: To explore the relationship between metal exposure level and blood pressure, so as to provide a scientific basis for verifying the relationship between metal exposure and elevated blood pressure among primary school students. Methods: In July 2022, a total of 555 students of second to sixth grade were selected by cluster random sampling method from two primary schools in Zhuxi County, Shiyan City, Hubei Province. A questionnaire survey was conducted to obtain the socio demographic characteristics and living habits of the participants. The height, weight, body mass index(BMI) and blood pressure were obtained by physical examination. At the same time, the urine of the subjects was collected, and the metal mass fraction in urine was detected by inductively coupled plasma mass spectrometry. The relationship between metal mass fraction in urine and blood pressure was analyzed by generalized linear regression. Results: The detection rate of elevated blood pressure in primary school students was 15.86% , and there was a statistically significant difference in the detection rate of elevated blood pressure among obese primary school students (yes:37.25%,no:13.69%, χ 2=19.28, P <0.01).There were statistically significant differences in BMI[15.80( 14.69 ， 17.92 )，17.87(15.49，20.89)kg/m 2] between the non elevated blood pressure group and the elevated blood pressure group of elementary school students ( Z =-4.67, P <0.01). The geometric mean mass fraction of zinc in urine was the highest ( 6 942.86 μg/g), titanium was the lowest (2.20 μg/g). Zinc and lead were positively correlated with elevated systolic blood pressure( β = 0.054 , 0.014), zinc and cadmium were positively correlated with elevated diastolic blood pressure ( β =0.038,0.029) ( P <0.05). Conclusions Metal zinc, lead and cadmium concentration are associated with elevated blood pressure. It is necessary to intervene and control the exposure of zinc, lead and cadmium in the environment to promote the blood pressure health of primary school students.

Objective To assess the influence of inter-implant distances on the accuracy of intraoral scanning im-pressions in vitro.Methods A master cast model with different inter-implant distances was scanned by laboratory and intraoral scanners,which were used as the reference and intraoral scan data.The distance and angular devia-tions of the scan bodies corresponding to the reference and intraoral digital scan standard tessellation language(STL)files were measured and calculated in a three-dimensional analysis software.The one-sample t-test,Spearman's correlation analysis,Brown-Forsythe F test,Games-Howell post-hoc test,and Levene's test were used for comparisons(α=0.05).Results The overall distance and angular deviations of the intraoral digital scan were(27.48±18.14)μm and(0.24±0.19)°,within clinically acceptable limits(P＜0.001).The inter-implant distances exhibited a significant positive correlation with both the scanning distance and angular deviations in terms of scanning trueness.The angular deviation differed significantly between the 1-2 group(8.13 mm)and the other distance groups.Additionally,inter-implant distances affected the precision of the intraoral scanner(P＜0.05).Conclusion The findings of this study indicate that intraoral scanning impressions of complete-arch implant-sup-ported prostheses are within clinically acceptable ranges of accuracy.Inter-implant distances≤8.13 mm can result in a higher accuracy of intraoral scanning.Increased inter-implant distances can adversely affect intraoral scanning accuracy.

Abernethy malformation， also known as congenital portosystemic shunts， is rare in clinical practice， with less than 300 cases reported in the global literature up to 2019. The disease can have serious complications such as pulmonary hypertension， liver tumor， and liver failure and tends to have an extremely poor prognosis， and early diagnosis and active and effective treatment can reduce and delay the onset of complications. In this case， portography combined with balloon occlusion helped to display the underdeveloped slender portal vein with dysplasia， so that the child who was formerly misdiagnosed with type Ⅰ Abernethy malformation was diagnosed with type Ⅱ Abernethy malformation， and then the child was successfully treated by transcatheter closure. This article gives a detailed report of this case.

OBJECTIVE To establish a total quality management system for pharmacy intravenous admixture services （PIVAS）， in order to promote the standardization， accuracy and rationalization of clinical intravenous infusion. METHODS Based on information system in PIVAS， the management system and quality monitoring items of the whole process before， during and after PIVAS infusion preparation were formulated. The quality control and quality improvement were carried out regularly with quality management tools and methods such as PDCA （plan， do， check， process） cycle， quality control circle， and root cause analysis. The main quality control indexes of PIVAS were retrospectively analyzed before （in 2019） and after PDCA cycle management （in 2020 and 2021）. RESULTS The indexes of quality monitoring in the whole process of PIVAS infusion preparation， such as the score of drug quality management， the drug residue qualification rate and the qualified rate of drug content in infusion， were increased from 92 points， 79%， 86.4% in 2019 to 99 points， 92%， 99.8% in 2021， respectively. The indexes of safe and rational drug use， such as the ratio of intravenous irrational medical orders， the rate of drug repercussion， the rate of antibiotics use， and the rate of TCM injection use decreased from 0.98%， 6.1%， 40.55%， 39.70% to 0.23%， 3.2%， 37.18%， 26.00%， respectively. CONCLUSIONS The established total quality management system for PIVAS can improve the quality management level in the infusion preparation process， improve the quality of infusion preparation and promote clinical safe and rational drug use.

