Calciumpillen tegen botontkalking zonder toegevoegde vitamines zorgen voor
aderverkalking, zo blijkt uit Brits onderzoek. Slikkers van calciumpillen lopen een
hoger risico op een hartinfarct, waarschuwden Engelse onderzoekers onlangs in het medische
tijdschrift British Medical Journal (BMJ). Ze versterken het proces van kalkafzetting
rond zogeheten elastinevezels in de vaatwanden.
Voedingsadviezen ter preventie en
behandeling van hart- en vaatziekten richten zich voornamelijk op een vermindering van de
inname van verzadigd vet, met als voornaamste doel het gehalte LDL-cholesterol te
verlagen. Welke andere voedingsmaatregelen dragen bij tot een beter bloedlipidenprofiel?
Zodra verzadigde vetten vervangen worden door koolhydraten, en dan vooral geraffineerde
koolhydraten, dan heeft dit ook een negatief effect op het bloedvetten profiel dat
bijdraagt aan de arteriosclerose, verminderde insulinegevoeligheid en overgewicht. Daarom
dienen voedingsadviezen, die het risico op hart- en vaatziekten moeten verlagen, de nadruk
te leggen op beperking van o.a. de inname van geraffineerde koolhydraten. Toename van
visceraal vet (vet rond de organen) is een bekende risicofactor voor diabetes type II en
hart- en vaatziekten. Fructoseconsumptie blijkt de typische kenmerken van het metabool
syndroom te verergeren. In vergelijking met glucose verhoogde fructose in een groep obese
personen de cholesterolsynthese in de lever. De insulinegevoeligheid werd minder en het
visceraal vet nam toe.
Radio - De VascuLuminator: een
Nederlandse topuitvinding
Woensdag 6 oktober werd in het Utrechts
Medisch Centrum een nieuwe Nederlandse uitvinding gepresenteerd: de VascuLuminator. De
bedenker is Ruud Verdaasdonk, hoofd afdeling fysica en medische technologie VUmc. De
VascuLuminator is: een navigatiesysteem om misprikken bij bloedafname te voorkomen.
Oximeter of Pulse-oximeter genoemd, is een
medisch hulpmiddel in de vorm van een Clip om via de vinger de hoeveelheid zuurstof
(saturatie) in het bloed te meten, een belangrijke graadmeter voor sporters,
longpatiënten, bergwandelaars, vliegsporters, EHBO-ers en stoppende rokers.
Behandeling voor zeldzame ernstige
bloedvatenziekte ontdekt
Onderzoekers van de Gentse universiteit
hebben samen met Parijse wetenschappers een behandeling ontdekt voor de zeldzame maar
ernstige bloedvatenziekte vasculair Ehlers Danlos Syndroom (vEDS).
Onderzoek doet vermoeden dat
‘mozaïek’ van gen-defecten vetgehalte in bloed sterk verhoogt
Een ‘mozaïek’ van
gemeenschappelijke en zeldzame deffecten in vier genen kan het vetgehalteniveau van het
bloed mogelijk verhogen tot een gevaarlijk niveau. Dit werd aangetoond door onderzoek.
Afwijking bij Maltese familie werpt
nieuw licht op bloedarmoede
Doorbraak in onderzoek kan sleutel zijn tot
aanpak van erfelijke bloedziekten
Onderzoekers van Erasmus MC hebben een
doorbraak geboekt in het onderzoek naar erfelijke bloedarmoede, waarbij zuurstof in het
bloed niet goed wordt getransporteerd. De onderzoekers hebben ontdekt dat ze het
zuurstoftransport mogelijk kunnen verbeteren door een bepaald bloedeiwit te bewerken. Ze
hebben dit ontdekt dankzij een Maltese familie met een afwijking aan dit eiwit. Dat maken
ze bekend in het augustusnummer van het toonaangevende tijdschrift Nature Genetics. De
doorbraak opent perspectieven voor de behandeling van mensen met erfelijke bloedarmoede.
Wereldwijd worden er elk jaar 300.000
nieuwe patiënten geboren. Ook in Nederland komt erfelijke bloedarmoede steeds vaker voor.
Het gaat hierbij vooral om mensen (en hun kinderen) afkomstig uit landen rond de
Middellandse zee. Zij lijden aan chronische bloedarmoede en moeten regelmatig
bloedtransfusies ondergaan. Onder erfelijke bloedarmoede vallen ernstige aandoeningen als
sikkelcelziekte en thalassemie. Bij sikkelcelziekte vervormen rode bloedcellen, wat kan
leiden tot verstopte bloedvaten. Ook kan de afwijking schade aan organen veroorzaken. Bij
thalassemie werken de rode bloedcellen niet goed en worden ze sneller afgebroken, waardoor
patiënten ernstige bloedarmoede krijgen. Het Erasmus MC heeft voor deze patiënten
inmiddels een speciale sikkelcel polikliniek.
De doorbraak in het onderzoek is mede te
danken aan een Maltese familie. Bij veel leden van deze familie is het bloedeiwit KLF1
minder actief. Dat eiwit regelt de aanmaak van de zuurstoftransporteur hemoglobine. De
afwijking bij de familie blijkt een gunstig bijeffect te hebben: hun bloed kan beter
zuurstof opnemen en transporteren. Die ontdekking kan de sleutel zijn tot een betere
behandeling van erfelijke bloedarmoede. 'Als patiënten hetzelfde KLF1-eiwit zouden hebben
als de Maltese familie, zou hun zuurstoftransport dus verbeteren. Dat zou de symptomen van
hun ziekte sterk verminderen. Ze zouden mogelijk een leven kunnen leiden zonder
bloedtransfusies', zegt Sjaak Philipsen, onderzoeker op de afdeling Celbiologie van
Erasmus MC.
Bij de Maltese familie werkt de aanmaak van
hemoglobine net als bij ongeboren baby's. Omdat baby's zuurstof uit het bloed van hun
moeder moeten halen, maken ze een vorm van hemoglobine aan die sterker bindt aan zuurstof
dan volwassen hemoglobine. Als het bloedeiwit KLF1 minder actief is (zoals bij de Maltese
familie), komt er meer 'baby-hemoglobine' (HbF) in het bloed. Daardoor verbeteren de
opname en het transport van zuurstof.
Het is de onderzoekers al gelukt om in het
laboratorium het eiwit in menselijke cellen zo te veranderen dat het dezelfde
eigenschappen vertoont als het eiwit van de Maltese familie. Dit is een grote doorbraak
waar wetenschappers wereldwijd al jaren naar uit kijken. Philipsen: 'Het is gelukt dankzij
de toepassing van nieuwe technieken. Vijf jaar geleden hadden we dit resultaat nog niet
kunnen behalen. Vervolgonderzoek moet uitwijzen of het ook lukt om het eiwit bij
patiënten zo te wijzigen dat de zuurstofopname en transport verbeteren.'
Deep Vein Thrombosis
Te lage bloeddruk vervuilt het
lichaam
Met een te lage bloeddruk komt het bloed
met zijn voedingsstoffen niet diep genoeg in de haarvaatjes van onze weefsels. De cellen
krijgen zo niet de stoffen die ze nodig hebben. Bovendien kunnen ze hun afvalstoffen niet
kwijt omdat er geen druk is om die weg te voeren, naar het lymfesysteem toe. Dit vervuilt
ons lichaam. Lichaamscellen die tekorten hebben terwijl hun afval zich opstapelt kunnen
niet goed functioneren en bezorgen het lichaam stress.
In haar promotieonderzoek wilde Mirjam
Meltzer het fibrinolytisch systeem beter begrijpen. Dat is verantwoordelijk voor het
afbreken van bloedstolsels en speelt een rol bij het ontstaan van hartinfarct en veneuze
trombose.
Meltzer analyseerde de resultaten van twee
grote studies waaraan ongeveer 2000 patienten met veneuze trombose, 600 patienten met een
eerste hartinfarct en evenveel controlepersonen aan deelnamen. Zij ontdekte dat personen
met een verlengde 'lysis-tijd' een hoger risico hebben op een hartinfarct of veneuze
trombose. Een langere lysis-tijd wil zeggen dat die mensen er langer over doen een
bloedstolsel op te lossen.
Ook zag Meltzer dat bepaalde
fibrinolytische eiwitten verband houden met arteriele en veneuze trombose. In de toekomst
zouden de resultaten van haar onderzoek gebruikt kunnen worden voor het ontwikkelen van
medicatie voor de behandeling van trombose.
Spugende bloedvaten
Minuscule aderen in de hersenen kennen een
ingenieuze manier om vuil kwijt te raken: ze spugen het uit. Zo voorkomen ze dat
bloedpropjes of klonten cholesterol een gevaarlijke opstopping veroorzaken.
Onderzoekers van het Erasmus MC hebben
ontdekt hoe nieuwe bloedvaten ontstaan. Ook zijn genen gevonden die daarbij een rol
spelen. De ontdekkingen kunnen helpen bij het bestrijden van kanker en hart- en
vaatziekten. Onderzoeker Robert Herpers promoveert woensdag 31 maart op de bevindingen.
Genen
Herpers heeft gekeken welke genen actief zijn in de bloedvatwand. Vervolgens heeft hij
onderzocht wat die genen precies doen en welke zorgen voor de groei en aanleg van nieuwe
bloedvaten. Zo heeft Herpers vastgelegd hoe aders en slagaders met elkaar samengaan
wanneer bepaalde genen niet goed functioneren.
Groeien
De resultaten kunnen bijdragen aan een betere behandeling van hart- en vaatziekten.
