Heat transfer coefficients for liquid hydrogen turbopumps

Empirical equations were derived to establish the appropriate heat transfer coefficients as functions of the temperature drops and heat transfer rates for a wide range of convective and boiling conditions at different locations in a liquid hydrogen turbopump

Noise reduction in gravitational wave interferometers using feedback

We show that the quantum locking scheme recently proposed by Courty {\it et al.} [Phys. Rev. Lett. {\bf 90}, 083601 (2003)] for the reduction of back action noise is able to significantly improve the sensitivity of the next generation of gravitational wave interferometers.Comment: 12 pages, 2 figures, in print in the Special Issue of J. Opt. B on Fluctuations and Noise in Photonics and Quantum Optic

Investigating the Contribution of Mature Collagen Crosslinks to Cooked Meat Toughness Using a Stewed Beef Shank Model

Objective: The objective of this study was to investigate mature collagen crosslink densities and their relationship to connective tissue texture using a stewed beef shank model. Study Description: Connective tissue texture, Warner-Bratzler shear force, and collagen content and characteristics were measured for six different beef shank cuts from eight U.S. Department of Agriculture Low Choice beef carcasses (n = 48). Results: Deep digital flexor from the foreshank had the toughest connective tissue texture, greatest Warner-Bratzler shear force value, most cooked collagen content, one of the greatest insoluble collagen percentages, as well as greatest raw and cooked pyridinoline densities among all the beef shank cuts (P \u3c 0.05). Correlation analysis showed that cooked collagen content, percent insoluble collagen, as well as raw pyridinoline densities had positive correlations with connective tissue texture (r = 0.550, 0.498, and 0.560, respectively; P \u3c 0.01) and Warner-Bratzler shear force (r = 0.615, 0.392 and 0.730, respectively; P \u3c 0.05). The Bottom Line: Pyridinoline is a heat stable collagen crosslink that is difficult to degrade even with extensive heat treatment. As a result, raw pyridinoline density is a good indicator for heat insoluble collagen content, cooked beef connective tissue texture, and ultimately, tenderness in beef cuts with high concentration of connective tissue prepared with moist heat cookery

A Preliminary Investigation of the Contribution of Different Tenderness Factors to Beef Loin, Tri-tip, and Heel Tenderness

Objective: The objective is to better understand the contribution of each tenderness factor to the perception of tenderness of three specific beef muscles with similar tenderness ratings. Study Description: Longissimus lumborum (loin), tensor fascia latae (tri-tip), and gastrocnemius (heel) were collected from 10 U.S. Department of Agriculture low Choice beef carcasses and assigned to a 5- or 21-day aging period (n = 60). Steaks from each aging period from each subprimal were assigned to one of three assays: 1) trained sensory analysis; 2) objective tenderness evaluation (Warner-Bratzler shear force); or 3) physiochemical analysis (sarcomere length, proteolysis, intramuscular fat content, collagen crosslink, and content). Results: Sarcomere length, troponin-T degradation, collagen content, mature collagen crosslink density, intramuscular lipid content, and trained panel analysis were measured. Correlation analysis indicated each muscle has a specific tenderness factor that contributed to the overall tenderness evaluated by trained panelists. The equations indicated Longissimus lumborum tenderness was driven by lipid content (P \u3c 0.05) and that Tensor fascia latae tenderness was driven by collagen content (P \u3c 0.05). Gastrocnemius tenderness was driven by proteolysis (P \u3c 0.01), and only collagen content can be casually used as an overall tenderness predictor for all three cuts. The Bottom Line: Each muscle showed a unique tenderness factor profile. Loin is inherently tender, and tri-tip has the makings for a tender cut as seen by our biochemical analysis, yet panelists rated tri-tip to have similar overall tenderness as heel, an inherently tough muscle

An Investigation on the Influence of Various Biochemical Tenderness Factors on Eight Different Bovine Muscles

