Journal articles: 'Alpha-enhanced'

1

Druliner, J. D., F. W. Hobbs, and W. C. Seide. "Concerning enhanced reactivities of .alpha.-keto hydroperoxides." Journal of Organic Chemistry 53, no. 3 (February 1988): 700–702. http://dx.doi.org/10.1021/jo00238a044.

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2

Addleman, R. S., M. J. O'Hara, J. W. Grate, and O. B. Egorov. "Chemically enhanced alpha-energy spectroscopy in liquids." Journal of Radioanalytical and Nuclear Chemistry 263, no. 2 (January 2005): 291–94. http://dx.doi.org/10.1007/s10967-005-0051-z.

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3

Oettinger, C. W., L. A. Bland, J. C. Oliver, M. J. Arduino, S. K. McAllister, and M. S. Favero. "The effect of uremia on tumor necrosis factor-alpha release after an in vitro whole-blood endotoxin challenge." Journal of the American Society of Nephrology 4, no. 11 (May 1994): 1890–95. http://dx.doi.org/10.1681/asn.v4111890.

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Uremia has been associated with immunologic aberrations, including anergy, increased susceptibility to infections, and reduced phagocytic activity of polymorphonuclear leukocytes. In this study, cytokine release in uremic and nonuremic blood after in vitro endotoxin stimulation was studied. Blood from nonuremic controls, chronic renal failure patients not on dialysis, and chronic hemodialysis patients predialysis and postdialysis was spiked with 10 ng/mL of Escherichia coli endotoxin and incubated for 2 and 26 h. Plasma tumor necrosis factor-alpha (TNF alpha) concentrations were determined by ELISA after each incubation period. To further study which uremic blood component may be responsible for enhanced release of TNF alpha, plasma and cellular components of chronic renal failure patients and controls were switched and then given an in vitro endotoxin stimulation (1 ng/mL). It was found that (1) TNF alpha release is enhanced by uremia and is exacerbated with progressive declines in renal function, (2) enhanced TNF alpha release is related to a blood cellular phenomenon induced by uremia, and (3) enhanced TNF alpha release in hemodialysis patients is associated with a prolonged stimulation and/or reduced plasma elimination of TNF alpha.

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4

Lajat, S., Z. Tanfin, G. Guillon, and S. Harbon. "Modulation of phospholipase C pathway and level of Gq alpha/G11 alpha in rat myometrium during gestation." American Journal of Physiology-Cell Physiology 271, no. 3 (September 1, 1996): C895—C904. http://dx.doi.org/10.1152/ajpcell.1996.271.3.c895.

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The regulation of the receptor-G protein-phospholipase C (PLC) cascade was investigated in rat myometrium at midgestation (day 12) and at term (day 21) comparatively to the estrogen-treated tissue (day 0). Carbachol-mediated generation of [3H]inositol phosphates was insensitive to pertussis toxin and was enhanced at days 12 and 21 two- and threefold, respectively, with no alteration of muscarinic sites (M3 subtype). A similar increase could be detected in the production of inositol 1,4,5-trisphosphate, indicating the stimulation of a PLC degrading phosphatidylinositol 4,5-bisphosphate. AlF4- also enhanced PLC activation during gestation, suggesting pregnancy-related regulations that bypass receptor activation. Immunoreactive G proteins, Gq alpha and G11 alpha, and PLC-beta 3 were detected in all myometrial preparations. The amount of PLC-beta 3 was similar in day 0 and day 21 myometrium, although decreasing by 75% at midgestation. Of significance was the increased amount of Gq alpha in day 12 and day 21 myometrium (3- and 2-fold, respectively) which coincided with the enhanced phosphoinositide breakdown. The upregulation of Gq alpha may contribute to the enhanced PLC activity during pregnancy and at term.

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5

White, R. E., and G. O. Carrier. "Enhanced vascular alpha-adrenergic neuroeffector system in diabetes: importance of calcium." American Journal of Physiology-Heart and Circulatory Physiology 255, no. 5 (November 1, 1988): H1036—H1042. http://dx.doi.org/10.1152/ajpheart.1988.255.5.h1036.

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Mesenteric arteries from streptozotocin (STZ)-diabetic rats developed greater contractile force in response to norepinephrine and related alpha-agonists than arteries from age-matched controls. Subsequent experiments attempted to define the mechanisms underlying these findings. Transmural nerve stimulation of mesenteric arteries from both groups of animals revealed a similar optimal frequency and voltage of stimulation; however, arteries from STZ-diabetic rats developed greater contractile force than controls. Second, determination of selective alpha-adrenergic antagonist affinities (pA2 values) revealed qualitatively similar postjunctional alpha 1-adrenoceptors in both groups of arteries. Third, disruption of the endothelium did not abolish the enhanced responsiveness of arteries from STZ-diabetic rats. In contrast, the increased vascular responsiveness in STZ-diabetes was associated with a greater dependency on extracellular calcium, with no change in the response to alpha-agonist-induced release of calcium from cellular stores. Thus the enhanced responsiveness of mesenteric arteries from STZ-diabetic rats to alpha-adrenergic agonists cannot be attributed to neuronal deterioration, altered postjunctional alpha-adrenoceptor subtypes, endothelium degeneration, or enhanced release of intracellular calcium but is associated with a greater dependency on extracellular calcium.

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6

John, R., R. Henley, and D. Shankland. "Evaluation of an enhanced luminescence assay for alpha-fetoprotein." Clinical Chemistry 32, no. 11 (November 1, 1986): 2066–69. http://dx.doi.org/10.1093/clinchem/32.11.2066.

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Abstract We evaluated a two-site enhanced luminescence immunoenzymometric assay (Amerlite; Amersham International) for alpha-fetoprotein (AFP) in maternal serum and amniotic fluid. The assay is rapid, involving two incubations totalling 4 h. The working range of the assay for serum AFP is 5.5 to 750 kilo-int. units/L (CV less than 10%), with a sensitivity of detection of 0.2 kilo-int. unit/L. The regression equation for the Amerlite assay (y) and our in-house RIA procedure (x) was y = 0.816x + 2.9 (n = 142, r = 0.96). Analytical recovery of added AFP (code 72/227) at three concentrations was 86.7%. Serum AFP concentrations were measured at 15 to 18 weeks of gestation in subjects with normal pregnancies and in subjects whose pregnancies resulted in open neural tube defects; all of the latter had serum AFP concentrations greater than 2.5 multiples of the median. We find the Amerlite system to be an efficient, reliable system for screening for open neural tube defects without use of hazardous radioactive labels.

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7

Shu, San-Ging. "Alpha-gamma equalization-enhanced hand radiographic image segmentation scheme." Optical Engineering 48, no. 10 (October 1, 2009): 107001. http://dx.doi.org/10.1117/1.3242852.

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8

Worley, Christopher G., Richard W. Linton, and Edward T. Samulski. "Electric-Field-Enhanced Self-Assembly of .alpha.-helical polypeptides." Langmuir 11, no. 10 (October 1995): 3805–10. http://dx.doi.org/10.1021/la00010a034.

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9

Dubois, Aurelie, Catherine François, Veronique Descamps, Carole Fournier, Czeslaw Wychowski, Jean Dubuisson, Sandrine Castelain, and Gilles Duverlie. "Enhanced anti-HCV activity of interferon alpha 17 subtype." Virology Journal 6, no. 1 (2009): 70. http://dx.doi.org/10.1186/1743-422x-6-70.

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10

Luo, Y., X. Chen, W. C. DeWolf, and M. A. OʼDonnell. "BCG EXPRESSING HUMAN INTERFERON-ALPHA 2B DEMONSTRATES ENHANCED IMMUNOGENICITY." Journla of Immunotherapy 22, no. 5 (September 1999): 463. http://dx.doi.org/10.1097/00002371-199909000-00046.

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11

Lamers, A. E., G. Flik, and S. E. Bonga. "A specific role for TRH in release of diacetyl alpha-MSH in tilapia stressed by acid water." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 267, no. 5 (November 1, 1994): R1302—R1308. http://dx.doi.org/10.1152/ajpregu.1994.267.5.r1302.

