Miracle-dz/UniFAR-FTUs huggingface dataset:
Titanium dioxide induced inflammation in the small intestine.

AIM To investigate the effects of titanium dioxide (TiO₂) nanoparticles (NPTiO₂) and microparticles (MPTiO₂) on the inflammatory response in the small intestine of mice. METHODS Bl 57/6 male mice received distilled water suspensions containing TiO₂ (100 mg/kg body weight) as NPTiO₂ (66 nm), or MPTiO₂ (260 nm) by gavage for 10 d, once a day; the control group received only distilled water. At the end of the treatment the duodenum, jejunum and ileum were extracted for assessment of cytokines, inflammatory cells and titanium content. The cytokines interleukin (IL)-1b, IL-4, IL-6, IL-8, IL-10, IL-12, IL-13, IL-17, IL-23, tumor necrosis factor-α (TNF-α), intracellular interferon-γ (IFN-γ) and transforming growth factor-β (TGF-β) were evaluated by enzyme-linked immunosorbent assay in segments of jejunum and ileum (mucosa and underlying muscular tissue). CD4+ and CD8+ T cells, natural killer cells, and dendritic cells were evaluated in duodenum, jejunum and ileum samples fixed in 10% formalin by immunohistochemistry. The titanium content was determined by inductively coupled plasma atomic emission spectrometry. RESULTS We found increased levels of T CD4+ cells (cells/mm²) in duodenum: NP 1240 ± 139.4, MP 1070 ± 154.7 vs 458 ± 50.39 (P < 0.01); jejunum: NP 908.4 ± 130.3, MP 813.8 ± 103.8 vs 526.6 ± 61.43 (P < 0.05); and ileum: NP 818.60 ± 123.0, MP 640.1 ± 32.75 vs 466.9 ± 22.4 (P < 0.05). In comparison to the control group, the groups receiving TiO₂ showed a statistically significant increase in the levels of the inflammatory cytokines IL-12, IL-4, IL-23, TNF-α, IFN-γ and TGF-β. The cytokine production was more pronounced in the ileum (mean ± SE): IL-12: NP 33.98 ± 11.76, MP 74.11 ± 25.65 vs 19.06 ± 3.92 (P < 0.05); IL-4: NP 17.36 ± 9.96, MP 22.94 ± 7.47 vs 2.19 ± 0.65 (P < 0.05); IL-23: NP 157.20 ± 75.80, MP 134.50 ± 38.31 vs 22.34 ± 5.81 (P < 0.05); TNFα: NP 3.71 ± 1.33, MP 5.44 ± 1.67 vs 0.99 ± 019 (P < 0.05); IFNγ: NP 15.85 ± 9.99, MP 34.08 ± 11.44 vs 2.81 ± 0.69 (P < 0.05); and TGF-β: NP 780.70 ± 318.50, MP 1409.00 ± 502.20 vs 205.50 ± 63.93 (P < 0.05). CONCLUSION Our findings indicate that TiO₂ particles induce a Th1-mediated inflammatory response in the small bowel in mice.
A whole-process WiFi security perception software system

A whole-process WiFi security perception software system is designed in this paper based on the analysis of client's wireless access process, it consists of three modules to protect user from security threats during the pre-connection, connection and after-connection. The system could detects WiFi environment and shows with 3D effect, marking the Rogue AP, which is found out by multi-factors analysis techniques. During the connection, it inspired by the idea of Fog Computing, sending fake traffic to protect PSK from sniffing. After connection, the system detects Deauth attack in time, and traces the attacker. Finally, The software functionalities is realized, all the suspicious points are displayed on the User Interface (UI). The corresponding experimental testing shows that it could protect the surf in the WiFi environment effectively.
Phase III, double-blind, controlled trial of atamestane plus toremifene compared with letrozole in postmenopausal women with advanced receptor-positive breast cancer.

