Causes and global, regional, and national burdens of traumatic brain injury from 1990 to 2019.

PURPOSE: Traumatic brain injury (TBI), currently a major global public health problem, imposes a significant economic burden on society and families. We aimed to quantify and predict the incidence and severity of TBI by analyzing its incidence, prevalence, and years lived with disability (YLDs). The epidemiological changes in TBI from 1990 to 2019 were described and updated to provide a reference for developing prevention, treatment, and incidence-reducing measures for TBI. METHODS: A secondary analysis was performed on the incidence, prevalence, and YLDs of TBI by sex, age group, and region (n = 21,204 countries and territories) between 1990 and 2019 using the Global Burden of Diseases, Injuries, and Risk Factors Study 2019. Proportions in the age-standardized incidence rate due to underlying causes of TBI and proportions of minor and moderate or severe TBI were also reported. RESULTS: In 2019, there were 27.16 million (95% uncertainty intervals (UI): 23.36 - 31.42) new cases of TBI worldwide, with age-standardized incidence and prevalence rates of 346 per 100,000 population (95% UI: 298-401) and 599 per 100,000 population (95% UI: 573-627), respectively. From 1990 to 2019, there were no significant trends in global age-standardized incidence (estimated annual percentage changes: -0.11%, 95% UI: -0.18% - -0.04%) or prevalence (estimated annual percentage changes: 0.01%, 95% UI: -0.04% - 0.06%). TBI caused 7.08 million (95% UI: 5.00 - 9.59) YLDs in 2019, with age-standardized rates of 86.5 per 100,000 population (95% UI: 61.1 - 117.2). In 2019, the countries with higher incidence rates were mainly distributed in Central Europe, Eastern Europe, and Australia. The 2019 global age-standardized incidence rate was higher in males than in females. The 2019 global incidence of moderate and severe TBI was 182.7 per 100,000 population, accounting for 52.8% of all TBI, with falls and road traffic injuries being the main causes in most regions. CONCLUSIONS: The incidence of moderate and severe TBI was slightly higher in 2019, and TBI still accounts for a significant portion of the global injury burden. The likelihood of moderate to severe TBI and the trend of major injury under each injury cause from 1990 to 2019 and the characteristics of injury mechanisms in each age group are presented, providing a basis for further research on injury causes in each age group and the future establishment of corresponding policies and protective measures.

Prognostic Prediction Value and Biological Functions of Non-Apoptotic Regulated Cell Death Genes in Lung Adenocarcinoma.

Objective To explore the potential biological functions and prognostic prediction values of non-apoptotic regulated cell death genes (NARCDs) in lung adenocarcinoma.Methods Transcriptome data of lung adenocarcinoma were downloaded from The Cancer Genome Atlas and Gene Expression Omnibus databases. We identified differentially expressed NARCDs between lung adenocarcinoma tissues and normal tissues with R software. NARCDs signature was constructed with univariate Cox regression analysis and the least absolute shrinkage and selection operator Cox regression. The prognostic predictive capacity of NARCDs signature was assessed by Kaplan-Meier survival curve, receiver operating characteristic curve, and univariate and multivariate Cox regression analyses. Functional enrichment of NARCDs signature was analyzed with gene set variation analysis, Gene Ontology, and Kyoto Encyclopedia of Genes and Genomes. In addition, differences in tumor mutational burden, tumor microenvironment, tumor immune dysfunction and exclusion score, and chemotherapeutic drug sensitivity were analyzed between the high and low NARCDs score groups. Finally, a protein-protein interaction network of NARCDs and immune-related genes was constructed by STRING and Cytoscape software. Results We identified 34 differentially expressed NARCDs associated with the prognosis, of which 16 genes (ATIC, AURKA, CA9, ITGB4, DDIT4, CDK5R1, CAV1, RRM2, GAPDH, SRXN1, NLRC4, GLS2, ADRB2, CX3CL1, GDF15, and ADRA1A) were selected to construct a NARCDs signature. NARCDs signature was identified as an independent prognostic factor (P < 0.001). Functional analysis showed that there were significant differences in mismatch repair, p53 signaling pathway, and cell cycle between the high NARCDs score group and low NARCDs score group (all P < 0.05). The NARCDs low score group had lower tumor mutational burden, higher immune score, higher tumor immune dysfunction and exclusion score, and lower drug sensitivity (all P < 0.05). In addition, the 10 hub genes (CXCL5, TLR4, JUN, IL6, CCL2, CXCL2, ILA, IFNG, IL33, and GAPDH) in protein-protein interaction network of NARCDs and immune-related genes were all immune-related genes. Conclusion The NARCDs prognostic signature based on the above 16 genes is an independent prognostic factor, which can effectively predict the clinical prognosis of patients of lung adenocarcinoma and provide help for clinical treatment.

