Miracle-dz/UniFAR-FTUs huggingface dataset:
Galectin-1-Matured Human Monocyte-Derived Dendritic Cells Have Enhanced Migration through Extracellular Matrix1

Dendritic cells (DCs) are potent mediators of the immune response, and can be activated by exogenous pathogen components. Galectin-1 is a member of the conserved β-galactoside-binding lectin family that binds galactoside residues on cell surface glycoconjugates. Galectin-1 is known to play a role in immune regulation via action on multiple immune cells. However, its effects on human DCs are unknown. In this study, we show that galectin-1 induces a phenotypic and functional maturation in human monocyte-derived DCs (MDDCs) similar to but distinct from the activity of the exogenous pathogen stimuli, LPS. Immature human MDDCs exposed to galectin-1 up-regulated cell surface markers characteristic of DC maturation (CD40, CD83, CD86, and HLA-DR), secreted high levels of IL-6 and TNF-α, stimulated T cell proliferation, and showed reduced endocytic capacity, similar to LPS-matured MDDCs. However, unlike LPS-matured DCs, galectin-1-treated MDDCs did not produce the Th1-polarizing cytokine IL-12. Microarray analysis revealed that in addition to modulating many of the same DC maturation genes as LPS, galectin-1 also uniquely up-regulated a significant subset of genes related to cell migration through the extracellular matrix (ECM). Indeed, compared with LPS, galectin-1-treated human MDDCs exhibited significantly better chemotactic migration through Matrigel, an in vitro ECM model. Our findings show that galectin-1 is a novel endogenous activator of human MDDCs that up-regulates a significant subset of genes distinct from those regulated by a model exogenous stimulus (LPS). One unique effect of galectin-1 is to increase DC migration through the ECM, suggesting that galectin-1 may be an important component in initiating an immune response.
Propofol inhibits lipopolysaccharide-induced lung epithelial cell injury by reducing hypoxia-inducible factor-1alpha expression.

BACKGROUND Lipopolysaccharide (LPS) may activate hypoxia-inducible factor (HIF)-1α, which up-regulates cytokine expression and the lethality of LPS-induced shock. We investigated the effect of propofol on HIF-1α expression and acute lung injury in LPS-treated mice. METHODS A series of both positive and negative control experiments were performed. We injected BALB/C mice with propofol or vehicle i.p. immediately and 12 h after an LPS challenge. After 24 h, we examined the lung wet/dry weight ratio, neutrophil infiltration, and HIF-1α mRNA expression and inflammatory cytokines in the lung tissue. Survival was determined for 48 h after LPS injection. In vitro, we determined the responses of A549 cells, with and without HIF-1α silenced, to treatment with LPS alone and LPS plus propofol. RESULTS Propofol prolonged survival and attenuated acute lung injury and decreased the expression of HIF-1α, interleukin (IL)-6, keratinocyte-derived chemokine, and tumour necrosis factor-alpha (TNF-α) in the lungs of endotoxaemic mice. In HIF-1α knockdown-A549 cells, LPS-induced TNF-α, IL-6, and the pro-apoptotic gene, BNIP3 expression and apoptosis were reduced. Propofol, but not an inhibitor of nuclear factor κB, reduced HIF-1α expression in LPS-stimulated A549 cells. Propofol also down-regulated, in A549 cells, the expression of IL-6, IL-8, and TNF-α, Bcl-2/adenovirus E1B 19 kDa interacting protein 3 (BNIP3), and apoptosis. CONCLUSIONS Propofol reduces apoptosis in LPS-stimulated lung epithelial cells by decreasing HIF-1α, BNIP3, and cytokine production. Using propofol to inhibit HIF-1α expression may protect against the acute lung injury caused by LPS-induced sepsis.
Wing Musculature Reconstruction in Extinct Flightless Auks (Pinguinus and Mancalla) Reveals Incomplete Convergence with Penguins (Spheniscidae) Due to Differing Ancestral States

