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Journal articles on the topic 'MAC'

Author: Grafiati

Published: 4 June 2021

Last updated: 30 July 2024

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1

Salameh, Ahlam Ibrahim, Vernon A. Ruffin, and Walter F. Boron. "Effects of metabolic acidosis on intracellular pH responses in multiple cell types." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 307, no. 12 (December 15, 2014): R1413—R1427. http://dx.doi.org/10.1152/ajpregu.00154.2014.

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Metabolic acidosis (MAc), a decrease in extracellular pH (pHo) caused by a decrease in [HCO3−]o at a fixed [CO2]o, is a common clinical condition and causes intracellular pH (pHi) to fall. Although previous work has suggested that MAc-induced decreases in pHi (ΔpHi) differ among cell types, what is not clear is the extent to which these differences are the result of the wide variety of methodologies employed by various investigators. In the present study, we evaluated the effects of two sequential MAc challenges (MAc1 and MAc2) on pHi in 10 cell types/lines: primary-cultured hippocampal (HCN) neurons and astrocytes (HCA), primary-cultured medullary raphé (MRN) neurons, and astrocytes (MRA), CT26 colon cancer, the C2C12 skeletal muscles, primary-cultured bone marrow-derived macrophages (BMDM) and dendritic cells (BMDC), Ink4a/ARF-null melanocytes, and XB-2 keratinocytes. We monitor pHi using ratiometric fluorescence imaging of 2′,7′-bis-(2-carboxyethyl)-5-(and-6)-carboxyfluorescein while imposing MAc: lowering (pHo) from 7.4 to 7.2 by decreasing [HCO3−]o from 22 to 14 mM at 5% CO2 for 7 min. After MAc1, we return cells to the control solution for 10 min and impose MAc2. Using our definition of MAc resistance [(ΔpHi/ΔpHo) ≤ 40%], during MAc1, ∼70% of CT26 and ∼50% of C2C12 are MAc-resistant, whereas the other cell types are predominantly MAc-sensitive. During MAc2, some cells adapt [(ΔpHi/ΔpHo)2 < (ΔpHi/ΔpHo)1], particularly HCA, C2C12, and BMDC. Most maintain consistent responses [(ΔpHi/ΔpHo)2 ≅ (ΔpHi/ΔpHo)1], and a few decompensate [(ΔpHi/ΔpHo)2>(ΔpHi/ΔpHo)1], particularly HCN, C2C12, and XB-2. Thus, responses to twin MAc challenges depend both on the individual cell and cell type.

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2

Nagano, Hiroaki, Takeshi Kinjo, Jiro Fujita, and Tomoo Kishaba. "Radiological findings in nontuberculous mycobacterial pulmonary diseases: A comparison between the Mycobacterium avium complex and the Mycobacterium abscessus complex." PLOS ONE 17, no. 7 (July 21, 2022): e0271660. http://dx.doi.org/10.1371/journal.pone.0271660.

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The Mycobacterium abscessus complex (MABC) comprises rapidly growing mycobacteria and has received increasing attention recently, with an increasing number of associated infections reported worldwide. However, the clinical features of MABC pulmonary disease (MABC-PD), especially in terms of the chest computed tomography (CT) findings, are not fully understood. Thus, this retrospective, cross-sectional study aimed to evaluate the clinical background and chest high-resolution CT (HRCT) findings of MABC-PD in comparison with those of Mycobacterium avium complex PD (MAC-PD). Accordingly, 36 patients with MABC-PD and 65 patients with MAC-PD (defined according to the American Thoracic Society criteria), who were newly diagnosed at four major hospitals in Okinawa (Japan) between January 2012 and December 2017, were analyzed. With respect to their clinical background, only cardiovascular diseases were significantly more common in patients with MABC-PD than in those with MAC-PD (38.9% vs. 18.5%, p = 0.0245). HRCT revealed a significantly higher incidence of low attenuation in patients with MABC-PD than in those with MAC-PD (63.9% vs. 10.8%, p<0.0001). On analyzing only never-smokers (20 and 47 patients with MABC-PD and MAC-PD, respectively), this significant difference remained (65.0% vs. 8.5%, p<0.0001), suggesting MABC infection itself caused low attenuation. In terms of the distribution of abnormal shadows, the involvement of the right lower, left upper, and left lower lobes was more common in patients with MABC-PD than in those with MAC-PD. Furthermore, the mean number of involved lung lobes was significantly higher in patients with MABC-PD than in those with MAC-PD (5.6 vs. 4.7, p<0.001). Although further studies are needed, we assume that the aforementioned radiological features of MABC-PD are due to the high virulence of MABC.

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3

Lin, Kimberly, Lingjun Zhang, Michael Kong, Maojing Yang, Yinghua Chen, Earl Poptic, Melanie Hoffner, Jijun Xu, Connie Tam, and Feng Lin. "Development of an anti-human complement C6 monoclonal antibody that inhibits the assembly of membrane attack complexes." Blood Advances 4, no. 9 (May 11, 2020): 2049–57. http://dx.doi.org/10.1182/bloodadvances.2020001690.

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Abstract Membrane attack complexes (MACs; C5b-9) assembled after complement activation can directly injure self-tissues, leading to various diseases. Eculizumab, a monoclonal antibody (mAb) against complement component C5, is being used in the clinic to treat diseases in which MAC-mediated tissue damage is a primary cause. However, C5 is not a selective target for MAC assembly inhibition, and some patients respond incompletely or not at all to the eculizumab treatment. Therefore, C6, the next essential component in the terminal pathway of complement activation, may be an alternative target for the selective inhibition of MAC formation. Surprisingly, few reports describe a functional blockade of C6 using a specific mAb. Here, we report the development of an anti-human C6 mAb (clone 1C9) that recognizes C6 both in free circulation and within C5b6 complexes. This mAb blocked C7 binding to C5b6 complexes and consequently inhibited MAC formation and protected affected paroxysmal nocturnal hemoglobinuria patient red blood cells from MAC-mediated damage in vitro. In addition, this mAb cross-reacts with rhesus monkey but not mouse complement C6. Finally, 1C9 significantly reduced human complement–mediated intravascular hemolysis in vivo in a mouse model. These results suggest that the anti-C6 mAb holds promise as a new therapeutic agent that selectively targets MAC for many complement-mediated pathological conditions.

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4

Diamond, M. S., and T. A. Springer. "A subpopulation of Mac-1 (CD11b/CD18) molecules mediates neutrophil adhesion to ICAM-1 and fibrinogen." Journal of Cell Biology 120, no. 2 (January 15, 1993): 545–56. http://dx.doi.org/10.1083/jcb.120.2.545.

