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.

Cerebral Protection of Intraoperative Infusion of Dexmedetomidine in Patients with Chronic Cerebrovascular Stenosis Undergoing Endovascular Interventional Therapies: A Prospective Randomized Controlled Trial.

BACKGROUND: To investigate the cerebral protective effect of intraoperative dexmedetomidine infusion on patients with chronic cerebral vascular stenosis receiving endovascular interventional therapy. METHODS: Sixty patients with carotid artery or cerebral artery stenosis or occlusion stenting under elective general anesthesia were divided into dexmedetomidine group (group D) and normal saline group (group N). Group D was given dexmedetomidine loading dose 1.0 µg/kg after peripheral vein opening for 10 min, and then adjusted infusion rate to 0.5 µg/kg/h until stopped 30 min before end. RESULTS: At 7 days after operation, the contents of S100ß, neuron-specific enolase (NSE) and interleukin-6 (IL-6) in group D were apparently lower than those in group N (P < 0.05), while the contents of IL-1ß and tumor necrosis factor-α in 2 groups showed no statistical significance (P > 0.05). Additionally, at 4 days and 7 days after operation, the scores of Mini-Mental State Scale (MMSE) and Wechsler Memory Scale (WMS) in group D were significantly higher than those in group N (P < 0.05). Thirty days after surgery, the cerebral hemodynamic indexes (relative mean transit time, relative time to peak) in group D were significantly improved, and obviously better than those in group N (P < 0.05). CONCLUSIONS: The S-100ß, NSE, and inflammatory mediator IL-6 in group D were significantly decreased compared with group N, the MMSE and WMS cognitive function scores, and the cerebral blood perfusion were apparently improved in group D, clarifying dexmedetomidine has protective effect on nerve tissue injury by inhibiting inflammation.

[Current Status and New Drugs Progress in the Treatment of Relapsed and Refractory Acute Myeloid Leukemia--Review].

The overall therapeutic outcome of acute myeloid leukemia (AML) is poor, and relapse and refractory are the main reasons for treatment failure. Leukemia cells of relapsed and refractory AML (R/R-AML) patients are usually resistant to conventional chemotherapy, and new treatment regimens are urgently needed to further improve the survival rate and prolong the survival time of these patients.There are no recommended unified treatment regimens other than entering clinical trials.At present,the main options are salvage chemotherapy and hematopoietic stem cell transplantation (HSCT), and HSCT is the only possible cure for R/R-AML, but the prognosis of most of these patients is still poor.In recent years,the treatment status of AML has progressed rapidly, and the new therapies are emerging, many new drugs have become the research focus. Some progress has been made in improving chemosensitivity and overcoming chemoresistance by combining the new drugs with the original chemotherapeutic drugs, which provide a new treatment option and improve the overall prognosis for R/R-AML patients. This article will review the current treatment status and the latest progress in new drug research of R/R-AML.

Time-series analysis in imatinib-resistant chronic myeloid leukemia K562-cells under different drug treatments.

Chronic myeloid leukemia (CML) is characterized by the accumulation of active BCR-ABL protein. Imatinib is the first-line treatment of CML; however, many patients are resistant to this drug. In this study, we aimed to compare the differences in expression patterns and functions of time-series genes in imatinib-resistant CML cells under different drug treatments. GSE24946 was downloaded from the GEO database, which included 17 samples of K562-r cells with (n=12) or without drug administration (n=5). Three drug treatment groups were considered for this study: arsenic trioxide (ATO), AMN107, and ATO+AMN107. Each group had one sample at each time point (3, 12, 24, and 48 h). Time-series genes with a ratio of standard deviation/average (coefficient of variation) >0.15 were screened, and their expression patterns were revealed based on Short Time-series Expression Miner (STEM). Then, the functional enrichment analysis of time-series genes in each group was performed using DAVID, and the genes enriched in the top ten functional categories were extracted to detect their expression patterns. Different time-series genes were identified in the three groups, and most of them were enriched in the ribosome and oxidative phosphorylation pathways. Time-series genes in the three treatment groups had different expression patterns and functions. Time-series genes in the ATO group (e.g. CCNA2 and DAB2) were significantly associated with cell adhesion, those in the AMN107 group were related to cellular carbohydrate metabolic process, while those in the ATO+AMN107 group (e.g. AP2M1) were significantly related to cell proliferation and antigen processing. In imatinib-resistant CML cells, ATO could influence genes related to cell adhesion, AMN107 might affect genes involved in cellular carbohydrate metabolism, and the combination therapy might regulate genes involved in cell proliferation.

