Gotowa bibliografia na temat „940.1/8”

This study considered the Sabah traditional bamboo musical instrument, sompoton. The fast Fourier transform (FFT) of sompoton was determined via a Pico oscilloscope. All three sompotons displayed almost similar fundamental frequencies. The individual tubes 1, 2, 3, 4, 5, 6, and 8 (except tube 7) of sompoton I, II, and III produced the fundamental frequency (in hertz) as 924, 758, 655, 589, 449, 407, 537, as 954, 779, 655, 614, 469, 387, 552, and as 944, 820, 655, 635, 407, 407, and 552, respectively. The averaged frequency obtained from the three sompotons (with the diatonic frequency and note in bracket) was 940.6 (932.3-A5# tube 1), 785.6 (783.9-G5 tube 2), 655 (659.2-E5 tube 3), 612.6 (622.2-D5# tube 4), 547 (554.3-C5# tube 8), 441.6 (440-A4 tube 5), and 400.3 (392-G4 tube 6). The tunings were remarkably similar in the tonal relationships. The pitch of the drone tube (tube 6) repeated an octave higher at tube 2, the intervals of perfect 4th higher at tube 8, and the intervals of perfect 5th higher at tube 4 were always found. The standard deviations of the fundamental pitch from the three sompotons for tube 1, 2, 3, 4, 5, 6, and 8 were 15.3, 31.5, 0.0, 9.2, 31.6, 11.5, and 8.7, respectively.

Background:Semaphorin 4D (SEMA4D) / CD100, known as a subfamily of axonal guidance proteins, has also been reported to act as an immunoregulator in several infectious and inflammatory diseases [1]. Sjögren’s syndrome (SS) is a systemic autoimmune disease that primarily affects the exocrine glands by infiltrated lymphocytes resulting in dryness of mouth and eyes. IL-17 was reported to impair the integrity of tight junction barrier and attenuate the expression of aquaporin 5 (AQP5), causing salivary gland dysfunction in SS [2].Objectives:This study was aimed to evaluate the role of SEMA4D in patients with SS and investigate the effect of SEMA4D on human salivary gland epithelial cell (SGEC) and T cell.Methods:Soluble SEMA4D levels in plasma were measured by enzyme-linked immunosorbent assay (ELISA) from patients with SS, non-SS sicca and healthy controls. Immortalized human SGECs, originated from acini (NS-SV-AC) and duct (NS-SV-DC), were used to evaluate the effects of SEMA4D. CD4+T cells from human peripheral blood were isolated to determine the secretion of cytokines in response to SEMA4D. IFN-γ and IL-17 were used to determine the effects on AQP5 expression of SGEC.Results:The levels of soluble SEMA4D in plasma were increased in patients with SS (median [interquartile range]: 1221.3 [393.5] pg/mL) compared to non-SS sicca (940.2 [355.1] pg/mL,p= 0.006) or healthy controls (909.5 [108.0] pg/mL,p <0.0001). The levels of soluble SEMA4D in plasma were correlated with the levels of several autoantibodies including anti-SSA (Spearman’s rho = 0.358,p= 0.006), anti-SSB (rho = 0.350,p= 0.007), and anti-muscarinic receptor 3 (M3R) Ab (rho = 0.495,p< 0.001), and also correlated with total IgG (rho = 0.431,p= 0.002). SEMA4D-stimulated SGECs showed decreased expression of tight junctions such as occludin and Zo-1. CD4+T cells secreted IFN-γ (p= 0.025), IL-17 (p= 0.028), and IL-21 (p= 0.007) with SEMA4D stimulation. IFN-γ and IL-17 decreased AQP5 expression in SGECs.Conclusion:SEMA4D contributed to decreased expression of tight junction in SGECs. SEMA4D induced production of IFN-γ and IL-17 in CD4+T cells and these cytokine decreased AQP5 expression in SGECs.References:[1]Worzfeld T, Offermanns S. Nat Rev Drug Discov. 2014;13(8):603-21.[2]Bhattarai KR, Junjappa R, Handigund M, Kim HR, Chae HJ. Autoimmun Rev. 2018;17(4):376-90.Disclosure of Interests:None declared

