James Adjaye

The paper uses iPSC-derived liver cells to show SAHA reduces Z-alpha-1-antitrypsin polymers by increasing chaperone expression in AATD models.

The paper identifies gene expression signatures and pathways associated with APOL1-mediated kidney disease using transcriptome data and cellular models.

This study uses blood vessel organoids to model systemic sclerosis vasculopathy and fibrosis, showing that SSc serum induces epigenetic and molecular changes linked to endothelial dysfunction and potential therapeutic targets.

The paper identifies 344 genes with overlapping expression in human podocytes and brain, associated with synaptic signaling and cell projections, using gene expression analysis and pathway mapping.

This study shows DPP4 inhibition alters metabolism and inflammation pathways in steatotic hiPSC-derived HLCs, suggesting potential therapeutic benefits for MAFLD.

This study shows that CSB-deficient iPSCs have impaired DNA repair and stress responses after BPDE exposure, highlighting CSB's role in genome stability during development.

This study identifies upregulated proteins in SCD patients with proteinuria and links them to inflammation and kidney injury via the TGFβ-p53 axis in podocyte cultures.

This paper rejuvenates a renal progenitor cell line to model APOL1-mediated kidney inflammation and fibrosis, showing Baricitinib can mitigate IFN-gamma-induced effects.

This study shows human urine-derived SIX2-positive renal progenitor cells reduce kidney fibrosis in an IRI mouse model but do not fully restore kidney function within 21 days.

This study examines how nephrotoxins and oxidants affect the differentiation and function of iPSC-derived renal proximal tubular cells, finding that differentiating cells are highly sensitive to these agents.

This study examines BPDE toxicity in hiPSCs and NPCs, revealing hiPSCs are more sensitive to BPDE with enhanced p53-mediated DNA damage response, and NBS patient cells show reduced apoptosis.

The paper presents a pipeline using scRNA-seq data to deconvolute and estimate cell type fractions in bulk transcriptome data from organoids.

This study uses human iPSC-derived neuronal cultures exposed to hemozoin to show activation of DNA damage, p38 MAPK, and neurodegenerative pathways similar to cerebral malaria.

The paper identifies evolutionarily conserved genes and pathways in human and mouse musculoskeletal progenitors through RNA-sequencing analysis and pathway enrichment.

This study uses human iPSC-derived brain organoids to show that unconjugated bilirubin induces neuro-inflammation in a model of Crigler Najjar Syndrome.

This study identifies cytokine biomarkers in urine that can detect AKI early and suggests their role in regulating TP53 and SIRT1 pathways.

The paper identifies gender-specific and gender-independent cytokine markers in urine from Ghanaian CKD patients, suggesting potential biomarkers for early detection.

This study uses NBS patient-derived cerebral organoids to show that impaired p53-mediated DNA damage response contributes to microcephaly by causing neuronal apoptosis and disrupted neurogenesis.

This study analyzes transcriptome data from Plasmodium falciparum infections to identify neurological sequelae associated with different severities of malaria.

This study uses thyroid hormones to mature hepatocyte-like cells derived from iPSCs, showing improved expression of adult markers and reduced fetal markers.

The paper performs a meta-analysis of RNA-sequencing data from human lung epithelial cells to identify genes co-expressed with ACE2 and related biological processes in SARS-CoV-2 infection.

This study performs a phylogenetic analysis of SARS-CoV-2 sequences from West Africa, finding multiple introductions and suggesting latent circulation of earlier clades before first registered cases.

This study uses iPSC-derived neuronal cultures with the TREM2 R47H variant to construct an Aβ-induced gene regulatory network, identifying ER-stress as a potential causal factor in LOAD.

This paper identifies and characterizes human urine-derived renal progenitor cells, revealing their molecular identity, reprogramming potential, and gene regulatory mechanisms for self-renewal and differentiation.