scholarly journals Estimation of lead in blood donors of Dakshina Kannada population in relation to smoking

2018 ◽  
Vol 30 (4) ◽  
pp. 212
Author(s):  
A. Hashim ◽  
Fathima Haneena ◽  
C.S. Muhammed Rashid
Keyword(s):  
2014 ◽  
Vol 77 (8) ◽  
pp. 426-440 ◽  
Author(s):  
Carmen Freire ◽  
Rosalina Jorge Koifman ◽  
Denys Fujimoto ◽  
Vanessa Cristina de Oliveira Souza ◽  
Fernando Barbosa Jr. ◽  
...  

1996 ◽  
Vol 6 (1) ◽  
pp. 31-36 ◽  
Author(s):  
F. M. Cowan ◽  
A. M. Johnson ◽  
J. Wadsworth ◽  
M. Brennan

Author(s):  
Melek Yanasik ◽  
Fatma Savran Oguz ◽  
Sevgi Kalayoglu Besisik ◽  
Mukadder Huslu ◽  
Gulyuz Ozturk ◽  
...  
Keyword(s):  

2014 ◽  
Vol 52 (01) ◽  
Author(s):  
A Kempinska ◽  
M Krawczyk ◽  
M Klak ◽  
M Blatkiewicz ◽  
F Lammert ◽  
...  

1995 ◽  
Vol 74 (05) ◽  
pp. 1271-1275 ◽  
Author(s):  
C M A Henkens ◽  
V J J Bom ◽  
W van der Schaaf ◽  
P M Pelsma ◽  
C Th Smit Sibinga ◽  
...  

SummaryWe measured total and free protein S (PS), protein C (PC) and factor X (FX) in 393 healthy blood donors to assess differences in relation to sex, hormonal state and age. All measured proteins were lower in women as compared to men, as were levels in premenopausal women as compared to postmenopausal women. Multiple regression analysis showed that both age and subgroup (men, pre- and postmenopausal women) were of significance for the levels of total and free PS and PC, the subgroup effect being caused by the differences between the premenopausal women and the other groups. This indicates a role of sex-hormones, most likely estrogens, in the regulation of levels of pro- and anticoagulant factors under physiologic conditions. These differences should be taken into account in daily clinical practice and may necessitate different normal ranges for men, pre- and postmenopausal women.


1996 ◽  
Vol 76 (06) ◽  
pp. 1004-1008 ◽  
Author(s):  
R C Tait ◽  
Isobel D Walker ◽  
J A Conkie ◽  
S I A M Islam ◽  
Frances McCall

SummaryDespite many reports of individuals with congenital plasminogen deficiency and thrombosis, there is still uncertainty whether heterozygous deficiency represents a real thrombophilic risk factor or simply a coincidental finding. We have addressed this issue by testing for plasminogen deficiency in a cohort of 9611 blood donors. Out of 66 donors with reduced plasminogen activity on two occasions 28 were shown to have a familial deficiency state (including 3 with dysplasminogen-aemia). Our observed prevalence rate for familial plasminogen deficiency, calculated at 2.9/1000 (95% Cl = 1.9-4.2 per 1000), was not significantly different from that calculated from published reports of congenital plasminogen deficiency in thrombotic cohorts (5.4/1000). Furthermore, with only two exceptions, all 80 donors and relatives with familial deficiency were asymptomatic with regard to thrombosis -including a 29 year old donor with suspected compound heterozygous hypoplasminogenaemia. These findings add further weight to the argument that familial heterozygous plasminogen deficiency, at least in isolation, does not constitute a significant thrombotic risk factor. However, it remains uncertain whether plasminogen deficiency, when combined with other thrombophilic conditions, may become more clinically important.


1997 ◽  
Vol 77 (05) ◽  
pp. 0856-0861 ◽  
Author(s):  
N Abuaf ◽  
S Laperche ◽  
B Rajoely ◽  
R Carsique ◽  
A Deschamps ◽  
...  

