Changes in esophagus interstitial cells of Cajal in response to acute stress.

BACKGROUND: Thoracic trauma is common, and traffic accident-related traumatic injury can cause acute stress leading to esophageal motility disorders. Interstitial cells of Cajal (ICCs) are regarded as gastrointestinal pacemaker cells. AIM: This study explored the mechanism underlying changes in lower esophagus ICCs under acute stress conditions. METHODS: Fifty adult rabbits, randomly divided into one healthy control and four study groups, were subjected to right chest puncture using a Hopkinson bar. Thereafter, one group was immediately subjected to lower esophagectomy, whereas the other three groups were maintained for 24, 48 and 72 h after puncture and subjected to lower esophagectomy. Immunohistochemistry was used to detect ICC distribution, morphology and density, and TUNEL assays were used to determine ICC apoptosis. Enzyme-linked immunosorbent assays (ELISAs) were used to measure cortisol, epinephrine, dopamine, IL-9, cholecystokinin (CCK) and vasoactive intestinal peptide (VIP). Western blotting and RT-PCR were performed to detect changes in SCF/c-kit and nNOS pathways. RESULTS: After puncture, lung tissue was hemorrhaged, alveoli in puncture areas were destroyed, esophageal pH was decreased, and serum cortisol, epinephrine and dopamine levels increased. ICC numbers increased and apoptotic ICCs decreased in all stress groups after puncture (all p < .01). IL-9, CCK and VIP levels in lower esophagus tissue were increased after puncture (all p < .01). Moreover, SCF/c-kit and nNOS pathways were upregulated in response to stress (all p < .01). CONCLUSIONS: Acute stress promotes increases in lower esophageal ICCs that might affect esophagus ICC functions and esophageal motility.

Pathophysiological changes and injury markers for acute lung injury from blunt impact in infant rabbits.

Background: Traffic accidents, particularly blunt impacts, cause serious injuries in children. We aimed to assess inflammatory and injury responses in infant rabbits subjected to acute lung injury resulting from blunt impact, with the goal of identifying potential circulatory injury markers. Methods: Forty 4-week-old infant rabbits were subjected to a right chest impact using a Hopkinson bar with 2,600 g. Computed tomography was employed to assess injury severity. Pathological changes were observed using hematoxylin and eosin staining in the control, 0, 24, and 72 h groups, post-injury. Immunohistochemistry was used to examine surfactant protein A (SP-A) changes in right lung tissues and upper main bronchi. Serum levels of interleukin-6 (IL-6), IL-8, and SP-A were measured using ELISA within 24 h post-injury in the control, 0 h, and 24 h groups. Results: Following blunt injury, significant increases were observed in blood white blood cell count (F = 101.556, P < 0.01) and neutrophil percentage (F = 104.228, P < 0.01), which gradually decreased after 24 and 72 h. The lung wet/dry weight ratio indicated significant edema (F = 79.677, P < 0.01), corroborated by hematoxylin and eosin staining showing edema, exudation, and marked granulocyte infiltration in the control, 0 h, 24 h and 72 h groups. SP-A levels decreased rapidly at 0 h, and recovered between 24 and 72 h in the right lung tissues (F = 6.7, P < 0.05), left lung (F = 15.825, P < 0.05) and upper main bronchi (F = 59.552, P < 0.01). The ELISA results showed increasing trends for the control and 0 h groups, while decreasing trends were observed in 24 h group for IL-6 (F = 58.328, P < 0.01) and IL-8 (F = 41.802, P < 0.01). Conversely, SP-A exhibited a decreasing trend in the control and 0 h groups but increased in the serum of 24 h group (F = 52.629, P < 0.01). Discussion: In cases of direct chest trauma in infant rabbits, particularly mild injuries without rib fractures. SP-A levels correlated with pathological changes across all groups and may serve as biomarkers for pediatric blunt lung impact.

Impact of acute stress disorder on surfactant protein D levels in acute lung injury.

Many people sustain acute lung injuries in road traffic collisions, but few studies have dealt with such injuries in live models. This study aimed to explore the basic pathophysiological and inflammatory changes in adult rabbits following acute thoracic trauma. We randomly assigned 50 rabbits to control and injury groups. Rabbits in the injury group were subjected to right chest pressure (2600 g) using a Hopkinson bar. Measurements were taken in the control group and 0, 24, 48, and 72 h after injury in the injury group. Injury severity was evaluated in gross view; with haematoxylin and eosin (H&E) staining; and through the serum changes of tumor necrosis factor alpha (TNF-α), surfactant protein D (SP-D), and neutrophils. Secretion changes in SP-D in right lung injured tissues were estimated by western blotting and qPCR. Serum TNF-α levels increased rapidly immediately after injury, gradually recovering after 24, 48, and 72 h (p < 0.01). The percentage of neutrophils in the accompanying blood showed a consistent trend. Gross necropsy and H&E staining indicated different levels of bleeding, alveoli exudation, and inflammatory transformation after impact. ELISA depicted the same trend in circulation (F = 22.902, p < 0.01). Western blotting showed that SP-D protein levels in tissues decreased at 0 h and increased at 24, 48, and 72 h. We demonstrate the feasibility of a model of impact lung injury. Primary impact caused injury without external signs. Inflammation began immediately, and the lungs began recovering at 24, 48, and 72 h, as shown by increased SP-D levels in circulation and tissues.With complaints of ALI and inflammation, SP-D may be a potential biomarker after chest trauma.