PURPOSE To compare time to progression (TTP) with a steroidal aromatase inhibitor (AI) atamestane (ATA) combined with toremifene (TOR; complete estrogen blockade) versus letrozole (LET) in receptor-positive advanced breast cancer (ABC). PATIENTS AND METHODS Eligibility included postmenopausal receptor-positive ABC and adjuvant hormonal therapy completed more than 12 months prior to study entry. Participants received daily ATA 500 mg with TOR 60 mg (ATA + TOR), or letrozole 2.5 mg (LET). The primary end point was TTP, whereas secondary objectives included objective response (OR), overall survival (OS), and time to treatment failure (TTF). The study had 80% power to detect a 25% increase in TTP assuming a TTP of 9.4 months in the LET population. RESULTS A total of 865 patients were randomly assigned (434 to ATA + TOR and 431 to LET) in 60 centers in the United States, Canada, Russia, and Ukraine. Baseline characteristics were balanced. Median TTP was identical in the two arms at 11.2 months (P < .92). Median TTF was similar at 9.24 months (ATA + TOR) versus 10.44 months (LET). The hazard ratios (LET/ATA + TOR) were 1.00 (95% CI, 0.92 to 1.08) for TTP, 0.99 (95% CI, 0.92 to 1.06) for TTF, and 0.98 (95% CI, 0.87 to 1.11) for OS. OR occurred in 30% of patients receiving ATA + TOR and in 36% of patients receiving LET (P < .1). Adverse events (AEs) were similar for patients receiving ATA + TOR versus LET, and serious AEs were 10% v 11%, respectively. CONCLUSION TTP for patients receiving ATA + TOR was identical to that for patients receiving LET, representing the first endocrine therapy comparable to LET in ABC. Unlike in the Anastrozole, Tamoxifen, and Combined trial, addition of an antiestrogen did not decrease efficacy of the AI. Future studies of AIs in combination with more effective selective estrogen receptor modulators or selective receptor downregulators is warranted.
FTY720, a novel immunosuppressant, induces sequestration of circulating mature lymphocytes by acceleration of lymphocyte homing in rats, III. Increase in frequency of CD62L‐positive T cells in Peyer’s patches by FTY720‐induced lymphocyte homing

FTY720, a novel immunosuppressant, sequesters circulating mature lymphocytes, especially T cells, within lymph nodes and Peyer’s patches by accelerating lymphocyte homing, and thereby causes lymphocyte depletion in the blood. The FTY720‐induced acceleration of lymphocyte homing appears to be mediated by lymphocyte homing receptors including CD62L, CD49d/β7, and CD11a/CD18. In this study, expressions of CD62L, CD49d and CD11a on T cells in the peripheral blood, lymph nodes and Peyer’s patches were analysed by flow cytometry in rats given FTY720 (1 mg/kg) orally. FTY720 markedly decreased the number of peripheral blood T cells, while not affecting CD62L, CD49d and CD11a expressions at 1–3 hr after administration. In contrast, both the frequency of CD62L‐positive T cells and intensity of CD62L expression on T cells were increased in Peyer’s patches but not lymph nodes at 3 hr after administration of FTY720. CD49d and CD11a expressions on T cells were unaffected by FTY720 in both Peyer’s patches and lymph nodes at the same point in time. On the other hand, analysis of lymphocyte homing with calcein‐labelled lymphocytes and anti‐CD62L monoclonal antibody (mAb) confirmed that FTY720 predominantly increased CD62L‐dependent lymphocyte homing to Peyer’s patches. These findings indicate that FTY720 increases the frequency of CD62L‐positive T cells by accelerating CD62L‐predominant homing in Peyer’s patches.
Angiopoietin-1 Reduces VEGF-Stimulated Leukocyte Adhesion to Endothelial Cells by Reducing ICAM-1, VCAM-1, and E-Selectin Expression

