Background: Abdominal and thoracic CT provide a valuable opportunity for osteoporosis screening regardless of the clinical indication for imaging. Purpose: To establish reference normative ranges for first lumbar vertebra (L1) trabecular attenuation values across all adult ages to measure bone mineral density (BMD) at routine CT. Materials and Methods: Reference data were constructed from 20 374 abdominal and/or thoracic CT examinations performed at 120 kV. Data were derived from adults (mean age, 60 years 6 12 [standard deviation]; 56.1% [11 428 of 20 374] women). CT examinations were performed with (n = 4263) or without (n = 16 111) intravenous contrast agent administration for a variety of unrelated clinical indications between 2000 and 2018. L1 Hounsfield unit measurement was obtained either with a customized automated tool (n = 11 270) or manually by individual readers (n = 9104). The effects of patient age, sex, contrast agent, and manual regionof-interest versus fully automated L1 Hounsfield unit measurement were assessed using multivariable logistic regression analysis. Results: Mean L1 attenuation decreased linearly with age at a rate of 2.5 HU per year, averaging 226 HU 6 44 for patients younger than 30 years and 89 HU 6 38 for patients 90 years or older. Women had a higher mean L1 attenuation compared with men (P , .008) until menopause, after which both groups had similar values. Administration of intravenous contrast agent resulted in negligible differences in mean L1 attenuation values except in patients younger than 40 years. The fully automated method resulted in measurements that were average 21 HU higher compared with manual measurement (P , .004); at intrapatient subanalysis, this difference was related to the level of transverse measurement used (midvertebra vs off-midline level). Conclusion: Normative ranges of L1 vertebra trabecular attenuation were established across all adult ages, and these can serve as a quick reference at routine CT to identify adults with low bone mineral density who are at risk for osteoporosis.

Inflammation is essential for host defense but can cause tissue damage and organ failure if unchecked. How the inflammation is resolved remains elusive. Here we report that the transcription factor Miz1 was required for terminating lipopolysaccharide (LPS)-induced inflammation. Genetic disruption of the Miz1 POZ domain, which is essential for its transactivation or repression activity, resulted in hyper-inflammation, lung injury and increased mortality in LPS-treated mice while reduced bacterial load and mortality in mice with Pseudomonas aeruginosa pneumonia. Loss of the Miz1 POZ domain prolonged pro-inflammatory cytokine expression. Upon stimulation, Miz1 was phosphorylated at Ser178, which is required for recruiting histone deacetylase 1 to repress transcription of C/EBP-δ, an amplifier of inflammation. Our data provide a long-sought mechanism underlying resolution of LPS-induced inflammation.

The family is a highly conserved gene group that regulates cell-cell interaction, embryogenesis, and tissue commitment. This review summarizes the existing data on the third subtype of the family, Notch3. The role of Notch3 in different types of cancers is discussed, as well as implications of its modification and new strategies to affect Notch3 signaling activity.

Disease stage, positive margins, skull base involvement, perineural invasion, time to recurrence, and location of metastasis, but not nodal involvement, could serve as poor prognostic factors in ACC.

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