Philip Morris
Passive Smoking Severely Decreases Platelet Sensitivity to Antiaggregatory Prostaglandins
Fields
- Author
- Kefalides, A.
- Sinzinger, H.
- Area
- SCIENTIFIC AFFAIRS/BLACK LATERAL OLD S&T
- Type
- PSCI, PUBLICATION SCIENTIFIC
- FOOT, FOOTNOTES
- Site
- R529
- Named Organization
- Fonds Zur Forderung Wissenschaftlichen F
- Master ID
- 2023511661/2307
- 2023511661-2307 Environmental Tobacco Smoke and Heart Disease
- 2023511710 the Relationship of Passive Smoking to Various Health Outcomes Among Seventh-Day Adventists in California.
- 2023511714-1718 Passive Smoking and the Risk of Heart Attack or Coronary Death
- 2023511722-1727 Effects of Passive Smoking on Ischemic Heart Disease Mortality of Nonsmokers A Prospective Study
- 2023511728 Erratum
- 2023511729 'effects of Passive Smoking on Ischemic Heart Disease Mortality of Nonsmokers: A Prospective Study'
- 2023511730 the First Author Replies
- 2023511734-1737
- 2023511738-1744 Passive Smoking in Females and Coronary Heart Disease
- 2023511749-1756 Original Contributions Heart Disease Mortality in Nonsmokers Living with Smokers
- 2023511760-1781 Lung Cancer in Japan: Effects of Nutrition and Passive Smoking
- 2023511785-1789 Passive Smoking and Cardiorespiratory Health in A General Population in the West of Scotland
- 2023511790 Passive Smoking and Cardiorespiratory Health in Scotland
- 2023511791-1792 Passive Smoking and Cardiorespiratory Health in Scotland
- 2023511793-1795 Passive Smoking and Cardiorespiratory Health in Scotland
- 2023511800-1802 Public Health Briefs Passive Smoking and 20-Year Cardiovascular Disease Mortality Among Nonsmoking Wives, Evans County, Georgia
- 2023511806-1816 Relationship of Passive Smoking to Risk of Lung Cancer and Other Smoking-Associated Diseases
- 2023511818 Increased Incidence of Heart Attacks in Nonsmoking Women Married to Smokers
- 2023511822-1824 Cvd Epidemiology Newsletter
- 2023511829-1841 Original Contributions Effects of Passive Smoking in the Multiple Risk Factor Intervention Trial
- 2023511842 Re: 'effects of Passive Smoking in the Multiple Risk Factor Intervention Trial'
- 2023511843-1844 Re: 'effects of Passive Smoking in the Multiple Risk Factor Intervention Trial'
- 2023511845 Re: 'effects of Passive Smoking in the Multiple Risk Factor Intervention Trial'
- 2023511846 the Authors Reply
- 2023511849-1853 Smoking As A Risk Factor for Cerebral Ischemia
- 2023511857-1862 Urinary Cotinine Measurement in Patients with Buerger's Disease - Effects of Active and Passive Smoking on the Disease Process
- 2023511865-1881 An Estimate of Adult Mortality in the United States From Passive Smoking
- 2023511882 Editorial Cardiovascular Risks of Environmental Tobacco Smoke
- 2023511883-1887 An Estimate of Adult Mortality in the United States From Passive Smoking: A Response
- 2023511888-1890 An Estimate of Adult Mortality in the United States From Passive Smoking: A Response
- 2023511891-1892 Ischemic Heart Disease: Response to Lee
- 2023511893-1895 Rebuttal to Lee / Katzenstein Commentary on Passive Smoking Risk
- 2023511896-1899 An Estimate of Adult Mortality in the United States From Passive Smoking: A Response
