Objective Forecasting the seasonality and trend of pulmonary tuberculosis is important for the rational allocation of health resources; however, this foresting is often hampered by inappropriate prediction methods. In this study, we performed validation research by comparing the accuracy of the autoregressive integrated moving average (ARIMA) model and the back-propagation neural network (BPNN) model in a southeastern province of China. Methods We applied the data from 462,214 notified pulmonary tuberculosis cases registered from January 2005 to December 2015 in Jiangsu Province to modulate and construct the ARIMA and BPNN models. Cases registered in 2016 were used to assess the prediction accuracy of the models. The root mean square error (RMSE), mean absolute percentage error (MAPE), mean absolute error (MAE) and mean error rate (MER) were used to evaluate the model fitting and forecasting effect. Results During 2005-2015, the annual pulmonary tuberculosis notification rate in Jiangsu Province was 56.35/100,000, ranging from 40.85/100,000 to 79.36/100,000. Through screening and comparison, the ARIMA (0, 1, 2) (0, 1, 1)12 and BPNN (3-9-1) were defined as the optimal fitting models. In the fitting dataset, the RMSE, MAPE, MAE and MER were 0.3901, 6.0498, 0.2740 and 0.0608, respectively, for the ARIMA (0, 1, 2) (0, 1, 1)12 model, 0.3236, 6.0113, 0.2508 and 0.0587, respectively, for the BPNN model. In the forecasting dataset, the RMSE, MAPE, MAE and MER were 0.1758, 4.6041, 0.1368 and 0.0444, respectively, for the ARIMA (0, 1, 2) (0, 1, 1)12 model, and 0.1382, 3.2172, 0.1018 and 0.0330, respectively, for the BPNN model. Conclusion Both the ARIMA and BPNN models can be used to predict the seasonality and trend of pulmonary tuberculosis in the Chinese population, but the BPNN model shows better performance. Applying statistical techniques by considering local characteristics may enable more accurate mathematical modeling.

/pdf/forecasting-the-seasonality-and-trend-of-pulmonary-f48rkw8itg.pdf

Forecasting the seasonality and trend of pulmonary tuberculosis in Jiangsu Province of China using advanced statistical time-series analyses

Vitamin D is a pro-hormone characterized by an intricate metabolism and regulation. It is well known for its role in calcium and phosphate metabolism, and in bone health. However, several studies have assessed a huge number of extra-skeletal functions, ranging from cell proliferation in some oncogenic pathways to antioxidant and immunomodulatory functions. Vitamin D exerts its role by binding to VDRs (vitamin D receptors), which are located in many different tissues. Moreover, VDRs are able to bind hundreds of genomic loci, modulating the expression of various primary target genes. Interestingly, plenty of gene polymorphisms regarding VDRs are described, each one carrying a potential influence against gene expression, with relapses in several chronic diseases and metabolic complications. In this review, we provide an overview of the genetic aspects of vitamin D and VDR, emphasizing the gene regulation of vitamin D, and the genetic modulation of VDR target genes. In addition, we briefly summarize the rare genetic disease linked to vitamin D metabolism. 

Vitamin D: An Overview of Gene Regulation, Ranging from Metabolism to Genomic Effects

Epigenetics regulate gene function without any alteration in the DNA sequence. The epigenetics represent one of the most important regulators in different cellular processes and have initially been developed in microorganisms as a protective strategy. The evaluation of the epigenetic mechanisms is also important in achieving an efficient control strategy in tuberculosis (TB). TB is one of the most significant epidemiological concerns in human history. Despite several in vivo and in vitro studies that have evaluated different epigenetic modifications in TB, many aspects of the association between epigenetics and TB are not fully understood. The current paper is aimed at reviewing our knowledge on histone modifications and DNA methylation modifications, as well as miRNAs regulation in TB.

The inter-talk between Mycobacterium tuberculosis and the epigenetic mechanisms.

Background The expression of progestin and adipoQ receptor 3 (PAQR3) is generally downregulated in multiple tumors, which is associated with tumor progression and poor prognosis. Methods The clinical value of PAQR3 was analyzed using various databases and in 60 patients with non-small cell lung cancer (NSCLC). In addition, cell counting kit-8 (CCK-8), colony formation, and flow cytometry assays were used to evaluate the effect of PAQR3 on the growth of NSCLC cells in vitro. Gene set enrichment analysis (GSEA) was performed to investigate the possible mechanism through which PAQR3 is involved in the progression of lung cancer. Furthermore, western blotting was employed to verify the relevant mechanism. Results The expression of PAQR3 was decreased in 60 NSCLC patients and was related to the histological subtype, lymph node metastasis, tumor size, and diagnosis of NSCLC. Patients with lung adenocarcinoma with increased PAQR3 expression tended to have a better prognosis. Besides, PAQR3 inhibited proliferation, clone formation, and cycle transition in NSCLC cells, but induced apoptosis. The results of GSEA showed that PAQR3 regulated the progression of lung cancer by affecting cell cycle, DNA replication, and the p53 signaling pathway. We confirmed that PAQR3 overexpression inhibited the expression of NF-κB, while it increased the expression of p53, phospho-p53, and Bax. On the contrary, PAQR3 inhibition played an opposite role in these proteins. Conclusion PAQR3 inhibited the growth of NSCLC cells through the NF-κB/P53/Bax signaling pathway and might be a new target for diagnosis and treatment.