The mechanism and progress of ferroptosis in pancreatic cancer.

Pancreatic cancer is one of the deadliest cancers in the world, causing hundreds of thousands of deaths worldwide annually. Because of late diagnosis, rapid metastasis and drug resistance to chemotherapy, pancreatic cancer has a poor prognosis. Although the treatment of pancreatic cancer has made tremendous progress, the options for effective treatment are still limited, and new treatment methods are in crying needs to improve prognosis in clinic. Ferroptosis is an iron-dependent non-apoptotic cell death mode, which is mediated by lipid peroxidation and iron accumulation. Ferroptosis plays a momentous role in regulating different cancers in recent years, such as breast cancer, hepatocellular carcinoma, lung cancer and pancreatic cancer. In this present review, we elaborate on the regulatory mechanisms and signaling pathways of ferroptosis in pancreatic cancer, with the intention of delivering directions and new ideas for the treatment of pancreatic cancer.

Changed epidemiology of anthrax and molecular characteristics of Bacillus anthracis in Inner Mongolia Autonomous Region, China.

Anthrax is a natural foci disease in Inner Mongolia, which poses a severe threat to public health. In this study, the incidence number, rate and constituent ratio were used to describe the epidemiological characteristics of anthrax in the region from 1956-2018. The molecular correlation and genetic characteristics of the strains were investigated using canonical single nucleotide polymorphisms (CanSNP), multiple-locus variable-number tandem repeat analysis (MLVA-15) and whole genome sequencing (WGS). The epidemiological characteristics of anthrax in Inner Mongolia have altered significantly. The incidence of anthrax has decreased annually without vaccination, and the regional distribution of anthrax gradually transferred from central and western regions to the eastern. Moreover, the occupation distribution evolved from multiple early occupations to predominated by farmers and herdsmen. This change is closely related to policy factors and to changes in the means of production and the living habits of the local population. This indicates that reformulating the control and prevention strategies is essential. Both A. Br. Ames and A. Br. 001/002 subgroups were the predominant CanSNP genotypes of Bacillus anthracis in Inner Mongolia. A total of 36 strains constituted six shared MLVA-15 genotypes, suggesting an epidemiological link between the strains of each shared genotype. The six shared genotypes ([GT1, 9, 11 and 15] and [GT8 and 12]) consisting of 2-7 strains confirmed the occurrence of multiple point outbreaks and cross-regional transmission caused by multiple common sources of infection. Phylogenetic analysis based on the WGS core genome showed that strains from this study formed an independent clade (C.V.), and they were positioned close to each other, suggesting a common origin. Further comparison analysis should be performed to ascertain the geographic origin of these strains.

Study on the mechanism of anti-MIRI action of total flavones of Fructus Chorspondiatis by PET/CT imaging.