Maternal circulating concentrations of tumor necrosis factor-alpha, leptin, and adiponectin in gestational diabetes mellitus: a systematic review and meta-analysis.

Gestational diabetes mellitus (GDM) is one of the most common pregnancy complications. Inflammation may play a role in the pathogenesis of GDM. We performed a systematic review and meta-analysis to determine whether maternal serum concentration of tumor necrosis factor-alpha (TNF-α), leptin, and adiponectin were associated with GDM. A systematic search of PubMed and Medline was undertaken. In total, 27 trials were evaluated by meta-analyses using the software Review Manager 5.0. The results showed that maternal TNF-α (P = 0.0003) and leptin (P < 0.00001) concentrations were significantly higher in GDM patients versus controls. However, maternal adiponectin (P < 0.00001) concentration was significantly lower in GDM patients compared with controls. Subgroup analysis taking in consideration the effect of obesity on maternal adipokine levels showed that circulating levels of TNF-α and leptin remained elevated in GDM patients compared to their body mass index (BMI) matched controls, and adiponectin level remained depressed in GDM individuals. Our findings strengthen the clinical evidence that GDM is accompanied by exaggerated inflammatory responses.

Increase of beta-amyloid and C-reactive protein in liver transplant recipients with postoperative cognitive dysfunction.

BACKGROUND: Postoperative cognitive dysfunction (POCD) is an adverse condition characterized by declined cognitive functions following surgeries and anesthesia. POCD has been associated with increased hospital stay and mortality. There are histological similarities to Alzheimer's disease. Most early studies were conducted in patients receiving cardiac surgery. Since there is no information about POCD in liver transplant recipients, we measured the incidence of POCD in patients after liver transplantation and examined the correlation between neurological dysfunction and biological markers of dementia-based diseases. METHODS: We studied 25 patients who had a liver transplan-tation between July 2008 and February 2009. Patients with prior encephalopathy or risk factors associated with the development of POCD were excluded from the study. Five validated neuropsychiatric tests were used for diagnosis. The diagnosis was based on one standard deviation decline in two of the five neuropsychiatric tests. The correlation between patient variables and the development of POCD was examined. Serum levels of beta-amyloid and C-reactive protein were measured by standard ELISA and compared between patients with and without POCD. RESULTS: POCD was present in 11 (44%) of the 25 patients. Patients with POCD had significantly higher MELD scores, were more often Child-Pugh class C and received more blood transfusion during surgery. The serum beta-amyloid protein and C-reactive protein concentrations were significantly increased at 24 hours after surgery in the POCD group. CONCLUSIONS: The incidence of POCD in our group of liver transplant patients was greater than that reported in other surgical patients. The increase in the serum biomarkers of dementia in the POCD patients supports the hypothesis that chronic cognitive defects are due to a process similar to that seen in Alzheimer's disease.

In vitro cartilage production using an extracellular matrix-derived scaffold and bone marrow-derived mesenchymal stem cells.

