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1.
PLoS One ; 14(10): e0222777, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31584956

RESUMO

BACKGROUND: Previous studies have documented that disordered eating is associated with a wide range of impaired physical and mental health conditions among children and adolescents. The relationship between disordered eating and health-related quality of life (HRQOL) has been predominantly examined in children and adolescents who are overweight or obese or suffer from chronic illnesses. In the last decade, several studies have been conducted to investigate the relationship between disordered eating and HRQOL among school and community children and adolescents. No systematic review or meta-analysis has synthesized the findings from these population-based studies. The purpose of this systematic review and meta-analysis was to synthesize the relationship between disordered eating and HRQOL among the general population of children and adolescents. METHODS: We performed a computer search for the English language literature using the databases PUBMED, EMBASE and PSYCINFO to retrieve eligible studies published between 1946 and August 9, 2018. We also searched the relevant articles using PubMed related article search features and manually examined the reference lists of the retrieved full text articles selected from the database search. The association between disordered eating and HRQOL was synthesized using both a qualitative method and a meta-analysis. The review was conducted adhering to the Preferred Reporting Items for Systematic reviews and Meta-Analyses (PRISMA) guidelines. RESULTS: We identified eight studies that met the inclusion criteria and were included in the final synthesis. The studies included six cross-sectional studies and two longitudinal studies. The systematic review found that disordered eating attitudes and behaviors were associated with lower HRQOL among children and adolescents. Children and adolescents with bulimia nervosa (BN), binge eating disorder (BED), purging disorder (PD) and other eating disorder symptoms had poorer HRQOL than their healthy peers without the eating disorder conditions. The meta-analysis using four out of the eight studies showed that disordered eating was significantly associated with poor psychosocial health and lower overall HRQOL among children and adolescents. CONCLUSION: The present review reveals that disordered eating behaviors and eating disorders are associated with decreased HRQOL in children and adolescents. More prospective studies are needed to ascertain the directions in the relationship between disordered eating and HRQOL among children and adolescents. The findings of this review suggest that health programs for promoting healthy eating and reducing disordered eating behaviors among school children and adolescents may help to enhance the HRQOL and overall health status of these individuals.

2.
EBioMedicine ; 48: 203-211, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31629678

RESUMO

BACKGROUND: We previously conducted a systematic field synopsis of 1059 breast cancer candidate gene studies and investigated 279 genetic variants, 51 of which showed associations. The major limitation of this work was the small sample size, even pooling data from all 1059 studies. Thereafter, genome-wide association studies (GWAS) have accumulated data for hundreds of thousands of subjects. It's necessary to re-evaluate these variants in large GWAS datasets. METHODS: Of these 279 variants, data were obtained for 228 from GWAS conducted within the Asian Breast Cancer Consortium (24,206 cases and 24,775 controls) and the Breast Cancer Association Consortium (122,977 cases and 105,974 controls of European ancestry). Meta-analyses were conducted to combine the results from these two datasets. FINDINGS: Of those 228 variants, an association was observed for 12 variants in 10 genes at a Bonferroni-corrected threshold of P < 2·19 × 10-4. The associations for four variants reached P < 5 × 10-8 and have been reported by previous GWAS, including rs6435074 and rs6723097 (CASP8), rs17879961 (CHEK2) and rs2853669 (TERT). The remaining eight variants were rs676387 (HSD17B1), rs762551 (CYP1A2), rs1045485 (CASP8), rs9340799 (ESR1), rs7931342 (CHR11), rs1050450 (GPX1), rs13010627 (CASP10) and rs9344 (CCND1). Further investigating these 10 genes identified associations for two additional variants at P < 5 × 10-8, including rs4793090 (near HSD17B1), and rs9210 (near CYP1A2), which have not been identified by previous GWAS. INTERPRETATION: Though most candidate gene variants were not associated with breast cancer risk, we found 14 variants showing an association. Our findings warrant further functional investigation of these variants. FUND: National Institutes of Health.

