Miracle-dz/UniFAR-FTUs huggingface dataset:
Fulminant community-acquired Acinetobacter baumannii pneumonia as a distinct clinical syndrome.

STUDY OBJECTIVES Acinetobacter baumannii (AB) is an important cause of hospital-acquired pneumonia (HAP), and an uncommon but important cause of community-acquired pneumonia (CAP) with high mortality. To better characterize CAP-AB, we compared its clinical features and outcomes with a control group of HAP-AB patients. METHODS This is a retrospective case-control study comparing CAP-AB and HAP-AB patients, which was performed at United Christian Hospital between July 2000 and December 2003. RESULTS There were 19 cases of CAP-AB and 74 cases of HAP-AB. When compared with the HAP-AB group, the CAP-AB group had more ever-smokers (84.3% vs 55.4%, respectively; p = 0.031), more COPD patients (63.2% vs 29.7%, respectively; p = 0.014), and fewer median days of hospitalization (HAP-AB group, median, 0 days; CAP-AB group, 0 days [range, 0 to 30 days]; p = 0.049) in the previous year. The CAP-AB group had more patients with positive blood culture findings (31.6% vs 0%, respectively; p < 0.001), a higher frequency of ARDS (84.2% vs 17.6%, respectively; p < 0.001), and disseminated intravascular coagulation (DIC) (57.9% vs 8.1%, respectively; p < 0.001). The median survival time was only 8 days in the CAP-AB group, vs 103 days in the HAP-AB group (p = 0.003). Factors associated with the higher mortality in the CAP-AB group included the presence of AB bacteremia (p = 0.040), platelet count of < 120 x 10(9) cells/L (p = 0.026), pH < 7.35 on presentation (p = 0.047), and the presence of DIC (p = 0.004). CONCLUSIONS CAP-AB appears to be a unique clinical entity with a high incidence of bacteremia, ARDS, DIC, and death, when compared to HAP-AB. Further studies are needed to investigate the mechanism of the fulminant nature of CAP-AB.
The Impact of Modified Instructions on Ego-Level Scores: A Psychometric Hazard or Indication of Optimal Ego Level?

Various modified instructions have different effects on the Washington University Sentence Completion Test for Ego Development (Loevinger, 1985). These effects were reviewed and 2 alternative explanations were explored: The "measurement unreliability explanation" versus the "optimal level explanation. " Both explanations were systematically studied in 2 test-retest experiments with the Sentence Completion Test for Children and Youths (Westenberg, Treffers, & Drewes, 1998). The modified instructions were to make a favorable impression on the tester ("fake good" condition) or to complete the sentences in as adult and mature a manner as one can ("be mature" condition). Both experiments were conducted with 9- to 15-year-old children and adolescents (N = 127, 128). As was anticipated, neither the fake good nor the be mature condition yielded higher (or lower) reliability indexes as compared to the standard instructions, hence discounting the measurement unreliability explanation. Also as expected, the fake good condition did not yield significantly higher ego-level scores, whereas the be mature condition did yield significantly higher ego-level scores. The former instructions did not convey information relevant to the construct or measure of ego development, whereas the latter instructions did convey information relevant for raising ego-level scores. It is argued that the higher scores under the be mature instructions might reflect the respondents' "optimal" ego level (best functioning), whereas the ego-level score under the standard instructions might reflect their "functional" level (normal functioning).
Reduced microvascular and myocardial damage in patients with acute myocardial infarction and preinfarction angina.

