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1 gated their antioxidative, antimicrobial and haemolytic activities and their interactions with model
2 we investigated the virulence properties and haemolytic activities of these 2 clonal types using in v
3               Significantly higher levels of haemolytic activity (approximately 16-fold) were observe
4                    Virulence assay indicated haemolytic activity and biofilm formation by the test ba
5 lysing (lecithinase) activity, 1.5 times the haemolytic activity and over seven times the activity to
6 nce of both the major secreted protein and a haemolytic activity from the mutant signalled that the L
7 EF demonstrated that it is CylE that confers haemolytic activity in E. coli.
8 tein of Borrelia burgdorferi by means of its haemolytic activity in Escherichia coli.
9                                              Haemolytic activity in the mutant laboratory strains cou
10 fic lipase that contributes to lipolytic and haemolytic activity in vitro and is required for optimal
11 es tested, H. pinifolia recorded the minimum haemolytic activity of 2.07+/-0.63% at 1000 mug/ml conce
12 ontrast, the reduced concentration and lower haemolytic activity of emm type 1.0 SLO led to transloca
13 ffect on enzymatic activity, it inhibits the haemolytic activity of PlcHR2.
14 580) failed to prevent the contact-dependent haemolytic activity of Shigella.
15 of band 3 function significantly reduced the haemolytic activity of streptolysin S, and dramatically
16                                          The haemolytic activity of the compounds was evaluated again
17  Phe69Cys substitutions markedly reduced the haemolytic activity of the enzyme, our work suggests tha
18                                     Enhanced haemolytic activity of the luxS strain was also shown to
19     Remarkably, LukSF-PV inhibition of LukED haemolytic activity on both human and murine erythrocyte
20                                          The haemolytic activity was erythrocyte-species specific, wi
21                                          The haemolytic activity was shown to be highly protease sens
22 s in cylB, cylF and cylH retaining wild-type haemolytic activity were identified in all strains.
23 response to growth phase, including enhanced haemolytic activity, and a dramatic reduction in the exp
24 ive mutations in vitro, including changes in haemolytic activity, antibiotic susceptibility, and meta
25 e third class had nearly wild-type levels of haemolytic activity, but had a decrease in protein half-
26 e protein which stabilized BlyA and enhanced haemolytic activity.
27 strain, designated 35000-3, lacks detectable haemolytic activity.
28       The first class had a severe defect in haemolytic activity.
29 ytotoxic (brine shrimp leathality assay) and haemolytic activity.
30         In addition, Cyt toxins also display haemolytic activity.
31 cytosolic pool of Ply void of any detectable haemolytic activity.
32 agA in group G streptococcus eliminated beta-haemolytic activity.
33 genetic basis for group G streptococcus beta-haemolytic activity.
34           The fibronectin/fibrinogen-binding/haemolytic-activity/streptokinase-regulator-X (FasX) sRN
35 encoding gene fibronectin/fibrinogen-binding/haemolytic-activity/streptokinase-regulator-X (fasX) wer
36 5% of patients) being pyrexia and autoimmune haemolytic anaemia (seven [7%] each), pneumonia (six [6%
37        Further all the patients with chronic haemolytic anaemia and alcoholic cirrhosis had black pig
38 cretion of 5-oxoproline, metabolic acidosis, haemolytic anaemia and central nervous system damage.
39 ive longer, the chronic effects of sustained haemolytic anaemia and episodic vaso-occlusive events dr
40 angement with leukocytosis, lactic acidosis, haemolytic anaemia and hyperbilirubinemia.
41 opment beginning at about 9 months of severe haemolytic anaemia and several malignant cancers, both o
42  to be clinically important, protect against haemolytic anaemia in hepatitis-C-infected patients rece
43 ations in PIEZO1 cause an autosomal dominant haemolytic anaemia in humans called dehydrated hereditar
44  is erythrocyte age and dose-dependent acute haemolytic anaemia in individuals with glucose-6-phospha
45 erocytosis (HS) is the most common inherited haemolytic anaemia in Northern Europeans.
46 ss the substantial morbidity associated with haemolytic anaemia in sickle cell disease.
47                                          The haemolytic anaemia is characterized by an increase in er
48 ominant role of complement in disease is the haemolytic anaemia of paroxysmal nocturnal haemoglobinur
49  did not have refractory disease, autoimmune haemolytic anaemia requiring treatment, chronic or activ
50 active hepatitis B or C infection; or active haemolytic anaemia were excluded.
51 gressive renal failure, thrombocytopenia and haemolytic anaemia which is a condition rarely seen in a
52                               There was less haemolytic anaemia with fludarabine plus cyclophosphamid
53 ckle cell disease, a debilitating, inherited haemolytic anaemia with premature morbidity and mortalit
54  cause of chronic congenital non-spherocytic haemolytic anaemia worldwide, with an estimated prevalen
55 erse events; one of these deaths (autoimmune haemolytic anaemia) was possibly related to venetoclax.
