Miracle-dz/UniFAR-FTUs huggingface dataset:
Pilot Study of SIgA as a Stress Maker with Repetitive Saliva Collection

Recent studies investigating the impacts on human internal physiological states of the psychological intervention have revealed close relationship and sensitive interaction between human body and mind. For example, various human secretory immune and endocrine substances, such as immunoglobulin A and cortisol, are temporary enhanced by acute stressful tasks or stressful events in daily life (e.g., Ader, Felten & Cohen, 2001). This field of study has drastically advanced over the last decade with development in molecular analysis techniques, forming truly inter-disciplinary scientific field covering psychology, physiology, and cognitive science. Especially for cognitive science, it has recently revealed that such effects on human secretions are more than reflections of given psychological stimuli, because higher cognitive processes including ‘controllability’ can mediate those effects (e.g., Isowa, Ohira, & Murashima, 2006). This field of study is also marked as a developing methodology for the physiological evaluation of the human mental process. However, even though previous studies successfully observed physiological changes in the human body according to mental states, there is still small number of studies, and those reported results are inconsistent with each other. Moreover, few studies has been made investigating precise modulation in time series; most of the past studies assessed sample collections of human secretion, such as saliva, urine, and blood, just before and after psychological intervention, but not serially over experimental time period. Some reasons can be thought for that small numbers of sampling, such as acceptability of subjects for repetitive sampling especially for blood, cost of quantitative determination of secretory substances. Above all, regarding with saliva sampling, the change of mass of saliva by repetitive sampling accompanying with feedback effects of some kind cannot neglect. In this paper, we introduced a new method for saliva collection for repetitive sampling compared with conventional sampling method with ‘salivette’ cotton (described below), and conducted an experiment investigating the modulation of secretory Immunoglobulin A (SIgA), which is assumed to be one possible stress makers (Bosh, Ring, de Geus et al., 2002), assessed with a stressful task. Figure 1: SIgA concentration and Saliva with repetitive saliva collection by salivette.
Mercury Alters Endotoxin-Induced Inflammatory Cytokine Expression in Liver: Differential Roles of P38 and Extracellular Signal-Regulated Mitogen-Activated Protein Kinases

Mercury is a widespread metal in the environment and consequently large populations are currently exposed to low levels of mercury. Endotoxin, a component of the Gram-negative bacteria, promotes inflammatory responses. We recently reported that mercury modulates the production of nitric oxide and various inflammatory cytokines induced by endotoxin in a macrophage cell line (Nitric Oxide 2002, 7:67). The present study was designed to determine the impact of mercury on endotoxin-induced inflammatory cytokine expression and corresponding signal transduction in mouse liver. Male BALB/c mice were exposed continuously to 0, 0.3, 1.5, 7.5, or 37.5 ppm of mercury in drinking water for 14 days and at the end of the treatment periodlipopolysaccharide (LPS, 0.5 mg/kg) was injected intraperitoneally 2 hr prior to euthanasia. The doses of mercury and LPS did not cause hepatotoxicity as indicated by unaltered circulating alanine aminotransferase and aspartate aminotransferase levels. Mercury decreased liver glutathione (GSH) and with LPS additively decreased GSH. Mercury activated p38 mitogen-activated protein kinase (MAPK) and additively increased LPS-induced p38 MAPK phosphorylation. In contrast, mercury alone had no effect on activation of extracellular signal-regulated kinase (ERK) but inhibited LPS-induced ERK activation. Mercury increased the expression of tumor necrosis factor α (TNFα) and further potentiated LPS-induced TNFα expression. Mercury did not affect LPS-induced interleukin (IL)-1β expression but decreased LPS-induced IL-6 expression. Results indicated that low levels of mercury augment LPS-induced TNFα expression by altering GSH and p38 MAPK. Mercury modulates LPS-induced p38 and ERK activation and downstream TNFα and IL-6 expression in mouse liver.
Exploiting Type 3 Complement Receptor for TNF-α Suppression, Immune Evasion, and Progressive Pulmonary Fungal Infection1