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We report that a subpopulation (10%) of the Mac-1 (CD1 1b/CD18) molecules on activated neutrophils mediates adhesion to ICAM-1 and fibrinogen. We describe a novel mAb (CBRM1/5) that binds to an activation-specific neoepitope on a subset of Mac-1 molecules on neutrophils and monocytes after stimulation with chemoattractants or phorobol esters but does not recognize Mac-1 on resting myeloid cells. CBRM1/5 immunoprecipitates a subpopulation of Mac-1 molecules from detergent lysates of neutrophils, binds to immunoaffinity-purified Mac-1, and localizes to the I domain on the alpha chain of Mac-1. Because CBRM1/5 recognizes a fraction of Mac-1 on activated neutrophils, but still blocks Mac-1-dependent adhesion to fibrinogen and ICAM-1, we suggest that only a small subset of Mac-1 molecules is competent to mediate adhesion.

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5

Kohl, S., L. S. Loo, F. S. Schmalstieg, and D. C. Anderson. "The genetic deficiency of leukocyte surface glycoprotein Mac-1, LFA-1, p150,95 in humans is associated with defective antibody-dependent cellular cytotoxicity in vitro and defective protection against herpes simplex virus infection in vivo." Journal of Immunology 137, no. 5 (September 1, 1986): 1688–94. http://dx.doi.org/10.4049/jimmunol.137.5.1688.

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Abstract The role of the Mac-1, LFA-1, p150,95 leukocyte glycoprotein family in mediating antiviral host defense was investigated by utilizing mononuclear cells (MC) obtained from eight patients with a genetic deficiency of Mac-1, LFA-1, and p150,95, and normal MC incubated with subunit-specific monoclonal antibodies (MAb) directed against these glycoproteins. As shown with an in vitro chromium-release cytotoxicity assay to herpes simplex virus (HSV)-infected Chang liver target cells, MC of these patients with the severe phenotype or normal MC preincubated with a combination of MAb against Mac-1 glycoprotein subunits were deficient in antibody-dependent cellular cytotoxicity (ADCC). When used individually, MAb directed at LFA-1-alpha or -beta also inhibited ADCC and natural killer cytotoxicity (NKC). In a single cell agarose assay, MC of Mac-1-deficient patients formed fewer effector-target cell conjugates in the presence of specific anti-HSV antibody. To investigate the in vitro contributions of these glycoproteins to cytotoxic host defense mechanisms, two in vivo adoptive transfer models were explored in which neonatal mice are protected against a lethal HSV challenge by normal human MC plus anti-HSV antibody (in vivo ADCC) or human interferon-alpha (NKC stimulated in vivo). In each model, MC from patients with "severe" or "moderate" phenotypes of Mac-1 deficiency, or normal MC incubated with a combination of anti-LFA-alpha, Mac-1-alpha, p150,95-alpha plus -beta MAb failed to protect neonatal mice against lethal HSV infection. These studies further indicate requirements for adhesion-dependent mechanisms in the mediation of MC-ADCC, and suggest that Mac-1-dependent cellular adhesive properties are necessary for normal cytotoxic functions in vivo in experimental models of human ADCC or interferon-stimulated NKC. These findings, in addition to the recognized occurrence of severe or even lethal viral infections in some Mac-1-deficient patients, suggest that glycoproteins of the Mac-1 family may be important determinants of antiviral host defense.

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6

Bush, Elizabeth. "Mac B., Kid Spy: Mac Undercover by Mac Barnett." Bulletin of the Center for Children's Books 72, no. 1 (2018): 7–8. http://dx.doi.org/10.1353/bcc.2018.0548.

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7

Meiyasa, F., N. Taringan, K. U. Henggu, Y. R. Tega, S. Ndahawali, K. E. Zulfamy, M. N. B. Saputro, and I. Priyastiti. "Biological activities of macroalgae in the Moudulung waters: bioactive compounds and antioxidant activity." Food Research 8, no. 1 (January 13, 2024): 82–91. http://dx.doi.org/10.26656/fr.2017.8(1).050.

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This study aimed to determine the bioactive compounds and antioxidant activity of macroalgae in Moudolung Waters. The bioactive compounds in seven samples of macroalgae were extracted with methanol. Analysis of macroalgae bioactive compounds was carried out qualitatively by determining the presence of bioactive compounds including alkaloids, flavonoids, saponins, tannins, phenol hydroquinone, and steroids/ terpenoids. antioxidant activity was carried out using the DPPH (2,2-diphenyl-1-picrylhydrazyl-hydrate) method. Data were analyzed descriptively using Microsoft Excel and all data are expressed as mean. The results showed that these seven macroalgae species have bioactive compounds such as alkaloids, flavonoids, saponins, tannins, phenol hydroquinone, and steroids/terpenoids which function as antioxidants. The highest antioxidant activity was the MA6 (Turbinaria ornate) followed by MA1 (Hormopysa triquetra), MA4 (Ulva flexuosa syn. Enteromorpha flexuosa), MA5 (Eucheuma spinosum), MA2 (Sargassum muticum), MA3 (Gracilaria corticate), and MA7 (Ulva reticulata) were 75.25 mg/mL, 90.31 mg/mL, 134.52 mg/mL, 200.22 mg/mL, 216.91 mg/mL, 259.16 mg/mL, and 270.42 mg/mL, respectively. The results suggested that Turbinaria ornate and Hormopysa triquetra could be used as an important substitute for functional ingredients in foods and pharmaceuticals or nutraceuticals.

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8

Maya, Togolani Godfrey, Erick Vitus Komba, Gloria Ivy Mensah, Peter Masunga Mbelele, Stella George Mpagama, Sayoki Godfrey Mfinanga, Kennedy Kwasi Addo, and Rudovick Reuben Kazwala. "Drug susceptibility profiles and factors associated with non-tuberculous mycobacteria species circulating among patients diagnosed with pulmonary tuberculosis in Tanzania." PLOS ONE 17, no. 3 (March 24, 2022): e0265358. http://dx.doi.org/10.1371/journal.pone.0265358.