Abstract Exposure to particulate matter (PM) is an environmental determinant of chronic lung- and cardiovascular disease (CVD). Gene array expression analysis in rats exposed to PM showed a marked increase in tissue factor in the lung (Kooter et al, Inhal Toxicol.2005;17(1):53–65). We hypothesised that pro-inflammatory effects of PM would affect the cardiovascular system, in part through a prothrombotic action. To functionally characterize such effects we determined tissue factor (TF) activity and effects on thrombin generation in tissues from animals challenged with PM. Spontaneous hypertensive rats (SHR) rats were exposed via intratracheal instillation to different concentrations of PM collected from a highway tunnel (road tunnel dust: 0.3–1–3–10 mg PM/kg bodyweight (BW)) for 4 and 48 hours. For comparison we also tested organ- homogenates of mice that received 2 mg/kg endotoxin i.p. for 6 hours, as a well characterized inflammation driven prothrombotic animal model. Tissue factor activities show an increase with increasing concentrations of road tunnel dust. For 10mg/kg BW there is a significant difference both after 4 and 48 hours of exposure compared to controls (1044.5 ± 471.6, 1020.8 ± 61.6 vs. 397 ± 231.1 pM, p<0.02 ). For comparison, tissue factor activity in lungs of endotoxemic mice (25.8 ± 5.28 pM) was significantly higher than in lungs of control mice (12.7 ± 1.73 pM, p<0.05), whereas the activity in other organs (brain, heart, spleen, liver, kidney) was comparable between both groups. TF in the lung is known to increase under inflammatory conditions. We adapted the Calibrated Automated Thrombogram (CAT) that measures the thrombin generating potential in human platelet poor plasma (PPP) so that we were able to add tissue homogenates and measure the effect on thrombin generation. There is an 8-fold reduction in the endogenous thrombin potential (ETP) upon addition of lung homogenate from untreated rats and mice compared to the ETP of pooled PPP from 80 healthy volunteers (174.5 ± 61 vs. 1436.6 ± 112 nM min). We established that this inhibition is primarily due to the presence of thrombomodulin in the lungs, becausethe inhibitory effect was absent in protein C deficient human plasma andlungs from TM pro/pro mice that have a 100-fold reduction in thrombomodulin cofactor activity show a complete recovery of the ETP (1685.5 ± 208.8 nM min). With increasing concentrations of road tunnel dust the ETP increases with significant differences at 10mg/kg BW after 4 hours (389.5 ± 147.7 vs. 174.5 ± 61 for saline, p<0.05). After 48 hours the ETP augments further for the highest concentrations (1440.7 ± 288.8 nM min vs. saline: 163.9 ± 64 nM min, p<0.0001). This indicates a concentration- and time dependent reduction in thrombomodulin activity after PM exposure. Endotoxin challenge caused an increase in ETP (940.8 ± 523.1 vs. 194.3 ± 158.7nM min) for lung homogenates, whereas no changes were observed for brain (1794.8 ± 49.6 vs. 1801.8 ± 42.8 nM min) and heart (784.6±90 vs. 873.8 ± 74.3 nM min) compared to control tissues. The combination of these measurements indicates that the procoagulant state in the lungs after exposure to PM is related to inflammation and can be (partially) explained by the ratio of tissue factor and thrombomodulin activities in these organs.

T‐type voltage gated Ca2+ channels (VGCC) have been hypothesized to control spontaneous transient outward currents (STOCs) through large‐conductance Ca2+‐activated K+ channels (BKCa) and contribute to the negative‐feedback regulation of myogenic tone. We tested this hypothesis in superior epigastric arteries (SEAs) isolated from male C57BL‐6 mice. SEAs were isolated and enzymatically dissociated to obtain single smooth muscle cells for whole‐cell recording of paxilline‐sensitive (PAX, 1 μM) STOCs at −30 mV, or cannulated and studied by pressure myography (80 cm H2O, 37°C). The T‐type blocker Ni2+ (30 μM) had no effect on STOC amplitude (20.1±1.7 pA vs. 20.6±1.7 pA; n = 12, p > 0.05), but increased STOC frequency (0.79±0.15 Hz vs. 1.21±0.22 Hz; n = 12, p < 0.05). While Ni2+ produced concentration‐dependent constriction of isolated, pressurized SEAs (logEC50 = −5.6±0.1; Emax = 40±3% constriction), block of BKCa with PAX had no effect on vasoconstriction induced by 30 μM Ni2+ (before PAX = 44±11% constriction vs. in the presence of 1μM PAX = 47±11% constriction; n = 6, p > 0.05). In contrast to Ni2+, the non‐selective T‐type blocker, mibefradil, produced vasodilation (logEC50‐ = −6.9±0.2; Emax = 74±8% dilation), whereas the putative T‐type blocker, ML218, had no significant effect on myogenic tone between 10nM and 10μM (n=6–7, p > 0.05). Our data do not support a role for T‐type VGCC in the negative‐feedback regulation of myogenic tone and suggest that Ni2+ may constrict murine SEAs by means other than block of T‐type VGCC.Support or Funding InformationSupported by PO1‐HL070687 and ASPET‐SURF to B. Mullan