Objective: Beef tenderness is a complex palatability trait with many tenderness-contributing components. The objective of this study is to understand the relative contribution of each tenderness component to eight different beef muscles. Study Description: Top sirloin butt, ribeye, brisket, flank, knuckle, eye of round, mock tender, and shoulder clod were collected from 10 U.S. Department of Agriculture high choice beef carcasses and assigned to a 2- or 21-day aging period (n = 160). Protein degradation, collagen content, mature collagen crosslink density, intramuscular lipid content, pH, shear force, and trained sensory panel analysis were determined. A Pearson correlation analysis was used to determine the relationship between each tenderness contributor measured in this study to the overall tenderness evaluated by the trained panelist. Results: Overall tenderness of ribeye, flank, eye of round, and shoulder clod were largely driven by the protein degradation of muscle fibers (effect of aging). On the other hand, overall tenderness for brisket was determined by collagen content and crosslink density (effect from connective tissue). Finally, overall tenderness of top sirloin butt was strongly correlated with lipid content. When all the cuts were combined together and analyzed as a whole (n = 160), all of the biochemical measurements conducted in this study played a small but important role as an overall tenderness contributor. The Bottom Line: Results from this study filled in some of the knowledge gap on the relative contribution of each tenderness component to the overall perception of tenderness from each cut. The industry can utilize this information to provide tenderness management strategies for each cut as well as improve the robustness of current tenderness predicting technology

Differential Expression of CD163 on Monocyte Subsets in Healthy and HIV-1 Infected Individuals

CD163, a haptoglobin-hemoglobin (Hp-Hb) scavenger receptor, expressed by monocytes and macrophages, is important in resolution of inflammation. Age-related non-AIDS co-morbidities in HIV-infected individuals, particularly dementia and cardiovascular disease, result in part from effects of HIV-1 infection on monocyte and macrophage biology. CD163 co-expression on CD14+CD16++ monocytes has been proposed as a useful biomarker for HIV-1 disease progression and the presence of HIV associated dementia. Here we investigated CD163 expression on monocyte subsets ex vivo, on cultured macrophages, and soluble in plasma, in the setting of HIV-1 infection. Whole blood immunophenotyping revealed CD163 expression on CD14++CD16- monocytes but not on CD14+CD16++ monocytes (P = 0.004), supported by CD163 mRNA levels. Incubation with M-CSF induced CD163 protein expression on CD14+CD16++ monocytes to the same extent as CD14++CD16− monocytes. CD163 expression on CD14++CD16+ monocytes from HIV-infected subjects was significantly higher than from uninfected individuals, with a trend towards increased expression on CD14++CD16− monocytes (P = 0.019 and 0.069 respectively), which is accounted for by HIV-1 therapy including protease inhibitors. Shedding of CD163 was shown to predominantly occur from the CD14++CD16− subset after Ficoll isolation and LPS stimulation. Soluble CD163 concentration in plasma from HIV-1 infected donors was similar to HIV-1 uninfected donors. Monocyte CD163 expression in HIV-1 infected patients showed a complicated relationship with classical measures of disease progression. Our findings clarify technical issues regarding CD163 expression on monocyte subsets and further elucidates its role in HIV-associated inflammation by demonstrating that CD163 is readily lost from CD14++CD16− monocytes and induced in pro-inflammatory CD14+CD16++ monocytes by M-CSF. Our data show that all monocyte subsets are potentially capable of differentiating into CD163-expressing anti-inflammatory macrophages given appropriate stimuli. Levels of CD163 expression on monocytes may be a potential biomarker reflecting efforts by the immune system to resolve immune activation and inflammation in HIV-infected individuals

Differential Expression of CD163 on Monocyte Subsets in Healthy and HIV-1 Infected Individuals

CD163, a haptoglobin-hemoglobin (Hp-Hb) scavenger receptor, expressed by monocytes and macrophages, is important in resolution of inflammation. Age-related non-AIDS co-morbidities in HIV-infected individuals, particularly dementia and cardiovascular disease, result in part from effects of HIV-1 infection on monocyte and macrophage biology. CD163 co-expression on CD14+CD16++ monocytes has been proposed as a useful biomarker for HIV-1 disease progression and the presence of HIV associated dementia. Here we investigated CD163 expression on monocyte subsets ex vivo, on cultured macrophages, and soluble in plasma, in the setting of HIV-1 infection. Whole blood immunophenotyping revealed CD163 expression on CD14++CD16- monocytes but not on CD14+CD16++ monocytes (P = 0.004), supported by CD163 mRNA levels. Incubation with M-CSF induced CD163 protein expression on CD14+CD16++ monocytes to the same extent as CD14++CD16− monocytes. CD163 expression on CD14++CD16+ monocytes from HIV-infected subjects was significantly higher than from uninfected individuals, with a trend towards increased expression on CD14++CD16− monocytes (P = 0.019 and 0.069 respectively), which is accounted for by HIV-1 therapy including protease inhibitors. Shedding of CD163 was shown to predominantly occur from the CD14++CD16− subset after Ficoll isolation and LPS stimulation. Soluble CD163 concentration in plasma from HIV-1 infected donors was similar to HIV-1 uninfected donors. Monocyte CD163 expression in HIV-1 infected patients showed a complicated relationship with classical measures of disease progression. Our findings clarify technical issues regarding CD163 expression on monocyte subsets and further elucidates its role in HIV-associated inflammation by demonstrating that CD163 is readily lost from CD14++CD16− monocytes and induced in pro-inflammatory CD14+CD16++ monocytes by M-CSF. Our data show that all monocyte subsets are potentially capable of differentiating into CD163-expressing anti-inflammatory macrophages given appropriate stimuli. Levels of CD163 expression on monocytes may be a potential biomarker reflecting efforts by the immune system to resolve immune activation and inflammation in HIV-infected individuals

