Cutaneous dysbiosis characterizes the post-allogeneic hematopoietic stem cell transplantation period.

Gut dysbiosis is linked to mortality and the development of graft-versus-host disease (GVHD) after hematopoietic stem cell transplantation (HSCT), but the impact of cutaneous dysbiosis remains unexplored. We performed a pilot observational study and obtained retroauricular and forearm skin swabs from 12 adult patients prior to conditioning chemotherapy/radiation, and at 1-week, 1-month and 3-months after allogeneic HSCT, and performed shotgun metagenomic sequencing. The cutaneous microbiome among HSCT patients was enriched for gram-negative bacteria such as E coli and Pseudomonas, fungi, and viruses.

Using routine primary care data in research: (in)efficient case studies and perspectives from the Asthma UK Centre for Applied Research.

Aim: We aimed to identify enablers and barriers of using primary care routine data for healthcare research, to formulate recommendations for improving efficiency in knowledge discovery.

Background: Data recorded routinely in primary care can be used for estimating the impact of interventions provided within routine care for all people who are clinically eligible. Despite official promotion of 'efficient trial designs', anecdotally researchers in the Asthma UK Centre for Applied Research (AUKCAR) have encountered multiple barriers to accessing and using routine data.

An overview of proactive monitoring and management of respiratory issues in ataxia-telangiectasia in a specialist and shared care pediatric clinic.

Ataxia-telangiectasia (A-T) is an ultrarare autosomal recessive disorder and occurs in all racial and ethnic backgrounds. Clinically, children and young people with A-T are affected by sinopulmonary infections, neurological deterioration with concomitant bulbar dysfunction, increased sensitivity to ionizing radiation, immunodeficiency, a decline in lung function, chronic liver disease, endocrine abnormalities, cutaneous and deep-organ granulomatosis, and early death. Pulmonary complications become more frequent in the second decade of life and are a leading cause of death in individuals with A-T.

In defence of ferroptosis.

Rampant phospholipid peroxidation initiated by iron causes ferroptosis unless this is restrained by cellular defences. Ferroptosis is increasingly implicated in a host of diseases, and unlike other cell death programs the physiological initiation of ferroptosis is conceived to occur not by an endogenous executioner, but by the withdrawal of cellular guardians that otherwise constantly oppose ferroptosis induction. Here, we profile key ferroptotic defence strategies including iron regulation, phospholipid modulation and enzymes and metabolite systems: glutathione reductase (GR), Ferroptosis suppressor protein 1 (FSP1), NAD(P)H Quinone Dehydrogenase 1 (NQO1), Dihydrofolate reductase (DHFR), retinal reductases and retinal dehydrogenases (RDH) and thioredoxin reductases (TR).