56 n ratio, ineffective erythropoiesis, chronic haemolytic anaemia, compensatory haemopoietic expansion,
57                Repeated sickling and ongoing haemolytic anaemia, even when subclinical, lead to paren
58 racterised by ineffective erythropoiesis and haemolytic anaemia, leading to long-term complications,
59                        Patients with chronic haemolytic anaemia, such as in thalassaemia, require rep
60  by the triad of non-immune microangiopathic haemolytic anaemia, thrombocytopenia, and acute kidney i
61        Clinically, this disease manifests as haemolytic anaemia, thrombocytopenia, and renal insuffic
62 zed by thrombocytopenia and microangiopathic haemolytic anaemia, was almost universally fatal until t
63 f the most important of these is RBV-induced haemolytic anaemia, which affects most patients and is s
64             PK deficiency results in chronic haemolytic anaemia, with wide ranging and serious conseq
65 ted to erythrocytes and only associated with haemolytic anaemia.
66 rocytic red blood cell morphology and severe haemolytic anaemia.
67 t not Ppara(-/-) mice from PHZ-induced acute haemolytic anaemia.
68 ap mutations associated with non-spherocytic haemolytic anaemia.
69 g for immune thrombocytopenia and autoimmune haemolytic anaemias (AIHAs).
70 erization, in membrane insertion and also in haemolytic and insecticidal activities.
71 ted integrations in cylE were invariably non-haemolytic and non-cytolytic, a finding confirmed by in
72 biofilm, anticancer, anti-inflammatory, anti-haemolytic, and anti-hyperpigmentation activities.
73 aly,weight loss, life-threatening autoimmune haemolytic anemia and hemophagocytosis.
74 en rupture, or to cure refractory autoimmune haemolytic anemia.
75                                          The haemolytic/cytolytic activity of the cylE allelic exchan
76                      Genetic analysis of the haemolytic determinant revealed two borrelia haemolysin
77 tion in antenatal management and outcomes in haemolytic disease of the fetus and newborn between site
78                                  Advances in haemolytic disease of the fetus and newborn have led to
79 variations in the management and outcomes of haemolytic disease of the fetus and newborn in at-risk p
80                        2443 pregnancies with haemolytic disease of the fetus and newborn treated betw
81 udy, data from cases with moderate or severe haemolytic disease of the fetus and newborn were retriev
82                    Up to 88% of infants with haemolytic disease of the fetus and newborn who are trea
83 on is the second most common cause of severe haemolytic disease of the fetus and newborn, after anti-
84 , and subsequent prevention of Rhesus (Rh) D haemolytic disease of the fetus and newborn, is the most
85 after intrauterine transfusion treatment for haemolytic disease of the fetus and newborn.
86 as part of the postnatal treatment of severe haemolytic disease of the fetus and newborn.
87 vention of postnatal anaemia in infants with haemolytic disease of the fetus and newborn.
88  of erythrocyte transfusions in infants with haemolytic disease of the fetus and newborn.
89 unoglobulin (Anti-D Ig) prophylaxis prevents haemolytic disease of the fetus and newborn.
90   Eligible participants had pregnancies with haemolytic disease of the fetus that led to fetal death
91 e has significantly reduced the incidence of haemolytic disease of the foetus and newborn previously
92                            Here, we show non-haemolytic enterotoxin (NHE) from the neglected human fo
93 olates from emerging MTs differed in growth, haemolytic, epithelial infection, and murine colonisatio
94 t, a non-acylated, enzymatically active, non-haemolytic form of AC toxin is able to increase cAMP, re
95 nts with underlying medical conditions, beta-haemolytic group G streptococcus can produce necrotising
96                                         beta-haemolytic group G streptococcus was the sole microbial
97 crotising soft tissue infections due to beta-haemolytic group G streptococcus.
98          Group A streptococcus (GAS), a beta-haemolytic human pathogen, expresses a NEAT protein, Shr
99 i, and a transformant was identified as beta-haemolytic on blood agar.
100            The peptides studied did not show haemolytic or antimicrobial activities, except P#4 (AAGG
101                                     The beta-haemolytic phenotype of group G streptococcus is produce
102 he long-standing mystery of the variable non-haemolytic phenotype of its immediate parent, RN450.
103                    We show here that the non-haemolytic phenotype of RN4220 is caused by an extra A r
104 issociation between agr activity and the non-haemolytic phenotype of RN4220, and has solved the long-
105 eptolysin S (SLS) produces the hallmark beta-haemolytic phenotype produced by GAS.
