A study on the co- and adjacent channel protection requirements for mobile satellite ACSSB modulation

Samples of speech modulated by narrowband frequency modulation (NBFM) (cellular) and amplitude companded single sideband (ACSSB) radios were subjected to simulated co- and adjacent channel interference environments typical of proposed frequency division multiple access (FDMA) mobile satellite systems. These samples were then listened to by a group of evaluators whose subjective responses to the samples were used to produce a series of graphs showing the relationship between subjective acceptability, carrier to noise density (C/No), carrier to interference ratio (C/I), and frequency offset. The results show that in a mobile satellite environment, ACSSB deteriorates more slowly than NBFM. The co- and adjacent channel protection ratios for both modulation techniques were roughly the same, even though the mechanism for signal deterioration is different

Recent technical advances in general purpose mobile Satcom aviation terminals

A second general aviation amplitude companded single sideband (ACSSB) aeronautical terminal was developed for use with the Ontario Air Ambulance Service (OAAS). This terminal is designed to have automatic call set up and take down and to interface with the Public Service Telephone Network (PSTN) through a ground earth station hub controller. The terminal has integrated RF and microprocessor hardware which allows such functions as beam steering and automatic frequency control to be software controlled. The terminal uses a conformal patch array system to provide almost full azimuthal coverage. Antenna beam steering is executed without relying on aircraft supplied orientation information

Correlation of bone density of individual jaw sections according to Hounsfield with the length of the adentiary section in the cone-beam computer tomography program

Aim. To study the existence of a relationship between the density of bone tissue and the length of the edentulous part of the tooth row. Materials and methods. Evaluation of the density of the spongy substance of the jaws by the maximum and average value of HU. The density of cancellous bone was evaluated only in the areas available for implant placement. The groups consisted of the localization and extent of the dentition defect. Statistical methods included the estimation of the arithmetic mean (M), standard deviation (σ), error of the mean (m), confidence interval (95 % CI), estimation of the median (Me) and interquartile range ([Q1; Q2]), Student’s test (t criterion). Results. Maximum and average indicators of cancellous bone density in defects of the upper (562.4 [347.1; 777.8] and 301.5 [163.0; 439.9], respectively (р = 0.84) and lower (1379.0 [1116.2; 1641.9] HU and 848.6 [630.6; 1066.6] HU, respectively, p = 0.96) jaws in the areas of molars and premolars with “large” defects are significantly different from the indicators “small” defects (299.7 [176.9; 422.4] and 642.6 [470.4; 814.9], 1061.1 [866.5; 1255.7] and 608.3 [440.5; 776.1, respectively). The average bone density of the alveolar process of the upper jaw is almost the same in defects of different lengths. The average density of the cancellous bone of the alveolar part of the lower jaw in “large” defects has significant differences from “average” ones (p = 0.02) and “small” (p = 0.005) defects. Conclusions. The average density of cancellous bone of the alveolar part of the lower jaw in “large” defects has significant differences from “medium” (p = 0.02) and “small” (p = 0.005) defects, and regardless of the extent of the dentition defect corresponds to class D3 (350–850 HU) according to the Misch classification. The average density of cancellous bone of the alveolar process of the upper jaw in the areas of molars and premolars does not have significant differences depending on the extent of the dentition defect and corresponds to class D4 (150–350 HU) according to the Misch classification. Since one class includes a large range of values, the clinical classification of Misch does not allow taking into account individual bone density indicators that have statistically significant differences in different areas of the dentition

Oxidative stress is associated with suspected non-alcoholic fatty liver disease and all-cause mortality in the general population

