Does the National Fitness Policy Promote National Health?-An Empirical Study from China.

The influence of national health level in the stability and sustainable development of national society is increasingly prominent. The purpose of this study is to examine whether, when, and how national fitness policies exert influence on national health. Panel data from 2008 to 2017 of 30 Chinese provinces (cities) (except the Tibet autonomous region) were used to systematically reveal the direct impact of national fitness policies on national health and its characteristics in different regions, as well as the interaction mechanisms of human capital and finance health expenditures in public sports. This study found that first, national fitness policies had a positive effect on adult health. Second, sports human capital weakens the health effect of national fitness policies, while public finance health expenditures strengthen this effect. Lastly, the health effect of national fitness policies varies significantly across regions due to uneven regional economic development, and the differences in the effects on different age groups (adults and children) are equally pronounced. This study suggests that national fitness public service system and diverse national fitness plans improving national health level are important for a new dynamic balance and high quality coordinated development in both Chinese economic growth and social welfare.

MLL3 suppresses tumorigenesis through regulating TNS3 enhancer activity.

MLL3 is a histone H3K4 methyltransferase that is frequently mutated in cancer, but the underlying molecular mechanisms remain elusive. Here, we found that MLL3 depletion by CRISPR/sgRNA significantly enhanced cell migration, but did not elevate the proliferation rate of cancer cells. Through RNA-Seq and ChIP-Seq approaches, we identified TNS3 as the potential target gene for MLL3. MLL3 depletion caused downregulation of H3K4me1 and H3K27ac on an enhancer ~ 7 kb ahead of TNS3. 3C assay indicated the identified enhancer interacts with TNS3 promoter and repression of enhancer activity by dCas9-KRAB system impaired TNS3 expression. Exogenous expression of TNS3 in MLL3 deficient cells completely blocked the enhanced cell migration phenotype. Taken together, our study revealed a novel mechanism for MLL3 in suppressing cancer, which may provide novel targets for diagnosis or drug development.

Clinical nurses' nasogastric feeding practices in adults: a multicenter cross-sectional survey in China.

OBJECTIVE: We aimed to investigate practices of nasogastric tube (NGT) intubation and feeding for adults by clinical nurses in China. METHODS: A self-designed and validated questionnaire comprising 30 questions was distributed to 560 clinical nurses in three comprehensive hospitals of Xiamen, China. The questionnaire covered participants' demographic characteristics, NGT placement, administration of enteral nutrition (EN), and monitoring or management of feeding intolerance. RESULTS: A total 464 (82.9%) questionnaires were completed; 36.2% of nurses used nose-ear-xiphoid and 79.5% forehead-xiphoid measurement to define the internal length of the NGT. Many participants still used traditional methods to confirm NGT placement (auscultation of injected air 50.2%, bubble test 34.7% and observing feeding tube aspirate 34.3%). Bolus feeding was the most commonly used technique to administer EN. A total 97.0% of all nurses used syringes to measure gastric residual volume (GRV), and 62.7% measured GRV every 4-8 hours. The most frequently used GRV threshold values were 200 mL (44.6%) and 150 mL (25.2%). Most nurses stopped feeding immediately when encountering high GRV (84.3%) or diarrhea (45.0%). The nasogastric feeding practices of many clinical nurses were not consistent with international guidelines. CONCLUSIONS: Our study can provide an impetus for nursing administrators to revise their nasogastric feeding procedures, to promote compliance with evidence-based guidelines.

Association of maximum standardized uptake value with occult mediastinal lymph node metastases in cN0 non-small cell lung cancer.

OBJECTIVES: The management of non-small cell lung cancer (NSCLC) relies on the tumour-node-metastasis (TNM) stage, and the treatment regimen differs based on the N status. Positron emission tomography-computed tomography (PET-CT) has emerged as a powerful imaging tool for the detection of various cancers with a relatively low false-negative rate. We explored predictors to identify false-negative N2 disease in PET-CT. METHODS: A total of 284 consecutive cN0 patients with peripheral NSCLC who underwent PET-CT scans followed by curative intent resections were enrolled as a training set to identify predictors of occult N2 metastases by multivariable analysis. The accuracy and cut-off values for the predictors were calculated using a receiver operating characteristic curve. Clinical and pathological data were analysed retrospectively. An additional 151 patients were collected as a test set to validate the results, including the occult N2 rate and accuracy. RESULTS: In total, 8.5% (24/284) PET-CT-diagnosed N0 NSCLC cases had pathologically diagnosed N2 metastases. The SUVmax of the primary tumour was a unique independent risk factor for occult N2 NSCLC [P = 0.003, 95% confidence interval = 0.81-0.96, odds ratio (OR) = 0.88]. Occult N2 metastases occurred more frequently in the subcarinal (16/24) and right lower paratracheal lymph nodes (12/24). Accordingly, we divided the patients into two groups by SUVmax: the occult N2 rates in the SUVmax of <2.6 and SUVmax of ≥2.6 groups were 1.0% (1/100) and 12.5% (23/184), respectively (P = 0.001). In the test set, the occult N2 incidence rate was 9.3% (14/151), with the highest rates occurring in the subcarinal (9/14) and right lower paratracheal lymph nodes (6/14). In the two groups defined by SUVmax, the occult N2 rates were 4% (2/50) and 11.9% (12/101), respectively. CONCLUSIONS: The SUVmax of the primary tumour was an independent risk factor for occult N2 metastases in NSCLC patients diagnosed as clinical N0 by PET-CT. SUVmax of ≥2.6 of the primary tumour may indicate the risk of N2 metastases, and invasive mediastinal staging techniques or comprehensive therapy should not be ignored in these patients.