- 2023511900-1906 An Estimate of Adult Mortality in the United States From Passive Smoking: A Response to Criticism
- 2023511908-1911 Deaths From Lung Cancer and Ischemic Heart Disease Due to Passive Smoking in New Zealand
- 2023511912 Deaths From Lung Cancer and Ischemic Heart Disease Due to Passive Smoking in New Zealand
- 2023511913 Passive Smoking in New Zealand
- 2023511914 Passive Smoking in New Zealand
- 2023511915 Passive Smoking in New Zealand
- 2023511916 Passive Smoking and Passive Thinking
- 2023511918-1937 Cardiovascular Diseases and the Work Environment A Critical Review of the Epidemiological Literature on Chemical Factors
- 2023511939-1950 Clinical Progress Series Passive Smoking and Heart Disease Epidemiology, Physiology, and Biochemistry
- 2023511952-1957 Review Passive Smoking and the Risk of Heart Disease
- 2023511958-1961 Aha Medical / Scientific Statement Position Statement Environmental Tobacco Smoke and Cardiovascular Disease A Position Paper From the Council on Cardiopulmonary and Critical Care, American Heart Association
- 2023511965-1983 the Health Consequences of Involuntary Smoking A Report of the Surgeon General
- 2023511985-1998 Environmental Tobacco Smoke Measuring Exposures and Assessing Health Effects
- 2023512000-2015 Environmental Tobacco Smoke Proceedings of the International Symposium at Mcgill University 890000 Environmental Tobacco Smoke and Cardiovascular Disease: A Critique of the Epidemiological Literature and Recommendations for Future Research
- 2023512016-2028 Panel Discussion on Cardiovascular Disease
- 2023512030-2037 Indoor Air Quality and Ventilation Environmental Tobacco Smoke (Ets) and Cardiovascular Disease
- 2023512039-2054 A Critique of the Methods Used to Assess the Toxic Effects on Man of Combustion Products.
- 2023512056-2066 Coronary Heart Disease and Involuntary Smoking
- 2023512068-2077 7. Environmental Tobacco Smoke and Coronary Heart Disease
- 2023512079-2088 Environmental Tobacco Smoke and Coronary Heart Disease
- 2023512090-2091 Editorial Give A Dog-End A Bad Name
- 2023512093-2108 Weaknesses in Recent Risk Assessments of Environmental Tobacco Smoke
- 2023512110-2129 Environmental Tobacco Smoke and Mortality A Detailed Review of Epidemiological Evidence Relating Environmental Tobacco Smoke to the Risk of Cancer, Heart Disease and Other Causes of Death in Adults Who Have Never Smoked - 5 Heart Disease
- 2023512131-2155 Environmental Tobacco Smoke Exposure and Occupational Heart Disease
- 2023512157-2171 Passive Smoking and Coronary Artery Disease. Biological Plausibility and Severity of Effect
- 2023512173-2180 Carbon Monoxide and Cardiovascular Disease: An Analysis of the Weight of Evidence
- 2023512185-2189 the Effects of Passive Inhalation of Cigarette Smoke on Excercise Performance
- 2023512192-2195 Effect of Passive Smoking on Angina Pectoris
- 2023512199-2202
- 2023512203-2213 Effect of 'passive' Smoking on the Physical Load Tolerance of Coronary Heart Disease Patients
- 2023512216-2220 Indoor Passive Smoking: Its Effect on Cardiac Performance
- 2023512227-2230 Platelet Sensitivity to Prostacyclin in Smokers and Non-Smokers
- 2023512233-2237 Besitzen Passivraucher Ein Erhohtes Thromboserisiko?