Background & Aims: Non-alcoholic fatty liver disease (NAFLD) is characterized by excessive lipid accumulation, inflammation and an imbalanced redox homeostasis. We hypothesized that systemic free thiol levels, as a proxy of systemic oxidative stress, are associated with NAFLD. Methods: Protein-adjusted serum free thiol concentrations were determined in participants from the Prevention of Renal and Vascular End-Stage Disease (PREVEND) cohort study (n = 5562). Suspected NAFLD was defined by the Fatty Liver Index (FLI ≥ 60) and Hepatic Steatosis Index (HSI > 36). Results: Protein-adjusted serum free thiols were significantly reduced in subjects with FLI ≥ 60 (n = 1651). In multivariable logistic regression analyses, protein-adjusted serum free thiols were associated with NAFLD (FLI ≥ 60) (OR per doubling of concentration: 0.78 [95% CI 0.64-0.96], P =.016) even when adjusted for potential confounding factors, including systolic blood pressure, diabetes, current smoking, use of alcohol and total cholesterol (OR 0.80 [95% CI 0.65-0.99], P =.04). This association lost its significance (OR 0.94 [95% CI 0.73-1.21], P =.65) after additional adjustment for high-sensitive C-reactive protein. Stratified analyses showed significantly differential associations of protein-adjusted serum free thiol concentrations with suspected NAFLD for gender (P <.02), hypertension (P <.001) and hypercholesterolemia (P <.003). Longitudinally, protein-adjusted serum free thiols were significantly associated with the risk of all-cause mortality in subjects with NAFLD (FLI ≥ 60) (HR 0.27 [95% CI 0.17-0.45], P <.001). Conclusion: Protein-adjusted serum free thiol levels are reduced and significantly associated with all-cause mortality in subjects with suspected NAFLD. Quantification of free thiols may be a promising, minimally invasive strategy to improve detection of NAFLD and associated risk of all-cause mortality in the general population

Collagen release by human hepatic stellate cells requires vitamin C and is efficiently blocked by hydroxylase inhibition

Liver fibrosis is characterized by the accumulation of extracellular matrix proteins, mainly composed of collagen. Hepatic stellate cells (HSCs) mediate liver fibrosis by secreting collagen. Vitamin C (ascorbic acid) is a cofactor of prolyl-hydroxylases that modify newly synthesized collagen on the route for secretion. Unlike most animals, humans cannot synthesize ascorbic acid and its role in liver fibrosis remains unclear. Here, we determined the effect of ascorbic acid and prolyl-hydroxylase inhibition on collagen production and secretion by human HSCs. Primary human HSCs (p-hHSCs) and the human HSCscell line LX-2 were treated with ascorbic acid, transforming growth factor-beta (TGFβ) and/or the pan-hydroxylase inhibitor dimethyloxalylglycine (DMOG). Expression of collagen-I was analyzed by RT-qPCR (COL1A1), Western blotting, and immunofluorescence microscopy. Collagen secretion was determined in the medium by Western blotting for collagen-I and by HPLC for hydroxyproline concentrations. Expression of solute carrier family 23 members 1 and 2 (SLC23A1/SLC23A2), encoding sodium-dependent vitamin C transporters 1 and 2 (SVCT1/SVCT2) was quantified in healthy and cirrhotic human tissue. In the absence of ascorbic acid, collagen-I accumulated intracellularly in p-hHSCs and LX-2 cells, which was potentiated by TGFβ. Ascorbic acid co-treatment strongly promoted collagen-I excretion and enhanced extracellular hydroxyproline concentrations, without affecting collagen-I (COL1A1) mRNA levels. DMOG inhibited collagen-I release even in the presence of ascorbic acid and suppressed COL1A1 and alpha-smooth muscle actin (αSMA/ACTA2) mRNA levels, also under hypoxic conditions. Hepatocytes express both ascorbic acid transporters, while p-hHSCs and LX-2 express the only SVCT2, which is selectively enhanced in cirrhotic livers. Human HSCs rely on ascorbic acid for the efficient secretion of collagen-I, which can be effectively blocked by hydroxylase antagonists, revealing new therapeutic targets to treat liver fibrosis

Sediment-laden sea ice in southern Hudson Bay: Entrainment, transport, and biogeochemical implications