TNF-α is crucial in defense against intracellular microbes. Host immune cells use type 3 complement receptors (CR3) to regulate excess TNF-α production during physiological clearance of apoptotic cells. BAD1, a virulence factor of Blastomyces dermatitidis, is displayed on yeast and released during infection. BAD1 binds yeast to macrophages (Mφ) via CR3 and CD14 and suppresses TNF-α, which is required for resistance. We investigated whether blastomyces adhesin 1 (BAD1) exploits host receptors for immune deviation and pathogen survival. Soluble BAD1 rapidly entered Mφ, accumulated intracellularly by 10 min after introduction to cells, and trafficked to early and late endosomes. Inhibition of receptor recycling by monodansyl cadaverine blocked association of BAD1 with Mφ and reversed TNF-α suppression in vitro. Inhibition of BAD1 uptake with cytochalasin D and FcR-redirected delivery of soluble BAD1 as Ag-Ab complexes or of wild-type yeast opsonized with IgG similarly reversed TNF-α suppression. Hence, receptor-mediated entry of BAD1 is requisite in TNF-α suppression, and the route of entry is critical. Binding of soluble BAD1 to Mφ of CR3−/− and CD14−/− mice was reduced to 50 and 33%, respectively, of that in wild-type mice. Mφ of CR3−/− and CD14−/− mice resisted soluble BAD1 TNF-α suppression in vitro, but, in contrast to CR3−/− cells, CD14−/− cells were still subject to suppression mediated by surface BAD1 on wild-type yeast. CR3−/− mice resisted both infection and TNF-α suppression in vivo, in contrast to wild-type and CD14−/− mice. BAD1 of B. dermatitidis thus co-opts normal host cell physiology by exploiting CR3 to subdue TNF-α production and foster pathogen survival.
Fifty Years of Vehicle Routing

The Vehicle Routing Problem (VRP) was introduced 50 years ago by Dantzig and Ramser under the title “The Truck Dispatching Problem. ” The study of the VRP has given rise to major developments in the fields of exact algorithms and heuristics. In particular, highly sophisticated exact mathematical programming decomposition algorithms and powerful metaheuristics for the VRP have been put forward in recent years. The purpose of this article is to provide a brief account of this development.
Multiple Rare Alleles Contribute to Low Plasma Levels of HDL Cholesterol

Heritable variation in complex traits is generally considered to be conferred by common DNA sequence polymorphisms. We tested whether rare DNA sequence variants collectively contribute to variation in plasma levels of highdensity lipoprotein cholesterol (HDL-C). We sequenced three candidate genes (ABCA1, APOA1, and LCAT) that cause Mendelian forms of low HDL-C levels in individuals from a population-based study. Nonsynonymous sequence variants were significantly more common (16% versus 2%) in individuals with low HDL-C (95th percentile). Similar findings were obtained in an independent population, and biochemical studies indicated that most sequence variants in the low HDL-C group were functionally important. Thus, rare alleles with major phenotypic effects contribute significantly to low plasma HDL-C levels in the general population.
Channel-Aware Quantization for Decentralized BLUE via Energy-Constrained Wireless Sensor Networks

Bit assignment for local sensor data quantization in the decentralized best-linear-unbiased-estimation (BLUE) scenario is widely addressed in the signal processing research for wireless sensor networks. When the timely knowledge of the instantaneous sensor noise variance (for implementing the BLUE fusion rule) is too costly to obtain, one plausible alternative is to exploit the associated statistical characterization. Related such proposals, however, do not explicitly take into account the communication link impairments such as channel fading. In this paper we extend the current results to the more realistic case when signal transmission is subject to the fading effect. We show that the optimal bit allocation problem can be reformulated in the form of convex optimization, and then derive an analytical solution. Through numerical simulation the proposed solution is seen to outperform the uniform energy allocation scheme. instead optimize an associated tractable lower bound. It is shown that, even in the presence of channel fading, the problem can be formulated as convex optimization and is then analytically solved. Numerical simulation shows that, in the low-energy regime, the proposed method yields smaller average MSE, and at the same time achieves at least 10 % energy reduction, when compared with the uniform energy allocation scheme. In the high-energy case, even though the MSE performances of the two methods are roughly the same, the energy saving attained by the proposed method will be more than 60 %. The rest of this paper is organized as follows. Section II is the preliminary. Section III shows that main analytical result and the related numerical study. Section IV briefly concludes this paper.
Maximum-likelihood estimation of OFDM carrier frequency offset for fading channels