3.
Artigo em Inglês | MEDLINE | ID: mdl-31642792

RESUMO

BACKGROUND: Laryngeal Squamous Cell Carcinoma (LSCC) is a malignant epithelial tumor with poor prognosis and its incidence rate increases recently. rLj-RGD3, a recombinant protein cloned from the buccal gland of Lampetra japonica, contains three RGD motifs which could bind to integrins on the tumor cells. METHODS: MTT assay was used to detect the inhibitory rate of viability. Giemsa's staining assay was used to observe the morphological changes of cells. Hoechst 33258 and TUNEL staining assay, DNA ladder assay were used to examine the apoptotic. Western blot assay was applied to detect the change of integrin signal pathway. Wound-healing assay, migration and invasion assay were used to detect the mobility of Hep2 cells. H&E staining assay was used to show the arrangement of the Hep2 cells in the solid tumor tissues. RESULTS: In the present study, rLj-RGD3 was shown to inhibit the viability of LSCC Hep2 cells in vitro by inducing apoptosis with an IC50 of 1.23µM. Western blot showed the apoptosis of Hep2 cells induced by rLj-RGD3 was depend on integrin-FAK-Akt pathway. Wound healing, transwells, and western blot assays in vitro showed rLj-RGD3 suppressed the migration and invasion of Hep2 cells by integrin-FAK-paxillin/PLC pathway which could also affect the cytoskeleton arrangement in Hep2 cells. In vivo studies, rLj-RGD3 inhibited the growth, tumor volume and weight, as well as disturbed the tissue structure of the solid tumors in xenograft models of BALB/c nude mice without reducing their body weights. CONCLUSION: These results suggested that rLj-RGD3 is an effective and safe suppressor on the growth and metastasis of LSCC Hep2 cells from both in vitro and in vivo experiments, rLj-RGD3 might be expected to become a novel anti-tumor drug to treat LSCC patients in the near future.

4.
JAMA Oncol ; 2019 Sep 19.
Artigo em Inglês | MEDLINE | ID: mdl-31536134

RESUMO

Importance: Survival differences between male and female patients with breast cancer have been reported, but the underlying factors associated with the disparity have not been fully studied. This understanding is fundamental to developing strategies for cancer treatment and survivorship care. Objective: To compare mortality between male and female patients with breast cancer and quantitatively evaluate the factors associated with sex-based disparity in mortality. Design, Setting, and Participants: This large, nationwide, registry-based cohort study used the National Cancer Database to identify and obtain data on patients who received a breast cancer diagnosis between January 1, 2004, and December 31, 2014. After exclusions, the final study population comprised 1 816 733 patients. Statistical analyses were conducted from September 1, 2018, to January 15, 2019. Main Outcomes and Measures: The primary outcome was overall survival. Secondary outcomes were 3-year and 5-year mortality. Mortality differences were evaluated by Kaplan-Meier analysis. The roles of race/ethnicity, clinical characteristics, treatments, and access-to-care factors in the association between sex and mortality were estimated by nested Cox proportional hazards regression models with adjustment for age. Results: In total, 16 025 male (mean [SD] age, 63.3 [13.0] years) and 1 800 708 female (mean [SD] age, 59.9 [13.3] years) patients with breast cancer were included in the study. Compared with female patients, male patients had higher mortality across all stages. For men, the overall survival rate was 45.8% (95% CI, 49.5-54.0; P < .001), the 3-year rate was 86.4% (95% CI, 85.9-87.0; P < .001), and the 5-year rate was 77.6% (95% CI, 76.8-78.3; P < .001). For women, the overall survival rate was 60.4% (95% CI, 58.7-62.0; P < .001), the 3-year rate was 91.7% (95% CI, 91.7-91.8; P < .001), and the 5-year rate was 86.4% (95% CI, 86.4-86.5; P < .001). Overall, clinical characteristics and undertreatments were associated with a 63.3% excess mortality rate for male patients. A higher proportion of excess deaths in men were explained by these factors in the first 3 years after breast cancer diagnosis (66.0%) and in all patients with early-stage cancer (30.5% for stage I and 13.6% for stage II). However, sex remained a significant factor associated with overall mortality (adjusted hazard ratio [HR], 1.19; 95% CI, 1.16-1.23) as well as mortality at 3-year (adjusted HR, 1.15; 95% CI, 1.10-1.21) and 5-year (adjusted HR, 1.19; 95% CI, 1.14-1.23) analyses, even after adjustment for clinical characteristics, treatment factors, age, race/ethnicity, and access to care. Conclusions and Relevance: This study found that mortality after cancer diagnosis was higher among male patients with breast cancer compared with their female counterparts. Such disparity appeared to persist after accounting for clinical characteristics, treatment factors, and access to care, suggesting that other factors (particularly additional biological attributes, treatment compliance, and lifestyle factors) should be identified to help in eliminating this disparity.