During a research expedition in Hudson Bay in June 2018, vast areas of thick (>10 m), deformed sediment-laden sea ice were encountered unexpectedly in southern Hudson Bay and presented difficult navigation conditions for the Canadian Coast Guard Ship Amundsen. An aerial survey of one of these floes revealed a maximum ridge height of 4.6 m and an average freeboard of 2.2 m, which corresponds to an estimated total thickness of 18 m, far greater than expected within a seasonal ice cover. Samples of the upper portion of the ice floe revealed that it was isothermal and fresh in areas with sediment present on the surface. Fine-grained sediment and larger rocks were visible on the ice surface, while a pronounced sediment band was observed in an ice core. Initial speculation was that this ice had formed in the highly dynamic Nelson River estuary from freshwater, but δ^{18}O isotopic analysis revealed a marine origin. In southern Hudson Bay, significant tidal forcing promotes both sediment resuspension and new ice formation within a flaw lead, which we speculate promotes the formation of this sediment-laden sea ice. Historic satellite imagery shows that sediment-laden sea ice is typical of southern Hudson Bay, varying in areal extent from 47 to 118 km2 during June. Based on an average sediment particle concentration of 0.1 mg mL^{–1} in sea ice, an areal extent of 51,924 km2 in June 2018, and an estimated regional end-of-winter ice thickness of 1.5 m, we conservatively estimated that a total sediment load of 7.8 × 106 t, or 150 t km^{–2}, was entrained within sea ice in southern Hudson Bay during winter 2018. As sediments can alter carbon concentrations and light transmission within sea ice, these first observations of this ice type in Hudson Bay imply biogeochemical impacts for the marine system

Anti-tumor activity against multiple myeloma by combination of KW-2478, an Hsp90 inhibitor, with bortezomib

Heat shock protein 90 (Hsp90) is a promising target for anti-tumor therapy. We previously reported the anti-tumor activity of a novel Hsp90 inhibitor, KW-2478, in multiple myeloma (MM) as a single agent. In this study, we examined the combinational effect of KW-2478 and bortezomib, a proteasome inhibitor, in vitro and in vivo. In vitro, KW-2478 enhanced bortezomib-induced cell growth inhibition, both in MM cell lines and primary patient MM cells. The combination of KW-2478 and bortezomib also induced caspase activation in MM cell lines. Interestingly, the combination synergistically enhanced the expression of Hsp70B, a homolog of Hsp70, in human MM cells and peripheral blood mononuclear cells, indicating Hsp70B could be a surrogate biomarker for the combination of Hsp90 and proteasome inhibitors. In vivo, the combination of KW-2478 with bortezomib showed synergistic anti-tumor activity without significant body weight loss in a subcutaneously inoculated human myeloma model. Furthermore, the combination also showed synergistic reduction of tumor burden in bone marrow in an orthotopic myeloma model. Our results strongly suggest that combination of KW-2478 with bortezomib could exhibit enhanced anti-tumor activity against human myeloma

Structural Basis for GTP-Dependent Dimerization of Hydrogenase Maturation Factor HypB

Maturation of [NiFe]-hydrogenase requires the insertion of iron, cyanide and carbon monoxide, followed by nickel, to the catalytic core of the enzyme. Hydrogenase maturation factor HypB is a metal-binding GTPase that is essential for the nickel delivery to the hydrogenase. Here we report the crystal structure of Archeoglobus fulgidus HypB (AfHypB) in apo-form. We showed that AfHypB recognizes guanine nucleotide using Asp-194 on the G5 loop despite having a non-canonical NKxA G4-motif. Structural comparison with the GTPγS-bound Methanocaldococcus jannaschii HypB identifies conformational changes in the switch I region, which bring an invariant Asp-72 to form an intermolecular salt-bridge with another invariant residue Lys-148 upon GTP binding. Substitution of K148A abolished GTP-dependent dimerization of AfHypB, but had no significant effect on the guanine nucleotide binding and on the intrinsic GTPase activity. In vivo complementation study in Escherichia coli showed that the invariant lysine residue is required for in vivo maturation of hydrogenase. Taken together, our results suggest that GTP-dependent dimerization of HypB is essential for hydrogenase maturation. It is likely that a nickel ion is loaded to an extra metal binding site at the dimeric interface of GTP-bound HypB and transferred to the hydrogenase upon GTP hydrolysis