Effectiveness of a Teach-Back Education Program on Perioperative Pain in Patients With Lung Cancer: An Intervention Study Using Behavior Change Wheel.

OBJECTIVE: To assess the effect of a teach-back educational intervention using Behavior Change Wheel (BCW) framework on perioperative pain among patients with lung cancer. METHODS: A prospective quasi-experimental study was conducted in 88 patients with lung cancer from a tertiary hospital in China. According to the order of admission, they were allocated to either control group or intervention group, with 44 patients in each group. Patients in the control group received routine nursing care, while patients in the intervention group were given a teach-back education program based on BCW framework. The visual analog scale (VAS) was adopted to evaluate patients' pain on the day of surgery (T0), 1 (T1), 2 (T2), and 3 (T3) days after surgery. We also recorded the use of patient-controlled analgesia (PCA), the length of hospital stay, and the degree of patients' satisfaction. RESULTS: Rest pain, pain when coughing, and pain during activity that patients in the intervention group experienced were significantly less severe than those in the control group on T0 and T1. The pain when coughing in the intervention group was also significantly milder on T2 and T3. In addition, the number of self-control time, use duration, and total dose of PCA were significantly lower in the intervention group. Moreover, patients' satisfaction of nursing service was significantly higher in the intervention group. CONCLUSION: A teach-back education program based on BCW framework was effective in pain management among the perioperative patients with lung cancer. This study demonstrates the application of teach-back method and the BCW in the development of patient education intervention to mitigate perioperative pain.

Temperature-Dependent Spontaneous Resolution of a Tetrahedral Chiral-at-Nickel(II) Complex under Supramolecular Control.

Although stereochemical control of carbon centers is a well-established technique in modern synthetic chemistry, that of tetrahedral metal complexes with a stereogenic metal center remains difficult due to the dynamic nature of their coordination bonds. Here we report the synthesis of a tetrahedral d8 high-spin chiral-at-nickel(II) complex composed exclusively of achiral ligands and the supramolecular control of its temperature-dependent spontaneous resolution in crystals. Under certain conditions, complex molecules with the same absolute configuration of the nickel(II) center grow into conglomerate crystals with a helically arranged structure due to intermolecular hydrogen bonding. This process is highly spontaneous, does not require any chiral sources, and is closely related to the origin of homochirality in biological systems. The obtained enantiopure nickel(II) complex will be a new type of redox-active chiral source for asymmetric synthetic chemistry.

A retrospective cohort study of disease-related risk factors for central venous catheter-related symptomatic thrombosis in intensive care unit inpatients.

ABSTRACT: Central venous catheters (CVC) are widely used in critically ill patients given their benefits in monitoring vital signs, treatment administration, and renal replacement therapy in intensive care unit (ICU) patients, but these catheters have the potential to induce symptomatic catheter-related venous thrombosis (CRVT). This study reported the rate of symptomatic CRVT in ICU patients receiving CVC and analyzed the disease-related risk factors for symptomatic CRVT in ICU patients.A retrospective analysis was performed on the consecutive ICU 1643 critically ill patients with CVCs inserted from January 2015 to December 2019. Symptomatic CRVT was confirmed by ultrasound. CVCs were divided into 2 groups based on the presence of symptomatic CRVT, and the variables were extracted from the electronic medical record system. Logistic univariate and multivariate regression analyses were used to determine the disease-related risk factors of symptomatic CRVT.A total of 209 symptomatic CRVT events occurred among 2114 catheters. The rate of CRVT was 9.5 per 1000 catheter days. Univariate analysis revealed that trauma, major surgery, heart failure, respiratory failure, and severe acute pancreatitis were risk factors for symptomatic CRVT in the ICU. Multivariate analysis showed that trauma (odds ratio [OR], 2.046; 95% confidence interval [CI] [1.325-3.160], P = .001), major surgery (OR, 2.457; 95% CI [1.641-3.679], P = .000), and heart failure (OR, 2.087; 95% CI [1.401-3.111], P = .000) were independent disease-related risk factors for symptomatic CRVT in ICU. The C-statistic for this model was 0.61 (95% CI [0.57-0.65], P = .000).The incidence rate of symptomatic CRVT in the ICU population was 9.5 per 1000 catheter days. Trauma, major surgery, and heart failure are independent disease-related risk factors of symptomatic CRVT.

Long noncoding RNA NEAT1 sponges miR-129 to modulate renal fibrosis by regulation of collagen type I.

