Academic literature on the topic 'Hemolytic-assay'

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Journal articles on the topic "Hemolytic-assay"

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Yamada, S., T. Aiba, A. Hattori, T. Suzuki, S. L. Asa, and K. Kovacs. "Reverse Hemolytic Plaque Assay." Pathology - Research and Practice 187, no. 5 (June 1991): 546–51. http://dx.doi.org/10.1016/s0344-0338(11)80140-8.

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Xiao, Hang, Yu-bin Xu, Xia Liu, and De-qiang Dou. "Hemolytic assay for Huangqi Injection." Chinese Herbal Medicines 8, no. 1 (January 2016): 61–66. http://dx.doi.org/10.1016/s1674-6384(16)60009-6.

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Ekdahl, Kristina N., Dan Norberg, Anders A. Bengtsson, Gunnar Sturfelt, Ulf R. Nilsson, and Bo Nilsson. "Use of Serum or Buffer-Changed EDTA-Plasma in a Rapid, Inexpensive, and Easy-To-Perform Hemolytic Complement Assay for Differential Diagnosis of Systemic Lupus Erythematosus and Monitoring of Patients with the Disease." Clinical and Vaccine Immunology 14, no. 5 (March 7, 2007): 549–55. http://dx.doi.org/10.1128/cvi.00486-06.

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ABSTRACT We previously described a simplified quantitative hemolytic assay for classical pathway (CP) hemolytic function in serum that has been shown to correlate with the 50% hemolytic complement (CH50) assay. In the present study, we used this assay to compare CP functions; plasma levels of C3, C4, and C3dg; and ratios of C3dg to C3 in healthy individuals and patients with systemic lupus erythematosus (SLE) or rheumatoid arthritis (RA) with different degrees of complement activation. A significant depression in CP function and levels of C4 and C3 and increased C3dg levels and C3dg/C3 ratios were observed in the SLE patients. In patients with RA, CP function was normal, whereas C3, C4, and C3dg levels and the C3dg/C3 ratio were elevated. The SLE results are compatible with systemic complement consumption, whereas the RA data suggest an acute-phase reaction with a normal C3 catabolic rate. To facilitate the handling of patient samples, we also developed a method to restore the hemolytic function of EDTA-plasma by transferring it to Veronal-buffered saline containing the thrombin inhibitor lepirudin. This process inhibits coagulation and enables complement activation, allowing a longer time lag between sample harvesting and testing. These results, combined with previous correlation studies, suggest that the CP hemolytic assay can effectively replace the CH50 assay for routine SLE differential diagnosis and monitoring of disease activity.
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Tenner, Andrea J., and Michael M. Frank. "A Sensitive Specific Hemolytic Assay for Proenzyme C1." Complement 4, no. 1 (1987): 42–52. http://dx.doi.org/10.1159/000463006.

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Yamada, Shozo. "The reverse hemolytic plaque assay in endocrine pathology." Endocrine Pathology 1, no. 3 (September 1990): 129–31. http://dx.doi.org/10.1007/bf02915389.

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Boyanton, Bobby L., Elizabeth M. Darnell, Anne E. Prada, Dana M. Hansz, and Barbara Robinson-Dunn. "Evaluation of the Lyra Direct Strep Assay To Detect Group A Streptococcus and Group C and G Beta-Hemolytic Streptococcus from Pharyngeal Specimens: TABLE 1." Journal of Clinical Microbiology 54, no. 1 (October 21, 2015): 175–77. http://dx.doi.org/10.1128/jcm.02405-15.

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The Lyra Direct strep assay was compared to culture for its ability to detectStreptococcusgroup A and β-hemolytic groups C/G using rapid antigen-negative pharyngeal specimens (n= 161). The Lyra assay correctly detected all β-hemolytic streptococci (group A,n= 19; group C/G,n= 5). In batch mode, the Lyra assay reduced intralaboratory turnaround time by 60% (18.1 h versus 45.0 h) but increased hands-on time by 96% (3 min 16 s versus 1 min 40 s per specimen).
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Mhatre, A., and W. P. Aston. "A simple hemolytic assay for bovine complement component C3." Veterinary Immunology and Immunopathology 15, no. 3 (June 1987): 239–51. http://dx.doi.org/10.1016/0165-2427(87)90086-9.