BACKGROUND After acute myocardial infarction, the presence of ischemic preconditioning as a result of preinfarction angina has a protective role, limiting necrosis extent and guaranteeing greater myocardial functional recovery. The relationship between preinfarction angina, microvascular reflow, and myocardial function is poorly known. We hypothesized that after acute myocardial infarction patients with preinfarction angina have both microvascular integrity and myocardial function preservation. METHODS AND RESULTS In 51 patients with a first acute myocardial infarction, we noninvasively assessed microvascular perfusion and coronary flow reserve with intravenous myocardial contrast echocardiography and investigated myocardial contractile recovery with low-dose dobutamine and 90-day follow-up echocardiography. Typical angina was present in 25 patients and absent in 26 patients during the 7 days preceding the myocardial infarction. Compared with those patients without preinfarction angina, patients with preinfarction angina showed a greater microvascular reflow extent and coronary flow reserve (respectively, 25.2% +/- 22.8% vs 48.3% +/- 23.3%, P <.05, and 3.44 +/- 0.75 vs 1.95 +/- 0.67, P <.0001), a better regional myocardial function, as expressed with wall motion score index in the risk area at dobutamine (1.67 +/- 0.61 vs 2.10 +/- 0.43, P <.005) and at follow-up (1.72 +/- 0.56 vs 2.22 +/- 0.40, P <.0001) echocardiogram, despite being similar in the first echocardiogram (2.60 +/- 0.28 vs 2.63 +/- 0.28, P = not significant), and significantly less pronounced left ventricular dilation at follow-up. CONCLUSION Presence of preinfarction angina, because of the preconditioning effect, reduces myocardial damage and favors myocardial viability, limiting left ventricular remodeling. This beneficial effect seems to be at least partly mediated by the more preserved microvascular integrity and functional vasodilation after acute myocardial infarction.
Exercise training reduces peripheral arterial stiffness and myocardial oxygen demand in young prehypertensive subjects.

BACKGROUND Large artery stiffness is a major risk factor for the development of hypertension and cardiovascular disease. Persistent prehypertension accelerates the progression of arterial stiffness. METHODS Forty-three unmedicated prehypertensive (systolic blood pressure (SBP) = 120-139 mm Hg or diastolic blood pressure (DBP) = 80-89 mm Hg) men and women and 15 normotensive time-matched control subjects (NMTCs; n = 15) aged 18-35 years of age met screening requirements and participated in the study. Prehypertensive subjects were randomly assigned to a resistance exercise training (PHRT; n = 15), endurance exercise training (PHET; n = 13) or time-control group (PHTC; n = 15). Treatment groups performed exercise training 3 days per week for 8 weeks. Pulse wave analysis, pulse wave velocity (PWV), and central and peripheral blood pressures were evaluated before and after exercise intervention or time-matched control. RESULTS PHRT and PHET reduced resting SBP by 9.6±3.6mm Hg and 11.9±3.4mm Hg, respectively, and DBP by 8.0±5.1mm Hg and 7.2±3.4mm Hg, respectively (P < 0.05). PHRT and PHET decreased augmentation index (AIx) by 7.5% ± 2.8% and 8.1% ± 3.2% (P < 0.05), AIx@75 by 8.0% ± 3.2% and 9.2% ± 3.8% (P < 0.05), and left ventricular wasted pressure energy, an index of extra left ventricular myocardial oxygen requirement due to early systolic wave reflection, by 573±161 dynes s/cm(2) and 612±167 dynes s/cm(2) (P < 0.05), respectively. PHRT and PHET reduced carotid-radial PWV by 1.02±0.32 m/sec and 0.92±0.36 m/sec (P < 0.05) and femoral-distal PWV by 1.04±0.31 m/sec and 1.34±0.33 m/sec (P < 0.05), respectively. No significant changes were observed in the time-control groups. CONCLUSIONS This study suggests that both resistance and endurance exercise alone effectively reduce peripheral arterial stiffness, central blood pressures, augmentation index, and myocardial oxygen demand in young prehypertensive subjects.
GABAergic/Glutamatergic–Glial/Neuronal Interaction Contributes to Rapid Adaptation in Pacinian Corpuscles

Pacinian corpuscles (PCs) are tactile receptors composed of a nerve ending (neurite) that is encapsulated by layers of lamellar cells. PCs are classified as primary mechanoreceptors because there is no synapse between the transductive membrane and the site of action-potential generation. These touch receptors respond in a rapidly adapting manner to sustained pressure (indentation or displacement), which until now was believed to be attributable solely to the mechanical properties of the capsule. However, evidence of positive immunoreactivity for GABA receptors on the neurite, as well as evidence for gene expression of synaptobrevin in the lamellar cells led to the hypothesis that GABAergic inhibition originating from the lamellar cells is involved in the rapid adaptation process of PCs. Electrophysiological data from isolated PCs demonstrates that, in the presence of either gabazine or picrotoxin (GABA receptor antagonists), many action potentials appear during the static portion of a sustained indentation stimulus (similar to slowly adapting receptors) and that these “static” spikes completely disappear in the presence of GABA. It was consequently hypothesized that glutamate, released by either the neurite itself or the lamellar cells, caused these action potentials. Indeed, the glutamate receptor blocker kynurenate either decreased or totally eliminated the static spikes. Together, these results suggest that GABA, emanating from the modified Schwann cells of the capsule, inhibits glutamatergic excitation during the static portion of sustained pressure, thus forming a “mechanochemical,” rather than purely mechanical, rapid adaptation response. This glial–neuronal interaction is a completely novel finding for the PC.
Aspect Diversity in Moths Revisited