/pdf/paqr3-inhibits-non-small-cell-lung-cancer-growth-by-58zxillnc5.pdf

PAQR3 Inhibits Non-small Cell Lung Cancer Growth by Regulating the NF-κB/p53/Bax Axis.

Deficiency in circulatory vitamin D level and vitamin D receptor DNA methylation could be associated with weakened innate immune response and increased susceptibility to tuberculosis (TB) disease in children. Therefore, we aimed to study the effect of vitamin D receptor (VDR) gene methylation on plasma vitamin D level and the expression of the VDR gene in children with active-TB disease. A cross-sectional comparative study was conducted in 43 children with active-TB and 33 healthy control children (HC). The vitamin D level was measured in plasma, while the levels of VDR gene promoter methylation and VDR gene expression were measured in peripheral blood. Children with active-TB showed a significantly lower median vitamin D level than HC [Cases 17.18 ng/mL (IQR, 8.3-18.6 ng/mL); HC 41.34 ng/mL (IQR, 40.2-43.49 ng/mL) (p<0.0001)] and decreased mRNA expression level of VDR gene [Cases 0.51 (IQR, 0.40-0.70); HC 1.06 (IQR, 0.8-1.2) (p<0.0001)] and increased VDR DNA methylation [Cases 75% (IQR, 50-75%); HC 10% (IQR, 10-25%) (p<0.0001)]. The VDR hypermethylation is significantly associated with reduced vitamin D level and decreased expression level of VDR gene. Therefore this inverse association could be involved in the impairment in the VDR mediated cytolytic and antimicrobial effector cell response in pediatric TB disease.

Methylation Status of VDR Gene and its Association with Vitamin D Status and VDR Gene Expression in Pediatric Tuberculosis Disease.

A variety of abnormalities in vitamin D metabolism have been reported in patients with active tuberculosis. However, intervention trials have produced inconsistent results. We hypothesized that genetic and epigenetic changes in the key genes of the vitamin D metabolic pathway may partly explain the differences between studies. We performed a case-control study followed by a prospective cohort study. We recruited 122 patients with pulmonary tuberculosis and 118 healthy controls. The serum 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D levels were measured. The methylation of the promoter regions of key genes in the vitamin D metabolic pathway (CYP24A1, CYP27A1, CYP27B1, CYP2R1, and VDR) was detected using the Illumina MiSeq platform. The specific methylation profiles were examined as epigenetic biomarkers. The sensitivity, specificity, and receiver operating characteristic (ROC) curves were used to estimate the predictive value of the biomarkers. The baseline serum 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D concentrations in the cases were significantly lower than those in the controls (51.60 ± 27.25 nmol/L vs. 117.50 ± 75.50 nmol/L, Z = − 8.515, P < 0.001; 82.63 ± 51.43 pmol/L vs. 94.02 ± 49.26 pmol/L, Z = − 2.165, P = 0.03). We sequenced 310 CpG sites in five candidate genes. After Bonferroni correction, there were 55 differentially methylated CpG sites between cases and controls; 41.5% were in the CYP27B1 gene, 31.7% were in the CYP24A1 gene, 14.7% were in the VDR gene, and 12.3% were in the CYP27A1 gene. When we designated the CpG sites that remained significant after the Bonferroni correction as the biomarkers, the area under the curve (AUC) for the cumulative methylation was 0.810 (95% CI 0.754–0.866). There was an interaction between CYP27A1 methylation level and 1,25-dihydroxyvitamin D concentration associated with the risk of TB (ORinteraction = 4.11, 95% CI 1.26–13.36, P = 0.019). The serum 1,25-dihydroxyvitamin D concentration at the end of the intensive treatment stage was related to a patient’s prognosis (P = 0.008). There were 23 CpG sites that were individually related to the treatment outcomes, but the relationships were not significant after the Bonferroni correction. Both serum vitamin D concentrations and the methylation levels of key genes in the vitamin D metabolic pathway are related to the risk and prognosis of tuberculosis.

/pdf/vitamin-d-and-the-promoter-methylation-of-its-metabolic-8puf8jh014.pdf

Vitamin D and the promoter methylation of its metabolic pathway genes in association with the risk and prognosis of tuberculosis

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Vitamin D and the promoter methylation of its metabolic pathway genes in association with the risk and prognosis of tuberculosis