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Background While most Non-tuberculous mycobacteria (NTM) are saprophytic, several species have been associated with human diseases, from localized infection to disseminated diseases. Pulmonary NTM infections lead to TB-like disease called NTM pulmonary disease (NTM-PD). Due to variation in treatment options among NTM species, it is necessary to identify the species and determine drug susceptibility profiles to inform the choice of appropriate regimen for the disease. Design A total of 188 culture-positive isolates from patients diagnosed with TB were screened for NTM at the Central Tuberculosis Reference Laboratory. All NTM were further speciated using GenoType® Mycobacterium—Common Mycobacterium and Additional species (GenoType® CM/AS) kit. Mycobacteria avium complex (MAC) and Mycobacteria abscessus complex (MABC) which could not be identified with the test to species were subjected to GenoType® Mycobacteria NTM-DR for further speciation. Using the same test, identified MAC and MABC were genotyped to determine the drug susceptibility profile for each isolate to macrolide and aminoglycosides. Results Of all isolates identified as mycobacteria, 24 (13%) were NTM. Fifteen isolates could be identified to species level of which prevalent species was M. avium sub. intracellulare 4 (27%). A total of 10 isolates were MAC (n = 6) and MABC (n = 4) were subjected to GenoType® Mycobacteria NTM-DR for determination of macrolide and aminoglycoside susceptibility. Three of the four MABC had a mutation at the T28 position of the erm (41). All MAC were susceptible to both drugs. Conclusion In this study, MAC was the most frequently isolated NTM species followed by MABC. While all MAC and MABC identified, were susceptible to aminoglycosides, three MABC were resistant to the macrolides due to mutation at position 28 of the erm (41) gene. For this, it is important for clinicians need to rule out NTM, understand species and their drug susceptibility for optimal case management.

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9

Jeong, Byeong-Ho, Kyeongman Jeon, Hye Yun Park, Seong Mi Moon, Su-Young Kim, Soo-Youn Lee, Sung Jae Shin, Charles L. Daley, and Won-Jung Koh. "Peak Plasma Concentration of Azithromycin and Treatment Responses in Mycobacterium avium Complex Lung Disease." Antimicrobial Agents and Chemotherapy 60, no. 10 (August 1, 2016): 6076–83. http://dx.doi.org/10.1128/aac.00770-16.

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ABSTRACTMacrolides, such as azithromycin (AZM) and clarithromycin, are the cornerstones of treatment forMycobacterium aviumcomplex lung disease (MAC-LD). Current guidelines recommend daily therapy with AZM for cavitary MAC-LD and intermittent therapy for noncavitary MAC-LD, but the effectiveness of these regimens has not been thoroughly investigated. This study evaluated associations between microbiological response and estimated peak plasma concentrations (Cmax) of AZM. The AZMCmaxwas measured in patients receiving daily therapy (250 mg of AZM daily,n= 77) or intermittent therapy (500 mg of AZM three times weekly,n= 89) for MAC-LD and daily therapy forMycobacterium abscessuscomplex LD (MABC-LD) (250 mg of AZM daily,n= 55). The AZMCmaxwas lower with the daily regimen for MAC-LD (median, 0.24 μg/ml) than with the intermittent regimen for MAC-LD (median, 0.65 μg/ml;P< 0.001) or daily therapy for MABC-LD (median, 0.53 μg/ml;P< 0.001). After adjusting for confounding factors, AZMCmaxwas independently associated with favorable microbiological responses in MAC-LD patients receiving a daily regimen (adjusted odds ratio [aOR], 1.58; 95% confidence interval [CI], 1.01 to 2.48;P= 0.044) but not an intermittent regimen (aOR, 0.85; 95% CI, 0.58 to 1.23,P= 0.379). With the daily AZM-based multidrug regimen for MAC-LD, a low AZMCmaxwas common, whereas a higher AZMCmaxwas associated with favorable microbiologic responses. The results also suggested that the addition of rifampin may lower AZMCmax. When a daily AZM-based multidrug regimen is used for treating severe MAC-LD, such as cavitary disease, the currently recommended AZM dose might be suboptimal. (This study has been registered at ClinicalTrials.gov under identifier NCT00970801.)

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10

Crockett-Torabi, E., B. Sulenbarger, C. W. Smith, and J. C. Fantone. "Activation of human neutrophils through L-selectin and Mac-1 molecules." Journal of Immunology 154, no. 5 (March 1, 1995): 2291–302. http://dx.doi.org/10.4049/jimmunol.154.5.2291.

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Abstract The effect of selective cell activation through L-selectin and Mac-1 molecules cross-linking on neutrophil superoxide anion (O2-) generation and changes in intracellular calcium [Ca2+]i was investigated. Cross-linking of L-selectin using different mAbs induced a rapid and transient increase in [Ca2+]i and O2- generation by neutrophils that were dependent on the extent of L-selectin cross-linking and mAb epitope binding. In addition, cross-linking of L-selectin induced an up-regulation of surface Mac-1 expression on neutrophils. Cross-linking of Mac-1 molecules with mAb also induced significant changes in [Ca2+]i levels and O2- generation by neutrophils, which was also dependent on the epitope binding by mAb. Pretreatment of neutrophils with LPS caused a marked decrease in the expression of L-selectin molecules and significant inhibition (i.e., 59 +/- 4%) of anti-L-selectin mAb-dependent O2- generation and [Ca2+]i signal. In contrast, LPS pretreatment caused a significant up-regulation of Mac-1 molecules on neutrophil and enhanced O2- generation by neutrophils. The data indicate that cross-linking of L-selectin and Mac-1 initiates changes in [Ca2+]i and O2- production in neutrophils and suggest that these distinct adhesion molecules independently may play important regulatory roles in modulating neutrophil-endothelial cell interactions, transmigration, and neutrophil function at sites of tissue injury.

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11

Johnson, Kaeli, Oliver Dong, and Xin Li. "The evolutionarily conserved MOS4-associated complex." Open Life Sciences 6, no. 5 (October 1, 2011): 776–84. http://dx.doi.org/10.2478/s11535-011-0043-7.

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AbstractRecent work in plant immunity has shown that MOS4, a known intermediate in R protein mediated resistance, is a core member of the nuclear MOS4-associated complex (MAC). This complex is highly conserved in eukaryotes, as orthologous complexes known as the CDC5L-SNEVPrp19-Pso4 complex and the Nineteen complex (NTC) were previously identified in human and yeast, respectively. The involvement of these complexes in pre-mRNA splicing and spliceosome assembly suggests that the MAC probably has a similar function in plants. Double mutants of any two MAC components are lethal, whereas single mutants of the MAC core components mos4, Atcdc5, mac3, and prl1 are all viable and display pleiotropic defects. This suggests that while the MAC is required for some essential biological function such as splicing, individual MAC components are not crucial for complex functionality and likely have regulatory roles in other biological processes such as plant immunity and flowering time control. Future studies on MAC components in Arabidopsis will provide further insight into the regulatory mechanisms of the MAC on specific biological processes.