Ricklefs and O’Rourke compared the diversity of appearance (aspect diversity) in samples of moths attracted to ultraviolet lights in Colorado, Arizona, and Panama. The more species‐rich Panamanian assemblage of moths exhibited proportionately greater diversity of color and form, which supported stronger frequency‐dependent selection by predators to diversify the strategies that moths adopt to achieve crypsis in an ecological space composed of resting backgrounds. Comparable analyses of 15 additional samples obtained from Ecuador to Canada fail to support Ricklefs and O’Rourke’s original result. In the present analysis, two measures of the volume of aspect space were unrelated to the number of species per sample and did not differ between temperate and tropical localities. Either frequency‐dependent (apostatic) selection is not a powerful force in diversifying moth appearance, or it does not vary with latitude, or potential resting backgrounds and cryptic strategies are similarly constrained in temperate and tropical regions.
A model of student engagement : identifying engagement triggers in Dutch higher vocational education

Increasing student engagement remains a challenge for educators: although there is large volume of research studies and published articles, the choice of successful pedagogical interventions with the aim of increasing student engagement remains difficult. The purpose of this study was to improve our understanding of student engagement and the factors that activate and prompt students to put effort into their studies. An online Student Satisfaction Survey was administered in which 4,992 or 24.4% of the total student population at Avans University of Applied Sciences returned useable responses. These led to the identification of engagement types and specific engagement triggers. Significantly different engagement types , and engagement triggers were found among full-time and part-time students, first-year and upper-level students, as well as students from differing faculties. These findings hold a number of implications. Administrators need to take into account student engagement as one of the possible strategic focal points in the palette of university initiatives in attempting to increase student retention. Durkheim' s work on suicide and Bourdieu' s theory of social capital are explored to broaden the understanding student retention: Durkheim's four types of suicide as possible analogues and Bourdieu's theory of social capital as a possible variable for students' academic success. Therefore, university policies surrounding student engagement should not focus solely on the student's behaviour, but also on the interaction between students and the university. Furthermore, educational policies regarding the pedagogical climate within the university need to support student engagement.
Granulocyte Colony-Stimulating Factor Improves Motor Function in Rats Developing Compression Myelopathy

Study Design. Basic animal research. Objective. The effects of granulocyte colony-stimulating factor (G-CSF) were assessed in a rat chronic spinal cord compression model to explore the potential of G-CSF as a pharmacological treatment for cervical spondylotic myelopathy. Summary of Background Data. G-CSF is a hematopoietic cytokine used clinically to treat neutropenia. Recently, neuroprotective effects of G-CSF have been reported in spinal cord disorders. Methods. To introduce the chronic cervical cord compression, thin polyurethane sheets were implanted under C5-C6 laminae of rats and gradually expanded by absorbing water. This model reproduces delayed compressive myelopathy of the cervical spine. In sham operations, the sheets were immediately removed. G-CSF (15 &mgr;g/kg) or normal saline (NS) was administered subcutaneously 5 days a week. Experimental groups were sham operation given NS; cord compression given NS; and cord compression given G-CSF. To assess motor functions, rotarod performance, and grip strength were measured. Twenty-six weeks after surgery, cervical spinal cords were examined histopathologically. In the prevention experiment, G-CSF or NS administration was started immediately after surgery. In the treatment experiment, their administration was started 8 weeks after surgery. In another experiment, in three groups in the prevention experiment, terminal deoxynucleotidyl transferase–mediated deoxyuridine triphosphate–biotin nick end labeling staining was performed to assess apoptotic cell death at 8 weeks after surgery. Results. In the prevention experiment, administration of G-CSF preserved the motor functions and motor neurons throughout the 26 weeks, and significantly decreased the number of apoptotic cells at 8 weeks. In the treatment experiment, G-CSF administration from 8 weeks after surgery markedly restored the motor function temporarily to a level equal to the sham group. Conclusion. G-CSF prevents the decline in motor functions and preserves motor neurons in the rat chronic cord compression model. G-CSF also improves motor function in the progressive phase of compression myelopathy. Level of Evidence: N/A
Effect of stretching on gene expression of beta1 integrin and focal adhesion kinase and on chondrogenesis through cell-extracellular matrix interactions.