This study aimed to explore the anti-glioma effect of natural compound pterostilbene(PTE) through regulating pyroptosis and apoptosis pathways, and to analyze the possible anti-glioma pathways and targets of PTE by network pharmacology and molecular docking. In this study, the action targets of PTE and the glioma targets were obtained by network pharmacology to construct a target network and a protein-protein interaction(PPI) network to predict the possible action targets of PTE against glioma. Molecular docking was performed on the core targets by AutoDock and the action pathways of PTE against glioma were predicted by enrichment analysis. In addition, the effect of PTE on the viability of U87MG and GL261 glioma cells was detected by CCK-8 assay. Clone formation assay and cell scratching assay were used to explore the effect of different concentrations of PTE on the proliferation and migration, respectively of glioma cells. Hoechst staining was used to observe PTE-induced apoptosis in glioma cells. The changes in mitochondrial membrane potential were detected by JC-1 staining. The pyroptosis-inducing effect of PTE on glioma cells was observed by inverted microscopy and lactate dehydrogenase(LDH) assay. Hoechst 33342/PI dual staining assay was performed to detect the integrity of glioma cell membranes. The expressions of pyroptosis and apoptosis-related proteins in glioma cells after PTE induction were determined by Western blot. In this study, 37 anti-glioma targets of PTE were obtained, and enrichment analysis suggested that PTE exerted anti-glioma effects through various signaling pathways including cancer pathway, proteoglycan in cancer, PI3K/AKT pathway, and apoptosis regulatory pathway. Molecular docking revealed that PTE had good binding activity with the main targets. Compared with the control group, PTE significantly reduced the viability as well as the proliferation, migration and adhesion abilities of U87MG and GL261 cells; it induced the apoptosis of the two glioma cells and the decrease of mitochondrial membrane potential in U87MG cells, and the effects increased with the increase of drug concentration. Compared with the conditions in the control group, glioma cells in the PTE group had increased pyroptosis-specific appearance and gradually increased LDH release; the number of PI positive cells was significantly elevated with the increase of PTE concentration as revealed by Hoechst 33342/PI staining; the expression levels of apoptosis-related factors cleaved PARP1 and B-cell lymphoma-2(Bcl-2) associated X(BAX) in the PTE group were markedly up-regulated, while the expression level of Bcl-2 was markedly down-regulated; the activation levels of pyroptosis-related proteins cleaved caspase-3 and gasdermin E-N(GSDME-N) had a remarkable rise in the PTE group, while no significant changes were found in the activation levels of gasdermin D-N(GSDMD-N) and cleaved caspase-1. In summary, PTE plays an anti-glioma role by inhibiting cell viability, proliferation, and migration and activating the caspase-3/GSDME-mediated pyroptosis pathway and mitochondrial apoptosis pathway.
Pyroptosis ; Caspase 3/metabolism* ; Network Pharmacology ; Gasdermins ; Molecular Docking Simulation ; Phosphatidylinositol 3-Kinases/metabolism* ; Apoptosis ; Proto-Oncogene Proteins c-bcl-2/metabolism*

Pyroptosis， an atypical new cell death mode other than apoptosis and necrosis， has been discovered in recent years. Pyroptosis depends on the cleavage of gasdermins （GSDMs） by Caspases. The activated GSDMs act on the plasma membrane to form a perforation， which results in cell lysis and triggers inflammation and immune response. Pyroptosis can be induced by four distinct signaling pathways， including canonical and non-canonical inflammasome pathways， apoptosis-associated Caspases-mediated pathway， and granzyme pathway. In these signaling pathways， GSDMs are the executors of pyroptosis. Pyroptosis is associated with the death of tumor cells and the inflammatory damage of normal tissues. Recent studies have demonstrated that moderate pyroptosis can lead to tumor cell death to exert an anti-tumor effect， and meanwhile stimulate the tumor immune microenvironment， while it can promote tumor development. Despite the good performance， drug-based anti-tumor therapies such as tumor immunotherapy， chemotherapy， and targeted therapy have some shortcomings such as drug resistance， recurrence， and damage to normal tissues. The latest research shows that a variety of natural compounds have anti-tumor effects in the auxiliary treatment of tumors by mediating the pyroptosis pathways in a multi-target and multi-pathway manner， which provide new ideas for the study of anti-tumor therapy. We reviewed the molecular mechanism of pyroptosis and the regulatory role of pyroptosis in tumors and tumor immune microenvironment， and summarized the recent research progress in the natural medicinal components regulating pyroptosis in anti-tumor therapy， with a view to providing ideas for the research on the anti-tumor therapy based on pyroptosis.

