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.

Predicting Severity in Hypertriglyceridemia-Induced Acute Pancreatitis: The Role of Neutrophils, Calcium, and Apolipoproteins.

BACKGROUND Hypertriglyceridemia-induced acute pancreatitis (HTG-AP), representing 10% of all acute pancreatitis cases, is characterized by younger onset age and more severe progression, often leading to higher ICU admission rates. This condition poses a significant challenge due to its rapid progression and the potential for severe complications, including multiple organ failure. HTG-AP is distinct from other forms of pancreatitis, such as those caused by cholelithiasis or alcohol, in terms of clinical presentation and outcomes. It's essential to identify early markers that can predict the severity of HTG-AP to improve patient management and outcomes. MATERIAL AND METHODS This study divided 127 HTG-AP patients into mild acute pancreatitis (MAP, n=71) and moderate-to-severe acute pancreatitis (MSAP/SAP, n=56) groups. Blood biological indicators within the first 24 hours of admission were analyzed. Risk factors for HTG-AP progression were determined using binary logistic regression and ROC curves. RESULTS Elevated levels of HCT, NLR, TBI, DBI, AST, Cre, and AMS were noted in the MSAP/SAP group, with lower levels of LYM, Na⁺, Ca²âº, ApoA, and ApoB compared to the MAP group (p<0.05). NEUT%, Ca²âº, ApoA, and ApoB were significantly linked with HTG-AP severity. Their combined ROC analysis yielded an area of 0.81, with a sensitivity of 61.8% and specificity of 90%. CONCLUSIONS NEUT%, Ca²âº, ApoA, and ApoB are significant risk factors for progressing to MSAP/SAP in HTG-AP. Their combined assessment provides a reliable predictive measure for early intervention in patients at risk of severe progression.

Overexpression of SP1 restores autophagy to alleviate acute renal injury induced by ischemia-reperfusion through the miR-205/PTEN/Akt pathway.

BACKGROUND: Acute kidney injury (AKI) is a major kidney disease with poor clinical outcome. SP1, a well-known transcription factor, plays a critical role in AKI and subsequent kidney repair through the regulation of various cell biologic processes. However, the underlying mechanism of SP1 in these pathological processes remain largely unknown. METHODS: An in vitro HK-2 cells with anoxia-reoxygenation injury model (In vitro simulated ischemic injury disease) and an in vivo rat renal ischemia-reperfusion injury model were used in this study. The expression levels of SP1, miR-205 and PTEN were detected by RT-qPCR, and the protein expression levels of SP1, p62, PTEN, AKT, p-AKT, LC3II, LC3I and Beclin-1 were assayed by western blot. Cell proliferation was assessed by MTT assay, and the cell apoptosis was detected by flow cytometry. The secretions of IL-6 and TNF-α were detected by ELISA. The targeted relationship between miR-205 and PTEN was confirmed by dual luciferase report assay. The expression and positioning of LC-3 were observed by immunofluorescence staining. TUNEL staining was used to detect cell apoptosis and immunohistochemical analysis was used to evaluate the expression of SP1 in renal tissue after ischemia-reperfusion injury in rats. RESULTS: The expression of PTEN was upregulated while SP1 and miR-205 were downregulated in renal ischemia-reperfusion injury. Overexpression of SP1 protected renal tubule cell against injury induced by ischemia-reperfusion via miR-205/PTEN/Akt pathway mediated autophagy. Overexpression of SP1 attenuated renal ischemia-reperfusion injury in rats. CONCLUSIONS: SP1 overexpression restored autophagy to alleviate acute renal injury induced by ischemia-reperfusion through the miR-205/PTEN/Akt pathway.

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.

[Effects of recruitment maneuver in prone position on hemodynamics in patients with severe pulmonary infection].