BACKGROUND: To investigate anti myocardial ischemia/reperfusion injury (MIRI) action of total flavones of Fructus Chorspondiatis (TFFC) in rats by 13N-ammonia micro PET/CT imaging, etc. METHODS: Male Sprague-Dawley rats were randomly divided into 6 groups. Micro PET/CT imaging was performed before and after modeling to calculate the volume (VOI) and SUVmean of myocardial ischemic area. The oxidative stress index [(superoxide dismutase (SOD), malondialdehyde (MDA)] and the marker enzymes [creatine kinase (CK), lactate dehydrogenase (LDH)] of myocardial injury were detected. The pathological changes of myocardial were observed via HE staining. A MIRI model of rat cardiomyocytes in vitro was established, the damage and apoptosis of myocardial cells in each group were observed, and the apoptosis rate of cardiomyocytes was detected. RESULTS: The imaging viscosities of the imaging agents were observed at 24 and 48 h in each group. The VOI of 24 h imaging was (6.33±2.02), (6.01±1.56) and (3.32±0.86) mm3, respectively. The VOI of 48 h imaging was (3.31±1.33), (2.61±1.01) and (1.32±0.58) mm3. The 72 h imaging medium and high dose group recovered, while the low dose group still saw sparseness with (1.26±0.68) mm3 VOI. The ischemic (SUVmean) gradually increased with time. Metabolism gradually recovered (F=121.82, 450.82, 435.75, P<0.05). The three doses of TFFC can eliminate free radicals and reduce the damage of myocardial injury. Amongst them, the high-dose group had a better effect on SOD, and the middle-dose group had a better effect on MDA and LDH. The low-dose group affected CK, and a significant difference was observed compared with the control group (P<0.05). After administration, the morphology of myocardial cells in each dose group was improved to some extent. Nuclear pyknosis, rupture, the apoptosis rate, etc. were significantly reduced, the number of cells increased. The high dose group showed the most obvious improvement. CONCLUSIONS: The PET/CT imaging method can detect non-invasive, in vivo and dynamic MIRI, and can accurately evaluate the protective effect of traditional Mongolian medicine TFFC on MIRI. The Anti-MIRI of TFFC can scavenge free radicals, reduce oxidative stress damage, inhibit apoptosis, affect the activity of related enzymes.

The N-terminal polypeptide derived from vMIP-II exerts its antitumor activity in human breast cancer through CXCR4/miR-7-5p/Skp2 pathway.

Breast cancer is a malignant tumor with the highest incidence in women of the world. CXCR4 and Skp2 are highly expressed in breast cancer cells and CXCR4 was positively correlated with Skp2 by interference or overexpression. The microRNA array was used to detect the differentially expressed spectrum of micro RNAs in breast cancer cells the changes of miR-7-5p after CXCR4 inhibitor (NT21MP) treatment to block the CXCR4/SDF-1 pathway was founded. MiR-7-5p has been found to be correlated with Skp2 in various tumors in the literature, and Skp2 expression can be regulated by transfection with miR-7-5p mimics or inhibitors. The expression level of miR-7-5p was upregulated or downregulated after CXCR4 interference or overexpression. Combined with the correlation between CXCR4 and miR-7-5p in the chip results, CXCR4 may regulate Skp2 through miR-7-5p. Epithelial cells have the morphological characteristics of mesenchymal cells for some reason called epithelial-mesenchymal transformation (EMT). Transfection of miR-7-5p mimics into drug-resistant cells reduced Skp2 levels, decreased the expression of Vimentin, Snail, and slug, and increased the expression of E-cadherin. CXCR4 inhibitor (NT21MP) can reverse the EMT changes caused by miR-7-5p inhibitor. Similarly, in vivo results suggesting that CXCR4 inhibitors can reverse the EMT phenotype of drug-resistant breast cancer cells through the CXCR4/miR-7-5p/Skp2 pathway. In summary, the CXCR4/miR-7-5p/Skp2 signaling pathway plays an important role in the progression of breast cancer. This study provides a theoretical basis for the treatment of breast cancer by targeting the CXCR4 pathway.

Long noncoding RNA H19 acts as a miR-340-3p sponge to promote epithelial-mesenchymal transition by regulating YWHAZ expression in paclitaxel-resistant breast cancer cells.