- 2023512241-2244 Passive Smoking Affects Endothelium and Platelets
- 2023512247-2253 Lipoprotein and Oxygen Transport Alterations in Passive Smoking Preadolescent Children the Mcv Twin Study
- 2023512256-2257 Abstracts of the 30th Annual Conference on Cardiovascular Disease Epidemiology Children's Hdl-Chol: the Effects of Tobacco: Smoking, Smokeless and Parental Smoking
- 2023512261-2266 Passive Smoking Alters Lipid Profiles in Adolescents
- 2023512269-2274 Serum Lipids & Lipoprotein Profiles of Cigarette Smokers & Passive Smokers
- 2023512278-2279 8th Worldconference on Tobacco or Health Building A Tobacco-Free World 920330 - 920403 Buenos Aires - Argentina Abstracts, Posters and Videos. Serum Lipoproteins in Nonsmokers Chronically Exposed to Tobacco Smoke in the Workplace
- 2023512282 the Association Between Carotid Arterial Wall Thickness and Active and Passive Cigarette Smoking
- 2023512285 Passive Smoking and Carotid Artery Wall Thickness: the Aric Study
- 2023512290-2297 Passive Smoking Increases Experimental Atherosclerosis in Cholesterol-Fed Rabbits
- 2023512300-2301 Supplement to Circulation Abstracts From the 65th Scientific Sessions New Orleans Convention Center New Orleans, Louisiana 921116 - 921119
- 2023512304-2307 Association of Passive Smoking with Increased Coronary Heart Disease Risk Is Not Explained by Elevation of Leucocyte Count
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392
PRETARATIONS USED IN TH! CDLLitORaSTIY£ STSlDY
Preparanon
Subtype HBeAV
anu-HBe Serunv
plasma State.
8pIA9 ,d ann-HSe Serum I Freezedned
A .d HBeAg Serum L,qurd
B ad antt-HBe Ptasma
Lquad
C ay HBeAg I
Serum Llqutd
D ry antrHBe Serum Liquid
E av HBeeSg Serum ~ L+qutd
F ad HBe-ig Serum L Liquid
Gt ad aato-HBe Serum Freeze dried
'fnqa.ed Den.e.Rsfirenci Pretarsr+s er'He'eluu ~ Surfaas AwrrRn.
tCoOed duMrorea( 1111rnuA Ilsieearee Map.ruon
Twelve laboratories contnbuted data from a total of 31 aamys. All
parttapanes used solid phase ndiotrttmunoassays-the 'AL'SRIA
II~' commercial kit (Abbott) :tn six, a ttsodifiatloaof the cornmercul
kit in two.t and the reantrung fotu laboratones used their local
method.
aassy,data were analysed using the standard method: of parallel'
lineaisays:° potencies ofthe samples were expressed'relattve to the
proposed standard. For each sample, potencv ratios from replicate
assan of Individual laboratona were combined by taking their
geometric rrlntts. The frequency distributions of'these valiies are
shown in the figure.
No obvious dlffereneY were found between estimates obtained
from laboratories using duYercnt forms of radiouttmunoassav.
There was reasonable agreement between the potencv estimates
obtained bv the different laboratories. The potency estimates
obtained for the coded duplicate of the standard (sample G)'were
remarkably close to unity. Furthermore, there was betteragreemenr
between latlorntona for the potency of sample G than for the other
samplei: Nevertheless, the variation found between potency
estimates of the individual coded prepantlons for the different
laboratories were cotsstdered to be smallitn practtcal'rerms:.
In 1982 the National Biological Standards Board authorlsed the
atablishtnenr of the preparation coded' 8015,49 as the British
Reference Preparatson of Hepanns B Surface .jnugen ( HtAg), with
an assigned unttage of 100 unsts per ampoule.
The Hepatitis qdvuay Group has recommendefl° thar all
donations ofblood destttsed [o contrtbute to protcat iracttonauon ar
'Hopus R. Rar S. Joraan T. t4an AD. tmqrwaet eeenem.er a H R~i~.rreenrne.+~+n
co0uet<rcWn4waun,ur..ns{eem JC"..Par_ IIM0:7]:.Ip-2)a Finnv01. Sotrtel nrt4a,. W.bpra6arae, iraeC.
L:xrdonGruTin. I9Ta
A4na.rvCyrwy on Toruq.iar rM Presence oi Hep.rnrr.ta.arraua Anrisen ana
AnnawdeTlrq:repon. Irr 1
I , F r -irt- 7
j
P-Me ~ I of .ol- t
Fs.qaseaey df.rribsi.r .(p.e.aey . etim.aarx s.mpt.. A-Gia
term. eif proy...d nf.ese.e.pe.paatioa
Each box deroeea the mea.n potenirv obtnmed bv une Iaborato" br
radtotmmuna.ua'open boees (Abbott commercrai kit). hatched boxes.