5.
Food Chem Toxicol ; 134: 110831, 2019 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-31545996

RESUMO

Bee pollens constitute a large number of flavonoids and thus possess great medicinal value. However different varieties of bee pollen flavonoids vary with different species and their content also differ greatly in different region. Herein, the aim of present research is to establish a method based on high performance liquid chromatography (HPLC) for quantitative analysis of flavonoids compounds and chemical fingerprint analysis of bee pollen. Five batches of rape bee pollen collected from different region of China and particularly six bee pollen species obtained in Anhui were used to establish the fingerprint. The feasibility and advantages of the used HPLC fingerprint were verified for its similarity evaluation by systematically comparing chromatograms with professional analytical software. The similarities of liquid chromatography fingerprints for five batches of rape bee pollen were more than 0.994 while six batches of different species of bee pollen were lower than 0.810. In quantitative analysis, the six compounds showed good regression (R ≥ 0.9964) within the test ranges, and all the values for the RSD were lower than 2%. The developed HPLC fingerprint method was found simple, reliable, and it was validated for the quality control and identification of bee pollen. Additionally, simultaneous quantification of six flavonoids ingredients in the bee pollen samples was conducted to reveal the variation in their content. The results indicated that the HPLC fingerprint, as a characteristic distinguishing method combining similarity evaluation and quantification analysis, can be successfully used to assess the quality and also to identify the authenticity of bee pollen.

6.
Toxicol Appl Pharmacol ; 381: 114729, 2019 Oct 15.
Artigo em Inglês | MEDLINE | ID: mdl-31445927

RESUMO

The PI3K/AKT signaling pathway is one of the most frequently activated signaling networks in human cancers and has become a valuable target in anticancer therapy. However, accumulating reports suggest that adverse effects such as severe liver injury and inflammation may accompany treatment with pan-PI3K and pan-AKT inhibitors. Our prior work has demonstrated that activation of the PI3K/AKT pathway has a protective role in Fas- or TNFα-induced hepatocytic cell death and liver injury. We postulated that PI3K or AKT inhibitors may exacerbate liver damage via the death factor-mediated hepatocyte apoptosis. In this study we found that several drugs targeting PI3K/AKT either clinically used or in clinical trials sensitized hepatocytes to agonistic anti-Fas antibody- or TNFα-induced apoptosis and significantly shortened the survival of mice in in vivo liver damage models. The PI3K or AKT inhibitors promoted Fas aggregation, inhibited the expression of cellular FLICE-inhibitory protein S and L (FLIPL/S), and enhanced procaspase-8 activation. Conversely, cotreatment with the AKT specific activator SC79 reversed these effects. Taken together, these findings suggest that PI3K or AKT inhibitors may render hepatocytes hypersensitive to Fas- or TNFα-induced apoptosis and liver injury.