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After exposure of tilapia for 7 days to low-pH water, plasma thyrotropin-releasing hormone (TRH) levels were elevated, and the melanocyte-stimulating hormone (MSH) cells in the pituitary pars intermedia had increased in size and showed enhanced synthetic and secretory activity. The MSH cells became more sensitive to TRH but not to corticotropin-releasing hormone (CRH). Stimulation by TRH (but not by CRH) of the MSH cells of tilapia exposed to low pH specifically enhanced the release of diacetyl alpha-MSH, the most potent corticotropic form of alpha-MSH. Acute stress imposed by handling and confinement for 1 h elevated the plasma cortisol level but did not affect blood plasma alpha-MSH levels. We conclude that stimulation by TRH is pivotal for an enhanced release of diacetyl alpha-MSH during low-pH adaptation. These results are further evidence of a role for TRH and alpha-MSH in the activation of the hypothalamopituitary-interrenal axis during adaptation to low pH.

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12

Suda, T., R. Murray, C. Guidos, and A. Zlotnik. "Growth-promoting activity of IL-1 alpha, IL-6, and tumor necrosis factor-alpha in combination with IL-2, IL-4, or IL-7 on murine thymocytes. Differential effects on CD4/CD8 subsets and on CD3+/CD3- double-negative thymocytes." Journal of Immunology 144, no. 8 (April 15, 1990): 3039–45. http://dx.doi.org/10.4049/jimmunol.144.8.3039.

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Abstract Many cytokines (including IL-1, IL-2, IL-4, IL-6, and TNF-alpha) have been shown to induce thymocyte proliferation in the presence of PHA. In this report, we demonstrate that certain cytokine combinations induce thymocyte proliferation in the absence of artificial comitogens. IL-1 alpha, IL-6, and TNF-alpha enhanced the proliferation of whole unseparated thymocytes in the presence of IL-2, whereas none of them induced thymocyte proliferation alone. In contrast, of these three enhancing cytokines, only IL-6 enhanced IL-4-induced proliferation. We also separated thymocytes into four groups based on their expression of CD4 and CD8, and investigated their responses to various cytokines. The results indicate that each cytokine combination affects different thymocyte subsets; thus, IL-1 alpha enhanced the proliferation of CD4-CD8- double negative (DN) thymocytes more efficiently than IL-6 in the presence of IL-2, whereas IL-6 enhanced the responses of CD4+CD8- and CD4-CD8+ single positive (SP) thymocytes to IL-2 or IL-4 better than IL-1 alpha. TNF-alpha enhanced the proliferation of both DN and both SP subsets in the presence of IL-2 and/or IL-7. None of these combinations induced the proliferation of CD4+CD8+ double positive thymocytes. Finally, DN were separated into CD3+ and CD3- populations and their responsiveness was investigated, because recent reports strongly suggest that CD3+ DN thymocytes are a mature subset of different lineage rather than precursors of SP thymocytes. CD3+ DN proliferated in response to IL-7, TNF-alpha + IL-2, and IL-1 + IL-2. CD3- DN did not respond to IL-7 or to IL-1 + IL-2, but did respond to TNF-alpha + IL-2. Finally, we detected TNF-alpha production by a cloned line of thymic macrophages, as well as by DN adult thymocytes. These results suggest that cytokines alone are capable of potent growth stimuli for thymocytes, and indicate that different combinations of these molecules act selectively on thymocytes at different developmental stages.

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13

Sibley, L. D., L. B. Adams, Y. Fukutomi, and J. L. Krahenbuhl. "Tumor necrosis factor-alpha triggers antitoxoplasmal activity of IFN-gamma primed macrophages." Journal of Immunology 147, no. 7 (October 1, 1991): 2340–45. http://dx.doi.org/10.4049/jimmunol.147.7.2340.

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Abstract IFN-gamma is an important mediator of cellular resistance against microbial pathogens and tumor cells due in part to its potent capacity to activate macrophages for enhanced cytotoxicity. The present study demonstrates that TNF-alpha regulates the expression of enhanced antimicrobial activity by triggering IFN-gamma primed macrophages to kill or inhibit intracellular Toxoplasma gondii. Resident mouse macrophages stimulated with rIFN-gamma at levels up to 2500 U/ml failed to display enhanced antitoxoplasmal activity when cultured in vitro under low endotoxin conditions (less than 10 pg/ml), but were triggered by addition of small amounts of LPS (0.1 ng/ml). A similar requirement for LPS as a second signal necessary to trigger antitoxoplasmal activity was observed when IFN-gamma was administered to mice in vivo. The essential nature of this triggering step allowed us to explore the role of cytokines that act as endogenous regulators of macrophage activation. rTNF-alpha, although unable to confer antitoxoplasmal activity when used alone to treat macrophages, was capable of triggering IFN-gamma-primed macrophages cultured under low endotoxin conditions. The ability of TNF-alpha to trigger IFN-gamma-primed macrophages was blocked by rabbit anti-TNF-alpha polyclonal antisera but was not affected by polymyxin B indicating that TNF-alpha triggering was not due to contamination with LPS. Collectively, these findings demonstrate that TNF-alpha performs an important regulatory role in the expression of enhanced anti-microbial activity by IFN-gamma-primed macrophages.

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14

Hyman, A. L., and P. J. Kadowitz. "Enhancement of alpha- and beta-adrenoceptor responses by elevations in vascular tone in pulmonary circulation." American Journal of Physiology-Heart and Circulatory Physiology 250, no. 6 (June 1, 1986): H1109—H1116. http://dx.doi.org/10.1152/ajpheart.1986.250.6.h1109.

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The influence of increases in vascular tone on responses to selective alpha 1- and alpha 2-adrenoceptor agonists, norepinephrine, epinephrine, and isoproterenol was investigated in the feline pulmonary vascular bed. Under resting tone conditions with constant pulmonary blood flow and left atrial pressure, intralobar injections of the alpha 1-adrenoceptor agonists, phenylephrine and methoxamine, and the alpha 2-adrenoceptor agonists, UK 14304 and B-HT 933, increased lobar arterial pressure. When pulmonary vascular resistance was raised to a high steady level, vasoconstrictor responses to the alpha 2-adrenoceptor agonists were markedly increased, responses to methoxamine were increased to a lesser extent, and pressor responses to phenylephrine and epinephrine were reversed. These vasodilator responses to phenylephrine and epinephrine at elevated vascular tone were blocked by propranolol. Moreover, after beta-adrenoceptor blockade, vasoconstrictor responses to phenylephrine, epinephrine, and norepinephrine were also greater at elevated tone than at resting tone. Vasodilator responses to the beta-adrenoceptor stimulant, isoproterenol, were enhanced at higher levels of vasoconstrictor tone and were blocked by propranolol and by albuterol, a selective beta 2-adrenoceptor antagonist. The enhanced vasoconstrictor responses to the alpha 2-adrenoceptor agonists were selectively blocked by yohimbine, whereas the enhanced responses to the alpha 1-adrenoceptor agonists and, for the most part, the vasoconstrictor responses to norepinephrine and epinephrine, were blocked by prazosin. The present data support the hypothesis that postjunctional alpha 1- and alpha 2-adrenoceptors mediating vasoconstriction and beta 2-adrenoceptors mediating vasodilation are present in the feline pulmonary vascular bed.(ABSTRACT TRUNCATED AT 250 WORDS)

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15

Gao, A. G., F. P. Lindberg, J. M. Dimitry, E. J. Brown, and W. A. Frazier. "Thrombospondin modulates alpha v beta 3 function through integrin-associated protein." Journal of Cell Biology 135, no. 2 (October 15, 1996): 533–44. http://dx.doi.org/10.1083/jcb.135.2.533.

