A disease-targeted picture book for children with Henoch-Schonlein purpura nephritis: A quasi-experimental study.

BACKGROUND: Children with Henoch-Schonlein purpura nephritis are frequently burdened with psychological problems besides disease treatment and adherence. Currently, there is a shortage of appropriate and effective educational materials to facilitate physical and psychological recovery. OBJECTIVES: To examine a picture book for the effectiveness of disease-related knowledge, coping strategies, resilience, quality of life and depressive symptoms in children with Henoch-Schonlein purpura nephritis in China. DESIGN: A quasi-experimental design with repeated measures was adopted. The control group received standard care. The intervention group received the standard care plus a free picture book. This disease-specific picture book narrated the story of two rabbits diagnosed with Henoch-Schonlein purpura nephritis who underwent a series of examinations, faced difficulties taking medication, and eventually recovered. PARTICIPANTS: The study recruited 60 children diagnosed with Henoch-Schonlein purpura nephritis. MEASUREMENTS: Disease-related knowledge, resilience, coping strategies, depression and paediatric quality of life were measured at baseline, the third day, the first month and the third month after recruitment. The acceptability of the picture book was evaluated at the last data-collection point. RESULTS: The data showed that children in the intervention group demonstrated higher levels of knowledge (p < 0.001), less usage of emotional coping strategies (p = 0.003), reduced depressive symptoms (p = 0.003), improved psychological resilience (p < 0.001), and better quality of life (p < 0.046) than those in the control group in the third month. Most children (83.3%) in the intervention group were satisfied with the picture book. CONCLUSIONS: The targeted picture book is an effective educational tool for improving clinical outcomes and was highly accepted by children.

Did the universal zero-markup drug policy lower healthcare expenditures? Evidence from Changde, China.

BACKGROUND: The zero-markup drug policy (also known as the universal zero-markup drug policy (UZMDP)) was implemented in stages beginning with primary healthcare facilities in 2009 and eventually encompassing city public hospitals in 2016. This policy has been a central pillar of Chinese health reforms. While the literature has examined the impacts of this policy on healthcare utilization and expenditures, a more comprehensive and detailed assessment is warranted. The purpose of this paper is to explore the impacts of the UZMDP on inpatient and outpatient visits as well as on both aggregate healthcare expenditures and its various components (including drug, diagnosis, laboratory, and medical consumables expenditures). METHODS: A pre-post design was applied to a dataset extracted from the Changde Municipal Human Resource and Social Security Bureau comprising discharge data on 27,246 inpatients and encounter data on 48,282 outpatients in Changde city, Hunan province, China. The pre-UZMDP period for the city public hospitals was defined as the period from October 2015 to September 2016, while the post-UZMDP period was defined as the period from October 2016 to September 2017. Difference-in-Difference negative binomial and Tobit regression models were employed to evaluate the impacts of the UZMDP on healthcare utilization and expenditures, respectively. RESULTS: Four key findings flow from our assessment of the impacts of the UZMDP: first, outpatient and inpatient visits increased by 8.89 % and 9.39 %, respectively; second, average annual inpatient and outpatient drug expenditures fell by 4,349.00 CNY and 1,262.00 CNY, respectively; third, average annual expenditures on other categories of healthcare expenditures increased by 2,500.83 CNY, 417.10 CNY, 122.98 CNY, and 143.50 CNY for aggregate inpatient, inpatient diagnosis, inpatient laboratory, and outpatient medical consumables expenditures, respectively; and fourth, men and older individuals tended to have more inpatient and outpatient visits than their counterparts. CONCLUSIONS: Although the UZMDP was effective in reducing both inpatient and outpatient drug expenditures, it led to a sharp rise in other expenditure categories. Policy decision makers are advised to undertake efforts to contain the growth in total healthcare expenditures, in general, as well as to evaluate the offsetting effects of the policy on non-drug components of care.

Molecular Subtypes Based on the Stemness Index Predict Prognosis in Glioma Patients.

