Miracle-dz/UniFAR-FTUs huggingface dataset:
Isolation of heterothallic haploid and auxotrophic mutants of Schizosaccharomyces japonicus

The fission yeast Schizosaccharomyces japonicus var. japonicus belong to the genus Schizosaccharomyces, together with Schizosaccharomyces pombe, which has been well studied as a model organism. In contrast, Sz. japonicus is poorly characterized and genetic tools were yet to be developed. We here report the isolation of the heterothallic haploids NIG2017, NIG2025 and NIG2028, which were derivatives of a Sz. japonicus homothallic strain (NIG2008). Based on the genomic sequence of Sz. japonicus, released by the Broad Institute, we found that Sz. japonicus also possesses orthologues of the mating‐type genes of Sz. pombe; two mat‐M (−) and two mat‐P (+) genes. As expected, heterothallic strains were defective in one of the Sz. japonicus mat genes (matsj). We confirmed that NIG2017 and NIG2025 strains only expressed mRNA from the matsj‐P genes, while homothallic strains expressed both matsj‐M and matsj‐P. Although the NIG2028 strain expressed both gene products, matsj‐P was found mutated, which may have conferred the heterothallic phenotype of the mutant. Thus, we concluded that these were stable heterothallic strains. We designated NIG2017 and NIG2025 as h+ and NIG 2028 as h−, respectively. We also found additional h− strains (NIG5872 and NIG5873) that arose from the cross between NIG2017 and NIG2028 derivatives. In addition to that, we have constructed a ura4sj‐deleted strain and an ade6sj‐mutated strain. We used these heterothallic strains and the auxotroph strains to perform spore dissection analysis to determine the genetic distances between several loci, and found that the mating type loci and ade6sj locus were linked to centromeres. Copyright © 2009 John Wiley & Sons, Ltd.
A dialogue system for multimodal human-robot interaction

This paper presents a POMDP-based dialogue system for multimodal human-robot interaction (HRI). Our aim is to exploit a dialogical paradigm to allow a natural and robust interaction between the human and the robot. The proposed dialogue system should improve the robustness and the flexibility of the overall interactive system, including multimodal fusion, interpretation, and decision-making. The dialogue is represented as a Partially Observable Markov Decision Process (POMDPs) to cast the inherent communication ambiguity and noise into the dialogue model. POMDPs have been used in spoken dialogue systems, mainly for tourist information services, but their application to multimodal human-robot interaction is novel. This paper presents the proposed model for dialogue representation and the methodology used to compute a dialogue strategy. The whole architecture has been integrated on a mobile robot platform and has bee n tested in a human-robot interaction scenario to assess the overall performances with respect to baseline controllers.
Assessment of the Sensitizing Potential of Processed Peanut Proteins in Brown Norway Rats: Roasting Does Not Enhance Allergenicity

Background IgE-binding of process-modified foods or proteins is the most common method for examination of how food processing affects allergenicity of food allergens. How processing affects sensitization capacity is generally studied by administration of purified food proteins or food extracts and not allergens present in their natural food matrix. Objectives The aim was to investigate if thermal processing increases sensitization potential of whole peanuts via the oral route. In parallel, the effect of heating on sensitization potential of the major peanut allergen Ara h 1 was assessed via the intraperitoneal route. Methods Sensitization potential of processed peanut products and Ara h 1 was examined in Brown Norway (BN) rats by oral administration of blanched or oil-roasted peanuts or peanut butter or by intraperitoneal immunization of purified native (N-), heated (H-) or heat glycated (G-)Ara h 1. Levels of specific IgG and IgE were determined by ELISA and IgE functionality was examined by rat basophilic leukemia (RBL) cell assay. Results In rats dosed orally, roasted peanuts induced significant higher levels of specific IgE to NAra h 1 and 2 than blanched peanuts or peanut butter but with the lowest level of RBL degranulation. However, extract from roasted peanuts was found to be a superior elicitor of RBL degranulation. Process-modified Ara h 1 had similar sensitizing capacity as NAra h 1 but specific IgE reacted more readily with process-modified Ara h 1 than with native. Conclusions Peanut products induce functional specific IgE when dosed orally to BN rats. Roasted peanuts do not have a higher sensitizing capacity than blanched peanuts. In spite of this, extract from roasted peanuts is a superior elicitor of RBL cell degranulation irrespectively of the peanut product used for sensitization. The results also suggest that new epitopes are formed or disclosed by heating Ara h 1 without glucose.
Extent of pharmacovigilance among resident doctors in Edo and Lagos states of Nigeria

