Optimizing B-lines on lung ultrasound: an in-vitro to in-vivo pilot study with clinical implications.

B-lines on lung ultrasound (US) are the hallmark of pulmonary edema. It is unknown if ultrasound machine settings or probe type matter. We created an in-vitro gelatin model. Using lung presets as baseline, five blinded investigators assessed the impact of 32 distinct settings on B-line visibility based on a Likert-Scale (LS) from 0 to10 (< 5 worse, > 5 better) separately for two probes. The experiment was then repeated in-vivo in a patient with known pulmonary edema. Based on a multivariable regression LS-ratings were similar when comparing the in-vitro versus in-vivo experiment (P = 0.16; partial R2 = 0.2%) and when using the curvilinear versus linear probe (P = 0.69; partial R2 = 0.02%) but significantly different across machine settings (P < 0.0001; partial R2 = 34.4%). Limited by its pilot character, our study suggests that (1) certain US-machine settings heavily impact B-line visibility, with no clear difference between probes; (2) in-vitro models are a valid and practical alternative to more challenging patient-based research; (3) there is significant potential to improve B-line visibility and thus diagnostic yield in the clinical setting by using lung presets, centering the focal zone at the pleural line and increasing the distal time gain compensation, most of which are (in our experience) rarely done.

Macrophage-derived apoptotic bodies promote the proliferation of the recipient cells via shuttling microRNA-221/222.

Bacterial pneumonia is a common and serious clinical entity. Alveolar epithelial cells and alveolar macrophages are the first line of defense in the innate immunity against bacterial pathogens. Epithelial cells are known to release chemokines/cytokines that recruit and activate phagocytic cells. However, the signals sent from alveolar macrophages back to the lung epithelial cells remain largely unexplored. We found that LPS, a well-recognized stimulator derived from gram-negative (G-) bacteria, rapidly and robustly induces the secretion of macrophage-derived extracellular vesicles (EVs). The main type of EVs found in the early stages after LPS stimulation are apoptotic bodies (ABs) and not microvesicles (MVs) or exosomes (Exos). Furthermore, LPS markedly up-regulate the levels of a repertoire of microRNAs (miRNAs) in the macrophage-derived ABs, including miR-221 and miR-222. Functionally, the LPS-induced, macrophage-derived ABs promote the proliferation of malignant and/or normal lung epithelial cells. We next directly transfected miR-221 and/or miR-222 inhibitors into the LPS-induced ABs. Deletion of miR-221/222 in ABs significantly reduces the AB-mediated proliferation of lung epithelial cells. Mechanistically, AB-shuttling miR-221/222 promote cell growth by modulating cyclin-dependent kinase inhibitor 1B (CDKN1B) pathways. Collectively, LPS-induced, macrophage-derived ABs promote the proliferation of their recipient epithelial cells, partially via AB-shuttling miRNAs.

Myocarditis along with acute ischaemic cerebellar, pontine and lacunar infarction following viper bite.

Cerebrovascular complications are rare following viper bites. A 65-year-old man presented with loss of consciousness and developed haemiparesis following a viper bite. Coagulation parameters were severely deranged. MRI showed acute ischaemic infarction on the left side in the precentral and postcentral gyrus, hemipons and cerebellum. Troponin T was elevated and transient left bundle branch block was seen. The patient had a good outcome following treatment with Anti Snake Venom and supportive therapy. Possible mechanisms of infarction are discussed.