ATM and IRAK1 orchestrate two distinct mechanisms of NF-κB activation in response to DNA damage.

DNA damage in cells induces the expression of inflammatory genes. However, the mechanism by which cells initiate an innate immune response in the presence of DNA lesions blocking transcription remains unknown. Here we find that genotoxic stresses lead to an acute activation of the transcription factor NF-κB through two distinct pathways, each triggered by different types of DNA lesions and coordinated by either ataxia-telangiectasia mutated (ATM) or IRAK1 kinases.

Tetrodotoxin toxicity: an increasing threat.

A man aged in his sixties presented to the emergency department with vomiting, dizziness and generalised weakness preceded by perioral and peripheral paraesthesias for several hours. He did not speak English and was visiting from overseas. Examination revealed multidirectional nystagmus, subtle bilateral ptosis, marked bilateral upper limb dysmetria and heel-shin ataxia, with mild proximal limb weakness.

Statewide neurology inpatient whole body and brain 18F-fluorodeoxyglucose positron emission tomography utilisation patterns demonstrate avenues for optimisation.

18F-fluorodeoxyglucose positron emission tomography (18F-FDG PET) can provide unique insights; however, access may be difficult. In this 2-year statewide study of all neurology inpatient admissions, 27.9% (41/147) of PET (any field of view) demonstrated significant abnormalities.

Locally advanced/metastatic non-small-cell lung cancer in Lebanon: focus on ALK tyrosine kinase inhibitors.

Treatment of non-small-cell lung cancers (NSCLC) has evolved over the last decade. According to studies, the use of targeted therapies has significantly increased the life expectancy of patients. Moreover, ALK-tyrosine kinase inhibitors (ALK-TKIs) have improved clinical outcomes.

PRC2-EZH1 contributes to circadian gene expression by orchestrating chromatin states and RNA polymerase II complex stability.

Circadian rhythmicity of gene expression is a conserved feature of cell physiology. This involves fine-tuning between transcriptional and post-transcriptional mechanisms and strongly depends on the metabolic state of the cell. Together these processes guarantee an adaptive plasticity of tissue-specific genetic programs.