IMPROVING VTE RISK ASSESSMENT IN HOSPITALISED PATIENTS IN A TERTIARY CARE HOSPITAL IN IRELAND.

Background: The initial baseline audit showed that only 24% of patients had a documented VTE- RA, this demonstrated an urgent need to improve VTE-RA in hospitalised patients. This quality improvement project (QIP) aimed to achieve 90% compliance in completing the VTE-RA tool and embedding this process into practice. Several measures were carried out which included the development of a TP policy, VTE-RA tool, education sessions and monthly point prevalence audits incorporating Plan, Do, Study, Act (PDSA) cycles.

Induced pluripotent stem cells in companion animals: how can we move the field forward?

Following a one medicine approach, the development of regenerative therapies for human patients leads to innovative treatments for animals, while pre-clinical studies on animals provide knowledge to advance human medicine. Among many different biological products under investigation, stem cells are among the most prominent. Mesenchymal stromal cells (MSCs) are extensively investigated, but they present challenges such as senescence and limited differentiation ability.

Calculated Globulin as a potential screening tool for paraproteinemia to aid in the early diagnosis of Multiple Myeloma.

Background: Multiple Myeloma (MM) is a haematological malignancy with increasing global incidence. Diagnosis of MM should be initiated at the primary care level to achieve the best patient outcome. However, this can be delayed due to nonspecific presenting symptoms, such as back pain and fatigue.

Minimal Residual Disease in Multiple Myeloma: Potential for Blood-Based Methods to Monitor Disease.

In recent years, the life expectancy of Multiple Myeloma (MM) patients has substantially improved, but this cancer remains incurable with increasing incidence in the developed world. Most MM patients will eventually relapse due to residual drug-resistant cancerous cells that survive treatment, commonly referred to as minimal residual disease (MRD). Methods to improve MRD detection in MM patients are generating considerable interest as a means of monitoring patients' response to treatment.

Targeting JAK-STAT Signalling Alters PsA Synovial Fibroblast Pro-Inflammatory and Metabolic Function.

Objectives: Psoriatic arthritis (PsA) is a chronic inflammatory disease associated with psoriasis. Janus Kinase inhibitors (JAKi) have emerged as an encouraging class of drugs for the treatment of PsA. Here, we compare the effect of four JAKi on primary PsA synovial fibroblasts (PsAFLS) activation, metabolic function, and invasive and migratory capacity.

Derivation of four iPSC lines from a male ASD patient carrying a deletion in the middle coding region of NRXN1α gene (NUIGi039-A and NUIGi039-B) and a male sibling control (NUIGi040-A and NUIGi040-B).

NRXN1 deletions are commonly found in autism spectrum disorder (ASD) and other neurodevelopmental/neuropsychiatric disorders. Derivation of induced pluripotent stem cells (iPSCs) from different diseases involving different deletion regions are essential, as NRXN1 may produce thousands of splicing variants. We report here the derivation of iPSCs from a sibling control and an ASD proband carrying de novo heterozygous deletions in the middle region of NRXN1, using a non-integrating Sendai viral kit.

Derivation of iPSC lines from two patients with autism spectrum disorder carrying NRXN1α deletion (NUIGi041-A, NUIG041-B; NUIGi045-A) and one sibling control (NUIGi042-A, NUIGi042-B).

NRXN1 encodes thousands of splicing variants categorized into long NRXN1α, short NRXN1β and extremely short NRXN1γ, which exert differential roles in neuronal excitation/inhibition. NRXN1α deletions are common in autism spectrum disorder (ASD) and other neurodevelopmental/neuropsychiatric disorders. We derived induced pluripotent stem cells (iPSCs) from one sibling control and two ASD probands carrying NRXN1α, using non-integrating Sendai viral method.

Targeting mitochondrial dysfunction in MAIT cells limits IL-17 production in obesity.

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Mucosal-Associated Invariant T Cells Display Diminished Effector Capacity in Oesophageal Adenocarcinoma.

Oesophageal adenocarcinoma (OAC) is an aggressive malignancy with poor prognosis, and incidence is increasing rapidly in the Western world. Mucosal-associated invariant T (MAIT) cells recognize bacterial metabolites and kill infected cells, yet their role in OAC is unknown. We aimed to elucidate the role of MAIT cells during cancer development by characterizing the frequency, phenotype, and function of MAIT cells in human blood and tissues, from OAC and its pre-malignant inflammatory condition Barrett's oesophagus (BO).

Obesity Reduces mTORC1 Activity in Mucosal-Associated Invariant T Cells, Driving Defective Metabolic and Functional Responses.

Obesity underpins the development of numerous chronic diseases, such as type II diabetes mellitus. It is well established that obesity negatively alters immune cell frequencies and functions. Mucosal-associated invariant T (MAIT) cells are a population of innate T cells, which we have previously reported are dysregulated in obesity, with altered circulating and adipose tissue frequencies and a reduction in their IFN-γ production, which is a critical effector function of MAIT cells in host defense.

ER stress signaling has an activating transcription factor 6α (ATF6)-dependent "off-switch".

In response to an accumulation of unfolded proteins in the endoplasmic reticulum (ER) lumen, three ER transmembrane signaling proteins, inositol-requiring enzyme 1 (IRE1), PRKR-like ER kinase (PERK), and activating transcription factor 6α (ATF6α), are activated. These proteins initiate a signaling and transcriptional network termed the unfolded protein response (UPR), which re-establishes cellular proteostasis. When this restoration fails, however, cells undergo apoptosis.