Development of a blended teaching quality evaluation scale (BTQES) for undergraduate nursing based on the Context, Input, Process and Product (CIPP) evaluation model: A cross-sectional survey.

OBJECTIVE: Developing a nursing undergraduate blended teaching quality evaluation tool based on the Context, Input, Process and Product model and evaluating its reliability and validity. BACKGROUND: Blended teaching is a commonly used teaching method in medical education, but there are limited tools available to effectively measure the quality of blended teaching. DESIGN: A Delphi study and cross-sectional study. METHODS: Using the Context, Input, Process and Product model as the theoretical framework, a questionnaire was developed through literature review, expert consultation and pre-survey. From April to July 2023, 448 students from a certain university were selected as the research subjects and the questionnaire was examined for reliability and validity through a survey method. RESULTS: The blended teaching quality evaluation scale with 35 items includes four dimensions Context, Input, Process and Product. The content validity and reliability of the blended teaching quality evaluation scale are both good, with a content validity index of 0.934 for the total scale and a content validity index of 0.750-1.00 for each item. The SEM shows that χ2/df = 6.89, RMSEA = 0.115, CFI = 0.882, NFI=0.865, RFI= 0.855, IFI = 0.882, TLI = 0.873. The Cronbach's α coefficient of the total scale is 0.991 and the Cronbach's α coefficient for each dimension is 0.944-0.984. CONCLUSION: The scale is based on the characteristics of blended learning and quality evaluation covers all aspects of teaching. It can accurately evaluate the quality of teaching, evaluate the problems in the teaching process based on the teaching quality score and propose reasonable teaching improvement suggestions based on the weak links in the teaching process.

[Retracted] Tunicamycin inhibits colon carcinoma growth and aggressiveness via modulation of the ERK­JNK­mediated AKT/mTOR signaling pathway.

Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that certain of the Transwell invasion and migration assay data shown in Fig. 1B and C were strikingly similar to data appearing in different form in other articles written by different authors at different research institutes, which had either already been published or were under consideration for publication at around the same time. Owing to the fact that the contentious data in the above article had already been published prior to its submission to Molecular Medicine Reports, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 17: 4203­4212, 2018; DOI: 10.3892/mmr.2018.8444].

Survival benefit of primary and metastatic tumor resection for colon cancer with liver metastases: A population based, propensity score-matched study.

Background: Colon cancer remains one of the most common malignancies and we aimed to evaluate whether surgery has an effect on the survival of metastatic colon patients. Methods: We analyzed 7,583 metastatic colon patients from the Surveillance, Epidemiology, between January 2010 and December 2015. Using Cox proportional hazards models and Kaplan-Meier curves, the overall survival rate (OS) and cancer-specific survival rate and End Results (SEER) registry (CSS) months (m) were evaluated with corresponding 95% confidence intervals (95% CIs). Propensity score matching (PSM) was performed to adjust for potential baseline confounding of all comparison groups. Results: In general, receiving both primary and metastatic tumor resection (PMTR) remarkably improved OS and CSS compared with only primary tumor resection (PTR) after PS matching (PSM) (P < 0.05), with a significantly improved OS (HR = 0.74, 95%CI = 0.69-0.80) and CSS (HR = 0.71, 95%CI = 0.66-0.76) in all stage M1 colon patients. The stratification analysis indicated a significant difference between OS and CSS in M1a and M1b stages. After PSM, PMTR was found to be associated with remarkably improved OS and CSS for patients with liver metastases but not associated with OS and CSS of patients with lung metastases in both M1a and M1b stage. Conclusions: The results from this large SEER cohort supported PMTR might improve the survival of colon patients with liver metastases on the basis of chemotherapy.

Establishment and verification of a nomogram prediction model of hypertension risk in Xinjiang Kazakhs.