OBJECTIVE: To evaluate effects of recruitment maneuver in prone position on hemodynamics in patients with severe pulmonary infection, based on the protective pulmonary ventilation strategy. METHODS: Ninety-seven cases with severe pulmonary infection admitted to intensive care unit (ICU) of Ganzhou City People's Hospital undergoing mechanical ventilation were involved. Volume controlled ventilation mode with small tidal volume (8 ml/kg) and positive end-expiratory pressure (PEEP) of 6 cm H(2)O [1 cm H(2)O = 0.098 kPa] was conducted. Each patient underwent recruitment maneuver in supine position and then in prone position [PEEP 20 cm H(2)O+pressure control (PC) 20 cm H(2)O]. Heart rate (HR), mean arterial pressure (MAP), pulse oxygen saturation [SpO(2)] and blood gas analysis data were recorded before and after recruitment maneuver in either position. A double-lumen venous catheter was inserted into internal jugular vein or subclavian vein, and a pulse index contour cardiac output (PiCCO) catheter was introduced into femoral artery. Cardiac index (CI), stroke volume index (SVI), systemic vascular resistance index (SVRI), intra-thoracic blood volume index (ITBVI), extra vascular lung water index (EVLWI), global end-diastolic volume index (GEDVI), global ejection fraction (GEF), stroke volume variation (SVV) and central vein pressure (CVP) were monitored. RESULTS: (1) Compared with data before recruitment maneuver, there were no significant differences in HR and MAP after supine position and prone position recruitment maneuver, but significant differences in SpO(2) were found between before and after recruitment maneuver when patients' position was changed (supine position: 0.954 ± 0.032 vs. 0.917 ± 0.025, P < 0.05; prone position: 0.982 ± 0.028 vs. 0.936 ± 0.039, P < 0.05). SpO(2) was higher in prone position recruitment maneuver (P < 0.05). (2) Compared with data before recruitment maneuver, CI [L×min(-1)×m(-2)], SVI (ml/m(2)), GEDVI (ml/m(2)) and GEF were decreased significantly during recruitment maneuver (supine position: CI 3.2 ± 0.4 vs. 3.8 ± 0.6, SVI 32.4 ± 5.6 vs. 38.8 ± 6.5, GEDVI 689 ± 44 vs. 766 ± 32, GEF 0.267 ± 0.039 vs. 0.305 ± 0.056; prone position: CI 3.1 ± 0.5 vs. 3.6 ± 0.4, SVI 31.2 ± 5.8 vs. 37.3 ± 5.0, GEDVI 678 ± 41 vs. 758 ± 36, GEF 0.268 ± 0.040 vs. 0.288 ± 0.053, all P < 0.05), and CVP [cm H(2)O] and SVV were significantly increased [supine position: CVP 10.7 ± 1.5 vs. 8.2 ± 2.5, SVV (11.2 ± 3.3)% vs. (8.3 ± 4.7)%; prone position: CVP 10.3 ± 1.8 vs. 8.1 ± 2.5, SVV (12.7 ± 3.4)% vs. (9.1 ± 3.6)%, all P < 0.05], but they returned to the level of that before recruitment maneuver soon after termination of recruitment maneuver. There were no significant differences in SVRI, ITBVI and EVLWI between before and after recruitment maneuver in both positions. There were also no significant differences in above parameters between two positions. CONCLUSIONS: Based on the lung protective ventilation strategy of small tidal volume with PEEP, oxygenation was improved and SpO(2) was increased significantly when prone position ventilation combined with lung recruitment method was used in severe pulmonary infection patients. The effect of recruitment maneuver during prone position on hemodynamics was slight, except a temporary decrease of SVI and GEF just during recruitment maneuver.

Saturated hydrogen saline protects rats from acute lung injury induced by paraquat.

BACKGROUND: Paraquat (PQ) intoxication causes lung oxidative stress damage. Saturated hydrogen saline, a newly explored antioxidant, has been documented to play a powerful antioxidant role in preventing oxidative stress damage. This study aimed to investigate the protective effects and the possible mechanisms of intoxication on rats with acute lung injury (ALI) caused by paraquat poisoning. METHODS: Thirty PQ poisoned rats were randomly divided into a PQ intoxication group (intoxication group), a saturated hydrogen saline intervention group (intervention group), and a control group, with 10 rats in each group. The first two groups accepted an intragastric administration of PQ at a dose of 50 mg/kg for every single rat, and the control group was fed with a same volume of normal saline. Five mL/kg of saturated hydrogen saline was given to the intervention group three times a day by peritoneal injection for three days after intoxication. Arterial blood gas was detected on the third day. The rats were executed and their lungs were taken for measurement of wet dry weight ratio, homogenate malondialdehyde (MDA), and 8-hydroxy-2'-deoxyguanosine (8-OhdG). Histological changes of the lungs were also observed. RESULTS: Compared with the control group, the intoxication group had more serious hypoxemia, greater wet/dry weight ratio, higher MDA level, higher expression of 8-OhdG and more severe lung damage (P<0.01 or P<0.05). However, after intervention with saturated hydrogen saline, poisoned animals turned to have lighter hypoxemia, smaller wet/dry weight ratio, lower MDA level, lower expression of 8-OhdG, and milder lung damage (P<0.01 or P<0.05). CONCLUSIONS: Saturated hydrogen saline is effective in preventing acute lung injury caused by PQ. Possibly, it can neutralize toxic oxygen radicals selectively and alleviate the oxidative stress injury induced by PQ.