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12

van Spriel, Annemiek B., Jeanette H. W. Leusen, Marjolein van Egmond, Henry B. P. M. Dijkman, Karel J. M. Assmann, Tanya N. Mayadas, and Jan G. J. van de Winkel. "Mac-1 (CD11b/CD18) is essential for Fc receptor–mediated neutrophil cytotoxicity and immunologic synapse formation." Blood 97, no. 8 (April 15, 2001): 2478–86. http://dx.doi.org/10.1182/blood.v97.8.2478.

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Abstract Receptors for human immunoglobulin (Ig)G and IgA initiate potent cytolysis of antibody (Ab)-coated targets by polymorphonuclear leukocytes (PMNs). Mac-1 (complement receptor type 3, CD11b/CD18) has previously been implicated in receptor cooperation with Fc receptors (FcRs). The role of Mac-1 in FcR-mediated lysis of tumor cells was characterized by studying normal human PMNs, Mac-1–deficient mouse PMNs, and mouse PMNs transgenic for human FcR. All PMNs efficiently phagocytosed Ab-coated particles. However, antibody-dependent cellular cytotoxicity (ADCC) was abrogated in Mac-1−/− PMNs and in human PMNs blocked with anti–Mac-1 monoclonal Ab (mAb). Mac-1−/− PMNs were unable to spread on Ab-opsonized target cells and other Ab-coated surfaces. Confocal laser scanning and electron microscopy revealed a striking difference in immunologic synapse formation between Mac-1−/− and wild-type PMNs. Also, respiratory burst activity could be measured outside membrane-enclosed compartments by using Mac-1−/− PMNs bound to Ab-coated tumor cells, in contrast to wild-type PMNs. In summary, these data document an absolute requirement of Mac-1 for FcR-mediated PMN cytotoxicity toward tumor targets. Mac-1−/− PMNs exhibit defective spreading on Ab-coated targets, impaired formation of immunologic synapses, and absent tumor cytolysis.

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13

Nolte, D., R. Hecht, P. Schmid, A. Botzlar, M. D. Menger, C. Neumueller, F. Sinowatz, D. Vestweber, and K. Messmer. "Role of Mac-1 and ICAM-1 in ischemia-reperfusion injury in a microcirculation model of BALB/C mice." American Journal of Physiology-Heart and Circulatory Physiology 267, no. 4 (October 1, 1994): H1320—H1328. http://dx.doi.org/10.1152/ajpheart.1994.267.4.h1320.

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The leukocyte beta 2-integrin Mac-1 (CD11b/CD18) and its endothelial ligand intercellular adhesion molecule 1 (ICAM-1) are involved in leukocyte adhesion to and macromolecular leakage from postcapillary venules during inflammatory reactions. Both events are also encountered after ischemia-reperfusion of striated muscle, suggesting a central role of both adhesion proteins in reperfusion injury. Using intravital fluorescence microscopy and a microcirculation model in awake BALB/C mice, we investigated the effects of monoclonal antibodies (MAb) and Fab fragments to Mac-1 and MAb to ICAM-1 on leukocyte-endothelium interaction and macromolecular leakage of fluorescein isothiocyanate-dextran (1.5 x 10(5) mol wt) in striated skin muscle after 3 h of ischemia followed by reperfusion. We demonstrated that administration of MAb and Fab to Mac-1 before reperfusion was as effective as administration of MAb to ICAM-1, which was found to be significantly upregulated in the postischemic tissue by immunohistochemical analysis, in preventing postischemic leukocyte adhesion to and macromolecular leakage from postcapillary venules, whereas postischemic leukocyte rolling was not affected after MAb administration. Postischemic capillary perfusion was efficiently preserved in animals treated with anti-Mac-1 and anti-ICAM-1 MAb compared with animals receiving the isotype-matched control antibodies.(ABSTRACT TRUNCATED AT 250 WORDS)

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Ding, A., S. D. Wright, and C. Nathan. "Activation of mouse peritoneal macrophages by monoclonal antibodies to Mac-1 (complement receptor type 3)." Journal of Experimental Medicine 165, no. 3 (March 1, 1987): 733–49. http://dx.doi.org/10.1084/jem.165.3.733.

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Several features of activation of mouse peritoneal macrophages were elicited by 1-2-d exposure to submicrogram concentrations of anti-Mac-1 (M1/70), a rat monoclonal antibody that reacts with the alpha chain of complement receptor type 3 (Mac-1). The changes induced included enhanced capacity to secrete H2O2 when triggered with PMA, decreased secretion of proteins, increased expression of Ia antigen and decreased phagocytosis of particles. These changes closely resembled those induced by rIFN-gamma in type, extent, and time course. The concentration of M1/70 IgG resulting in 50% of the maximal activation of macrophage H2O2-releasing capacity averaged 0.18 +/- 0.03 micrograms/ml. This activation was not blocked by anti-FcR mAb, and could be reproduced with M18/2, a mAb against beta chain of Mac-1, suggesting that a direct ligation of Mac-1 with mAb was responsible for the activation. Neither depletion of T cells nor addition of neutralizing Abs to IFN-gamma or TNF-alpha prevented M1/70-mediated macrophage activation. Moreover, F(ab')2 of M1/70, or plating of macrophages on C3bi-coated surfaces, inhibited the activation of macrophages by rIFN-gamma. These findings suggest that Mac-1 (CR3) may play an important role in macrophage activation.

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15

Goepfert, Christine, Nadine Regenscheit, Vanessa Schumacher, Simone Roos, Christophe Rossier, Corinne Baehler, Sarah Schmitt, and Horst Posthaus. "Mycobacterium aviumSubsp.aviumInfection in Four Veal Calves: Differentiation from Intestinal Tuberculosis." BioMed Research International 2014 (2014): 1–5. http://dx.doi.org/10.1155/2014/715841.

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Mycobacterium aviumsubsp.avium(Maa) is an intracellular pathogen belonging to theMycobacterium avium-intracellularecomplex (MAC). Reservoirs of MAC are the natural environment, wildlife and domestic animals. In adult bovine, MAC infections are typically caused byMycobacterium aviumsubsp.paratuberculosis(Map). Maa infections in bovine are rarely reported but may cause clinical disease and pathological lesions similar to those observed in paratuberculosis or those induced by members of theMycobacterium tuberculosiscomplex (MTBC). Therefore, differentiation of MAC from MTBC infection should be attempted, especially if unusual mycobacterial lesions are encountered. Four veal calves from a fattening farm dying with clinical signs of otitis media, fever, and weight loss were submitted for necropsy. Samples from affected organs were taken for histologic investigation, bacteriologic culture, and bacterial specification using PCR. Macroscopic thickening of the intestinal mucosa was induced by granulomatous enteritis and colitis. Intracytoplasmic acid-fast bacteria were detected by Ziehl-Neelsen stains and PCR revealed positive results forMycobacterium aviumsubsp.avium. Clinical and pathological changes of Maa infection in veal calves had features ofMycobacterium aviumsubsp.paratuberculosisand the MTBC. Therefore,Mycobacterium tuberculosiscomplex infection should be considered in cases of granulomatous enteritis in calves.

