4 research outputs found
Iron Behaving Badly: Inappropriate Iron Chelation as a Major Contributor to the Aetiology of Vascular and Other Progressive Inflammatory and Degenerative Diseases
- Author
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- The Long-Term Intervention with Pravastatin in Ischaemic Disease (LIPID) Study Group
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- ZZ Chong
- Publication venue
- Publication date
- 09/08/2008
- Field of study
The production of peroxide and superoxide is an inevitable consequence of
aerobic metabolism, and while these particular "reactive oxygen species" (ROSs)
can exhibit a number of biological effects, they are not of themselves
excessively reactive and thus they are not especially damaging at physiological
concentrations. However, their reactions with poorly liganded iron species can
lead to the catalytic production of the very reactive and dangerous hydroxyl
radical, which is exceptionally damaging, and a major cause of chronic
inflammation. We review the considerable and wide-ranging evidence for the
involvement of this combination of (su)peroxide and poorly liganded iron in a
large number of physiological and indeed pathological processes and
inflammatory disorders, especially those involving the progressive degradation
of cellular and organismal performance. These diseases share a great many
similarities and thus might be considered to have a common cause (i.e.
iron-catalysed free radical and especially hydroxyl radical generation). The
studies reviewed include those focused on a series of cardiovascular, metabolic
and neurological diseases, where iron can be found at the sites of plaques and
lesions, as well as studies showing the significance of iron to aging and
longevity. The effective chelation of iron by natural or synthetic ligands is
thus of major physiological (and potentially therapeutic) importance. As
systems properties, we need to recognise that physiological observables have
multiple molecular causes, and studying them in isolation leads to inconsistent
patterns of apparent causality when it is the simultaneous combination of
multiple factors that is responsible. This explains, for instance, the
decidedly mixed effects of antioxidants that have been observed, etc...Comment: 159 pages, including 9 Figs and 2184 reference
Single-dose administration and the influence of the timing of the booster dose on immunogenicity and efficacy of ChAdOx1 nCoV-19 (AZD1222) vaccine: a pooled analysis of four randomised trials.
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- Elsevier
- Publication date
- 01/02/2021
- Field of study
BACKGROUND: The ChAdOx1 nCoV-19 (AZD1222) vaccine has been approved for emergency use by the UK regulatory authority, Medicines and Healthcare products Regulatory Agency, with a regimen of two standard doses given with an interval of 4-12 weeks. The planned roll-out in the UK will involve vaccinating people in high-risk categories with their first dose immediately, and delivering the second dose 12 weeks later. Here, we provide both a further prespecified pooled analysis of trials of ChAdOx1 nCoV-19 and exploratory analyses of the impact on immunogenicity and efficacy of extending the interval between priming and booster doses. In addition, we show the immunogenicity and protection afforded by the first dose, before a booster dose has been offered. METHODS: We present data from three single-blind randomised controlled trials-one phase 1/2 study in the UK (COV001), one phase 2/3 study in the UK (COV002), and a phase 3 study in Brazil (COV003)-and one double-blind phase 1/2 study in South Africa (COV005). As previously described, individuals 18 years and older were randomly assigned 1:1 to receive two standard doses of ChAdOx1 nCoV-19 (5 × 1010 viral particles) or a control vaccine or saline placebo. In the UK trial, a subset of participants received a lower dose (2·2 × 1010 viral particles) of the ChAdOx1 nCoV-19 for the first dose. The primary outcome was virologically confirmed symptomatic COVID-19 disease, defined as a nucleic acid amplification test (NAAT)-positive swab combined with at least one qualifying symptom (fever ≥37·8°C, cough, shortness of breath, or anosmia or ageusia) more than 14 days after the second dose. Secondary efficacy analyses included cases occuring at least 22 days after the first dose. Antibody responses measured by immunoassay and by pseudovirus neutralisation were exploratory outcomes. All cases of COVID-19 with a NAAT-positive swab were adjudicated for inclusion in the analysis by a masked independent endpoint review committee. The primary analysis included all participants who were SARS-CoV-2 N protein seronegative at baseline, had had at least 14 days of follow-up after the second dose, and had no evidence of previous SARS-CoV-2 infection from NAAT swabs. Safety was assessed in all participants who received at least one dose. The four trials are registered at ISRCTN89951424 (COV003) and ClinicalTrials.gov, NCT04324606 (COV001), NCT04400838 (COV002), and NCT04444674 (COV005). FINDINGS: Between April 23 and Dec 6, 2020, 24 422 participants were recruited and vaccinated across the four studies, of whom 17 178 were included in the primary analysis (8597 receiving ChAdOx1 nCoV-19 and 8581 receiving control vaccine). The data cutoff for these analyses was Dec 7, 2020. 