Ibudilast, a Pharmacologic Phosphodiesterase Inhibitor, Prevents Human Immunodeficiency Virus-1 Tat-Mediated Activation of Microglial Cells

Human Immunodeficiency Virus-1 (HIV-1)-associated neurocognitive disorders (HAND) occur, in part, due to the inflammatory response to viral proteins, such as the HIV-1 transactivator of transcription (Tat), in the central nervous system (CNS). Given the need for novel adjunctive therapies for HAND, we hypothesized that ibudilast would inhibit Tat-induced excess production of pro-inflammatory cytokines, such as tumor necrosis factor-alpha (TNFα) in microglial cells. Ibudilast is a non-selective cyclic AMP phosphodiesterase inhibitor that has recently shown promise as a treatment for neuropathic pain via its ability to attenuate glial cell activation. Accordingly, here we demonstrate that pre-treatment of both human and mouse microglial cells with increasing doses of ibudilast inhibited Tat-induced synthesis of TNFα by microglial cells in a manner dependent on serine/threonine protein phosphatase activity. Ibudilast had no effect on Tat-induced p38 MAP kinase activation, and blockade of adenosine A2A receptor activation did not reverse ibudilast's inhibition of Tat-induced TNFα production. Interestingly, ibudilast reduced Tat-mediated transcription of TNFα, via modulation of nuclear factor-kappa B (NF-κB) signaling, as shown by transcriptional activity of NF-κB and analysis of inhibitor of kappa B alpha (IκBα) stability. Together, our findings shed light on the mechanism of ibudilast's inhibition of Tat-induced TNFα production in microglial cells and may implicate ibudilast as a potential novel adjunctive therapy for the management of HAND

Nuclear Factor-Kappa B Family Member RelB Inhibits Human Immunodeficiency Virus-1 Tat-Induced Tumor Necrosis Factor-Alpha Production

Human Immunodeficiency Virus-1 (HIV-1)-associated neurocognitive disorder (HAND) is likely neuroinflammatory in origin, believed to be triggered by inflammatory and oxidative stress responses to cytokines and HIV protein gene products such as the HIV transactivator of transcription (Tat). Here we demonstrate increased messenger RNA for nuclear factor-kappa B (NF-κB) family member, transcription factor RelB, in the brain of doxycycline-induced Tat transgenic mice, and increased RelB synthesis in Tat-exposed microglial cells. Since genetic ablation of RelB in mice leads to multi-organ inflammation, we hypothesized that Tat-induced, newly synthesized RelB inhibits cytokine production by microglial cells, possibly through the formation of transcriptionally inactive RelB/RelA complexes. Indeed, tumor necrosis factor-alpha (TNFα) production in monocytes isolated from RelB deficient mice was significantly higher than in monocytes isolated from RelB expressing controls. Moreover, RelB overexpression in microglial cells inhibited Tat-induced TNFα synthesis in a manner that involved transcriptional repression of the TNFα promoter, and increased phosphorylation of RelA at serine 276, a prerequisite for increased RelB/RelA protein interactions. The Rel-homology-domain within RelB was necessary for this interaction. Overexpression of RelA itself, in turn, significantly increased TNFα promoter activity, an effect that was completely blocked by RelB overexpression. We conclude that RelB regulates TNFα cytokine synthesis by competitive interference binding with RelA, which leads to downregulation of TNFα production. Moreover, because Tat activates both RelB and TNFα in microglia, and because Tat induces inflammatory TNFα synthesis via NF-κB, we posit that RelB serves as a cryoprotective, anti-inflammatory, counter-regulatory mechanism for pathogenic NF-κB activation. These findings identify a novel regulatory pathway for controlling HIV-induced microglial activation and cytokine production that may have important therapeutic implications for the management of HAND