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Integrin-associated protein (IAP) is a receptor for the carboxyl-terminal "cell-binding domain" (CBD) of thrombospondin 1 (TS1). IAP associates with alpha v beta 3 integrin and mAbs against IAP inhibit certain integrin functions. Here we examine the effects of the TS1 CBD and 4N1K (KRFYVVMWKK), a cell-binding peptide derived from it, on the adhesion and spreading on vitronectin (VN) of C32 human melanoma cells which express IAP, alpha v beta 3, and alpha v beta 5. Cells adhere to VN at low surface densities via alpha v beta 5 and spread very slowly while adhesion to higher density VN involves both alpha v beta 5 and alpha v beta 3 and results in rapid spreading. Spreading of the cells, but not adhesion, on sparse VN coatings is markedly enhanced by the presence of soluble TS1, the recombinant CBD and 4N1K, but not the "mutant" peptide 4NGG, KRFYGGMWKK, which fails to bind IAP. This enhanced spreading is completely blocked by mAb LM609 against alpha v beta 3 and the anti-IAP mAb B6H12. Correlated with this enhanced spreading is increased tyrosine phosphorylation of focal adhesion kinase (FAK), paxillin, and a protein of ca. 90 kD. The enhanced spreading induced by TS1 and 4N1K and the constitutive spreading on higher density VN are both blocked by calphostin C (100 nM), wortmannin (10 nM), and tyrosine kinase inhibitors. In contrast, pertussis toxin specifically blocks only the TS1 stimulated spreading on low density VN, indicating that IAP exerts its effects on signal transduction via a heterotrimeric Gi protein acting upstream of a common cell spreading pathway which includes PI-3 kinase, PKC, and tyrosine kinases.

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Gong, J. H., H. Sprenger, F. Hinder, A. Bender, A. Schmidt, S. Horch, M. Nain, and D. Gemsa. "Influenza A virus infection of macrophages. Enhanced tumor necrosis factor-alpha (TNF-alpha) gene expression and lipopolysaccharide-triggered TNF-alpha release." Journal of Immunology 147, no. 10 (November 15, 1991): 3507–13. http://dx.doi.org/10.4049/jimmunol.147.10.3507.

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Abstract We have previously shown that infection of macrophages by influenza A virus is capable of priming for a high TNF-alpha production in response to LPS. The present study was designed to examine in more detail TNF-alpha gene expression and TNF-alpha protein release of virus-infected, murine PU5-1.8 macrophages in the presence or absence of low and by itself rather inefficient concentrations of LPS (10 ng/ml). Although influenza A virus infection alone induced a massive TNF-alpha mRNA accumulation, translation into the bioactive TNF-alpha protein was low as intra- and extracellularly determined by bioassay, specific ELISA and Western blot. However, when LPS was added simultaneously or up to 4 h after infection, a high TNF-alpha production was initiated. The virus-induced TNF-alpha mRNA accumulation appeared to be due to both transcriptional and post-transcriptional changes: an enhanced TNF-alpha gene transcription as determined by nuclear run-on transcription assay and a markedly prolonged half-life of TNF-alpha mRNA as shown in actinomycin D-treated macrophages. These findings imply that influenza A virus may 1) either directly or indirectly stimulate TNF-alpha gene transcription activators or may interfere with labile transcription repressor proteins and 2) may stabilize TNF-alpha mRNA by delaying its degradation. Both mechanisms, taken together, prime influenza A virus-infected macrophages for a high TNF-alpha release in response to LPS which, as clinical cases show, may adversely affect patients with combined influenza A virus and bacterial infections.

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17

Heidenreich, S., J. H. Gong, A. Schmidt, M. Nain, and D. Gemsa. "Macrophage activation by granulocyte/macrophage colony-stimulating factor. Priming for enhanced release of tumor necrosis factor-alpha and prostaglandin E2." Journal of Immunology 143, no. 4 (August 15, 1989): 1198–205. http://dx.doi.org/10.4049/jimmunol.143.4.1198.

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Abstract The macrophage-activating properties of murine recombinant granulocyte-macrophage (GM)-CSF were studied in murine peritoneal macrophages with respect to metabolism, endocytosis, PGE2 and TNF-alpha release, and tumor cytotoxicity. GM-CSF was found to be a potent stimulus for RNA and protein synthesis, glucose consumption, pinocytosis, and FcR-independent phagocytosis. Macrophages were activated by GM-CSF to kill TNF-alpha-insensitive Eb lymphoma cells but failed to generate cytotoxicity against TNF-alpha-sensitive L929 cells. Although GM-CSF alone was incapable of stimulating TNF-alpha release, it primed macrophages for elevated TNF-alpha production in response to IFN-gamma plus LPS. The priming effect of GM-CSF disappeared upon longer incubation (greater than 12 h) and was followed by a strongly reduced responsiveness to stimuli that release TNF-alpha. Late-stage suppression could be reverted by treatment with the cyclooxygenase blocker indomethacin, and GM-CSF-induced priming for enhanced TNF-alpha release was entirely restored. The responsible arachidonic acid product mediating suppression was found to be PGE2, because 1) GM-CSF-primed macrophages released enhanced amounts of PGE2 and 2) indomethacin-restored macrophages were again suppressed when exogenous PGE2 was added back in amounts produced by GM-CSF-primed macrophages. Although GM-CSF potently induced TNF-alpha gene transcription by 20 h of treatment, PGE2 interfered with translation into the secreted TNF-alpha protein. These data show that GM-CSF is capable of priming for the enhanced release of two factors, initially for TNF-alpha and subsequently for PGE2. The temporally delayed generation of these two mediators suggests an autoregulatory circuit in which the later produced PGE2 limits GM-CSF-induced macrophage activation.

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18

Morley, S. J., and V. M. Pain. "Translational regulation during activation of porcine peripheral blood lymphocytes: association and phosphorylation of the α and γ subunits of the initiation factor complex eIF-4F." Biochemical Journal 312, no. 2 (December 1, 1995): 627–35. http://dx.doi.org/10.1042/bj3120627.

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Mature peripheral blood lymphocytes exist in a resting state both in vivo and when maintained in culture, exhibiting low translation rates consistent with their non-proliferative state. Previously we have shown that activation of these quiescent cells with either phorbol ester or concanavalin A leads to a rapid increase in the rate of protein synthesis and phosphate-labelling of initiation factor eIF-4 alpha [Morley, Rau, Kay and Pain (1993) Eur. J. Biochem. 218, 39-48]. We now show that neither the early enhanced translation rate nor the early increased phosphate-labelling of eIF-4 alpha requires the activity of the 70 kDa form of ribosomal protein S6 kinase. In addition, we demonstrate that eIF-4 gamma is phosphorylated in response to cell activation, an event which is correlated with phosphorylation of eIF-4 alpha and enhanced eIF-4F complex formation. In these studies, isoelectric focusing and immunoblot analysis of eIF-4 alpha indicate that phosphate-labelling of eIF-4 alpha following cell activation reflects a modest increase in steady-state phosphorylation, mediated by the enhanced activity of eIF-4 alpha kinase(s) and inhibition of eIF-4 alpha phosphatase activity. In the resting cell, eIF-4 alpha is associated with heat- and acid-stable insulin-responsive protein (PHAS-I; 4E-BP1); following acute stimulation with phorbol ester, there is a 40% decrease in the amount of PHAS-I associated with eIF-4 alpha. Incubation of anti-PHAS-I immunoprecipitates with extracts containing activated or immunprecipitated mitogen-activated protein kinase resulted in a small increase in phosphorylation of recovered PHAS-I and a modest release of eIF-4 alpha from the PHAS-I-eIF-4 alpha complex. These data suggest a possible role for PHAS-I in the regulation of eIF-4F complex formation and the rate of translation in primary cells.

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19

Webb, D. S., and T. L. Gerrard. "IFN-alpha and IFN-gamma can affect both monocytes and tumor cells to modulate monocyte-mediated cytotoxicity." Journal of Immunology 144, no. 9 (May 1, 1990): 3643–48. http://dx.doi.org/10.4049/jimmunol.144.9.3643.