ABSTRACT: Hypertension is the main risk factor for cardiovascular and renal diseases. It is of great importance to develop effective risk prediction models to identify high-risk groups of hypertension. This study is to establish and verify a nomogram model for predicting the risk of hypertension among Kazakh herders in Xinjiang, China.This is a prospective cohort study. Totally, 5327 Kazakh herders from the Nanshan pastoral area of Xinjiang were enrolled. They were randomly divided into the modeling set of 3729 cases (70%) and the validation set of 1598 cases (30%). In the modeling set, univariate analysis, least absolute shrinkage and selection operator regression and multivariate Logistic regression were used to analyze the influencing factors of hypertension, and a nomogram prediction model was constructed. We then validated the model in the validation set, and evaluated the accuracy of the model using receiver operating characteristic and calibration curve.Based on univariate analysis, least absolute shrinkage and selection operator regression and multivariate logistic regression analysis, we identified 14 independent predictors of hypertension in the modeling set, including age, smoking, alcohol consumption, baseline body mass index, baseline diastolic blood pressure, baseline systolic blood pressure, daily salt intake, yak-butter intake, daily oil intake, fruit and vegetable intake, low-density lipoprotein, cholesterol, abdominal circumference, and family history. The area under the receiver operating characteristic curve of the modeling set and the verification set was 0.803 and 0.809, respectively. Moreover, the calibration curve showed a higher agreement between the nomogram prediction and the actual observation of hypertension.The risk prediction nomogram model has good predictive ability and could be used as an effective tool for the risk prediction of hypertension among Kazakh herders in Xinjiang.

The pregnancy-related anxiety characteristics in women with gestational diabetes mellitus: why should we care?

BACKGROUND: Gestational diabetes mellitus (GDM) is very commonly-seen in clinical settings, and GDM patients may have higher levels of anxiety. It's necessary to evaluate the anxiety level and potentially influencing factors in patients with GDM, to provide insights for the management of anxiety of GDM patients. METHODS: Patients with GDM treated in our hospital from May, 2018 to May, 2020 were included. We evaluated the characteristics of patients and the scores of pregnancy-related anxiety scale for anxiety level, vulnerable personality style questionnaire (VPSQ) for personality, general self-efficacy scale (GSES) for self-efficacy, social support rating scale (SSRS) for social support level. Logistic regression analyses were conducted to identify the potential influencing factors of anxiety in GDM patients. RESULTS: A total of 386 GDM patients were included, the incidence of anxiety in patients with GDM was 59.07%. Anxiety was positively correlated with the susceptible personality (r = 0.604, p = 0.023), and it was negatively correlated with self-efficacy and social support (r = -0.586 and -0.598 respectively, all p < 0.05). The education level, monthly income, abnormal pregnancy (miscarriage, premature rupture of membranes) and cesarean section history and first pregnancy were the independent influencing factors for the anxiety in the patients with GDM (all p < 0.05). CONCLUSIONS: The anxiety of GDM patients is very common, early care and interventions are warranted for those patients with abnormal pregnancy and cesarean section history, first pregnancy, lower education level, and less monthly income.

miRNA-138-5p suppresses cigarette smoke-induced apoptosis in testicular cells by targeting Caspase-3 through the Bcl-2 signaling pathway.

Long-term cigarette smoking (CS) can cause testicular toxicity, which interferes with normal spermatogenesis and leads to male infertility. One possible mechanism for this is the activation of the apoptosis signaling pathway, which leads to the irreversible apoptosis of testicular cells. However, the exact mechanism for this is not completely understood. Cell viability, cell apoptosis, and lactate dehydrogenase release assays were performed to elucidate the function of micro RNA (miRNA) in the pathogenesis of male testicular cell injury induced by CS. The results suggested that testicular cell injury was associated with CS both in vitro and in vivo. CS extract (CSE)-treated Leydig and Sertoli cells showed noticeable apoptosis. Based on the results of Agilent miRNA microarray and bioinformatics analyses, miRNA-138-5p was used in subsequent experiments. Quantitative polymerase chain reaction and Western blot assays showed a negative correlation between miR-138-5p and Caspase-3 expression. Transfection of miR-138-5p mimic significantly inhibited apoptosis and downregulated the expression of Caspase-3 in TM3 and TM4 cells. Furthermore, a dual-luciferase reporter assay demonstrated that miR-138-5p directly targeted Caspase-3 to regulate the apoptosis of testicular cells mediated by CSE. In addition, overexpression of miR-138-5p markedly downregulated the expression of p53 and Bak, which played critical roles in the Bcl-2 pathway. These results demonstrate that miRNA-138-5p inhibits CS-induced apoptosis in testicular cells by targeting Caspase-3 through the Bcl-2 signaling pathway.