SummaryIn HIV-1 infection, an increased prevalence of anticardiolipin autoantibodies (aCL) and lupus anticoagulant (LA) has been described. In order to see if these antibodies are isolated or, like in autoimmune diseases, associated with hematological disorders and with antibodies to other phospholipids and to proteins of coagulation, we investigated 3 groups of patients: 1. 342 HIV-1 infected patients, 2. 145 control patients including 61 systemic lupus erythematosus (SLE) patients, 58 patients with a connective tissue disease, 15 patients with stroke, 11 patients with syphilis and 3.100 blood donors. In HIV-1 infection antiprothrombin (aPrT) antibodies were present in 25% of patients, the prevalence of antiphosphatidylcholine antibodies (aPC) (50%) was almost as high as aCL (64%), and 39% had both antibodies. Absorption on liposomes of the latter revealed an heterogeneous mixture of aCL and aPC or cross-reacting antibodies. In contrast with SLE, anti-β2-glycoprotein I (4%), LA (1%), biological false positive test for syphilis (0.3%), thrombosis (p <0.001) were uncommon. In HIV-1 infection, antiphospholipid antibodies do not associate with features linked to them in SLE or syphilis.


1966 ◽  
Vol 16 (01/02) ◽  
pp. 001-017 ◽  
Author(s):  
W Berg ◽  
K Korsan-Bengtsen ◽  
J Ygge

SummaryA one-stage lysis time system containing fibrinogen, streptokinase, thrombin, and a known, small amount of plasminogen was used to determine plasminogen in plasma.The known amount of plasminogen was added to the system in order to keep the lysis times relatively short when a highly diluted plasma was tested. High dilutions of plasma were used to reduce the influence of the plasma inhibitors.The calculation of the plasminogen concentration was made on the basis of the correlation: “plasminogen = fibrinogen/lysis time” which was valid in the system. The method allowed determination of plasminogen in plasma with varying fibrinogen concentrations, as the fibrinogen concentration in plasma was considered in the calculation.The presence of “spontaneous” plasmin activity in the plasma did not influence the plasminogen determination. Estimated by this method, the plasminogen content in plasma from 32 blood donors aged 25-45 years was 13.1 ±2.4 casein u/ml. The error of a single determination was 0.3 casein u/ml. The plasminogen content in plasma, determined with the present method, is about 3-4 times higher than the content found when a caseinolytic method is used.


1979 ◽  
Author(s):  
R. Kotitschke ◽  
J. Scharrer

F.VIII R:Ag was determined by quantitative immunelectrophoresis (I.E.) with a prefabricated system. The prefabricated system consists of a monospecific f.VIII rabbit antiserum in agarose on a plastic plate for the one and two dimensional immunelectrophoresis. The lognormal distribution of the f.VIII R:Ag concentration in the normal population was confirmed (for n=70 the f.VIII R:Ag in % of normal is = 95.4 ± 31.9). Among the normal population there was no significant difference between blood donors (one blood donation in 8 weeks; for n=43 the f.VIII R:Ag in % of normal is = 95.9 ± 34.0) and non blood donors (n=27;f.VIII R:Ag = 94.6 ± 28.4 %). The f.VIII R:Ag concentration in acute hepatitis B ranged from normal to raised values (for n=10, a factor of 1.8 times of normal was found) and was normal again after health recovery (n=10, the factor was 1.0). in chronic hepatitis the f.VIII R:Ag concentration was raised in the majority of the cases (for n=10, the factor was 3.8). Out of 22 carrier sera 20 showed reduced, 2 elevated levels of the f.VIII R:Ag concentration. in 5 sera no f.VIII R:Ag could be demonstrated. The f.VIII R:Ag concentration was normal for n=10, reduced for n=20 and elevated for n=6 in non A-non B hepatitis (n=36). Contrary to results found in the literature no difference in the electrophoretic mobility of the f.VIII R:Ag was found between hepatitis patients sera and normal sera.


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