Systematic attention to adverse drug reactions (ADRs) started with the thalidomide disaster in the early 60s of the 20th century. In 1968 ten countries supported a spontaneous reporting system for ADR and collaborated with the WHO pilot research project for international drug monitoring. This survey was conducted to determine the level of awareness of resident doctors about ADRs reporting, the extent of their involvement in pharmacovigilance activities and to build a useful data base that will improve the quality of health care in Nigeria.
Content of Waking Life Events and of Nightmare Themes

Examined the relationship of incidence of 3 types of nightmare themes to incidence of specific events listed in the Social Readjustment Rating Scale and in the Life Events Inventory. The former list of events was administered to 98 and the latter to 56 part-time college students. Information on nightmares' content was available for both samples. Events and nightmare themes were retrospectively reported for the last 6 mo. No significant relationships were found between specific types of nightmare content and specific events. Persons who experienced more events of the Life Events Inventory also reported more nightmare themes, however, similar relationship was not observed for events listed in the readjustment scale.
Mammalian Mitogen-activated Protein Kinase Pathways Are Regulated through Formation of Specific Kinase-Activator Complexes*

Mammalian cells contain at least three signaling systems which are structurally related to the mitogen-activated protein kinase (MAPK) pathway. Growth factors acting through Ras primarily stimulate the Raf/MEK/MAPK cascade of protein kinases. In contrast, many stress-related signals such as heat shock, inflammatory cytokines, and hyperosmolarity induce the MEKK/SEK(MKK4)/SAPK(JNK) and/or the MKK3 or MKK6/p38hog pathways. Physiological agonists of these pathway types are either qualitatively or quantitatively distinct, suggesting few common proximal signaling elements, although past studies performed in vitro, or in cells using transient over-expression, reveal interaction between the components of all three pathways. These studies suggest a high degree of cross-talk apparently not seen in vivo. We have examined the possible molecular basis of the differing agonist profiles of these three MAPK pathways. We report preferential association between MAP kinases and their activators in eukaryotic cells. Furthermore, using the yeast 2-hybrid system, we show that association between these components can occur independent of additional eukaryotic proteins. We show that SAPK(JNK) or p38hog activation is specifically impaired by co-expression of cognate dominant negative MAP kinase kinase mutants, demonstrating functional specificity at this level. Further divergence and insulation of the stress pathways occurs proximal to the MAPK kinases since activation of the MAPK kinase kinase MEKK results in SAPK(JNK) activation but does not cause p38hog phosphorylation. Therefore, in intact cells, the three MAPK pathways may be independently regulated and their components show specificity in their interaction with cognate cascade members. The degree of intermolecular specificity suggests that mammalian MAPK signaling pathways may remain distinct without the need for specific scaffolding proteins to sequester components of individual pathways.
The Hematological and Molecular Spectrum of α-Thalassemias in Turkey: The Hacettepe Experience

