5 research outputs found
Rocketdyne LOX bearing tester program
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The cause, or causes, for the Space Shuttle Main Engine ball wear were unknown, however, several mechanisms were suspected. Two testers were designed and built for operation in liquid oxygen to empirically gain insight into the problems and iterate solutions in a timely and cost efficient manner independent of engine testing. Schedules and test plans were developed that defined a test matrix consisting of parametric variations of loading, cooling or vapor margin, cage lubrication, material, and geometry studies. Initial test results indicated that the low pressure pump thrust bearing surface distress is a function of high axial load. Initial high pressure turbopump bearing tests produced the wear phenomenon observed in the turbopump and identified an inadequate vapor margin problem and a coolant flowrate sensitivity issue. These tests provided calibration data of analytical model predictions to give high confidence in the positive impact of future turbopump design modification for flight. Various modifications will be evaluated in these testers, since similar turbopump conditions can be produced and the benefit of the modification will be quantified in measured wear life comparisons
Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease
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- Zineldine A.
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- Publication venue
- 'Massachusetts Medical Society'
- Publication date
- 01/01/2017
- Field of study
Background: Experimental and clinical data suggest that reducing inflammation without affecting lipid levels may reduce the risk of cardiovascular disease. Yet, the inflammatory hypothesis of atherothrombosis has remained unproved. Methods: We conducted a randomized, double-blind trial of canakinumab, a therapeutic monoclonal antibody targeting interleukin-1β, involving 10,061 patients with previous myocardial infarction and a high-sensitivity C-reactive protein level of 2 mg or more per liter. The trial compared three doses of canakinumab (50 mg, 150 mg, and 300 mg, administered subcutaneously every 3 months) with placebo. The primary efficacy end point was nonfatal myocardial infarction, nonfatal stroke, or cardiovascular death. RESULTS: At 48 months, the median reduction from baseline in the high-sensitivity C-reactive protein level was 26 percentage points greater in the group that received the 50-mg dose of canakinumab, 37 percentage points greater in the 150-mg group, and 41 percentage points greater in the 300-mg group than in the placebo group. Canakinumab did not reduce lipid levels from baseline. At a median follow-up of 3.7 years, the incidence rate for the primary end point was 4.50 events per 100 person-years in the placebo group, 4.11 events per 100 person-years in the 50-mg group, 3.86 events per 100 person-years in the 150-mg group, and 3.90 events per 100 person-years in the 300-mg group. The hazard ratios as compared with placebo were as follows: in the 50-mg group, 0.93 (95% confidence interval [CI], 0.80 to 1.07; P = 0.30); in the 150-mg group, 0.85 (95% CI, 0.74 to 0.98; P = 0.021); and in the 300-mg group, 0.86 (95% CI, 0.75 to 0.99; P = 0.031). The 150-mg dose, but not the other doses, met the prespecified multiplicity-adjusted threshold for statistical significance for the primary end point and the secondary end point that additionally included hospitalization for unstable angina that led to urgent revascularization (hazard ratio vs. placebo, 0.83; 95% CI, 0.73 to 0.95; P = 0.005). Canakinumab was associated with a higher incidence of fatal infection than was placebo. There was no significant difference in all-cause mortality (hazard ratio for all canakinumab doses vs. placebo, 0.94; 95% CI, 0.83 to 1.06; P = 0.31). Conclusions: Antiinflammatory therapy targeting the interleukin-1β innate immunity pathway with canakinumab at a dose of 150 mg every 3 months led to a significantly lower rate of recurrent cardiovascular events than placebo, independent of lipid-level lowering. (Funded by Novartis; CANTOS ClinicalTrials.gov number, NCT01327846.
Casemix, management, and mortality of patients receiving emergency neurosurgery for traumatic brain injury in the Global Neurotrauma Outcomes Study: a prospective observational cohort study
- Author
- Abbas G.
- Abdallah O. I.
- Abdel-Lateef A.
- Abdifatah K.
- Abdullateef A.
- Abeygunaratne R.
- Aboellil M.
- Adam A.