(modtficaanao(Abbon lurt. Cifled boees lorher methorls) ~
THEL1 vCET.Al.'GUST 14. 1982
Y.H.S: fraenonatsoo centres should' be tested bw techniques that
give a'"paitlve" result for a concentration of:2 BntLSh units oi'
HBaAg'ml. Subsequently a funher.study was carrted out to esttmate
the detection hmtts, reiattve to the British Reference Prepantton, of'
methods used bv the participants. Preliminary results have shown
that labontones in the study detecred~ the presence of 5epantu
antigen at a concentration of 0 i uruts/ml. In some laboratories as
little as 0- 125 unstvttil could be routinely detected. Thus the assav
methods Inedm the study should rullv fulfil the recommendatton
of the Hepatitis Xdvtsorv Group.
We.rhank the Colla.rng for parrmctp¢nnf in the srudrDnEtuaoethBouil
IBirntsn{hamh Dr C. H Camcron ano Dr D S. Dane tLondonl: Dr R. )
Cn.faedlCathlkel;DnR.HopttnslElmburyhl:DrR:S.LnerndDr8 S
CatoAndfi (ElstreeR Dr Ataryret Supran ILondonl Dr P. PNton:me:
ILondank Dr E. G. Wlleeler and Dr 4': 1 Jenktns tBrentwoodc Prot: AJ.
Zuekerm.n. DrHaui Snuth, and Dr.H. Bo.errnan I Londonc Dr R. I Gererv
(Betbeada: C.S.A.); Prof R: Thomsaen. Dr: R' lierlrch, and Dr K Lcelea
(G3tttnjen. West Gerasanvl:.andDr P J CamptieiL.standardsprocessinq
saetwn- V.LB.S.C.. +haorr;anased the.lutnFutton oi,the ampoailcn.
Nxrrol!lerarre rw aWO9cal.
s[arbNa aMcanrrp. ,
Lonorr YWSaRa
V.ALERIE SE.iGRUATL
.4WRAG FERGUsQ.
D. 11 \'1rlliRiTH
G. C. S..HIZD
Nddlesa H a.p wai.Nfteal. Smoa:
Lonoon 1st C. H. C.tmF.RU%
PASSIVE SMOKING SEVERELY DECREASES
PLATELET SE.'9SCTfYITY TO A:P7TIAGGREGATORY
PROSTAGLANDINS
Sta,-tn the editorlal (,Aarch 6. p. 548) and'tnahe ensuing carre-
spotsdence on passtve smoking the risk of the development of
atherosclerosis has norbeen mentioned. Cnpubiishedstudla(H! S:
and 0: Burghuber; and E. Walter) suggest that plateleu function is
severely u7ected in urwken, and (here ts some evidence ehar
cigarette smoking msght exert Irs action via dtmtnnhal vasculltr
prostacyclln (PGI=) svnthesu ' and decreased senstt tvttv of platelets
to antugsregatorq protraglandlns, ' We have looked'at the erTeas of
passive smoktng on platelet senstttvtty.
We measured platelet sensltlvttv to the anruggregatory
prostagiandins (E11 I_, D.) before, during, and after passive
smoking tn esghcmale and'fbur female smokers aged 22-31'and in
eight male and'one female non-smokers aged 24-30 In a 18 m3
room thtrty cigarettes of a strong brand ('Gi(anes') were smoked by
testers, to give a smoke concentration calculated to resemble that in
diseea, restaurants, and the like. The rest sublens were exposed to
the smoke for 15 rnut: Blood was sampled immediately before and at
the end of the smoking penod and 20 and 60 mtn afterwards froma
Lvbttal vein without occlusion, uuh 38"/e sodlum ctrrae as
annewgulant. f'Platelet senslttvtt y as nsp ressed as I nko ( t he amount
of PG' in tsglml platelet rich plasma necnurv to halve the
aggregarwn Induced by I wrnoUl .a1)P);
Passive smoking (table) reduced platelet senstnvtry to the
antuggregatory PGs, being much more severe tn non-smokers than
tnsmokess. 20 mtts afterpasstve smoking, platelet senstavttv staned
to return to basal values and Ihls happened more qulcklv in non-
smokers. However, the baseline values in smokers were
siptfantly lower (p<001p than those in non,smokers.