Breast cancer (BC) is the leading cause of cancer-related death in women worldwide and one of the most prevalent malignancy. In recent years, increasing evidence had illuminated that long noncoding RNAs (lncRNAs) serve as critical factors in multiple tumor progression, including BC. Emerging references had indicated that the lncRNA H19 acts as significant roles in tumor progression and epithelial-mesenchymal transition (EMT). However, the underlying molecular mechanisms and biological roles of H19 in BC invasion, metastasis and EMT are still unclear. In this study, it was detected that the expression level of H19 was increased in BC paclitaxel-resistant (PR) cells subline (MCF-7/PR) in comparison with MCF-7 parental cells. In vitro, there were demonstrated that H19 overexpression promoted BC cells proliferation, metastasis, invasion and EMT procedures, and suppressed cells apoptosis. Whereas, H19 suppression resulted in the contrary biological effects. Besides, bioinformatics tools and dual-luciferase reporters assays indicated that miR-340-3p could act as a potential target gene of H19, the underlying mechanism studies proved that H19 could act as a competing endogenous RNA (ceRNA) via competitively binding miR-340-3p to promote BC cell proliferation, metastasis and EMT by regulating tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein zeta (YWHAZ) and potentiate the Wnt/ß-catenin signaling in BC cells. In summary, our findings demonstrated that H19 could act as a ceRNA in BC progression, metastasis and EMT through modulating miR-340-3p/YWHAZ axis and activating the canonical Wnt/ß-catenin signaling pathway, indicating that H19 might act as an underlying therapeutic target and prognostic biomarker for BC therapy.

Spatiotemporal analysis of hand, foot and mouth disease data using time-lag geographically-weighted regression.

Hand, Foot, and Mouth Disease (HFMD) is a common and widespread infectious disease. Previous studies have presented evidence that climate factors, including the monthly averages of temperature, relative humidity, air pressure, wind speed and Cumulative Risk (CR) all have a strong influence on the transmission of HFMD. In this paper, the monthly time-lag geographically- weighted regression model was constructed to investigate the spatiotemporal variations of effect of climate factors on HFMD occurrence in Inner Mongolia Autonomous Region, China. From the spatial and temporal perspectives, the spatial and temporal variations of effect of climate factors on HFMD incidence are described respectively. The results indicate that the effect of climate factors on HFMD incidence shows very different spatial patterns and time trends. The findings may provide not only an indepth understanding of spatiotemporal variation patterns of the effect of climate factors on HFMD occurrence, but also provide helpful evidence for making measures of HFMD prevention and control and implementing appropriate public health interventions at the county level in different seasons.

Long noncoding RNA AC073284.4 suppresses epithelial-mesenchymal transition by sponging miR-18b-5p in paclitaxel-resistant breast cancer cells.

Breast cancer (BC) is the most prevalent malignant cancer in the world, is the leading cause of cancer-related death female. Recently, there is accumulating evidence that long noncoding RNAs (lncRNAs) might as an important role in the progression of BC. (epithelial-mesenchymal transition (EMT) is considered to play a vital role in tumor cells migration and invasion. Nevertheless, the entire biological mechanisms and functions of lncRNAs in tumor migration, invasion, and EMT remain uncertain. In the present research, we observed that the expression of lncRNA AC073284.4 was downregulated in BC paclitaxel-resistant (PR) cells (MCF-7/PR) and tissues. Bioinformatics analysis predicted that miR-18b-5p was a direct target of AC073284.4, which has been validated by dual-luciferase reporter gene assay. We further proved that AC073284.4 could directly bind to miR-18b-5p and relieve the suppression for dedicator of cytokinesis protein 4 (DOCK4). Furthermore, the underlying functional experiments demonstrated that AC073284.4 might sponge miR-18b-5p to attenuate the invasion, metastasis, and EMT of BC cell through upregulating DOCK4 expression. In summary, AC073284.4 might serve as a competing endogenous RNA (ceRNA) in BC progression via modulating miR-18b-5p/DOCK4 axis, which weakens EMT and migration of BC. These results suggesting that AC073284.4 might function as a potential novel diagnostic biomarker in the progression of BC.

The N-terminal polypeptide derived from viral macrophage inflammatory protein II reverses breast cancer epithelial-to-mesenchymal transition via a PDGFRα-dependent mechanism.