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Reis, Kathleen J. "A hemolytic assay for the measurement of equine complement." Veterinary Immunology and Immunopathology 23, no. 1-2 (November 1989): 129–37. http://dx.doi.org/10.1016/0165-2427(89)90115-3.

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Munkvad, S., J. Jespersen, J. Sidelmann, and J. Gram. "Specific, sensitive, precise, and rapid functional chromogenic assay of activated first complement component (C1) in plasma." Clinical Chemistry 36, no. 7 (July 1, 1990): 1305–11. http://dx.doi.org/10.1093/clinchem/36.7.1305.

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Abstract We present a new functional assay for the first complement component (C1) in plasma, based on its activation by inhibition of the C1-esterase inhibitor (C1-inh) when monospecific antiserum to C1-inh is added to the plasma. After maximal activation, we can determine the concentration of activated C1 by using an amidolytic rate assay with a chromogenic substrate. We have optimized the assay conditions with respect to incubation time, concentration of antiserum to C1-inh, ionic strength, and pH. Our method determines specifically the concentration in plasma of free activated C1, not complexes of activated C1 with C1-inh, and is not influenced by the concentration of C1-inh in the test sample. Concentrations of C1 correlated significantly with activities determined by a hemolytic assay (r = 0.55, t = 4.09, P less than 0.001). The estimated interassay CV was 5% and the intra-assay CV was 1%. The sensitivity, imprecision, and practical test performance of our assay are superior to those of conventionally used hemolytic assays.
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Naveed, Khalid, Aqeel Javeed, Muhammad Ashraf, Amjad Riaz, Aamir Ghafoor, and Adeel Sattar. "Effect of nabumetone on humoral immune responses in mice." Arquivo Brasileiro de Medicina Veterinária e Zootecnia 72, no. 3 (May 2020): 915–20. http://dx.doi.org/10.1590/1678-4162-11460.

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ABSTRACT Nabumetone is used to reduce the pain and inflammation in rheumatoid arthritis. In the current study, immunomodulatory effect of Nabumetone is investigated in mice. The control group was administered normal saline orally as placebo. Nabumetone was administered orally via gavage in two treatment groups at 14mg/kg.b.w. doses and 28mg/kgb.w., respectively. Haemagglutination (HA) assay, Jerne hemolytic plaque and mice lethality assays were applied. In HA assay, the titer was significantly decreased in Nabumetone treatment groups (P< 0.001). In Jerne hemolytic plaque formation assay, there was a significant reduction (P< 0.001) in number of plaques in Nabumetone treated groups when compared with control. In mice lethality assay, there was a significant difference in mortality ratio of mice in control and Nabumetone treated groups (P< 0.001). Therefore, it is concluded that Nabumetone suppresses the humoral immune response in mice.
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Dissertations / Theses on the topic "Hemolytic-assay"

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Tran, An Xuong. "Measuring the Changes in Tumor Necrosis Factor-Alpha (TNF-α) from Secretory Populations of U937 Monocytic Cells during Differentiation." Digital Commons @ East Tennessee State University, 2002. https://dc.etsu.edu/etd/685.

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Tumor necrosis factor-alpha (TNF-α) is a cytokine produced primarily by macrophages during acute inflammation. In this study we examined the differential effect of retinoic acid (RA) and phorbol 12-myristate 13-acetate (PMA) on the induction of TNF-α secretion from U937 monocytic cell populations by using the reverse hemolytic plaque assay (RHPA). The RHPA will allow us to investigate both changes in TNF-α secreting populations as well as monitor the relative amount of TNF-α released from individual cells. Our results indicate that treatment of U937 cells with RA (10-6M) moderately increases the secreting cell populations, and dramatically enhances the amount of TNF-α secreted from cells already committed to secretion. In contrast, treatment with PMA (250ng/ml) drastically increased the secreting population, but only slightly increasing the amount of TNF-α released. These results suggest that induction of TNF-α secretion from U937 cells occurs by different pathways.
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Smith, Dorinda Ann. "The Development and Application of a Hemolytic Plaque Forming Cell Assay (PFC) and a Cytotoxic T-Lymphocyte Assay (CTL) in Tilapia (Oreochromis niloticus) for Immunotoxicity Risk Assessment of Environmental Contaminants." Thesis, Virginia Tech, 1998. http://hdl.handle.net/10919/36948.