Objective: The spectrum of α-thalassemias correlates well with the number of affected α-globin genes. Additionally, combinations of the several non-deletional types of mutations with a large trans deletion comprising the 2 α-globin genes have an impact on the clinical severity. The objective of this study was to analyze the hematological and molecular data of 35 patients with Hb H disease from a single center in order to identify the genotypes of Hb H disease and genotype-phenotype correlations. Materials and Methods: Herein, we report the hematological and mutational spectrum of patients with Hb H disease (n=35). Additionally, genotypes of α-gene mutations of 78 individuals, who were referred to our institution for α-gene screening, were analyzed. Results: Supporting the previous data from Turkey, -α3. 7 was the most common mutation among patients with Hb H disease (62.8%) and in the other 78 subjects (39.7%). Of the patients with Hb H disease, the most common genotypes were -α3. 7/--20.5, -α3. 7/--26.5, and -α3. 7/--17.5 in 10 (28.6%), 6 (17.1%), and 6 (17.1%) patients, respectively. Another small deletion, -4.2 alpha, and several non-deletional types of α-gene mutations, namely α (-5nt): IVS-I donor site (GAG.GTG.AGG->GAG.G-----); α (PA-2): AATAAA>AATGGA, and α (cd59): GGC->GAC, were found to be associated with Hb H disease when present at trans loci of one of the large deletions given above. The combinations consisting of 1 non-deletional and 1 of the large deletional types of mutations (αTα/--) at trans loci were found to result in a more severe phenotype compared to the genotypes composed of 1 small trans deletion of a large deletion (-α/--). The combination of α (Cd59) and -- in trans was associated with severe phenotype and the disease was associated with an increase in Hb Bart’s level with null Hb H. In spite of the presence of 2 intact α-globin genes, homozygosity for PA-2 mutation resulted in severe Hb H disease. Conclusion: This study indicated that Hb H disease is not rare in Turkey and its genotype is quite heterogeneous.
highlighted topics Cellular Responses to Mechanical Stress Invited Review: Pulmonary capillary stress failure

West, B. Invited Review: Pulmonary capillary stress failure. J Appl Physiol 89: 2483–2489, 2000. —The pulmonary blood-gas barrier is an extraordinary bioengineering structure because of its vast area but extreme thinness. Despite this, almost no attention has been given to its mechanical properties. The remarkable area and thinness come about because gas exchange occurs by passive diffusion. However, the barrier also needs to be immensely strong to withstand the very high stresses in the capillary wall when capillary pressure rises during exercise. The strength of the thin region of the barrier comes from type IV collagen in the basement membranes. When the stresses in the capillary walls rise to high levels, ultrastructural changes occur in the barrier, a condition known as stress failure. Physiological conditions that alter the properties of the barrier include severe exercise in elite human athletes. Animals that have been selectively bred for high aerobic activity, such as Thoroughbred racehorses, consistently break their pulmonary capillaries during galloping. Pathophysiological conditions causing stress failure include high-altitude pulmonary edema and overinﬂation of the lung, which frequently occurs with mechanical ventilation. Remodeling of the capillary wall occurs in response to increased wall stress in diseases such as mitral stenosis. The barrier is able to maintain its extreme thickness with sufﬁcient strength as a result of continual regulation of its wall structure. How it does this is a central problem in lung biology.
The stability of magnesite in the transition zone and the lower mantle as function of oxygen fugacity

The oxygen fugacity at which magnesite (MgCO3) is reduced to diamond in a typical mantle assemblage has been determined between 16 and 45 GPa and 1500–1700°C in experiments employing a multianvil device. This oxygen fugacity for carbonate stability, measured using a sliding redox sensor that employs IrFe alloy, was found to be greater than 2 log units above the iron‐wüstite oxygen buffer (ΔIW+2). Reversal experiments employing FeNi alloy confirmed complete oxidation of Ni in the presence of magnesite and diamond even at 45 GPa. As the oxygen fugacity of the transition zone and lower mantle is most likely at or below the IW buffer, mantle carbon, if distributed relatively homogeneously, is unlikely to be hosted in carbonates throughout most of the mantle but is more likely present as diamond, methane, Fe‐rich carbide or as a carbon‐component dissolved in Fe‐Ni metal. The existence of carbonate at these depths would imply the presence of unusually oxidized regions of the deeper mantle. Such regions could form in the deeper mantle from an influx of subduction related carbonate melt, which would reduce by causing oxidation of the surrounding silicates. Due to changes in the degree of oxidation of the surrounding mantle such melts could potentially travel further in the transition zone mantle than in the lower mantle. The results do not exclude the possibility that carbonate could coexist with Fe‐Ni metal or carbide at the very base of the lower mantle.
ThinkerBelle EEG amplifying dress

