• Journal of Trauma and Injury
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• v.25 no.4
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• pp.217-222
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• 2012

Purpose: Diaphragmatic rupture following trauma is often an associated and missed injury. This report is about our experience with treating traumatic diaphragmatic rupture (TDR). Methods: From January 2007 to September 2012, 18 patients who had a diaphragmatic rupture due to blunt trauma or penetrating injury underwent an operation for diaphragmatic rupture at our hospital. We retrospectively reviewed their medical records, including demographic factors, initial vital signs, associated injuries, interval between trauma and diagnosis, injured side of the diaphragm, diagnostic tools, surgical method or approaches, operative time, herniated organs, complications, and mortality. Results: The average age of the patients was 43 years, and 16 patients were male. Causes of trauma included motor vehicle crashes (n=7), falls (n=7), and stab wounds (n=5). The TDR was right-sided in 6 patients and left-sided in 12. The diagnosis was made by using a chest X-ray (n=3), and thorax or upper abdominal computed tomography (n=15). Ten(10) patients were diagnosed within 12 hours. A thoracotomy was performed in 8 patients, a video-assisted thoracoscopic surgery in 4 patients, a laparotomy in 3 patients, and a sternotomy in one patient. Herniated organs were the omentum (n=11), stomach (n=8), spleen and colon (n=6), and liver (n=6). Eighteen diaphragmatic injuries were repaired primarily. Seven patients underwent ventilator care, and two of them had pneumonia and acute respiratory distress syndrome. There were no operative mortalities. Conclusion: Early diagnosis and surgical treatment determine the successful management of TDR with or without the herniation of abdominal organs. The surgical approach to TDR is chosen based on accompanying organ injuries and the injured side.

• International Journal of Stem Cells
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• v.16 no.2
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• pp.191-201
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• 2023

Background and Objectives: O-cyclic phytosphingosine-1-phosphate (cP1P) is a synthetic chemical and has a structure like sphingosine-1-phosphate (S1P). S1P is known to promote cell migration, invasion, proliferation, and anti-apoptosis through hippocampal signals. However, S1P mediated cellular-, molecular mechanism is still remained in the lung. Acute lung injury (ALI) and its severe form acute respiratory distress syndrome (ARDS) are characterized by excessive immune response, increased vascular permeability, alveolar-peritoneal barrier collapse, and edema. In this study, we determined whether cP1P primed human dermal derived mesenchymal stem cells (hdMSCs) ameliorate lung injury and its therapeutic pathway in ALI mice. Methods and Results: cP1P treatment significantly stimulated MSC migration and invasion ability. In cytokine array, secretion of vascular-related factors was increased in cP1P primed hdMSCs (hdMSC^cP1P), and cP1P treatment induced inhibition of Lats while increased phosphorylation of Yap. We next determined whether hdMSC^cP1P reduce inflammatory response in LPS exposed mice. hdMSC^cP1P further decreased infiltration of macrophage and neutrophil, and release of TNF-α, IL-1β, and IL-6 were reduced rather than naïve hdMSC treatment. In addition, phosphorylation of STAT1 and expression of iNOS were significantly decreased in the lungs of MSC^cP1P treated mice. Conclusions: Taken together, these data suggest that cP1P treatment enhances hdMSC migration in regulation of Hippo signaling and MSC^cP1P provide a therapeutic potential for ALI/ARDS treatment.

• Tuberculosis and Respiratory Diseases
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• v.44 no.6
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• pp.1343-1352
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• 1997