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Schreiber, Melvyn H. "MAC." Academic Radiology 7, no. 6 (June 2000): 456. http://dx.doi.org/10.1016/s1076-6332(00)80389-x.

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Fang, Zhihan, Yu Yang, Shuai Wang, Boyang Fu, Zixing Song, Fan Zhang, and Desheng Zhang. "MAC." Proceedings of the ACM on Interactive, Mobile, Wearable and Ubiquitous Technologies 3, no. 2 (June 21, 2019): 1–24. http://dx.doi.org/10.1145/3328913.

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Issekutz, T. B. "In vivo blood monocyte migration to acute inflammatory reactions, IL-1 alpha, TNF-alpha, IFN-gamma, and C5a utilizes LFA-1, Mac-1, and VLA-4. The relative importance of each integrin." Journal of Immunology 154, no. 12 (June 15, 1995): 6533–40. http://dx.doi.org/10.4049/jimmunol.154.12.6533.

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Abstract The role of the monocyte integrins, Mac-1, LFA-1, and VLA-4, on the adhesion of rat blood monocytes to rat microvascular endothelial cells in vitro and the importance of these receptors in monocyte migration to inflammation in vivo were evaluated. Monocyte adhesion to cytokine (IL-1, IFN-gamma, and TNF-alpha)-stimulated endothelial cells was mediated by Mac-1, LFA-1, and VLA-4, but Mac-1 appeared to be less important than LFA-1 or VLA-4. After i.v. injection, large numbers of 51Cr-labeled blood monocytes migrated within 2 h to dermal inflammatory sites induced by C5a, IL-1 alpha, IFN-gamma, TNF-alpha, LPS, and poly inosinic:cytidylic acid. Anti-Mac-1 mAb treatment had no effect, whereas anti-LFA-1 inhibited migration to C5a and the cytokines by 20 to 40%. Blocking both Mac-1 and LFA-1 decreased monocyte accumulation by 50 to 70% to all stimuli. Anti-VLA-4 inhibited monocyte migration to IL-1 alpha, IFN-gamma, TNF-alpha, and LPS, but not to C5a. Combining anti-Mac-1 with anti-VLA-4 did not increase this inhibition, whereas blocking VLA-4 and LFA-1 together further suppressed (60-85%) migration. Combined treatment with mAb to all three integrins inhibited > 98% of the monocyte migration to the inflammatory stimuli. In conclusion: 1) 51Cr blood monocytes can be used to quantify monocyte migration to inflammatory reactions in the rat. 2) Monocytes use Mac-1, LFA-1, and VLA-4 for in vitro adhesion and in vivo migration to cutaneous inflammation, and these integrins are essential for normal migration because blockade of all three virtually abolishes monocyte accumulation. 3) Mac-1 plays a less important role than LFA-1, as LFA-1 appears to substitute for Mac-1, and VLA-4 and LFA-1 can mediate much of the adhesion and migration. 4) The initiating inflammatory stimulus also modifies monocyte integrin usage, supporting the multistep combinatorial model of leukocyte extravasation.

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Hendrix, Christian, Myah McCrary, Rong Hou, and Getahun Abate. "Diagnosis and Management of Pulmonary NTM with a Focus on Mycobacterium avium Complex and Mycobacterium abscessus: Challenges and Prospects." Microorganisms 11, no. 1 (December 23, 2022): 47. http://dx.doi.org/10.3390/microorganisms11010047.

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Background: Nontuberculous mycobacteria (NTM) are ubiquitous. NTM can affect different organs and may cause disseminated diseases, but the pulmonary form is the most common form. Pulmonary NTM is commonly seen in patients with underlying diseases. Pulmonary Mycobacterium avium complex (MAC) is the most common NTM disease and M. abscessus (MAB) is the most challenging to treat. This review is prepared with the following objectives: (a) to evaluate new methods available for the diagnosis of pulmonary MAC or MAB, (b) to assess advances in developing new therapeutics and their impact on treatment of pulmonary MAC or MAB, and (c) to evaluate the prospects of preventive strategies including vaccines against pulmonary MAC or MAB. Methods: A literature search was conducted using PubMed/MEDLINE and multiple search terms. The search was restricted to the English language and human studies. The database query resulted in a total of 197 publications. After the title and abstract review, 64 articles were included in this analysis. Results: The guidelines by the American Thoracic Society (ATS), European Respiratory Society (ERS), European Society of Clinical Microbiology and Infectious Diseases (ESCMID), and Infectious Diseases Society of America (IDSA) are widely applicable. The guidelines are based on expert opinion and there may be a need to broaden criteria to include those with underlying lung diseases who may not fulfill some of the criteria as ‘probable cases’ for better follow up and management. Some cases with only one culture-positive sputum sample or suggestive histology without a positive culture may benefit from new methods of confirming NTM infection. Amikacin liposomal inhalation suspension (ALIS), gallium containing compounds and immunotherapies will have potential in the management of pulmonary MAC and MAB. Conclusions: the prevalence of pulmonary NTM is increasing. The efforts to optimize diagnosis and treatment of pulmonary NTM are encouraging. There is still a need to develop new diagnostics and therapeutics.

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Zhang, Li, Sébastien Paul, Franck Dumeignil, and Benjamin Katryniok. "Selective Oxidation of Isobutane to Methacrylic Acid and Methacrolein: A Critical Review." Catalysts 11, no. 7 (June 25, 2021): 769. http://dx.doi.org/10.3390/catal11070769.

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Selective oxidation of isobutane to methacrolein (MAC) and methacrylic acid (MAA) has received great interest both in the chemical industry and in academic research. The advantages of this reaction originate not only from the low cost of the starting material and reduced process complexity, but also from limiting the use of toxic reactants and the production of wastes. Successive studies and reports have shown that heteropolycompounds (HPCs) with Keggin structure (under the form of partially neutralized acids with increased stability) can selectively convert isobutane to MAA and MAC due to their strong and tunable acidity and redox properties. This review hence aims to discuss the Keggin-type HPCs that have been used in recent years to catalyze the oxidation of isobutane to MAA and MAC, and to review alternative metal oxides with proper redox properties for the same reaction. In addition, the influence of the main reaction conditions will be discussed.