Herpers: "Bij mensen die een hartinfarct hebben gehad stroomt er onvoldoende bloed
naar het hart, omdat de slagaders beschadigd zijn. Door nieuwe bloedvaten te laten
groeien, zijn die problemen mogelijk op te lossen."
Gevoelig
De kennis over bloedvaten helpt ook bij de bestrijding van bepaalde vormen van kanker.
Sommige tumoren scheiden stoffen uit die ervoor zorgen dat bloed- en lymfevaten van en
naar de tumor groeien. Daardoor krijgen de gezwellen meer 'voeding', groeien ze sneller en
is de kans op uitzaaiingen groter. Herpers heeft een gen (delta-like 4) gevonden dat
regelt hoe gevoelig de bloedvaten zijn voor dergelijke stoffen.
Omeprazol en bloedverdunner gaan
niet samen
De 'bloedverdunner' clopidogrel (Plavix),
die onder andere aan dialysepatiënten voorgeschreven wordt om stolling in de shunt te
voorkomen, kan beter niet tegelijk met de maagzuurremmer omeprazol gebruikt worden.
Risico's antistollingsmedicijnen
beter te voorspellen
In Nederland slikken maar liefst 360.000
mensen antistollingsmedicijnen, bijvoorbeeld om het risico op een hartinfarct of een
beroerte te verminderen. Een kwart van de patiënten kampt met sterke schommelingen in
bloedwaarden, waardoor de medicijnen minder effectief worden, en de kans op ernstige
bijwerkingen stijgt. UMCG-onderzoeker Nic Veeger ontdekte dat de eerste dertig dagen van
de behandeling voorspellen of iemand goed reageert op medicijnen. Bovendien is een kleine,
ongevaarlijke bloeding kort na de start van de behandeling een teken dat een patiënt
later grote problemen krijgt. Veeger promoveert 17 februari 2010 aan de Rijksuniversiteit
Groningen.
Bij langdurige antistollingsbehandeling
wordt gebruik gemaakt van vitamine K antagonisten. Vitamine K is voor een belangrijke deel
verantwoordelijk voor de aanmaak van stollingsfactoren in het bloed. Een stof die vitamine
K remt (een antagonist) kan daarom een goed antistollingsmiddel zijn. Vitamine K
antagonisten werden 60 jaar geleden geregistreerd als antistollingsmiddel. Inmiddels slikt
meer dan twee procent van de Nederlandse bevolking deze medicijnen, en het gebruik neemt
nog altijd toe. Onder meer de vergrijzing en de toename van obesitas spelen daarbij een
rol.
Een kwart vraagt extra aandacht
Uit het onderzoek van Veeger blijkt dat zo'n driekwart van de patiënten zeer goed is
geholpen met vitamine K antagonisten als fenprocoumon en acenocoumarol. Zij moeten
weliswaar regelmatig (1 à 2 keer per maand) ter controle naar de trombosedienst, maar de
mate van stolling van hun bloed blijft tussen de 45 en 65% van de tijd tussen
streefwaarden, zo blijkt. Bij een kwart van de patiënten zijn de stollingswaarden
maximaal 45% van de tijd in het streefgebied. Deze patiënten hebben een verhoogde kans op
trombo-embolie (een bloedprop) dat een beroerte kan veroorzaken, of een ernstige bloeding.
Risico's beter inschatten
Het is van groot belang dat snel duidelijk is of een patiënt tot de risicogroep behoort
die slecht instelbaar is. Veeger ontdekte twee goede voorspellers. Ten eerste blijkt dat
de eerste 30 dagen van de behandeling een goede indicatie geeft voor het verdere verloop
van de behandeling. Ten tweede blijkt een kleine, ongevaarlijke bloeding kort na de start
van de behandeling een voorspeller te zijn voor grotere problemen later in het traject.
Veeger: "Aan de hand van deze voorspellers kunnen hoogrisicopatiënten vroegtijdig
opgespoord worden. Door extra maatregelen en eventuele aanpassing van de behandeling kan
ook voor deze groep mogelijk een beter resultaat worden bereikt."
Kansen door nieuwe medicijnen
Internationaal zijn nieuwe antistollingsmedicijnen in opkomst. Een aantal hiervan zal naar
verwachting snel op de Nederlandse markt worden toegelaten. Veeger: "Het is nog
vroeg, maar voor patiënten die niet goed op de bestaande medicijnen reageren, bieden deze
nieuwe medicijnen wellicht uitkomst." Of de nieuwe medicijnen voor alle patiënten
zoveel voordeel zal bieden, is echter nog maar de vraag. Veeger: "Therapietrouw is
heel belangrijk bij het gebruik van antistollingsmedicijnen. In Nederland hebben we een
zeer effectief systeem van gespecialiseerde trombosediensten en is de therapietrouw erg
hoog. Bij de nieuwe medicijnen hoeft de patiënt niet meer door de trombosedienst
gecontroleerd te worden. Dit is een groot voordeel, maar de kans is groot dat dan de
therapietrouw afneemt. De werkzaamheid van de nieuwe medicijnen wordt hierdoor nadelig
beïnvloed. Daarom moet dit voor de Nederlandse situatie nog uitgebreid worden
onderzocht."
Vernieuwend onderzoek
Eerder onderzoek naar de effectiviteit van antistollingsmedicijnen was veelal gericht op
gemiddelde risico's onder grotere aantallen patiënten. Vernieuwend aan Veegers onderzoek
is dat voor de individuele patiënt de risico's op langere termijn in kaart werden
gebracht. Veeger analyseerde het verloop van bloedwaarden over langere tijd van in totaal
zo'n zesduizend patiënten.
New York Stem Cell Foundation
partner hoofdauteur van studie naar het creëren van bloedcellen uit stamcellen
Daylon James, Ph.D., van het Weill Cornell
Medisch College is hoofdauteur van een studie die voorwaarden moet definiëren voor het
aanmaken van een voorraad (?) cellen die geschikt zijn voor therapeutisch gebruik. Dr.
James en zijn collega's hebben een menselijk embryonaal stamcellen lijn ontwikkeld die
gebruikt kan worden om celproduktie en -activiteit te meten.
Risico op scheuren slagader in buik
beter op te sporen
Ontdekking: blaas meetinstrument te
gebruiken voor opsporen aneurysma’s in buikslagader. Een eenvoudige aanpassing aan
een instrument dat het volume van de blaas meet, stelt artsen in staat verwijdingen op te
sporen in slagaders in de buik van patiënten. Deze vondst is van levensbelang voor
patiënten met een dergelijke verwijding (aneurysma) in de buikslagader die elk moment zou
kunnen scheuren. Radosav Vidakovic kwam tot deze ontdekking tijdens zijn promotieonderzoek
binnen het Erasmus MC, waarop hij gisteren is gepromoveerd.
Het grote gevaar van een verwijding van de
buikslagader is dat de wand van de slagader op de plek van de verwijding zo zwak wordt,
dat de slagader scheurt (ruptuur). Dit kan de patiënt het leven kosten. Om een ruptuur te
voorkomen, moet het aneurysma worden verholpen door middel van een operatie. Hiertoe is
het van belang te kunnen meten of er bij een patiënt sprake is van een aneurysma in de
buikslagader. De blaasscan blijkt nu een heel eenvoudige en zeer effectieve methode om in
de algemene bevolking patiënten op te sporen met een verhoogd risico op aneurysma’s.
De blaasscan is een instrument waarmee
vanaf de buitenkant van het lichaam het blaasvolume gemeten kan worden. Hierbij wordt met
behulp van geluidsignalen onderzocht of een holte in het lichaam, in dit geval de blaas,
gevuld is met vloeistof. In plaats van de blaas keek Vidakovic in zijn onderzoek naar een
verwijding van de buikslagader, die met bloed is gevuld. De blaasscan is voor het opsporen
van aneurysma’s aangepast en vormt een snel, accuraat en betrouwbaar instrument.
Hiermee kunnen, zonder tussenkomst van een gespecialiseerd echografist, risicopatiënten
worden onderzocht op de aanwezigheid van aneurysma’s in de buikslagader. Waar nodig
kan de patiënt daarna worden doorverwezen voor verdere behandeling.
In Nederland worden jaarlijks 4536
patiënten geopereerd aan een aneurysma in de buikslagader, waarvan 904 met spoed wegens
een ruptuur. Vanwege de acute situatie die dan ontstaat, loopt de sterfte van de operatie
in die spoedgevallen zelfs op tot meer dan 50%. Bij een aneurysma van de buikslagader gaat
het om een plaatselijke verwijding die 50% groter is dan de normale diameter van de aorta.
De aandoening komt het meest voor bij mannen ouder dan 60 jaar. Naast geslacht en leeftijd
zijn risicofactoren een familiegeschiedenis met anuerysmatisch vaatlijden, roken, hoge
bloeddruk en overgewicht.
Nieuwe techniek voor behandeling
van etalagebenen spaart slagader
In haar proefschrift onderzoekt Suzanne
Gisbertz een nieuwe operatietechniek (remote endarteriectomie) voor patienten met een
afgesloten slagader in het bovenbeen en klachten van etalagebenen. Bij deze nieuwe
techniek wordt de oorspronkelijke slagader met een minimaal invasieve techniek van
binnenuit schoongemaakt, waardoor de slagader behouden blijft. In een gerandomiseerd
onderzoek vergeleek Gisbertz de nieuwe techniek met de standaard-aanpak, een
bypassoperatie in het been. Na drie jaar blijkt de slagader nog open te zijn in 47 procent
van de patienten die met via de nieuwe techniek geopereerd zijn, tegen 60 procent in de
bypassgroep. Het verschil tussen beide groepen is niet significant. Daarnaast onderzocht
Gisbertz het weefsel van de aderverkalking in relatie tot alcoholconsumptie en hart- en
vaatincidenten. Uit haar resultaten blijkt dat patienten met vaatlijden die alcohol
gebruiken minder vaak overlijden aan cardiovasculaire ziekten. Ook zien we dat van deze
patienten het weefsel minder ontstekingscellen en een minder vet laat zien. Dit is nooit
eerder aangetoond.
