Urinomas can occur after renal trauma or perforation of the collecting system during an endosurgical procedure. However, spontaneous urinomas are very rare. Here we report a case of a spontaneous perinephric urinoma following the removal of a Foley catheter in an 18-year-old girl with acute kidney injury caused by septic shock. The patient had been treated for septic shock, acute kidney injury, and acute respiratory distress syndrome, and had a Foley catheter in place for seven days. After Foley catheter removal, the patient complained of consistent voiding difficulty. An abdominal computed tomography scan showed a large amount of left perinephric fluid, and the aspirated fluid included urothelial cells, confirming the diagnosis of a urinoma. The urinoma was successfully treated by insertion of a double-J stent into the left ureter. This report discusses the available literature on urinomas, and their clinical features, diagnosis, and treatment.
The coronavirus disease 2019 (COVID-19) pandemic has become a public health emergency of global concern. In China, traditional Chinese medicine has been widely administered to COVID-19 patients without sufficient evidence. To evaluate the efficacy of Shenhuang Granule (SHG) for treating critically ill patients with COVID-19, we included in this study 118 patients who were admitted to the ICU of Tongji Hospital between January 28, 2020 and March 28, 2020. Among these patients, 33 (27.9%) received standard care plus SHG (treatment group) and 85 (72.1%) received standard care alone (control group). Enrolled patients had a median (IQR) age of 68 (57-75) years, and most (79 [67.1%]) were men. At end point of this study, 83 (70.3%) had died in ICU, 29 (24.5%) had been discharged from ICU, and 6 patients (5.2%) were still in ICU. Compared with control group, mortality was significantly lower in treatment group (45.4% vs. 80%, p < .001). Patients in treatment group were less likely to develop acute respiratory distress syndrome (ARDS) (12 [36.3%] vs. 54 [63.5%], p = 0.012) and cardiac injury (5 [15.1%] vs. 32 [37.6%], p = 0.026), and less likely to receive mechanical ventilation (22 [66.7%] vs. 72 [84.7%], p = 0.028) than those in control group. The median time from ICU admission to discharge was shorter in treatment group (32 [20-73] days vs. 76 [63-79] days, p = 0.0074). These findings suggest that SHG treatment as a complementary therapy might be effective for critically ill adults with COVID-19 and warrant further clinical trials.
Jae Min Lee;Kwang Hyun Chung;Jin Myung Park;Sang Hyub Lee;Ji Kon Ryu;Yong-Tae Kim
Journal of Digestive Cancer Research
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v.2
no.1
/
pp.28-31
/
2014
Pancreatic cancer is a highly aggressive cancer with poor prognosis. Although, gemcitabine is the current standard regimen as first-line chemotherapy for advanced pancreatic cancer, effective regimens of second-line chemotherapy after gemcitabine failure have not been established yet. We report a case of gemcitabine refractory pancreatic cancer treated with second-line chemotherapy with FOLFIRINOX regimen. A 57-year-old-woman visited our hospital for pancreatic body mass detected by computed tomography (CT). The patient underwent distal pancreatectomy and splenectomy and the pathologic results after surgery demonstrated adenocarcinoma. Follow-up was performed after surgery and CT and positron emission tomography (PET) 4 months after surgery revealed multiple hepatic metastases. The patient underwent first-line chemotherapy with gemcitabine and erlotinib for recurred pancreatic cancer. However, CT after 7 cycles of the chemotherapy showed the progression of multiple hepatic metastases and switch to second-line chemotherapy with FOLFIRINOX was initiated. CT after 16 cycles of the FOLFIRINOX showed the complete remission of multiple hepatic metastases. The patient was admitted for infective endocarditis with septic pneumonia 17 months after the initiation of FOLFIRINOX. However, the patients died from the progression of septic embolism and acute respiratory distress syndrome.
Su Hwan Lee;Ju Hye Shin;Min Woo Park;Junhyung Kim;Kyung Soo Chung;Sungwon Na;Ji-Hwan Ryu;Jin Hwa Lee;Moo Suk Park;Young Sam Kim;Jong-Seok Moon
IMMUNE NETWORK
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v.22
no.2
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pp.18.1-18.15
/
2022
Dysfunction of mitochondrial metabolism is implicated in cellular injury and cell death. While mitochondrial dysfunction is associated with lung injury by lung inflammation, the mechanism by which the impairment of mitochondrial ATP synthesis regulates necroptosis during acute lung injury (ALI) by lung inflammation is unclear. Here, we showed that the impairment of mitochondrial ATP synthesis induces receptor interacting serine/threonine kinase 3 (RIPK3)-dependent necroptosis during lung injury by lung inflammation. We found that the impairment of mitochondrial ATP synthesis by oligomycin, an inhibitor of ATP synthase, resulted in increased lung injury and RIPK3 levels in lung tissues during lung inflammation by LPS in mice. The elevated RIPK3 and RIPK3 phosphorylation levels by oligomycin resulted in high mixed lineage kinase domain-like (MLKL) phosphorylation, the terminal molecule in necroptotic cell death pathway, in lung epithelial cells during lung inflammation. Moreover, the levels of protein in bronchoalveolar lavage fluid (BALF) were increased by the activation of necroptosis via oligomycin during lung inflammation. Furthermore, the levels of ATP5A, a catalytic subunit of the mitochondrial ATP synthase complex for ATP synthesis, were reduced in lung epithelial cells of lung tissues from patients with acute respiratory distress syndrome (ARDS), the most severe form of ALI. The levels of RIPK3, RIPK3 phosphorylation and MLKL phosphorylation were elevated in lung epithelial cells in patients with ARDS. Our results suggest that the impairment of mitochondrial ATP synthesis induces RIPK3-dependent necroptosis in lung epithelial cells during lung injury by lung inflammation.
