Metabologia -

Omicron-derived SARS-CoV2 variants (exemplified most recently by XBB1.5(1)) are highly adept at evading immunity against vaccines and infection with previous variants and many parts of the world are c...

A multi-omic study links gut bacteria, microbial metabolites, and changes in heart function, pointing to biological relationships that could reshape how researchers investigate heart failure progression. Study: Gut microbiome shifts in chronic systolic heart failure are associated with disease severity and clinical improvement. Image Credit: Lightspring / Shutterstock A recent study published in the journal Nature Cardiovascular Research suggests that alterations in the gut microbiome in chronic systolic heart failure (HF) due to nonischemic cardiomyopathy (NICM) are associated with disease severity and clinical improvement. The researchers found that Bifidobacterium, some strains of which produced indole-3-propionic acid (IPA) in laboratory experiments, may play a role in HF. In particular, greater Bifidobacterium abundance was associated with milder disease and improved functional status, while higher circulating IPA and predicted microbial butyrate production were associated with milder HF measures. HF patients experience considerable morbidity and an increased risk of death. The condition is becoming more prevalent, and disease trajectories vary, while the mechanisms underlying disease progression remain poorly understood. The gut microbiome contributes to several biological pathways, but its role in chronic HF remains unclear. Most previous studies were cross-sectional, with small sample sizes and limited functional profiling. About the study In the present...

The PsychAD Consortium investigates the biological mechanisms behind neuropsychiatric symptoms in Alzheimer’s disease, related dementias, and serious mental ...

West Nile virus (WNV) is one of the leading causes of arthropod-transmitted encephalitis in the world, yet its effects on neurons, the principal target of WNV in the brain, remain poorly defined. Here we establish and use Ngn2-induced human iPSC-derived glutamatergic neurons to define the neuronal response to WNV through integrated temporal proteomics and transcriptomics. Temporal multi-omic profiling revealed that infection activated innate immunity and the Unfolded Protein Response while suppressing axonogenesis and synaptic programs. WNV infection also disrupted calcium homeostasis, reduced STMN2 abundance, and promoted cytoplasmic redistribution of TDP-43. Applying this neuronal model to characterize contemporary California isolates, we identified LA24, a lineage 1 strain that replicates efficiently in non-neuronal cell lines but is selectively attenuated in neurons, with reduced viral burden in the brain and attenuated pathogenicity in mice. Together, these findings uncover neuron-specific signatures of WNV pathogenesis and demonstrate that neuronal replication phenotypes can reveal strain-dependent virulence differences not captured by conventional cell lines.

<p xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" class="first" dir="auto" id="d18425570e83">The increasing availability of multi-omic data offers unprecedented opportunities to characterize…

Con il termine “cold case” si indicano i casi irrisolti: quei crimini dei quali le indagini non sono venute a capo e che si considerano ormai abbandonati perché il tempo trascorso è ormai troppo per…

West Nile virus (WNV) is one of the leading causes of arthropod-transmitted encephalitis in the world, yet its effects on neurons, the principal target of WNV in the brain, remain poorly defined. Here we establish and use Ngn2-induced human iPSC-derived glutamatergic neurons to define the neuronal response to WNV through integrated temporal proteomics and transcriptomics. Temporal multi-omic profiling revealed that infection activated innate immunity and the Unfolded Protein Response while suppressing axonogenesis and synaptic programs. WNV infection also disrupted calcium homeostasis, reduced STMN2 abundance, and promoted cytoplasmic redistribution of TDP-43. Applying this neuronal model to characterize contemporary California isolates, we identified LA24, a lineage 1 strain that replicates efficiently in non-neuronal cell lines but is selectively attenuated in neurons, with reduced viral burden in the brain and attenuated pathogenicity in mice. Together, these findings uncover neuron-specific signatures of WNV pathogenesis and demonstrate that neuronal replication phenotypes can reveal strain-dependent virulence differences not captured by conventional cell lines.