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Abstract IFN-alpha and IFN-gamma were found to enhance monocyte-mediated activity by acting on both tumor cells and monocytes. The addition of IFN-alpha or IFN-gamma enhanced the monocyte-mediated cytotoxicity of the human melanoma cell line, A375, as well as the human colon carcinoma cell line, HT-29. However, IFN-alpha generally induced more monocyte-mediated lysis of the A375 cells, whereas IFN-gamma induced more monocyte-mediated lysis of the HT-29 cells. These differences are, in part, due to the direct effects of the IFN on the tumor cells. Pretreatment of A375 cells with either IFN-alpha or IFN-gamma significantly enhanced their susceptibility to lysis by untreated monocytes. However, only IFN-gamma pretreatment of HT-29 cells enhanced the lysis of these cells by untreated monocytes. Differences were also observed in the activation of monocytes by IFN-alpha vs IFN-gamma with respect to their ability to induce soluble cytotoxic factors. We found that the addition of IFN-gamma and tumor cells (either the A375 or HT-29 cells) to monocytes induced TNF release, whereas IFN-alpha or IFN-gamma alone or IFN-alpha and tumor cells had no effect. Despite its presence, TNF did not appear to play a major role in the killing of either tumor cell line. However, inhibitors of H2O2-myeloperoxidase system suppressed both IFN-alpha- and IFN-gamma-induced cytotoxicity of the HT-29 cells. Thus IFN-alpha and IFN-gamma can induce both similar and distinct mechanisms of cytotoxicity in monocytes. In addition, both IFN types can increase the susceptibility of tumor cells to lysis by untreated monocytes, although sensitivity to IFN-alpha vs IFN-gamma may vary with different tumor cell lines. These differences observed between IFN-alpha and IFN-gamma on monocytes and tumor cells could have important implications for the clinical use of these cytokines.

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MOGUTNOV, B. M., N. V. PASETCHNIK, and E. I. ESTRIN. "Enhanced Plasticity of a Tool Steel Near .ALPHA.-.GAMMA. Transformation." ISIJ International 45, no. 5 (2005): 700–705. http://dx.doi.org/10.2355/isijinternational.45.700.

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21

Cuillière, Marie-Louise, Mounia Abbadi, Claire Molé, Paul Montagne, Marie-Christine Béné, and Gilbert Faure. "Microparticle-Enhanced Nephelometric Immunoassay of Alpha-Lactalbumin in Human Milk." Journal of Immunoassay 18, no. 1 (February 1997): 97–109. http://dx.doi.org/10.1080/01971529708005806.

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&NA;. "Enhanced response of anogenital warts with interferon alpha 2B + podophyllin." Inpharma Weekly &NA;, no. 756 (September 1990): 12–13. http://dx.doi.org/10.2165/00128413-199007560-00037.

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23

Konkle, B. A., S. S. Shapiro, A. S. Asch, and R. L. Nachman. "Cytokine-enhanced expression of glycoprotein Ib alpha in human endothelium." Journal of Biological Chemistry 265, no. 32 (November 1990): 19833–38. http://dx.doi.org/10.1016/s0021-9258(17)45448-2.

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Kim, H. K., J. Titze, M. Schoffler, F. Trinter, M. Waitz, J. Voigtsberger, H. Sann, et al. "Enhanced production of low energy electrons by alpha particle impact." Proceedings of the National Academy of Sciences 108, no. 29 (July 5, 2011): 11821–24. http://dx.doi.org/10.1073/pnas.1104382108.

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25

Gevaert, P., C. Bachert, G. Holtappels, C. P. Novo, J. Van der Heyden, L. Fransen, S. Depraetere, H. Walter, P. Cauwenberge, and J. Tavernier. "Enhanced soluble interleukin-5 receptor alpha expression in nasal polyposis." Allergy 58, no. 5 (May 2003): 371–79. http://dx.doi.org/10.1034/j.1398-9995.2003.00110.x.

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26

Castro, Pedro M., Patrícia Baptista, Giampaolo Zuccheri, Ana Raquel Madureira, Bruno Sarmento, and Manuela E. Pintado. "Film-nanoparticle composite for enhanced oral delivery of alpha-casozepine." Colloids and Surfaces B: Biointerfaces 181 (September 2019): 149–57. http://dx.doi.org/10.1016/j.colsurfb.2019.05.029.

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27

Prickett, Todd D., and David L. Brautigan. "Cytokine Activation of p38 Mitogen-Activated Protein Kinase and Apoptosis Is Opposed by alpha-4 Targeting of Protein Phosphatase 2A for Site-Specific Dephosphorylation of MEK3." Molecular and Cellular Biology 27, no. 12 (April 16, 2007): 4217–27. http://dx.doi.org/10.1128/mcb.00067-07.

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ABSTRACT alpha-4 is an essential gene and is a dominant antiapoptotic factor in various tissues that is a regulatory subunit for type 2A protein phosphatases. A multiplexed phosphorylation site screen revealed that knockdown of alpha-4 by small interfering RNA (siRNA) increased p38 mitogen-activated protein kinase (MAPK) and c-Jun phosphorylation without changes in JNK or ERK. FLAG-alpha-4 coprecipitated hemagglutinin-MEK3 plus endogenous protein phosphatase 2A (PP2A) and selectively enhanced dephosphorylation of Thr193, but not Ser189, in the activation loop of MEK3. Overexpression of alpha-4 suppressed p38 MAPK activation in response to tumor necrosis factor alpha (TNF-α). The alpha-4 dominant-negative domain (DND) (residues 220 to 340) associated with MEK3, but not PP2A, and its overexpression sensitized cells to activation of p38 MAPK by TNF-α and interleukin-1β, but not by ansiomycin or sorbitol. The response was diminished by nocodazole or by siRNA knockdown of the Opitz syndrome protein Mid1 that binds alpha-4 to microtubules. Interference by alpha-4 DND or alpha-4 siRNA increased caspase 3/7 activation in response to TNF-α. Growth of transformed cells in soft agar was enhanced by alpha-4 and suppressed by alpha-4 DND. The results show that alpha-4 targets PP2A activity to MEK3 to suppress p38 MAPK activation by cytokines, thereby inhibiting apoptosis and anoikis.

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Noritomi, Hidetaka, Jumpei Nishigami, Nobuyuki Endo, Satoru Kato, and Katsumi Uchiyama. "Influence of Water Activity on Protease Adsorbed on Biochar in Organic Solvents." Journal of Materials Science Research 6, no. 4 (September 28, 2017): 96. http://dx.doi.org/10.5539/jmsr.v6n4p96.

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We have found that the organic solvent-resistance of Alpha-chymotrypsin (Alpha-CT) is enhanced by adsorbing Alpha-CT onto bamboo charcoal powder (BCP), which is obtained by pyrolyzing bamboo waste under nitrogen atmosphere, and is markedly dependent on the thermodynamic water activity (aw) in organic solvents. When BCP-adsorbed Alpha-CT was immersed in acetonitrile at an appropriate water activity, it effectively enhanced the transesterification of N-acetyl-L-tyrosine ethyl ester (N-Ac-Tyr-OEt) with n-butanol (BuOH) to produce N-acetyl-L-tyrosine butyl ester (N-Ac-Tyr-OBu), compared to the hydrolysis of N-Ac-Tyr-OEt with water to give N-acetyl-L-tyrosine (N-Ac-Tyr-OH). When the water activity was 0.28, the initial rate of transesterification catalyzed by BCP-adsorbed Alpha-CT was about sixty times greater than that catalyzed by free Alpha-CT. Regarding the reaction selectivity which is defined as a ratio of the initial rate of transesterification to that of hydrolysis, BCP-adsorbed α-CT was much superior to free Alpha-CT. The catalytic activity of BCP-adsorbed Alpha-CT was markedly dependent on the reaction temperature. Furthermore, concerning the thermal stability at 50 oC, the half-life of BCP-adsorbed Alpha-CT exhibited 3.8-fold, compared to that of free Alpha-CT.

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29

Nath, K. A., E. O. Ngo, R. P. Hebbel, A. J. Croatt, B. Zhou, and L. M. Nutter. "alpha-Ketoacids scavenge H2O2 in vitro and in vivo and reduce menadione-induced DNA injury and cytotoxicity." American Journal of Physiology-Cell Physiology 268, no. 1 (January 1, 1995): C227—C236. http://dx.doi.org/10.1152/ajpcell.1995.268.1.c227.