Phenylethanol Glycosides Protect Myocardial Hypertrophy Induced by Abdominal Aortic Constriction via ECE-1 Demethylation Inhibition and PI3K/PKB/eNOS Pathway Enhancement.

Phenylethanol glycosides (CPhGs) are the core material basis of pharmacological activity in Cistanche tubulosa and have a variety of pharmacological effects. However, it is unclear whether CPhGs have an ameliorative effect on pressure overload-induced myocardial hypertrophy. In this study, male SD rats weighing (200 ± 20) g were established cardiac hypertrophy models by abdominal aortic coarctation (AAC). After operation, the rats were gavaged with corresponding medicine for 6 weeks (CPhGs 125, 250, and 500 mg/kg/d and valsartan 8.3 mg/kg/d). Echocardiography, heart weight index (HWI), cross-sectional area of cardiomyocytes (CSCA), fibrosis area, plasma endothelin 1(ET-1), and proinflammatory factors levels were detected. Our results showed that different CPhGs dosage decreased left ventricular posterior wall thickness (LVPWT), left ventricular end-diastolic diameter (LVED), HWI, CSCA, fibrosis area, ET-1, proinflammatory factors, arterial natriuretic peptide (ANP), brain natriuretic peptide (BNP), endothelin converting enzyme 1(ECE-1) mRNA levels, cyclooxygenase 2 (COX-2), high mobility group box 1 (HMGB-1) protein levels, and ECE-1 demethylation level while increasing left ventricular ejection fractions (LVEF), left ventricular fractional shortening (LVFS), phosphorylated phosphatidylinositol 3-kinase (p-PI3K), phosphorylated protein kinase B (p-PKB), and phosphorylated endothelial nitric oxide synthetase (p-eNOS). The indexes of CPhGs 250 and 500 mg/kg group were significantly different from AAC group; compared with valsartan group (AV), the indexes of CPhGs 500 mg/kg group were not significantly different. In conclusion, CPhGs ameliorated myocardial hypertrophy rats by AAC, which may be related to ECE-1 demethylation inhibition and PI3K/PKB/eNOS enhancement.

The Phenylethanol Glycoside Liposome Inhibits PDGF-Induced HSC Activation via Regulation of the FAK/PI3K/Akt Signaling Pathway.

Cistanche tubulosa is a traditional Chinese herbal medicine that is widely used to regulate immunity, and phenylethanol glycosides (CPhGs) are among the primary components responsible for this activity. However, the application of CPhGs is negatively affected by their poor absorption and low oral utilization. Targeted drug delivery is an important development direction for pharmaceutics. Previous studies have indicated that CPhGs could block the conduction of the signaling pathways in TGF-ß1/smad and inhibit the activation of hepatic stellate cells (HSCs). The aim of this study was to evaluate the anti-hepatic fibrosis effect of CPhG liposomes by inhibiting HSC activation, promoting apoptosis, blocking the cell cycle, suppressing the conduction of signaling pathways in focal adhesion kinase(FAK)/phosphatidylinositol-3-kinase(PI3K)/protein kinase B(Akt), and determining their in vitro hepatoprotective activity. In vitro release studies demonstrated that CPhG liposomes have a sustained release effect compared to drug CPhGs. HSC proliferation was inhibited after treatment with the CPhG liposomes (29.45, 14.72, 7.36 µg/mL), with IC50 values of 42.54 µg/mL in the MTT assay. Different concentrations of the CPhG liposomes could inhibit HSC proliferation, promote apoptosis, and block the cell cycle. The MTT method showed an obvious inhibition of HSC proliferation after CPhG liposome and Recombinant Rat Platelet-derived growth factor-BB(rrPDGF-BB) treatment. The levels of collagen-1, metallopeptidase inhibitor 1 (TIMP-1), α smooth muscle actin (α-SMA), and phosphorylated PI3K/Akt were downregulated, and matrix metalloproteinase-1 (MMP-1) was upregulated, by pretreatment with different concentrations of CPhG liposomes. Moreover, 29.45 µg/mL of CPhG liposomes could decrease the expression of the FAK protein and the phosphorylated PI3K and Akt protein downstream of FAK by overexpression of the FAK gene. This experiment suggests that CPhG liposomes may inhibit the activation of HSCs by inhibiting FAK and then reducing the expression of phosphorylated Akt/PI3K, thereby providing new insights into the application of CPhGs for liver fibrosis.