NT21MP, a 21-residue peptide derived from the viral macrophage inflammatory protein II, competed effectively with the natural ligand of CXC chemokine receptor 4 (CXCR4), stromal cell-derived factor 1-alpha, to induce apoptosis and inhibit growth in breast cancer. Its role in tumor epithelial-to-mesenchymal transition (EMT) regulation remains unknown. In this study, we evaluated the reversal of EMT upon NT21MP treatment and examined its role in the inhibition of EMT in breast cancer. The parental cells of breast cancer (SKBR-3 and MCF-7) and paclitaxel-resistant (SKBR-3 PR and MCF-7 PR) cells were studied in vitro and in combined immunodeficient mice. The mice injected with SKBR-3 PR cells were treated with NT21MP through the tail vein or intraperitoneally with paclitaxel or saline. Sections from tumors were evaluated for tumor weight and EMT markers based on Western blot. In vitro, the effects of NT21MP, CXCR4 and PDGFRα on tumor EMT were assessed by relative quantitative real-time reverse transcription-polymerase chain reaction, western blot and biological activity in breast cancer cell lines expressing high or low levels of CXCR4. Our results illustrated that NT21MP could reverse the phenotype of EMT in paclitaxel-resistant cells. Furthermore, we found that NT21MP governed PR-mediated EMT partly due to controlling platelet-derived growth factors A and B (PDGFA and PDGFB) and their receptor (PDGFRα). More importantly, NT21MP down-regulated AKT and ERK1/2 activity, which were activated by PDGFRα, and eventually reversed the EMT. Together, these results indicated that CXCR4 overexpression drives acquired paclitaxel resistance, partly by activating the PDGFA and PDGFB/PDGFRα autocrine signaling loops that activate AKT and ERK1/2. Inhibition of the oncogenic EMT process by targeting CXCR4/PDGFRα-mediated pathways using NT21MP may provide a novel therapeutic approach towards breast cancer.

[Effects of sewage sludge compost on the growth and element uptake of Neolamarckia cadamba seedlings]. / æ±¡æ³¥å †è‚¥å¯¹é»„æ¢æœ¨å¹¼è‹—ç”Ÿé•¿å’Œå ƒç´ å¸æ”¶çš„å½±å“.

Sewage sludge compost (SSC) is rich in organic matter and nutrient elements indispensable to plant growth. Utilizing SSC as seedling growing substrate is generally recognized as a new ecological method for utilization of sewage sludge. We investigated impacts of SSC treatments including 0% (CK), 25% (T1), 50% (T2), 75% (T3), and 100% (T4) on the growth and nutrient uptake of Neolamarckia cadamba seedlings in a 7-month pot experiment. The changes in element contents in substrate after pot experiment were also addressed. Results showed the SSC treatments had significant impacts on the growth of N. cadamba seedlings. The seedlings in T4 treatment grew abnormally and all died in two weeks after transplanting. Seedling height, ground diameter and biomass in T1, T2 and T3 treatments were significantly higher than CK, with those in T2 being the best among all treatments. Seedlings in T2 and T3 treatments took up significantly more N, P, K, Cu, Zn, Pb and Cd, while those in T1 treatment absorbed significantly more N and Pb than CK. The heavy metal uptake amount of each treatment exhibited the order of Zn＞Cu＞Pb＞Cd. At the end of the pot experiment, the contents of organic matter, N, P and K in growing substrate were still relatively high, and a certain portion of heavy metals still remained in the substrate, but with lower contents than the standards set for agricultural usage-oriented sewage sludge, indicating that the post-experiment substrate may be reused.

Clearance of serum solutes by hemofiltration in dogs with severe heat stroke.

BACKGROUND: We have previously reported that hemofiltration (HF) may be an effective additional means of treating heat stroke when rapid cooling is not effective. METHODS: Dogs were assigned to a heat stroke (control) or heat stroke + hemofiltration (HF) group (n = 8 each group). After heat stroke induction, dogs in the HF group received HF for 3 h. Serum concentrations of interleukin (IL)-10, tumor necrosis factor (TNF)-α, IL-6, blood urea nitrogen (BUN) and creatinine were measured at baseline and 1, 2, and 3 h after heat stroke. Clearance rates of solutes were determined 1, 2, and 3 h after the start of HF. RESULTS: Serum concentrations of all solutes tended to increase with time after heat stroke in the control group, but decreased (BUN, creatinine) or remained relatively unchanged (TNF-α, IL-6, IL-10) with time in the HF group. Concentrations of all solutes were significantly lower in the HF group compared with the control group at 2 and 3 h (P < 0.05). Clearance rates for small molecular weight solutes were high, while those for larger molecular weight solutes were low. CONCLUSION: HF prevents heat stroke-induced increases in serum cytokine concentrations and is effective for clearing small molecular weight solutes from serum, but less effective for clearing larger molecular weight solutes, including TNF-α, IL-6, and IL-10.