- Adams R.
- Adeleye A.
- Adeleye A. O.
- Adeolu A.
- Adji N. K.
- Afianti N.
- Agarwal S.
- Aghadi I. K.
- Aguilar P. M. M.
- Ahmad S. R.
- Ahmed D.
- Ahmed N.
- Aizaz H.
- Aji Y. K.
- Al-Habib A.
- Alamri A.
- Alberto A. J. M.
- Alcocer L. A.
- Alfaro L. G.
- Alhourani A.
- Ali S. M. R.
- Alkherayf F.
- AlMenabbawy A.
- Alshareef A.
- Aminullah M. A. S.
- Amjad M.
- Amorim R. L. O. D.
- Anbazhagan S.
- Andrade A.
- Antar W.
- Anyomih T. T. K.
- Aoun S.
- Apriawan T.
- Armocida D.
- Arnold P.
- Arraez M.
- Assefa T.
- Asser A.
- Athiththan S. P.
- Attanayake D.
- Aung M. M.
- Avi A.
- Ayala V. E. A.
- Azab M.
- Azam G.
- Azharuddin M.
- Badejo O.
- Badran M.
- Baig A. A.
- Baig R. A.
- Bajaj A.
- Bajamal A. H.
- Baker P.
- Bala R.
- Balasa A.
- Balchin R.
- Balogun J.
- Ban V. S.
- Bandi B. K. R.
- Bandyopadhyay S.
- Bank M.
- Barthelemy E.
- Bashford T.
- Bashir M. T.
- Basso L. S.
- Basu S.
- Batista A.
- Bauer M.
- Bavishi D.
- Beane A.
- Bejell S.
- Belachew A.
- Belli A.
- Belouaer A.
- Bendahane N. E. A.
- Benjamin O.
- Benslimane Y.
- Benyaiche C.
- Bernucci C.
- Berra L. V.
- Bhebe A.
- Biluts H.
- Bimpis A.
- Blanaru D.
- Bonfim J. C.
- Borba L. A. B.
- Borcek A. O.
- Borotto E.
- Bouhuwaish A. E. M.
- Bourilhon F.
- Brachini G.
- Breedon J.
- Broger M.
- Brunetto G. M. F.
- Bruzzaniti P.
- Budohoska N.
- Budohoski K.
- Burhan H.
- Calatroni M. L.
- Camargo C.
- Cappai P. F.
- Cardali S. M.
- Castano-Leon A. M.
- Cederberg D.
- Celaya M.
- Cenzato M.
- Challa L. M.
- Charest D.
- Chaurasia B.
- Chenna R.
- Cherian I.
- Ching'o J. H.
- Chotai T.
- Choudhary A.
- Choudhary N.
- Choumin F.
- Cigic T.
- Ciro J.
- Clark D.
- Conti C.
- Correa A. C. D. S.
- Cossu G.
- Couto M. P.
- Cruz A.
- D'Aliberti G. A.
- D'Silva D.
- Dampha L.
- Daniel R. T.
- Dapaah A.
- Darbar A.
- Dascalu G.
- Dauda H. A.
- Davies O.
- Delgado-Babiano A.
- Dengl M.
- Despotovic M.
- Devi B. I.
- Devi I.
- Dias C.
- Dirar M.
- Dissanayake M.
- Djimbaye H.
- Dockrell S.
- Dolachee A.
- Dolgopolova J.
- Dolgun M.
- Dow A.
- Drusiani D.
- Dugan A.
- Duong D. T.
- Duong T. K.
- Dziedzic T.
- Ebrahim A.
- El Fatemi N.
- El Helou A. E.
- El Maaqili R. E.
- El Mostarchid B. E.
- El Ouahabi A. E.
- El-Fiki A.
- El-Garci A.
- El-Ghandour N. M. F.
- El-shazly M.
- El-Sobky O.
- Elbaroody M.
- Elhadi M.