Differentiation of skeletal tissues, such as bone, ligament and cartilage, is regulated by complex interaction between genetic and epigenetic factors. In the present study, we attempted to elucidate the possible role of cell-extracellular matrix (ECM) adhesion on the inhibitory regulation in chondrogenesis responding to the tension force. The midpalatal suture cartilages in rats were expanded by orthopedic force. In situ hybridization for type I and II collagens, immunohistochemical analysis for fibronectin, alpha5 and beta1 integrins, paxillin, and vinculin, and cytochemical staining for actin were used to demonstrate the phenotypic change of chondrocytes. Immunohistochemical analysis for phosphorylation and nuclear translocation of extracellular signal-regulated kinase (ERK)-1/2 was performed. The role of the cell-ECM adhesion in the response of the chondroprogenitor cells to mechanical stress and the regulation of gene expression of focal adhesion kinase (FAK) and integrins were analyzed by using an in vitro system. A fibrous suture tissue replaced the midpalatal suture cartilage by the expansive force application for 14 days. The active osteoblasts that line the surface of bone matrix in the newly formed suture tissue strongly expressed the type I collagen gene, whereas they did not express the type II collagen gene. Although the numbers of precartilaginous cells expressing alpha5 and beta1 integrin increased, the immunoreactivity of alpha5 integrin in each cell was maintained at the same level throughout the experimental period. During the early response of midpalatal suture cartilage cells to expansive stimulation, formation of stress fibers, reorganization of focal adhesion contacts immunoreactive to a vinculin-specific antibody, and phosphorylation and nuclear translocation of ERK-1/2 were observed. In vitro experiments were in agreement with the results from the in vivo study, i.e. the inhibited expression of type II collagen and upregulation in integrin expression. The arginine-glycine-aspartic acid-containing peptide completely rescued chondrogenesis from tension-mediated inhibition. Thus, we conclude that stretching activates gene expression of beta1 integrin and FAK and inhibits chondrogenesis through cell-ECM interactions of chondroprogenitor cells.
Membrane Type 1 Matrix Metalloproteinase-associated Degradation of Tissue Inhibitor of Metalloproteinase 2 in Human Tumor Cell Lines*

Tissue inhibitor of metalloproteinase 2 (TIMP-2) is required for the membrane type 1 matrix metalloproteinase (MT1-MMP)-dependent activation of pro-MMP-2 on the cell surface. MT1-MMP-bound TIMP-2 has been shown to function as a receptor for secreted pro-MMP-2, resulting in the formation of a trimolecular complex. In the presence of uncomplexed active MT1-MMP, the prodomain of cell surface-associated MMP-2 is cleaved, and activated MMP-2 is released. However, the behavior of MT1-MMP-bound TIMP-2 during MMP-2 activation is currently unknown. In this study,125I-labeled recombinant TIMP-2 (125I-rTIMP-2) was used to investigate the fate of TIMP-2 during pro-MMP-2 activation by HT1080 and transfected A2058 cells. HT1080 and A2058 cells transfected with MT1-MMP cDNA (but not vector-transfected A2058 cells) were able to bind125I-rTIMP-2, to activate pro-MMP-2, and to process MT1-MMP into an inactive 43-kDa form. Under these conditions,125I-rTIMP-2 bound to the cell surface was rapidly internalized and degraded in intracellular organelles through a bafilomycin A1-sensitive mechanism, and125I-bearing low molecular mass fragment(s) were released in the culture medium. These different processes were inhibited by hydroxamic acid-based synthetic MMP inhibitors and rTIMP-2, but not by rTIMP-1 or cysteine, serine, or aspartic proteinase inhibitors. These results support the concept that the MT1-MMP-dependent internalization and degradation of TIMP-2 by some tumor cells might be involved in the regulation of pericellular proteolysis.
General Strategies to Design Nanometer Flip-Flops in the Energy-Delay Space

