Corneal Refractive Surgery Considerations in Patients With History of Orthokeratology.

Objective: To review the current literature describing corneal changes observed with orthokeratology (ortho-k) use and to formulate preliminary recommendations for these patients seeking corneal refractive surgery.

Methods: The literature search was conducted through the PubMed, Scopus, and Ovid databases through June 4, 2024, for articles regarding corneal physiological, tomographic, and biomechanical changes secondary to ortho-k use.

Results: Forty-one articles were found describing several changes associated with ortho-k use, including higher corneal staining, central corneal epithelial thinning and midperipheral thickening, increased higher-order aberrations, decreased contrast sensitivity, reduced corneal hysteresis and corneal resistance factor, and alterations in the tear proteome.

Caring as the unacknowledged matrix of evidence-based nursing.

In this article, we explicate evidence-based nursing (EBN), critically appraise its framework and respond to nurses' concern that EBN sidelines the caring elements of nursing practice. We use resources from care ethics, especially Vrinda Dalmiya's work that considers care as crucial for both epistemology and ethics, to show how EBN is compatible with, and indeed can be enhanced by, the caring aspects of nursing practice. We demonstrate that caring can act as a bridge between 'external' evidence and the other pillars of the EBN framework: clinical expertise; patient preferences and values.

The roles of intratumour heterogeneity in the biology and treatment of pancreatic ductal adenocarcinoma.

Intratumour heterogeneity (ITH) has become an important focus of cancer research in recent years. ITH describes the cellular variation that enables tumour evolution, including tumour progression, metastasis and resistance to treatment. The selection and expansion of genetically distinct treatment-resistant cancer cell clones provides one explanation for treatment failure.

Glycan degradation promotes macroautophagy.

Macroautophagy promotes cellular homeostasis by delivering cytoplasmic constituents to lysosomes for degradation [Mizushima, 20, 521-527 (2018)]. However, while most studies have focused on the mechanisms of protein degradation during this process, we report here that macroautophagy also depends on glycan degradation via the glycosidase, α-l-fucosidase 1 (FUCA1), which removes fucose from glycans. We show that cells lacking FUCA1 accumulate lysosomal glycans, which is associated with impaired autophagic flux.

Automated quality control and cell identification of droplet-based single-cell data using dropkick.

A major challenge for droplet-based single-cell sequencing technologies is distinguishing true cells from uninformative barcodes in data sets with disparate library sizes confounded by high technical noise (i.e., batch-specific ambient RNA).

CD9 identifies pancreatic cancer stem cells and modulates glutamine metabolism to fuel tumour growth.

Pancreatic ductal adenocarcinoma (PDAC) shows great cellular heterogeneity, with pronounced epithelial and mesenchymal cancer cell populations. However, the cellular hierarchy underlying PDAC cell diversity is unknown. Here we identify the tetraspanin CD9 as a marker of PDAC tumour-initiating cells.

MDH1 and MPP7 Regulate Autophagy in Pancreatic Ductal Adenocarcinoma.

Pancreatic ductal adenocarcinoma (PDAC) is driven by metabolic changes in pancreatic cells caused by oncogenic mutations and dysregulation of p53. PDAC cell lines and PDAC-derived xenografts grow as a result of altered metabolic pathways, changes in stroma, and autophagy. Selective targeting and inhibition of one of these may open avenues for the development of new therapeutic strategies.

Tissue curvature and apicobasal mechanical tension imbalance instruct cancer morphogenesis.

Tubular epithelia are a basic building block of organs and a common site of cancer occurrence. During tumorigenesis, transformed cells overproliferate and epithelial architecture is disrupted. However, the biophysical parameters that underlie the adoption of abnormal tumour tissue shapes are unknown.

The nuclear transport receptor Importin-11 is a tumor suppressor that maintains PTEN protein.

Phosphatase and tensin homologue (PTEN) protein levels are critical for tumor suppression. However, the search for a recurrent cancer-associated gene alteration that causes PTEN degradation has remained futile. In this study, we show that Importin-11 (Ipo11) is a transport receptor for PTEN that is required to physically separate PTEN from elements of the PTEN degradation machinery.

Cross-species conservation of complementary amino acid-ribonucleobase interactions and their potential for ribosome-free encoding.

The role of amino acid-RNA nucleobase interactions in the evolution of RNA translation and protein-mRNA autoregulation remains an open area of research. We describe the inference of pairwise amino acid-RNA nucleobase interaction preferences using structural data from known RNA-protein complexes. We observed significant matching between an amino acid's nucleobase affinity and corresponding codon content in both the standard genetic code and mitochondrial variants.

MYC Drives Pten/Trp53-Deficient Proliferation and Metastasis due to IL6 Secretion and AKT Suppression via PHLPP2.

Unlabelled: We have recently recapitulated metastasis of human PTEN/TP53-mutant prostate cancer in the mouse using the RapidCaP system. Surprisingly, we found that this metastasis is driven by MYC, and not AKT, activation. Here, we show that cell-cell communication by IL6 drives the AKT-MYC switch through activation of the AKT-suppressing phosphatase PHLPP2, when PTEN and p53 are lost together, but not separately.

Prostaglandin metabolite induces inhibition of TRPA1 and channel-dependent nociception.

Background: The Transient Receptor Potential (TRP) ion channel TRPA1 is a key player in pain pathways. Irritant chemicals activate ion channel TRPA1 via covalent modification of N-terminal cysteines. We and others have shown that 15-Deoxy-Δ12, 14-prostaglandin J2 (15d-PGJ2) similarly activates TRPA1 and causes channel-dependent nociception.