7.
J Surg Res ; 245: 265-272, 2019 Aug 14.
Artigo em Inglês | MEDLINE | ID: mdl-31421372

RESUMO

BACKGROUND: Although insurance and race-based survival disparities in colon cancer are well studied, little is known regarding how these survival disparities are impacted by type of treating facility. MATERIALS AND METHODS: This is a retrospective cohort study of 433,997 patients diagnosed with colon adenocarcinoma using the National Cancer Database (NCDB). Using Cox proportional hazard analyses, we assessed overall survival (OS) as a function of race, insurance status, and treating facility, after adjusting for demographic and clinical factors. We also assessed differences in OS according to race and insurance status stratified by treating facility type. RESULTS: OS was significantly diminished for blacks (hazard ratio [HR], 1.09; 95% confidence interval [CI], 1.07-1.10; P < 0.001) and increased for patients of other race (primarily Asians; HR, 0.76; 95% CI, 0.74-0.78) compared with whites. Patients with private insurance had improved OS compared with uninsured (HR, 1.28; 95% CI, 1.25-1.31; P < 0.001), Medicaid (HR, 1.35; 95% CI, 1.33-1.38; P < 0.001) and Medicare (HR, 1.13, 95% CI, 1.12-1.15; P < 0.001) patients. Compared with patients treated at comprehensive community programs, patients treated at academic centers (ACs) had improved OS (HR, 0.86; 95% CI, 0.85-0.88; P < 0.001). When stratified by type of treating facility, racial disparities were not mitigated for patients treated at ACs compared with other facilities (P = 0.266 for interaction). At ACs, patients with Medicaid had persistent OS disparities compared with patients with private insurance (HR, 1.12; 95% CI, 1.09-1.15; P < 0.001), although these disparities were significantly diminished compared with patients treated at other facilities (HR, 1.41; 95% CI, 1.38-1.45; P < 0.001). CONCLUSIONS: Other race, private insurance, and treatment at AC were independently associated with improved OS in patients with colon cancer. Medicaid-based, but not race-based, survival disparities are reduced at ACs compared with other facilities.

8.
J Urol ; 202(6): 1217-1223, 2019 12.
Artigo em Inglês | MEDLINE | ID: mdl-31430246

RESUMO

PURPOSE: High animal protein intake is a risk factor for nephrolithiasis. Whether plant based sources of protein are associated with kidney stone risk is not well studied. We examined the association of animal and plant protein intake with the risk of incident kidney stones in Shanghai, China. MATERIALS AND METHODS: Dietary intakes were obtained from a validated food frequency questionnaire at baseline. Self-reported stone events were ascertained at baseline and at followup visits. Multivariable Cox regression models were used to evaluate the associations of protein intake with the incident stone risk. RESULTS: During 319,211 and 696,950 person-years of followup 1,451 men and 1,202 women, respectively, reported incident stones. The average ± SD intake of animal and plant protein standardized to 2,000 kcal was 31.3 ± 13.7 and 48.4 ± 7.2 gm per day in women, and 30.8 ± 13.3 and 51.3 ± 7.6 gm per day, respectively, in men. On multivariable analysis participants in the highest quintiles of animal and nondairy animal protein intake showed an increased risk of incident stones compared to those in the lowest quintiles (HR 1.16, 95% CI 1.01-1.32, p=0.03 vs HR 1.14, 95% CI 1.01-1.30, p=0.04). Compared to the lowest quintile the highest intake quintiles of the animal-to-plant protein ratios and the nondairy animal-to-plant protein ratios were positively associated with stone risk (HR 1.17, 95% CI 1.03-1.33, p=0.02 and HR 1.20, 95% CI 1.06-1.36, p=0.005, respectively). No association was observed with plant protein intake (ptrend=0.14). CONCLUSIONS: In this population with a relatively low animal protein intake and a high plant protein intake, a greater animal protein intake was associated with a kidney stone risk. Increasing the proportion of plant protein relative to animal protein appeared protective against the risk.