Youngheon Park;Jimin Jang;Jooyeon Lee;Hyosin Baek;Jaehyun Park;Sang-Ryul Cha;Se Bi Lee;Sunghun Na;Jae-Woo Kwon;Seok-Ho Hong;Se-Ran Yang
International Journal of Stem Cells
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v.16
no.2
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pp.191-201
/
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 (hdMSCcP1P), and cP1P treatment induced inhibition of Lats while increased phosphorylation of Yap. We next determined whether hdMSCcP1P reduce inflammatory response in LPS exposed mice. hdMSCcP1P 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 MSCcP1P treated mice. Conclusions: Taken together, these data suggest that cP1P treatment enhances hdMSC migration in regulation of Hippo signaling and MSCcP1P provide a therapeutic potential for ALI/ARDS treatment.
The Journal of the Convergence on Culture Technology
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v.10
no.2
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pp.215-224
/
2024
The purpose of this study was to examine research trends related to neonatal simulation practice education of domestic nursing students. It was a descriptive research study. For literature collection, a total of 17 journals were selected as a result of a search using ('Newborn Simulation') AND ('Nursing Student' OR 'Nursing College Student' OR 'Student Nurse') in 6 domestic electronic databases. The research results showed that it started with 7 journals from 2011 to 2015 and decreased slightly to 5 journals from 2016 to 2020 and 5 journals from 2021 to 2023. The research design was mostly quantitative with a total of 16 journals(94%). Among them, there were 15 intervention journals(88%), 1 descriptive research journals(6%), and 1 mixed method journals(6%). The key topics in simulation practice were high-risk newborns with 9 journals(52%), respiratory distress syndrome in neonatal intensive care units appeared with 3 journals(18%), neonatal care with 3 journals(18%), normal newborn care with 1 journal(6%), and neonatal emergency airway care with 1 journals(6%). The main outcome variables were clinical performance, accounting for 5 journals(19.2%), followed by practice satisfaction 3 journals(11.5%). clinical competency and practice satisfaction were found to have significant positive effects. In conclusion, various research methods are required, such as expansion of nursing students' neonatal simulation practice education, repeated research, and qualitative research.
Backgraound : There have been many reports on the pathogenesis of sepsis-induced acute respiratory distress syndrome(ARDS) but, the precise mechanism has not been elucidated. This study examined the protective effect of an inhibition of platelet activating factor(PAF) remodeling and the adhesion molecule on the oxidative stress of the lungs in rats with an endotoxin induced acute lung injury(ALI). Methods : ALI was induced in Sprague-Dawley rats by instilling an E-coli endotoxin into the trachea. Ketotifen and fucoidan were used respectively to inhibit PAF remodeling and adhesion molecule. The lung leak index, lung myeloperoxidase(MPO) activity, bronchoalveolar lavage(BAL) fluid neutrophil count and lyso PAF acetyltransferase activity(AT), were measured and an ultrastructural study and cytochemical electron microscopy were performed. Results : The lung leak index, lung MPO activity, BAL fluid neutrophil count and lyso PAF AT activity was higher in the endotoxin-treated rats. In addition, severe destruction of the pulmonary architecture and increased hydrogen peroxide production were identified. These changes were reversed by ketotifen. However, fucoidan did not appear to have any protective effects. Conclusion : The inhibition of PAF remodeling appeared to be effective in decreasing the endotoxin-induced ALI. In addition, this effect might be derived from the inhibition of neutrophilic oxidative stress. However, the inhibition of the adhesion molecules by fucoidan appeared to be ineffective in decreasing the endotoxin-induced ALI.
