The impact of otitis media on speech production in children: A systematic review.

Introduction: Otitis Media (OM) is one of the most common infections in young children and can create fluctuating hearing loss. Despite the commonality of this condition, there is a lack of conclusive evidence on its impact on speech production outcomes. Therefore, the aim of this systematic review was to identify the impact of otitis media on speech production in children.

A transparent approach: Openness in forensic science reporting.

There have been numerous calls for increased transparency and disclosure in forensic science. However, there is a paucity of guidance on how to achieve this transparency in reports, and the impacts it may have on criminal justice proceedings. We describe one multi-disciplinary forensic laboratory's journey to fully transparent reporting, disclosing matters of scientific relevance and importance.

Metabolic control of adaptive β-cell proliferation by the protein deacetylase SIRT2.

Selective and controlled expansion of endogenous β-cells has been pursued as a potential therapy for diabetes. Ideally, such therapies would preserve feedback control of β-cell proliferation to avoid excessive β-cell expansion and an increased risk of hypoglycemia. Here, we identified a regulator of β-cell proliferation whose inactivation results in controlled β-cell expansion: the protein deacetylase Sirtuin 2 (SIRT2).

Efficacy of IAPP suppression in mouse and human islets by GLP-1 analogue conjugated antisense oligonucleotide.

Insulin resistance is the major risk factor for Type 2 diabetes (T2D). In vulnerable individuals, insulin resistance induces a progressive loss of insulin secretion with islet pathology revealing a partial deficit of beta cells and islet amyloid derived from islet amyloid polypeptide (IAPP). IAPP is co-expressed and secreted with insulin by beta cells, expression of both proteins being upregulated in response to insulin resistance.

S-nitrosylated TDP-43 triggers aggregation, cell-to-cell spread, and neurotoxicity in hiPSCs and in vivo models of ALS/FTD.

Rare genetic mutations result in aggregation and spreading of cognate proteins in neurodegenerative disorders; however, in the absence of mutation (i.e., in the vast majority of "sporadic" cases), mechanisms for protein misfolding/aggregation remain largely unknown.