AbstractGasoline vapour emission is hazardous to both human health and the ecosystem and also results in capital loss, altogether revealing the necessity of its recovery. Some ZIF‐8–Pebax flat nanocomposite membranes were fabricated by the method of solution casting and used for gasoline vapour recovery as represented by n‐hexane vapour/nitrogen separation. Microporous ZIF‐8 nanoparticles were synthesized and characterized by Fourier transform infrared (FTIR) and Brunauer–Emmett–Teller (BET) analysis. BET results revealed specific surface area, total volume, and average pore diameter of 940.8 m2 · g−1, 0.36 cm3 · g−1, and 1.54 nm, respectively. Pure nitrogen and n‐hexane vapour/nitrogen gas mixture permeabilities were measured through the membranes. There was a decline in both permeation rate and selectivity up to 5.0 wt.% of ZIF‐8 loading and the next increment at their higher loadings to considerably more values that the pristine membrane. The maximum n‐hexane vapour permeability and selectivity at 10.0 wt.% loading of ZIF‐8 nanoparticles, the feed flow rate of 173 mL · min−1, and permeate side pressure of −200 mbar were observed as 280.1 Barrer and 106.7, respectively, revealing 60.0% and 36.9% improvements compared with those of the pristine Pebax membrane. Observed 86%–92% n‐hexane vapour recovery approves the successful application of the ZIF‐8–Pebax nanocomposite membranes for n‐hexane/nitrogen separation. The long‐term separation performance of 5.0 wt.% ZIF‐8 loaded nanocomposite membrane was improved by 76.5% compared with that of the pristine Pebax membrane.

Abstract Objective To investigate the clinical features of multicentric reticulohistiocytosis (MRH). Methods The clinical manifestations, laboratory examination results and histologic characteristics of eleven patients with MRH were collected and compared with those of 33 patients with rheumatoid arthritis. Results In total, 72.7% of the MRH patients were women. The median age was 46 years (range 33–84 years). Diagnosed by specific pathologic features, all MRH patients exhibited cutaneous involvement. The dorsa of the hands, arms, face and auricle were the most commonly affected areas. Nodules were also located on the legs, scalp, trunk, neck, and even the hypoglossis and buccal mucosa. Ten MRH patients (90.9%) had symmetric polyarthritis. Compared with rheumatoid arthritis (RA) patients, MRH patients were more likely to have distal interphalangeal joint (DIP) involvement (63.6% vs 24.2%, P = 0.017) and less likely to have elbow (36.4% vs 72.7%, P = 0.003), ankle (45.5% vs 93.9%, P < 0.001) and metacarpophalangeal joint (MCP) (36.4% vs 78.8%, P = 0.009) involvement. Positivity for rheumatoid factor (RF) (36.4% vs 84.6%, P = 0.001) and anti-CCP antibody (9.1% vs 81.8%, P = 0.000), as well as the median RF titer [43.8 (31.7–61.0) vs 175.4 (21.3–940.3), P = 0.021], in MRH patients was lower than in RA patients. Elevation of the erythrocyte sedimentation rate (ESR) was also less common in MRH patients than in RA patients (36.4% vs 72.7%, P = 0.030). After treatment with median- to large-dose corticosteroids and disease-modifying antirheumatic drugs, 8 patients achieved complete remission and 2 patients partial remission (skin lesions ameliorated, joint lesions not ameliorated). Conclusion Always pathologically diagnosed, MRH is a systemic disease involving RA-like erosive polyarthritis and a specific distribution of skin nodules characterized by "coral beads". More DIP involvement and less elbow, ankle and MCP involvement are seen in MRH than in RA. In addition, less positivity and lower-titer RF, uncommon presence of anti-CCP antibodies and ESR elevation may be helpful to distinguish MRH from RA.