BACKGROUND: Cartilage repair is a challenging research area because of the limited healing capacity of adult articular cartilage. We had previously developed a natural, human cartilage extracellular matrix (ECM)-derived scaffold for in vivo cartilage tissue engineering in nude mice. However, before these scaffolds can be used in clinical applications in vivo, the in vitro effects should be further explored. METHODS: We produced cartilage in vitro using a natural cartilage ECM-derived scaffold. The scaffolds were fabricated by combining a decellularization procedure with a freeze-drying technique and were characterized by scanning electron microscopy (SEM), micro-computed tomography (micro-CT), histological staining, cytotoxicity assay, biochemical and biomechanical analysis. After being chondrogenically induced, the induction results of BMSCs were analyzed by histology and Immunohisto-chemistry. The attachment and viability assessment of the cells on scaffolds were analyzed using SEM and LIVE/DEAD staining. Cell-scaffold constructs cultured in vitro for 1 week and 3 weeks were analyzed using histological and immunohistochemical methods. RESULTS: SEM and micro-CT revealed a 3-D interconnected porous structure. The majority of the cartilage ECM was found in the scaffold following the removal of cellular debris, and stained positive for safranin O and collagen II. Viability staining indicated no cytotoxic effects of the scaffold. Biochemical analysis showed that collagen content was (708.2-44.7) µg/mg, with GAG (254.7 ± 25.9) µg/mg. Mechanical testing showed the compression moduli (E) were (1.226 ± 0.288) and (0.052 ± 0.007) MPa in dry and wet conditions, respectively. Isolated canine bone marrow-derived stem cells (BMSCs) were induced down a chondrogenic pathway, labeled with PKH26, and seeded onto the scaffold. Immunofluorescent staining of the cell-scaffold constructs indicated that chondrocyte-like cells were derived from seeded BMSCs and excreted ECM. The cell-scaffold constructs contained pink, smooth and translucent cartilage-like tissue after 3 weeks of culture. We observed evenly distributed cartilage ECM proteoglycans and collagen type II around seeded BMSCs on the surface and inside the pores throughout the scaffold. CONCLUSION: This study suggests that a cartilage ECM scaffold holds much promise for in vitro cartilage tissue engineering.

Novel cartilage-derived biomimetic scaffold for human nucleus pulposus regeneration: a promising therapeutic strategy for symptomatic degenerative disc diseases.

Because current therapies have not always been successful and effective, the possibility of regenerating the nucleus pulposus (NP) through a tissue-engineered construct offers a novel therapeutic possibility for symptomatic degenerative disc diseases (DDDs). However, more research is necessary to identify the optimal scaffold, cell type and mixture of signal factors needed for NP regeneration. Numerous possible scaffolds for NP regeneration have been investigated; they have many shortcomings in common. Various biological scaffolds derived from decellularized tissue and organs have been successfully used in tissue engineering and received approval for use in humans. Regretfully, harvesting of human NP is difficult and only small amounts can be obtained. The macromolecules of cartilage, which include collagen and proteoglycan aggrecan, are similar to those of the extracellular matrix of immature NP. Recent studies have shown that adipose-derived stem cells (ADSC) can be induced to develop NP-like phenotypes when stimulated by appropriate signals. We thus reasonably postulated that an ideal NP scaffold for tissue engineering could be fabricated from decellularized cartilage matrix (DCM). Furthermore, a combination of ADSCs and DCM-derived biomimetic scaffolds would be advantageous in NP tissue engineering and, in the long run, could become an effective treatment option for symptomatic DDD.

Intestinal absorption mechanisms of prenylated flavonoids present in the heat-processed Epimedium koreanum Nakai (Yin Yanghuo).

PURPOSE: The purpose is to determine absorption mechanism of five bioactive prenylated flavonoids (baohuoside I, icariin, epimedine A, B, and C) present in heat-processed Epimedium koreanum Nakai (Yin Yanghuo). METHODS: Transport of five prenylated flavonoids present in heat-processed herbs were studied in the human intestinal Caco-2 model and the perfused rat intestinal model. RESULTS: In the perfused rat intestinal model, prenylated flavonoids with a monoglucosidic bond (e.g., icariin) was rapidly hydrolyzed into corresponding metabolites (e.g., baohuoside I). In the Caco-2 model, apical to basolateral permeability of a monoglycoside baohuoside I (1.46 x 10(-6) cm/sec) was more than 2 folds greater than four prenylated flavonoids with 2 or more sugar moieties (<0.6 x 10(-6) cm/sec). The slow apical to basolateral transport of baohuoside I was the result of efflux. This efflux was carrier-mediated and active since its transport was vectorial, concentration- and temperature-dependent with activation energies greater than 15 kcal/mol. Efflux of baohuoside I was significantly suppressed by inhibitors of BCRP and MRP2, whereas efflux of icariin was significantly inhibited only by p-glycoprotein inhibitor verapamil. Because YHH is often heat-processed for better efficacy, we determined and found the optimal condition for increasing contents of more bioavailable flavonoids (i.e., baohuoside I) to be 160-170 degrees C for 5-7 min. CONCLUSIONS: Poor bioavailability of prenylated flavonoids results from their poor intrinsic permeation and transporter-mediated efflux. Heat processing parameters may be optimized to preserve the herb's bioavailable flavonoids, which help retain and improve its efficacy during processing.