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We demonstrate that alpha-ketoacids reduce and, in some instances, abrogate menadione-induced DNA damage and cytotoxicity in the human breast cancer cell line, MCF7. We confirm that alpha-ketoacids quench the copious amounts of H2O2 generated by menadione while these alpha-ketoacids undergo nonenzymatic oxidative decarboxylation; our data thus support enhanced H2O2 production as an important pathway for menadione-induced DNA damage and cytotoxicity. We also demonstrate that alpha-ketoacids scavenge H2O2 generated by mitochondria and microsomes when these organelles are exposed to menadione; additionally, alpha-ketoacids protect oxidant-vulnerable enzymes against functional impairment induced by H2O2. Finally, we provide the first in vivo demonstration that acute elevations in concentrations of alpha-ketoacids in rat tissues and urine scavenge H2O2. We conclude that enhanced H2O2 production is a major pathway for menadione-induced DNA damage and cytotoxicity and that the diverse alpha-ketoacids present within the cell must be considered, along with glutathione peroxidase and catalase, as part of the intracellular antioxidant defense mechanisms that regulate the ambient levels of H2O2.

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30

Chu, C. T., T. D. Oury, J. J. Enghild, and S. V. Pizzo. "Adjuvant-free in vivo targeting. Antigen delivery by alpha 2-macroglobulin enhances antibody formation." Journal of Immunology 152, no. 4 (February 15, 1994): 1538–45. http://dx.doi.org/10.4049/jimmunol.152.4.1538.

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Abstract The proteinase "inhibitor" alpha 2-macroglobulin (alpha 2M) is able to entrap and form covalent linkages with diverse proteins during a transient proteinase-activated state. These complexes are rapidly endocytosed after binding to receptors present on macrophages and other cells. We have previously shown that compared to free hen egg lysozyme (HEL), alpha 2M-complexed HEL undergoes enhanced macrophage uptake, processing, and presentation to T hybridoma clones in vitro. Inasmuch as it is not clear whether T hybridoma responses accurately reflect primary immune responses in vivo, we studied antibody production in rabbits using two Ag complexed with either human alpha 2M (H alpha 2M) or a homologous protein purified from rabbit plasma, alpha 1-macroglobulin (R alpha 1M). Pathogen-free NZW rabbits received s.c. injections with adjuvant-free preparations of free HEL or porcine pancreatic elastase (PPE), H alpha 2M-HEL-PPE complexes, R alpha 1M-HEL-PPE complexes, or mixtures of the uncomplexed proteins. Complexing the Ag to alpha 2M resulted in 10 to 500-fold higher IgG titers compared to uncomplexed controls. Injection of Ag complexed to either H alpha 2M or R alpha 1M resulted in levels of anti-HEL IgG comparable to those elicited by emulsification in CFA. Inasmuch as inflammatory proteinases such as neutrophil elastase can initiate covalent complex formation with alpha 2M, we propose that "proteinase-activated" alpha 2M may mediate receptor-enhanced Ag uptake by macrophages, resulting in augmented Ag processing and antibody production.

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31

Hanemaaijer, R., P. Koolwijk, L. le Clercq, W. J. A. de Vree, and V. W. M. van Hinsbergh. "Regulation of matrix metalloproteinase expression in human vein and microvascular endothelial cells. Effects of tumour necrosis factor α, interleukin 1 and phorbol ester." Biochemical Journal 296, no. 3 (December 15, 1993): 803–9. http://dx.doi.org/10.1042/bj2960803.

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Matrix metalloproteinases (MMPs) play a role in tissue remodelling and angiogenesis. We have investigated the expression and regulation of MMP-1 (interstitial collagenase), MMP-2 (gelatinase A), MMP-3 (stromelysin 1), MMP-7 (matrilysin), MMP-9 (gelatinase B) and their inhibitors TIMP-1 and TIMP-2 in human umbilical vein, femoral vein and microvascular endothelial cells, and compared these data with those obtained with human synovial fibroblasts. Non-stimulated vein endothelial cells expressed the mRNAs for MMP-1, MMP-2, TIMP-1 and TIMP-2. MMP-3 mRNA and protein were undetectable or only weakly expressed, but could be stimulated by the inflammatory mediator tumour necrosis factor alpha (TNF alpha). The expression of MMP-3 and MMP-1 was further enhanced by phorbol 12-myristate 13-acetate (PMA). Phorbol ester also induced TIMP-1 and MMP-9, the expression of the latter being further enhanced by TNF alpha or interleukin 1 alpha (IL-1 alpha). Similar stimulatory effects were observed in microvascular endothelial cells. Hence the inflammatory mediator TNF alpha induces/enhances the production of several matrix metalloproteinases in human endothelial cells. On the other hand, MMP-2 and TIMP-2 were not affected or were affected in a variable way by TNF alpha and/or phorbol ester, suggesting a dissimilar regulation of these proteins. The cyclic AMP-enhancing agent forskolin affected the production of MMPs in a cell-type-specific way. In human vein endothelial cells it enhanced the PMA-mediated induction of MMP-9, whereas it suppressed this induction in human microvascular endothelial cells and in synovial fibroblasts. On the other hand, forskolin suppressed the PMA-mediated induction of MMP-1 and MMP-3 in synovial fibroblasts, while it enhanced or did not affect this induction in various types of human endothelial cells. These observations may have implications for future pharmacological intervention in angiogenesis.

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32

Benveniste, E. N., J. Kwon, W. J. Chung, J. Sampson, K. Pandya, and L. P. Tang. "Differential modulation of astrocyte cytokine gene expression by TGF-beta." Journal of Immunology 153, no. 11 (December 1, 1994): 5210–21. http://dx.doi.org/10.4049/jimmunol.153.11.5210.

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Abstract In this study, we demonstrate that TGF-beta inhibits TNF-alpha expression, and induces/enhances IL-6 expression by primary rat astrocytes. Treatment of astrocytes with TGF-beta alone had no effect on TNF-alpha mRNA or protein expression; however, TGF-beta suppressed induction of TNF-alpha expression by three different stimuli (IFN-gamma/LPS, IFN-gamma/IL-1 beta, TNF-alpha) at both the protein and mRNA level. The extent of TGF-beta-mediated inhibition was greatest when astrocytes were pretreated with TGF-beta for 6 to 24 h, then exposed to the inducing stimuli. Inhibition of TNF-alpha mRNA steady-state levels by TGF-beta was a result of inhibition of TNF-alpha gene transcription, rather than degradation of the TNF-alpha message. In contrast, TGF-beta alone induced expression of IL-6 by astrocytes and synergized with two other cytokines, IL-1 beta and TNF-alpha, for enhanced IL-6 expression. TGF-beta-induced/enhanced IL-6 expression was mediated by transcriptional activation of the IL-6 gene. These results indicate that TGF-beta is an important regulator of cytokine production by astrocytes under inflammatory conditions in the brain.

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33

Ahmed Amin, Sahar. "Alpha activity emitted from leaves and roots of beetroot plant planted in enhanced soil with fertilizers." International Journal of Physical Research 8, no. 2 (September 2, 2020): 50. http://dx.doi.org/10.14419/ijpr.v8i2.31029.

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This study is to assesses radioactive materials transported to the beetroot plants grow in different fertilized soil. Equivalent weights of fertilizers were added to the soil prior the plantation. The alpha track densities were estimated utilizing solid state nuclear track detector (SSNTDs), CR-39. The obtained results show that alpha track densities in Beetroot plants in the lower and upper sides of plant leaves were varied from 67.62 Tr.cm−2 to 101.83 Tr.cm−2 and from 45.35 Tr.cm−2 to 94.67 Tr.cm−2 with mean values of 89.96 Tr.cm−2 and 68.48 Tr.cm−2, respectively. Alpha track densities were also measured in the samples of the enhanced plantation soil with fertilizers and in the whole parts of the Beetroot plant which were planted in these soils. These values were compared with alpha track densities obtained from fertilizer samples in the previous studies. The lower face of leaves gives higher α-particles activity than that obtained from the upper face. As well as, the alpha activity from the plants planted in soils enhanced with phosphate compost was found greater as contrast with that planted in a soil enhanced with organic fertilizer. The utilization of organic fertilizer don't cause much risks like contrasted with phosphate fertilizers. Therefore, the alpha activity depends on the nature of fertilizers added to the soil.

