ligand 1 (PD-L1) blockade with an agonistic regimen that induces 4-1BB costimulation during chronic LCMV infection. There is a boosting effect in the rescue of LCMV-specific CD8 T cell responses after dual treatment with PD-L1 blockade and 4-1BB agonistic Abs when the amount and timing of 4-1BB costimulation are carefully controlled. When PD-L1–blocking Abs are given together with a single low dose of anti–4-1BB agonistic Abs, there is an enhanced and stable expansion of viral-specific CD8 T cells. Conversely, when blocking Abs to PD-L1 are given with a repetitive high dose of anti–4-1BB, there is an initial synergistic expansion of viral-specific CD8 T cells by day 7, followed by dramatic apoptosis by day 14. Viral control paralleled CD8 T cell kinetics after dual treatment. By day 7 posttreatment, viral titers were lower in both of the combined regimens (compared with PD-L1 blockade alone). However, whereas the high dose of anti–4-1BB plus PD-L1 blockade resulted in rebound of viral titers to original levels, the low dose of anti–4-1BB plus PD-L1 blockade resulted in a stable reduction of viral loads. These findings demonstrate the importance of carefully manipulating the balance between activating and inhibitory signals to enhance T cell responses during chronic infection.
Single Channel Speech Enhancement Using Adaptive Soft-Thresholding with Bivariate EMD

This paper presents a novel data adaptive thresholding approach to single channel speech enhancement. The noisy speech signal and fractional Gaussian noise (fGn) are combined to produce the complex signal. The fGn is generated using the noise variance roughly estimated from the noisy speech signal. Bivariate empirical mode decomposition (bEMD) is employed to decompose the complex signal into a finite number of complex-valued intrinsic mode functions (IMFs). The real and imaginary parts of the IMFs represent the IMFs of observed speech and fGn, respectively. Each IMF is divided into short time frames for local processing. The variance of IMF of fGn calculated within a frame is used as the reference term to classify corresponding noisy speech frame into noise and signal dominant frames. Only the noise dominant frames are soft-thresholded to reduce the noise effects. Then, all the frames as well as IMFs of speech are combined, yielding the enhanced speech signal. The experimental results show the improved performance of the proposed algorithm compared to the recently reported methods.
Everybody's Different: A positive approach to teaching about health, puberty, body image, nutrition, self-esteem and obesity prevention

Weight and body image concerns in children and adolescents are increasing. Overall body dissatisfaction in young people has increased dramatically in the last few decades, with a heightened prevalence of dieting, eating disorders, obsessive exercise and steroid abuse. Everybody's Different details how to apply a proven self-esteem approach in schools, community settings and clinical situations to improve body image conceptions, prevent eating disorders and obesity, and foster health, nutrition and physical activity in young people.
Serum Amyloid A Activates the NLRP3 Inflammasome and Promotes Th17 Allergic Asthma in Mice

IL-1β is a cytokine critical to several inflammatory diseases in which pathogenic Th17 responses are implicated. Activation of the NLRP3 inflammasome by microbial and environmental stimuli can enable the caspase-1–dependent processing and secretion of IL-1β. The acute-phase protein serum amyloid A (SAA) is highly induced during inflammatory responses, wherein it participates in systemic modulation of innate and adaptive immune responses. Elevated levels of IL-1β, SAA, and IL-17 are present in subjects with severe allergic asthma, yet the mechanistic relationship among these mediators has yet to be identified. In this study, we demonstrate that Saa3 is expressed in the lungs of mice exposed to several mixed Th2/Th17-polarizing allergic sensitization regimens. SAA instillation into the lungs elicits robust TLR2-, MyD88-, and IL-1–dependent pulmonary neutrophilic inflammation. Furthermore, SAA drives production of IL-1α, IL-1β, IL-6, IL-23, and PGE2, causes dendritic cell (DC) maturation, and requires TLR2, MyD88, and the NLRP3 inflammasome for secretion of IL-1β by DCs and macrophages. CD4+ T cells polyclonally stimulated in the presence of conditioned media from SAA-exposed DCs produced IL-17, and the capacity of polyclonally stimulated splenocytes to secrete IL-17 is dependent upon IL-1, TLR2, and the NLRP3 inflammasome. Additionally, in a model of allergic airway inflammation, administration of SAA to the lungs functions as an adjuvant to sensitize mice to inhaled OVA, resulting in leukocyte influx after Ag challenge and a predominance of IL-17 production from restimulated splenocytes that is dependent upon IL-1R signaling.
The role of Information Technology in service innovation in the two different quadrants of the service-process matrix

This study's objective was to explore the role of Information Technology (IT) in service innovation in the two different quadrants of the service-process matrix, mass service and service shop. This study's findings illustrate that IT afford a major opportunity for differentiating- and efficiency-increasing service innovations for service organisations in the mass service quadrant of the service-process matrix, and a major opportunity for differentiating or customising service innovations in the service shop quadrant of the matrix. However, IT provides more opportunity for differentiating-service innovations than efficiency-increasing service innovations in the service shop quadrant of the matrix.
MicroRNA-127 Inhibits Lung Inflammation by Targeting IgG Fcγ Receptor I