Despite longstanding interest in convergent evolution, factors that result in deviations from fully convergent phenotypes remain poorly understood. In birds, the evolution of flightless wing-propelled diving has emerged as a classic example of convergence, having arisen in disparate lineages including penguins (Sphenisciformes) and auks (Pan-Alcidae, Charadriiformes). Nevertheless, little is known about the functional anatomy of the wings of flightless auks because all such taxa are extinct, and their morphology is almost exclusively represented by skeletal remains. Here, in order to re-evaluate the extent of evolutionary convergence among flightless wing-propelled divers, wing muscles and ligaments were reconstructed in two extinct flightless auks, representing independent transitions to flightlessness: Pinguinus impennis (a crown-group alcid), and Mancalla (a stem-group alcid). Extensive anatomical data were gathered from dissections of 12 species of extant charadriiforms and 4 aequornithine waterbirds including a penguin. It was found that the wings of both flightless auk taxa were characterized by an increased mechanical advantage of wing elevator/retractor muscles, and decreased mobility of distal wing joints, both of which are likely advantageous for wing-propelled diving and parallel similar functional specializations in penguins. However, the conformations of individual muscles and ligaments underlying these specializations differ markedly between penguins and flightless auks, instead resembling those in each respective group’s close relatives. Thus, the wings of these flightless wing-propelled divers can be described as convergent as overall functional units, but are incompletely convergent at lower levels of anatomical organization—a result of retaining differing conditions from each group’s respective volant ancestors. Detailed investigations such as this one may indicate that, even in the face of similar functional demands, courses of phenotypic evolution are dictated to an important degree by ancestral starting points.
A New Technique for Mobility Extraction in MOSFETs in the Presence of Prominent Gate Oxide Trapping: Application to InGaAs MOSFETs

In the presence of prominent gate oxide trapping, the conventional technique for channel mobility extraction in MOSFETs based on <inline-formula> <tex-math notation="LaTeX">${I}$ </tex-math></inline-formula>–<inline-formula> <tex-math notation="LaTeX">${V}/{C}$ </tex-math></inline-formula>–<inline-formula> <tex-math notation="LaTeX">${V}$ </tex-math></inline-formula> measurements becomes inadequate. This is the consequence of two different effects associated with oxide traps: gate voltage stretch-out and electron trapping and detrapping in the oxide at the megahertz (MHz)-range frequencies that are commonly utilized. In thin-channel planar InGaAs MOSFETs, both effects are observed and found to result in a severe overestimation of mobile charge and subsequently an underestimation of mobility using <inline-formula> <tex-math notation="LaTeX">${I}$ </tex-math></inline-formula>–<inline-formula> <tex-math notation="LaTeX">${V}/{C}$ </tex-math></inline-formula>–<inline-formula> <tex-math notation="LaTeX">${V}$ </tex-math></inline-formula>. To address this issue, we demonstrate a new mobility extraction technique (RF-<inline-formula> <tex-math notation="LaTeX">${I}_{D}$ </tex-math></inline-formula>) based on concurrent <inline-formula> <tex-math notation="LaTeX">${I}$ </tex-math></inline-formula>–<inline-formula> <tex-math notation="LaTeX">${V}$ </tex-math></inline-formula> and <inline-formula> <tex-math notation="LaTeX">${S}$ </tex-math></inline-formula>-parameter measurement in the gigahertz (GHz) regime that is largely immune to oxide trapping. Excellent agreement with Hall measurements as well as with theoretical predictions from Poisson–Schrodinger simulations gives confidence to the new technique. Importantly, the new technique is not limited to InGaAs planar MOSFETs, but applies to any device geometry and any material system. Promising mobility ~1100 cm<sup>2</sup>/<inline-formula> <tex-math notation="LaTeX">$\text{V}\cdot \text{s}$ </tex-math></inline-formula> is found in quantum-well planar InGaAs MOSFETs with a 4-nm-thick channel.
PU.1 and C/EBPα/β convert fibroblasts into macrophage-like cells

Earlier work has shown that the transcription factor C/EBPα induced a transdifferentiation of committed lymphoid precursors into macrophages in a process requiring endogenous PU.1. Here we have examined the effects of PU.1 and C/EBPα on fibroblasts, a cell type distantly related to blood cells and akin to myoblasts, adipocytes, osteoblasts, and chondroblasts. The combination of the two factors, as well as PU.1 and C/EBPβ, induced the up-regulation of macrophage/hematopoietic cell surface markers in a large proportion of NIH 3T3 cells. They also up-regulated these markers in mouse embryo- and adult skin-derived fibroblasts. Based on cell morphology, activation of macrophage-associated genes, and extinction of fibroblast-associated genes, cell lines containing an attenuated form of PU.1 and C/EBPα acquired a macrophage-like phenotype. The lines also display macrophage functions: They phagocytose small particles and bacteria, mount a partial inflammatory response, and exhibit strict CSF-1 dependence for growth. The myeloid conversion is primarily induced by PU.1, with C/EBPα acting as a modulator of macrophage-specific gene expression. Our data suggest that it might become possible to induce the transdifferentiation of skin-derived fibroblasts into cell types desirable for tissue regeneration.
Do Test Formats in Reading Comprehension Affect Second-Language Students' Test Performance Differently?