Tunicamycin inhibits colon carcinoma growth and aggressiveness via modulation of the ERK-JNK-mediated AKT/mTOR signaling pathway.

Epidemiology and evidence have demonstrated that colon carcinoma is one of the most common gastrointestinal tumors in the clinic. Reports have suggested that Tunicamycin significantly inhibits aggressiveness of colon carcinoma cells by promotion of apoptosis. In the present study, the inhibitory effect of tunicamycin on colon cancer cells and the potential underlying molecular mechanism was investigated. Western blotting, immunohistochemistry, apoptotic assays and immunofluorescence were used to analyze the therapeutic effects of tunicamycin on apoptosis, growth, aggressiveness and cell cycle of colon tumor cells, by downregulation of fibronectin, vimentin and E­cadherin expression levels. In vitro experiments demonstrated that tunicamycin significantly inhibited growth, migration and invasion of colon carcinoma cells. In addition, tunicamycin administration promoted apoptosis of colon carcinoma cells via upregulation of apoptotic protease activating factor 1 and cytochrome c expression levels, which are proteins that have a role in mitochondrial apoptosis signaling. Cell cycle assays revealed that tunicamycin suppressed proliferation and arrested S phase entry of colon carcinoma cells. Mechanistic analysis demonstrated that tunicamycin reduced expression and phosphorylation levels of extracellular signal­regulated kinase (ERK), c­JUN N­terminal kinase (JNK) and protein kinase B (AKT), and inhibited mammalian target of rapamycin (mTOR) expression levels in colon carcinoma cells. Endogenous overexpression of ERK inhibited tunicamycin­mediated downregulation of JNK, AKT and mTOR expression, which further blocked tunicamycin­mediated inhibition of growth and aggressiveness of colon carcinoma. In vivo assays revealed that tunicamycin treatment significantly inhibited tumor growth and promoted apoptosis, which led to long­term survival of tumor­bearing mice compared with the control group. In conclusion, these results suggested that tunicamycin may inhibit growth and aggressiveness of colon cancer via the ERK­JNK­mediated AKT/mTOR signaling pathway, and suggested that tunicamycin may be a potential anti­cancer agent for colon carcinoma therapy.

Epithelial­mesenchymal transition in colorectal carcinoma cells is mediated by DEK/IMP3.

To investigate the inhibitory effects of DEK/insulin­like growth factor II mRNA binding protein 3 (IMP3) on epithelial­mesenchymal transition (EMT) in colorectal carcinoma cells. SW620 and SW480 cell lines were selected. DEK­interfering lentivirus was transfected to knockdown DEK expression. Subsequently, MTT assays and flow cytometry were utilized to measure cell viability, and apoptosis, respectively. Cell invasion was detected using a Transwell assay. Quantitative polymerase chain reaction and western blot analysis were used to detect the expression of E­cadherin, vimentin, and matrix metalloproteinase (MMP)­9. Compared with the blank control, cells transfected with DEK­interfering lentivirus demonstrated a remarkable reduction in cell viability (P<0.05). The apoptotic rate in the DEK­interfering lentivirus group was significantly enhanced compared with the blank control group (P<0.05). In the DEK­interfering lentivirus group, the expression of E­cadherin was significantly elevated (P<0.05), while the expression of vimentin and MMP­9 were significantly reduced in both cell lines (P<0.05). The results of the present study demonstrated that EMT of colorectal carcinoma cells was partially mediated by DEK, which likely affected the invasive ability of colorectal carcinoma cells. In addition, cell proliferation and apoptosis were susceptible to DEK silencing. The current study has provided experimental evidence for the treatment of colorectal carcinoma using DEK silencing.

Cigarette smoke induces rat testicular injury via mitochondrial apoptotic pathway.