Beeldvorming groei bloedvaten:
mogelijkheden voor detectie en follow up van kanker
Om te kunnen groeien, hebben tumoren
bloedvaten nodig. De stof VEGF, die geproduceerd wordt door de tumor, is betrokken bij de
nieuwvorming van bloedvaten. Promovendus Wouter Nagengast ontwikkelde een methode om VEGF
in het lichaam met beeldvormende technieken in kaart te brengen. De promovendus laat zien
dat tumoren, zowel pre-klinisch als in de kliniek, met behulp van deze methode kunnen
worden gedetecteerd. Ook vond Nagengast in pre-klinische modellen aanwijzingen dat
VEGF-imaging kan helpen om de effectiviteit van angiogeneseremmers (kankermedicijnen die
vaatnieuwvorming tegengaan) in kaart te brengen. Of deze beeldvormende techniek ook bij
mensen gebruikt kan worden om de effectiviteit van behandelingen te monitoren, wordt
momenteel nader onderzocht.
ANCA-geassocieerde vasculitis (AAV) is een
zeldzame ziekte, waarbij de kleinste bloedvaten ontstoken raken. De ontsteking is het
gevolg van een ontsporing van het immuunsysteem. Bij AAV wordt, net als bij een aantal
andere auto-immuunziekten, het eigen lichaam door het afweerapparaat als
“vreemd” herkend. Kenmerkend voor de AAV is de aanwezigheid van ANCA,
antistoffen gericht tegen een specifieke groep witte bloedcellen, de neutrofiele
granulocyten. Promovendus Jan-Stephan Sanders brengt nauwgezet enkele risicofactoren voor
ontstekingsreacties in kaart. Ook ontdekte hij enkele markers die aangeven dat het risico
ontstekingen vergroot is. Hiermee maakt zijn onderzoek nauwkeuriger diagnose mogelijk.
Dagelijkse meting van de hoeveelheid bloed in de bloedvaten is behulpzaam om het optreden
van ondervulling van de vaten na een subarachnoïdale hersenbloeding (SAB) te voorkomen.
Hiermee kan mogelijk het ontstaan van hersenschade na een SAB worden voorkomen. Het
bijhouden van de vochtbalans en de interpretatie van diverse parameters van de
bloedsomloop zijn gebruikelijke methoden om het vochtbeleid na een SAB te sturen en te
pogen om de vullingstoestand normaal te houden.
Reinier Hoff laat in zijn proefschrift
echter zien dat deze methoden geen betrouwbare informatie geven over de daadwerkelijke
vullingstoestand en dat bij gebruik van deze methoden ondervulling nog veel voorkomt.
Wanneer nu het vochtbeleid wordt gestuurd op basis van dagelijkse metingen van het bloed
in de vaten, blijkt het beter mogelijk om de vullingstoestand normaal te houden, aldus
Hoff. Of hiermee ook daadwerkelijk de uitkomst voor de patiënten na een SAB wordt
verbeterd is nog niet duidelijk.
Universiteit Utrecht
Schade aan bloedvaten en
eindorganen hangen nauw samen
Aandoeningen aan eindorganen als de nieren
en het hart staan veelal niet op zichzelf,
maar kunnen mede veroorzaakt worden door veranderingen in de bloedvaten binnen of
buiten deze organen. Het wetenschappelijk inzicht in deze samenhang groeit. Nadir Ulu
bracht de samenhang in kaart tussen vasculaire dysfunctie enerzijds, en schade aan de
nieren en het hart anderzijds. Uit zijn onderzoek blijkt dat pathologische veranderingen
in de bloedvaten een centrale rol spelen bij het ontstaan van schade in deze eindorganen.
Op zijn beurt veroorzaakt de orgaanschade weer disfunctie van de bloedvaten, waardoor een
vicieuze cirkel ontstaat.
In onderstaand filmpje laat Arjen Witzel
het effect van GSM zien op je bloedcellen. Eindelijk denkt Witzel het antwoord te
hebben op de vraag waarom hij ziek wordt van al die elektromagnetische straling van de GSM
en UMTS zenders.
Groene thee component kan bijdragen
aan het behoud opgeslagen
bloedplaatjes en weefsels
In twee afzonderlijke studies is gebleken
dat een belangrijke component in groene thee, epigallocatechin-3-O-gallate (EGCG),
verlenging van de houdbaarheid van bloedplaatjes, gecryopreserveerde huid en weefsels
bewerkstelligd. Gepubliceerd in Cell Transplantation. Zie ook: Link
De twee complementaire studies hebben
aangetoond dat EGCG, een groene thee polyfenol dat bekend staat om zijn sterke
anti-oxidatieve eigenschappen, de levensduur van bloedplaatjes verlengd. Dr. Suong-Hyn
Hyon, auteur van beide studies en universitair hoofddocent bij het Instituut voor Medische
Wetenschappen Frontier in Kyoto Japan, stelt dat het exacte mechanisme waarmee EGCG werkt
nog niet bekend is.
Echter een aantal van de activiteiten van
EGCG zijn waarschijnlijk gerelateerd aan het oppervlakte bindend vermogen. Met gebruik van
standaard bloedbank procedures is de houdbaarheid voor bloedplaatjes cellen beperkt tot
vijf dagen (internationaal) of drie dagen volgens Japanse normen. Tijdens de opslag,
ondergaan bloedplaatjes biochemische, structurele en functionele veranderingen. Daarnaast
kan de membraam integriteit de homeostatische functies, zoals samenklontering en de
affiniteit voor oppervlaktereceptoren beïnvloeden.
Toen EGCG werd toegevoegd aan bloedplaatjes
concentraten waren de aggregatie en stollingfuncties tot zeker 6 dagen actief. Dit is
wellicht toe te schrijven aan EGCG antioxidatieve vermogen. Aangenomen wordt dat EGCG de
activatie van bloedplaatjes functies remt en aan de oppervlakte de proteïnen en vetten
beschermd tegen oxidatie. "Later konden de functies van de oppervlakte moleculen
worden hersteld door wassen/spoelen", constateerde Dr. Hyon. "GCG kan leiden tot
een remming op de voorgeprogrammeerde celdood (apoptosis) en minder celdood, met een
potentieel bruikbare methode om de levensduur van de cellen te verlengen."
Fred de Groot
Gezonde bloedvaten zouden vetgroei
kunnen voorkomen
De epitheelcellen van bloedvaten staan
bekend om het feit dat ze belangrijk zijn voor het behoud van de gezondheid, maar
onderzoekers aan de Indiana University School of Medicine zijn van mening dat deze cellen
een niet te vermoeden taak uit voeren, namelijk het handhaven van de ontwikkeling van
vetcellen. Hun bevindingen worden gerapporteerd in het septembernummer van het tijdschrift
'Stem Cells'.
De onderzoekers vonden dat de voorlopers
van stamcellen een duidelijk verminderde neiging hebben tot de ontwikkeling van vetcellen
wanneer deze in direct contact worden gebracht met gezonde endotheel cellen die zich in de
bloedvaten bevinden.
"De sleutel tot deze ontdekking was
onze recente observatie dat deze cellen, ook wel bekend als 'vetweefsel stromale cellen',
in vetweefsel in zeer nauw contact staan met endotheelcellen in kleine bloed- en
haarvate," zei Dr Keith L. March, co-hoofdonderzoeker van de studie en directeur van
'Indiana Center for Vascular Biology and Medicine (ICVBM)'.
"Nadat we hadden deze link hadden
herkend tussen endotheelcellen en stromale cellen, was het een logische stap om te vragen
hoe deze cellen elkaar kunnen beïnvloeden," zei March, die ook professor is van
medicina, physiology and biomedical engineering aan de 'IU School of Medicine and Krannert
Institute of Cardiology'.
March en zijn collega's doen onderzoek naar
het gebruik van de bouwstenen uit de natuur, de zogenoemde vetweefsel stamcellen, die ze
uit vetcellen weten te halen. Hun onderzoek kijkt naar manieren om vasculaire (vaat)
ziekten te behandelen, waarbij vetweefsel stamcellen worden gebruikt als middel voor de
groei van nieuwe bloedvaten als behandeling voor perifere (niet centraal gelegen)
vaataandoeningen.
Wanneer vetweefsel stamcellen werden
vermengd met endotheelcellen, hadden deze minder kans zich te ontwikkelen tot vetcellen,
zei Gangaraju Rajashekhar, hoofdauteur van het tijdschriftartikel en als onderzoeker
verbonden aan de 'Indiana Center for Vascular Biology and Medicine'.
"Wat we ontdekten was dat
endotheelcellen eiwitten afgeven, de zogenoemde Wnt eiwitten. Om specifieker te zijn, deze
spelen een belangrijke rol in het blokkeren van de ontwikkeling van vetcellen. Want
eiwitten reguleren de ontwikkeling en differentiatie in veel soorten weefsels en zouden
zelfs een rol kunnen spelen bij het verouderen", zei Rajashekhar.
De onderzoekers zeggen wel dat er meer
onderzoek nodig is om te bepalen of de reparatie van ongezonde endotheelcellen ook kan
helpen om vetgroei te controleren.
"We weten nu dat endotheelcellen in de
cellen van bloedvaten helpen bij het vertellen wat de vetweefsel stamcellen moeten
doen", zei Matthias Clauss, een ICVBM co-hoofdonderzoeker van de studie en een
hoogleraar voor cellulaire en integratieve fysiologie aan de 'IE School of Medicine'.