Colorectal cancer mortality in Inner Mongolia between 2008 and 2012.

AIM: To determine the extent of colorectal cancer (CRC) mortality and the association between demographic characteristics and CRC mortality in Inner Mongolia. METHODS: Data were collected from the Death Registry System, maintained by the Inner Mongolia Centers for Disease Control and Prevention, from 2008 to 2012. Deaths were classified according to the International Classification of Disease, 10(th) Revision. Years of life lost, average years of life lost (AYLL), and mortality were calculated over the five years between 2008 and 2012. A conditional logistic regression model was used to analyze the association between marital status, occupational status, education level, area of residence, and the risk of CRC. RESULTS: The AYLL of CRC was 17.39 years. The average mortality of CRC was 5.6/100000. People living in urban areas and having a higher education level had a significantly higher risk of CRC (OR = 1.74 and 95%CI: 1.29-2.35, P < 0.001 and OR = 2.39, 95%CI: 1.76-3.25, P < 0.001, respectively). People who were employed had a lower risk of CRC (OR = 0.64, 95%CI: 0.48-0.86, P = 0.003). The mortality of CRC was positively correlated with the education level (P < 0.001). No statistically significant association was observed between marital status and CRC risk (P = 0.259). CONCLUSION: Living in urban areas, higher education level and unemployment are associated with CRC mortality in Inner Mongolia.

[The pathogenic spectrum of hand, foot and mouth disease and molecular characterizations of human enterovirus 71 in Inner Mongolia autonomous region in 2010].

To study the pathogenic spectrum of hand, foot and mouth disease (HFMD) and the molecular characterizations of human enteroviruses 71 (HEV71) isolated from the clinical specimens of HFMD patients in Inner Mongolia in 2010. A total of 921 clinical specimens including stools and throat swabs were collected from HFMD patients in outpatient service in Inner Mongolia and then viral isolation was performed, the positive viral isolates were identified by using the real-time PCR method (detecting EV, HEV71 and CVA16 in a single tube), and VP4 and VP1 coding region amplification and sequencing was performed with the viral isolates that were identified as non-HEV71, non-CVA16 HEVs. A total of 153 viruses were isolated form 921 clinical specimens, the positive rate was 16.61%, of which 61 (39.87%) were HEV71, 82 (53.59%) were CVA16, 7 (6.53%) were other HEVs(6 were CVB4 and 1 was polio vaccine virus type II) and 3 (1.96%) were adenoviruses. Nine viruses were isolated from severe cases, of which 6 were HEV71 and 3 were CVA16. Thirty two HEV71 isolates were selected from the patients presenting mild symptoms and the patients presenting severe symptoms randomly, and the VP1 coding regions of represented HEV71 isolates were amplified and sequenced. Finally the phylogenetic tree was constructed among the VP1 coding regions of the different genotypes and subgenotypes of HEV71 strains. The nucleotide acid and amino acid of 32 represented HEV71 strains in Inner Mongolia were closed to HEV71 strains isolated from mainland China since 2007, especially from Beijing in 2008, and it showed that all HEV71 strains clustered within the C4a evolution branch of C4 subgenotype. There was slight difference in the nucleotide and the amino acid sequence in VP1 region among the 32 Inner Mongolia HEV71 strains, the identity were 96.4%-100% and 98.14%-100%, respectively, and there was a little difference in the nucleotide acid sequence between the HEV71 strains from Inner Mongolia in 2010 and in 2007, the identity was from 96.95% to 97.87%. Thirty two HEV71 strains were in different lineages in the phylogenetic tree, and it indicated that these strains belonged to many different viral transmission chains. HEV71 and CVA16 were the main pathogens of HFMD in Inner Mongolia in 2010 and most severe cases were caused by HEV71. All the HEV71 strains circulated in Inner Mongolia belonged to C4a evolution branch within C4 subgenotype. Phylogenetic analysis revealed that 2010 Inner Mongolia HEV71 strains were located in different lineages, and had more nucleotide identity with 2008 Beijing HEV71 strains than with 2007 Inner Mongolia HEV71 strains. This indicated that Inner Mongolia HEV71 strains had not evolved independently, but co-evolved with the HEV71 strains in other provinces in mainland China.

