ABSTRACT
OBJECTIVE: Computed tomography (CT)-guided lipiodol marking is one of the targeting methods for resecting small pulmonary nodules or ground-glass nodules in video-assisted thoracic surgery (VATS). However, lipiodol spreading during marking has not been assessed, practically. In this study, we examined the clinical significance and the influence of lipiodol spreading on surgery. METHODS: From April 2010 to March 2021, 176 pulmonary nodules in 167 patients were marked with lipiodol under CT guided before VATS. The marking images after lipiodol injection were classified into "Spread" and "non-Spread." Lung resection was sequentially performed on the same day. RESULTS: All target nodules were successfully resected in VATS. In the classification of marking images, Spread was 32 (18%), non-Spread was 144 (82%). There was a significant difference in duration of surgery (mean; 138.7 min vs. 118.3 min, p = 0.0496) and amount of bleeding (mean; 32.7 g vs. 11.2 g, p = 0.0173). Provided that limited to the data of wedge resections without intrathoracic pleural adhesion (n = 117), there was no significant difference in duration of surgery (mean; 104.8 min vs. 99.6 min, p = 0.48), amount of bleeding (mean; 4.9 g vs. 5.3 g, p = 0.58). In the multivariate logistic regression analysis, the risk factor of lipiodol spreading was intrathoracic pleural adhesion (odds ratio: 3.16, 95% confidence interval: 1.12-8.97, p = 0.03). There was no relationship between marking image and complication rate. CONCLUSIONS: Lipiodol spreading did not directly influence surgery and complication. However, it was a sign of intrathoracic pleural adhesion, which could lead to increased duration of surgery and amount of bleeding.
Subject(s)
Lung Neoplasms , Multiple Pulmonary Nodules , Pleural Diseases , Solitary Pulmonary Nodule , Humans , Ethiodized Oil , Lung Neoplasms/diagnostic imaging , Lung Neoplasms/surgery , Multiple Pulmonary Nodules/diagnostic imaging , Multiple Pulmonary Nodules/surgery , Thoracic Surgery, Video-Assisted/adverse effects , Thoracic Surgery, Video-Assisted/methods , Tomography, X-Ray Computed/methods , Solitary Pulmonary Nodule/diagnostic imaging , Solitary Pulmonary Nodule/surgery , Retrospective StudiesABSTRACT
BACKGROUND: Lipid-metabolizing enzymes and their metabolites affect inflammation and fibrosis, but their roles in chronic kidney disease (CKD) have not been completely understood. METHODS: To clarify their role in CKD, we measured the mRNA levels of major lipid-metabolizing enzymes in 5/6 nephrectomized (Nx) kidneys of C57BL/6 J mice. Mediator lipidomics was performed to reveal lipid profiles of CKD kidneys. RESULTS: In 5/6 Nx kidneys, both mRNA and protein levels of Alox15 were higher when compared with those in sham kidneys. With respect to in situ hybridization, the mRNA level of Alox15 was higher in renal tubules of 5/6 Nx kidneys. To examine the role of Alox15 in CKD pathogenesis, we performed 5/6 Nx on Alox15-/- mice. Alox15-/- CKD mice exhibited better renal functions than wild-type mice. Interstitial fibrosis was also inhibited in Alox15-/- CKD mice. Mediator lipidomics revealed that Alox15-/- CKD mouse kidneys had significantly higher levels of PGD2 than the control. To investigate the effects of PGD2 on renal fibrosis, we administered PGD2 to TGF-ß1-stimulated NRK-52E cells and HK-2 cells, which lead to a dose-dependent suppression of type I collagen and αSMA in both cell lines. CONCLUSION: Increased PGD2 in Alox15-/- CKD mouse kidneys could inhibit fibrosis, thereby resulting in CKD improvement. Thus, Alox15 inhibition and PGD2 administration may be novel therapeutic targets for CKD.
Subject(s)
Arachidonate 12-Lipoxygenase/genetics , Arachidonate 15-Lipoxygenase/genetics , Kidney/pathology , Lipid Metabolism/genetics , Prostaglandin D2/genetics , Renal Insufficiency, Chronic/genetics , Renal Insufficiency, Chronic/physiopathology , Actins/genetics , Actins/metabolism , Animals , Arachidonate 12-Lipoxygenase/metabolism , Arachidonate 15-Lipoxygenase/metabolism , Cell Line , Collagen Type I/genetics , Collagen Type I/metabolism , Collagen Type I, alpha 1 Chain , Fibrosis , Humans , Intramolecular Oxidoreductases/genetics , Kidney/metabolism , Kidney Tubules, Proximal/metabolism , Lipocalins/genetics , Male , Mice, Inbred C57BL , Nephrectomy , Prostaglandin D2/pharmacology , RNA, Messenger/metabolism , Renal Insufficiency, Chronic/pathologyABSTRACT
Type 4 Bartter syndrome (BS) is caused by genetic mutations in barttin, which is coded for by BSND. Barttin serves as the ß-subunit of the ClC-K chloride (Cl-) channel, which is widely expressed in distal nephrons. Type 4 BS is characterized by severely impaired reabsorption of salt, which may cause polyuria, hypokalemia, and metabolic alkalosis. Calcineurin inhibitors reportedly induce renal salt retention and hyperkalemia by enhancing the phosphorylation of the sodium (Na+)-potassium (K+)-2Cl- cotransporter (NKCC2) and Na+-Cl- cotransporter (NCC). In addition, we have previously reported that tacrolimus, a calcineurin inhibitor, increases the levels of phosphorylated NCC. In this study, we administered tacrolimus to barttin hypomorphic (Bsndneo/neo) mice, a murine model of type 4 BS that exhibits polyuria, hypokalemia, and metabolic alkalosis. Administration of tacrolimus increased the serum K+ level and suppressed urinary K+ excretion. Furthermore, after treatment with tacrolimus, Bsndneo/neo mice increased levels of phosphorylated NCC and NKCC2. We conclude that tacrolimus partially improves clinical phenotypes of Bsndneo/neo mice, and that calcineurin inhibitors might be effective for treating type 4 BS.