"Wat we nog niet weten is hoe de
vorming van vetcellen de opmaak van bloedvatcellen beinvloedt", zei Clauss.
"Onze huidige hypothese is dat endotheeldisfunctie de ontwikkeling van vetcellen
bevordert, vergezeld door de groei van nieuwe bloedvaten. Wij hopen spoedig deze cyclus te
kunnen onderbreken."
Dit onderzoek zou kunnen leiden tot nieuwe
mogelijkheden voor de behandeling van hart-en vaatziekten en zou ook artsen kunnen helpen
te voorzien van een ander wapen in de strijd tegen obesitas.
Voor meer informatie over ICVBM onderzoek, kijk op: http://www.vascularbiomed.iu.edu/.
Pittsburgh Researchers Identify
Population of Adult Stem Cells Found in Blood Vessels With Broad Ability To Regenerate
Other Tissues
In a promising finding for the field of regenerative medicine, stem cell researchers at
Children’s Hospital of Pittsburgh of UPMC have identified a source of adult stem
cells found on the walls of blood vessels with the unlimited potential to differentiate
into human tissues such as bone, cartilage and muscle. The scientists, led by Bruno
Péault, PhD, deputy director of the Stem Cell Research Center at Children’s
Hospital, identified cells known as pericytes that are multipotent, meaning they have
broad developmental potential. Pericytes are found on the walls of small blood vessels
such as capillaries and microvessels throughout the body and have the potential to be
extracted and grown into many types of tissues, according to the study. “This finding
marks the first direct evidence of the source of multipotent adult stem cells known as
mesenchymal stem cells. We believe pericytes represent one of the most promising sources
of multipotent stem cells that scientists have been searching for in the quest to make
regenerative medicine possible,” Dr. Péault said. “The encouraging aspect of
this source is that blood vessels are the one structure that all tissues in the human body
have in common. These cells can be extracted easily and painlessly from convenient sources
such as fat tissue, dental pulp, umbilical cord and placental tissue, then grown in
culture to large numbers and, possibly, re-injected into the patient to heal a broken
bone, a failing joint or an injured muscle.”
Backpack straps can decrease blood
flow in the shoulder and arm
In some professions -- such as the military, firefighting and mountain rescue -- the load
of a backpack may equal as much as 60 percent of adult body weight. A new study finds that
even light loads can decrease upper extremity blood flow and may result in a loss of fine
motor control and increased fatigue.
Twin findings raise hopes of
improved anemia treatments
A new understanding of how red blood cell production is controlled could lead to
improvements in the treatment of the blood disorder anemia, according to West Australian
medical researchers.
Blood vessels - The pied piper for
growing nerve cells
Researchers at Johns Hopkins have discovered that blood vessels in the head can guide
growing facial nerve cells with blood pressure controlling proteins. The findings, which
suggest that blood vessels throughout the body might have the same power of persuasion
over many nerves, are published this week in Nature.
Clues to How Blood Forms in
Life’s Earliest Stages
Guillermo García-Cardeña, director of the Laboratory for Systems Biology of the Center
for Excellence in Vascular Biology at Brigham and Women's Hospital (BWH) and George Q.
Daley, MD, PhD, director of the Stem Cell Transplantation Program at Children’s
Hospital Boston (CHB), along with scientists from the Indiana University School of
Medicine, intrigued by the appearance of blood progenitors in the wall of the developing
aorta soon after the heart starts beating, investigated the effects of mechanical
stimulation on blood formation in cultured mouse embryonic stem cells. Their findings
appear in the May 13, 2009 issue of Nature. They showed that shear stress - the frictional
force of fluid flow on the surface of cells lining the embryonic aorta - increases the
expression of master regulators of blood formation, including Runx1, and of genetic
markers found in blood stem cells. Shear stress also increased formation of colonies of
progenitor cells that give rise to specific lineages of blood cells (red cells,
lymphocytes, etc.). These findings demonstrate that biomechanical forces promote blood
formation. García-Cardeña, Daley and colleagues also studied mouse embryos with a
mutation that prevented initiation of the heartbeat. These embryos had a sharp reduction
in progenitor blood cell colonies, along with reduced expression of genetic markers of
blood stem cells. When specific cells from the mutant embryos were exposed in vitro to
shear stress, markers of blood stem cells and numbers of blood cell colonies were
restored. Finally, the team showed that when nitric oxide production was inhibited, in
both cell cultures and live mouse embryos, the effects of shear stress on blood progenitor
colony formation were reduced.
Have the patient’s coronary vessels, heart valves or myocardial muscle changed
abnormally? Doctors can verify this and administer the necessary therapy with the help of
a catheter, which is inserted into the body through a small incision in the groin area and
pushed to the heart through the vascular system. A metal guide wire inside the catheter
serves as a navigational aid. It is pulled and turned by the physician to steer and guide
the catheter. At the same time the catheter’s position in the vascular system has to
be monitored. This task is performed by X-rays, which penetrate the patient and show
exactly where the catheter is. The problem with this computer tomography method is that it
exposes the patient to quite a high dose of radiation. In addition, a contrast medium has
to be injected into the patient’s body in order to make the vascular system and the
soft tissue visible on the X-ray images. Researchers at the Fraunhofer Institute for
Production Technology IPT in Aachen have now found a way of avoiding both the radiation
and the contrast medium. In collaboration with colleagues at Philips and University
Hospital Aachen, they have developed a guide wire made of glass-fiber-reinforced plastic.
“Because the guide wire is made of plastic the imaging can be performed by magnetic
resonance tomography instead of computer tomography,” says IPT scientist Adrian
Schütte. “This is not possible with metal guide wires as the metal wire acts as an
antenna and heats up too much – this would damage the vessels, and could cause
proteins to clot.” Magnetic resonance tomography has many advantages for doctors and
patients. It does not produce ionizing radiation like computer tomography, and soft tissue
is clearly visible, so there is no need for a contrast medium.
By applying cutting-edge techniques in single-molecule manipulation, researchers at
Harvard University have uncovered a fundamental feedback mechanism that the body uses to
regulate the clotting of blood. The finding, which could lead to a new physical,
quantitative, and predictive model of how the body works to respond to injury, has
implications for the treatment of bleeding disorders.
Queen's chemist designs new
'catch-and-tell' molecules
A Queen’s scientist, whose research is now used worldwide in blood analysing
equipment, has made another important discovery. Recently announced as the winner of the
Royal Society of Chemistry’s (RSC) Sensors Award for 2008, Professor A. Prasanna de
Silva, has created ‘intelligent’ molecules. The discovery is based on previous
pioneering research by Professor De Silva and his colleagues at Queen’s, which
created ‘catch and tell’ sensor molecules that send out light signals when they
catch chemicals in blood. That technology helped create blood diagnostic cassettes which
have achieved sales of over $50 million worldwide. Used in hospitals, ambulances and
veterinary offices the cassettes are used to quickly monitor blood for levels of common
salt components such as sodium, potassium and calcium.
Most people know that cranberry juice can help lower the risk of urinary infections, at
least in some cases. But in 2003, doctors found what appeared to be a less beneficial side
effect.
IGC-associated scientists discover
new mechanism that regulates formation of blood vessels
Researchers in one of the external groups of the IGC, have discovered a novel mechanism
which regulates the process whereby new blood vessels are formed and wounds heal,
including chronic wounds, such as those found in diabetic patients and those suffering
from morbid obesity. These findings, by Sérgio Dias and his team, are to appear in the
new issue of the journal PLoS ONE(*), and have implications for the development of new
therapeutic approaches to healing damaged blood vessels and building new ones. Working at
the Centro de Investigação e Patobiologia Molecular of the Portuguese Institute of
Oncology Francisco Gentil, in Lisbon, the Neoangiogenesis groupshowed that the cells that
make new blood vessels (called endothelial cells) are stimulated by an intracellular
signalling pathway, mediated by the protein Notch. The formation of new blood vessels is a
crucial step in wound healing: the newly-formed vessels allow anti-inflammatory proteins
to reach the wound site, improve oxygenation of the damaged tissue and carry essential
nutrients for the re-structuring of the tissue, that is, the skin.
Over the past decade a number of studies have found that, rather than saving lives, blood
transfusions can actually harm patients. Most experts now agree that the problem isn't so
much the risk of blood-borne infectious diseases such as HIV, but the transfused blood
itself. Now, some surgeons and anesthetists are questioning whether every patient should
get the same "bloodless surgery" techniques that are used for Jehovah's
Witnesses -- who shun blood transfusions.
Oceans, plants, and humans - closer
than you think
If you look at our “family tree” you will find that apes are our
“parents”, plants are our “grandparents”, and the sun and sea our
“great grandparents”.
No Proof Found That Genetic Testing
Helps Prevent Blood Clots
According to a new report by the Department of Health & Human Services' (HHS) Agency
for Healthcare Research and Quality (AHRQ), there is insufficient evidence to conclude
that genetic testing for two gene mutations in adults with a history of blood clots helps
to prevent a condition known as deep-vein thrombosis or to improve other clinical
outcomes. The report, a summary of which will be published in the June 17 issue of JAMA,
also failed to find any benefit from genetic testing of family members of patients who
have at least one of the two mutations—known as Factor V Leiden (FVL) and prothrombin
G20210A—as well as a history of deep-vein thrombosis. As many as 600,000 Americans
each year may have deep-vein thrombosis—blood clots that form in the legs or pelvis.