Background : Heat-treated cells are known to be protected from lysis by TNF, which is considered to play a central role in the pathogenesis of sepsis-induced acute lung injury. The objective of the study was to investigate the effect of heat shock response by heat-pretreatment on the acute lung injury of the rats induced by intratracheally administered TNF-$\alpha$, Methods : We intratracheally instilled either saline or TNF (R&D, 500ng) with and without heat pretreatment in Sprague-Dawley rats weighing 250~350 g. The heated rats were raised their rectal temperature to $41^{\circ}C$ and was maintained thereafter for 13 minutes at 18 h before intratracheal administration of saline or TNF. After 5 h of intratracheal treatment, lung leak, lung myeloperoxidase activity (MPO) and heat shock proteins were measured in rats. Lung leak index was defined as counts per minute of $I^{25}$ in the right lung divided by counts per minutes of $I^{25}$ in 1.0 ml of blood. All data are expressed as means ${\pm}$SE. Results : There is no difference in acute lung leak index ($0.099{\pm}0.024$ vs $0.123{\pm}0.005$) among the rats given saline intratracheally with and without heat pretreatment, but MPO activity showed a decreased tendency in heat-pretreated rats ($4.58{\pm}0.79\;U/g$) compared with heat-unpretreated rats ($7.32{\pm}0.97\;U/g$) (P=0.064). Rats administered TNF intratracheally with heat-pretreatment had decreased lung leak index ($0.137{\pm}0.012$) and lung MPO activity ($5.51{\pm}1.04\;U/g$) compared with those of heat-unpretreated and TNF-administered rats ($0.186{\pm}0.016$, $14.34{\pm}1.22\;U/g$) (P<0.05 in each). There were no significant difference of lung leak index and MPO activity between TNF-treated rats with heat-pretreatment and saline-treated rats with and without heat-pretreatment. Conclusion : The heat shock response attenuated neutrophil recruitment and acute lung leak induced by intratracheal instillation of TNF-in rats.

• The Journal of the Korea institute of electronic communication sciences
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• v.8 no.11
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• pp.1785-1792
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• 2013

For patients suffering from spinal cord injuries, both of the possibility of having complications with the respiratory system and the related fatal rate are still high, while pneumonia is the most important cause of these fatalities. This research was carried out to find out what effects does a breathing exercise have on the respiratory functions and the improvement in the quality of life. The study was carried out for male patients suffering cervical spinal cord injuries for the purpose of inspiratory muscle strengthening. The objects of the study were 17 non-smoking-at-present male patients with C4 to C6 cervical spinal cord injuries. They had practiced inspiratory muscle strengthening training for three times a week for six weeks. The quality of life and the dyspnea (breathing difficulty) were self-measured before and after the training. As a result, the change in respiratory function was only significantly reduced (p<0.01) within the chronic group. In terms of the changes in the quality of life, the sub-acute group has only seen a significant improvement (p<0.05) for the VT(vitality), while the chronic group has seen significant improvements(p<0.05, p<0.01) in: GH(general health); BP(back pain); and VT(vitality). In this research, the inspiratory muscle strengthening has reduced the dyspnea (breathing difficulties) and improved the quality of life.

• Journal of Chest Surgery
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• v.35 no.5
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• pp.343-349
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• 2002

background: In an attempt to investigate the role of oxidants in the activation of phospholipase $A_2$(PLA$_2$) and endogenous oxidative stress in the lung. acute inflammatory lung injury was induced by the instillation of hydrogen peroxide into the trachea of Sprague-Dawley rats. Material and Method: To prove the hypothesis thats released oxidants from neutrophils activate the PLA$_2$ retrogradely, activities of PLA$_2$ and lysoplatelet activating factor acetyltransferase(lysoPAF AT) were assayed i hours after instillation of hydrogen peroxide. In addition, to confirm the impairing effects of the activation of PLA$_2$ associated with endogenous oxidative stress, lung weight/body weight ratio(L$\times$10$^{-3}$ B), protein contents(mg/two lungs) in bronchoalveolar lavage(BAL) were measured. As neutrophilic respiratory burst has been known to play a pivotal role in the genesis of endogenous oxidative stress associated with acute inflammatory lung injury, BAL neutrophils counts and level of lung myelperoxidase(MPO) were measured after hydorgen peroxide insult. Morphological and histochemical studies were also performed to identify the effect of the endogenous oxidative stress. Result: Five hours after hydrogen peroxide instillation, lungs showed marked infiltration of neutrophils and increased weight. Protein contents in BAL increased significantly compared to those of normal rats. PLA$_2$ activity was enhanced in the hydrogen peroxide instilled group. Interestingly, the accelerated production of platelet activating factor(PAF) was confirmed by the increased activity of lysoPAF AT in the $H_2O$$_2$ employed lung. Morphologically, light microscopic findings of lungs after instillation of hydrogen peroxide showed atelectasis and infiltration of inflammatory cells, which was thought to be caused by lipid mediators produced by PLA$_2$ activation. In cerium chloride cytochemical electron microscopy, dense deposits of cerrous perhydroxide were identified. In contrast, no deposit of cerrous perhydroxide was found in the normal lung.

