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Abstract Schizophrenia is associated with hippocampal volumetric changes, yet the genetic mechanisms linking schizophrenia to alterations in hippocampal volume and its subfields remain poorly understood. We analyzed the largest available GWAS summary statistics for schizophrenia (53,386 cases, 77,258 controls) and hippocampal volumetric traits (33,224 individuals).
1 Introduction Cirrhotic portal hypertension (CPH) is an important driving force behind the occurrence and development of various cirrhotic complications, including ascites, gastroesophageal variceal haemorrhage and hepatic encephalopathy, which are leading causes of death and liver transplantation worldwide [1]. The prime determinants of CPH are increased intrahepatic vascular resistance and expanded splanchnic blood flow [2].
At any given BMI, different genetic obesity risks do not change the metabolome Obesity is a heterogeneous phenotype that is crudely measured by body mass index (BMI). There is a need for a more precise yet portable method of phenotyping and categorizing risk in large numbers of people with obesity to advance clinical care and drug development. Here, we used non-targeted metabolomics and whole-genome sequencing to identify metabolic and genetic signatures of obesity.
Profound perturbation of the human metabolome by obesity Elizabeth T Cirulli, Lining Guo, Christine Leon Swisher, Naisha Shah, Lei Huang, Lori A Napier, Ewen F Kirkness, Tim D Spector, C. Thomas Caskey, Bernard Thorens, J. Craig Venter, Amalio Telenti bioRxiv 298224; doi: https://doi.org/10.1101/298224
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