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The prospect of utilizing the cichlid teleost tilapia (Oreochromis niloticus) as an alternative experimental model to mammals for immunotoxicity risk assessment is currently being proposed. As such, the National Toxicology Program's (NTP) standard battery of rodent immunotoxicity assays is being developed for use in this fish species. Included in the testing series are the hemolytic plaque forming cell (PFC) and the cytotoxic T-lymphocyte (CTL) assays, quantitative indicators of antibody production and cell-mediated activity, respectively. The assays were modified in consideration of specific tilapian immune parameters, then tested using fourteen environmental contaminants or drugs, ten of which are classified by the NTP as immunotoxic in rodents. Reduced antibody production via a decrease in plaque number was observed in response to exposure of tilapia to eight of the nine humoral immunotoxicants, and five of the five non-immunotoxicants. Under specific immunization circumstances, immunostimulation (also a response to immunotoxicity) was noted via an increase in plaque number in benzo[a]pyrene (B[a]P) exposed fish using the PFC assay, a result noted in rodents as well. Reduced T-cell recognition and lysis of allogeneic tilapian lymphocytes via a decrease in the percentage of specific 51Chromium (51Cr) release was observed in response to exposure of tilapia to the nine of the ten cell-mediated immunotoxicants, and four of the four non-immunotoxicants. Although the normal teleost immune responsiveness was slightly weaker than seen with mice under comparable conditions (presumably due to differences in antibody structure and decreased cells counts), tilapia were found to exhibit well-defined humoral and cell-mediated immune responses, and responses to immunotoxic and non-immunotoxic chemicals comparable to the rodent model.
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Book chapters on the topic "Hemolytic-assay"

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Mondal, Haimanti, John Thomas, and Natarajan Amaresan. "Assay of Hemolytic Activity." In Springer Protocols Handbooks, 187–89. New York, NY: Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-3032-7_24.

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Sam-Yellowe, Tobili Y. "Exercise 7: Hemolytic Plaque Assay (The Jerne Plaque Assay)." In Immunology: Overview and Laboratory Manual, 281–87. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-64686-8_31.

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Chabannes, Melchior, Véronique Frémeaux-Bacchi, and Sophie Chauvet. "Detection of C3 Nephritic Factor by Hemolytic Assay." In The Complement System, 147–58. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1016-9_15.

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Khullar, Poonam, Lavanya Tandon, Rajpreet Kaur, and Divya Mandial. "Hemolytic Assay of Biocompatible Nanomaterials in Drug Delivery Systems." In Research Methods and Applications in Chemical and Biological Engineering, 97–132. Series statement: AAP research notes on chemical engineering: Apple Academic Press, 2019. http://dx.doi.org/10.1201/9780429424137-8.

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"Hemolytic Plaque Assay." In Encyclopedia of Immunotoxicology, 372. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-54596-2_100226.

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Bernheimer, Alan W. "[30] Assay of hemolytic toxins." In Microbial Toxins: Tools in Enzymology, 213–17. Elsevier, 1988. http://dx.doi.org/10.1016/s0076-6879(88)65033-6.

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Usha, Usha. "Estimation of Complement C3, C4 and Hemolytic Assay for Serum Complement." In Manual of Immunopathological Techniques, 68. Jaypee Brothers Medical Publishers (P) Ltd., 2014. http://dx.doi.org/10.5005/jp/books/12385_12.

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Croxton, Thomas L., William McD Armstrong, and Nira Ben-Jonathan. "Patch clamp recording from anterior pituitary cells identified by reverse hemolytic plaque assay." In Methods in Enzymology, 144–66. Elsevier, 1989. http://dx.doi.org/10.1016/0076-6879(89)68011-1.