ObjectiveTo study the inhibitory effect of polyphyllin Ⅰ （PPI） on the growth of colorectal cancer cells and its molecular mechanism. MethodRKO cells were cultured and divided into a blank group and PPI treatment groups with concentrations of 0.6， 0.8， 1.0 μmol·L^-1， respectively. HRT18 cells were cultured and divided into a blank group and PPI treatment groups with concentrations of 1.2， 1.4， 1.6 μmol·L^-1， respectively. The effects of PPI on the proliferation and morphology of colorectal cancer were detected by cell proliferation toxicity assay， trypan blue exclusion assay， plate clone formation assay， and confocal high-intension cell imaging analysis system. Flow cytometry was used to detect the apoptosis rate of colorectal cancer cells. The pQCXIP-GFP-LC3 plasmid transfection assay was used to detect the formation of autophagosomes in colorectal cancer cells after PPI treatment. Western blot was used to detect the expression of apoptosis-related proteins Caspase-3， Caspase-8， and poly ADP ribose polymerase （PARP）， the expression of autophagy related protein LC3Ⅱ， and the expression and phosphorylation of Hippo signaling pathway proteins LATS1 and YAP. In the plvx-Flag-YAP plasmid transfection assay， YAP was overexpressed and treated with PPI， and the proliferation of colorectal cancer cells was detected by cytotoxicity assay. The expression of LC3Ⅱ and PARP in colorectal cancer cells was detected by Western blot. SwissADME predicted pharmacokinetic parameters of PPI. ResultAs compared with the blank group， the survival rate and clone formation ability of colorectal cancer cells in the PPI group were significantly decreased （P<0.01）， the cell area of colorectal cancer cells in the PPI group was significantly decreased， and the roundness of colorectal cancer cells was significantly increased （P<0.01）. As compared with the blank group， the apoptosis rate of colorectal cancer cells in PPI treatment groupw was significantly increased （P<0.01）， the expression of apoptotic proteins Caspase-3 and Caspase-8 protein precursor in PPI treatment groups was decreased， and the cleavage of PARP was increased （P<0.01）. As compared with the blank group， the expression level of autophagy-related protein LC3Ⅱ in colorectal cancer cells in PPI treatment groups was significantly increased， and the formation of autophagosomes was promoted （P<0.01）. As compared with the blank group， the expression of YAP protein in colorectal cancer cells in PPI treatment groups was significantly decreased， and the expressions of phosphorylated LATS1 and YAP were significantly increased （P<0.01）. As compared with the blank group， overexpression of YAP could significantly antagonize the effect of PPI on apoptosis， autophagy activation， and proliferation inhibition of colorectal cancer cells. SwissADME simulation results showed that PPI had good drug like activity. ConclusionPPI can induce apoptosis and autophagy of colorectal cancer cells through targeted activation of Hippo signaling pathway， thereby inhibiting their proliferation.

Objective To monitor the indoor radon concentration of urban residents in Shiyan, China, and to analyze the related influencing factors. Methods From April to July, 2019, RSKS standard detectors were used to measure the indoor radon concentration of 125 households in Shiyan, and the results were analyzed. Results The indoor radon concentration of residents in Shiyan showed a skewed distribution, ranging from 13.8 to 145 Bq/m³, and M (P₂₅,P₇₅) was 38.3 (29.0,62.0) Bq/m³. The estimated annual effective dose of radon and radon daughters from inhalation was 0.52-5.50 mSv, and M (P₂₅,P₇₅) was 1.45 (1.10, 2.36) mSv, which was consistent with literature. Building structure (H = 14.10, P < 0.001), floor (H = 24.41, P < 0.001), and geographical region (H = 8.963, P < 0.05) were influencing factors of indoor radon concentration, and the differences were significant. Conclusion The indoor radon concentration of urban residents in Shiyan is lower than the national standard limit. However, in daily life, it is still necessary to take appropriate measures to reduce the concentration of indoor radon as much as possible.

【Objective】 To investigate the related viral markers of HBV DNA reactive samples among voluntary blood donors in Shiyan area, so as to provide some reference for donor re-entry. 【Methods】 From August 2019 to June 2021, 78 samples with HBV DNA reactivity from voluntary blood donors in our blood station were collected, and they were further detected for HBV viral markers(using chemiluminescence assays), nucleic acid testing(NAT) of virus quantification and sequencing analysis. 【Results】 Forty-seven (60.3%)out of 78 HBV DNA reactive samples were from repeated blood donors, and 56.4%(44/78)of them were over 45 years old. Among the five viral markers of hepatitis B, 37.2%(29/78) were positive for anti-HBs alone, 19.2%(15/78) were positive for anti-HBe+ anti-HBc and anti-HBs+ anti-HBe+ anti-HBc, and 11.5% (9/78) were all items negative.A total of 62.8%(49/78) of samples were detected by NAT quantification and seven samples had been successfully sequenced for HBV. 【Conclusion】 NAT can effectively minimize the missed detection of HBsAg methodology and reduce the risk of HBV transmission through blood. The re-entry of HBV DNA reactive blood donors should be treated with care.

