Miracle-dz/UniFAR-FTUs huggingface dataset:
Anaphase B

Anaphase B spindle elongation is characterized by the sliding apart of overlapping antiparallel interpolar (ip) microtubules (MTs) as the two opposite spindle poles separate, pulling along disjoined sister chromatids, thereby contributing to chromosome segregation and the propagation of all cellular life. The major biochemical “modules” that cooperate to mediate pole–pole separation include: (i) midzone pushing or (ii) braking by MT crosslinkers, such as kinesin-5 motors, which facilitate or restrict the outward sliding of antiparallel interpolar MTs (ipMTs); (iii) cortical pulling by disassembling astral MTs (aMTs) and/or dynein motors that pull aMTs outwards; (iv) ipMT plus end dynamics, notably net polymerization; and (v) ipMT minus end depolymerization manifest as poleward flux. The differential combination of these modules in different cell types produces diversity in the anaphase B mechanism. Combinations of antagonist modules can create a force balance that maintains the dynamic pre-anaphase B spindle at constant length. Tipping such a force balance at anaphase B onset can initiate and control the rate of spindle elongation. The activities of the basic motor filament components of the anaphase B machinery are controlled by a network of non-motor MT-associated proteins (MAPs), for example the key MT cross-linker, Ase1p/PRC1, and various cell-cycle kinases, phosphatases, and proteases. This review focuses on the molecular mechanisms of anaphase B spindle elongation in eukaryotic cells and briefly mentions bacterial DNA segregation systems that operate by spindle elongation.
Structural Network Disorganization in Subjects at Clinical High Risk for Psychosis

Abstract Previous network studies in chronic schizophrenia patients revealed impaired structural organization of the brain’s rich-club members, a set of highly interconnected hub regions that play an important integrative role for global brain communication. Moreover, impaired rich-club connectivity has also been found in unaffected siblings of schizophrenia patients, suggesting that abnormal rich-club connectivity is related to familiar, possibly reflecting genetic, vulnerability for schizophrenia. However, no study has yet investigated whether structural rich-club organization is also impaired in individuals with a clinical risk syndrome for psychosis. Diffusion tensor imaging and probabilistic tractography was used to construct structural whole-brain networks in 24 healthy controls and 24 subjects with an at-risk mental state (ARMS). Graph theory was applied to quantify the structural rich-club organization and global network properties. ARMS subjects revealed a significantly altered structural rich-club organization compared with the control group. The disruption of rich-club organization was associated with the severity of negative psychotic symptoms and led to an elevated level of modularity in ARMS subjects. This study shows that abnormal structural rich-club organization is already evident in clinical high-risk subjects for psychosis and further demonstrates the impact of rich-club disorganization on global network communication. Together with previous evidence in chronic schizophrenia patients and unaffected siblings, our findings suggest that abnormal structural rich-club organization may reflect an endophenotypic marker of psychosis.
Altered cytological parameters in buccal cells from individuals with mild cognitive impairment and Alzheimer's disease

Previous studies have shown that mild cognitive impairment (MCI) may be reflective of the early stages of more pronounced neurodegenerative disorders such as Alzheimer's disease (AD). There is a need for a minimally invasive and inexpensive diagnostic to identify those who exhibit cellular pathology indicative of MCI and AD risk so that they can be prioritized for primary preventative measures. The hypothesis was that a minimally invasive approach using cytological markers in isolated buccal mucosa cells can be used to identify individuals of both MCI and AD. An automated buccal cell assay was developed using laser scanning cytometry (LSC) to measure buccal cell type ratios, nuclear DNA content and shape, and neutral lipid content of buccal cells from clinically diagnosed AD (n = 13) and MCI (n = 13) patients prior to treatment compared to age‐ and gender‐matched controls (n = 26). DNA content was significantly higher in all cell types in both MCI (P < 0.01) and AD (P < 0.05) compared with controls mainly due to an increase in >2N nuclei. Abnormal nuclear shape (circularity) was significantly increased in transitional cells in MCI (P < 0.001) and AD (P < 0.01) when compared to controls. In contrast, neutral lipid content (as measured by Oil red O “ORO” staining) of buccal cells was significantly lower in the MCI group (P < 0.05) compared with the control group. The ratio of DNA content/ORO in buccal basal cells for both MCI and AD was significantly higher compared to the control group, with ratios for MCI being approximately 2.8‐fold greater (P < 0.01) and AD approximately 2.3‐fold greater (P < 0.05) than the control group. Furthermore, there was a strong negative correlation between buccal cell DNA content and ORO content in the AD group (r2 = 0.75, P < 0.0001) but not in MCI or controls. The changes in the buccal cell cytome observed in this study could prove useful as potential biomarkers in identifying individuals with an increased risk of developing MCI and eventually AD. © 2014 International Society for Advancement of Cytometry
Clustering Algorithms