Background: Endotoxin or lipopolysaccharide(LPS) can prime phagocytic cells such as polymorphonuclear leukocytes, monocytes or animal peritoneal macrophages to generate increased amounts of secretory products such as oxygen free radicals and tumor necrosis factor, which play an important role in developing adult respiratory distress syndrome in gram negative sepsis. Human alveolar macrophages(HAM) are continuously exposed to various stimuli inhaled into the alveoli, and the response to LPS might be different in HAM. Therefore, we investigated the effect of LPS pre-exposure on HAM adhered to plastic surface and A549 cell(type II human alveolar epithelial cell line) monolayer. Methods: HAM were isolated from bronchoalveolar lavage fluid from normal lung of the patients with localized lung cancer and esophageal cancer. LPS was exposed to HAM for 2hrs before or after adherence to plastic surface of 24-well Linbro plate and A549 cell monolayer. And then HAM was stimulated with PMA(phorbol myristate acetate) or fMLP(N-formyl-methionylleucyl-phenylalanine). The amount of hydrogen peroxide($H_2O_2$) production in the supernatant was measured on the principle of peroxidase-dependent oxidation of phenol red by hydrogen peroxide. Results: LPS pre-exposure could not enhance $H_2O_2$ production in neither HAM adhered to plastic surface nor one to A549 cell monolayer. But LPS even in the absence of PMA or fMLP stimulation directly increased $H_2O_2$ release in HAM if added after the adherence to A549 cell monolayer. Conclusion: Endotoxin does not prime HAM, but may directly activate HAM adhered to alveolar epithelial cells. Further investagation will be necessary.
Background : In acute lung injury, activated neutrophils play an important role in tissue damage. For neutrophils to participate in lung inflammation, chemotactic factors released from mononuclear phagocytes are needed to bring these cells to the local site of inflammation, with interleukin-8 (IL-8) being one of the most specific and important chemotactic factors for neutrophils. IL-8 also induces the expression of adhesion molecules and activates neutrophils to release various inflammatory mediators. Lipopolysaccharide(LPS) is one of the most important causes of adult respiratory distress syndrome and can cause release of many inflammatory cytokines including IL-8 leading to acute lung injury. But little is known about the regulatory mechanism of LPS-induced IL-8 gene expression in mononuclear phagocytes. Method : Human alveolar macrophages(HAM) and peripleral blood monocytes(PBMC) were isolated from healthy volunteers. Time and dose relationship of LPS-induced IL-8 mRNA expression was observed by Northern blot analysis. To evaluate the regulatory mechanism of LPS-induced IL-8 gene expression, pretreatment of actinomycin D(AD, $5{\mu}g/ml$) and cycloheximide(CHX, $5{\mu}g/ml$) was done and Northern blot analysis for IL-8 mRNA and ELISA for immunoreactive IL-8 protein in culture supernatant were performed. Results : 1) In HAM, dose and time dependent LPS-induced IL-8 mRNA expression was observed with peak mRNA level at 8 hours post-stimulation. 2) In PBMC, dose and time dependent LPS-induced IL-8 mRNA expression was also observed with peak mRNA level at 4 hours post-stimulation. 3) AD decreased expression of LPS-induced IL-8 gene expression at both mRNAand protein levels in both types of cells. 4) CHX decreased expression of LPS-induced IL-8 gene expression at protein level in both cell types but in HAM, superinduction of IL-8 mRNA was observed while decreased expression of IL-8 mRNA was observed in PBMC. Conclusion : Time and dose dependent LPS-induced IL-8 gene expression was observed in mononuclear phagocytes which is at least partly regulated pretranslationally. LPS-induced IL-8 mRNA expression in HAM needs no de novo protein synthesis and may be under the control of a labile repressor protein while de novo protein synthesis may be needed in PBMC.
Huh, Jin Won;Lim, Chae-Man;Jegal, Yang-Jin;Lee, Sang Do;Kim, Woo Sung;Kim, Dong Soon;Kim, Won Dong;Koh, Youn Suck
Tuberculosis and Respiratory Diseases
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v.52
no.4
/
pp.376-384
/
2002
Background : The mortality from acute respiratory distress syndrome(ARDS) in the late stage, which is characterized by progressive pulmonary fibroproliferation, is ${\geq}80%$. Although previous prospective trials failed to show a survival benefit of steroid therapy in early ARDS, recently, a few of reports have described the survival benefit of the long-term use of steroid in patients with late ARDS. In this study, we analyzed the effect of steroid therapy on patients with late ARDS retrospectively in a single. Medral intensive care unit (MICU). Methods : Over a 3-year period, the medical records of 48 ARDS patients who had been on mechanical ventilation more than 8 days were reviewed. 14 patients were treated by the long-term use of methylprednisolone and another 34 patients served as a control. Both groups were comparable regarding clinical and physiologic data lung injury score(LIS), multiple organ failure score, APACHE III and SAPS II score. Because steroid was instituted after 8 days of advanced mechanical ventilatory support in average, we arbitrarily defined the $8^{th}$ day of ARDS as first day of the study. Results : Initially, the groups had similar PF($PaO_2/FiO_2$) ratio, LIS, APACHE III and SAPS II score. By 7th day after the start of steroid therapy, there were significant improvements in PF ratio, LIS, APACHE III and SAPS II score. The mortality in the steroid treated group was significantly lower(42.9% vs 73.5%, p<0.05). Conclusion : Although the data of this study was retrospective and was not randomized, in order to improve the patient's outcomes, steroid therapy should be considered in late ARDS patients. However, prospective trials are needed to define the indication and the effect of steroid therapy in late ARDS.
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