The molecular mechanisms of acute lung injury are incompletely understood. MicroRNAs (miRNAs) are crucial biological regulators that act by suppressing their target genes and are involved in a variety of pathophysiologic processes. miR-127 appears to be downregulated during lung injury. We set out to investigate the role of miR-127 in lung injury and inflammation. Expression of miR-127 significantly reduced cytokine release by macrophages. Looking into the mechanisms of regulation of inflammation by miR-127, we found that IgG FcγRI (CD64) was a target of miR-127, as evidenced by reduced CD64 protein expression in macrophages overexpressing miR-127. Furthermore, miR-127 significantly reduced the luciferase activity with a reporter construct containing the native 3′ untranslated region of CD64. Importantly, we demonstrated that miR-127 attenuated lung inflammation in an IgG immune complex model in vivo. Collectively, these data show that miR-127 targets macrophage CD64 expression and promotes the reduction of lung inflammation. Understanding how miRNAs regulate lung inflammation may represent an attractive way to control inflammation induced by infectious or noninfectious lung injury.
Ubiquitination of CD86 Is a Key Mechanism in Regulating Antigen Presentation by Dendritic Cells

Dendritic cells (DCs) require costimulatory molecules such as CD86 to efficiently activate T cells for the induction of adaptive immunity. DCs maintain minimal levels of CD86 expression at rest, but upregulate levels upon LPS stimulation. LPS-stimulated DCs produce the immune suppressive cytokine IL-10 that acts in an autocrine manner to regulate CD86 levels. Interestingly, the underlying molecular mechanism behind the tight control of CD86 is not completely understood. In this study, we report that CD86 is ubiquitinated in DCs via MARCH1 E3 ubiquitin ligase and that this ubiquitination plays a key role in CD86 regulation. Ubiquitination at lysine 267 played the most critical role for this regulation. CD86 is ubiquitinated in MARCH1-deficient DCs to a much lesser degree than in wild-type DCs, which also correlated with a significant increase in CD86 expression. Importantly, CD86 is continuously ubiquitinated in DCs following activation by LPS, and this was due to the autocrine IL-10 inhibition of MARCH1 downregulation. Accordingly, DCs lacking MARCH1 and DCs expressing ubiquitination-resistant mutant CD86 both failed to regulate CD86 in response to autocrine IL-10. DCs expressing ubiquitination-resistant mutant CD86 failed to control their T cell-activating abilities at rest as well as in response to autocrine IL-10. These studies suggest that ubiquitination serves as an important mechanism by which DCs control CD86 expression and regulate their Ag-presenting functions.
The Size of the Plasmacytoid Dendritic Cell Compartment Is a Multigenic Trait Dominated by a Locus on Mouse Chromosome 7

Plasmacytoid dendritic cells (pDC) compose one of the many distinct dendritic cell subsets. The primary function of pDC is to potently produce type 1 IFNs upon stimulation, which is highly relevant in antiviral responses. Consequently, the ability to manipulate the size of the pDC compartment in vivo may increase the capacity to clear viral infections. In an attempt to identify genetic loci affecting the size of the pDC compartment, defined by both the proportion and absolute number of pDC, we undertook an unbiased genetic approach. Linkage analysis using inbred mouse strains identified a locus on chromosome 7 (Pdcc1) significantly linked to both the proportion and the absolute number of pDC in the spleen. Moreover, loci on either chromosome 11 (Pdcc2) or 9 (Pdcc3) modified the effect of Pdcc1 on chromosome 7 for the proportion and absolute number of pDC, respectively. Further analysis using mice congenic for chromosome 7 confirmed Pdcc1, demonstrating that variation within this genetic interval can regulate the size of the pDC compartment. Finally, mixed bone marrow chimera experiments showed that both the proportion and the absolute number of pDC are regulated by cell-intrinsic hematopoietic factors. Our findings highlight the multigenic regulation of the size of the pDC compartment and will facilitate the identification of genes linked to this trait.
HER2/HER3 Signaling Regulates NK Cell-Mediated Cytotoxicity via MHC Class I Chain-Related Molecule A and B Expression in Human Breast Cancer Cell Lines

Overexpression of the receptor tyrosine kinases HER2 and HER3 is associated with a poor prognosis in several types of cancer. Presently, HER2- as well as HER3-targeted therapies are in clinical practice or evaluated within clinical trials, including treatment with mAbs mediating growth inhibition and/or activation of Ab-induced innate or adaptive cellular immunity. A better understanding of how HER2/HER3 signaling in tumors influences cellular immune mechanisms is therefore warranted. In this study, we demonstrate that HER2/HER3 signaling regulates the expression of MHC class I-related chain A and B (MICA and MICB) in breast cancer cell lines. The MICA and MICB (MICA/B) molecules act as key ligands for the activating receptor NK group 2, member D (NKG2D) and promote NK cell-mediated recognition and cytolysis. Genetic silencing of HER3 but not HER2 downregulated the expression of MICA/B, and HER3 overexpression significantly enhanced MICA expression. Among the major pathways activated by HER2/HER3 signaling, the PI3K/AKT pathway was shown to predominantly regulate MICA/B expression. Treatment with the HER3-specific ligand neuregulin 1β promoted the expression in a process that was antagonized by pharmacological and genetic interference with HER3 but not by the ataxia-telangiectasia–mutated (ATM) and ATM and Rad3-related protein kinases inhibitor caffeine. These observations further emphasize that HER2/HER3 signaling directly, and not via genotoxic stress, regulates MICA/B expression. As anticipated, stimulating HER2/HER3 enhanced the NKG2D-MICA/B–dependent NK cell-mediated cytotoxicity. Taken together, we conclude that signaling via the HER2/HER3 pathway in breast carcinoma cell lines may lead to enhanced NKG2D-MICA/B recognition by NK cells and T cells.