This study aims to investigate the effect of ethoxysanguinarine(Eth) on cisplatin(DDP)-resistant human gastric cancer cells and decipher the underlying mechanism. The human gastric cancer cell line SGC7901 and the DDP-resistant cell line SGC7901/DDP were used as the cell models. Western blot was employed to determine the expression levels of multidrug resistance-related proteins, and methyl thiazolyl tetrazolium(MTT) assay to detect the proliferation of SGC7901 and SGC7901/DDP cells exposed to DDP. After treatment with different concentrations of Eth, the proliferation of SGC7901 and SGC7901/DDP cells was detected by MTT assay, trypan blue exclusion assay, colony formation assay, and high-content imaging and analysis system. The apoptosis of SGC7901/DDP cells was detected by flow cytometry with Annexin V-FITC/PI staining. GFP-LC3 transfection was carried out to detect the effect of Eth on the autophagy of SGC7901/DDP cells. The expression levels of the multidrug resistance-related protein P-glycoprotein(P-gp), the apoptosis-related proteins [caspase-9, caspase-3, and poly(ADP-ribose) polymerase(PARP)], the autophagy-related protein light chain 3-Ⅱ(LC3-Ⅱ), the key effectors [mammalian target of rapamycin(mTOR), 70 kDa ribosomal protein S6 kinase(P70 S6 K), and 4 E binding protein 1(4 E-BP1)] of the mammalian target of rapamycin complex 1(mTORC1) signaling pathway, cancerous inhibitor of protein phosphatase 2A(CIP2A), and protein kinase B(Akt) were measured by Western blot. The mRNA level of CIP2A in the SGC7901/DDP cells exposed to Eth for 24 h was analyzed by RT-qPCR. After SGC7901/DDP cells were transfected with CIP2A expression vector pcDNA3.1-HA-CIP2A and treated with different concentrations of Eth, MTT assay was used to determine the prolife-ration of SGC7901/DDP cells and Western blot to detect the expression levels of related proteins. The interaction sites of Eth and CIP2A were predicted by molecular docking. The affinity between Eth and CIP2A was determined by drug affinity responsive target stability(DARTS) assay. The pharmacokinetic properties and drug-like activity of Eth were predicted by SwissADME. The results indicated that SGC7901/DDP cells were more sensitive to Eth than SGC7901 cells. Eth significantly inhibited proliferation and colony formation and changed the morphology, roundness, and area of SGC7901/DDP cells. Eth treatment caused the nucleus shrinking and significantly increased the apoptosis rate of the cells. Furthermore, Eth down-regulated the expression of caspase-9 and caspase-3 precursors and promoted the cleavage of PARP, which suggested that Eth induced the apoptosis of SGC7901/DDP cells. The GFP-LC3 in Eth-treated cells showed speckled aggregation. The up-regulated expression of LC3-Ⅱ by Eth indicated that Eth activated the autophagy of SGC7901/DDP cells. Eth down-regulated the expression of P-gp, the phosphorylation of mTOR, P70 S6K, and 4E-BP1, the expression of CIP2A, and the phosphorylation of Akt. Additionally, it increased the activity of PP2A, and had no significant effect on the expression of CIP2A in SGC7901/DDP cells. CIP2A overexpression antagonized the inhibition of cell proliferation and the activation of autophagy by Eth. Molecular docking suggested that Eth bound to CIP2A. The results of DARTS assay further proved the above binding effect. Eth has potential drug-like activity. The above results demonstrated that Eth inhibited the proliferation, induced the apoptosis, and activated the autophagy of SGC7901/DDP cells by targeting CIP2A and then down-regulating PP2A/mTORC1 signaling pathway. This study provided a new target for the treatment of cisplatin-resistant gastric cancer.
Humans ; Cisplatin/therapeutic use* ; Caspase 9/metabolism* ; Proto-Oncogene Proteins c-akt/metabolism* ; Caspase 3/metabolism* ; Stomach Neoplasms/metabolism* ; Drug Resistance, Neoplasm ; Antineoplastic Agents/therapeutic use* ; Molecular Docking Simulation ; Poly(ADP-ribose) Polymerase Inhibitors/therapeutic use* ; Autophagy ; Apoptosis ; Cell Proliferation ; Apoptosis Regulatory Proteins/metabolism* ; Mechanistic Target of Rapamycin Complex 1/metabolism* ; Cell Line, Tumor