The condition occurs most commonly in people who are sedentary for a long period of time,
such as when recovering from surgery or traveling long distances. The true number of
people who develop a pulmonary embolism is unknown, but AHRQ data for hospital patients
show that 258,000 individuals were diagnosed with the condition in 2006, and 20,000 died
as a result. "While genetic testing shows great promise to improve treatment and
prevent disease, this report clearly shows that we need more research and evidence to
achieve its full potential," said AHRQ Director Carolyn M. Clancy, M.D. "But
people can help reduce their likelihood of developing a blood clot by talking with their
doctor about precautions." The evidence report was requested and supported by the
Office of Public Health Genomics (OPHG) at HHS' Centers for Disease Control and
Prevention. The Evaluation of Genomic Applications in Practice and Prevention (EGAPP)
Working Group, established by OPHG in 2005, will use this evidence report and other
evidence to make recommendations on the validity and utility of genetic tests for FVL and
prothrombin G20210A. This report, titled Outcomes of Genetic Testing in Adults with a
History of Venous Thromboembolism, is the fifth evidence report requested for EGAPP.
Researchers Devise Means to Create
Blood By Indentifying Earliest Stem Cells
Johns Hopkins researchers have discovered the earliest form of human blood stem cells and
deciphered the mechanism by which these embryonic stem cells replicate and grow. They also
found a surprising biological marker that pinpoints these stem cells, which serve as the
progenitors for red blood cells and lymphocytes. The biochemical marker,
angiotensin-converting enzyme (ACE), is well known for its role in the regulation of blood
pressure, blood vessel growth, and inflammation. ACE inhibitors are already widely used to
treat hypertension and congestive heart failure, and the findings are, the researchers
say, likely to hold promise for developing new treatments for heart diseases, anemias,
leukemia and other blood cancers, and autoimmune diseases because they show for the first
time that ACE plays a fundamental role in the very early growth and development of human
blood cells. “We figured out how to get the ‘mother’ of all blood stem
cells with the right culture conditions,” says Elias Zambidis, M.D., Ph.D., of the
Institute of Cell Engineering at the Johns Hopkins University School of Medicine and the
Division of Pediatric Oncology at the Sidney Kimmel Comprehensive Cancer Center at Johns
Hopkins. “There is real hope that in the future we can grow billions of blood cells
at will to treat blood-related disorders, and just as critically if not more so,
we’ve got ACE as a ‘new’ old marker to guide our work,” Zambidis adds.
Controlling the green stuff in snot could help treat heart disease, reveals Professor
Michael Davies from the Faculty of Medicine and the Heart Research Institute. In an
exciting discovery, researchers from The University of Sydney, the Free Radical Centre at
the Heart Research Institute (HRI), and the Queensland University of Technology have found
agents that could stop the progression of heart disease by preventing damage by an enzyme
also found in snot."It might sound disgusting, but the same goop that makes snot
green gets dumped in our arteries during heart disease", Professor Davies. Snot
appears green due to the presence of the enzyme, myeloperoxidase.
Leaky blood vessels may cause fifth
of strokes, study suggests
One in five strokes may be caused by a weakening of the tiny arteries in the brain, a
study has found. New research shows that the brain damage caused by lacunar strokes -
which occur in tiny rather than large arteries - may be caused by a gradual weakening of
the artery wall. It was previously thought that this type of stroke was caused only by
reduced blood flow to the brain. Scientists at the University of Edinburgh believe that
this weakening occurs in the protective lining of the small arteries - known as the
blood-brain barrier - which stops potentially harmful substances getting into the brain.
The research involved two groups of stroke patients - one with lacunar stroke and one with
the large artery type. Both groups were injected with magnetic dye before having brain
scans that showed how the dye travelled through their blood vessels. In the lacunar
patients, more dye leaked out of the blood vessels into the brain than was the case in the
other group. This could only have happened if the dye were able to leak through the
protective barrier.
Blood vessel cells are instructed
to form tube-like structures
How do blood vessel cells understand that they should organise themselves in tubes and not
in layers? A research group from Uppsala University shows for the first time that a
special type of “instructor” molecule is needed to accomplish this. These
findings, published in the scientific journal Blood, might be an important step towards
using stem cells to build new organs. In order for a body to develop and function the
cells in the body must be able to organise themselves in relation to each other. The way
in which cells are arranged depends on the organ where they are located. Blood vessel
cells need to form three-dimensional, tube-like structures that can transport blood. But
how do blood vessel cells know that they should do that? An important part of the
communication between cells and their environment is the use of growth factors. These are
proteins that bind to receptors on the surface of the cell that receives the information.
When the receptor in turn forms a complex with other proteins, on the inside of the cell,
the read-out from the DNA can be altered. The information has “arrived”.
Scientists at the University of Bonn have discovered a new rare type of hemoglobin.
Hemoglobin transports oxygen in the red blood corpuscles. When bound to oxygen it changes
color. The new hemoglobin type appears optically to be transporting little oxygen.
Measurements of the blood oxygen level therefore present a similar picture to patients
suffering from an inherited cardiac defect.
For years, researchers have known that high blood pressure causes blood vessels to
contract and low blood pressure causes blood vessels to relax. Until recently, however,
researchers did not have the tools to determine the exact proteins responsible for this
phenomenon. Now, using atomic force microscopy - a microscope with very high resolution -
and isolating blood vessels outside the body, University of Missouri researchers have
identified a protein that plays an important role in the control of tissue blood flow and
vascular resistance. This new knowledge brings researchers one step closer to
understanding vascular diseases, such as high blood pressure, diabetes and other vascular
problems. “This study provides new insights that clarify the role of specific
proteins and the vascular smooth muscle cells that control the mechanical activity of
blood vessels,” said Gerald Meininger, professor and director of MU’s Dalton
Cardiovascular Research Center. “We have identified an important receptor that is
responsible for the ability of small arteries in the body. This research provides new
clues for the cause of vascular diseases, such as high blood pressure and diabetes and may
be used in the future as a possible therapeutic target.”
Last step leading to blood cell
formation elucidated
These new insights represent an important contribution to future clinical therapeutic
approaches. The study was published in the prestigious science journal Nature and will be
a central topic of the international symposium on the molecular mechanisms of
hematopoiesis, which will take place in Munich from April 2nd to 4th. The findings on the
molecular mechanisms of blood formation (hematopoiesis) will be presented in Munich at the
international symposium "Molecular Mechanisms of Normal and Malignant
Hematopoiesis" from April 2nd to 4th. A question that has puzzled researchers for
decades could now be solved: How are the first blood cells generated in the embryo? In
particular, Dr. Timm Schroeder, research group leader at the Institute of Stem Cell
Research of Helmholtz Zentrum Muenchen and his team found out that a special type of
endothelial cells exists that can transform themselves into blood cells. Endothelial cells
line the interior surface of blood vessels. Dr. Timm Schroeder explained "It is
extremely difficult to investigate the blood cell generation process. It occurs only very
briefly, hidden from view in the embryo within the mother's uterus." The scientists
first had to create the technical means to continually observe the transformation process
of endothelial cells into blood cells on the single-cell level over a longer period of
time. Dr. Schroeder and his colleagues developed novel bioimaging techniques with which
the behavior of large numbers of individual cells can be recorded and tracked. They
combined optimized microscopy, incubation and imaging technology as well as novel software
programs to track individual cells in time-lapse videos with sophisticated cell
purification and cell culture techniques. Thus, the scientists could observe the behavior
of many differentiating mesodermal cells over a period of up to one week. By carefully
analyzing thousands of cells and the molecules expressed by them, Dr. Schroeder and PhD
student Hanna Eilken were able to detect several very rare endothelial cells that indeed
transformed themselves into blood cells.
Blood transfusions may do more harm than good for a majority of patients because banked
blood begins to lose a key gas almost immediately after it is donated, researchers said
Monday.
Scientists at the University of Bonn have discovered a new rare type of haemo-globin.
Haemoglobin transports oxygen in the red blood corpuscles. When bound to oxygen it changes
colour. The new haemoglobin type appears optically to be transporting little oxygen.
Measurements of the blood oxygen level therefore present a similar picture to patients
suffering from an inherited cardiac defect. After examining two patients, the scientists
now understand that the new type of haemoglobin distorts the level of oxygen measured. The
scientists have named the type 'Haemoglobin Bonn'. They have published their discovery in
the current issue of the scientific journal 'Clinical Chemistry'.
In initial testing, the Ingber lab combined Candida albicans with blood and the antibody
coated iron beads. The solution was then filtered through their system, a dialysis like
device with electromagnets and up to 80 percent of the bead-pathogen complex were removed.
Bonn study shows that people with anxiety disorders tend to suffer from increased blood
clotting. f you are "frightened stiff", not only does the intense fear seem to
paralyse the body, it may even retard the blood flow. A study by medical scientists at the
University of Bonn has shown that people with an acute anxiety disorder tend to suffer
from higher levels of blood clotting than the psychologically healthy population. This
finding may explain why patients with anxiety problems are at greater risk of dying from
heart disease ? by a factor of one to four times. "The blood froze in my veins"
or "My blood curdled" these common figures of speech can be taken literally,
according to the latest studies. Indeed, more literally than some of us would like. For it
turns out that intense fear and panic attacks can really make our blood clot and increase
the risk of thrombosis or heart attack. Earlier studies showed that stress and anxiety can
influence coagulation. However, they were based almost entirely on questionnaire surveys
of healthy subjects. In contrast, the Bonn-based research team around Franziska Geiser
(from the Clinic and Policlinic for Psychosomatic Medicine and Psychotherapy) and Ursula
Harbrecht (from the Institute of Experimental Haematology and Transfusion Medicine) have
been the first to conduct a very careful examination of coagulation in patients with
anxiety disorders.