9.
Cancer Res ; 79(18): 4592-4598, 2019 Sep 15.
Artigo em Inglês | MEDLINE | ID: mdl-31337649

RESUMO

Several blood protein biomarkers have been associated with prostate cancer risk. However, most studies assessed only a small number of biomarkers and/or included a small sample size. To identify novel protein biomarkers of prostate cancer risk, we studied 79,194 cases and 61,112 controls of European ancestry, included in the PRACTICAL/ELLIPSE consortia, using genetic instruments of protein quantitative trait loci for 1,478 plasma proteins. A total of 31 proteins were associated with prostate cancer risk including proteins encoded by GSTP1, whose methylation level was shown previously to be associated with prostate cancer risk, and MSMB, SPINT2, IGF2R, and CTSS, which were previously implicated as potential target genes of prostate cancer risk variants identified in genome-wide association studies. A total of 18 proteins inversely correlated and 13 positively correlated with prostate cancer risk. For 28 of the identified proteins, gene somatic changes of short indels, splice site, nonsense, or missense mutations were detected in patients with prostate cancer in The Cancer Genome Atlas. Pathway enrichment analysis showed that relevant genes were significantly enriched in cancer-related pathways. In conclusion, this study identifies 31 candidates of protein biomarkers for prostate cancer risk and provides new insights into the biology and genetics of prostate tumorigenesis. SIGNIFICANCE: Integration of genomics and proteomics data identifies biomarkers associated with prostate cancer risk.

10.
Int J Cancer ; 2019 Jul 02.
Artigo em Inglês | MEDLINE | ID: mdl-31265136

RESUMO

A small number of circulating proteins have been reported to be associated with breast cancer risk, with inconsistent results. Herein, we attempted to identify novel protein biomarkers for breast cancer via the integration of genomics and proteomics data. In the Breast Cancer Association Consortium (BCAC), with 122,977 cases and 105,974 controls of European descendants, we evaluated the associations of the genetically predicted concentrations of >1,400 circulating proteins with breast cancer risk. We used data from a large-scale protein quantitative trait loci (pQTL) analysis as our study instrument. Summary statistics for these pQTL variants related to breast cancer risk were obtained from the BCAC and used to estimate odds ratios (OR) for each protein using the inverse-variance weighted method. We identified 56 proteins significantly associated with breast cancer risk by instrumental analysis (false discovery rate <0.05). Of these, the concentrations of 32 were influenced by variants close to a breast cancer susceptibility locus (ABO, 9q34.2). Many of these proteins, such as insulin receptor, insulin-like growth factor receptor 1 and other membrane receptors (OR: 0.82-1.18, p values: 6.96 × 10-4 -3.28 × 10-8 ), are linked to insulin resistance and estrogen receptor signaling pathways. Proteins identified at other loci include those involved in biological processes such as alcohol and lipid metabolism, proteolysis, apoptosis, immune regulation and cell motility and proliferation. Consistent associations were observed for 22 proteins in the UK Biobank data (p < 0.05). The study identifies potential novel biomarkers for breast cancer, but further investigation is needed to replicate our findings.

12.
Oncogene ; 38(28): 5747, 2019 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-31182792

RESUMO

A correction to this paper has been published and can be accessed via a link at the top of the paper.

13.
J Natl Cancer Inst ; 2019 May 29.
Artigo em Inglês | MEDLINE | ID: mdl-31143935

RESUMO

BACKGROUND: DNA methylation plays a critical role in breast cancer development. Previous studies have identified DNA methylation marks in white blood cells as promising biomarkers for breast cancer. However, these studies were limited by low statistical power and potential biases. Utilizing a new methodology, we investigated DNA methylation marks for their associations with breast cancer risk. METHODS: Statistical models were built to predict levels of DNA methylation marks using genetic data and DNA methylation data from HumanMethylation450 BeadChip from the Framingham Heart Study (N=1,595). The prediction models were validated using data from the Women's Health Initiative (N=883). We applied these models to genome-wide association study (GWAS) data of 122,977 breast cancer cases and 105,974 controls to evaluate if the genetically predicted DNA methylation levels at CpGs are associated with breast cancer risk. All statistical tests were two-sided. RESULTS: Of the 62,938 CpG sites (CpGs) investigated, statistically significant associations with breast cancer risk were observed for 450 CpGs at a Bonferroni-corrected threshold of P<7.94 × 10-7, including 45 CpGs residing in 18 genomic regions which have not previously been associated with breast cancer risk. Of the remaining 405 CpGs located within 500 kilobase flaking regions of 70 GWAS-identified breast cancer risk variants, the associations for 11 CpGs were independent of GWAS-identified variants. Integrative analyses of genetic, DNA methylation and gene expression data found that 38 CpGs may affect breast cancer risk through regulating expression of 21 genes. CONCLUSION: Our new methodology can identify novel DNA methylation biomarkers for breast cancer risk and can be applied to other diseases.