A decrease In platelet sensitivity is the maror deterrrttnant of
haemouanc re;ulatton' and mav thus be responsible for early
changes preceding stherosclerosls.5 In combination with our
1.Uwa I ~eeeN~r A ERret elnKarne on i ne fenn.er-n si R+wae.elrn rn ru aena. 1 n,
Y(i G.lM1.rrqrara i Fieenae. i W I>; ae.vr 41
wGW A. Rdalisa A. aveyrueer O. 5ronnqrr H. Pvdn aA. Innaen:e of z.,.< andp.ree tero" enppreter
rnunnr+,o anr r.qreprn.. pnrqundw uw nrum.
r0ea.0ee.ea !. u rwWen aM Mn-e/rwen Is 1' r. G.l Pnrr,yuwl+aIFue.. IwSl arr m7
1. Auen.Yl O. s~.auMer H. l'ernanen an PUncMnwetrn.nY t3ranruurre.ra.ucne
Rv.apa.CUr IAlrerrnluney.eit I: a'- T.n.-l ]rrAe I N I. Yl 112 - 1S
a SSanqar. H Rar.r. 1.ScMenrwrer6PtarNn .eneu,m- r« am~mesnon
qertqLa6rs u cavmr.nen d,ur aeo.wvn uapna t+R*om Anr,Na.e..r
INL aL- aro-s7
4. Smarww H: RW.nan I. Q41salra K. PaclNneer U. P,asw.P 1'aluao( pt+reler
.r,ers m wa.arepreo.pruaYtanMmiPGi . PG.E.. K'.D - SJ p.nemi
.wa..mr7au.,nraresqa u.aun{ ye Pmr.yu.enu...w.u laa.r. 7: I_S,t2.
2~2~5~22 23

fHELANCETAL'GL'ST 14. 1982
tL%TELET SE.ySITtt'ITY IEFOREANDAFTER PASStvE SMOKING
PG I Scfore End 20 min j, 60 mm
,ti'o+uwokm I 1
1. 1 26a011 2 16s0r21' 116=0~21 35z019
1'
s, te7_3,1 i32-5_.2. I2e2z4-1 ~2
47:28
D- ~2 7x3 6 556b5-3 51.3s42 M6z4-1
Sin.ir,rr
l. 1i5a0-26 I I20lo019 206c0-IB l93z023
E, 27-8m?3 306c3i 3t.0o4 II 29-1_29'
ID. ~ u- 9:a I I ' sa6_4s s9e:3r 45-2z1-e
ReWrs.a ne PG,mn oweia run .plmm... .MtrnsSE.~t.
pCL 01.
findings of deaessed PGi2 formation in umbilical artmesia bt+bia
born to mothers who smoked° the severe changes we found after
pautvrstnolung, apectally trt nonsmokers, point to an important
risk in nonsmokers exposedi to cigarette smoke for a long time.,
.Uthough not much is known about the long-term tnfluence of
passive smoking nn the rtsk for development of atherosclerosis, our
dYta do indicate that passive cigarette smoking, besides being an
important soctal' issue. may be a health problem too.
Q'e thank Vsna Vlouralis and'.%1ana l:anellopoui6s for lechmcal rawtancc
and Claudu D.aak fnr.secrer anavhe lo. The srudy. ~.u supportedbd a granl of
[he Fonds aur Fdrderung der wwenschafduchen Fonehunt;..