Model for new generation of blood
vessels challenged
In-growth and new generation of blood vessels, which must take place if a wound is to heal
or a tumor is to grow, have been thought to occur through a branching and further growth
of a vessel against a chemical gradient of growth factors. Now a research team at Uppsala
University and its University Hospital has shown that mechanical forces are considerably
more important than was previously thought. The findings, published today in the journal
Nature Medicine, open up a new field for developing treatments. New generation of blood
vessels takes place in normal physiological processes, such as when a wound heals,
children grow, or the mucous membrane of the womb is built up to be able to receive a
fertilized egg. It is also a crucial mechanism in tumor diseases, rheumatism, and certain
eye disorders, for example. How new generation and in-growth of blood vessels takes place
has not been fully understood. It has been assumed that the mechanisms are the same as
those that occur in embryonic development, which is probably a great over-simplification.
The formation of the vascular system in the fetus takes place in a well-organized and
reproducible way, which means that we all have blood vessel systems that look very much
the same. On the other hand, new generation of vessels in wound healing and tumor growth,
for example, occurs in a chaotic environment where it is difficult to see that there would
be well-defined gradients of growth factors, and it has not been possible to find evidence
of any. "Unlike these previous models, our findings show that in wound healing,
in-growth of new blood vessels takes place via mechanical forces that pull already
existing blood vessels into the wound when it heals," says Pär Gerwins, who directed
the study and is a physician and interventional radiologist at Uppsala University Hospital
as well as a researcher with the Department of Medical Biochemistry and Microbiology at
Uppsala University.
Genetic Abnormality May Increase
Risk of Blood Disorders
Researchers at Memorial Sloan-Kettering Cancer Center (MSKCC) have shown for the first
time that a tendency to develop some blood disorders may be inherited. Their research,
published online today in Nature Genetics, identifies a common genetic sequence
abnormality that enhances the likelihood of acquiring a mutation in a gene linked to
certain blood diseases. The investigators carried out a genome-wide study to identify
inherited DNA sequence changes that frequently occur in patients with myeloproliferative
neoplasms, in which several types of blood cells are excessively produced in the bone
marrow. They found that an inherited alteration in the gene for JAK2 - a protein with
enzymatic activity that is linked to the abnormal production of blood cells - is more
common in patients with these disorders. Importantly, patients who inherited this JAK2
alteration were predisposed to acquiring another JAK2 mutation on the same DNA strand.
According to the research, these mutations do not arise randomly, but are specifically
determined by the DNA sequence.
Experts reach consensus on
diagnosis and treatment of bleeding disorders in women
Because bleeding from the reproductive tract is a naturally occurring event during
menstruation and childbirth, women who exhibit menorrhagia, or excessive bleeding after
their menstrual cycle, may have underlying diseases that are underdiagnosed. In order to
address important issues related to the diagnosis and management of reproductive tract
bleeding in women with bleeding disorders, a consensus conference was convened. Results
are published in the July 2009 issue of the American Journal of Obstetrics &
Gynecology. The goals of the consensus conference were to highlight the problems these
women experience and to provide clinical information and recommend strategies to guide
practicing obstetricians and gynecologists. Where the international panel of experts in
obstetrics, gynecology and hematology reached consensus, recommendations were made. Von
Willebrand Disease (VWD) is the most common inherited bleeding disorder. VWD results from
a deficiency in, or a dysfunction of, von Willebrand factor (VWF), a protein necessary for
normal platelet adhesion and protection of factor VIII (FVIII) from proteolysis in the
circulation. The prevalence of menorrhagia in women with VWD is 74-92%. Although the
majority of women who present with menorrhagia do not have a bleeding disorder, the
conference participants identified more than a dozen symptoms that suggest further
evaluation, including menorrhagia since puberty, a family history of a bleeding disorder,
and personal history of one, but usually several, of the following symptoms: nosebleeds
(generally bilateral for more than 10 minutes), more than once in the past year; notable
bruising without injury (and with bruises >2 cm in diameter); minor wound bleeding from
trivial cuts lasting for more than 5 minutes; or prolonged or excessive bleeding following
dental extraction.
FDA Scientists Warn About Bleeding
Risk of Bayer's Blood-Thinning Drug
The FDA has publicly released documents from science reviewers expressing concern over the
blood-thinning drug rivaroxaban, marketed by Bayer AG and Johnson & Johnson (J&J)
as Xarelto in Canada and Europe. The drug has yet to receive regulatory approval in the
United States, but an application is pending.
Heart patients are often given two or three different drugs to prevent life-threatening
blood clots but these combinations can double, triple or even quadruple the risk of
stomach or intestinal bleeding, U.S. researchers said on Tuesday.
Blood transfusions carried out after cardiac surgery could be unnecessary and might cause
health complications for patients. Thanks to a £1 million grant by the National Institute
for Health Research Health Technology Assessment (NIHR HTA) programme a new research study
will investigate this issue. In the UK, cardiac surgery uses almost ten per cent of all
donor blood. Although the benefits of red cell blood transfusions for managing
life-threatening bleeding are clear, the majority of decisions to transfuse after surgery
are made on the basis of a patient’s haemoglobin level (a measure of the ability of
the blood to transport oxygen around the body). The level that causes a doctor to
transfuse a patient varies widely and research in non-cardiac surgical fields has shown
that lowering the level that ‘triggers’ transfusion reduces complications as
well as the use of blood. Barnaby Reeves, Professorial Research Fellow in Health Services
Research at the University of Bristol and Gavin Murphy, Walport Consultant Senior Lecturer
in Cardiac Surgery at University Hospitals Bristol NHS Foundation Trust will lead the
study.
MDCT Angiography Helps Lead to
Successful Treatment of Patients with Severely Blocked Arteries in the Legs
MDCT angiography leads to accurate recommendations for successful treatment of patients
with critical limb ischemia, sometimes allowing the patients to avoid more complicated
surgery, according to a study performed at the Medical University of Vienna, Vienna,
Austria. The study included 28 patients with severely blocked peripheral arteries. MDCT
angiography indicated that nine patients should undergo non-surgical endovascular
treatment such as percutaneous angioplasties or stent placement. Seven patients had
surgery and two had a combination of treatments. “MDCT angiography identified the
correct treatment in 18 patients,” said Rudiger Schernthaner, MD, lead author of the
study. In addition, MDCT angiography indicated that ten patients could or did not need to
undergo any treatment. “The reported incidence of peripheral arterial occlusive
disease (PAOD) is 15.5 cases per 1,000 person-years, and the prevalence is 4.5% among men
older than 55,” he said.
Mayo Researchers Explore Issues
Related to Multiple Myeloma Treatment
Multiple myeloma (MM) is a cancer of plasma cells that affects approximately 3 in 100,000
people each year. Although there is no cure for this disease, researchers have developed
treatments that help relieve pain, control complications, and slow the progress of MM in
many patients. Unfortunately, some of the most effective therapies also have toxic side
effects that can pose serious health risks and reduce quality of life. In the October
issue of Mayo Clinic Proceedings, two articles authored by Mayo researchers address the
issue of how to balance the risks and benefits associated with MM treatments.
By applying cutting-edge techniques in single-molecule manipulation, researchers at
Harvard University have uncovered a fundamental feedback mechanism that the body uses to
regulate the clotting of blood. The finding, which could lead to a new physical,
quantitative, and predictive model of how the body works to respond to injury, has
implications for the treatment of bleeding disorders. A team, co-led by Timothy A.
Springer, Latham Family Professor of Pathology at Harvard Medical School and Children's
Hospital Boston, and Wesley P. Wong, Rowland Junior Fellow and a Principal Investigator at
the Rowland Institute at Harvard, reported its discovery about the molecular basis for the
feedback loop responsible for hemostasis in the June 5th issue of Science. "The human
body has an incredible ability to heal from life's scrapes and bruises," explains
Wong. "A central aspect of this response to damage is the ability to bring bleeding
to end, a process known as hemostasis. Yet regulating hemostasis is a complex balancing
act." Too much hemostatic activity can lead to an excess of blood clots, resulting in
a potentially deadly condition known as thrombosis. If too little hemostatic activity
occurs in the body, a person may bleed to death. To achieve the proper balance, the body
relies on a largely mechanical feedback system that relies on the miniscule forces applied
by the circulation system on a molecular "force sensor" known as the A2 domain
of the blood clotting protein von Willebrand factor (VWF). By manipulating single
molecules of this A2 domain, the researchers found that the A2 domain acts as a highly
sensitive force sensor, responding to very weak tensile forces by unfolding, and losing
much of its complex three-dimensional organization. This unfolding event allows the
cutting of the molecule by an enzyme known as ADAMTS13. "In the body, these cutting
events decrease hemostatic potential and also enable blood clots to be trimmed in size.
The system is so finely tuned that the A2 shear sensor is able to regulate the size of VWF
within the blood stream, maintaining the optimal size for responding properly to
traumas," says Wong.
Discovery of natural compounds that
could slow blood vessel growth
Inside a cell it is so crowded that a certain protein from borrelia winds up being
crunched. From having been like an oblong rugby football, it gets bent and then collapses
into a lump. At this point a previously hidden part appears, known to trigger the
formation of antibodies. This explains how Borrelia can be diagnosed, a process that was
previously unknown. Congestion in the cell environment forces the protein V1sE, which
exists in borrelia bacteria, to change shape. Like a jack-in-the-box, an antigen- a
substance alien to the body -then pops up, prompting the body to start producing
antibodies. It is precisely the prevalence of these antibodies that physicians often use
to diagnose borrelia. Until today, we have had no knowledge of how these antibodies are
produced, since the antigen is hidden in the original form of the V1sE protein. “We
suspect that the changes in the shape of the protein are nature’s own origami to
control what functions the protein should have in specific circumstances. In this way
different parts can be exposed, roughly as in the jumping fleas made of folded paper that
children play with,” says Pernilla Wittung-Stafshede, who was recently named
professor of biological chemistry at Umeå University in Sweden.