Expression of copper metabolism-related genes is associated with the tumor immune microenvironment and predicts the prognosis of hepatocellular carcinoma.

Background: Copper metabolism dysfunction has been found to be associated with the progression of various malignant tumors. The aim of this study is to explore the prognostic value of copper metabolism-related genes (CMRGs) in hepatocellular carcinoma (HCC) and their impact on the immune microenvironment. Methods: We identified differentially expressed CMRGs in cancer and adjacent samples of HCC from The Cancer Genome Atlas (TCGA). Consensus clustering was performed to distinguish subgroups, and TIMER and CIBERSORT were applied to analyze the tumor immune microenvironment (TIME). We used the least absolute shrinkage and selection operator (LASSO) and multivariate Cox regression analysis to establish a prognostic risk model for CMRGs. Gene set enrichment analysis (GSEA) was performed to elucidate potential signaling mechanisms associated with the risk group, as well as to determine and compare the tumor mutation burden (TMB), immune cell infiltration levels, and immune checkpoint of the identified risk groups. Results: Two subgroups with significantly different survival rates were identified, with a better prognosis associated with high immune scores, high abundance of immune-infiltrating cells, and a relatively higher immune status. A prognostic risk model based on five CMRGs was constructed, which showed significant prognostic value. When combined with clinical feature column charts, this model can predict the prognosis of patients with HCC. Functional enrichment analysis showed that the low-risk group was enriched in a large number of metabolic pathways, while the high and low-risk groups exhibited different TMB and differential expression of immune checkpoint genes. The established model was validated in an independent International Cancer Genome Consortium (ICGC) dataset. Conclusions: The results indicate that the expression of CMRGs is associated with the prognosis of HCC and the tumor microenvironment, and can serve as a predictive indicator for evaluating the prognosis of HCC.

Comprehensive analysis of the association between inflammation indexes and complications in patients undergoing pancreaticoduodenectomy.

Background: During clinical practice, routine blood tests are commonly performed following pancreaticoduodenectomy (PD). However, the relationship between blood cell counts, inflammation-related indices, and postoperative complications remains unclear. Method: We conducted a retrospective study, including patients who underwent PD from October 2018 to July 2023 at the First Hospital of Chongqing Medical University, and compared baseline characteristics and clinical outcomes among different groups. Neutrophil count (NC), platelet count (PLT), lymphocyte count (LC), systemic immune-inflammation index (SII), platelet-to-lymphocyte ratio (PLR), neutrophil-to-lymphocyte ratio (NLR), and the product of platelet count and neutrophil count (PPN) were derived from postoperative blood test results. We investigated the association between these indicators and outcomes using multivariable logistic regression and restricted cubic spline analysis. The predictive performance of these indicators was assessed by the area under the curve (AUC) of the receiver operating characteristic (ROC) curve and decision curve analysis (DCA). Result: A total of 232 patients were included in this study. Multivariate logistic regression and restricted cubic spline analysis showed that all indicators, except for PLT, were associated with clinical postoperative pancreatic fistula (POPF). SII, NLR, and NC were linked to surgical site infection (SSI), while SII, NLR, and PLR were correlated with CD3 complication. PLT levels were related to postoperative hemorrhage. SII (AUC: 0.729), NLR (AUC: 0.713), and NC (AUC: 0.706) effectively predicted clinical POPF. Conclusion: In patients undergoing PD, postoperative inflammation-related indices and blood cell counts are associated with various complications. NLR and PLT can serve as primary indicators post-surgery for monitoring complications.

Distribution of interstitial cells of Cajal in the Esophagus and change in distribution after thoracic trauma.

Interstitial cells of Cajal (ICCs) function as pacemaker cells in the gastrointestinal tract. Acute thoracic trauma is a common and lethal cause of death due to physical trauma caused by traffic accidents. This study aimed to explore the distribution of esophageal ICCs and distribution changes observed after acute thoracic trauma. Thirty rabbits were randomly divided into a control group and two study groups. The control group animals underwent an esophagectomy. All animals in the study groups underwent right chest puncture using the Hopkinson bar technique. The study groups were subjected to esophagectomy 24 and 72 h after chest puncture. Distribution, morphology, and density of esophageal ICCs were detected using transmission electron microscopy, toluidine blue staining, and immunohistochemistry. Apoptosis of esophageal ICCs was evaluated using the terminal deoxynucleotidyl transferase (TdT) dUTP Nick-End Labeling assay. Western blotting and reverse transcription polymerase chain reaction were used to detect changes in the SCF/c-kit signaling pathway. Esophageal ICCs distribution and SCF/c-kit signal pathway decreased from the upper part to the lower part in both physiological state and after thoracic trauma. In contrast, death of ICCs increased from the upper part to the lower part, both in physiological and injured state (P < 0.05). After thoracic trauma, increased ICCs and decreased death of ICCs in all parts of the esophagus (P < 0.05) were observed. The observed distribution and changes in esophageal ICCs would have an impact on motility and motility disorders of the esophagus.