Focus issue: Artificial intelligence in medical physics.

Performance of an artificial intelligence tool with real-time clinical workflow integration - Detection of intracranial hemorrhage and pulmonary embolism.

Assessing perspectives on artificial intelligence applications to gastroenterology

Hopes and Hypes for Artificial Intelligence in Colorectal Cancer Screening

Strengths and Weaknesses of an Artificial Intelligence Polyp Detection Program as Assessed by a High-Detecting Endoscopist

Weakly-supervised deep learning models in computational pathology

Maximising the Opportunities of Artificial Intelligence for People Living With Cancer

Climate Change and the Health of the Public

The Image Gently in Dentistry campaign: promotion of responsible use of maxillofacial radiology in dentistry for children.

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Sky blue or murky waters: The diagnostic utility of methylene blue

Artificial Intelligence in Magnetic Resonance Imaging: A Feasible Practice?

Decoding the Enigma of Urticaria and Angioedema

Surveying the clinical practice of treatment adaptation and motion management in particle therapy.

Processing of NF-kappaB2 precursor protein p100 to generate p52 is tightly controlled, which is important for proper function of NF-kappaB. Accordingly, constitutive processing of p100, caused by the loss of its C-terminal processing inhibitory domain due to nfkappab2 gene rearrangements, is associated with the development of various lymphomas and leukemia. In contrast to the physiological processing of p100 triggered by NF-kappaB-inducing kinase (NIK) and its downstream kinase, IkappaB kinase alpha (IKKalpha), which requires the E3 ligase, beta-transducin repeat-containing protein (beta-TrCP), and occurs only in the cytoplasm, the constitutive processing of p100 is independent of beta-TrCP but rather is regulated by the nuclear shuttling of p100. Here, we show that constitutive processing of p100 also requires IKKalpha, but not IKKbeta (IkappaB kinase beta) or IKKgamma (IkappaB kinase gamma). It seems that NIK is also dispensable for this pathogenic processing of p100. These results demonstrate a general role of IKKalpha in p100 processing under both physiological and pathogenic conditions. Additionally, we find that IKKalpha is not required for the nuclear translocation of p100. Thus, these results also indicate that p100 nuclear translocation is not sufficient for the constitutive processing of p100.

Resuscitation highlights in 2011