An understanding of the causative mechanisms of the harmful effects of cigarette smoke on the male reproductive system remains incomplete. Here, we investigated three different inhaled cigarette smoke doses over five different exposure durations to identify how the testis is affected. The effects of cigarette smoke exposure on testicular germ cells were characterized by morphological changes and a significant elevation in the number of apoptotic cells. Caspase 3 activation increased dramatically after cigarette smoke exposure, accompanied by significant time-dependent expression of the pro-apoptotic proteins Bak (B cell lymphoma/leukemia 2 [Bcl-2] homologous antagonist killer), Bcl2l11 (a BH3 domain-only protein related to Bcl-2), Apaf1 (Apoptotic protease-activating factor-1), and Caspase 9. Conversely, the abundance of anti-apoptotic Bcl2l2 decreased. Taken together, our findings suggest that extensive inhalation of cigarette smoke damages testicular germ cells through the induction of the mitochondrial apoptotic pathway through the Bcl-2 protein family.

Hepatoprotective Effects of Nicotiflorin from Nymphaea candida against Concanavalin A-Induced and D-Galactosamine-Induced Liver Injury in Mice.

Nymphaea candida was used to treat hepatitis in Ugyhur medicine, and nicotiflorin (kaempferol 3-O-ß-rutinoside) is the main characteristic component in this plant [...].

Anti-arthritic Effects of Total Flavonoids from Juniperus sabina on Complete Freund's Adjuvant Induced Arthritis in Rats.

CONTEXT: Twigs and leaves of Juniperus sabina L. have been traditionally used as the medicinal herb in China for the treatment of many ailments including rheumatoid arthritis (RA). AIMS: To confirm the therapeutic effect of total flavonoids from J. sabina (JSTF) on RA-induced by Complete Freund's Adjuvant (CFA) in rats. SETTINGS AND DESIGN: Wistar rats (200 ± 20 g) were immunized by intradermal injection of 0.1 mL of CFA into the right hind metatarsal footpad. JSTF was administered orally at the dose of 125,250 and 500 mg/kg on 14 days after the induction of adjuvant arthritis. Tripterygium glycoside (20 mg/kg) was used as a positive control. Paw swelling, arthritic score, body weight loss, serum cytokines, inflammatory mediators, and histological change were measured. RESULTS: We found that JSTF could ameliorate paw swelling of CFA rats, and significantly inhibit arthritic score (P < 0.05). The overproduction of tumor necrosis factor alpha and interleukin 1beta were remarkably suppressed in the serum of JSTF (125,500 mg/kg) treated rats (P < 0.05). Histopathological studies also showed a marked decrease of synovial inflammatory infiltration and synovial lining hyperplasia in the joints of JSTF-treated animals. Six flavonoids were isolated and from JSTF by various chromatographic methods and identified as follows: Catechin, quercitrin, isoquercitrin, isoscutellarein 7-O-ß-D-xylopyranoside, isoscutellarein 7-O-ß-D-xylopyranose-(1 → 3)-α-L-rhamnoside, and rutin. CONCLUSIONS: These results suggest the potential therapeutically effect of JSTF as an anti-arthritis agent toward CFA-induced arthritis in rats, and verified therapeutic applications of J. sabina on RA in folk medicine. SUMMARY: Twigs and leaves of Juniperus sabina L. have been traditionally used as the medicinal herb in China for the treatment of rheumatoid arthritisJSTF could ameliorate paw swelling of CFA rats, and significantly inhibit arthritic scoreHistopathological studies showed a marked decrease of synovial inflammatory infiltration and synovial lining hyperplasia in the joints of JSTF-treated animalsSix flavonoids were isolated and from JSTF including: Catechin, quercitrin, isoquercitrin, isoscutellarein 7-O-ß-D-xylopyranoside, isoscutellarein 7-O-ß-D-xylopyranose-(1 → 3)-α-L- rhamnoside, and rutin. Abbreviations used: JSTF: Total flavonoids from Juniperus sabina; CFA: Complete Freund's Adjuvant; TG: Tripterygium glycoside; TNF-α: Tumor necrosis factor alpha; IL-1ß: Interleukin 1beta; IL-6: Interleukin 6; H and E: Hematoxylin and eosin.

Phenylethanol Glycosides from Cistanche tubulosa Suppress Hepatic Stellate Cell Activation and Block the Conduction of Signaling Pathways in TGF-ß1/smad as Potential Anti-Hepatic Fibrosis Agents.