Large-scale testing in English affects second-language students not only greatly but also differently than first-language learners. The research literature reports that confounding factors in such large-scale testing such as varying test formats may differentially affect the performance of students from diverse backgrounds. An investigation of test performance between ESL/ELD students and non- ESL/ELD students on the Ontario Secondary School Literacy Test (OSSLT) was performed to investigate whether test formats in reading comprehension affected the two groups differently. The results indicate that the overall pattern of difficulty levels on the three test formats were the same between ESL/ELD students and non-ESL/ELD students, except that ESL/ELD students performed substantially lower on each format and that more variability was found among ESL/ELD students. Further, discriminant analysis results indicated that only the multiplechoice questions obtained a significant discriminant coefficient in differentiating the two groups. The results suggest a lack of association between test formats and test performance.
Exfoliated mesothelial cell and CA-125 in automated peritoneal dialysis (APD) and continuous ambulatory peritoneal dialysis (CAPD) patients.

OBJECTIVE Automated peritoneal dialysis (APD) becomes the first option for peritoneal dialysis, nowadays overtaking continuous ambulatory peritoneal dialysis (CAPD) in many countries. The comparison of peritoneal membrane alteration in CAPD and APD is inconclusive. The authors therefore compared the peritoneal membrane changes in patients undergoing CAPD and APD. MATERIAL AND METHOD In naive end stage renal disease patients, the choice of PD modes (CAPD or APD) was dependent on the patient's decision. Thirty-six CAPD and 25APD patients with a total of 287 patient-months were compared. The peritoneal mass parameter, exfoliated mesothelial cell (MTC) and dialysate CA-125, as well as modified peritoneal equilibrium test (mPET) with 4.25% dextrose solution was simultaneously evaluated at 1 and 6 month follow-up. RESULTS Although the peritoneal function (as measured by D/P creatinine, D/D0 glucose, sodium dipping, and dialysate protein loss), adequacy, serum albumin, nutritional status, and residual renal function showed no significant differences between groups at 1 and 6 months, CA-125 but not MTC was higher in APD compared with CAPD at the first month of PD beginning. Due to the single time-point measurement limitation, the authors compared the peritoneal mass parameter differences between 1 and 6 month. During 6-month follow-up, CA-125 decreased 30 +/- 5% vs. 7 +/- 5% and MTC decreased 5 +/- 12% vs. 40 +/- 11% in APD and CAPD, respectively. The higher CA-125 reduction in APD and greater changes of MTC in CAPD suggested that there was less viable mesothelial cell in APD compared with CAPD. CONCLUSION The authors observed that both APD and CAPD damaged peritoneum. However, there might be higher peritoneal injury in APD patients. The proper randomization study in longer follow-up period is mandatory to confirm this observation.
Unsplinted implants and teeth supporting maxillary removable partial dentures retained by telescopic crowns: a retrospective study with >6 years of follow-up.

OBJECTIVES Data regarding tooth- and implant-supported maxillary removable partial dentures (TIRPDs) are scarce. The objective of this research was to perform a retrospective evaluation of the clinical long-term outcome of maxillary TIRPDs rigidly retained via telescopic crowns in patients undergoing supportive post-implant therapy (SIT). MATERIAL AND METHODS The inclusion criteria were met by 26 patients restored with maxillary TIRPDs between 1997 and 2011 in a private practice. Primary crowns (Marburg double crowns, MDCs) on teeth were cemented, whereas those on implants were screw-retained. Using patient records and data from a cross-sectional clinical examination in 2013, the survival rates of the teeth, implants and prostheses, together with the biological and technical complications, were analyzed. RESULTS After 6.12 ± 3.80 (range: 2-16) years of loading, 23 non-smoking patients with 23 dentures supported by 60 implants and 66 teeth were available for assessment. Nine teeth (survival rate: 86.36%) were lost, whereas 1 implant (survival rate: 98.36%) failed because of peri-implantitis. Although 30 implants (50%) in 16 patients (69.57%) showed bleeding on probing (BOP+), no further peri-implantitis was observed. The mean peri-implant probing depth (PPD) was 3.68 ± 0.71 mm. All dentures were functional and required technical maintenance efforts amounting to 0.128 treatments per patient per year (T/P/Y). CONCLUSIONS Within the limitations of this study, we conclude that TIRPDs retained via MDCs may represent a viable treatment option for patients with residual maxillary teeth.
The expression of L‐type voltage‐gated calcium channels in retinal photoreceptors is under circadian control