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- Publication venue
- 'Elsevier BV'
- Publication date
- 01/01/2022
- Field of study
Physico-chemical characteristics of rice (Oryza Sativa L.) grain imparting resistance and their association with development of rice weevil, Sitophilus oryzae (L.)Â (Coleoptera:Curculionidae)
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- A Ramputha
- A Wenda-Piesik
- AA Osipitan
- AL Marsaro JĂşnior
- AR Souza
- ASA Saad
- B Morallo-Rejesus
- BB Singh
- Bergvinson DJ Garcia-Lara
- BM Ribeiro
- BO Juliano
- C Antunes
- C Haine
- CM Smith
- D Kossou
- D Piesik
- D Seshagiri Rao
- DB Bottega
- DB Reddy
- DR Krishna
- E Ahmad
- EN Chijindu
- F Abebe
- F Hossain
- F Segrove
- FM Lara
- G Sahoo
- GS Prasad
- I Gudrups
- I Mohammad
- IE Nwana
- J Campbell
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- J Siwale
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- KJ Hong
- KK Kalsa
- LJ Bamaiyi
- LL Peters
- LP Ribeiro
- LP Soujanya
- LS Fontes
- M Nagpal
- MO Ashamo
- MS Murad
- NES Lale
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- NL Naveena
- OH Lowry
- P Dobie
- P Dobie
- PA Stevens
- PS Soumia
- RF Ewer
- RW Howe
- SE Lee
- SI Nwaubani
- T Keba
- V Stejskal
- WH McGaughey
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- Field of study
Antiinflammatory therapy with canakinumab for atherosclerotic disease
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- Publication venue
- 'Massachusetts Medical Society'
- Publication date
- Field of study
BACKGROUND: Experimental and clinical data suggest that reducing inflammation without affecting lipid levels may reduce the risk of cardiovascular disease. Yet, the inflammatory hypothesis of atherothrombosis has remained unproved. METHODS: We conducted a randomized, double-blind trial of canakinumab, a therapeutic monoclonal antibody targeting interleukin-1β, involving 10,061 patients with previous myocardial infarction and a high-sensitivity C-reactive protein level of 2 mg or more per liter. The trial compared three doses of canakinumab (50 mg, 150 mg, and 300 mg, administered subcutaneously every 3 months) with placebo. The primary efficacy end point was nonfatal myocardial infarction, nonfatal stroke, or cardiovascular death. RESULTS: At 48 months, the median reduction from baseline in the high-sensitivity C-reactive protein level was 26 percentage points greater in the group that received the 50-mg dose of canakinumab, 37 percentage points greater in the 150-mg group, and 41 percentage points greater in the 300-mg group than in the placebo group. Canakinumab did not reduce lipid levels from baseline. At a median follow-up of 3.7 years, the incidence rate for the primary end point was 4.50 events per 100 person-years in the placebo group, 4.11 events per 100 person-years in the 50-mg group, 3.86 events per 100 person-years in the 150-mg group, and 3.90 events per 100 person-years in the 300-mg group. The hazard ratios as compared with placebo were as follows: in the 50-mg group, 0.93 (95% confidence interval [CI], 0.80 to 1.07; P=0.30); in the 150-mg group, 0.85 (95% CI, 0.74 to 0.98; P=0.021); and in the 300-mg group, 0.86 (95% CI, 0.75 to 0.99; P=0.031). The 150-mg dose, but not the other doses, met the prespecified multiplicity-adjusted threshold for statistical significance for the primary end point and the secondary end point that additionally included hospitalization for unstable angina that led to urgent revascularization (hazard ratio vs. placebo, 0.83; 95% CI, 0.73 to 0.95; P=0.005). Canakinumab was associated with a higher incidence of fatal infection than was placebo. There was no significant difference in all-cause mortality (hazard ratio for all canakinumab doses vs. placebo, 0.94; 95% CI, 0.83 to 1.06; P=0.31). CONCLUSIONS: Antiinflammatory therapy targeting the interleukin-1β innate immunity pathway with canakinumab at a dose of 150 mg every 3 months led to a significantly lower rate of recurrent cardiovascular events than placebo, independent of lipid-level lowering. Copyright © 2017 Massachusetts Medical Society