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IMPERIALE, B. R., R. D. MOYANO, A. B. DI GIULIO, M. A. ROMERO, M. F. ALVARADO PINEDO, M. P. SANTANGELO, G. E. TRAVERÍA, N. S. MORCILLO, and M. I. ROMANO. "Genetic diversity ofMycobacterium aviumcomplex strains isolated in Argentina by MIRU-VNTR." Epidemiology and Infection 145, no. 7 (February 7, 2017): 1382–91. http://dx.doi.org/10.1017/s0950268817000139.

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SUMMARYMycobacterium aviumsp.avium(MAA),M. aviumsp.hominissuis(MAH), andM. aviumsp.paratuberculosis(MAP) are the main members of theM. aviumcomplex (MAC) causing diseases in several hosts. The aim of this study was to describe the genetic diversity of MAC isolated from different hosts. Twenty-six MAH and 61 MAP isolates were recovered from humans and cattle, respectively. GenoType CM®and IS1311-PCR were used to identifyMycobacteriumspecies. The IS901-PCR was used to differentiate between MAH and MAA, while IS900-PCR was used to identify MAP. Genotyping was performed using a mycobacterial interspersed repetitive-unit-variable-number tandem-repeat (MIRU-VNTR) scheme (loci: 292, X3, 25, 47, 3, 7, 10, 32) and patterns (INMV) were assigned according to the MAC-INMV database (http://mac-inmv.tours.inra.fr/). Twenty-two (22/26, 84·6%) MAH isolates were genotyped and 16 were grouped into the following, INMV 92, INMV 121, INMV 97, INMV 103, INMV 50, and INMV 40. The loci X3 and 25 showed the largest diversity (D: 0·5844), and the global discriminatory index (Hunter and Gaston discriminatory index, HGDI) was 0·9300. MAP (100%) isolates were grouped into INMV 1, INMV 2, INMV 11, INMV 8, and INMV 5. The HGDI was 0·6984 and loci 292 and 7 had the largestD(0·6980 and 0·5050). MAH presented a higherDwhen compared with MAP. The MIRU-VNTR was a useful tool to describe the genetic diversity of both MAH and MAP as well as to identify six new MAH patterns that were conveniently reported to the MAC-INMV database. It was also demonstrated that, in the geographical region studied, human MAC cases were produced by MAH as there was no MAA found among the human clinical samples.

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Springer, T. A., L. J. Miller, and D. C. Anderson. "p150,95, the third member of the Mac-1, LFA-1 human leukocyte adhesion glycoprotein family." Journal of Immunology 136, no. 1 (January 1, 1986): 240–45. http://dx.doi.org/10.4049/jimmunol.136.1.240.

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Abstract Monoclonal antibodies specific for p150,95, a third member of the Mac-1 and lymphocyte function-associated antigen-1 (LFA-1) leukocyte adhesion protein family, have been identified and used to study the biochemistry and cellular expression of p150,95. p150,95 is a noncovalently associated heterodimer containing alpha X and beta subunits of Mr = 150,000 and 95,000 respectively. Findings suggest that the p150,95 alpha X beta complex shares a common beta subunit with the alpha L beta LFA-1 and alpha M beta Mac-1 complexes. Co-precipitation experiments demonstrated identity between the p150,95 molecule precipitated by anti-beta MAb and by p150,95-specific MAb. Patients with a previously demonstrated genetic deficiency in Mac-1 and LFA-1 fail to express p150,95. Deficiency of the Mac-1, LFA-1, and p150,95 alpha beta complexes on the surface of patient cells appears due to a defect in the common beta subunit. The lack of cross-reaction of p150,95-specific MAb with LFA-1 and Mac-1, which appear to utilize identical beta subunits, suggests that the determinant is specified by the alpha X rather than the beta subunit of p150,95. The data suggest that alpha X is yet a third member of a family of alpha subunit proteins that associate with a common beta subunit, are differentially regulated in leukocyte differentiation, and function in adhesion reactions. p150,95 is normally expressed on blood monocytes and granulocytes. Chemoattractants such as f-Met-Leu-Phe stimulate a rapid, fivefold increase in surface expression that is not dependent on protein synthesis and appears to reflect mobilization of an intracellular latent pool. The intimate relation between the lack of chemoattractant-stimulated upregulation of p150,95 and Mac-1 by patient granulocytes and their failure to upregulate adhesiveness to these same stimuli in vitro, or to diapedese and migrate into inflammatory sites in vivo, is discussed.

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HUANG, LIBO, LI SHEN, YASHUAI LV, ZHIYING WANG, and KUI DAI. "MAC OR NON-MAC: NOT A PROBLEM." Journal of Circuits, Systems and Computers 23, no. 05 (May 8, 2014): 1450068. http://dx.doi.org/10.1142/s0218126614500686.

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Multicore designs have become the dominant organization for future high performance microprocessors. Instead of increasing cache sizes, clock frequencies, pipeline depths or register file (RF) ports, multicore designs tend to make each processor core simple but highly efficient. This new dimension for improving performance and power efficiency in multicore requires us to rethink processor architecture. Multiply-accumulate (MAC) operation is such a performance improvement technique that needs to be reviewed. MAC operation is the fundamentals of many DSP and multimedia applications, but it tends to be awkward to implement in an orthogonal instruction set architecture (ISA) because of operand bandwidth problem, instruction encoding problem, and hardware cost problem. So a big question is that whether we should support MAC or not in high-efficiency processor designs? This paper does a comparative study on this question and introduce data bandwidth relaxing techniques to eliminate narrow bandwidth provided by two-port RFs. The trade-off are also made to solve the instruction coding and hardware cost problem. So, the new design wisdom becomes that if you support multiply (MUL) operation, then support MAC operation.

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Anderson, D. C., L. J. Miller, F. C. Schmalstieg, R. Rothlein, and T. A. Springer. "Contributions of the Mac-1 glycoprotein family to adherence-dependent granulocyte functions: structure-function assessments employing subunit-specific monoclonal antibodies." Journal of Immunology 137, no. 1 (July 1, 1986): 15–27. http://dx.doi.org/10.4049/jimmunol.137.1.15.