• Tuberculosis and Respiratory Diseases
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• v.54 no.5
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• pp.532-541
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• 2003

Background : Phospholipase $A_2$ ($PLA_2$) has been known to be involved in the pathogenesis of acute lung injury (ALI) including ARDS. Since doxycycline has the property of inhibiting secretory group II $PLA_2$, the therapeutic effect of doxycycline hyclate was investigated for gut ischemia/reperfusion (I/R)-induced ALI in Sprague-Dawley rats. Methods : ALI was induced in Sprague-Dawley rats by clamping of the superior mesenteric artery for 60 min, followed by 120 min of reperfusion. To confirm the pathogenetic mechanisms of this ALI associated with neutrophilic oxidative stress, we measured bronchoalveolar lavage (BAL) protein content and lung MPO, and performed cyto-chemical electron microscopy for detection of free radicals, assay of $PLA_2$ activity and cytochrome-c reduction assay. Results : In gut I/R-induced ALI rats, protein leakage, pulmonary neutrophil accumulation, free radical production and lung $PLA_2$ activity were all increased. These effects were reversed by doxycycline hyclate. Conclusion : Doxycycline appears to be effective in ameliorating the gut I/R-induced ALI by inhibiting $PLA_2$, thereby decreasing the production of free radicals from neutrophils.

• Journal of the Korean Society of Radiology
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• v.82 no.1
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• pp.244-249
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• 2021

A 53-year-old woman presented with dyspnea. She had undergone extended thymectomy for an invasive thymoma two months prior. CT revealed numerous small nodules in the lung. After that, she deteriorated owing to acute respiratory distress syndrome (ARDS), and the vascular surgeon planned veno-venous extracorporeal membrane oxygenation (ECMO). During percutaneous cannulation through the left femoral vein, a vascular injury was suspected, and the patient's vital signs became unstable. Diagnostic angiography showed a ruptured left common iliac vein, and the bleeding was stopped by placement of a stent-graft. May-Thurner syndrome was diagnosed on abdominal CT. Here, we report a rare case of ECMO-related vascular injury in a patient with an unrecognized anatomical variant, May-Thurner syndrome.

• Journal of The Korean Society of Clinical Toxicology
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• v.10 no.2
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• pp.91-96
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• 2012

Purpose: A retrospective study with a literature review was conducted to identify the clinical characteristics and prognosis after the acute ingestion of glacial acetic acid. Methods: The medical records of 20 patients,who had presented to the emergency department of Ajou University Hospital complaining of the acute ingestion of glacial acetic acid between January 2006 and December 2011, were examined retrospectively. Results: Among the 172 patients admitted for caustics injury, 20 patients ingested glacial acetic acid. The mean age of the patients was $55{\pm}23.5$, and the mean volume of the acid was $84.5{\pm}71.3$ ml. The clinical features included 1) oral ulcers in 12 patients (63.2%), 2) respiratory difficulties in 11 patients (57.9%), 3) oliguria in 8 patients (42.1%), 4) renal toxicity in 7 patients (36.8%), 5) hepatic failure in 7 patients (36.8%), 6) disseminated intravascular boagulopathyin 7 patients (36.8%), 7) low blood pressure in 8 patients (42.1%), and 8) mental changes in 9 patients (47.4%). Ten patients required endotracheal intubation. Nine patients were admitted to the intensive care unit, and 5 patients expired. Conclusion: The ingestion of glacial acetic acid can cause severe symptoms, such as metabolic acidosis, multiple organ failure and upper airway swelling frequently and has a high mortality rate. Therefore, aggressive treatment, including endotracheal intubation, should be considered at the early stages.

• Tuberculosis and Respiratory Diseases
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• v.53 no.5
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• pp.519-529
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• 2002

