Laboratory evaluation of antiwear properties of motor oils

1973 ◽  
Vol 9 (11) ◽  
pp. 865-867
Author(s):  
F. N. Ermolov ◽  
M. A. Senichkin ◽  
P. G. Filatov
Keyword(s):  
Laboratory Evaluation ◽  
Antiwear Properties ◽  
Motor Oils

Laboratory evaluation of starting properties of motor oils

1988 ◽  
Vol 24 (11) ◽  
pp. 516-518
Author(s):  
V. N. Bauman ◽  
G. I. Shor ◽  
M. G. Arslanov ◽  
S. M. Kvait ◽  
V. L. Lashkhi ◽  
...  
Keyword(s):  
Laboratory Evaluation ◽  
Motor Oils

Effect of shale-tar additives on antiwear properties of motor oils

1975 ◽  
Vol 11 (12) ◽  
pp. 973-975
Author(s):  
N. I. Zelenin ◽  
E. I. Gulin ◽  
V. S. Demchenko ◽  
E. E. Nikitin ◽  
D. P. Yakubo
Keyword(s):  
Antiwear Properties ◽  
Motor Oils

Qualification test method for rating antiwear properties of motor oils in cam/lifter unit

1976 ◽  
Vol 12 (8) ◽  
pp. 633-636
Author(s):  
B. M. Bunakov ◽  
M. A. Grigor'ev ◽  
V. S. Zavel'skii ◽  
B. M. Kogan
Keyword(s):  
Test Method ◽  
Qualification Test ◽  
Qualification Test Method ◽  
Antiwear Properties ◽  
Motor Oils

Influence of phase composition of ash from additives on antiwear properties of motor oils

1977 ◽  
Vol 13 (4) ◽  
pp. 278-282
Author(s):  
P. G. Filatov ◽  
N. V. Shchegolev ◽  
L. A. Voinova
Keyword(s):  
Phase Composition ◽  
Antiwear Properties ◽  
Motor Oils

Laboratory study of antiwear properties of motor oils

1976 ◽  
Vol 12 (7) ◽  
pp. 560-563
Author(s):  
L. A. Al'tshuler ◽  
I. F. Blagovidov ◽  
V. P. Lapin ◽  
F. G. Sidlyaronok ◽  
G. I. Shor
Keyword(s):  
Laboratory Study ◽  
Antiwear Properties ◽  
Motor Oils

Clinical features and outcome of acquired haemophilia A

2010 ◽  
Vol 30 (03) ◽  
pp. 156-161 ◽  
Author(s):  
R. Gheisari ◽  
B. Bomke ◽  
T. Hoffmann ◽  
R. E. Scharf
Keyword(s):  
Respiratory Diseases ◽  
Care Center ◽  
Treatment Algorithm ◽  
Early Death ◽  
Underlying Disease ◽  
Pulmonary Sarcoidosis ◽  
Relative Increase ◽  
Laboratory Evaluation ◽  
Haemophilia A ◽  
Acquired Haemophilia

SummaryWe have performed a monocenter study on 29 consecutive patients with acquired haemophilia A who were referred for diagnosis and treatment to the Düsseldorf Haemophilia Comprehensive Care Center between March 2001 and February 2010. Patients, methods: 18 men (age: 44–86 years) and 11 women (age: 20–83 years). For laboratory evaluation, a standardized staged protocol of aPTT, FVIII : C activity and concentration, mixing studies with patient and normal plasma, and quantification of inhibitor titers (Bethesda assay) was used. Diagnostic work-up included elaborate examinations for any underlying disease. Results: In 18 (62%) of the 29 patients with acquired haemophilia A, an underlying disorder was identified, including 9 patients with respiratory diseases (31%), 7 patients with autoimmune disorders (24%), one with malignancy, and one with postpartum state, while in 11 patients (38%) acquired haemophilia A remained idiopathic. Haemotherapy of bleeding, suppression or elimination of the inhibitor, and induction of immunotolerance to endogenous FVIII:C were performed according to a treatment algorithm. Predefined clinical endpoints were control of bleeding, eradication of the inhibitor, complete or partial remission (CR, PR), relapse, or early death (≤30 days). Of the 29 patients in total, 22 individuals achieved CR (76%), three had PR, one relapsed, and three died within 30 days (one of acute myocardial infarction while on anti-haemorrhagic treatment, one of sepsis while on immunosuppression due to active acquired haemophilia A, one of lung bleeding in association with pre-existing pulmonary sarcoidosis). Conclusion: This monocenter study demonstrates that control of life-threatening bleeding, eradication of the inhibitor, and induction of tolerance to endogenous FVIII have significantly improved the clinical outcome of acquired haemophilia A. Our data also suggest a shift in underlying disorders associated with acquired haemophilia A, whereby, in comparison to published studies, a relative increase in the proportion of patients with respiratory diseases is present.