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Abstract MAb directed at the alpha-subunits of Mac-1 (alpha M), LFA-1 (alpha L), p150,95 (alpha X), or their common beta-subunit were used to characterize the contributions of the Mac-1 glycoprotein family to granulocyte adherence reactions. Inhibitory effects of these MAb in incubation experiments with normal granulocytes indicated distinct adhesive contributions of each subunit. Significantly greater adherence, and inhibition of adherence by anti alpha M, alpha X, and beta MAb, was observed under chemotactic conditions designed to "up-regulate" the surface expression of the alpha M beta and alpha X beta complexes. Adherence to protein-coated glass and binding of albumin-coated latex beads were significantly inhibited by anti-beta greater than anti-alpha M (OKM-10, M1/70, LM2/1.6 and OKM-1) greater than anti-alpha X greater than anti-alpha L MAb, but no effects of anti-HLA, AB, or anti-CR-1 MAb were evident. A similar rank order of inhibition was observed in granulocyte aggregation assays in response to C5a, PMA, or f-Met-Leu-Phe. Significant inhibition of directed migration by anti-beta or anti-alpha M (OKM-1 or OKM-10) MAb was observed in subagarose but not Boyden chemotaxis assays; inhibition was dependent on a continuous cell exposure to anti-Mac-1 alpha or beta during the assay, suggesting that a continuum of new Mac-1 expression is required for directed translocation. Phagocytosis of Oil-Red-O paraffin or zymosan selectively opsonized with C3-derived ligands was significantly inhibited by anti-alpha M MAb (OKM-10 greater than LM2/1.6 greater than M1/70 greater than OKM-1) or by combinations of anti-alpha M + anti-CR-1 MAb, but only minimal inhibitory effects of anti-beta MAb and no effects of anti-alpha L or anti-alpha X MAb were seen. Similarly, complement-dependent phagocytosis-associated lactoferrin release, ingestion, and intracellular killing of Staphylococcus aureus 502A, and binding of iC3b-opsonized SRBC, were significantly inhibited by anti-alpha M (OKM-10, M1/70) or combinations of anti-alpha M + anti-CR-1 MAb, but not by anti-beta, alpha L, or alpha X MAb. Notably, none of the anti-Mac-1 MAb demonstrated inhibitory effects in assays of adherence-independent functions including shape change, specific f-Met-Leu-3H-Phe binding, O-2 generation, chemiluminescence evolution, or lactoferrin release in response to PMA.(ABSTRACT TRUNCATED AT 400 WORDS)

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Graham, I. L., and E. J. Brown. "Extracellular calcium results in a conformational change in Mac-1 (CD11b/CD18) on neutrophils. Differentiation of adhesion and phagocytosis functions of Mac-1." Journal of Immunology 146, no. 2 (January 15, 1991): 685–91. http://dx.doi.org/10.4049/jimmunol.146.2.685.

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Abstract Mac-1 is a leukocyte integrin involved in multiple adhesion phenomena and also in the phagocytosis of particles that are bound via CR1 and the IgG FcR. We examined the divalent cation requirements for the Mac-1-dependent processes of adhesion and receptor-mediated phagocytosis. With phorbol ester stimulation, both processes occurred in the absence of extracellular Ca+2. In Ca+2-containing buffer, IB4, an anti-beta 2 mAb, inhibited both adhesion and CR1-mediated ingestion. In the absence of Ca+2, IB4 no longer had any effect on ingestion, although it continued to inhibit adhesion to protein-coated plastic completely. This demonstrates that the role of Mac-1 in adhesion is distinct from its role in phagocytosis. In addition, 1) IB4 did not change intracellular Ca+2 homeostasis; 2) as little as 300 nM free extracellular Ca+2 could restore the ability of IB4 to inhibit ingestion; and 3) in the absence of extracellular Ca+2, Mac-1 was more susceptible to enzymatic cleavage. Together these data suggest a Ca+2-dependent conformational change in Mac-1, which allows distinction of the roles of Mac-1 in phagocytosis and adhesion.

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26

Wang, Li, Xubin Zheng, Jun Ma, Jin Gu, and Wei Sha. "Comparative Proteomic Analysis of Exosomes Derived from Patients Infected with Non-Tuberculous Mycobacterium and Mycobacterium tuberculosis." Microorganisms 11, no. 9 (September 17, 2023): 2334. http://dx.doi.org/10.3390/microorganisms11092334.

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The non-tuberculous mycobacterium (NTM) is a very troublesome opportunistic pathogen, placing a heavy burden on public health. The pathogenesis of NTM pulmonary infection is not well-revealed yet, and its diagnosis is always challenging. This study aimed to use a comprehensive proteomics analysis of plasma exosomes to distinguish patients with rapidly growing NTM M. abscessus (MAB), slowly growing NTM M. intracellulare (MAC), and Mycobacterium tuberculosis (MTB). The identified protein components were quantified with label-free proteomics and determined with a bioinformatics analysis. The complement and coagulation were significantly enriched in patients with Mycobacterium infection, and a total of 24 proteins were observed with up-regulation, which included C1R, C1S, C2, MASP2, C4B, C8B, C9, etc. Of them, 18 proteins were significantly up-regulated in patients with MAB, while 6 and 10 were up-regulated in patients with MAC or MTB, respectively. Moreover, MAB infection was also related to the HIF-1 signaling pathway and phagosome processes, and MTB infection was associated with the p53 signaling pathway. This study provided a comprehensive description of the exosome proteome in the plasma of patients infected with MAB, MAC, and MTB and revealed potential diagnostic and differential diagnostic markers.

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Tandjaoui, Djamel, Messaoud Doudou, and Imed Romdhani. "FH-MAC." International Journal of Grid and High Performance Computing 1, no. 4 (October 2009): 40–56. http://dx.doi.org/10.4018/jghpc.2009070804.

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In this article, the authors propose a new hybrid MAC protocol named H-MAC for wireless mesh networks. This protocol combines CSMA and TDMA schemes according to the contention level. In addition, it exploits channel diversity and provides a medium access control method that ensures the QoS requirements. Using ns-2 simulator, we have implemented and compared H-MAC with other MAC protocol used in Wireless Network. The results showed that H-MAC performs better compared to Z-MAC, IEEE 802.11 and LCM-MAC.

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Baudrillard, Jean. "Mac intox." Lignes 29, no. 3 (1996): 203. http://dx.doi.org/10.3917/lignes0.029.0203.

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29

Baxell, R. "Mac Paps." History Workshop Journal 68, no. 1 (September 1, 2009): 251–59. http://dx.doi.org/10.1093/hwj/dbp013.

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30

Qin, Fei, and John E. Mitchell. "AS-MAC." ACM Transactions on Sensor Networks 10, no. 1 (November 2013): 1–29. http://dx.doi.org/10.1145/2529921.

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31

Frances Webber. "Mac users." Socialist Lawyer, no. 66 (2014): 46. http://dx.doi.org/10.13169/socialistlawyer.66.0046a.