In this paper, a general and complete design flow for nanometer flip-flops (FFs) is presented. The proposed design methodology permits to optimize FFs under constraints within the energy-delay space through extensive adoption of the Logical Effort method, which also allows for defining the bounds in the design space search. Transistors sizing is rigorously discussed by referring to cases that occur in practical designs. Appropriate metrics with clear physical meaning are proposed and various interesting properties are derived from circuit analysis. A well-defined design procedure is derived that can be easily automated with commercial CAD tools. In contrast to previous works, the impact of local interconnections is explicitly accounted for in the design loop, as is required in nanometer CMOS technologies. A case study is discussed in detail to exemplify the application of the proposed methodology. Extensive simulations for a typical FF in a 65-nm CMOS technology are presented to show the whole design procedure and validate the underlying assumptions.
Stability analysis of a general family of nonlinear positive discrete time-delay systems

ABSTRACT In this paper, we propose a new approach to analyse the stability of a general family of nonlinear positive discrete time-delay systems. First, we introduce a new class of nonlinear positive discrete time-delay systems, which generalises some existing discrete time-delay systems. Second, through a new technique that relies on the comparison and mathematical induction method, we establish explicit criteria for stability and instability of the systems. Three numerical examples are given to illustrate the feasibility of the obtained results.
Multiple cis Regulatory Elements Control RANTES Promoter Activity in Alveolar Epithelial Cells Infected with Respiratory Syncytial Virus

ABSTRACT Respiratory syncytial virus (RSV) produces intense pulmonary inflammation, in part through its ability to induce chemokine synthesis in infected airway epithelial cells. RANTES (regulated upon activation, normally T-cell expressed and presumably secreted) is a CC chemokine which recruits and activates monocytes, lymphocytes, and eosinophils, all cell types present in the lung inflammatory infiltrate induced by RSV infection. In this study, we analyzed the mechanism of RSV-induced RANTES promoter activation in human type II alveolar epithelial cells (A549 cells). Promoter deletion and mutagenesis experiments indicate that RSV requires the presence of five different cisregulatory elements, located in the promoter fragment spanning from −220 to +55 nucleotides, corresponding to NF-κB, C/EBP, Jun/CREB/ATF, and interferon regulatory factor (IRF) binding sites. Although site mutations of the NF-κB, C/EBP, and CREB/AP-1 like sites reduce RSV-induced RANTES gene transcription to 50% or less, only mutations affecting IRF binding completely abolish RANTES inducibility. Supershift and microaffinity isolation assays were used to identify the different transcription factor family members whose DNA binding activity was RSV inducible. Expression of dominant negative mutants of these transcription factors further established their central role in virus-induced RANTES promoter activation. Our finding that the presence of multiple cis regulatory elements is required for full activation of the RANTES promoter in RSV-infected alveolar epithelial cells supports the enhanceosome model for RANTES gene transcription, which is absolutely dependent on binding of IRF transcription factors. The identification of regulatory mechanisms of RANTES gene expression is fundamental for rational design of inhibitors of RSV-induced lung inflammation.
CARDIOVASCULAR EFFECTS ASSOCIATED WITH AIR POLLUTION: POTENTIAL MECHANISMS AND METHODS OF TESTING

A recent series of epidemiologic reports have shown associations between fine particulate matter (PM) levels and increased cardiovascular morbidity and mortality. Elevated PM levels have been linked with cardiac events, including serious ventricular arrhythmias and myocardial infarction. A workshop brought together epidemiologists, cardiologists, and toxicologists from academia, government, and industry to examine plausible mechanisms that could be responsible for such effects, and to consider the armamentarium of noninvasive tests available to examine these relationships. Possible mechanisms considered by the participants include: (a) effects on the autonomic nervous system; (b) alterations on ion channel function in myocardial cells; (c) ischemic responses in the myocardium; and (d) inflammatory responses triggering endothelial dysfunction, atherosclerosis, and thrombosis. A large number of tests were identified to assess specific mechanistic pathways underlying the cardiovascular effects of air pollution and include: (a) autonomic control of the cardiovascular system assessed primarily by heart-rate variability; (b) myocardial substrate and vulnerability assessed by the electrocardiogram and estimations of ejection fraction and wall motion abnormalities in imaging studies; and (c) endothelial function, atherosclerosis, and thrombosis assessed by clotting parameters, cytokines, lipid profiles, and forearm blood flow. A variety of approaches ranging from molecular and genetic investigations to human clinical studies were recommended to further investigate the important epidemiologic associations.