Data mining tasks  Predictive vs descriptive tasks – Predictive tasks: predict the value of a particular attribute (the target variable) based on the values of other attributes – Descriptive tasks: derive patterns (correlations, trends, clusters, trajectories, and anomalies) that summarize the underlying relationships in data  Predictive modeling – The goal of predictive modeling is to learn a model that minimizes the error between the predicted and true values of the target variable – Classification: for discrete target variables – Regression: for continuous target variables  Cluster analysis – The goal is to find groups of similar observations/objects – Many clustering algorithms have been developed Applications of clustering in biology
c-Fos Expression in the Nucleus of the Solitary Tract in Response to Salt Stimulation in Rats

Salt signals in tongue are relayed to the nucleus of the solitary tract (NST). This signaling is very important to determine whether to swallow salt-related nutrition or not and suggests some implications in discrimination of salt concentration. Salt concentration-dependent electrical responses in the chorda tympani and the NST were well reported. But salt concentration-dependency and spatial distribution of c-Fos in the NST were not well established. In the present study, NaCl signaling in the NST was studied in urethane-anesthetized rats. The c-Fos immunoreactivity in the six different NST areas along the rostral-caudal axis and six subregions in each of bilateral NST were compared between applications of distilled water and different concentrations of NaCl to the tongue of experimental animals. From this study, salt stimulation with high concentration (1.0 M NaCl) induced significantly higher c-Fos expression in intermediate NST and dorsal-medial and dorsal-middle subregions of the NST compared to distilled water stimulation. The result represents the specific spatial distribution of salt taste perception in the NST.
Taxonomy of gamma‐ray burst optical light curves: identification of a salient class of early afterglows

The temporal behaviour of the early optical emission from gamma-ray burst afterglows can be divided into four classes: fast-rising with an early peak, slow-rising with a late peak, flat plateaus and rapid decays since first measurement. The fast-rising optical afterglows display correlations among peak flux, peak epoch and post-peak power-law decay index that can be explained with a structured outflow seen off-axis, but the shock origin (reverse or forward) of the optical emission cannot be determined. The afterglows with plateaus and slow rises may be accommodated by the same model, if observer location offsets are larger than for the fast-rising afterglows, or could be due to a long-lived injection of energy and/or ejecta in the blast wave. If better calibrated with more afterglows, the peak flux-peak epoch relation exhibited by the fast- and slow-rising optical light curves could provide a way to use this type of afterglows as standard candles.
Effects of the neonicotinoid insecticide, clothianidin, on the reproductive organ system in adult male rats

Abstract Clothianidin (CTD) is a novel, broad-spectrum insecticide. In the current study, it was aimed to study the effect of subchronic exposure to low doses of CTD (2, 8 and 24 mg/kg body weight/day) on the reproductive system in adult rats. CTD treatment did not significantly change serum testosterone level or sperm parameters (e.g. concentration, motility and morphology), but caused significant decreases in weights of epididymis, right cauda epididymis and seminal vesicles. CTD treatment did not cause sperm DNA fragmentation and did not change the apoptotic index in the seminiferous tubules and levels of α-tocopherol and glutathione, but increased the level of thiobarbituric acid-reactive substances and cholesterol levels significantly at all doses. CTD exposure caused significant elevations in palmitic, linoleic and arachidonic acids in testis in all CTD-exposed groups. There was a drop in 20:4/18:2 (arachidonic acid/linoleic acid) ratio and an increase in 18:1n-9/18:0 (oleic acid/stearic acid) ratios in all CTD groups, in comparison to the control group. In conclusion, CTD had little detectable detrimental effects on the reproductive system of male rats over the measured parameters.
Ankyrin G Membrane Partners Drive the Establishment and Maintenance of the Axon Initial Segment