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34

Yorio, T., R. D. Page, and L. W. Frazier. "Prostaglandin regulation of H+ secretion in amphibian epithelia." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 260, no. 5 (May 1, 1991): R866—R872. http://dx.doi.org/10.1152/ajpregu.1991.260.5.r866.

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The role of prostaglandins in regulating H+ excretion in amphibian epithelia was investigated. The abdominal skin of the southern leopard frog Rana pipiens and the urinary bladder of the toad Bufo marinus were used to measure proton excretion across their mucosal surface. Prostaglandin F2 alpha (PGF2 alpha) produced a dose-dependent inhibition of H+ excretion across the frog skin. Frogs pretreated with ibuprofen (30 mg.kg-1.day-1 for 3 days) showed an enhanced proton excretion similar to that observed when frogs are placed in chronic metabolic acidosis. The number of mitochondria-rich cells, the cells responsible for proton excretion, was also increased in frog skins after chronic metabolic acidosis or ibuprofen treatment. Mezerein and the phorbol ester 4 beta-phorbol 12-myristate 13-acetate (4 beta-PMA), activators of protein kinase C (PCK), decreased H+ excretion in frog skin, whereas the inactive phorbol 4 alpha-PMA was without an effect. The inhibition of proton excretion was similar to that observed with PGF2 alpha and suggested that the effects of PGF2 alpha and activation of PKC were mediated through a common pathway. Frogs pretreated with ibuprofen not only had an enhanced proton excretion rate but also had a decrease in cytosolic PKC activity. In another amphibian tissue, the toad urinary bladder, PGE2 inhibited proton excretion at low doses but enhanced H+ excretion at higher doses. Toads maintained under chronic metabolic acidosis had enhanced proton excretion rates and also had a threefold increase in cellular PGE2 concentration, which was consistent with the observation that PGE2 enhanced proton excretion at high doses.(ABSTRACT TRUNCATED AT 250 WORDS)

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35

Fujii, K., H. Kohrogi, H. Iwagoe, J. Hamamoto, N. Hirata, T. Yamaguchi, O. Kawano, and M. Ando. "Evidence that PGF2 alpha-induced contraction of isolated guinea pig bronchi is mediated in part by release of tachykinins." Journal of Applied Physiology 79, no. 5 (November 1, 1995): 1411–18. http://dx.doi.org/10.1152/jappl.1995.79.5.1411.

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To investigate whether prostaglandin F2 alpha (PGF2 alpha) stimulates the release of tachykinins and whether the tachykinins play a role in the PGF2 alpha-induced bronchial contraction, we examined the contractile response to PGF2 alpha in the presence or absence of a neutral endopeptidase (NEP) inhibitor phosphoramidon in the guinea pig main bronchus in vitro. Because NEP effectively cleaves tachykinins, we hypothesized that the inhibition of NEP would enhance a PGF2 alpha-induced bronchial contraction if PGF2 alpha stimulates the release of tachykinins. Phosphoramidon significantly enhanced the concentration-response curve to PGF2 alpha. And it also significantly enhanced 10(-5) M PGF2 alpha-induced contraction. The enhancement was significantly attenuated in tissues where the tachykinins had been depleted by treatment with capsaicin. Furthermore, the enhancement of contraction was also significantly attenuated in the presence of tachykinin antagonist FK-224 (10(-5) M). Tetrodotoxin, a sodium-channel blocker that blocks nerve conduction, did not affect the enhancement. From these results we conclude that 1) PGF2 alpha causes the release of tachykinin-like substances, 2) these substances play a role in bronchial contraction in tissues where NEP activity is inhibited, and 3) nerve conduction is not necessary for the release of these substances in the guinea pig bronchus.

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36

Mayer, A. M., R. A. Pittner, G. E. Lipscomb, and J. A. Spitzer. "Effect of in vivo TNF administration on superoxide production and PKC activity of rat alveolar macrophages." American Journal of Physiology-Lung Cellular and Molecular Physiology 264, no. 1 (January 1, 1993): L43—L52. http://dx.doi.org/10.1152/ajplung.1993.264.1.l43.

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After the intravenous injection of recombinant human tumor necrosis factor (TNF)-alpha (6.0 x 10(5) U) into rats, phorbol 12-myristate 13-acetate (PMA)-stimulated superoxide anion (O2-) secretion was enhanced in suspensions of alveolar macrophages (AM phi) compared with saline-treated controls. No enhancement of spontaneous, A23187-stimulated, or opsonized zymosan (OPZ)-stimulated O2- release was observed. Intratracheal injection of TNF-alpha (6.0 x 10(5) U) did not result in enhancement of spontaneous or A23187-, OPZ-, or PMA-stimulated O2- release. Although no TNF-alpha was detected in the bronchoalveolar lavage fluid, small quantities of TNF-alpha and/or other mediators secreted by polymorphonuclear leukocytes present in the lung capillaries, veins, and arteries may have leaked into the alveolar compartment and primed AM phi for enhanced PMA-stimulated O2- release. The respiratory burst in macrophages and neutrophils appears to be dependent on the translocation of protein kinase C. We have demonstrated protein kinase C translocation in both TNF-alpha- and saline-treated AM phi on PMA stimulation, although no differences were observed due to TNF-alpha treatment.

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37

Nedwin, G. E., L. P. Svedersky, T. S. Bringman, M. A. Palladino, and D. V. Goeddel. "Effect of interleukin 2, interferon-gamma, and mitogens on the production of tumor necrosis factors alpha and beta." Journal of Immunology 135, no. 4 (October 1, 1985): 2492–97. http://dx.doi.org/10.4049/jimmunol.135.4.2492.

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Abstract Human peripheral blood mononuclear cells (PBMC) were induced by recombinant interleukin 2 and mitogens to secrete two distinct cytotoxic polypeptides, tumor necrosis factor-alpha (TNF-alpha) and tumor necrosis factor-beta (TNF-beta), previously called lymphotoxin. Treatment of PBMC with recombinant human interleukin 2 (rIL 2) or mitogens in combination with recombinant human interferon-gamma (rIFN-gamma) resulted in augmented production of both TNF-alpha and TNF-beta. rIFN-gamma alone had no effect on production of either cytotoxic polypeptide. TNF-alpha was produced within 2 to 3 hr after induction and was the major cytotoxin produced by PBMC during the first 48 hr of culture, after which time TNF-beta became the predominant species. TNF-beta was first secreted into the media after 8 hr of induction. Enhanced levels of both TNF-alpha and TNF-beta were seen when the PBMC were separated into adherent and nonadherent cells. Both TNF-alpha and TNF-beta were induced in different tumor cell lines of hematopoietic origin. The results demonstrate that the production of TNF-alpha and TNF-beta can be enhanced by two lymphokines, IL 2 and IFN-gamma.

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38

Mishra, Hirdyesh, and Chris D. Geddes. "Metal-Enhanced S1 and Alpha- S1 Fluorescence: Effects of Far-Field Excitation Irradiance on Enhanced Fluorescence." Journal of Physical Chemistry C 118, no. 49 (December 3, 2014): 28791–96. http://dx.doi.org/10.1021/jp5092587.

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39

Boudignon-Proudhon, C., PM Patel, and LV Parise. "Phorbol ester enhances integrin alpha IIb beta 3-dependent adhesion of human erythroleukemic cells to activation-dependent monoclonal antibodies." Blood 87, no. 3 (February 1, 1996): 968–76. http://dx.doi.org/10.1182/blood.v87.3.968.bloodjournal873968.