Vascular endothelial growth factor (VEGF) and angiopoietin-1 (Ang1) are potent vasculogenic and angiogenic factors that hold promise as a means to produce therapeutic vascularization and angiogenesis. However, VEGF also acts as a proinflammatory cytokine by inducing adhesion molecules that bind leukocytes to endothelial cells, an initial and essential step toward inflammation. In the present study, we used human umbilical vascular endothelial cells (HUVECs) to examine the effect of Ang1 on VEGF-induced expression of three adhesion molecules: intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and E-selectin. Interestingly, Ang1 suppressed VEGF-induced expression of these adhesion molecules. Furthermore, Ang1 reduced VEGF-induced leukocyte adhesion to HUVECs. These results demonstrate that Ang1 counteracts VEGF-induced inflammation by reducing VEGF-induced endothelial adhesiveness.
MinK-KvLQT1 Fusion Proteins, Evidence for Multiple Stoichiometries of the Assembled I sK Channel*

I sK , a slowly activating delayed rectifier K+ current through channels formed by the assembly of two channel proteins KvLQT1 and MinK, modulates the repolarization of cardiac action potentials. Mutations that map to theKvLQT1 and minK genes account for more than 50% of an inherited cardiac disorder, the Long QT syndrome (Splawski, I., Tristani-Firouzi, M., Lehmann, M. H., Sanguinetti, M. C., and Keating, M. T. (1997) Nat. Genet. 17, 338–340). Despite the importance of these channels to human cardiac function, the molecular basis of their uniquely slow gating properties as well as the stoichiometry and interaction sites of these two subunits are still unclear. We have constructed several fusion channel proteins to begin investigating the stoichiometry of these two subunits and the role of voltage-dependent subunit assembly in channel gating. Functional properties of these constructs were measured using whole cell patch clamp recordings of transiently transfected Chinese hamster ovary cells. The constructs we tested are as follows: MK24 (C terminus of MinK linked to N terminus of KvLQT1); KK40 (a tandem homodimer of KvLQT1); and MKK44 (C terminus of MinK linked to N terminus of KK40). In control experiments (no DNA, control DNA, or only MinK), no time-dependent K+ current was observed. Expression of KvLQT1 or KK40 produced currents that activate and inactivate in a voltage-dependent manner as reported by others for KvLQT1. In contrast, expression of MK24 and MKK44 elicited current with activation kinetics and voltage dependence very similar to native I sK and identical to currents expressed by cells co-transfected with independent MinK and KvLQT1 cDNA. Expression of MK24 plus additional MinK significantly slows current kinetics. Our data raise the possibility 1) of multiple MinK/KvLQT1 stoichiometries and 2) indicate that uniquely slow kinetics ofI sK channels is due to voltage-dependent conformational changes of the channel protein and not to assembly of channel subunits.
T Helper Lymphocyte and Mast Cell Immunohistochemical Pattern in Nonceliac Gluten Sensitivity

Background and Aims Nonceliac gluten sensitivity (NCGS) is a gluten-related emerging condition. Since few data about NCGS histopathology is available, we assessed the markers of lymphocyte and innate immunity activation. Materials and Methods We retrieved duodenal biopsy samples of patients with NCGS diagnosis according to the Salerno criteria. We selected specimens of positive (seropositive celiac disease/Marsh 1-2 stage) and negative (normal microscopic picture) controls. Immunohistochemistry for CD3 (intraepithelial lymphocytes-IELs), CD4 (T helper lymphocytes), CD8 (T cytotoxic lymphocytes), and CD1a/CD117 (Langerhans/mast cells) was performed. ANOVA plus Bonferroni's tests were used for statistical analysis. Results Twenty NCGS, 16 celiac disease, and 16 negative controls were selected. CD3 in NCGS were higher than negative controls and lower than celiac disease (18.5 ± 6.4, 11.9 ± 2.8, and 40.8 ± 8.1 IELs/100 enterocytes; p < 0.001). CD4 were lower in NCGS than controls and celiac disease (31.0 ± 22.1, 72.5 ± 29.5, and 103.7 ± 15.7 cells/mm2; p < 0.001). CD8 in NCGS were similar to negative controls, but lower than celiac disease (14.0 ± 7.4 and 34.0 ± 7.1 IELs/100 enterocytes, p < 0.001). CD117 were higher in NCGS than celiac disease and negative controls (145.8 ± 49.9, 121.3 ± 13.1, and 113.5 ± 23.4 cells/mm2; p = 0.009). Conclusions The combination of CD4 and CD117, as well as IEL characterization, may be useful to support a clinical diagnosis of NCGS.
Clinical exercise testing in the normal thoroughbred racehorse.