.lihere.cierout Retearcf+ Gloua.,
t)tp.rtmem o(.NtdwJ PMwwe.-.
ana Alherateuraw uq Theannaut Rmorcn Grouo o('.Ine Auurun Aod.m.. o( Scunta
H. St:Y2aNGE)t
A-1(/901,.nn.. Auuna A. KEFALlD IS
EARLY TRE.9TMF1`fT OF OESOPHAGEAL YARBCFS
SIR,-Wliile we agree with Freeman and colleagues (;ilrlV 10,, p.
66) that vasopressin or its analogues may have a place in the
muugement,of acute vanceai bleeding, we believe its roirisat best
subs3dtary. Since the patients moar at risk are those wbo rebleed
early, the aun of management in vanceal bleeding should be to
prevent rebleeding as much as to control the presenting
haemorrhage. To this end we have developed a practice oftaanagLng
vartceal' bleeding which provides results equally as good as thoae
obtained with givpresstn by Freeman et ai. and which a11o serxs as a
basts for long-term management.
If bleeding u aatve, a Luston tube' is inflated in the gasatc
fundus and maintained on traaton. When rausctntion is efiected'
the vances are tmmediatel v iniected with sderosaar with the tube tn
sttu.,els there is no oesophageal balloon on ttus rube, usteetxon is not
techntally difficult and there u cheadvantage that a bloodless field
is obtained. Furthermorett seems likeiy rhat pressure on the gutnc
eariea aidi sclerosis by preventing retrograde flow ofsderoant. If
there is no active bleeding at the tstne of endoaopy the vances ars
tmected, without the tube. which an be passed Later if bleeding
becomes a difFirultu: Sclerosis is cottaaued fortnigbtly until vaneeal
obliteration is complete.
Since ad'opttng thu policy 18 mottths ago we have treated suttem
patients with acute vartceal bleeding. One died imtssed9ately on
admtsston to hospital before endoRcopy could be arrmed out. Of ebe
remausder. eight had sclerotherapy with the Lhton tube in sutn and
:even had it wtthout the rube. Of these p.nean, one rebled three
tnaa before dyusg of liver failure due to hepanc angtoaareo®a; the
other fourteen remain well, although two rebled'before tbe,rvanas
wQ2 obliterated.
While giypresstm trught be of vaHte in vancol bieedusg when
endoscopic sclerothenpv is unavailable, we believe that our simple
policy taay be of greater value in most general hospnals.,
Dep.rtmeetoi\SWrcuG.uroencen>IeRr. RJ..DtCTI!VSOr:kadensroxe t H.wo.nl: R BLHRLNs
Niu. Ra.G
C&OWW-60t p: _'QQ J. O: HL'tiTER
e. D+6r CS L:nreser Ch..Sua.nrer. H. SJaerCn,er K UmNO/ anen pra.m+etmienna,+sn u d~man..nal 1.
11.0- aeru ,e .wnen: .w tmMC L- I N I-e1
11 t.'.aeen R R. Tt,t ttntrVtnc+"uW os(nunt ,reume+n ag bl..d,a{ emooe.Al wrem.
Gur+wwt..,wer 1413. S4: 1-
393
ICOSAPE."tTAENOIC ACm AND
ISCHAEMIC HEART DISFaSE
StR.-Dr Jones and Dr DRVra Qul,v 24, p. 2211 diacuas the
decrease in circulating plaselets which various worsrrs have found
to be produced by fish oils. But they state that Hay ttnd colle.gua '
used' "a staulhr fish oil and EPA supplesaatt" to that uaed by
Thorngren and Gustafson.= There was a auaal da,fTerena. Hay a
RlL used "Wlsxepa" (,iiarfleet Refining Cotsspsny: a subtudury of
Imperial Foods), whtth is a refined deodoFtsed blead'of marine body
oils with added annoxtdanes: it contains about 20°1% of farry aads as
rtmnodontc (C20:Sr-3 or "EPA"), about 194% as ciupanodontc
(C22:6n- 3) and leu than 14L u cetolac (U2: le- 11). The firss two
are asenttall fatty aerdh and the third is tosu, at least to lower
antmals, being an isomer of eruac aad (C22:1 R-9) found in eertatn
rapaeed' oils, which cannot be oridised with ease by muscle
mitochondrta unless adaptation has occurred and therefbre causes
mvocardui fibrosis with sudden death. Thora;rert's volunteen,
however,, changed their usual Swedish diet for eleven wee'rs to
include "a predomtnatue of fish, mainly mackerel and sRlmon".
