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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.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.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.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.

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-β1-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.

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-β1-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. Supplementary Information The online version contains supplementary material available at 10.1007/s10157-021-02021-y.

Type 4 Bartter syndrome (BS) is caused by genetic mutations in barttin, which is coded for by BSND. Barttin serves as the β-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.

Clathrate formation and crystal structures of 3α, 7α, 12α-trihydroxy-5β-cholan-24-amide (cholamide) have been investigated. Cholamide forms inclusion compounds with various organic compounds having hydrogen-bond (H-bond) donors. X-Ray crystallographic studies showed that cholamide has bilayer structures with molecular channels. The crystal structures are quite similar to those of channel-type inclusion crystals of cholic acid. Steric dimensions of the host cavities are identical, but cholamide has an H-bond ‘hook’ on the wall of the channels, while cholic acid does not. This difference is correlated with not only the inclusion abilities but also the molecular structures. Two H-bond donors of the amide group yield a hydrophilic inclusion cavity that includes H-bond acceptors, and one H-bond donor of the carboxylic acid gives a lipophilic inclusion cavity that includes non-polar or less polar compounds.

Crystal structure of an inclusion crystal of cholanamide with aniline is described. Comparison of the crystal structure with that of the cholic acid clathrate reveals both hosts have quite similar assembly mode. However, the most smking difference is hydrogen bonding. Aniline is included in host lattice of cholanamide by triple hydrogen bonds, whereas in that of cholic acid by double weak hydrogen bonds. Difference of the molecular structure between them gives raise to change the host-guest hydrogen bonding.

Hyodeoxycholic acid forms inclusion crystals with aromatic amines such as pyridine, aniline and toluidines. The crystal structure of a 1:1 inclusion compound of hyodeoxycholic acid with pyridine was determined.

Hyodeoxycholic acid forms inclusion crystals with aromatic amines such as pyridine, aniline and toluidines. The crystal structure of a 1:1 inclusion compound of hyodeoxycholic acid with pyridine was determined.