Influence of oral comprehensive nursing intervention on mechanically ventilated patients in ICU: a randimized controlled study.

OBJECTIVE: To explore the effect of oral comprehensive nursing intervention on mechanically ventilated patients in ICU. METHODS: Select 76 cases of mechanically ventilated patients in severe ICU admitted to our hospital from January 2022 to October 2022 as the research objects, and divide them into the control group and the observation group according to the way the patients receive oral care. 38 cases each. The patients in the control group received routine nursing intervention, and the patients in the observation group received comprehensive oral nursing intervention on the basis of the nursing of the control group. The clinical index data, oropharyngeal hygiene, pH value, blood gas analysis index levels, and the occurrence and death of ventilator-associated pneumonia were compared between the two groups of patients. RESULTS: The hospitalization time of the two groups was compared (P > 0.05); the mechanical ventilation time and ICU stay time of the observation group were significantly lower than those of the control group (all, P < 0.05); the oral odor scores, The plaque index and soft scale index were significantly lower than those of the control group (all, P < 0.05); the pH value, PaO 2 value, and SpO 2 value of the observation group were significantly lower than those of the control group, and the PaCO 2 value was significantly higher than that of the control group. group (all, P < 0.05); the incidence of VAP in the control group was 55.26%, and the mortality rate was 15.79%, the incidence rate of VAP in the observation group was 21.05%, and the mortality rate was 2.63%, and the incidence rate and mortality rate of VAP in the observation group were significantly lower in the control group (all, P < 0.05). CONCLUSION: The application of nursing intervention can effectively promote the recovery of patients, improve the hygiene of patients' oropharynx, adjust the levels of pH and blood gas-related indicators in patients, and reduce VAP in patients. risk of morbidity and mortality.

Tumor-associated macrophages increase the proportion of cancer stem cells in lymphoma by secreting pleiotrophin.

Tumor-associated macrophages (TAMs) are closely related to the occurrence and development of lymphoma, but their mechanism is still unclear. Here we collected peripheral blood and lymphoma tissue from patients with diffuse large B lymphoma. Results showed that the proportion of TAMs in high-risk group was significantly higher than that in low-risk group. Moreover, the expressions of pleiotrophin (PTN), PTPRZ1 (PTN receptor) and ß-catenin in lymphoma tissues of high-risk group were also significantly higher than those in low-risk group. Correlation analysis showed that the proportion of TAMs in lymphocyte was positively correlated with the expression of PTN and PTPRZ1 in lymphoma tissue. In vitro experimental results showed that TAM promoted the invasion and proliferation of lymphoma cells by secreting PTN. We also found that TAMs increased the proportion of cancer stem cells in lymphoma. Animal experiments showed that TAMs promoted lymphoma growth. Both Ki-67 proliferation index and CD44+cancer stem cells increased significantly in TAM group. Blocking PTN or ß-catenin partly inhibited these effects of TAMs. In conclusion, TAMs increased the proportion of cancer stem cells through PTN/ß-catenin pathway in lymphoma.

CD150highTreg cells may attenuate graft versus host disease and intestinal cell apoptosis after hematopoietic stem cell transplantation.

Combined transplantation of regulatory T cells (Treg cells) may significantly attenuate graft versus host disease (GVHD) after hematopoietic stem cell transplantation (HSCT). Recent studies indicated that CD150+Treg cells could secret adenosine to maintain the quiescent status of HSCs. However, whether it is attributable to the attenuation of GVHD after HSCT is still unclear. In vitro studies revealed that CD150+Treg cells induced immune tolerance was comparable to that induced by CD150-Treg cells, but CD150+Treg cells can secret more adenosine, increase P-AMPK expression and regulate energy metabolism to induce the proliferation of HSC proliferation and inhibit their differentiation into dendritic cells. In this study, GVHD animal model was established, and combined transplantation of Treg cells and HSCs was performed. Results showed the survival time was significantly prolonged, the proliferation rate of HSCs increased significantly and the proportion of undifferentiated HSCs elevated significantly after CD150+Treg transplantation as compared to CD150-Treg transplantation. Immunohistochemistry revealed CD150+Treg cells could secret adenosine, activate AMPK expression and inhibit intestinal cell apoptosis and inflammation after HSCT. Taken together, this study indicates CD150+Treg cells can regulate energy metabolism to attenuate GVHD and intestinal cell apoptosis after HSCT.

Expression and role of TNIP2 in multiple organ dysfunction syndrome following severe trauma.

