An unstable patient with a large sucking chest wound managed with gauze packing for preventing tension and bleeding control before surgery in Korea: a case report.

This case report describes the management of a 51-year-old female patient who arrived at the emergency room with a stab wound to the upper right chest. Immediate medical interventions were undertaken, including blood transfusions and endotracheal intubation. To prevent tension and control bleeding, gauze packing was applied directly through the large open wound. Further surgical exploration identified a laceration in the lung, necessitating a right upper lobe resection. Postoperatively, the patient's vital signs stabilized, and she was subsequently discharged without complications. This case highlights the decision-making process in selecting between an emergency department thoracotomy and an operating room thoracotomy for patients with penetrating chest trauma. It also illustrates the role of gauze packing in managing tension and hemorrhage. In summary, gauze packing can be an effective interim measure for stabilizing patients with traumatic injuries, unstable vital signs, and large open chest wounds, particularly when a chest tube is already in place, to prevent tension and facilitate bleeding control prior to surgical intervention.

Sox17 Deficiency Promotes Pulmonary Arterial Hypertension via HGF/c-Met Signaling.

BACKGROUND: In large-scale genomic studies, Sox17, an endothelial-specific transcription factor, has been suggested as a putative causal gene of pulmonary arterial hypertension (PAH); however, its role and molecular mechanisms remain to be elucidated. We investigated the functional impacts and acting mechanisms of impaired Sox17 (SRY-related HMG-box17) pathway in PAH and explored its potential as a therapeutic target. METHODS: In adult mice, Sox17 deletion in pulmonary endothelial cells (ECs) induced PAH under hypoxia with high penetrance and severity, but not under normoxia. RESULTS: Key features of PAH, such as hypermuscularization, EC hyperplasia, and inflammation in lung arterioles, right ventricular hypertrophy, and elevated pulmonary arterial pressure, persisted even after long rest in normoxia. Mechanistically, transcriptomic profiling predicted that the combination of Sox17 deficiency and hypoxia activated c-Met signaling in lung ECs. HGF (hepatocyte grow factor), a ligand of c-Met, was upregulated in Sox17-deficient lung ECs. Pharmacologic inhibition of HGF/c-Met signaling attenuated and reversed the features of PAH in both preventive and therapeutic settings. Similar to findings in animal models, Sox17 levels in lung ECs were repressed in 26.7% of PAH patients (4 of 15), while those were robust in all 14 non-PAH controls. HGF levels in pulmonary arterioles were increased in 86.7% of patients with PAH (13 of 15), but none of the controls showed that pattern. CONCLUSIONS: The downregulation of Sox17 levels in pulmonary arterioles increases the susceptibility to PAH, particularly when exposed to hypoxia. Our findings suggest the reactive upregulation of HGF/c-Met signaling as a novel druggable target for PAH treatment.

The impact of COVID-19 on trauma patients and orthopedic trauma operations at a single focused training center for trauma in Korea.

Purpose: The objective of this study was to determine the effects of coronavirus disease 2019 (COVID-19) on the volume of trauma patients, the number of orthopedic trauma operations, and the severity of injuries. We also investigated the correlations between social distancing and these variables. Methods: This was a retrospective review of trauma patient cases at a single focused training center for trauma in Korea from January 2017 to April 2021. The COVID-19 group included patients treated from January 1 to April 30 in 2020 and 2021, and the control group included patients treated during the same months from 2017 to 2019. The volume of trauma patients according to the level of social distancing was evaluated among patients treated from August 2, 2020 to November 23, 2020. Results: The study included 3,032 patients who presented to the emergency department with traumatic injuries from January to April 2017 to 2021. The average number of patients was 646.7 and 546.0 in the control and COVID-19 groups, respectively. The percentage of patients injured in traffic accidents (TAs) decreased from 25.0% to 18.2% (P<0.0001). The proportions of in-car TAs and pedestrian TAs also decreased from 6.7% and 10.8% to 3.5% and 6.0%, respectively (P=0.0002 and P<0.0001). The percentage of bicycle TAs increased from 2.4% to 4.0% (P=0.0128). The proportion of patients with an Injury Severity Score above 15 and the mortality rate did not change significantly. As the level of social distancing increased, the number of trauma patients and the number of trauma injuries from TAs decreased. The number of orthopedic trauma operations also depended on the social distancing level. Conclusions: The number of trauma patients presenting to the emergency department decreased during the COVID-19 period. The volume of trauma patients and orthopedic trauma operations decreased as the social distance level increased.