To evaluate normal cardiorespiratory and metabolic responses of Thoroughbred horses to a standardised treadmill exercise test, we examined 28 horses ranging in age from 1 to 4 years. The group consisted of eight yearlings, eight 2-year-olds and twelve 3 and 4-year-olds. All horses except the yearlings were in training, and either racing or ready to race, at the time of examination. None of the horses had histories of performance problems. On the first day the horses received a full physical examination, resting electrocardiogram, upper respiratory tract endoscopy and either one or two acclimatisation runs on the treadmill. The following day they were given an exercise test on a treadmill inclined at 6 degrees (+10% slope). The test consisted of 3 min at 4 m/sec, 90 sec at 6 m/sec and 60 sec intervals at 8, 10, 11, 12 and 13 m/sec. During the last 15 sec of each step, blood samples were collected for plasma lactate determination, expired respiratory gases were obtained using an open flow mask system for measurement of oxygen uptake, and heart rate was measured using telemetry electrocardiogram. From these measurements, various derived values were calculated, which have been used by others as indices of exercise capacity. These values included: V200 (speed at HR of 200 bpm), VHRmax (speed at which horses reached maximum HR), VO2-200 (oxygen uptake at a HR of 200 bpm), VO2max (maximum oxygen uptake), VLA4 (speed at which horses reached a plasma lactate of 4 mmol/l) and HRLA4 (HR at which horses reached a plasma lactate of 4 mmol/l). The yearlings had significantly lower values than the older age groups for most of the derived values. (ABSTRACT TRUNCATED AT 250 WORDS)
Toxoplasma and schizophrenia

Research on infectious agents as a possible cause of schizophrenia has become prominent in the past decade. Toxoplasma gondii has emerged as a prime candidate for a variety of reasons; (i) many studies have reported that individuals with schizophrenia, compared to controls, have a higher prevalence of antibodies to T. gondii, (ii) some individuals with adult toxoplasmosis develop psychotic symptoms similar to those of schizophrenia, (iii) epidemiologically, there are many similarities between toxoplasmosis and schizophrenia, (iv) antipsychotic drugs known to be effective in schizophrenia also inhibit some parasites, including T. gondii, (v) Toxoplasma has been shown to induce elevated levels of dopamine in experimentally infected animals (elevated dopamine is commonly seen in individuals with schizophrenia) and (vi) studies have shown that individuals with schizophrenia, compared to controls, have had greater exposure to cats in childhood. A number of questions remain concerning a role for Toxoplasma in the aetiology of schizophrenia, including the roles of strain variation, the timing and source of infection, and the role of host genes in determining disease susceptibility. The establishment of a firm association between Toxoplasma and the aetiology of schizophrenia and related disorders would represent a major breakthrough in the understanding of these disorders and would lead to novel methods for their treatment and prevention.
The ADHD and Sleep Conundrum: A Review