Glioma is the common histological subtype of malignancy in the central nervous system, with high morbidity and mortality. Glioma cancer stem cells (CSCs) play essential roles in tumor recurrence and treatment resistance. Thus, exploring the stem cell-related genes and subtypes in glioma is important. In this study, we collected the RNA-sequencing (RNA-seq) data and clinical information of glioma patients from The Cancer Genome Atlas (TCGA) and Chinese Glioma Genome Atlas (CGGA) databases. With the differentially expressed genes (DEGs) and weighted gene correlation network analysis (WGCNA), we identified 86 mRNA expression-based stemness index (mRNAsi)-related genes in 583 samples from TCGA RNA-seq dataset. Furthermore, these samples from TCGA database could be divided into two significantly different subtypes with different prognoses based on the mRNAsi corresponding gene, which could also be validated in the CGGA database. The clinical characteristics and immune cell infiltrate distribution of the two stemness subtypes are different. Then, functional enrichment analyses were performed to identify the different gene ontology (GO) terms and pathways in the two different subtypes. Moreover, we constructed a stemness subtype-related risk score model and nomogram to predict the prognosis of glioma patients. Finally, we selected one gene (ETV2) from the risk score model for experimental validation. The results showed that ETV2 can contribute to the invasion, migration, and epithelial-mesenchymal transition (EMT) process of glioma. In conclusion, we identified two distinct molecular subtypes and potential therapeutic targets of glioma, which could provide new insights for the development of precision diagnosis and prognostic prediction for glioma patients.

Decreased MiR-30a promotes TGF-ß1-mediated arachnoid fibrosis in post-hemorrhagic hydrocephalus.

BACKGROUND: Fibrosis in the ventricular system is closely associated with post-hemorrhagic hydrocephalus (PHH). It is characterized by an expansion of the cerebral ventricles due to CSF accumulation following intraventricular hemorrhage (IVH). The activation of transforming growth factor-ß1 (TGF-ß1) may be involved in thrombin-induced arachnoid fibrosis. METHODS: A rat model of PHH was established by injection of autologous non-anticoagulated blood from the right femoral artery into the lateral ventricles. Differential expression of miR-30a was detected in rat arachnoid cells by RNA sequencing. AP-1, c-Fos, and TRAF3IP2 were knocked down in primary arachnoid cells, and the degree of arachnoid fibrosis was assessed. RESULTS: Decreased expression of miR-30a and increased expression of TRAF3IP2, TGF-ß1, and α-SMA were detected in the arachnoid cells of PHH rat. Besides, overexpression of miR-30a targets TRAF3IP2 mRNA 3'UTR and inhibits the expression of TRAF3IP2, TGF-ß1, and α-SMA in the primary arachnoid cells. Furthermore, TRAF3IP2 activates AP-1 to promote arachnoid fibrosis. The content of type I collagen in the primary arachnoid cells was reduced after the silencing of AP-1 and TRAF3IP2. CONCLUSIONS: This study identified a miR-30a-regulated mechanism of arachnoid fibrosis, suggesting a previously unrecognized contribution of miR-30a to the pathogenesis of fibrosis in the ventricular system. These results might provide a new target for the clinical diagnosis and treatment of PHH.

Current situation and distribution equality of public health resource in China.

BACKGROUND: The public health system has been developed in China for several years while no research explores its distribution. This research aims to describe the variation and equality of public health allocation from 2013 to 2018 and explore the source of inequality. METHODS: Data in this research was obtained from the China Health Statistics Yearbook 2014 to 2019 and the China Statistical Yearbook 2019. Four indicators were chosen in describing the development and current situation of the public health system. Three of them were used to evaluate allocation equality. 31 provinces were categorized into western, middle, and eastern groups based on geographical and economic conditions. Total allocation equality, inter- and intra-difference were all measured by the Theil index. RESULTS: All indicators showed a stably upwards trend except for the number of public health institutions. The allocation gap of the public health institution per km2 was larger than that per 10,000 capita. Theil index of three indicators continually rose from 2013 to 2018 and the inequality of public health institutions allocation was the highest one. The western region had the highest Theil index in technical personnel and beds allocation. Among the three regions, the western region contributed most to inequality. CONCLUSIONS: The public health workforces and institutions are still under the requirement of the National Medical and Health Service System Plan. From 2013 to 2018, the equality of public health resources stably decreases, which is mainly contributed by the internal difference within the western region. Further research should be done to explore the possible cause of the results. Problems founded in this research should be solved by multisectoral cooperation.

Development and Validation of a Tumor Mutation Burden-Related Immune Prognostic Model for Lower-Grade Glioma.

