Blodet ditt kan avsløre risiko for hjerte- og karsykdom

Researcher at CERG, Anja ByeNår du besøker fastlegen din kan du måle blant annet kolesterol og triglyserider i blod for å avdekke om du er i risikosonen for hjerte- og karsykdom. Sammen med informasjon om BMI, røykevaner og blodtrykk, kan fastlegen din bruke dette til å estimerer sannsynligheten for at du får hjerte- og karsykdom i løpet av de neste 10 årene. Det er flere risikokalkulatorer tilgjengelig i dag, og i Norge bruker fastlegene vanligvis NORRISK systemet, som er tilpasset den norske befolkningen. NORRISK bruker informasjon om alder, kjønn, røykevaner, systolisk blodtrykk og total kolesterol til å estimere den enkeltes risiko hjerte- og karsykdom. Den individuelle risikoen blir brukt som grunnlag for videre råd og behandling av pasientene.

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Cas9: the gene hacker that bites DNA

Jose Bianco MoreiraEvolutionary pressures forced all living species to adapt to challenging and hostile environments. Giraffes developed long necks that enable them to reach more food on top of trees, birds can fly to escape dangers from ground level and humans became smart enough to domesticate their previous predators. These characteristics evolved over millions of years as a result of random DNA mutations, which somehow conferred survival advantage to an organism that would then pass this “good mutation” to the next generations. Although these DNA alterations (mutations) are necessary for the evolution of species, their random nature sometimes gives rise to unwanted characteristics. This is the case of genetic diseases that have haunted humanity for centuries.

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We hear about them all the time, but what is a gene?

Nathan ScrimeourWe hear about them all the time – this gene causes a disease, or that gene is important for normal heart function. Most people could tell you that your genes are made of something called DNA, that you inherit them from your parents and pass them on to your children, and that they determine much of who you are and what you look like. But how do we get from genes to an entire organism, and what control do we have over our genes?

To answer these questions, we need a basic understanding of what is known as the “central dogma” of biology, which describes the one way flow of genetic information. While the reality is more complex than this, the flow can be simplified as such:

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Genetics and cardiovascular disease

Picture of DNAIn Western world, cardiovascular disease (CVD) is among the leading cause of premature death and a major cause of disability. Over the years, the knowledge of CVD risk factors clustering and their multiplicative interactions to promote CVD risk has led to the development of multivariable risk prediction algorithms to use in primary care settings. The guidelines for CVD prevention recommend that an individual’s risk of CVD is estimated by combining different risk factors into a numeric estimate of risk. Most of these risk prediction algorithms include well-known CVD risk factors such as: age, sex, hypertension, cholesterol, smoking, family history of CVD and diabetes mellitus. A variety of risk prediction algorithms are available, as charts, tables, computer programmes, and web-based tools.

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Skreddersydd trening til ditt DNA

DNA blåRead this post in English here!

Flere forskningsrapporter slår fast at genene våre spiller en viktig rolle for hvordan hver enkelt av oss responderer på forskjellige typer trening, dette snakket jeg om under NIH Fitness convention 15. november.

Den første store studien som viste variasjoner i treningsrespons kom i 1980. I denne studien deltok 720 personer på et treningsprogram som varte i 5 måneder, og forskerne målte maksimalt oksygenopptak (det beste målet på kondisjon) før og etter treningsperioden. Overaskende nok så de en enorm forskjell i endringer av oksygenopptak. Noen få gikk faktisk ned, mens andre økte enormt. Forskerne undersøkte også om utgangspunktet hadde noen betydning, altså hvor høyt oksygenopptak deltakerne hadde før du ble med på treningsprogrammet, men til toss for dette viste resultatene det samme. Forskerne konkluderte med at omtrent 10 % av befolkningen hadde liten eller ingen forbedring i oksygenopptak etter treningsperioden. I etterkant har studier vist at omtrent 50 % av variasjoner i treningsrespons skyldes arv.

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Targeted Nucleose Technology and knockout rats – guest lecture at NTNU

Yesterday Professor Aron Guerts from the Cardiovascular Research Center and Human Molecular Genetics Center at the Medical College of Wisconsin visited NTNU. Many of us visited his guest lecture, titled “Targeted Nuclease Technology: Empowering genetic engineering beyond the mouse”.

Over the past five to ten years, a suite of revolutionary tools has emerged and created a new field of “Genome Editing”. During the last 20 years, precision modification of a genome was basically restricted to the mouse model and their embryonic stem cells from a couple of common strains. Scientific progressions within the field have now made it possible to engineer precise mutations and genetic modifications to essentially any genome of any cell from any strain or species.

Photo: HeadSpin

Photo: HeadSpin

With the term Targeted Nuclease Technology (TNT), Guerts especially points to the three following discoveries:

  • The Zinc-Finger Nucleases (ZFNs), an artificial restricion enzyme improving the targeting of unique sequences within complex genomes.
  • Transcription activator-like effector nucleases (TALENs) – another restriction enzyme, generated by fusing a TAL effector DNA binding domain to a DNA cleavage domain. This type of enzymes cut DNA strands at a specific secuence. The advantage of transcription activator-like effectors (TALEs) is that they can be engineered to bind practically any desired DNA sequence. This enables genome editing when TALENs are introduced into cells.
  • RNA-Guided Nucleases (RGNs) (CRISPR/Cas9), programmable endonucleases also involved in targeted genome editing. 

These discoveries have vastly expanded the possibilities for both basic research of the genome and for promising therapeutic strategies. Guert’s research group at the Medical College of Wisconsin has explored the use of TNT to laboratory rat and mouse disease model strains to create resources of gene knock-out models, specific gene knock-in strains, and for generating conditional (Cre/loxP-based) knockout models.  When combined with other transgenic tools, they are now empowering rat researchers across the globe to address gene-centered hypotheses in widely studied physiological, pharmacological, biochemical, and behavioral model systems.

Guerts is a key contributor to this exciting technology development and was responsible for the world’s first targeted gene knockout rats. For  a more thorough description, you can read about the Knockout Rats in a Science article from 2009.

Maria Henningsen, CERG

Julekalenderens luke 12 – er trening ungdomskilden?

DNA grønnJa, det kan det være! Dette skyldes effekten på telomerene, som er en del av DNA-trådene våre. Forkorting av telomerene er an av de mest kjente aldringsteoriene, og det er faktisk disse vi snakker om når vi omtaler den biologiske klokken. Men vi har gode nyheter: trening kan gjøre at de opprettholder lengden, og virke som en buffer mot dårlig helse.

Dette visste Magnus Rom Jensen, som er dagens vinner. Gratulerer!

Vet du svaret på spørsmålet student Øyvind stiller idag – er det hjertets arbeidskapasitet som begrenser kondisjonen vår? Delta i kalenderen her!