Photoreceptors are non‐spiking neurons, and their synapses mediate the continuous release of neurotransmitters under the control of L‐type voltage‐gated calcium channels (VGCCs). Photoreceptors express endogenous circadian oscillators that play important roles in regulating photoreceptor physiology and function. Here, we report that the L‐type VGCCs in chick cone photoreceptors are under circadian control. The L‐type VGCC currents are greater when measured during the subjective night than during the subjective day. Using antibodies against the VGCCα1C and VGCCα1D subunits, we found that the immunofluorescence intensities of both VGCCα1C and VGCCα1D in photoreceptors are higher during the subjective night. However, the mRNA levels of VGCCα1D, but not VGCCα1C, are rhythmic. Nocturnal increases in L‐type VGCCs are blocked by manumycin A, PD98059, and KN93, which suggest that the circadian output pathway includes Ras, Erk, and calcium‐calmodulin dependent kinase II. In summary, four independent lines of evidence show that the L‐VGCCs in cone photoreceptors are under circadian control.
Cellular and Molecular Pathways of COVID-19 and Potential Points of Therapeutic Intervention

With the objective of linking early findings relating to the novel SARS-CoV-2 coronavirus with potentially informative findings from prior research literature and to promote investigation toward therapeutic response, a coherent cellular and molecular pathway is proposed for COVID-19. The pathway is consistent with a broad range of observed clinical features and biological markers and captures key mediators of pathophysiology. In this proposed pathway, membrane fusion and cytoplasmic entry of SARS-CoV-2 virus via ACE2 and TMPRSS2-expressing respiratory epithelial cells, including pulmonary type-II pneumocytes, provoke an initial immune response featuring inflammatory cytokine production coupled with a weak interferon response, particularly in IFN-λ–dependent epithelial defense. Differentiation of non-classic pathogenic T-cells and pro-inflammatory intermediate monocytes contributes to a skewed inflammatory profile, mediated by membrane-bound immune receptor subtypes (e.g., FcγRIIA) and downstream signaling pathways (e.g., NF-κB p65 and p38 MAPK), followed by chemotactic infiltration of monocyte-derived macrophages and neutrophils into lung tissue. Endothelial barrier degradation and capillary leakage contribute to alveolar cell damage. Inflammatory cytokine release, delayed neutrophil apoptosis, and NETosis contribute to pulmonary thrombosis and cytokine storm. These mechanisms are concordant with observed clinical markers in COVID-19, including high expression of inflammatory cytokines on the TNF-α/IL-6 axis, elevated neutrophil-to-lymphocyte ratio (NLR), diffuse alveolar damage via cell apoptosis in respiratory epithelia and vascular endothelia, elevated lactate dehydrogenase (LDH) and CRP, high production of neutrophil extracellular traps (NETs), depressed platelet count, and thrombosis. Although certain elements are likely to be revised as new findings emerge, the proposed pathway suggests multiple points of investigation for potential therapeutic interventions. Initial candidate interventions include prophylaxis to augment epithelial defense (e.g., AT1 receptor blockade, type III and type I interferons, melatonin, calcitriol, camostat, and lopinavir) and to reduce viral load (e.g., remdesivir, ivermectin, emetine, Abelson kinase inhibitors, dopamine D2 antagonists, and selective estrogen receptor modulators). Additional interventions focus on tempering inflammatory signaling and injury (e.g., dexamethasone, doxycycline, Ang1-7, estradiol, alpha blockers, and DHA/EPA, pasireotide), as well as inhibitors targeted toward molecular mediators of the maladaptive COVID-19 immune response (e.g., IL-6, TNF-α, IL-17, JAK, and CDK9).
Mast cells modulate acute ozone-induced inflammation of the murine lung.