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CROXTON, THOMAS L., WILLIAM McD ARMSTRONG, and NIRA BEN-JONATHAN. "Patch Clamp Recording from Anterior Pituitary Cells Identified by Reverse Hemolytic Plaque Assay." In Neuroendocrine Peptide Methodology, 481–502. Elsevier, 1989. http://dx.doi.org/10.1016/b978-0-12-185150-7.50038-5.

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Mohseni, Mojtaba, Benyamin Djawadi, and Noushin Khazaei. "Escherichia coli O157:H7 and Its Effect on Human Health." In Escherichia coli [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.101825.

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Escherichia coli (E. coli) has many serotypes. The O157:H7 E. coli serotype is the most prominent serotype of enterohemorrhagic E. coli. It produces the Shiga toxin, which is one of the most important virulent factors discovered till today and has different subtypes with different antigenic and molecular traits. Consumption of contaminated water, milk or even eating an uncooked raw meat can cause bloody diarrhea that can end up in a life-threatening disease, such as hemolytic uremic syndrome (HUS). This is a condition that affects endothelial cells in the blood vessels and leads to thrombocytopenic purpura (TTP) that can cause blood clots formation in small blood vessels. The E. coli O157:H7 can be isolated from patient’s stool and be identified by serological tests such as enzyme-linked immunosorbent assay (ELISA) and immunoblotting methods. This special strain of E. coli can be used as a biological weapon, as it can be so dangerous and has the ability to spread easily form person to person.
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Conference papers on the topic "Hemolytic-assay"

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SCHLEGEL, N., J. MOAKE, C. LOIRAT, M. F. HURTAUD, S. LEVY-TOLEDANO, and H. MATHIEU. "CHILDHOOD HEMOLYTIC UREMIC SYNDROME (HUS) : VON WILLEBRAND FACTOR (vWF) AND PLATELET AGGREGATING ACTIVITY (PAA) STUDIES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643475.

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It has been suggested that a vWF High Molecular Weight Multi-mers (HMWM) decrease or a PAA were involved in the pathogenesis of HUS. We have studied 8 children (6 girls,_2 boys; 7 months-8_1/2 years old) with HUS : plasma creatinine /μmol/l; mean(range)/=306 (105-524), hemoglobin (g/100ml)-7(6.3-7.8), schistocytes (%)=8(1-18), platelets (x103/mm3)-57(10-115). The vWF was studied quantitatively (antigen ; vWF RAg assay) and qualitatively (multimeric pattern : immunoblotting and autoradiography). PAA studied by incubating the patient's platelet poor plasma (RPR) with washed normal platelets (aggregometer, % light transmission) and confirmed by Thromboxane B2 (TXB2) assay and [14C] Serotonine release study. The PAA was characterized by studying the in vitro effect of several platelet aggregation inhibitors, Immunoglobulins (Igs) and Fresh Frozen Plasma (FFP) on the platelet aggregation.An increase of vWF RAg (%) was observed in 6 cases : mean:330, and possibly related with renal failure. A vWF HMWM decrease was found in 3 patients : 2/3 with associated infection(E.Coli, Pneumococcus), 1/3 with severe hemolysis. Two of these 3 patients had a favourable renal outcome and 1 a severe course (chronic hemodialysis, Arterial Thrombotic MicroAngiopathy at renal histology).An important PAA was evidenced only in 1 patient : post bone-marrow graft HUS during neuroblastoma(NB),arterial hypertension and chronic renal failure. This PAA was Ca++, TXB2 and cAMP dependent; it was moderately inhibited in vitro by Igs and FFP, but persisted after 5 days of Igs infusion (0.3g/Kg/day). Treatment with aspirin and dipyridamole (10mg/Kg/day each) suppressed the patient platelet auto-aggregation although the PAA persisted (follow up:10months). The PAA did not seem to be related with the NB (absence of GD2 ganglioside, specific marker of NB); it could be related with anti platelet antibodies. The coexistence of the two abnormalities could not be demonstrated in our patients.In conclusion, a vWF HMWM decrease was found in 3 out of 8 children patients with HUS. Its presence was not correlated with the severity of the disease. We could demonstrate the presence of PAA during childhood HUS in only 1 post bone-marrow graft case. The PAA characterization is useful for therapeutic decisions and contributes to a better pathogenetic understanding.
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