Results 191 to 200 of about 10,250,216 (364)

Clinical genetics [PDF]

open access: yesJournal of Medical Genetics, 1996
openaire   +2 more sources

Identifying knowledge deficiencies in genetics education among medical students and interns in Saudi Arabia- A cross-sectional study

open access: yesBMC Medical Education
Background Understanding genetics is crucial for medical students, particularly in Saudi Arabia, where genetic disorders are prevalent owing to high rates of consanguineous marriages.
Abeer F. Zakariyah   +5 more
doaj   +1 more source

Phenotype, origin and estimated prevalence of a common long QT syndrome mutation: a clinical, genealogical and molecular genetics study including Swedish R518X/KCNQ1families [PDF]

open access: gold, 2014
Annika Winbo   +6 more
openalex   +1 more source

A pilot eConsultation service in Eastern Ontario: bridging clinical genetics and primary care

open access: yesEuropean Journal of Human Genetics, 2019
Priya T. Bhola   +4 more
semanticscholar   +1 more source

Inhibition of CDK9 enhances AML cell death induced by combined venetoclax and azacitidine

open access: yesMolecular Oncology, EarlyView.
The CDK9 inhibitor AZD4573 downregulates c‐MYC and MCL‐1 to induce death of cytarabine (AraC)‐resistant AML cells. This enhances VEN + AZA‐induced cell death significantly more than any combination of two of the three drugs in AraC‐resistant AML cells.
Shuangshuang Wu   +18 more
wiley   +1 more source

Clinical genetics-it's polygenic. [PDF]

open access: yesEur J Hum Genet, 2021
McNeill A.
europepmc   +1 more source

A synthetic benzoxazine dimer derivative targets c‐Myc to inhibit colorectal cancer progression

open access: yesMolecular Oncology, EarlyView.
Benzoxazine dimer derivatives bind to the bHLH‐LZ region of c‐Myc, disrupting c‐Myc/MAX complexes, which are evaluated from SAR analysis. This increases ubiquitination and reduces cellular c‐Myc. Impairing DNA repair mechanisms is shown through proteomic analysis.
Nicharat Sriratanasak   +8 more
wiley   +1 more source

Adaptaquin is selectively toxic to glioma stem cells through disruption of iron and cholesterol metabolism

open access: yesMolecular Oncology, EarlyView.
Adaptaquin selectively kills glioma stem cells while sparing differentiated brain cells. Transcriptomic and proteomic analyses show Adaptaquin disrupts iron and cholesterol homeostasis, with iron chelation amplifying cytotoxicity via cholesterol depletion, mitochondrial dysfunction, and elevated reactive oxygen species.
Adrien M. Vaquié   +16 more
wiley   +1 more source

Clinical applications of schizophrenia genetics: genetic diagnosis, risk, and counseling in the molecular era

open access: yesThe Application of Clinical Genetics, 2012
Gregory Costain1,2, Anne S Bassett1–41Clinical Genetics Research Program, Centre for Addiction and Mental Health, 2Institute of Medical Science, University of Toronto, 3Division of Cardiology, Department of Medicine and Department of Psychiatry,
Costain G, Bassett AS
doaj  

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