In OFDM systems, significant performance degradation can result from a small carrier frequency offset, which may occur due to drift after an initial frequency acquisition. We consider the estimation of the frequency offset in the tracking mode, using demodulation decisions rather than training sequences. Both maximum-likelihood estimation and a simpler, iterative technique are considered. For a system with 128 subchannels, coherent QPSK modulation, and an exponentially decaying multipath-fading channel, our simulation results show that unbiased estimation with a standard deviation of less than 1% can be achieved within three iterations if the frequency offset is less than 15%. After the correction using the estimated frequency offset, the bit error rate of the demodulation decisions is no different from that without a frequency offset.
Survival of human enteroviruses in the Hawaiian ocean environment: evidence for virus-inactivating microorganisms

The stability of certain human enteroviruses in the Hawaiian ocean environment was examined. The present data indicated that the time for 90% reduction of poliovirus type 1 at 24 +/- 1 degree C in seawater samples obtained from different sites in Hawaii ranged from 24 to 48 h, and complete inactivation occurred within 72 to 96 h. The accumulated evidence also strongly indicated that a virus-inactivating agent(s) of a microbiological nature was present in both clean and sewage-polluted seawaters, but not in fresh, mountain stream waters. The antiviral activity was lost when the seawater samples were subjected to boiling, autoclaving, or filtration through a 0.22- or 0.45-micrometer, but not a 1.0-micrometer, membrane filter. That the antiviral activity of the seawater was related to the growth activities of microorganisms was corroborated by the observed effects of added nutrients, a lower temperature of incubation, and the presence of certain antibiotics. Other enteric viruses, such as coxsackie virus B-4 and echo virus-7, were also shown to be similarly inactivated in seawater.
TGF-&bgr; Superfamily Signaling in Muscle and Tendon Adaptation to Resistance Exercise

Numerous studies in muscle and tendon have identified a central role of the transforming growth factor-&bgr; (TGF-&bgr;) superfamily of cytokines in the regulation of extracellular matrix growth and remodeling, protein degradation, and cell proliferation and differentiation. We provide a novel framework for TGF-&bgr; and myostatin signaling in controlling the coordinated adaptation of both skeletal muscle and tendon tissue to resistance training.
Inquiry will examine transgender people’s access to healthcare

A parliamentary committee will investigate whether transgender people are being treated fairly, including their dealings with health services and access to gender reassignment treatment on the NHS. The Women and Equalities Committee’s inquiry into equality for transgender people—that is, people who identify with a gender different from the one assigned to them at birth—will also look at how current laws are operating, employment and workplace issues, transphobia and hate crime, and issues affecting …
THE TRANSFORMATION OF THE PLASMODIUM GALL INACEUM OOCYST IN AEDES AEGYPTI MOSQUITOES

Sporoblast and sporozoite formation from oocysts of the avian malarial parasite, Plasmodium gallinaceum, after the seventh day of infection in Aedes aegypti mosquitoes offers an interesting example of differentiation involving the appearance and modification of several cellular components. Sporoblast formation is preceded by (a) invaginations of the oocyst capsule into the oocyst cytoplasm, (b) subcapsular vacuolization and cleft formation, (c) the appearance of small tufts of capsule material on the previously noted invaginations, and (d) linear dense areas located just below the oocyst plasma membrane which predetermine the site of emerging sporozoites from the sporoblast. The subcapsular clefts subdivide the once-solid oocyst into sporoblast peninsula. Within the sporoblast, nuclei migrate from the random distribution seen in the solid oocyst and come to lie at the periphery of the sporoblast just below the linear dense areas noted in the earlier stage. A typical nuclear fiber apparatus occurs in most of the nuclei seen in random sections at this stage although such a fiber apparatus may occasionally be seen in the solid oocyst stage. The nucleus, its associated fiber apparatus, and the overlying dense area appear to induce the onset of sporozoite budding from the sporoblast as well as the formation of the sporozoite pellicular complex and the paired organelle precursor. Several mitochondria are present in each sporozoite, in contrast to the single mitochondrion seen in the merozoites of the erythrocytic and exoerythrocytic stages of avian malaria infection. The paired organelles and associated dense inclusion bodies are formed by condensation of an irregular meshwork of membranebound, coarse, dense material. The nature of small, particulate cytoplasmic inclusions is described.
Drift of Visually Induced Optostatic Torsion