Background : The therapeutic effects of surfactants on acute lung injury derive not only from their recruiting action on collapsed alveoli but also from their anti-inflammatory action in the alveolar sapce. This study evaluated the anti-inflammatory action of a surfactant in an acute lung injury model of rats by neutrophils were recollected from the BAL fluid and the NF-${\kappa}B$ activity of the neutrophilic nuclear protein was evaluated. Methods : Male Sprague-Dawley rats weighing approximately 300 gram were divided into 3 groups, which consisted of 6 rats respectively. In the control group, normal saline(3ml/kg) was instilled into the trachea twice with 30 minute interval. In two other groups, acute lung injury was induced by the intra-tracheal instillation of LPS(5mg/kg). Thirty minutes later, either a surfactant(ST group; 30mg/kg) or normal saline(NT group: 3ml/kg) was instilled via the trachea. Twenty-four hours after the LPS instillation, the BAL fluid was retrieved to measure the WBC count and cytokine(IL-$1{\beta}$ and IL-6) levels. The neutrophils were isolated from the BAL fluid and the nuclear protein was extracted to evaluate the NF-${\kappa}B$ activity using a eletrophoretic mobility shift assay(EMSA). Results : The WBC count of the BAL fluid of the ST group($3,221{\pm}1,914{\times}10^3/{\mu}l$) was higher than that of the control group($356{\pm}275{\times}10^3/{\mu}l$)(p<0.05) and lower than that of the NT group($5,561{\pm}1,757{\times}10^3/{\mu}l$)(p<0.05)). The BAL fluid level of IL-$1{\beta}$ from the NT group($2,064{\pm}1,082pg/ml$) was higher than those of the ST group($360{\pm}234pg/ml$)(p<0.05) and the control group(0pg/ml)p<0.05) and control group($49{\pm}62pg/ml$)(p<0.05). The NF-${\kappa}B$ activity of the neutrophilic nuclear protein in the ST group and NT group was similar. Conclusion : The surfactant, attenuates the alveolar inflammation in the acute lung injury of rats model. However, its anti-inflammatory action does no't appear to be mediated by the inhibition of NF-${\kappa}B$ activity.

• Tuberculosis and Respiratory Diseases
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• v.44 no.2
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• pp.379-390
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• 1997

Background : It has long been suggested that neutrophils and their products are implicated as the central mediators of the acute lung injuries. Contrary to the dominant role of neutrophils in ARDS, many cases of ARDS has occurred in the setting of severe neutropenia without pulmonary neutrophil infiltration. Therefore it is certain that effector cell(s) other than neutrophil play an important role in the pathogenesis of ARDS. This experiment was performed to define the mechanism of ARDS in the setting of neutropenia, 1) by comparing the severity of endotoxin-induced lung injury, 2) by measurement of hydrogen peroxide production and cytokine concentration in the bronchoalveolar lavage cells and fluids obtained from different rats with and without cyclophosphamide-pretreatment. Method : The male Sprague-Dawleys were divided into the normal control (NC)-, endotoxin (ETX)-, and cyclophosphamide (CPA)-group in which neutropenia was induced by injecting cyclophosphamide intraperitoneally. Acute lung injury was evoked by injecting lipopolysaccharide (LPS) into a tail vein. The bronchoalveolar lavage (BAL) was performed at 3 and 6 hour after administration of LPS to measure the change of cell counts and concentrations of protein and cytokines, tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6). Hydrogen peroxide (HPO) production from BAL cells was measured at 6 hour after LPS administration by phenol red microassay with and without zymosan stimulation. Results : The results were as follows. A change of leukocyte counts in the peripheral blood after treatment with CPA : More than 95% of total leukocytes and neutrophils were reduced after CPA administration, resulting in severe neutropenia. A change of BAL cells : In the ETX-group, the number of total cells (p < 0.01) and of macrophage and neutrophil (p < 0.05) were increased at 3 and 6 hour after LPS administration compared to those of NC-group. In the CPA-group, the number of total leukocyte and macrophage were not changed after LPS administration, but neutrophil counts were significantly reduced and it took part in less than 0.1% of total BAL cells (p < 0.01 vs NC-group). BAL cells in this group were almost all macrophages (99.7%). A change of protein concentration in the BALF : In the ETX-group, protein concentration was increased at 3 hour and was more increased at 6 hour after LPS administration (p < 0.05 and < 0.01 vs NC-group, respectively). In the CPA-group, it was also significantly elevated at 3 hour after LPS administration (p < 0.05 vs NC-group), but the value was statistically not different from that of ETX-group. The value measured at 6 hour after LPS administration in the CPA-group became lower than that of ETX-group (p < 0.05), but showed still a higher value compared to that of NC-group (p < 0.05). A change of cytokine concentration in the BALF : TNF -alpha and IL-6 were elevated in the ETX - and CPA-group compared to those of NC-group at both time intervals. There was no statistical difference in the values of both cytokines between the ETX- and CPA-groups. Measurement of hydrogen peroxide production from BAL cells : There was no intergroup difference of HPO production from resting cells. HPO production after incubation with opsonized zymosan was significantly elevated in all groups. The percent increment of HPO production was highest in the ETX-group (89.0%, p < 0.0008 vs NC-group), and was 42.85 in the CPA-group (p = 0.003 vs NC-group ). Conclusion : Acute lung injury in the setting of neutropenia might be caused by functional activation of resident alveolar macrophages.