All blood cell production in adults depends on the steady work of a vital gene that if
lost results in early bone marrow failure, Dartmouth Medical School cancer geneticists
have found. Their research reveals an unexpected role for the gene in sustaining the adult
blood-forming system, and opens novel strategies for targeting the gene, which is often
involved in a type of childhood leukemia.
Advanced image analysis can provide
better risk assessment in hardening of the arteries
Ultrasound examination of the carotid artery is a patient-friendly and inexpensive method
for assessing atherosclerosis and thereby predicting the risk of cardiovascular diseases.
Peter Holdfeldt, who recently defended his doctoral thesis at Chalmers University of
Technology in Sweden, has developed new analytical methods for ultrasound images that can
provide more reliable and more exact assessments of atherosclerosis. Cardiovascular
diseases brought on by hardening of the arteries are the most common cause of death in the
Western world. Hardening of the arteries means a thickening of the walls of blood vessels
and the appearance of so-called atherosclerotic plaque, which consist of stored fat, among
other things. With the aid of ultrasound images, it is possible to find individuals who
are at risk by measuring the thickness of the walls in the carotid artery. Another
ultrasound method is to analyze whether the character of various types of plaque can
predict the risk of cardiovascular diseases. Peter Holdfeldt has developed new and more
refined methods of image analysis that are based on dynamic programming.
"Measurements of the thickness of the walls of the carotid require the detection of
boundaries between different layers of tissue in the blood vessel," he says.
"Previously dynamic programming has been used to automatically detect boundaries in
still images. But the new method uses dynamic programming for detection in image sequences
of one and the same blood vessel instead."
By applying cutting-edge techniques in single-molecule manipulation, researchers at
Harvard University have uncovered a fundamental feedback mechanism that the body uses to
regulate the clotting of blood. The finding, which could lead to a new physical,
quantitative, and predictive model of how the body works to respond to injury, has
implications for the treatment of bleeding disorders.A team, co-led by Timothy A.
Springer, Latham Family Professor of Pathology at Harvard Medical School and Children's
Hospital Boston, and Wesley P. Wong, Rowland Junior Fellow and a principal investigator at
the Rowland Institute at Harvard, reports its discovery about the molecular basis for the
feedback loop responsible for hemostasis in the June 5 issue of Science. "The human
body has an incredible ability to heal from life's scrapes and bruises," explains
Wong. "A central aspect of this response to damage is the ability to bring bleeding
to an end, a process known as hemostasis
A rush of blood to the head --
anger increases blood flow
Mental stress causes carotid artery dilation and increases brain blood flow. A series of
ultrasound experiments, described in BioMed Central's open access journal Cardiovascular
Ultrasound, also found that this dilatory reflex was absent in people with high blood
pressure. Tasneem Naqvi and Hahn Hyuhn from the University of Southern California and
Cedars-Sinai Medical Center evaluated carotid artery reactivity and brain blood flow in
response to mental stress in 10 healthy young volunteers (aged between 19 and 27 years),
20 older healthy volunteers (aged 38 to 60 years) and in 28 patients with essential
hypertension (aged 38 to 64 years). They found that in healthy subjects, mental stress
caused vasodilation. This was accompanied by a net increase in brain blood flow. In
hypertensive subjects, mental stress produced no vasodilation and no significant change in
brain blood flow. During the experiments, the volunteers were set a series of tasks
designed to provoke mental stress, including reading, arithmetic and anger recall tests.
The researchers used ultrasound imaging to measure the effects of this activity on the
carotid artery and an artery within the brain, while also measuring blood pressure and
heart rate. According to Naqvi, "Inappropriate vasoconstriction, or lack of dilation
in response to mental stress in stable coronary heart disease, contributes to the genesis
of myocardial ischemia and confers an increased risk in patients with coronary artery
disease. It will be interesting to see whether the lack of mental stress induced dilation
we found defines subjects at increased risk of future cerebral events". Lack of
required blood flow increase to the brain during mental activities may potentially affect
cognition and cerebral performance during complex cerebral tasks.
A West Australian research team has made the world-first discovery a 'pied piper' molecule
within blood cells, called Liar, that leads other molecules into the nucleus of the cell,
and could offer a key in treating prostate, breast and colon cancers as well as leukemia.
Uncovered by two research groups at the Western Australian Institute for Medical Research
(WAIMR) led by Associate Professor Evan Ingley and Director Professor Peter Klinken, they
have also identified the function of a known cellular enzyme, Lyn, as a switch that 'turns
on' blood cell development. The findings are published in the April 16 issue of Blood, the
journal of the American Society of Hematology, the world's premier hematology journal.
Associate Professor Ingley said the findings were a leap forward in the understanding of
how blood cells develop and divide, which could offer them a key to turning off cancerous
cell growth. "LIAR is like a key, which opens a pathway into the nucleus of a blood
cell for a number of other molecules, allowing them to flow in – and these molecules
are what signal the cell to develop and divide," he said. "From here, if we
could control Liar, the hope is that we could use it to switch off the growth of abnormal,
or cancerous, cells. "Because Liar is present in every blood cell, this knowledge
could help treat a huge range of conditions and diseases, but where it has most potential
is in cancers of the prostate, breast, colon and blood where activity of the enzyme Lyn is
heightened." The focus of the team's investigations, Lyn has now been identified as
an enzyme which modifies proteins that triggers the cell to develop further.
Cartilage, bones and the internal walls of blood vessels can be created by using common
connective tissue cells from human skin. Researchers in reconstructive plastic surgery at
Linköping University have successfully manipulated these tissue cells to take on
different shapes depending on the medium they have been cultivated in.“This means
that it will be much easier to produce autologous tissue, which is tissue created from the
patient’s own body”, says Gunnar Kratz, Professor of Experimental Plastic
Surgery and team leader for the research group.The results of the group’s research
are now published in three simultaneous scientific articles. Bone, cartilage and blood
vessels are important components in reconstructive surgery, where damaged tissue needs to
be recreated. Minor fractures can heal spontaneously but for major bone damage and
cartilage injuries there is the need to transplant tissue from other parts of the
patient’s body. Different strategies have been attempted to instead grow autologous
tissue from stem cells, for example those present in bone marrow. These cells, however,
can be difficult to harvest, cultivate and store. Compared to these cells connective
tissue cells from human skin has great advantages. A small biopsy is often enough to
collect a sufficient amount of cells. “They are the ‘weed’ cells of the
body, very easy to collect and cultivate into the cell type required. They are also very
suitable to use to create a personal cell bank”, Gunnar Kratz says.
Weizmann Institute Scientists Show
White Blood Cells Move like Millipedes
How do white blood cells – immune system ‘soldiers’ – get to the site
of infection or injury? To do so, they must crawl swiftly along the lining of the blood
vessel – gripping it tightly to avoid being swept away in the blood flow – all
the while searching for temporary ‘road signs’ made of special adhesion
molecules that let them know where to cross the blood vessel barrier so they can get to
the damaged tissue. In research recently published in the journal Immunity, Prof. Ronen
Alon and his research student Ziv Shulman of the Weizmann Institute’s Immunology
Department show how white blood cells advance along the length of the endothelial cells
lining the blood vessels. Current opinion maintains that immune cells advance like
inchworms, but Alon’s new findings show that the rapid movement of the white blood
cells is more like that of millipedes. Rather than sticking front and back, folding and
extending to push itself forward, the cell creates numerous tiny ‘legs’ no more
than a micron in length – adhesion points, rich in adhesion molecules (named LFA-1)
that bind to partner adhesion molecules present on the surface of the blood vessels. Tens
of these legs attach and detach in sequence within seconds – allowing them to move
rapidly while keeping a good grip on the vessels’ sides.
Elevated level of certain protein
in urine linked to increased risk for blood clots
Preliminary research suggests that higher than normal levels of the protein albumin in
urine is associated with an increased risk for blood clots in the deep veins of the legs
or lungs (venous thromboembolism; VTE), according to a study in the May 6 issue of JAMA.
The overall incidence of VTE in developed countries is about 0.15 percent per year,
varying from less than 0.005 percent in individuals younger than 15 years to as high as
0.5 percent at 80 years of age. Known risk factors for VTE include stasis (a slowing of
the normal flow) of the blood and changes in the composition of the blood. However, in as
many as 50 percent of VTE cases, none of the known risk factors are present, according to
background information in the article. Microalbuminuria (albumin in urine; 30-300 mg per
24-hour urine collection) is associated with changes in the levels of several coagulation
proteins. The effect of coagulation disorders is more evident in the development of VTE
than of arterial thromboembolism (formation of a blood clot in the arterial system).
"Hence, in theory, a link between microalbuminuria and VTE is likely; however,
research addressing this issue has yet to be conducted," the authors write. Bakhtawar
K. Mahmoodi, B.Sc., of the University Medical Centre Groningen, the Netherlands, and
colleagues conducted a study to assess whether microalbuminuria is associated with VTE.
The ongoing, community-based study, started in 1997, includes all inhabitants of
Groningen, the Netherlands, (age 28 through 75 years [n = 85,421]) who were sent a postal
questionnaire and a vial to collect a urine sample for measurement of urinary albumin
concentration. Of those who responded (40,856), a group (8,592) including more
participants with higher levels of urinary albumin concentration completed screening at an
outpatient clinic. Screening data were collected on urinary albumin excretion (UAE) and
risk factors for cardiovascular and kidney disease.