Increase of Vδ2+ T Cells That Robustly Produce IL-17A in Advanced Abdominal Aortic Aneurysm Tissues.

Abdominal aortic aneurysm (AAA) is a chronic dilation of the aorta with a tendency to enlarge and eventually rupture, which constitutes a major cause of cardiovascular mortality. Although T-cell infiltrates have been observed in AAA, the cellular, phenotypic, and functional characteristics of these tissue-infiltrating T cells are not fully understood. Here, we investigated the proportional changes of T-cell subsets-including CD4+ T cells, CD8+ T cells, and γδ T cells-and their effector functions in AAAs. We found that Vδ2+ T cells were presented at a higher frequency in aortic aneurysmal tissue compared to normal aortic tissue and PBMCs from patients with AAA. In contrast, no differences were observed in the frequencies of CD4+, CD8+, and Vδ1+ T cells. Moreover, we observed that the Vδ2+ T cells from AAA tissue displayed immunophenotypes indicative of CCR5+ non-exhausted effector memory cells, with a decreased proportion of CD16+ cells. Finally, we found that these Vδ2+ T cells were the main source of IL-17A in abdominal aortic aneurysmal tissue. In conclusion, our results suggest that increased Vδ2+ T cells that robustly produce IL-17A in aortic aneurysmal tissue may contribute to AAA pathogenesis and progression.

Dll4 Suppresses Transcytosis for Arterial Blood-Retinal Barrier Homeostasis.

RATIONALE: Central nervous system has low vascular permeability by organizing tight junction (TJ) and limiting endothelial transcytosis. While TJ has long been considered to be responsible for vascular barrier in central nervous system, suppressed transcytosis in endothelial cells is now emerging as a complementary mechanism. Whether transcytosis regulation is independent of TJ and its dysregulation dominantly causes diseases associated with edema remain elusive. Dll4 signaling is important for various vascular contexts, but its role in the maintenance of vascular barrier in central nervous system remains unknown. OBJECTIVE: To find a TJ-independent regulatory mechanism selective for transcytosis and identify its dysregulation as a cause of pathological leakage. METHODS AND RESULTS: We studied transcytosis in the adult mouse retina with low vascular permeability and employed a hypertension-induced retinal edema model for its pathological implication. Both antibody-based and genetic inactivation of Dll4 or Notch1 induce hyperpermeability by increasing transcytosis without junctional destabilization in arterial endothelial cells, leading to nonhemorrhagic leakage predominantly in the superficial retinal layer. Endothelial Sox17 deletion represses Dll4 in retinal arteries, phenocopying Dll4 blocking-driven vascular leakage. Ang II (angiotensin II)-induced hypertension represses arterial Sox17 and Dll4, followed by transcytosis-driven retinal edema, which is rescued by a gain of Notch activity. Transcriptomic profiling of retinal endothelial cells suggests that Dll4 blocking activates SREBP1 (sterol regulatory element-binding protein 1)-mediated lipogenic transcription and enriches gene sets favorable for caveolae formation. Profiling also predicts the activation of VEGF (vascular endothelial growth factor) signaling by Dll4 blockade. Inhibition of SREBP1 or VEGF-VEGFR2 (VEGF receptor 2) signaling attenuates both Dll4 blockade-driven and hypertension-induced retinal leakage. CONCLUSIONS: In the retina, Sox17-Dll4-SREBP1 signaling axis controls transcytosis independently of TJ in superficial arteries among heterogeneous regulations for the whole vessels. Uncontrolled transcytosis via dysregulated Dll4 underlies pathological leakage in hypertensive retina and could be a therapeutic target for treating hypertension-associated retinal edema.