Severe trauma can result in secondary multiple organ dysfunction syndrome (MODS) and death. Inflammation response and oxidative stress promote the occurrence and development of MODS. TNFAIP3­interacting protein 2 (TNIP2), which can repress the activation of nuclear factor­κB (NF­κB) and may be involved in MODS progression, has not been studied in regards to MODS. The present study aimed to investigate the expression, role and mechanism of TNIP2 in MODS following severe trauma. The expression level of TNIP2 was initially detected in the blood of patients with MODS using reverse transcription­quantitative polymerase chain reaction and western blot assay. Then, to investigate the role of TNIP2 in MODS, a MODS rat model was conducted by trauma and the model rats were treated with TNIP2­plasmid (intraperitoneal injection). Blood levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH), blood urea nitrogen (BUN), creatine (Cr) and creatine kinase (CK); and tumor necrosis factor α (TNF­α), high­mobility group box 1 (HMGB­1), malondialdehyde (MDA) and total antioxidant capacity (TAC) in the different groups were assessed. In addition, activation of NF­κB was assessed by detecting the level of phospho­p65. The results showed that TNIP2 was significantly decreased in the blood of patients with MODS. TNIP2 was also significantly downregulated in the blood and the pulmonary, renal and hepatic tissues of MODS rats. The levels of ALT, AST, LDH, BUN, Cr and CK were markedly increased in the blood of MODS rats, and these increases were inhibited by TNIP2­plasmid administration. Moreover, blood levels of TNF­α, HMGB­1 and MDA were significantly increased in MODS rats, while TAC was notably decreased, and these changes were prevented by TNIP2­plasmid administration. Furthermore, it was found that activation of NF­κB induced by MODS was eliminated by TNIP2­plasmid. In conclusion, the data indicated that TNIP2 is significantly decreased in MODS following severe trauma, and it plays a protective role in MODS development by inhibiting the inflammation response and oxidative stress by preventing NF­κB activation.

MicroRNA-365 regulates the occurrence and immune response of sepsis following multiple trauma via interleukin-6.

In the present study, the expression of microRNA (miR)-365 and interleukin (IL)-6 in peripheral blood mononuclear cells and serum from patients with sepsis following multiple trauma has been investigated. A total of 26 patients with sepsis following multiple trauma were included as the experimental group, whereas 21 contemporaneous patients without sepsis following multiple trauma were included as the negative control group. The expression of IL-6 mRNA and miR-365 was determined by reverse transcription-quantitative polymerase chain reaction, and western blot analysis was used to measure IL-6 protein expression. ELISA was performed to determine the secretion of IL-6 protein. Following stimulation with lipopolysaccharide (LPS) for 24 h, THP-1 cells were used to examine the expression of miR-365 and the levels of IL-6 protein and mRNA in cells simulating sepsis. A dual luciferase reporter assay revealed that IL-6 mRNA was a direct target of miR-365. Patients with sepsis following multiple trauma exhibited significantly higher IL-6 mRNA and protein levels than patients without sepsis (P<0.05). In addition, miR-365 expression in patients with sepsis following trauma was significantly lower than in patients without sepsis (P<0.05). Similar effects were observed in THP-1 cells treated with LPS. The present study demonstrated that increased expression of IL-6 in patients with sepsis following multiple trauma is associated with decreased expression of miR-365. miR-365 may regulate the occurrence and immune response of sepsis following multiple trauma via IL-6. These results may elucidate agents for clinical diagnosis and treatment of the disease.

Association of CYP2E1 and NAT2 polymorphisms with lung cancer susceptibility among Mongolian and Han populations in the Inner Mongolian region.

PURPOSE: To explore associations of CYP2E1 and NAT2 polymorphisms with lung cancer susceptibility among Mongolian and Han populations in the Inner Mongolian region. MATERIALS AND METHODS: CYP2E1 and NAT2 polymorphisms were detected by PCR-RFLP in 930 lung cancer patients and 1000 controls. RESULTS: (1) Disequilibrium of the distribution of NAT2 polymorphism was found in lung cancer patients among Han and Mongolian populations (p=0.031). (2) Lung cancer risk was higher in individuals with c1, D allele of CYP2E1 RsaI/PstI, DraI polymorphisms and slow acetylation of NAT2 (c1 compared with c2, OR=1.382, 95%CI: 1.178- 1.587, p=0.003; D compared with C, OR=1.241, 95%CI: 1.053-1.419, P<0.001; slow acetylation compared with rapid acetylation, OR=1.359, 95%CI:1.042-1.768, p=0.056) (3) Compared with c2/c2 and rapid acetylation, c1/c1 together with slow acetylation synergetically increased risk of lung cancer 2.83 fold. (4) Smokers with CYP2E1 c1/c1, DD, and NAT2 slow acetylation have 2.365, 1.916, 1.841 fold lung cancer risk than others with c2/c2, CC and NAT2 rapid acetylation, respectively. (5) Han smokers with NAT2 slow acetylation have 1.974 fold lung cancer risk than others with rapid acetylation. CONCLUSIONS: Disequilibrium distribution of NAT2 polymorphism was found in lung cancer patients among Han and Mongolian populations. Besides, Han smokers with NAT2 slow acetylation may have higher lung cancer risk compared with rapid acetylation couterparts. CYP2E1 c1/ c1, DD and NAT2 slow acetylation, especially combined with smoking, contributes to the development of lung cancer. CYP2E1 c1/c1 or DD genotype and NAT2 slow acetylation have strong synergistic action in increasing lung cancer risk.