This paper describes the ThinkerBelle EEG Amplifying Dress, an emotive wearable, which uses EEG signals from a NeuroSky MindWave EEG headset to amplify data on a dress using fibre optic filament. The dress illuminates when it receives data from the headset and is designed for wear in evening social occasions. The paper also explains the motivation for creating this emotive wearable and it's audience. It charts the construction of the dress, the electronics, approach to programming and data, plus conclusions and next steps.
Mannose-binding lectin deficiency does not increase the prevalence of Helicobacter pylori seropositivity

Background Mannose-binding lectin is an immune molecule that can bind to pathogens and initiate the complement cascade. In certain clinical situations, often characterized by immune compromise, mannose-binding lectin deficiency can increase the risk of infectious complications. Helicobacter pylori is one of the most common human infections and can bind mannose-binding lectin. Therefore, we examined whether mannose-binding lectin status influences the prevalence of H. pylori infection. Methods Two distinct populations were targeted. The first consisted of 166 volunteer blood donors, the second included 108 peripheral blood stem cell donors. All were tested for serological evidence of H. pylori infection, and had their mannose-binding lectin status characterized by genotyping, and quantification of mannose-binding lectin mannan-binding level and C4-deposition function in plasma. Results H. pylori positive blood donors had higher blood mannose-binding lectin levels, as measured by C4 deposition (median 0.67 vs. 0.40, P=0.009, hazard ratio 2.82, 95% confidence interval 1.29–6.19) and mannan-binding assays (median 1.83 vs. 1.26, P=0.02, hazard ratio 1.28, 95% confidence interval 1.03–1.59). A trend was also found between the presence of an MBL2 coding mutation and a reduced prevalence of H. pylori. No significant associations were found in the second population. Conclusions Mannose-binding lectin deficiency does not increase the risk of H. pylori infection. The finding in one population that greater mannose-binding lectin activity might predispose to infection, suggests that this study should be repeated in other large cohorts of normal subjects.
The mRNA decay factor PAT1 functions in a pathway including MAP kinase 4 and immune receptor SUMM2

Multi‐layered defense responses are activated in plants upon recognition of invading pathogens. Transmembrane receptors recognize conserved pathogen‐associated molecular patterns (PAMPs) and activate MAP kinase cascades, which regulate changes in gene expression to produce appropriate immune responses. For example, Arabidopsis MAP kinase 4 (MPK4) regulates the expression of a subset of defense genes via at least one WRKY transcription factor. We report here that MPK4 is found in complexes in vivo with PAT1, a component of the mRNA decapping machinery. PAT1 is also phosphorylated by MPK4 and, upon flagellin PAMP treatment, PAT1 accumulates and localizes to cytoplasmic processing (P) bodies which are sites for mRNA decay. Pat1 mutants exhibit dwarfism and de‐repressed immunity dependent on the immune receptor SUMM2. Since mRNA decapping is a critical step in mRNA turnover, linking MPK4 to mRNA decay via PAT1 provides another mechanism by which MPK4 may rapidly instigate immune responses.
Slowing Down in Spatially Patterned Ecosystems at the Brink of Collapse

