Effect of mechanical ventilation guided by transpulmonary pressure in acute respiratory distress syndrome patients: a systematic review and meta-analysis of randomized control trials.

OBJECTIVE: This study aimed to investigate the effect of mechanical ventilation guided by transpulmonary pressure in patients diagnosed with acute respiratory distress syndrome (ARDS). MATERIALS AND METHODS: Randomized control trials of ARDS patients that received mechanical ventilation guided by transpulmonary pressure vs. mechanical ventilation guided by traditional lung protective ventilation strategies in adults were retrieved by two reviewers independently from PubMed, EMBASE, The Cochrane Library, The China National Knowledge Infrastructure, and WanFang database before October 2022. The protocol has been registered on PROSPERO (CRD42022307816). The primary outcome was mortality. The secondary outcomes included mechanical ventilation days, oxygenation function and ventilation parameters, hemodynamics, and cytokines level. RESULTS: Thirteen articles (819 patients) were finally included through our search strategy. The total mortality (RR, 0.68; 95% CI, 0.54-0.85; p = 0.0006) and mechanical ventilation days (MD, -2.77; 95% CI, -4.60 - -0.94; p = 0.003) reduced when compared with the control group. Patients in the transpulmonary pressure group had higher oxygen index (MD, 40.74; 95% CI 9.81-71.68, p = 0.010) and lung compliance (MD, 7.98; 95% CI 4.55-11.41, p < 0.00001). Positive end-expiratory pressure (PEEP) was higher in the transpulmonary pressure group (MD, 5.47; 95% CI, 3.59 - 7.35; p < 0.00001). The Interlukin-6 (IL-6) level in the control group decreased obviously compared with that in the transpulmonary pressure group (SMD, -2.03; 95% CI, -3.50 - -0.56; p = 0.007). CONCLUSIONS: Mechanical ventilation guided by transpulmonary pressure tended to have a beneficial prognosis on ARDS patients. Oxygenation and lung mechanics parameters were also improved. The clinical effect of mechanical ventilation directed by transpulmonary pressure was superior to the traditional lung protective ventilation strategies in ARDS patients.

Correlation among RKIP expression, NF-κB p65 levels, and T-lymphocyte subsets in gastric cardia adenocarcinoma.

The aim of this study was to characterize variations in Raf kinase inhibitor protein (RKIP) expression and related signaling molecules in gastric cardia adenocarcinoma. Cancerous and precancerous tissues were collected from patients with gastric cardia adenocarcinoma and normal tissue was collected from healthy controls. RKIP expression was detected in these tissues and the serum levels of NF-κB p65 and T-lymphocyte subsets were measured. Positive RKIP expression was higher in gastric cardia adenocarcinoma tissues than in precancerous tissues. The serum level of total NF-κB p65 was higher in patients with gastric cardia adenocarcinoma than in healthy controls. Levels of NF-κB p65 did not correlate with positive and negative expression of RKIP, but were higher in patients with lymph node metastasis than in those without it. The cellular immune function of the gastric cardia adenocarcinoma group was lower than in normal controls, particularly in cases with negative RKIP expression. RKIP is downregulated in gastric cardia adenocarcinoma tissues, which is related to the occurrence, progression, invasion, and metastasis of tumors. The possible mechanism for this may be the inhibition of NF-κB activity and cellular immune function, which allows for the escape of tumor cells from immune surveillance.

Alterations in pancreatic microcirculation and expression of endothelin-1 in a model of chronic pancreatitis.

Chronic pancreatitis (CP) is characterized by the presence of an inflammatory infiltrate with progressive destruction of acinar cells and fibrosis. The finding that endothelin-1 (ET-1), an endothelium-derived peptide having vasoconstrictive and mitogenic properties, reduces pancreatic blood flow (PBF) in normal rats suggested that the peptide may be associated with the reduced PBF seen in animal models of CP and with the morphological abnormalities of the disease. This study investigates changes in blood flow to the pancreas and other abdominal organs in a rat model of CP and compares ET-1 production in the pancreata of these rats and normal controls. CP was induced in male Wistar rats by the injection of oleic acid into the common bile/pancreatic duct. The radiolabeled microsphere technique was employed to measure blood flow to the pancreas, duodenum, liver, spleen, and kidneys. Immunohistochemistry was used to investigate the cellular production of ET-1. After 3 weeks, significant decreases were noted in body weight, pancreatic weight, and pancreatic DNA, amylase, and protein content in the animals with CP. PBF was reduced by 64% and duodenal blood flow by 80% relative to those in control animals. Hepatic and splenic blood flows were increased by 91 and 88%, respectively, compared to those in controls. A 50% decrease in renal blood flows were increased by 91 and 88%, respectively, compared to those in controls. A 50% decrease in renal blood flow was also seen in the experimental group after 3 weeks. Pancreata from animals with CP stained diffusely for ET-1 in the cytoplasm of vascular endothelial, acinar, and ductal cells. In the control pancreata, focal staining for ET-1 was observed only in acinar cells. This difference was significant in endothelial and ductal cells. There was weak staining of islet cells in both groups. The results suggest that elevation in local production of ET-1 may be associated with the morphological and hemodynamic changes of CP.