Cistanche tubulosa is a traditional Chinese herbal medicine widely used for regulating immunity and phenylethanol glycosides (CPhGs) are among the primary components responsible for this activity. Previous studies have indicated the preventive and therapeutic effects of CPhGs on bovine serum albumin (BSA)-induced hepatic fibrosis in rats. The aim of the study was to evaluate the anti-hepatic fibrosis effect of CPhGs and the monomers echinacoside and acteoside by inhibiting hepatic stellate cell (HSC) activation, blocking the conduction of signaling pathways in transforming growth factor-ß1 (TGF-ß1)/smad, and determine their in vitro hepatoprotective activity. HSC proliferation was obviously inhibited after treatment with CPhGs (100, 50 µg/mL)/echinacoside (500, 250, 125 µg/mL)/acteoside (6, 3 µg/mL), with IC50 values of 119.125, 520.345 and 6.999 µg/mL, respectively, in the MTT assay. Different concentrations of CPhGs/echinacoside/acteoside did not affect the cellular toxicity on HSC according to lactate dehydrogenase (LDH) measurements. Different concentrations of CPhGs/echinacoside/acteoside increased the mRNA level and protein expression of smad7, and decreased the mRNA levels of smad2, smad3 and the protein expression of smad2, phospho-smad2 (p-smad2), smad3, phospho-smad3 (p-smad3) in HSC. In summary, these results demonstrate that CPhGs/echinacoside/acteoside can block the conduction of the signaling pathways in TGF-ß1/smad, and inhibit the activation of HSC, suggesting that C. tubulosa may thus be a potential herbal medicine for the treatment of liver fibrosis.

Preventive effects of phenylethanol glycosides from Cistanche tubulosa on bovine serum albumin-induced hepatic fibrosis in rats.

BACKGROUND: Cistanche tubulosa is a traditional Chinese herbal medicine that is widely used for regulating immunity. Phenyl ethanol glycosides (CPhGs) from this plant are the primarily efficacious materials. This aim of this study was to evaluate the preventive and therapeutic effects of CPhGs on BSA-induced hepatic fibrosis in rats and related molecular mechanisms involving hepatic stellate cells. Biejiarangan (BJRG), another traditional Chinese herbal medicine, was used as a positive control. METHODS: In in vivo experiments, 75 SD rats were randomly divided into 6 groups: normal (distilled water-treated), model (BSA-treated), positive drug (BSA-treated + BJRG 600 mg/kg/day), and BSA-treated + CPhGs (125, 250, and 500 mg/kg/day) groups. The liver and spleen indices, serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), hexadecenoic acid (HA), laminin (LN), type III procollagen (PCIII), type IV collagen (IV-C), hydroxyproline (Hyp), and transforming growth factor ß 1 (TGF-ß 1) were measured in rat livers. Histopathological grades for liver fibrosis were assessed for each group using H&E and Masson's trichrome staining. The expression of TGF-ß 1, collagen I (Col-I) and collagen III (Col-III) were determined by an immunohistochemical staining method. These effects were further evaluated in vitro by determining expression levels of NF-κB p65 and Col-I by quantitative real-time PCR analyses. Col-I protein expression was also examined by western blotting. RESULTS: All dose groups (125, 250, and 500 mg/kg/day) of CPhGs significantly reduced the liver and spleen index, decreased ALT, AST, HA, LN, PCIII, IV-C serum levels, TGF-ß 1 content (P < 0.01, P < 0.01, and P < 0.01), and Hyp content. CPhGs also markedly alleviated the swelling of liver cells and effectively prevented hepatocyte necrosis and inflammatory cell infiltration. Immunohistochemical results showed that CPhGs significantly reduced the expression of TGF-ß 1 (P < 0.01, P < 0.01, and P < 0.01), Col- I, and Col-III. The in vitro effects of CPhGs (100, 75, 50, and 25 ug/ml) on HSC-T6 showed that CPhGs significantly reduced mRNA expression of NF-κB p65 and Col-I, and CPhGs also downregulated Col-I protein expression. CONCLUSIONS: CPhGs have a significant anti-hepatic fibrosis effect, and may be used as hepatoprotective agents for treatment of hepatic fibrosis.