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PurposeThis study aimed to develop and validate a scoring system based on a nomogram of common clinical metrics to discriminate between active pulmonary tuberculosis (APTB) and inactive pulmonary tuberculosis (IPTB).Patients and methodsA total of 1096 patients with pulmonary tuberculosis (PTB) admitted to Wuhan Jinyintan Hospital between January 2017 and December 2019 were included in this study. Of these patients with PTB, 744 were included in the training cohort (70%; 458 patients with APTB, and 286 patients with IPTB), and 352 were included in the validation cohort (30%; 220 patients with APTB, and 132 patients with IPTB). Data from 744 patients from the training cohort were used to establish the diagnostic model. Routine blood examination indices and biochemical indicators were collected to construct a diagnostic model using the nomogram, which was then transformed into a scoring system. Furthermore, data from 352 patients from the validation cohort were used to validate the scoring system.ResultsSix variables were selected to construct the prediction model. In the scoring system, the mean corpuscular volume, erythrocyte sedimentation rate, albumin level, adenosine deaminase level, monocyte-to-high-density lipoprotein ratio, and high-sensitivity C-reactive protein-to-lymphocyte ratio were 6, 4, 7, 5, 5, and 10, respectively. When the cut-off value was 15.5, the scoring system for recognizing APTB and IPTB exhibited excellent diagnostic performance. The area under the curve, specificity, and sensitivity of the training cohort were 0.919, 84.06%, and 86.36%, respectively, whereas those of the validation cohort were 0.900, 82.73, and 86.36%, respectively.ConclusionThis study successfully constructed a scoring system for distinguishing APTB from IPTB that performed well.

Acute lung injury(ALI)/acute respiratory distress syndrome(ARDS) is a form of acute-onset hypoxemic respiratory failure characterised by an acute, diffuse, inflammatory lung injury, and increased alveolar-capillary permeability, which is caused by a variety of pulmonary or nonpulmonary insults. Recently, aberrant mitochondria and mitochondrial DNA(mtDNA) level are associated with the development of ALI/ARDS, and plasma mtDNA level shows the potential to be a promising biomarker for clinical diagnosis and evaluation of lung injury severity. In mechanism, the mtDNA and its oxidised form, which are released from impaired mitochondria, play a crucial role in the inflammatory response and histopathological changes in the lung. In this review, we discuss mitochondrial outer membrane permeabilisation (MOMP), mitochondrial permeability transition pore(mPTP), extracellular vesicles (EVs), extracellular traps (ETs), and passive release as the principal mechanisms for the release of mitochondrial DNA into the cytoplasm and extracellular compartments respectively. Further, we explain how the released mtDNA and its oxidised form can induce inflammatory cytokine production and aggravate lung injury through the Toll-like receptor 9(TLR9) signalling, cytosolic cGAS-stimulator of interferon genes (STING) signalling (cGAS-STING) pathway, and inflammasomes activation. Additionally, we propose targeting mtDNA-mediated inflammatory pathways as a novel therapeutic approach for treating ALI/ARDS.