[In vitro stimulation of retinoic acid syndrome by rotary cell culture system and its relationship with expression of CXCR4 and SDF-1 alpha].

OBJECTIVE: To explore the molecular mechanism and prevention of retinoic acid syndrome (RAS). METHODS: SDF-1 alpha mRNA from healthy adult lung tissue was measured by RT-PCR, CXCR4 protein expression on the cell membrane of APL cells induced by ATRA (APL-ATRA) was tested by FCM, and the rotary cell culture system (RCCS) was used to build a modal for in vitro stimulation of APL-ATRA infiltrating human lung tissue. The ability of APL-ATRA in adhesion, migration and infiltration was observed by interference from DEX, Ara-C and DNR. RESULTS: The APL-ATRA cells could evidently infiltrate into normal lung tissue. Mean fluorescence intensity (MFI) of CXCR4 on the cell membrane of APL-ATRA cells was 30.6 +/- 1.8, which was much higher than that on unspecialized APL cells (9.8 +/- 4.2). SDF-1 alpha mRNA expression was detected positive in all 6 lung tissue. Contrary to the control groups, DEX could dramatically restrain the ability of APL-ATRA cells in adhesion and migration [(27.2 +/- 2.6)% vs. (46.0 +/- 3.0)%, (28.1 +/- 4.0)% vs. (48.2 +/- 3.0)%], while Ara-C and DNR could distinctly depress the ability in adhesion, migration and infiltration [(28.1 +/- 3.0)%, (30.2 +/- 3.2)% vs. (46.0 +/- 3.0)%; (29.0 +/- 4.0)%, (23.0 +/- 5.2)% vs. (48.2 +/- 3.0)%; (16.8 +/- 7.6)%, (17.1 +/- 6.0)% vs. (43.6 +/- 5.0)%]. CONCLUSION: In vitro APL-ATRA cells can infiltrate into the human lung tissue. High expression of CXCR4 on APL-ATRA and SDF-1 alpha in the lung tissue may be one of the molecular mechanisms of the lung infiltration and RAS. DEX, Ara-C and DNR can dramatically restrain the ability of APL-ATRA cells in adhesion, migration and infiltration.

[Expression of Runx2/Cbfa1 in the developing pulpo-dentinal complex of postnatal mice].

OBJECTIVE: To study the expression of Runx2/Cbfa1 in the developing dentin and differentiating odontoblasts. METHODS: A postnatal mice teeth developing model was built histologically. Immunohistochemical technique was adopted to determine the expression of Runx2/Cbfa1 in the developing pulpo-dentinal complex in mice. RESULTS: Runx2/Cbfa1 was merely present in predentin in the exact and before the 11th day's postnatal stages. Meanwhile, it was positively located in odontoblasts and dental pulp cells in root region, but negatively in coral part after the 11th day's stages. CONCLUSION: Runx2/Cbfa1 may play an important role in the deposing of tooth dentin and in the differentiating of odontoblasts and pulp cells.

[Effect of mitochondrial membrane potential in the neurotoxicity of artemether].

OBJECTIVE: To study the effect of mitochondrial membrane potential and cellular membrane permeability in the neurotoxicity of artemether. METHODS: Mitochondrial membrane potential and cellular membrane permeability in pheochromocytoma cell and primary cultured rat neuronal cell were measured by flow cytometry, using rhodamine 123(Rh123) and PI as fluorescent dye, respectively. Mitochondrial swelling was measured by spectrometer. RESULTS: Artemether could decrease the mitochondrial membrane potential and increase the cellular membrane permeability in both cell types in a dose-dependent manner. In addition, artemether led to mitochondrial swelling with dose-effect and time-effect relationships. CONCLUSION: The decrease of mitochondrial membrane potential plays an important role in the neurotoxicity of artemether. The drug can change the mitochondrial membrane potential and mitochondrial swelling by affecting the permeability transition pore complex located in the mitochondrial membrane, increasing cellular membrane permeability, causing an obstruction and finally leading to neurotoxicity.