Predicting the risk of critical transitions, such as the collapse of a population, is important in order to direct management efforts. In any system that is close to a critical transition, recovery upon small perturbations becomes slow, a phenomenon known as critical slowing down. It has been suggested that such slowing down may be detected indirectly through an increase in spatial and temporal correlation and variance. Here, we tested this idea in arid ecosystems, where vegetation may collapse to desert as a result of increasing water limitation. We used three models that describe desertification but differ in the spatial vegetation patterns they produce. In all models, recovery rate upon perturbation decreased before vegetation collapsed. However, in one of the models, slowing down failed to translate into rising variance and correlation. This is caused by the regular self-organized vegetation patterns produced by this model. This finding implies an important limitation of variance and correlation as indicators of critical transitions. However, changes in such self-organized patterns themselves are a reliable indicator of an upcoming transition. Our results illustrate that while critical slowing down may be a universal phenomenon at critical transitions, its detection through indirect indicators may have limitations in particular systems.
MEDULLARY BONE AND AVIAN CALCIUM REGULATION

Medullary bone forms in egg-laying birds in response to gonadal steroids and is the most overtly oestrogen-dependent of all bone types. It acts as a labile reservoir for the supply of eggshell calcium. Previous studies indicate that feeding calcium- and vitamin-D-deficient diets to chickens results in resorption of cortical rather than medullary bone. More recent studies in calcium-stressed quail hens question this hypothesis and suggest that during the first 2 weeks of dietary calcium depletion the medullary bone is resorbed while cortical bone volume remains intact. The role of the osteoclast in bone resorption is the focus of much research that has recently included studies of medullary bone osteoclasts. The functional morphology of the avian cells, i.e. changes from quiescent to active osteoclasts with ruffled borders, reflects the rapid changes in medullary bone turnover that occur during the egg-laying cycle. Unlike mammalian osteoclasts, those from avian sources generally appear refractory to inhibitory factors such as calcitonin or raised extracellular calcium concentration. However, medullary bone osteoclasts cultured in vitro for several days recover their ability to respond to the latter factor by increasing their levels of free cytosolic Ca2+, reducing tartrate-resistant acid phosphatase secretion and reducing their cell spread area. It is suggested that factors such as ambient calcium levels and prostaglandins may form part of a system of rapid local control for medullary bone osteoclast activity.
Antimicrobial-Sensing Proteins in Obesity and Type 2 Diabetes

Obesity is well known to be associated with a cluster of metabolic diseases such as dyslipidemia, hypertension, insulin resistance, type 2 diabetes, and atherosclerosis (1). Alterations of the innate immune system are increasingly recognized to be intrinsically linked to metabolic pathways in humans (2). Central to metabolic diseases is insulin resistance associated with a low-grade inflammatory status (3). The mechanisms through which proinflammatory cytokines, such as tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-1α, interact with cellular insulin signal transduction cascades have been better understood in the last few years (4–6). In vivo, a direct correlation between increased circulating proinflammatory cytokines and insulin resistance has been well demonstrated (3,7). The origin of this increased inflammatory activity in obesity and type 2 diabetes is virtually unknown. Immune system homeostasis is challenged by continuous external insults, such as saturated fatty acid–rich diets (8), pathogen-associated molecular patterns like lipopolysaccharide (LPS) (9), advanced glycation end products (AGEs) (10), burden of infection (11), and oxidative stress (12). These continuous insults could result in a chronic low level of inflammation associated with insulin resistance. Here, we review the potential significance of neutrophil dysfunction in subjects with type 2 diabetes and the consequence of altered antimicrobial-sensing protein profile in obesity-related metabolic disturbances. Given that 60–70% of blood leukocytes are granulocytes and over 90% of granulocytes are neutrophils, polymorphonuclear cells (PMNs) are the largest fraction of white blood cells. PMNs possess a variety of functions, including chemotaxis, adhesion to the endothelium and foreign agents, phagocytosis, and microbicidal activity. PMNs are able to penetrate and migrate into infected tissues and destroy invading microorganisms after internalization by producing multiple toxic agents such as reactive oxygen species (ROS), proteases (elastase), and proteins interfering with bacterial development. Chronic disease (such as type 2 diabetes), age-associated insulin resistance, nutrition, …