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Following platelet stimulation by agonists, integrin-alpha IIb beta 3 (or glycoprotein IIb-IIIa) is converted to an activated state that can bind soluble fibrinogen and mediate platelet aggregation. However, little is known about modulation of alpha IIb beta 3 in cell lines. In the present study, we show that agonist stimulation modulates alpha IIb beta 3-dependent adhesive properties of a human erythroleukemic (HEL) cell line. Brief treatment with phorbol 12-myristate 13-acetate (PMA) caused a significant increase in HEL cell adhesion to monoclonal antibodies (MoAbs) specific for activated alpha IIb beta 3 (PAC1 or pl- 55). This adhesion was inhibited by blocking MoAbs or peptides specific for alpha IIb beta 3, but not by anti-Fc gamma receptor-specific MoAb. Similarly, PMA enhanced HEL cell adhesion to immobilized fibrinogen by 10-fold. However, the activation-dependent ligands in solution (ie, PAC1, pl-55, or fibrinogen) did not inhibit the enhanced HEL cell adhesion to immobilized MoAbs PAC1 or pl-55 after PMA treatment. Thus, PMA may increase alpha IIb beta 3-dependent adhesion to immobilized activation-dependent antibodies and fibrinogen by increasing the local concentration of alpha IIb beta 3 to participate in low-affinity interactions, resulting in an increased avidity, changing the affinity state of alpha IIb beta 3, or both.

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40

Koyasu, S., Y. Tagaya, K. Sugie, S. Yonehara, J. Yodoi, and I. Yahara. "The expression of IL-2R alpha-chain is enhanced by activation of adenylate cyclase in large granular lymphocytes and natural killer cells." Journal of Immunology 146, no. 1 (January 1, 1991): 233–38. http://dx.doi.org/10.4049/jimmunol.146.1.233.

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Abstract An increase in intracellular cAMP level induced the expression of IL-2R alpha-chain, the 55-kDa component of IL-2R complex, in a human NK-like cell line, YT. We show here that forskolin also induces the expression of IL-2R alpha-chain on mouse large granular lymphocytes (LGL) but not on T cells. In contrast, treatment with a combination of phorbol ester and calcium ionophore, which is a strong inducer of IL-2R alpha-chain on T cells, does not induce the expression of the alpha-chain on LGL cells. Forskolin was shown to activate the transcription of IL-2R alpha-chain gene in YT cells as revealed by the chloramphenicol acetyltransferase assay. Chemical cross-linking experiments using radio-iodinated IL-2 also supported the enhanced expression of IL-2R alpha-chain by treatment with forskolin. In contrast to the alpha-chain, IL-2R beta-chain was not induced by forskolin as revealed by flow cytofluorometry with a mAb against the beta-chain molecule. These results indicate that the activation of adenylate cyclase induces or/and enhance the expression of IL-2R alpha-chain at the transcriptional level in LGL/NK cells including mouse LGL and human YT cell, which leads to the enhanced expression of high affinity IL-2 receptors.

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41

Jelinek, D. F., and P. E. Lipsky. "Enhancement of human B cell proliferation and differentiation by tumor necrosis factor-alpha and interleukin 1." Journal of Immunology 139, no. 9 (November 1, 1987): 2970–76. http://dx.doi.org/10.4049/jimmunol.139.9.2970.

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Abstract The role of tumor necrosis factor-alpha (TNF-alpha) in human B cell responses was examined and compared with that of interleukin (IL) 1 by assessing the ability of each cytokine to support proliferation and differentiation. Recombinant TNF-alpha (rTNF-alpha) and recombinant IL-1 (rIL-1) each enhanced the generation of immunoglobulin-secreting cells (ISC) in cultures of pokeweed mitogen-stimulated B cells incubated with T cells. To examine the direct effect of rTNF-alpha and rIL-1 on the responding B cell, highly purified peripheral blood B cells were stimulated with Cowan I Staphylococcus aureus (SA). In the absence of T cell factors, proliferation was minimal and there was no generation of ISC. Recombinant IL-2 (rIL-2) supported both responses. Although rTNF-alpha alone did not support SA-stimulated generation of ISC, it did increase SA-stimulated B cell DNA synthesis by two- to eightfold. In addition, rTNF-alpha augmented B cell proliferation in rIL-2 supported SA-stimulated cultures. Moreover, rTNF-alpha enhanced the generation of ISC stimulated by rIL-2 alone or rIL-2 and SA. rIL-1 also augmented DNA synthesis and generation of ISC by B cells stimulated with SA and rIL-2. However, rTNF-alpha enhanced proliferation and ISC generation in SA + rIL-2-stimulated cultures even when they were supplemented with saturating concentrations of rIL-1. Utilizing a two-stage culture system, it was found that the major effect of rTNF-alpha was to enhance responsiveness of SA-activated B cells to rIL-2, whereas it exerted only a minimal effect during initial stimulation. These results indicate that TNF-alpha as well as IL-1 augment B cell responsiveness. Moreover, the ability of rTNF-alpha to enhance B cell responsiveness was not an indirect effect resulting from the induction of Il-1 production by contaminating monocytes, but rather resulted from the delivery of a signal by rTNF-alpha directly to the responding B cell that promoted both proliferation and differentiation after initial activation. The data therefore indicate that human B cell responsiveness can be independently regulated by the action of two separate monocyte-derived cytokines.

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42

Kenny, D., H. L. Brooks, and D. C. Warltier. "Enhanced alpha-adrenergic vasoconstriction by n-3 fatty acids in conscious dogs." American Journal of Physiology-Heart and Circulatory Physiology 258, no. 6 (June 1, 1990): H1660—H1667. http://dx.doi.org/10.1152/ajpheart.1990.258.6.h1660.

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The effect of dietary fish oil supplementation on cardiac function and the pressor response to selective agonists of postjunctional alpha 1- and alpha 2-adrenoceptors was investigated in chronically instrumented dogs (n = 12). Following ganglionic, cholinergic, and beta-adrenergic blockade, dose responses to phenylephrine (0.3-1.2 micrograms/kg iv), a selective alpha 1-adrenoceptor agonist, and azepexole (B-HT 933, 5-20 micrograms/kg iv), a selective alpha 2-adrenoreceptor agonist, were obtained in conscious dogs. Fish oil capsules containing eicosapentaenoic acid (1.12 g) and docosahexaenoic acid (480 mg) were administered orally twice daily for 1 wk, and dose-response curves were repeated. Dose-response curves were again obtained 1 wk after fish oil was discontinued. Fish oil supplementation resulted in significantly (P less than 0.05) increased arterial pressure at rest, and after autonomic nervous system blockade there was an increase in peripheral vascular resistance. Cardiac output was reduced in fish oil-treated dogs during autonomic nervous system blockade. The pressor response to selective alpha 1- and alpha 2-adrenoceptor stimulation was increased secondary to elevated peripheral vascular resistance. Hemodynamics and exaggerated vascular reactivity returned to control 1 wk after dietary fish oil was discontinued. The results of this study demonstrate that dietary fish oil supplementation produces an increase in arterial pressure via peripheral vasoconstriction and that the vascular response to alpha-adrenergic stimulation is exaggerated.

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43

Hackett, R. J., L. S. Davis, and P. E. Lipsky. "Comparative effects of tumor necrosis factor-alpha and IL-1 beta on mitogen-induced T cell activation." Journal of Immunology 140, no. 8 (April 15, 1988): 2639–44. http://dx.doi.org/10.4049/jimmunol.140.8.2639.

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Abstract The effect of rTNF-alpha on human T cell function was examined and compared with that of rIL-1 beta by assessing the ability of each cytokine to support mitogen-induced proliferation, IL-2 production, and IL-2R expression. TNF-alpha and IL-1 beta each enhanced DNA synthesis induced by PHA or immobilized mAb to the CD3 molecular complex. In addition, each cytokine increased the number of cells entering the G1 phase of the cell cycle and augmented IL-2R expression. The combination of optimal concentrations of these factors supported these responses to a greater extent than either cytokine alone, suggesting that T cell responsiveness is independently regulated by the action of at least two separate monocyte derived cytokines. Whereas TNF-alpha had little effect, IL-1 beta augmented IL-2 mRNA expression and IL-2 production by mitogen-stimulated cells. Furthermore, IL-1 beta enhanced proliferation with increasing length of culture. Whereas TNF-alpha also enhanced proliferation late in culture, it was less effective in this regard than IL-1 beta. Thus, IL-1 beta and TNF-alpha augment mitogen-induced T cell proliferation by increasing the number of cells initially activated and by promoting subsequent cell cycle progression. They differ, however, in their capacity to promote IL-2 mRNA and IL-2 production and therefore ongoing T cell proliferation.