332 NAAT-positive infections met the primary endpoint of symptomatic infection more than 14 days after the second dose. Overall vaccine efficacy more than 14 days after the second dose was 66·7% (95% CI 57·4-74·0), with 84 (1·0%) cases in the 8597 participants in the ChAdOx1 nCoV-19 group and 248 (2·9%) in the 8581 participants in the control group. There were no hospital admissions for COVID-19 in the ChAdOx1 nCoV-19 group after the initial 21-day exclusion period, and 15 in the control group. 108 (0·9%) of 12 282 participants in the ChAdOx1 nCoV-19 group and 127 (1·1%) of 11 962 participants in the control group had serious adverse events. There were seven deaths considered unrelated to vaccination (two in the ChAdOx1 nCov-19 group and five in the control group), including one COVID-19-related death in one participant in the control group. Exploratory analyses showed that vaccine efficacy after a single standard dose of vaccine from day 22 to day 90 after vaccination was 76·0% (59·3-85·9). Our modelling analysis indicated that protection did not wane during this initial 3-month period. Similarly, antibody levels were maintained during this period with minimal waning by day 90 (geometric mean ratio [GMR] 0·66 [95% CI 0·59-0·74]). In the participants who received two standard doses, after the second dose, efficacy was higher in those with a longer prime-boost interval (vaccine efficacy 81·3% [95% CI 60·3-91·2] at ≥12 weeks) than in those with a short interval (vaccine efficacy 55·1% [33·0-69·9] at <6 weeks). These observations are supported by immunogenicity data that showed binding antibody responses more than two-fold higher after an interval of 12 or more weeks compared with an interval of less than 6 weeks in those who were aged 18-55 years (GMR 2·32 [2·01-2·68]). INTERPRETATION: The results of this primary analysis of two doses of ChAdOx1 nCoV-19 were consistent with those seen in the interim analysis of the trials and confirm that the vaccine is efficacious, with results varying by dose interval in exploratory analyses. A 3-month dose interval might have advantages over a programme with a short dose interval for roll-out of a pandemic vaccine to protect the largest number of individuals in the population as early as possible when supplies are scarce, while also improving protection after receiving a second dose. FUNDING: UK Research and Innovation, National Institutes of Health Research (NIHR), The Coalition for Epidemic Preparedness Innovations, the Bill & Melinda Gates Foundation, the Lemann Foundation, Rede D'Or, the Brava and Telles Foundation, NIHR Oxford Biomedical Research Centre, Thames Valley and South Midland's NIHR Clinical Research Network, and AstraZeneca
Role of K+ Channels in M2 Muscarinic Receptor-Mediated Inhibition of Noradrenaline Release From the Rat Stomach
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- Adams DJ Harper AA
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- Publication venue
- 'Japanese Pharmacological Society'
- Publication date
- 01/01/2004
- Field of study
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- Björse G
- Blaauw M
- Blackburn TM
- Blarquez O
- Blois JL
- Blois JL
- Blois JL
- Blois JL
- Blois JL
- Blois JL.
- Blois JL.
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- Blonder B
- Blonder B
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- Blonder B.
- Blonder B.
- Blytt A.
- Bobek P
- Bocherens H.
- Bogotá-Angel RG
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- Bond WJ
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- Booth RK
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- Borregaard MK
- Botkin DB
- Bottema S
- Bottema S.
- Boyd WE
- Boyer AG
- Boyle JF.
- Brachi B
- Bradley RS.
- Bradshaw EG
- Bradshaw RHW
- Bradshaw RHW
- Bradshaw RHW
- Bradshaw RHW
- Bradshaw RHW
- Bradshaw RHW
- Bradshaw RHW
- Bradshaw RHW
- Bradshaw RHW
- Bradshaw RHW
- Bradshaw RHW
- Bradshaw RHW
- Bradshaw RHW.
- Bradshaw RHW.
- Bradshaw RHW.
- Bradshaw RHW.
- Bradshaw RHW.
- Bradshaw RHW.
- Bradshaw WE
- Bramwell D
- Bramwell D
- Brede N
- Brewer S
- Brewer S
- Brewer S
- Brewer S
- Bridgewater P
- Brito-Morales I
- Britton AJ
- Britton AJ
- Britton AJ
- Brncic TM
- Brock WA
- Broennimann O
- Brook EJ
- Brooker RW
- Brown CD
- Brown KJ
- Brown KJ
- Brown SK
- Browne Ribeiro AT.
- Brugger SO
- Brussel T
- Buckley LB.
- Bunting L
- Bunting MJ
- Bunting MJ
- Bunting MJ
- Burke MJW
- Burney DA
- Burney DA
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- Burney DA
- Burney DA
- Burney DA
- Burney DA.
- Burney DA.
- Burney DA.
- Burney DA.
- Burney DA.
- Burney DA.