14.
J Vasc Access ; 20(6): 583-591, 2019 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-30919720

RESUMO

At present, central venous access devices (CVADs) are widely used in clinical practice. The reasons for CVAD obstruction caused by precipitated medication or lipids are increasingly complex. However, there is no clear treatment program for CVAD obstruction caused by precipitated medication or lipids. The target of this study was to analyze data regarding obstruction caused by precipitated medication or lipids in CVADs and to calculate the efficacy of different treatment methods. A systematic review with meta-analysis was conducted in alignment with the Preferred Reporting Items for Systematic Reviews and Meta-analyses (PRISMA) statement. The PubMed, Web of Science, EMBASE, Cochrane Library, CINAHL, and China National Knowledge Internet databases were searched for original research published before 2018. There were 1356 publications initially screened, with one additional study identified through snowballing. Seven studies met the inclusion criteria. The reasons for obstruction, except for clot formation, primarily included the following: mechanical complications; lipid deposition; mineral deposition; or drug precipitation. Meta-analysis showed that sodium hydroxide resulted in the highest recanalization rate in lipid deposition, followed by ethanol, and the difference was significant. The efficacy analysis revealed that hydrochloric acid and l-cysteine have similar effects on mineral deposition and drug precipitation. According to this review, the most effective methodology was shown to be the intravenous perfusion of sodium hydroxide in several treatments when the obstruction is caused by lipid deposition. In contrast, mineral deposition and drug deposition are best treated with l-cysteine to recover the patency of central venous access devices.

15.
Mol Ther Nucleic Acids ; 16: 105-117, 2019 Feb 20.
Artigo em Inglês | MEDLINE | ID: mdl-30861413

RESUMO

The important role of insulin-like growth factor-1 receptor (IGF-1R) in tumorigenesis has been well established. The classical model involves IGF-1R binding to IGF-1/2, the following activation of PI3K-Akt-signaling cascades, driving cell proliferation and apoptosis inhibition. Here we report a new signal transduction pathway of IGF-1R in the intestinal epithelium. Using heterozygous knockout mice (Igf1r+/-), we analyzed the expressions of viral RNA sensors MDA5 and RIG-I in the intestinal epithelium. Igf1r+/- mice exhibited higher MDA5 and RIG-I than wild-type (WT) mice, indicating that knockdown of IGF-1R could trigger MDA5 and RIG-I. IGF-1R knockdown-triggered MDA5 and RIG-I were further investigated in human colonic cancer cells. Increased MDA5 and RIG-I were clearly seen in the cytoplasm in cancer cells as well as normal human colonic cells with silenced IGF-1R. Notably, the upregulations of MDA5 and RIG-I was not affected by blockage of the PI3K-Akt pathway with LY294002. These results suggested a new signal transduction pathway of IGF-1R. Importantly, IGF-1R knockdown-triggered MDA5 and RIG-I resulted in colorectal cancer apoptosis through activation of the mitochondrial pathway. These in vitro observations were evidenced in the azoxymethane (AOM)-dextran sulfate sodium (DSS) colorectal cancer model of mice. In conclusion, knockdown of IGF-1R triggers viral RNA sensor MDA5- and RIG-I-mediated mitochondrial apoptosis in cancer cells.