The axon initial segment (AIS) is a specialized neuronal compartment that plays a key role in neuronal development and excitability. It concentrates multiple ion channels and cell adhesion molecules. The anchoring of these AIS membrane components is known to be highly dependent of the scaffold protein ankyrin G (ankG) but whether ankG membrane partners play a reciprocal role in ankG targeting and stabilization has not been studied yet. In cultured hippocampal neurons and cortical organotypic slices, we found that shRNA-mediated knockdown of ankG membrane partners led to a decrease of ankG concentration and perturbed the AIS formation and maintenance. These perturbations were rescued by expressing an AIS-targeted sodium channel, or a minimal construct containing the ankyrin-binding domain of Nav1.2 and a membrane anchor. We thus demonstrate that a tight and precocious association of ankG to its membrane partners is crucial for the establishment and maintenance of the AIS.
Eosinopenia as a Marker of Outcome in Acute Exacerbations of Chronic Obstructive Pulmonary Disease.

BACKGROUND Acute exacerbation of chronic obstructive pulmonary disease (AECOPD) is a common cause of hospitalization and mortality. Recent studies have shown the usefulness of eosinopenia in predicting the outcomes of patients admitted to the intensive care unit. This study examined the association of eosinopenia with the outcomes of patients with AECOPD. METHODS This is a prospective study. Patients with AECOPD were divided into two cohorts: patients with eosinopenia and those without eosinopenia. Duration of hospitalization, need of mechanical ventilation, in-hospital mortality, rehospitalization, or death within 30 days after discharge were compared between the two cohorts. Eosinopenia was defined as eosinophil count of >40 cells/mm(3). RESULTS Among 100 patients with AECOPD, 44 were eosinopenic and 56 were non-eosinopenic. Duration of hospitalization of patients with eosinopenia was 12.38 ± 9.85 days and that of patients without eosinopenia was 7.35 ± 5.68 days (p = 0.001). In all, 16 (36%) patients with eosinopenia and seven (12%) patients without eosinopenia needed mechanical ventilation (p = 0.005). In-hospital mortality rate among eosinopenic and noneosinopenic patients was 37.5% (12/44) and 7.6% (4/56), respectively (p = 0.006). Among 100 patients with AECOPD, 16 died in the hospital. Of these, 12 (27.27%) were eosinopenic and 4 (7.6%) were noneosinopenic (p = 0.006). The mean eosinophil count of patients who died in the hospital (n = 16) was 44.00 cells/ml whereas that of survivors (n = 84) was 107.41 cells/ml (p = 0.022). CONCLUSION We conclude that a significant relationship exists between eosinopenia and outcomes of patients with AECOPD. Thus, eosinopenia can be a useful, easy-to-measure, and inexpensive biomarker for predicting the prognosis of patients with AECOPD.
Connected subglacial lake drainage beneath Thwaites Glacier, West Antarctica

Abstract. We present conventional and swath altimetry data from CryoSat-2, revealing a system of subglacial lakes that drained between June 2013 and January 2014 under the central part of Thwaites Glacier, West Antarctica (TWG). Much of the drainage happened in less than 6 months, with an apparent connection between three lakes spanning more than 130 km. Hydro-potential analysis of the glacier bed shows a large number of small closed basins that should trap water produced by subglacial melt, although the observed large-scale motion of water suggests that water can sometimes locally move against the apparent potential gradient, at least during lake-drainage events. This shows that there are important limitations in the ability of hydro-potential maps to predict subglacial water flow. An interpretation based on a map of the melt rate suggests that lake drainages of this type should take place every 20–80 years, depending on the connectivity of the water flow at the bed. Although we observed an acceleration in the downstream part of TWG immediately before the start of the lake drainage, there is no clear connection between the drainage and any speed change of the glacier.
SOCS3 and IRS-1 gene expression differs between genotype 1 and genotype 2 hepatitis C virus-infected HepG2 cells