These fish have cetoietc actd as a predommant farty acid, anaivses
(in °70 of total actds) by Dr hlarv, Gale in our Instttute being:
O,i c2P3 C2: 6 Cr'. I
,%latkere/ Lknmert ,;n.ren,r) 12- I 11' 4 9.0
'.
Salrtan (.Sdiwm uiarl 10-'_ t li 11.3
The relevance of CZ2:1 fttry acids is that they probably decrease
the number of circulating plateias. McDonald and collesgtsa 1'fed
seven heaithv maies for 22 days with rapeseed oil containing 3946
eruclc acid (whtch supplied 38% total deetarv energy); tn.five of
them there was a marked fall in platelet count whsch returned lo
normal when their customarv diet was resumed:,On a traditional
Eskimo d7et fOr.. IDO dYVs (only sql, fish. andwater) mvpluelet
count deereased'from 226 0001/,1 to 52 0001/+1L and plateie'ts changed
morphologlallv to giant fonns: this diet was very high m.C20:5,
C22:6, and C22::. The first of these tended to displace atach-dontc
aad (C20:4n-6) us, for instance, the different phosplsoltptds of'
platelets' and cetoletc acid appeared in these as well as tn,
lipoprotetns. erythrocyte membnna, adipose tissue, and skeletall
muscie. But the dramatic utvease in bleeding time was prob.blv
aused'partlv by the alteration in the struaure and therefore fluwdttv
of the platelet membrana and'not only by the observed alterations
in prostanotds:l the former may also have contributed to the
decrease in platelet count since Hav et at. ' obtKrved a decruse on a
diet containing negligible cetoleu aad:
The references in ~ Jones and IDRna' Iener raise an impot'tant
question of nomenclature. They twue refer to mmnodon3c tbd
(C20:5n- 3), as "ercowpenranotc" T1sss word conatns three
errors-one aademtc, one areless (the secvad .'e" should be .'a"),
and one fundamental. The LLC.P.A.CI:L'.B. Commtsaton on
Biocheaual Vomenclature has decrreda in its asdom(or folly) thar
the Greek trcool (or the common Epic dsalea form itucool.) must
be anglictaed u"icoa" therebr dropping one or two epsilotu: so
"EPA" must be "IPA"' To be on the right side, Professor
Crawford and'colleagua" from the Royd College of Surgeons in a
current paper use both spellings in difftratt places. But trivial
names for fatty aads are useful; Ikkt w continue to nll'C20:5R-3
tu'nnodonac actd and C22:6w-3 cluprttodonsc acid.
Ih.ernw.rsuImrnwe ei Hrmr. Nl.mm..
Swr.n Cm,.t.ne..
As,MMn OS IuaA~ HCGN 5l.I.CLAIR
; HnCR.%S:.thra.r.V.S..rrR ER.ad.f..edrv,mwn.mnwni.or,on.v1- ucnmtn,cne.nrat.eae L.r., 1N:.,t2N-tp
:' Tlwen~ttn ~t. Gw,.urw A ERtta ef t 1-.wt ,wtast u aer4 t.ev.oonae..c
KW un.0it[Wee ~un.., i,~,b aN prew a~reta.mr li..t, IN I. i,. I IeP.fl.
1~. ~I:D,muaRE.. Reet t'.N. Lt11rrEL ti,nr Dl'ERtt, a n.mt.a.~ m.nvT /,ra
psnernrandDweO Mtn.m.er ni ,w.t mt.. 1. Prnttaunp o( Imenw,.eu
Rapercd Canenm i(:ar.. le:4l M\-ttle
+'. S.nc,rn M+l te.an.ten.aw a..n.,r...n a r E.a- m- In F,.,w.nII. R.
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