Global histone modification profiling reveals the epigenomic dynamics during malignant transformation in a four-stage breast cancer model.

BACKGROUND: Epigenetic regulation has emerged to be the critical steps for tumorigenesis and metastasis. Multiple histone methyltransferase and demethylase have been implicated as tumor suppressors or oncogenes recently. But the key epigenomic events in cancer cell transformation still remain poorly understood. METHODS: A breast cancer transformation model was established via stably expressing three oncogenes in primary breast epithelial cells. Chromatin immunoprecipitation followed by the next-generation sequencing of histone methylations was performed to determine epigenetic events during transformation. Western blot, quantitative RT-PCR, and immunostaining were used to determine gene expression in cells and tissues. RESULTS: Histones H3K9me2 and me3, two repressive marks of transcription, decrease in in vitro breast cancer cell model and in vivo clinical tissues. A survey of enzymes related with H3K9 methylation indicated that KDM3A/JMJD1A, a demethylase for H3K9me1 and me2, gradually increases during cancer transformation and is elevated in patient tissues. KDM3A/JMJD1A deficiency impairs the growth of tumors in nude mice and transformed cell lines. Genome-wide ChIP-seq analysis reveals that the boundaries of decreased H3K9me2 large organized chromatin K9 modifications (LOCKs) are enriched with cancer-related genes, such as MYC and PAX3. Further studies show that KDM3A/JMJD1A directly binds to these oncogenes and regulates their transcription by removing H3K9me2 mark. CONCLUSIONS: Our study demonstrates reduction of histones H3K9 me2 and me3, and elevation of KDM3A/JMJD1A as important events for breast cancer, and illustrates the dynamic epigenomic mechanisms during breast cancer transformation.

The selective activation of p53 target genes regulated by SMYD2 in BIX-01294 induced autophagy-related cell death.

Transcription regulation emerged to be one of the key mechanisms in regulating autophagy. Inhibitors of H3K9 methylation activates the expression of LC3B, as well as other autophagy-related genes, and promotes autophagy process. However, the detailed mechanisms of autophagy regulated by nuclear factors remain elusive. In this study, we performed a drug screen of SMYD2-/- cells and discovered that SMYD2 deficiency enhanced the cell death induced by BIX01294, an inhibitor of histone H3K9 methylation. BIX-01294 induces accumulation of LC3 II and autophagy-related cell death, but not caspase-dependent apoptosis. We profiled the global gene expression pattern after treatment with BIX-01294, in comparison with rapamycin. BIX-01294 selectively activates the downstream genes of p53 signaling, such as p21 and DOR, but not PUMA, a typical p53 target gene inducing apoptosis. BIX-01294 also induces other autophagy-related genes, such as ATG4A and ATG9A. SMYD2 is a methyltransferase for p53 and regulates its transcription activity. Its deficiency enhances the BIX-01294-induced autophagy-related cell death through transcriptionally promoting the expression of p53 target genes. Taken together, our data suggest BIX-01294 induces autophagy-related cell death and selectively activates p53 target genes, which is repressed by SMYD2 methyltransferase.

[Effect of shenfu injection on the stability of circulation during induction of general anesthesia for aged people].

OBJECTIVE: To observe the intervention of Shenfu Injection (SFI) on the hemodynamics and circulatory function during induction of general anesthesia for aged people, in order to optimize the medication of anesthesia inductive phase in aged people. METHODS: Sixty aged patients scheduled to receive general anesthesia were equally randomized into 2 groups, the SFI group and the control group. SFI via intravenous drip (1 mL/kg diluted with 5 mL/kg saline) was administered to the SFI group 15 min before anesthesia induction and to the control group, normal saline was administered instead. Then the induction and intubation were implemented. The systolic blood pressure (SBP), diastolic pressure (DBP), heart rate (HR), central venous pressure (CVP), pulse saturation oxygen (SpO2), and the ST segment of ECG were observed at the different time points of induction, i.e. at the time of entry into the operating room (T1), ending the medication (T2), before the induction (T3), showing the lowest SBP in induction (T4), before and after intubation (T5 and T5). The dose and frequency of atropine and ephedrine applied in the inductive phase were observed as well. RESULTS: As compared with the baseline values measured at T1, CVP elevated at T2, T3, and T6 (P < 0.05), SBP and DBP descended at T4, T5, T6 in both groups; HR accelerated at T2, T3, and T6 in the control group; and HR at T4, T5 and T6 in both groups were significantly different (P < 0.05 or P < 0.01). Inter-group comparisons showed significant difference between groups in CVP at T2 (P < 0.05); so did SBP, DBP and HR at T4, T5 and T6 (P < 0.05 or P < 0.01). CONCLUSION: Application of SFI in the inductive phase of general anesthesia in aged people could evidently reduce the fluctuation of hemodynamics to prevent the occurrence of myocardial ischemia and improve it definitely.