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32

Kim, M., S. Kannan, I. Lee, O. Sokolsky, and M. Viswanathan. "Java-MaC." Electronic Notes in Theoretical Computer Science 55, no. 2 (October 2001): 218–35. http://dx.doi.org/10.1016/s1571-0661(04)00254-3.

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33

Sani, Omeed, and Steven L. Shafer. "MAC Attack?" Anesthesiology 99, no. 6 (December 1, 2003): 1249–50. http://dx.doi.org/10.1097/00000542-200312000-00002.

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34

Sheldrake, Kevin. "Mac attack." New Scientist 205, no. 2746 (February 2010): 27. http://dx.doi.org/10.1016/s0262-4079(10)60300-4.

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35

Tanaka, Yutaka. "MAC system." Journal of the Institute of Television Engineers of Japan 44, no. 12 (1990): 1683–89. http://dx.doi.org/10.3169/itej1978.44.1683.

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36

Weissmann, Gerald. "Jimmy Mac." Nature Genetics 33, no. 4 (April 2003): 445–46. http://dx.doi.org/10.1038/ng0403-445.

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37

Liu, Chin-Jung, Pei Huang, and Li Xiao. "TAS-MAC." ACM Transactions on Sensor Networks 12, no. 1 (March 21, 2016): 1–30. http://dx.doi.org/10.1145/2835180.

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38

Dutta, Prabal, Stephen Dawson-Haggerty, Yin Chen, Chieh-Jan Mike Liang, and Andreas Terzis. "A-MAC." ACM Transactions on Sensor Networks 8, no. 4 (September 2012): 1–29. http://dx.doi.org/10.1145/2240116.2240119.

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39

Hong, Bryan Kun, Chandrika Kumar, and Richard A. Marottoli. "“MAC” Attack." American Journal of Medicine 122, no. 12 (December 2009): 1096–98. http://dx.doi.org/10.1016/j.amjmed.2009.07.005.

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40

Adelsheim, Rebecca. "Maximal Mac." Theater 53, no. 3 (November 1, 2023): 110–20. http://dx.doi.org/10.1215/01610775-10705097.

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41

Bharati, S., and Weihua Zhuang. "CAH-MAC: Cooperative ADHOC MAC for Vehicular Networks." IEEE Journal on Selected Areas in Communications 31, no. 9 (September 2013): 470–79. http://dx.doi.org/10.1109/jsac.2013.sup.0513042.

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42

Priya, B., and S. Solai Manohar. "EE-MAC: Energy Efficient Hybrid MAC for WSN." International Journal of Distributed Sensor Networks 9, no. 12 (January 2013): 526383. http://dx.doi.org/10.1155/2013/526383.

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43

Watfa, Mohamed K., Samir Selman, and Hovig Denkilkian. "UW-MAC: An underwater sensor network MAC protocol." International Journal of Communication Systems 23, no. 4 (November 25, 2009): 485–506. http://dx.doi.org/10.1002/dac.1086.

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44

Kilgore, K. S., J. P. Shen, B. F. Miller, P. A. Ward, and J. S. Warren. "Enhancement by the complement membrane attack complex of tumor necrosis factor-alpha-induced endothelial cell expression of E-selectin and ICAM-1." Journal of Immunology 155, no. 3 (August 1, 1995): 1434–41. http://dx.doi.org/10.4049/jimmunol.155.3.1434.

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Abstract Although TNF-alpha and several products of the activated complement system (e.g., C3b, iC3b, and C5a) are known to modulate endothelial cell function in vitro, relatively little is known about the potential modulatory role of the membrane attack complex (MAC) in endothelial cell activation. Using an in vitro neutrophil-endothelial adhesion assay and a quantitative whole cell ELISA to measure endothelial E-selectin and intracellular adhesion molecule-1 (ICAM-1) expression, we examined the modulatory role of the MAC in TNF-alpha-induced neutrophil-endothelial cell adhesive interactions. Activation of quiescent human umbilical vein endothelial cells (HUVECs) with TNF-alpha results in a concentration-dependent increase in neutrophil adhesion measured at 4 h. Assembly of sublytic concentrations of the MAC on endothelial cells did not result in changes in neutrophil-HUVEC adhesion measured at 4 h. Activation of HUVECs with TNF-alpha followed by assembly of the MAC resulted in a marked increase in neutrophil binding as compared with that observed in cells treated with TNF-alpha alone. Blocking studies of mAb revealed that in either TNF-alpha-stimulated or TNF-alpha and MAC-activated endothelial cells enhanced neutrophil binding was nearly entirely attributable to E-selectin and ICAM-1. This conclusion was further supported by a whole-cell ELISA, which provided evidence that the MAC augments TNF-alpha-induced up-regulation of both E-selectin and ICAM-1. This study provides data that support the conclusion that the distal complement system (MAC) can enhance TNF-alpha-induced proinflammatory endothelial cell functions.

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Gudnavar, Anand, and Manjanaik N. "IF-MAC: Improved Funneling MAC for Wireless Sensor Network." Science & Technology Journal 10, no. 1 (January 1, 2022): 49–55. http://dx.doi.org/10.22232/stj.2022.10.01.07.

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Mahlknecht, S., and M. Spinola Durante. "WUR-MAC: Energy efficient Wakeup Receiver based MAC Protocol." IFAC Proceedings Volumes 42, no. 3 (2009): 79–83. http://dx.doi.org/10.3182/20090520-3-kr-3006.00012.

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47

Injong Rhee, A. Warrier, M. Aia, Jeongki Min, and M. L. Sichitiu. "Z-MAC: A Hybrid MAC for Wireless Sensor Networks." IEEE/ACM Transactions on Networking 16, no. 3 (June 2008): 511–24. http://dx.doi.org/10.1109/tnet.2007.900704.

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Lee, Dongwon, and Sunmyeng Kim. "MPT-MAC: Multi-Packet Transmission MAC Protocol in UWASNs." Applied Mathematics & Information Sciences 11, no. 2 (March 1, 2017): 525–30. http://dx.doi.org/10.18576/amis/110223.

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49

McLarty, C. "SAUNDERS MAC LANE. Saunders Mac Lane: A Mathematical Autobiography." Philosophia Mathematica 15, no. 3 (March 12, 2007): 400–404. http://dx.doi.org/10.1093/philmat/nkm010.

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Knudsen, Lars R., and Chris J. Mitchell. "Analysis of 3gpp-MAC and two-key 3gpp-MAC." Discrete Applied Mathematics 128, no. 1 (May 2003): 181–91. http://dx.doi.org/10.1016/s0166-218x(02)00444-4.

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