Laboratory Evaluation and Clinical Characteristics of 2,132 Consecutive Unselected Patients with Venous Thromboembolism – Results of the Spanish Multicentric Study on Thrombophilia (EMET*-Study)

1997 ◽  
Vol 77 (03) ◽  
pp. 444-451 ◽  
Author(s):  
José Mateo ◽  
Artur Oliver ◽  
Montserrat Borrell ◽  
Núria Sala ◽  
Jordi Fontcuberta ◽  
...  
Keyword(s):  
Venous Thrombosis ◽  
Odds Ratio ◽  
Protein C ◽  
Protein S ◽  
Laboratory Evaluation ◽  
Clinical Factors ◽  
Recurrent Thrombosis ◽  
Heparin Cofactor Ii ◽  
Crude Odds Ratio ◽  
History Of

SummaryPrevious studies on the prevalence of biological abnormalities causing venous thrombosis and the clinical characteristics of thrombotic patients are conflicting. We conducted a prospective study on 2,132 consecutive evaluable patients with venous thromboembolism to determine the prevalence of biological causes. Antithrombin, protein C, protein S, plasminogen and heparin cofactor-II deficiencies, dysfibrinoge-nemia, lupus anticoagulant and antiphospholipid antibodies were investigated. The risk of any of these alterations in patients with familial, recurrent, spontaneous or juvenile venous thrombosis was assessed. The overall prevalence of protein deficiencies was 12.85% (274/2,132) and antiphospholipid antibodies were found in 4.08% (87/2,132). Ten patients (0.47%) had antithrombin deficiency, 68 (3.19%) protein C deficiency, 155 (7.27%) protein S deficiency, 16 (0.75%) plasminogen deficiency, 8 (0.38%) heparin cofactor-II deficiency and 1 had dysfib-rinogenemia. Combined deficiencies were found in 16 cases (0.75%). A protein deficiency was found in 69 of 303 (22.8%) patients with a family history of thrombosis and in 205/1,829 (11.2%) without a history (crude odds ratio 2.34, 95% Cl 1.72-3.17); in 119/665 (17.9%) patients with thrombosis before the age of 45 and in 153/1,425 (10.7%) after the age of 45 (crude odds ratio 1.81, 95% Cl 1.40-2.35); in 103/616 (16.7%) with spontaneous thrombosis and in 171/1,516 (11.3%) with secondary thrombosis (crude odds ratio 1.58, 95% Cl 1.21-2.06); in 68/358 (19.0%) with recurrent thrombosis and in 206/1,774 (11.6%) with a single episode (crude odds ratio 1.78,95% Cl 1.32-2.41). Patients with combined clinical factors had a higher risk of carrying some deficiency. Biological causes of venous thrombosis can be identified in 16.93% of unselected patients. Family history of thrombosis, juvenile, spontaneous and recurrent thrombosis are the main clinical factors which enhance the risk of a deficiency. Laboratory evaluation of thrombotic patients is advisable, especially if some of these clinical factors are present.

Sign in / Sign up

Export Citation Format

Share Document