[B1a and b1b evolutionary branch of coxsackie virus A16 co-prevailed in Inner Mongolia Autonomous Region].

To study on the molecular evolution of Coxsackie virus A16 (CVA16)isolated from clinical speci-mens of Hand, foot and mouth Disease( HFMD) patients in Inner Mongolia in 2010. A total of 921 clinical specimens including stools, throat swabs and vesicle fluids were collected from 888 HFMD patients in out-patient service in Inner Mongolia and viral isolation was then performed, the positive viral isolates were identified by using the real-time PCR method detecting CVA16. A total of 50 CVA16 isolates were selected from the patients presenting mild symptoms, severe symptoms and the death patients randomly, and the VP1 coding regions of representative CVA16 isolates were amplified and sequenced. Finally the phylogenetic tree was constructed among the VP1 coding regions of the different genotypes and subgenotypes of CVA16 strains. Eighty two viruses were isolated form 921 clinical specimens, the positive rate was 8. 90%, of which 3 viruses were isolated from severe cases and 1 viruses was from death cases. The nucleotide acid of 50 representative CVA16 strains in Inner Mongolia were closed to CVA16 strains isolated from mainland China since 1998, especially from Beijing in 2009 and from Henan in 2010, the identity were 96. 18% approximately 98. 88% and 94. 94a approximately 98. 76%, respectively. There was a little difference in the nucleotide acid between the CVA16 strains from Inner Mongolia in 2010 and in 2007, the identity were 91. 68% approximately 96. 52% The phylogenetic tree showed that all CVA16 strains clustered within Bla and B1b evolution branch of B1 genotype. There was slight difference in the nucleotide and the amino acid in VP1 region among the 50 Inner Mongolia CVA16 strains, the identity were 89. 99% approximately 100% and 98. 31% approximately 100%, respectively, indicating that these strains belonged to many different viral transmission chains. The CVA16 strains circulated in Inner Mongolia in 2010 were all belong to B1a and B1b evolution branch of B1 genotype, and the two evolutionary branchs of Coxsackie virus A16 were co-evolved and co-prevailed in Inner Mongolia Autonomous Region.

One-step bulk preparation of calcium carbonate nanotubes and its application in anticancer drug delivery.

Bulk fabrication of ordered hollow structural particles (HSPs) with large surface area and high biocompatibility simultaneously is critical for the practical application of HSPs in biosensing and drug delivery. In this article, we describe a smart approach for batch synthesis of calcium carbonate nanotubes (CCNTs) based on supported liquid membrane (SLM) with large surface area, excellent structural stability, prominent biocompatibility, and acid degradability. The products were characterized by transmission electron micrograph, X-ray diffraction, Fourier transform infrared spectra, UV-vis spectroscopy, zeta potential, and particle size distribution. The results showed that the tube-like structure facilitated podophyllotoxin (PPT) diffusion into the cavity of hollow structure, and the drug loading and encapsulation efficiency of CCNTs for PPT are as high as 38.5 and 64.4 wt.%, respectively. In vitro drug release study showed that PPT was released from the CCNTs in a pH-controlled and time-dependent manner. The treatment of HEK 293T and SGC 7901 cells demonstrated that PPT-loaded CCNTs were less toxic to normal cells and more effective in antitumor potency compared with free drugs. In addition, PPT-loaded CCNTs also enhanced the apoptotic process on tumor cells compared with the free drugs. This study not only provides a new kind of biocompatible and pH-sensitive nanomaterial as the feasible drug container and carrier but more importantly establishes a facile approach to synthesize novel hollow structural particles on a large scale based on SLM technology.

Effects of continuous haemofiltration on serum enzyme concentrations, endotoxemia, homeostasis and survival in dogs with severe heat stroke.