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44

Lehtonen, A., S. Matikainen, and I. Julkunen. "Interferons up-regulate STAT1, STAT2, and IRF family transcription factor gene expression in human peripheral blood mononuclear cells and macrophages." Journal of Immunology 159, no. 2 (July 15, 1997): 794–803. http://dx.doi.org/10.4049/jimmunol.159.2.794.

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Abstract IFN signaling is mediated by binding of IFNs to their receptors and subsequent activation of Janus tyrosine kinase (JAK)-STAT signaling pathway. Stimulation of cells with IFN-alpha leads to the assembly of IFN-stimulated gene factor 3 transcription factor complex formed by STAT1, STAT2, and p48 protein. IFN-gamma signaling is mediated by homodimeric STAT1 protein. Although these signaling molecules are expressed constitutively, there is also evidence of transcriptional regulation by IFNs. We have characterized the expression of STAT and IFN regulatory factor (IRF) family transcription factors in primary human blood mononuclear cells and macrophages in response to IFN-alpha and IFN-gamma stimulation. We show that IFN-alpha and IFN-gamma rapidly and efficiently enhanced STAT1, STAT2, p48, and IRF-1 gene expression. IFN-gamma induced IRF-1 gene expression more strongly than IFN-alpha. Stimulation experiments in the presence of protein synthesis inhibitor, cycloheximide, suggested that these genes were activated directly by IFNs. IRF-2 gene was apparently only weakly responsive to IFNs in these cells. When macrophages were pretreated with low doses of IFN-gamma and then stimulated with IFN-alpha, clearly enhanced formation of specific transcription factor complexes was detected. This suggests that higher intracellular levels of STAT1, STAT2, and p48 protein may result in enhanced signal transduction for cytokines utilizing these transcription factors.

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45

Nakano, Y., K. Onozuka, Y. Terada, H. Shinomiya, and M. Nakano. "Protective effect of recombinant tumor necrosis factor-alpha in murine salmonellosis." Journal of Immunology 144, no. 5 (March 1, 1990): 1935–41. http://dx.doi.org/10.4049/jimmunol.144.5.1935.

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Abstract The enhancement of resistance by i.p. administration of murine rTNF-alpha into mice against i.p. challenge with virulent Salmonella typhimurium was studied. Administration of TNF-alpha (5 x 10(4) U/mouse) into mice at 6 or 12 h before the challenge with S. typhimurium organisms enhanced the bactericidal capacity in the peritoneal cavities of the mice. The diminution of the infecting organism in the peritoneal cavities of the TNF-alpha-treated mice was not due to the systemic spread of the organism inasmuch as few organism were recovered from other areas such as the spleen and liver. The TNF-alpha treatment effected a slight increase of neutrophils in the peritoneal cavity, but did not effect an increase of macrophages, including Ia-bearing macrophages. The survival rate of mice infected with Salmonella was improved by the i.p. injection of TNF-alpha before infection. Co-administration of smaller doses of TNF-alpha (5 x 10(3) U) and murine rIFN-gamma (10(2) U) at 6 h before the challenge also effectively enhanced bactericidal activity and protectivity. The cooperative effect of TNF-alpha and IFN-gamma was only seen when these recombinant cytokines were injected together at the proper time before the challenge. Injection of rabbit anti-TNF-alpha serum abolished the effects of TNF-alpha and the cooperative effect of TNF-alpha and IFN-gamma. Furthermore, the serum could abolish the cooperative effect of IFN-gamma and LPS on bactericidal activity, suggesting participation of LPS-induced TNF-alpha in the cooperation.

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46

Bonner, J. C., A. Badgett, P. M. Lindroos, and P. G. Coin. "Basic fibroblast growth factor induces expression of the PDGF receptor-alpha on human bronchial smooth muscle cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 271, no. 6 (December 1, 1996): L880—L888. http://dx.doi.org/10.1152/ajplung.1996.271.6.l880.

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Bronchial smooth muscle cell (SMC) hyperplasia is a key feature in the pathology of asthma. Platelet-derived growth factor (PDGF) isoforms are SMC mitogens. We investigated the effect of basic fibroblast growth factor (bFGF), transforming growth factor-beta 1 (TGF-beta 1), interleukin-1 beta (IL-1 beta), and tumor necrosis factor-alpha (TNF-alpha) on the PDGF receptor system on human bronchial SMC from three different donors. bFGF induced gene expression of the PDGF alpha-receptor (PDGF-R alpha) approximately threefold without altering the PDGF beta-receptor (PDGF-R beta). IL-1 beta and TNF-alpha did not affect the PDGF receptor system. TGF-beta 1 downregulated PDGF-R alpha mRNA approximately 60% without changing PDGF-R beta mRNA levels. Receptor assays showed that bFGF increased the [125I]PDGF-AA binding site approximately twofold, whereas TGF-beta 1 reduced [125I]PDGF-AA binding approximately 60%. TGF-beta 1, but not latent TGF-beta 1, counteracted the bFGF-induced increase in [125I]PDGF-AA binding. PDGF-AA-stimulated tyrosine phosphorylation on the PDGF-R alpha was enhanced after treatment with bFGF, bFGF pretreatment enhanced the mitogenic response of SMC to PDGF-AA and PDGF-AB. These findings suggest that upregulation of the PDGF-R alpha by bFGF could contribute to SMC hyperplasia during chronic airway inflammation in asthma.

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47

Capotosto, Paolo, Claudio Babiloni, Gian Luca Romani, and Maurizio Corbetta. "Resting-state Modulation of Alpha Rhythms by Interference with Angular Gyrus Activity." Journal of Cognitive Neuroscience 26, no. 1 (January 2014): 107–19. http://dx.doi.org/10.1162/jocn_a_00460.

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The default mode network is active during restful wakefulness and suppressed during goal-driven behavior. We hypothesize that inhibitory interference with spontaneous ongoing, that is, not task-driven, activity in the angular gyrus (AG), one of the core regions of the default mode network, will enhance the dominant idling EEG alpha rhythms observed in the resting state. Fifteen right-handed healthy adult volunteers underwent to this study. Compared with sham stimulation, magnetic stimulation (1 Hz for 1 min) over both left and right AG, but not over FEF or intraparietal sulcus, core regions of the dorsal attention network, enhanced the dominant alpha power density (8–10 Hz) in occipitoparietal cortex. Furthermore, right AG-rTMS enhanced intrahemispheric alpha coherence (8–10 Hz). These results suggest that AG plays a causal role in the modulation of dominant low-frequency alpha rhythms in the resting-state condition.

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Vrysis, Lazaros, Leontios Hadjileontiadis, Iordanis Thoidis, Charalampos Dimoulas, and George Papanikolaou. "Enhanced Temporal Feature Integration in Audio Semantics via Alpha-Stable Modeling." Journal of the Audio Engineering Society 69, no. 4 (April 12, 2021): 227–37. http://dx.doi.org/10.17743/jaes.2021.0001.

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Almeida, Maria Leonor Silva, Larissa Marques Peres, and Kleber Melo Silva. "On applying an Enhanced Generalized Alpha Plane to shunt reactor protection." Electric Power Systems Research 212 (November 2022): 108387. http://dx.doi.org/10.1016/j.epsr.2022.108387.

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Manohar, Prasanth, Kodivery Muthukalianan Gothandam, Velu Rajesh Kannan, and Nachimuthu Ramesh. "ENHANCED AMYLOLYTIC ACTIVITY OF INTRACELLULAR alpha-AMYLASE PRODUCED BY BACILLUS TEQUILENSIS." Journal of Microbiology, Biotechnology and Food Sciences 6, no. 6 (June 1, 2017): 1314–18. http://dx.doi.org/10.15414/jmbfs.2017.6.6.1314-1318.

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Journal articles on the topic 'Alpha-enhanced'

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