Abstract Background: The poor response to antiviral treatment of hepatitis C virus (HCV)-infected patients with genotype 1b has been associated with a higher prevalence of metabolic syndrome. However, the molecular link between these clinical entities is not clear. The goal of this study was to clarify the role of genotype 1b and 2 in the genetic expression of suppressor of cytokine signaling 3 (SOCS3) and insulin receptor substrate 1 (IRS-1). Methods: We infected human hepatocellular carcinoma cell line (HepG2) cells with human HCV genotype 1b or 2 and measured the gene and protein expression of SOCS3 at various times. We also evaluated impairment in the insulin pathway by analysis of IRS-1 and phospho-AKT. For the control, we used HepG2 cell cultures treated with non-infectious serum. We also demonstrated the occurrence of HCV infection by the detection of both positive and negative strands in the cells and culture medium. To test infection of the HepG2 cells, we performed quantitative real-time polymerase chain reaction (qRT-PCR) of viral load at different time points. We analyzed the viral genotype in the pellet and supernatant. Results: At each time point, we found positive and negative strands in the infected cells, while in the medium we found positive, but no negative strands. We also detected the presence of the correct genotype in the medium. Two weeks following infection when the viral load was higher, we tested genotype 1b and 2 infected cells. SOCS3 gene expression was significantly higher in genotype 1b-infected cells (median 2.56; mean 2.82±0.59) compared with genotype 2 (median 1.34; mean 1.46±0.31) (p=0.04) and control cells (median 1.09; mean 1.02±0.11, p=0.02). There was no difference between cells exposed to genotype 2 and control cells. Conversely, IRS-1 was significantly lower in genotype 1b-infected cells (median 15.97; mean 15.45±0.67) compared with genotype 2-infected cells (median 16.45; mean 16.44±0.01, p=0.04). Statistically significant differences were seen when comparing the pAKT/AKT ratio in genotype 1b-infected cells (0.19±0.034) and not genotype 1b-infected (genotype 2-infected and non-infected) cells (0.253±0.004, p=0.03). This inverse regulation is compatible with interactions between the molecular expression of SOCS3, IRS-1 and phospho-AKT mediated by the genotype 1b virus. Conclusions: Up-regulation of the SOCS3 gene might be one of the mechanisms governing non-response to therapy and expression of insulin resistance mediated via a direct mechanism at this level of genotype 1b HCV. Clin Chem Lab Med 2009;47:1217–25.
Subunit selectivity and epitope characterization of mAbs directed against the GABAA/benzodiazepine receptor

mAbs bd 17, bd 24, and bd 28 raised against bovine cerebral gamma- aminobutyric acid (GABAA)/benzodiazepine receptors were analyzed for their ability to detect each of 12 GABAA receptor subunits expressed in cultured mammalian cells. Results showed that mAb bd 17 recognizes epitopes on both beta 2 and beta 3 subunits while mAb bd 24 is selective for the alpha 1 subunit of human and bovine, but not of rat origin. The latter antibody reacts with the rat alpha 1 subunit carrying an engineered Leu at position four, documenting the first epitope mapping of a GABAA receptor subunit-specific mAb. In contrast to mAbs bd 17 and bd 24, mAb bd 28 reacts with all GABAA receptor subunits tested but not with a glycine receptor subunit, suggesting the presence of shared epitopes on subunits of GABA-gated chloride channels.
The ICAP Framework: Linking Cognitive Engagement to Active Learning Outcomes

This article describes the ICAP framework that defines cognitive engagement activities on the basis of students’ overt behaviors and proposes that engagement behaviors can be categorized and differentiated into one of four modes: Interactive, Constructive, Active, and Passive. The ICAP hypothesis predicts that as students become more engaged with the learning materials, from passive to active to constructive to interactive, their learning will increase. We suggest possible knowledge-change processes that support the ICAP hypothesis and address the limitations and caveats of the hypothesis. In addition, empirical validation for the hypothesis is provided by examining laboratory and classroom studies that focus on three specific engagement activities: note taking, concept mapping and self-explaining. We also consider how ICAP can be used as a tool for explaining discrepant findings, dictate the proper choice of a control condition, and evaluate students’ outputs. Finally, we briefly compare ICAP to existing theories of learning.
The Mechanisms of Propofol-Mediated Hyperpolarization of In Situ Rat Mesenteric Vascular Smooth Muscle