Tumor mutation burden (TMB) is a useful biomarker to predict prognosis and the efficacy of immune checkpoint inhibitors (ICIs). In this study, we aimed to explore the prognostic value of TMB and the potential association between TMB and immune infiltration in lower-grade gliomas (LGGs). Somatic mutation and RNA-sequencing (RNA-seq) data were downloaded from the Cancer Genome Atlas (TCGA) database. TMB was calculated and patients were divided into high- and low-TMB groups. After performing differential analysis between high- and low-risk groups, we identified six hub TMB and immune-related genes that were correlated with overall survival in LGGs. Then, Gene Set Enrichment Analysis was performed to screen significantly enriched GO terms between the two groups. Moreover, an immune-related risk score system was developed by LASSO Cox analysis based on the six hub genes and was validated with the Chinese Glioma Genome Atlas dataset. Using the TIMER database, we further systematically analyzed the relationships between mutants of the six hub genes and immune infiltration levels, as well as the relationships between the immune-related risk score system and the immune microenvironment in LGGs. The results showed that TMB was negatively correlated with OS and high TMB might inhibit immune infiltration in LGGs. Furthermore, the risk score system could effectively stratify patients into low- and high-risk groups in both the training and validation datasets. Multivariate Cox analysis demonstrated that TMB was not an independent prognostic factor, but the risk score was. Higher infiltration of immune cells (B cells, CD4+ T cells, CD8+ T cells, neutrophils, macrophages, and dendritic cells) and higher levels of immune checkpoints (PD-1, CTLA-4, LAG-3, and TIM-3) were found in patients in the high-risk group. Finally, a novel nomogram model was constructed and evaluated to estimate the overall survival of LGG patients. In summary, our study provided new insights into immune infiltration in the tumor microenvironment and immunotherapies for LGGs.

Extracellular vesicles from human urine-derived stem cells inhibit glucocorticoid-induced osteonecrosis of the femoral head by transporting and releasing pro-angiogenic DMBT1 and anti-apoptotic TIMP1.

Osteonecrosis of the femoral head (ONFH) frequently occurs after glucocorticoid (GC) treatment. Extracellular vesicles (EVs) are important nano-sized paracrine mediators of intercellular crosstalk. This study aimed to determine whether EVs from human urine-derived stem cells (USC-EVs) could protect against GC-induced ONFH and focused on the impacts of USC-EVs on angiogenesis and apoptosis to explore the mechanism by which USC-EVs attenuated GC-induced ONFH. The results in vivo showed that the intravenous administration of USC-EVs at the early stage of GC exposure could rescue angiogenesis impairment, reduce apoptosis of trabecular bone and marrow cells, prevent trabecular bone destruction and improve bone microarchitecture in the femoral heads of rats. In vitro, USC-EVs reversed the GC-induced suppression of endothelial angiogenesis and activation of apoptosis. Deleted in malignant brain tumors 1 (DMBT1) and tissue inhibitor of metalloproteinases 1 (TIMP1) proteins were enriched in USC-EVs and essential for the USC-EVs-induced pro-angiogenic and anti-apoptotic effects in GC-treated cells, respectively. Knockdown of TIMP1 attenuated the protective effects of USC-EVs against GC-induced ONFH. Our study suggests that USC-EVs are a promising nano-sized agent for the prevention of GC-induced ONFH by delivering pro-angiogenic DMBT1 and anti-apoptotic TIMP1. STATEMENT OF SIGNIFICANCE: This study demonstrates that the intravenous injection of extracellular vesicles from human urine-derived stem cells (USC-EVs) at the early stage of glucocorticoid (GC) exposure efficiently protects the rats from the GC-induced osteonecrosis of the femoral head (ONFH). Moreover, this study identifies that the promotion of angiogenesis and inhibition of apoptosis by transferring pro-angiogenic DMBT1 and anti-apoptotic TIMP1 proteins contribute importantly to the USC-EVs-induced protective effects against GC-induced ONFH. This study suggests the promising prospect of USC-EVs as a new nano-sized agent for protecting against GC-induced ONFH, and the potential of DMBT1 and TIMP1 as the molecular targets for further augmenting the protective function of USC-EVs.

[Advances in research on the pathogenesis of hydrocephalus].

Hydrocephalus is a common neurological disease with complex etiology. It is characterized by the accumulation and continuous growth of cerebrospinal fluid in the ventricular system and subarachnoid space. Hydrocephalus can be caused by congenital genetic factors, brain trauma and cerebral hemorrhage. Through the efforts of many researchers, the pathogenesis of hydrocephalus is being completed, but it has not been fully explained. The imbalance of cerebrospinal fluid production and absorption into the sinus, and disorder of the cerebrospinal fluid circulation pathway or the osmotic pressure maintenance in the ventricle can lead to increased cerebrospinal fluid and ventricular dilatation.