106 investigated a potential link of shared beta-haemolytic phenotype to disease pathogenesis.
107 - and delta-haemolysins, and hence, in a non-haemolytic phenotype.
108  site, demonstrated attenuated lipolytic and haemolytic phenotypes when compared with the isogenic pa
109 old purification and characterization of the haemolytic phospholipase C (PLC) of Pseudomonas aerugino
110 ariants of Ply: a cell-wall restricted fully haemolytic Ply, and a cytosolic pool of Ply void of any
111                Therapeutic targeting of this haemolytic process may reduce microvascular obstruction
112 aperone PlcR2 affects both the enzymatic and haemolytic properties of PlcH.
113                         Exaggeration of this haemolytic response promoted RBC aggregation and microva
114                                              Haemolytic risk is dependent on treatment dose and patie
115                                        Their haemolytic risk when treated with 8-aminoquinolines has
116                               To predict the haemolytic risk, the amount of drug received from the br
117 ably higher predictive power of drug induced haemolytic risk.
118 orm a national-level index of relative G6PDd haemolytic risk.
119 , together with a national index of relative haemolytic risk.
120 coding the CylA and CylB system by the alpha-haemolytic S. gordonii is presented.
121 2 strain produced large quantities of highly haemolytic SLO that resulted in rapid development of sep
122 mediated illnesses secondary to group A beta-haemolytic streptococcal infections present with motor a
123 Cw6 and environmental triggers, such as beta-haemolytic streptococcal infections, are major determina
124                                         beta-haemolytic streptococci from all positive cultures were
125 with pharyngitis, 107 (24%) had group A beta-haemolytic streptococci on throat culture.
126 corded and a throat culture for group A beta-haemolytic streptococci was done.
127  may occur after infection with group A beta-haemolytic streptococci.
128 ysmal nocturnal haemoglobinuria and atypical haemolytic syndrome has revitalised efforts to target co
129                                              Haemolytic titres, total PlcH protein and beta-galactosi
130 e of eculizumab in the treatment of atypical haemolytic uraemic syndrome (aHUS) as well as the other
131           Most cases of diarrhoea-associated haemolytic uraemic syndrome (HUS) are caused by Shiga-to
132                                              Haemolytic uraemic syndrome (HUS) is a heterogeneous gro
133                                              Haemolytic uraemic syndrome (HUS), which is caused by Sh
134         The largest number of adult cases of haemolytic uraemic syndrome (HUS)/thrombotic thrombocyto
135 c E. coli isolates, including the historical haemolytic uraemic syndrome (HUSEC) E. coli HUSEC041 O10
136  and the treatment of shiga toxin associated haemolytic uraemic syndrome (STEC HUS) is also provided.
137                                              Haemolytic uraemic syndrome is a rarely seen in adults o
138                                              Haemolytic uraemic syndrome is a triad of progressive re
139 their proximity to conserved basic residues, haemolytic uraemic syndrome may result from a failure of
140 sed the large 2011 outbreak of diarrhoea and haemolytic uraemic syndrome secretes blended virulence f
141                The outbreak of diarrhoea and haemolytic uraemic syndrome that occurred in Germany in
142  non-bloody diarrhoea, haemorrhagic colitis, haemolytic uraemic syndrome, and death.
143 udies suggest that treatment may precipitate haemolytic uraemic syndrome, and other studies suggest n
144 aks associated with haemorrhagic colitis and haemolytic uraemic syndrome, which can be fatal.
145 icant, number of infected people develop the haemolytic uraemic syndrome, which is the most frequent
146 sual numbers of cases of bloody diarrhoea or haemolytic uraemic syndrome.
147 ysmal nocturnal haemoglobinuria and atypical haemolytic uraemic syndrome.
148 to lessen the risk of the development of the haemolytic uraemic syndrome.
149 istribution of mutations leading to atypical haemolytic uraemic syndrome.
150 ses diarrhoea, haemorrhagic colitis, and the haemolytic uraemic syndrome.
151  between SCR-16 to SCR-20 is associated with haemolytic uraemic syndrome.
152  some of which included fatalities caused by haemolytic uraemic syndrome.
153 lly thought of as immune-mediated, including haemolytic-uraemic syndrome, diabetic kidney disease and
154 loody diarrhea and acute renal failure(4,5) (haemolytic uremic syndrome).
155 ntified in a clinical isolate in which a non-haemolytic variant had arisen during the course of infec
156 ically heterogeneous in storage, and its non-haemolytic variants had the 8A mutation.
157 ng that ST615 harbours the expression of two haemolytic variants of Ply: a cell-wall restricted fully
158 homology to SlyA, originally thought to be a haemolytic virulence determinant in Salmonella typhimuri

 
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