Feasibility of utilizing mediastinal drains alone following esophageal cancer surgery: a retrospective study.

BACKGROUND: It was typically necessary to place a closed thoracic drainage tube for drainage following esophageal cancer surgery. Recently, the extra use of thoracic mediastinal drainage after esophageal cancer surgery had also become more common. However, it had not yet been determined whether mediastinal drains could be used alone following esophageal cancer surgery. METHODS: A total of 134 patients who underwent esophageal cancer surgery in our department between June 2020 and June 2023 were retrospectively analyzed. Among them, 34 patients received closed thoracic drainage (CTD), 58 patients received closed thoracic drainage combined with mediastinal drainage (CTD-MD), while 42 patients received postoperative mediastinal drainage (MD). The general condition, incidence of postoperative pulmonary complications, postoperative NRS score, and postoperative anastomotic leakage were compared. The Mann-Whitney U tests, Welch's t tests, one-way ANOVA, chi-square tests and Fisher's exact tests were applied. RESULTS: There was no significant difference in the incidence of postoperative hyperthermia, peak leukocytes, total drainage, hospitalization days and postoperative pulmonary complications between MD group and the other two groups. Interestingly, patients in the MD group experienced significantly lower postoperative pain compared to the other two groups. Additionally, abnormal postoperative drainage fluid could be detected early in this group. Furthermore, there was no significant change in the incidence of postoperative anastomotic leakage and the mortality rate of patients after the occurrence of anastomotic leakage in the MD group compared with the other two groups. CONCLUSIONS: Using mediastinal drain alone following esophageal cancer surgery was equally safe. Furthermore, it could substantially decrease postoperative pain, potentially replacing the closed thoracic drain in clinical practice.

Spleen contributes to chronic restraint stress-induced lung injury through splenic CD11b+ cells.

Chronic stress can induce lung injury. The spleen, as the largest peripheral immune organ, plays a crucial role in various lung diseases. Our previous study found that the spleen underwent significant changes during chronic restraint stress (CRS). However, the exact role of the spleen in CRS-induced lung injury remains unclear. In this study, we found that CRS could increase lung index. CRS could lead to alterations of the lungs such as destruction of alveolar wall, thickening of alveolar septa, dilation of pulmonary capillaries, and increased inflammatory cell infiltration. CRS increases the concentration of malondialdehyde (MDA), decreases the level of surfactant protein A (SP-A), and elevates the levels of pro-inflammatory factors (TNF-α, IL-6, and IL-1ß) in the lungs. Additionally, CRS could increase the proportions and numbers of CD11b+Ly6ChiLy6G- monocytes in the lung, while cannot alter proportions and numbers of CD3-NK1.1+ NK cells, CD3+CD4+ T cells, CD3+CD8+ T cells, and CD11b+Ly6G+ neutrophils. Moreover, the levels of inflammatory markers in lung tissues were positively correlated with the proportion of CD11b+Ly6ChiLy6G- monocytes. Interestingly, splenectomy inhibited CRS-induced lung injury and attenuated the alteration in the proportion of CD11b+Ly6ChiLy6G- monocytes in the lungs induced by CRS. Moreover, splenic CD11b+ cells, rather than splenic CD11b- cells, transfused into splenectomized mice, and subsequently exposed to CRS, can cause lung injury. These results suggest that CRS could induce lung injury and CD11b+Ly6ChiLy6G- monocytes aggregation in the lung. The spleen could contribute to CRS-induced lung injury. Furthermore, splenic CD11b+ cells might play an important role in CRS-induced lung injury.

[Fibroblast growth factor-1 inhibits Wnt/ß-catenin pathway during adipogenesis].

OBJECTIVE: To determine the time course and potential mechanism of fibroblast growth factor-1 (FGF-1) in the regulation of adipogenesis.
 METHODS: We cultured human Simpson-Golabi-Behmel syndrome (SGBS) pre-adipocytes with recombinant FGF-1 and harvested cells at various stages prior to and during differentiation; at cell proliferation (D-3), confluence (D0), early (D3), middle (D7) and mature (D14) stages of differentiation. We determined lipid accumulation in mature adipocytes by morphological observation and quantitative measurement of oil red O staining. We also examined the expression of adipogenic genes and related markers involved in the Wnt/ß-catenin pathway using quantitative Real-time PCR and Western blot.
 RESULTS: Compared to control SGBS cells, treatment with FGF-1 increased lipid accumulation; induced a sustained increase in the mRNA for peroxisome proliferater-activated receptor γ (PPARγ), glyceraldehyde-3-phosphate dehydrogenase (G3PDH), adiponectin and glucose transporter type 4 (GLUT4); and promoted a sustained decrease in expression of markers of the Wnt/ß-catenin pathway, ß-catenin and transcription factor 4 (TCF4).
 CONCLUSION: The adipogenic effects of FGF-1 are apparent throughout the whole priming and differentiation period in human SGBS pre-adipocytes. Furthermore, our results suggest that FGF-1 promotes adipogenesis, at least in part, via a sustained decrease in activity of the Wnt/ß-catenin pathway.