Blog Archives

Where portrait photos meet genetics and AI

June 13, 2019 – This is simply fascinating stuff. Researchers are testing neural networks that automatically combine portrait photos with genetic and phenotypic patient data in order to obtain definitive diagnosis of hereditary rare diseases, all with the help of artificial intelligence (AI).  

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CRISPR/Cas9 for the Treatment of Duchenne Muscular Dystrophy: Prime time already?

December 12, 2018 – The application of CRISPR/Cas9 based molecular technology in the field of gene editing (or genome editing) has recently had its exploded limelight exposure for a couple of reasons. The question arises if this exposure is earned or somewhat premature.

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Breast Cancer: Performance of prognostic signatures

February 17, 2018 – In a new study, published in JAMA Oncology online on February 15, 2018, a comparison of the performance of 6 prognostic signatures for estrogen receptor (ER) –positive breast cancer was performed in a secondary analysis of a randomized clinical trial.

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Theragenomics: Ivacaftor (Kalydeco) in the CFTR mutation-based treatment of cystic fibrosis (CF)

May 18, 2017 – Ivacaftor (Kalydeco) is a cystic fibrosis transmembrane conductance regulator (CFTR) potentiator indicated for the treatment of cystic fibrosis (CF) in patients age 2 years and older who are carriers one of the following mutations in the CFTR gene: G551D,

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Massaging of data and outcomes: Can we ever trust clinical trial outcomes reported by Pharma?

January 28, 2017 – One could call it a scandal. The dire reality is that what is described here could be widespread practice in the business of clinical trials performed and outcomes reported by Pharma, namely that only half of the truth may be told to patients,

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The antibody aducanumab reduces Aβ plaques in Alzheimer’s disease

alz-ad-iSeptember 09.  2016 – The pre-clinical animal model and Phase 1b placebo-controlled study in prodromal and mild Alzheimer Disease (AD) patients (n=165), both demonstrate that aducanumab reduced amyloid-beta in the brain and the reduction was dose-dependent. Amyloid-beta plaque is associated with the development of AD and it has for a long time been hypothesized that removing it may slow the clinical decline of people who have AD.

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