- Burrows MT
- Burrows MT
- Burthe SJ
- Bush MB
- Bush MB
- Bush MB
- Bush MB
- Bush MB
- Bush MB
- Bush MB
- Bush MB
- Bush MB
- Bush MB
- Bush MB
- Bush MB
- Bush MB
- Bush MB
- Bush MB
- Bush MB
- Bush MB
- Bush MB
- Bush MB.
- Bush MB.
- Caballero-Rodríguez D
- Cain ML
- Cain ML
- Calcote RR.
- Calder WJ
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- Camill P
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- Carstensen J
- Carter RN
- Carter VA
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- Caseldine CJ
- Castilla-Beltrán A
- Castilla-Beltrán A
- Castiñeira Latorre C
- Catalan J
- Catullo RA
- Cañellas-Boltà N
- Cañellas-Boltà N
- Chadwick OA
- Chalk TB
- Chamberlin TC.
- Chambers FM
- Chambers FM
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- Chandler MEJ.
- Chape S
- Chapin FS
- Chapin FS.
- Chase JM
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- Cheddadi R
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- Chepstow-Lusty A
- Chiarucci A
- Chu C-J
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- Cole A
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- Cole KL.
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- Coleman JS
- Colinvaux PA
- Colinvaux PA
- Colinvaux PA
- Colinvaux PA
- Colinvaux PA.
- Collier MJ
- Collignon AM
- Collins AF
- Colloff MJ
- Colombaroli D
- Colombaroli D
- Colombaroli D
- Colombaroli D
- Colombaroli D
- Colwell RK
- Comandini O
- Combourieu-Nebout N
- Conedera M
- Conedera M
- Connell JH
- Connell JH.
- Connor SE
- Connor SE
- Connor SE
- Connor SE
- Contamin R
- Cook ER
- Cook ER
- Cooper A
- Corlett RT
- Corlett RT
- Corlett RT.
- Corlett RT.
- Corner EJH.
- Correa-Metrio A
- Correa-Metrio A
- Correa-Metrio A
- Correa-Metrio A
- Cossart E
- Costanza R
- Costanza R
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- Cowles HC.
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- Crausbay SD
- Crawley MJ.
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- Croudace IW
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- Cui Q-Y
- Curtis JT.
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- Cázares E
- Côté IM
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- Dakos V
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- Davis BAS
- Davis MA.
- Davis MB
- Davis MB
- Davis MB
- Davis MB
- Davis MB
- Davis MB
- Davis MB
- Davis MB
- Davis MB
- Davis MB.
- Davis MB.
- Davis MB.
- Davis MB.
- Davis MB.
- Davis MB.
- Davis MB.
- Davis MB.
- Davis MB.
- Davis MB.
- Davis MB.
- Davis MB.
- Davis MB.
- Davis MB.
- Davis MB.
- Davis MB.
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- Davis RB
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- de Boer EJ
- de Boer EJ
- de Boer EJ
- de Lafontaine G
- de Lafontaine G
- de Nascimento L
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- de Witte LC
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- Delcourt HR
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- Delcourt PA
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- deMenocal P
- Denevan WM.
- Denham TP
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- Dickie IA
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- Dietl GP.
- Dillehay TD
- DiMichele WA
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- Dobrowski SZ
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- Dubois N
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- D’Antoni HL
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- Erdtman G
- Erdtman G.
- Erichsen EO
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- Espíndola A
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- Field MH
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- Figueroa-Rangel BL
- Finch J
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- Finsinger W
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- Firbas F.
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- Fischer JM
- Fisher CT
- Fitzpatrick MC
- Fitzpatrick MC
- Flagmeier M
- Flantua SGA
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- Flenley JR
- Flenley JR
- Flenley JR
- Flenley JR
- Flenley JR.
- Flenley JR.
- Flenley JR.
- Flenley JR.
- Flenley JR.
- Flessa KW
- Flessa KW
- Flessa KW.
- Fletcher M-S
- Fletcher M-S
- Fletcher M-S
- Fletcher M-S
- Foley JA
- Folke C
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- Forcier LK.
- Fordham DA
- Fordham DA
- Forest F
- Forman RTT
- Fortes GG
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- Fyfe RM.
- Fyfe RM.
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- Garzón MB
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- Gaüzère P
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- Gelorini V
- Giarrizzo E
- Gienapp P
- Giesecke T
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- Giesecke T
- Giesecke T
- Giesecke T
- Giesecke T
- Giesecke T
- Giesecke T
- Giesecke T
- Giesecke T
- Giesecke T
- Giesecke T.
- Giesecke T.
- Giesecke T.
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- Gilbert B
- Gilbert FS.
- Gill JL
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- Githumbi EN
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- Granoszewski W.
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- Hewitt GM.
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- Jacobson GL.
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