Previously, we reported that propofol hyperpolarizes vascular smooth muscle (VSM) cells of small arteries and veins. The current study was designed to determine whether propofol-mediated hyperpolarization is the result of specific effects on potassium channels known to exist in VSM and on steps in the intracellular nitric oxide (NO), cyclic guanosine monophosphate (cGMP), and cyclic adenosine monophosphate (cAMP) second messenger pathways. VSM transmembrane potentials (Em) were measured in situ in sympathetically denervated, small mesenteric arteries and veins of Sprague-Dawley rats. Effects of propofol on VSM Em were determined before and during superfusion with specific inhibitors of VSM calcium-activated (KCa), adenosine triphosphate-sensitive (KATP), voltage-dependent (Kv), and inward rectifying (KIR) potassium channels and with endogenous mediators of vasodilation. Propofol significantly hyperpolarized VSM in small mesenteric vessels. This hyperpolarization was abolished on inhibition of KCa and KATP channel activity and on inhibition of NO and cGMP (but not cAMP). Assuming a close inverse correlation between the magnitude of VSM Em and contractile force, these results suggest that propofol induces hyperpolarization and relaxation in denervated, small mesenteric vessels by activation of KCa and KATP channels. Such channel activation may be mediated by activation of NO and cGMP, but not cAMP, second messenger pathways.
Identification of Novel Laminin- and Fibronectin-binding Proteins by Far-Western Blot: Capturing the Adhesins of Streptococcus suis Type 2

Bacterial cell wall (CW) and extracellular (EC) proteins are often involved in interactions with extracellular matrix (ECM) proteins such as laminin (LN) and fibronectin (FN), which play important roles in adhesion and invasion. In this study, an efficient method combining proteomic analysis and Far-Western blotting assays was developed to screen directly for bacterial surface proteins with LN- and FN-binding capacity. With this approach, fifteen potential LN-binding proteins and five potential FN-binding proteins were identified from Streptococcus suis serotype 2 (SS2) CW and EC proteins. Nine newly identified proteins, including oligopeptide-binding protein OppA precursor (OppA), elongation factor Tu (EF-Tu), enolase, lactate dehydrogenase (LDH), fructose-bisphosphate aldolase (FBA), 3-ketoacyl-ACP reductase (KAR), Gly ceraldehyde-3-phosphate dehydrogenase (GAPDH), Inosine 5′-monophosphate dehydrogenase (IMPDH), and amino acid ABC transporter permease (ABC) were cloned, expressed, purified and further confirmed by Far-Western blotting and ELISA. Five proteins (OppA, EF-Tu, enolase, LDH, and FBA) exhibited specifically binding activity to both human LN and human FN. Furthermore, seven important recombinant proteins were selected and identified to have the ability to bind Hep-2 cells by the indirect immunofluorescent assay. In addition, four recombinant proteins, and their corresponding polyclonal antibodies, were observed to decrease SS2 adhesion to Hep-2 cells, which indicates that these proteins contribute to the adherence of SS2 to host cell surface. Collectively, these results show that the approach described here represents a useful tool for investigating the host-pathogen interactions.
A two-stage thermal modification of wood

Thermal modification or heat treatment is an effective method to improve the dimensional stability and biological durability of wood. An undesired side effect is the reduction of mechanical properties of wood, mainly due to the high temperatures involved (150-280°C). In this thesis the effects of heat treatment on wood properties are discussed in relation to anatomical and molecular changes found in wood after heat treatment. The results are based on investigations of a full-scale industrial heat treatment method under relative mild conditions (< 200°C) including a moist and dry treatment stage. Several changes and/or modifications of the main components of wood (cellulose, hemicelluloses and lignin) appear to be involved in the effects of heat treatment on important wood properties like dimensional stability, strength/stiffness and biological durability. Although the effect of heat treatment on the anatomical structure of wood is limited, changes have been found affecting the properties of wood. This thesis provides a better understanding of thermal modification, which probably contributes to a more controlled use of heat-treated wood in service conditions.