ABSTRACT. The relationship between attention-deficit hyperactivity disorder (ADHD) and sleep is a complex one that poses many challenges in clinical practice. Recent studies have helped to elucidate the nature of the brain mechanisms and neuromodulator systems underlying the theoretical associations among sleepiness, arousal, and attention. Studies of sleep disturbances in children with academic and behavioral problems have also underscored the role that primary sleep disorders such as obstructive sleep apnea hypopnea syndrome play in the clinical presentation of symptoms of inattention and behavioral dysregulation. In addition, new methodologies used in examining sleep and sleep patterns in children diagnosed with ADHD have shed further light on the prevalence, type, risk factors for, and impact of sleep disturbances in these children. The following discussion of the multilevel relationships among sleep quality and quantity, neurobehavioral functioning, and the clinical syndrome of ADHD expands on previous reviews of the literature and synthesizes what is currently known about the interaction of sleep and attention/arousal in children to propose possible underlying mechanisms, integrate more recent findings, and highlight important areas for future study. In addition, guidelines are provided for a clinical approach to evaluation and management of children with ADHD and sleep problems.
Disruption of CXC Motif Chemokine Ligand-14 in Mice Ameliorates Obesity-induced Insulin Resistance*

In obese individuals, white adipose tissue (WAT) is infiltrated by large numbers of macrophages, resulting in enhanced inflammatory responses that contribute to insulin resistance. Here we show that expression of the CXC motif chemokine ligand-14 (CXCL14), which targets tissue macrophages, is elevated in WAT of obese mice fed a high fat diet (HFD) compared with lean mice fed a regular diet. We found that HFD-fed CXCL14-deficient mice have impaired WAT macrophage mobilization and improved insulin responsiveness. Insulin-stimulated phosphorylation of Akt kinase in skeletal muscle was severely attenuated in HFD-fed CXCL14+/- mice but not in HFD-fed CXCL14-/- mice. The insulin-sensitive phenotype of CXCL14-/- mice after HFD feeding was prominent in female mice but not in male mice. HFD-fed CXCL14-/- mice were protected from hyperglycemia, hyperinsulinemia, and hypoadiponectinemia and did not exhibit increased levels of circulating retinol-binding protein-4 and increased expression of interleukin-6 in WAT. Transgenic overexpression of CXCL14 in skeletal muscle restored obesity-induced insulin resistance in CXCL14-/- mice. CXCL14 attenuated insulin-stimulated glucose uptake in cultured myocytes and to a lesser extent in cultured adipocytes. These results demonstrate that CXCL14 is a critical chemoattractant of WAT macrophages and a novel regulator of glucose metabolism that functions mainly in skeletal muscle.
The Effect of Reference Electrode Position in Cochlear Implants.

OBJECTIVE This study aims to evaluate the increase in power of cochlear implants (CI) as the reference electrode (RE) position changes. Patients in whom it is necessary to use the full power of the device to achieve the desired stimulation levels, this strategy will ensure that stimulation capability is maximized. MATERIALS AND METHODS The variability in RE placement in the temporal bone has a measurable effect on the electrical current, impedance, and power consumption, and if the electrode position has a functional effect on the stimulation intensity. The following three approaches were used: 1) classical circuit analysis, 2) 2-dimensional numerical simulations, and 3) real temporal bone measurements using a purpose-made CI. RESULTS The three approaches demonstrate a significant decrease in the current intensity and electrical resistance for distances that are closer to the intra-cochlear electrode. The results also demonstrate that to maintain a constant current, shorter distances require 33% less power. CONCLUSION Reference electrode position during surgery can make significant differences in CI power consumption and threshold intensity, which allows a more powerful stimulation in complicated patients (i.e., those with otosclerosis). This study presents an attractive perspective to surgeons, as it shows a way to decrease consumption that might result in a longer battery life or more power to be devoted to coding strategy performance.
[Gene therapy with tumor suppressor gene p53 and(or) p16 on the nude mice models of NSCLC in vivo].