AIM: To examine the effectiveness of continuous haemofiltration as a treatment for severe heat stroke in dogs. METHODS: Dogs were randomly allocated to a control or continuous haemofiltration group (both n=8). Heat stroke was induced by placing anaesthetised dogs in a high temperature cabin simulator. Upon confirmation of heat stroke (rectal temperature>42 °C, mean arterial pressure (MAP) decrease>25 mmHg), dogs were removed from the chamber and continuous haemofiltration was initiated and continued for 3h for dogs in the continuous haemofiltration group. Dogs in the control group were observed at room temperature. RESULTS: Rectal temperature, haemodynamics, pH, blood gases and electrolyte concentrations rapidly returned to baseline in the continuous haemofiltration group, but not the control group. After 3h, rectal temperature was 36.68±0.51 °C in the continuous haemofiltration group and 39.83±1.10 °C in the control group (P<0.05). Continuous haemofiltration prevented endotoxin and all serum enzyme concentrations from increasing and caused malondialdehyde concentrations to decrease. After 3h, endotoxin concentrations were 0.14±0.02 EU ml(-1) in the continuous haemofiltration group and 0.23±0.05 EU ml(-1) in the control group (P=0.003), while malondialdehyde concentrations were 4.86±0.61 mmol l(-1) in the continuous haemofiltration group and 8.63±0.66 mmol l(-1) in the control group (P<0.001). Five dogs died in the control group within 3h, whereas no dogs died in the continuous haemofiltration group. CONCLUSIONS: Continuous haemofiltration rapidly reduced body temperature, normalised haemodynamics and electrolytes, improved serum enzyme concentrations and increased survival in dogs with heat stroke. Continuous haemofiltration may be an effective treatment for heat stroke.

Mesoporous biocompatible and acid-degradable magnetic colloidal nanocrystal clusters with sustainable stability and high hydrophobic drug loading capacity.

Fabrication of magnetic particles (MPs) with high magnetization and large surface area simultaneously is critical for the application of MPs in bioseparation and drug delivery but remains a challenge. In this article, we describe an unprecedented approach to synthesize mesoporous magnetic colloidal nanocrystal clusters (MCNCs) stabilized by poly(γ-glutamic acid) (PGA) with high magnetization, large surface area (136 m(2)/g) and pore volume (0.57 cm(3)/g), excellent colloidal stability, prominent biocompatibility, and acid degradability. This result provides the important step toward the construction of a new family of MCNCs and demonstrates its capacity in a "magnetic motor" drug delivery system. Here, as an example, we explore the applicability of as-prepared mesoporous MCNCs as hydrophobic drug delivery vehicles (paclitaxel as model drug), and the resultant loading capacity is as high as 35.0 wt %. The antitumor efficacy measured by MTT assay is significantly enhanced, compared with free drugs. Thus, combined with their inherent high magnetization, the mesoporous MCNCs pave the way for applying magnetic targeting drug carriers in antitumor therapeutics.

The electrostatic interactions between nano-TiO(2) and trypsin inhibit the enzyme activity and change the secondary structure of trypsin.

In this work, the interaction between nano-TiO(2) and trypsin was investigated, and the mechanisms of the interaction were explored by the methods of UV-vis detection, circular dichroism (CD), and fluorescence. The results clearly demonstrated that nano-TiO(2) had an inhibitory effect on the enzyme activity. The activity was decreased to 64% of the untreated trypsin in the presence of 300 µg/ml nano-TiO(2). UV spectrometry proved that nano-TiO(2) had a strong physical absorption effect on trypsin, and the CD spectra revealed that the secondary structure of trypsin was partly destroyed while bound together with nano-TiO(2). The ratio of α-helix increased from 7.9% to 12.8% in the presence of 100 µg/ml TiO(2) while the ratio of ß-sheet decreased from 48.7% to 36.4%. Furthermore, the fluorescence spectrometry indicated that nano-TiO(2) could quench the intrinsic fluorescence of trypsin through static quenching. Meanwhile, the binding constant was calculated to be 1, and the process of binding of trypsin on nano-TiO(2) was a spontaneous molecular interaction procedure in which electrostatic interaction plays a major role. Our study was to provide a useful approach for evaluating the health risk of nanomaterials on level of proteins.