What separates dangerous blood
vessel plaques from benign ones
Researchers say they have evidence to explain what separates your average blood vessel
plaque from those that are at high risk for triggering the development of
dangerous—even fatal—blood clots. The findings in the May issue of Cell
Metabolism, a Cell Press publication, suggest that drugs designed to tackle a form of
cellular stress might be useful in treating heart disease, which is the number one killer
and getting worse, according to the researchers. "Just about everybody in our society
has atherosclerosis by the time we reach 20," said Ira Tabas of Columbia University
in New York. In atherosclerosis, lipid, inflammation and white blood cells known as
macrophages build up at various spots along blood vessel walls, he explained. The vast
majority of these lesions will never cause any problem whatsoever, but the rest—some
2 percent of all plaques—will eventually lead to the development of an acute blood
clot and to heart attack, sudden death, or stroke. "The billion dollar question is
why 98 percent cause no problem, and 2 percent do." Their report adds support to the
notion that so-called endoplasmic reticulum (ER) stress together with the body's natural
way of coping with that stress is one answer. The ER is a cellular component that serves
two major functions: it is the site where new proteins are made, folded, and transported,
and it is also the central storage depot for the cell's calcium and controls its release,
Tabas explained. When insults to the cell throw those functions off kilter, cells handle
the imbalance via a pathway known as the unfolded protein response (UPR). If times get
really tough, that pathway simply kills off the cells that are suffering. That decision to
die is commandeered by an ER stress effector known as CHOP. "When cells die, it's OK
as long as it's not en masse," Tabas said, noting that we lose billions of cells
every day. "It's a wonderful path to keep the ER in check, and by killing a cell here
and there because of uncorrectable ER stress, the pathway protects the whole organism. In
pathologies, however, this pathway gets overexuberant." Indeed, scientists are
increasingly coming to the realization that ER stress and the body's
"overexuberant" reaction to it are common features of aging, underlying
neurodegenerative disease, and diabetes, for example. In the case of atherosclerosis, ER
stress within plaques could lead to the massive death of cells—and of macrophages in
particular—leading to the generation of a structure called the "necrotic
core." Those necrotic cores are known to be a defining feature of plaques that are
vulnerable to rupture and blood clot formation. While earlier studies had suggested a
correlation between ER stress and vulnerable plaques, the new study is the first to show a
clear causal connection between the two, Tabas said. His group studied two separate
strains of mice, each carrying a specific genetic alteration that makes them especially
prone to develop atherosclerosis. The mice also lacked CHOP, disabling the prodeath branch
of the ER stress pathway.
Research at Columbia University
Medical Center shows why certain arterial plaques can turn deadly
A common misconception about arterial plaque is that it inevitably leads to a heart attack
or a stroke. New research at Columbia University Medical Center, however, sheds light on
why so few plaques in any given individual actually cause a problem. Furthermore, the
research has identified a key protein that may promote the conversion from benign to
dangerous plaques. While a vast majority of atherosclerotic lesions are relatively
harmless, the rest – some two percent of all plaques – eventually lead to an
acute blood clot and to heart attack, sudden death or stroke. What separates the average
blood vessel plaque from those that are at high risk for triggering the development of
dangerous – even fatal – blood clots, is the "billion dollar
question," says Columbia University Medical Center's Ira Tabas, M.D., Ph.D., whose
findings are presented in the cover story of the May issue of Cell Metabolism. Dr. Tabas
believes that the real danger from the fatty deposits lies not with their size, but with
what lies underneath the surface of the deposit. Like magma underneath a volcano,
rumblings in the core of a deposit, which contains dead cells, can break open the plaques.
Once the plaque ruptures, a blood clot in the lumen of the artery can form. "It is
this sudden clotting that restricts blood flow and can cause a heart attack, stroke, or
sudden cardiac death," Dr. Tabas says. "Just about everybody in our society has
atherosclerosis by the time we reach 20," Dr. Tabas added. "So the wave of the
future in treating atherosclerosis will be in preventing harmless lesions in young people
from becoming dangerous ones, or soothing dangerous plaques so they don't rupture as we
age." The best way to do that is unclear at the moment. Volatile plaques are
complicated, and there are likely many things that lead to instability and rupture. But a
graveyard – or necrotic core – of dead cells inside the plaque undoubtedly
contributes, Dr. Tabas says, because substances released by the dead cells tend to weaken
the cap covering the lesion and thereby trigger clot formation. The research by Dr. Tabas'
lab found that when a specific gene was deleted in two separate strains of
atherosclerosis-prone mice, the dangerous plaques were much smaller. The gene encodes a
protein that is part of a cell stress reaction that can lead to cell death. The work
raises the possibility that drugs designed to quiet this form of cellular stress might be
useful in treating heart disease, which is the number one killer in the United States and
becoming more prevalent.
Possible safer target for
anti-clotting drugs found
Researchers at the University of Illinois at Chicago College of Medicine have identified a
new molecular target in the process of blood clot formation, which seems to reduce
clotting without excessive bleeding, the common side-effect of anti-clotting agents.
Current US guidelines for the prescription of potent anticoagulants by surgeons who
perform joint replacement operations could be doing patients more harm than good,
according to Dr. Nigel Sharrock and his team from the Hospital for Special Surgery in New
York. Their paper was published in the March issue of Springer's journal Clinical
Orthopaedics and Related Research.
Study in Nature Medicine
establishes major new treatment target in diseased arteries
Removing a single protein prevents early damage in blood vessels from triggering a
later-stage, frequently lethal complication of atherosclerosis, according to research
published online today in the journal Nature Medicine. By eliminating the gene for a
signaling protein called cyclophilin A (CypA) from a strain of mice, researchers were able
to provide complete protection against abdominal aortic aneurysm (AAA). The aorta is the
main artery carrying blood from the heart, and AAA is a progressive outward dilation of
the aorta under the stress of blood pressure due to a breakdown in the vessel's structural
integrity. AAA leads to 15,000 deaths a year, mostly in aging men, when aneurysms rupture
to spill blood into the abdomen, a fatal event in 90 percent of cases. Adding to the
study's importance, AAA shares vital biochemical pathways with atherosclerosis, the
leading cause of heart attack and stroke. Thus, drugs that target CypA could potentially
address both AAA and atherosclerosis. When study mice were engineered to remove their CypA
gene, none from that group developed AAA in the face of the hypertension and high
cholesterol known to accelerate it. In contrast, 78 percent of mice with
"normal" amounts of CypA developed AAA under the same conditions, 35 percent
with a fatal rupture. The team also found high CypA levels in the rupture-prone vessels of
humans with AAA, and that major drugs like statins reduce CypA levels, which may partly
explain their benefit. "It is extremely unusual for the removal of one protein to
provide absolute protection, but it makes perfect sense because cyclophilin A promotes
three of the most destructive forces in blood vessels – oxidative stress,
inflammation and matrix degradation," said Bradford C. Berk, M.D., Ph.D., professor
of Medicine within the Aab Cardiovascular Research Institute at the University of
Rochester Medical Center, and senior author of the study. "We are working to design
anti-CypA drugs that will diminish the disease processes underlying AAA, atherosclerosis
and hypertension."
Bacteria can directly cause human blood and plasma to clot—a process that was
previously thought to have been lost during the course of vertebrate evolution, according
to new research at the University of Chicago, National Institute of Allergy and Infectious
Diseases, and Institut Pasteur in Paris. Their findings will be published online Nov. 2 in
Nature Chemical Biology. The discovery will improve scientists' understanding of
coagulation during bacterial infections and may lead to new clinical methods for treating
serious medical conditions such as sepsis and anthrax.
Study Finds Blood Cells Can Be
Reprogrammed to Act as Embryonic Stem Cells
In a recent study, U.S. researchers have reprogrammed cells found in circulating blood
into cells that are molecularly and functionally indistinguishable from embryonic stem
cells, a revolutionary achievement that provides a readily accessible source of stem cells
and an alternative to harvesting embryonic stem cells. The findings were prepublished
online in Blood, the official journal of the American Society of Hematology. Embryonic
stem cells have long been coveted for their potential to treat a multitude of diseases as
a result of their unique properties of nearly indefinite self-renewal and pluripotency
(the ability to develop into any type of cell in the body), but their use has been the
subject of political controversy. “Our findings provide the first proof that cells
from human blood can morph into stem cells,” said senior study author George Q.
Daley, MD, PhD, an investigator for the Howard Hughes Medical Institute at Children’s
Hospital, Boston. “Making pluripotent stem cells from blood, which is one of the
easiest tissues to obtain, provides an easy strategy for generating patient-specific stem
cells that are valuable research tools and may one day be used to treat a number of
diseases.” To generate induced pluripotent stem cells (dubbed iPS cells), blood was
collected from a 26-year-old male donor. From the blood sample, the researchers isolated
CD34+ cells, a type of stem cell that produces only blood cells, and cultured them in
growth factors for six days to increase their number. During the culture, the scientists
infected the CD34+ cells with viruses carrying reprogramming factors, genes normally
expressed in embryonic stem cells that can reset the blood cells to an embryonic state.
Colonies of cells exhibiting physical characteristics similar to embryonic stem (ES) cells
appeared about two weeks after the procedure. To determine whether these cells were also
functionally similar to ES cells, the scientists analyzed the CD34+ iPS cell lines to see
if they had acquired stem cell “markers,” the unique combination of proteins
that coat the cells’ surface and distinguish them from other types of cells. Indeed,
the iPS cell lines expressed the same markers as ES cells and further shared the capacity
to differentiate into a variety of specialized cell types.