The long noncoding RNA nuclear enriched abundant transcript 1 (NEAT1) has been reported to promote liver fibrosis progression. However, its molecular mechanism in renal fibrosis was not elucidated. In the present study, an in vitro model of renal fibrosis was established with HK-2 and HKC-8 cells treated with transforming growth factor-ß1. C57BL/6 mice were used for the in vivo model with unilateral ureteral obstruction. Our results indicated that NEAT1 and collagen type I levels were significantly upregulated, whereas miR-129 was obviously downregulated, in the progression of renal fibrosis. Meanwhile, NEAT1 knockdown or miR-129 overexpression inhibited collagen type I deposition, the epithelial-mesenchymal transition process, and the inflammation response to suppress renal fibrosis. NEAT1 directly targeted miR-129, and miR-129 directly bound to collagen type I. Downregulation of miR-129 reversed inhibition of renal fibrosis induced by NEAT1 silencing, and upregulation of collagen type I also reversed inhibition of renal fibrosis caused by miR-129 overexpression. NEAT1 knockdown alleviated renal fibrosis in mice subjected to unilateral ureteral obstruction. In conclusion, NEAT1 sponged miR-129 to modulate the epithelial-mesenchymal transition process and inflammation response of renal fibrosis by regulation of collagen type I. Our study indicates a novel role in the regulation of renal fibrosis and provides a new potential treatment target for renal fibrosis.

Silencing of MAP4K4 by short hairpin RNA suppresses proliferation, induces G1 cell cycle arrest and induces apoptosis in gastric cancer cells.

Gastric cancer (GC) is the second most common cause of cancer­associated mortality worldwide. Previous studies suggest that mitogen­activated protein kinase kinase kinase kinase isoform 4 (MAP4K4) is involved in cancer cell growth, apoptosis and migration. In the present study, bioinformatics analysis and reverse transcription­quantitative polymerase chain reaction were performed to determine if MAP4K4 was overexpressed in GC. The knockdown of MAP4K4 by RNA interference in GC cells markedly inhibited cell proliferation, which may be mediated by cell cycle arrest in the G1 phase. The silencing of MAP4K4 also induced cell apoptosis by increasing the ratio of Bax/Bcl­2. In addition, Notch signaling was markedly reduced by MAP4K4 silencing. The results of the present study suggested that inhibition of MAP4K4 may be a therapeutic strategy for GC.

Effect of RTKN on progression and metastasis of colon cancer in vitro.

Like many epithelial-derived cancers, colon cancer results from a multistep tumorigenic process. However, the detailed mechanisms involved in colon cancer formations are poorly characterized. In the present study, we investigated the role of RTKN in colon cancer and explored underlying mechanisms. The results showed that RTKN expression was significantly increased in colon cancer tissues when compared with the adjacent tissues of patients in Shanghai People's hospital and in TCGA independent dataset. Furthermore, silencing of RTKN inhibited cell proliferation, migration, invasion, and arrested cell cycle at G1 phase in LOVO cells. Bioinformatics analysis demonstrated that DNA replication and cell cycle were involved in the regulation of RTKN. MCM2/3/5, CDK1/2 and PCNA expression had a direct relationship with the reduction of RTKN. RTKN could affect the proliferation and metastasis of colon cancer by reducing expression of MCM2/3/5, CDK1/2 and PCNA, suggesting that RTKN was a potential target for treating colon cancer.

Ponicidin induces apoptosis via JAK2 and STAT3 signaling pathways in gastric carcinoma.

Ponicidin has a variety of biological effects such as immunoregulatory and anti-inflammatory functions as well as anti-viral functions especially in the upper respiratory tract infection. This study was aimed to elucidate the antitumor effect of ponicidin in gastric carcinoma MKN28 cells and the possible molecular mechanism involved. Cell viability was measured by the Cell Count Kit-8 (CCK8). Cell apoptosis was assessed by flow cytometry as well as cell cycle and reactive oxygen species (ROS) analysis. Western blot analysis was used to detect the active form of caspase-3 as well as Bax and B-cell lymphoma-2 (Bcl-2) expressions after cells were treated with different concentrations of ponicidin. The results revealed that ponicidin could inhibit the growth of MKN28 cells significantly in both a time- and dose-dependent manner. The cell cycle was blocked and ROS generation was increased after the cells were treated with ponicidin. Bcl-2 expression was down-regulated remarkably while Bax expression and the active form of caspase-3 were increased after apoptosis occurred. We therefore conclude that ponicidin exhibited significant growth inhibition of gastric carcinoma cell line MKN28 and induced apoptosis of MKN28 cells via the signaling pathway regulated by Janus kinase 2 (JAK2) and signal transducers and activators of transcription 3 (STAT3). Ponicidin may serve as a potential therapeutic agent for gastric carcinoma.