Purpose: Compensatory ocular torsion has been found in response to static tilted visual stimuli. The purpose was to investigate if visually induced ocular torsion is maintained during continuous stimulation and to reinvestigate the effect of stimuli tilt angle. Methods: Eye movements were recorded in 19 healthy individuals using a 3-D video oculography system. One visual stimulus was used in the tests, a photographic image of a city scene with spatial clues relevant for body posture. The scenes were tilted counterclockwise around a central pivot point from 0 to 15 degrees (test A), from 0 to 30 degrees (test B), and from 0 to 45 degrees (test C). Each tilted stimulus position was held static for 4 min, 40 sec. Results: A compensatory torsional response was found in all subjects and test conditions. No significant difference was found between the different stimuli tilt angles. The torsional response was not maintained but drifted back towards the reference position. Conclusions: Visually induced ocular torsion in response to a static tilted scene is not maintained, but drifts back towards the initial reference position. Higher cognitive functions such as imagination and attention certainly have an influence on the outcome.
MicroRNAs as regulators of epithelial-mesenchymal transition

Epithelial-mesenchymal transition (EMT) describes the molecular reprogramming and phenotypic changes involved in the conversion of polarised immotile epithelial cells to motile mesenchymal cells. This process allows the remodelling of tissues during embryonic development and is implicated in the promotion of tumor invasion and metastasis. Several recent studies have identified the miR-200 family and miR-205 as key regulators of EMT and enforcers of the epithelial phenotype. The miR-200 family participates in a signaling network with the E-cadherin transcriptional repressors ZEB1/δEF1 and ZEB2/SIP1, and TGF-β2 that is postulated to facilitate maintenance of stable epithelial or mesenchymal states but also allow reversible switching between these states in response to EMT effectors (such as TGF-β). This review summarizes these recent findings and their implications in both developmental EMT and tumor progression.
Toxoplasma Rhoptry Protein 16 (ROP16) Subverts Host Function by Direct Tyrosine Phosphorylation of STAT6*

The obligate intracellular parasite, Toxoplasma gondii, modulates host immunity in a variety of highly specific ways. Previous work revealed a polymorphic, injected parasite factor, ROP16, to be a key virulence determinant and regulator of host cell transcription. These properties were shown to be partially mediated by dysregulation of the host transcription factors STAT3 and STAT6, but the molecular mechanisms underlying this phenotype were unclear. Here, we use a Type I Toxoplasma strain deficient in ROP16 to show that ROP16 induces not only sustained activation but also an extremely rapid (within 1 min) initial activation of STAT6. Using recombinant wild-type and kinase-deficient ROP16, we demonstrate in vitro that ROP16 has intrinsic tyrosine kinase activity and is capable of directly phosphorylating the key tyrosine residue for STAT6 activation, Tyr641. Furthermore, ROP16 co-immunoprecipitates with STAT6 from infected cells. Taken together, these data strongly suggest that STAT6 is a direct substrate for ROP16 in vivo.
Left ventricular myocardium of heart as a 3D scheme

In this paper it will be shown that according to the scheme theory in algebraic geometry, human heart as an elastic body can be represented as a 3D scheme, on account of algebraic equations of the myocardial fibers as the local parts of the global scheme. It is possible that the fiber movements to be discussed here are identical with the so-called "myocardial fiber transactions"; however the information available to me regarding the latter is lacking in precision, that I can from no judgment in the matter. It is hoped that some enquirer may succeed shortly in this introduced scheme suggested here, which is so important in connection with the theory of schemes.
JAK2 and STAT3 activation contributes to neuronal damage following transient focal cerebral ischemia