We hypothesized that mast cells modulate lung inflammation that develops after acute ozone (O3) exposure. Two tests were done: (1) genetically mast-cell-deficient (WBB6F1-W/Wv, WCB6F1-SI/SId) and bone-marrow-transplanted W/Wv mice were exposed to O3 or filtered air, and the inflammatory responses were compared with those of mast-cell-sufficient congenic mice (WBB6F1-(+)/+, WCB6F1-(+)/+); (2) genetically O3-susceptible C57BL/6J mice were treated pharmacologically with putative mast-cell modulators or vehicle, and the O3-induced inflammatory responses were compared. Mice were exposed to 1.75 ppm O3 or air for 3 h, and lung inflammation was assessed by bronchoalveolar lavage (BAL) 6 and 24 h after exposure. Relative to O3-exposed W/Wv and SI/SId mice, the mean numbers of lavageable polymorphonuclear leukocytes (PMNs) and total BAL protein concentration (a marker of permeability) were significantly greater in the respective O3-exposed normal congenic +/+ mice (p < 0.05). Mast cells were reconstituted in W/Wv mice by transplantation of bone marrow cells from congenic +/+ mice, and O3-induced lung inflammation was assessed in the mast-cell-replete W/Wv mice. After O3 exposure, the changes in lavageable PMNs and total protein of mast-cell-replete W/Wv mice were not different from age-matched normal +/+ control mice, and they were significantly greater than those of sham-transplanted W/Wv mice (p < 0.05). Genetically susceptible C57BL/6J mice were pretreated with a mast-cell stabilizer (nedocromil sodium), secretagogue (compound 48/80), or vehicle, and the mice were exposed to O3. (ABSTRACT TRUNCATED AT 250 WORDS)
The effect of change of voltage acceleration on temperature activation of oxide breakdown for ultrathin oxides

We report the effect of change of voltage acceleration on temperature dependence of oxide breakdown for ultra-thin oxides below 6 nm. The time- or charge-to-breakdown (T/sub BD//Q/sub BD/) is directly measured over a wide range of temperatures (-30/spl deg/C to 200/spl deg/C) for several fixed voltages using different area capacitors and long-term stress. Using extensive experimental evidence, we unequivocally demonstrate that this strong temperature dependence of oxide breakdown on ultra-thin oxides is not a thickness effect as previously suggested at least for thickness range investigated in this work. It is a consequence of two experimental facts: 1) voltage-dependent voltage acceleration and 2) temperature-independent voltage acceleration within a fixed T/sub BD/ window. These results provide a coherent picture for T/sub BD/ in both voltage and temperature domains for ultra-thin oxides.
Assessment and Quantification of the Accuracy of Low- and High-Resolution Remote Sensing Data for Shoreline Monitoring

Τhe accuracy of low-resolution remote sensing data for monitoring shoreline evolution is the main issue that researchers have been trying to overcome in recent decades. The drawback of the Landsat satellite archive is its spatial resolution, which is appropriate only for low-scale mapping. The present study investigates the potentialities and limitations of remote sensing data and GIS techniques in shoreline evolution modeling, with a focus on two major aspects: (a) assessing and quantifying the accuracy of low- and high-resolution remote sensing data for shoreline mapping; and (b) calculating the divergence in the forecasting of coastline evolution based on low- and high-resolution datasets. Shorelines derived from diachronic Landsat images are compared with the corresponding shorelines derived from high-spatial-resolution airphotos or Worldview-2 images. The accuracy of each dataset is assessed, and the possibility of forecasting shoreline evolution is investigated. Two sandy beaches, named Kalamaki and Karnari, which are located in Northwestern Peloponnese, Greece, are used as test sites. It is proved that the shorelines derived from the Landsat data present a displacement error of between 6 and 11 m. The specific data are not suitable for the shoreline forecasting procedure and should not be used in related studies, as they yield less accurate results for the two study areas in comparison with the high-resolution data.
PARANOIA IN A NONCLINICAL POPULATION OF COLLEGE STUDENTS

The present study examined the incidence of paranoid ideation in a nonclinical population. A sample of 324 college students completed a questionnaire assessing their personal experiences of paranoia, with an emphasis on the cognitive, behavioral, and affective components of their experience. They also completed a general measure of paranoia in nonclinical samples, the Fenigstein and Vanable Paranoia Scale, and the Rosenberg Self-Esteem Scale. A total of 153 participants reported an experience of paranoia, which included a clear statement of planned intention to harm. This group scored significantly higher on the Paranoia Scale than those who reported no experience of paranoia. Furthermore, greater levels of paranoid ideation were associated with lower self-esteem. The present findings suggest that paranoia is a common human experience, and are consistent with the idea of continuity between normal and abnormal experience.