OBJECTIVE To investigate the effect of tumor suppressor gene p53 and(or) p16 treatment on the nude mice models of non-small cell lung cancer (NSCLC). METHODS Nude mice were injected subcutaneously with NSCLC cell line A549. 25 nude mice were randomly divided into 5 groups (control, SA, p53 gene, p16 gene, p53 + p16 genes), p53 and(or) p16 genes mediated by stearylamine/DOPE (SA liposome) were injected intratumorally alone or jointly. The size of tumor and survival period of nude mice were measured after treatment. RESULTS p53 and(or) p16 genes can obviously inhibit the growth of tumor. The difference was significant between control and treated groups, among which the combined p53 and p16 genes enhance the inhibiting effect more markedly. The survival period of tumor-bearing nude mice was prolonged after transfecting p53 gene or p16 gene alone, p53 and p16 genes jointly can prolong the survival period significantly. CONCLUSIONS Tumor suppressor gene p53 and(or) p16 in the replacement therapy of NSCLC are of potential clinical significance. The combination of p53 and p16 gene may have a greater antitumoral effect in vivo.
Interaction of Common Azole Antifungals with P Glycoprotein

ABSTRACT Both eucaryotic and procaryotic cells are resistant to a large number of antibiotics because of the activities of export transporters. The most studied transporter in the mammalian ATP-binding cassette transporter superfamily, P glycoprotein (P-gp), ejects many structurally unrelated amphiphilic and lipophilic xenobiotics. Observed clinical interactions and some in vitro studies suggest that azole antifungals may interact with P-gp. Such an interaction could both affect the disposition and exposure to azole antifungal therapeutics and partially explain the clinical drug interactions observed with some antifungals. Using a whole-cell assay in which the retention of a marker substrate is evaluated and quantified, we studied the abilities of the most widely prescribed orally administered azole antifungals to inhibit the function of this transporter. In a cell line presenting an overexpressed amount of the human P-gp transporter, itraconazole and ketoconazole inhibited P-gp function with 50% inhibitory concentrations (IC50s) of ∼2 and ∼6 μM, respectively. Cyclosporin A was inhibitory with an IC50 of 1.4 μM in this system. Uniquely, fluconazole had no effect in this assay, a result consistent with known clinical interactions. The effects of these azole antifungals on ATP consumption by P-gp (representing transport activity) were also assessed, and the Km values were congruent with the IC50s. Therefore, exposure of tissue to the azole antifungals may be modulated by human P-gp, and the clinical interactions of azole antifungals with other drugs may be due, in part, to inhibition of P-gp transport.
Role of norepinephrine in hepatic gluconeogenesis: evidence of aging and training effects.

This study examined the relationship among the sympathetic neurotransmitter norepinephrine (NE), hepatic gluconeogenesis, and glyconeogenesis in 63 (30 trained and 33 untrained) young (7 mo), middle-aged (15 mo), and old (25 mo) male Fischer 344 rats. Animals were trained 1 h/day, 5 days/wk for 10 wk at treadmill speeds of 75% of age-specific maximal capacity. Liver sections, removed at rest, were sliced and incubated in [14C]lactic acid and 0, 0.5, 1.0, 3.0, or 6.0 ng/ml NE. The rate of [14C]lactate incorporation into glucose was significantly greater in young compared with old animals in both training groups and at all NE concentrations. All trained animals had greater rates of glucose production from lactate than their untrained counterparts at 0.5, 1.0, 3.0, and 6.0 ng/ml NE. At each NE concentration, the old rats showed the lowest rates of glycogen synthesis from lactate. The untrained rats in all age groups were the least responsive to increases in NE concentration. Total hepatic glycogen synthase activity exhibited age-related declines as the young and middle-aged had significantly greater total activity compared with the old animals: 620.4 +/- 27.5, 590.0 +/- 37.9, and 436.3 +/- 44.5 disintegrations/min, respectively. No differences with training were found in total activity. The percent of glycogen synthase in the active form was significantly greater in young compared with old in both the trained (48.6 +/- 2.0 vs. 40.0 +/- 1.3% active) and untrained animals (44.7 +/- 2.2 vs. 35.4 +/- 1.5% active). (ABSTRACT TRUNCATED AT 250 WORDS)