Increased levels of interleukin‐6 (IL‐6) play a role in post‐ischemic cerebral inflammation. IL‐6 binding to its receptors induces phosphorylation of the receptor associated janus kinases (JAKs), and the down‐stream signal transducer and activator of transcription (STAT) family of transcription factors, which amplify the IL‐6 signal transduction. We evaluated the functional significance of JAK2 and STAT3 activation in focal ischemia‐induced neuronal damage. Transient middle cerebral artery occlusion in adult rats led to increased JAK2 and STAT3 phosphorylation in the ipsilateral cortex and striatum after 6–72 h of reperfusion. Fluorescent immunohistochemistry with cell specific markers (NeuN for neurons, glial fibrillary acidic protein for reactive astrocytes and ED1/OX42 for activated macrophages/microglia) showed that both pJAK2 and pSTAT3 staining is predominantly localized in the macrophages/microglia in the post‐ischemic brain. Intracerebroventricular infusion of rats with AG490 (a JAK2 phosphorylation inhibitor) prevented the post‐ischemic JAK2 and STAT3 phosphorylation and significantly decreased the infarct volume, number of apoptotic cells and neurological deficits, compared to vehicle control. Furthermore, intracerebral injection of siRNA specific for STAT3 led to curtailed STAT3 mRNA expression and phosphorylation, decreased infarct volume, fewer apoptotic cells and improved neurological function following transient middle cerebral artery occlusion. These studies show that JAK2‐STAT3 activation plays a role in post‐ischemic brain damage.
Regulatory natural autoantibodies to apoptotic cells: pallbearers and protectors.

To provide effective host defense, a healthy immune system must recognize microbial threats and coordinate a protective inflammatory response. Yet the maintenance of overall homeostasis also dictates an absolute requirement for the efficient recognition and clearance of the host’s own dead and dying cells, and these functions must somehow also be balanced to avoid autoimmune disease. In recent studies we have characterized a class of naturally arising regulatory antibodies (NAbs) to oxidation-associated phospholipid antigens on apoptotic-cell (AC) membranes that discriminate apoptotic from healthy cells. When augmented by appropriate constant region effector functions, these antibodies enhance the phagocytic clearance of ACs, blunt inflammatory responses transduced by membrane and endosomal Toll-like receptors (TLRs), and block the development of inflammatory arthritis. These NAbs have also been implicated in lupus as well as atherosclerosis. We describe a model of immune homeostasis, termed the inhibitory dual receptor hypothesis, in which NAbs to ACs oppose the development of autoimmune and inflammatory disease.
Medication overuse headache

Medication overuse headache (MOH) has incited passionate debate among headache clinicians and researchers in recent years. The existence of MOH as a diagnostic category1 and as a potentially modifiable risk factor for headache chronification is well-recognized by most headache specialists.2 However, the greatest controversies seem to exist over whether medication overuse should be regarded as cause or consequence; and over the treatment strategies, including advice about withdrawal of frequently used symptomatic (acute pain relieving) medication and whether prophylactic treatment should be initiated during withdrawal or after detoxification.3,4 This ongoing debate is undoubtedly a symptom of a lack of high-quality evidence, as Scher et al.5 state in this issue of Neurology®. Other contributing factors include the difficulty of disentangling retrospectively the underlying primary headache type predating medication overuse and cultural differences regarding types of overused symptomatic medication. Most notably, the advice to patients to stop symptomatic medication that may provide transient benefits seems to counter the mission of headache practitioners to minimize pain.
Hypothalamic, other diencephalic, and telencephalic neurons that project to the dorsal midbrain

Neurons in the hypothalamus, other diencephalic regions, and the telencephalon which project to the mesencephalic central gray (CG) and the region lateral to it were demonstrated, in the rat, by the horseradish peroxidase retrograde neuroanatomical tracing method with diaminobenzidine and tetramethyl benzidine visualization reactions. The greatest concentrations of neurons that project to the dorsal mesencephalon were found in the ventromedial nucleus, particularly the anterior and ventrolateral subdivisions, in the dorsal premammillary nucleus, and in the zona incerta. Neurons that project to or lateral to the CG were also found in the laterocaudal hypothalamus, the dorsomedial hypothalamus, regions of the anterior hypothalamic area, specific areas of the cerebral cortex (32, 29, 8, 8A, 13, 14), and the central nucleus of the amygdala. Some neurons that project were also found in the preoptic area, septum, bed nucleus of the stria terminals, and the habenula.