James P. Higham

The paper compares left ventricular phenotypes across humans, chimpanzees, and macaques to identify structural and functional traits associated with higher stroke volume in humans.

This study examines how early life adversity affects adult behavior in free-ranging rhesus macaques, finding that ELA correlates with increased aggression, reduced grooming, and submissive behaviors.

This study shows that DNA methylation from fecal samples accurately reflects molecular aging in wild capuchin monkeys, revealing age-related epigenetic changes linked to cellular damage and inflammation.

The paper shows that age and early life adversity affect DNA methylation across tissues in macaques, with distinct but overlapping patterns.

This study validates fecal haptoglobin as a biomarker of inflammation in wild capuchin monkeys and finds environmental factors, not demographic or circadian variables, influence its concentrations.

The paper quantifies variation in primate social structures across 11 species, identifying distinct patterns in kin and rank biases and male-centered subgrouping.

This study profiles 5.3 million cells from 55 rhesus macaques across their lifespan to map age-related changes in brain cell types and identify molecular signatures linked to aging and Alzheimer's disease.

This study compares cardiac structure and function in free-ranging and captive rhesus macaques across age, finding that captive macaques show more pronounced age-related cardiac changes.

This study shows that early life adversity in rhesus macaques affects growth, reproductive timing, and lifetime reproductive success, with adversity intensifying trade-offs between growth and reproduction.

The paper investigates genetically based sperm discrimination in primates by examining vaginal immune responses and pH changes after mating with genetically similar males.

This study identifies MMP3, MMP8, and MMP9 as inducers of Ca2+ release in DRG neurons via PAR1 and PLC activation, revealing a novel role for MMP signaling in sensory neurons during inflammation.

The paper optimizes a reduced representation DNA methylation sequencing protocol for cost-effective, population-scale studies across species.

The paper examines how reduced social connectedness in older primates can mitigate infection risks from a hypothetical pathogen, showing age-related changes in social behavior affect disease dynamics.

The paper analyzes sex-biased gene expression in rhesus macaque brains to understand its evolutionary and biomedical implications, finding similarities with human patterns and associations with neurodevelopmental disorders.

This study correlates mouse digging behavior with human pain experience, showing that digging deficits reflect pain levels and that meloxicam is more effective than gabapentin in alleviating these deficits.

This study identifies Angiotensin II as a pro-nociceptive mediator in IBD by showing increased Agt expression and AT1 receptor activation in colonic neurons.

The paper shows that KV7 channel openers, but not SK/IK channel openers, reduce colonic afferent responses to noxious stimuli, suggesting KV7 channels as potential targets for abdominal pain treatment.

This study examines age-related changes in ocular features of rhesus macaques, finding associations between age and corneal thickness, axial length, refractive error, cataracts, and retinal drusen.

This study shows TNFα sensitizes colonic nociceptors via TNFR1 and p38 MAPK, enhancing responses to capsaicin and noxious distension.

The paper analyzes ACE2 gene sequences in strepsirrhine primates to assess their susceptibility to SARS-CoV-2, finding high variability and potential risk in some species.

The paper compares ACE2 variation across primates to assess susceptibility to SARS-CoV-2, finding that apes and African/Asian monkeys are highly susceptible while others show reduced risk.

This paper reviews rhesus macaques as a model for human ageing, showing shared gene regulatory signatures in immune ageing between macaques and humans.

This paper shows that reducing Ank2 expression in Drosophila neurons causes AD-like features, suggesting ANK1 may be a therapeutic target.