16.
Hua Xi Kou Qiang Yi Xue Za Zhi ; 37(1): 70-75, 2019 Feb 01.
Artigo em Chinês | MEDLINE | ID: mdl-30854823

RESUMO

OBJECTIVE: This work aimed to identify the risk factors of Helicobacter pylori (H. pylori) infection in preschool children and provide effective measures for the prevention and reduction of the incidence of H. pylori infections. METHODS: A total of 204 children from two kindergartens in Suzhou city were recruited through a questionnaire survey. Risk factors were selected through the single factor paired data χ² test and multiple factor Logistic regression analysis. Oral and gastric H. pylori infections were detected by using H. pylori saliva detection (HPS) and ¹³C-urea breath test (¹³C-UBT). Special toothpaste for H. pylori control was selected for oral cleaning. Oral H. pylori infection rates at 2 months after special toothpaste treatment were examined by using HPS. RESULTS: The high-risk factors of H. pylori infections among preschool children included poor personal hygiene habits, such as the nibbling of fingers and the avoidance of hand-washing before meals, diet, and parent's history of stomach disease. Among the 204 subjects enrolled in this study, 158 (77.45%), 37 (18.14%), and 28 (13.73%) were HPS positive, ¹³C-UBT positive, and HPS and ¹³C-UBT positive, respectively. The incidence of oral H. pylori infections was significantly higher than that of gastric H. pylori infections (P<0.01). The positive rate of infections significantly decreased after special toothpaste treatment (P<0.01). This result indicates that the intervention was effective. CONCLUSIONS: Children must receive education on good eating habits. Individualized dining habits or the use of public chopsticks must be implemented. H. pylori infections must be detected as early as possible. Specific toothpaste for oral cleaning must be selected. These approaches could drastically prevent or reduce the incidence of H. pylori infections among preschool children.


Assuntos
Infecções por Helicobacter , Helicobacter pylori , Testes Respiratórios , Pré-Escolar , Infecções por Helicobacter/epidemiologia , Humanos , Fatores de Risco , Ureia
17.
J Hazard Mater ; 369: 503-511, 2019 May 05.
Artigo em Inglês | MEDLINE | ID: mdl-30807990

RESUMO

As an industrial waste characterized by huge volume and high alkalinity, red mud has become a serious environmental problem. The reuse of red mud has been explored in previous studies, including as building materials and for soil and waste water treatment. In this study, an innovation was made for the reuse of red mud to create a synergistic effect. Red mud was first used in flue gas desulfurization (FGD), and then the desulfurized red mud was again reused to make a geopolymer material. By using one type of original red mud and three types of fly ash, this study revealed that with high alkalinity and desulfurization capacity, the red mud could serve as an excellent FGD sorbent. After FGD, the sodium sulfate in the desulfurized red mud acted as a chemical activator for geopolymer made with class C fly ash. A 25% increase in strength was observed between the geopolymers with the red mud after FGD and with the original one. There are no significant benefits of FGD on the class F fly ash-based geopolymers and further study is required.

18.
Zhongguo Dang Dai Er Ke Za Zhi ; 21(2): 139-143, 2019 Feb.
Artigo em Chinês | MEDLINE | ID: mdl-30782275

RESUMO

OBJECTIVE: To investigate the molecular epidemiological characteristics of norovirus (NoV) among children with acute gastroenteritis in Tianjin in 2017. METHODS: A total of 758 stool specimens were collected from the children with acute gastroenteritis possibly caused by viral infection in Tianjin Children's Hospital between January and December, 2017. Quantitative real-time RT-PCR was used for primary screening of NoV, and conventional RT-PCR was used for gene amplification, sequencing and genotype identification of the VP1 region of capsid protein in positive specimens. RESULTS: Among the 758 specimens, 241 (31.8%) were found to have GII NoV. Sequencing of the VP1 region of capsid protein in positive specimens showed that among the 241 specimens with GII NoV, 69 (28.6%) had GII.4 subtype, 51 (21.2%) had GII.3 subtype, 24 (10.0%) had GII.2 subtype, and 18 (7.5%) had other subtypes. There was a significant difference in NoV detection rate between different age groups (P=0.018), and the 1- <4 years group had the highest NoV detection rate (37.3%). There was also a significant difference in NoV detection rate across seasons (P<0.001), and there was a highest NoV detection rate in winter (48.1%). Twenty-seven children (3.6%) had co-infections with NoV and rotavirus. CONCLUSIONS: NoV is one of the major pathogens of the children with acute gastroenteritis from Tianjin in 2017. GII genotype, especially GII.4 subtype, is the prevalent strain. NoV infection is commonly seen in children less than 4 years and reaches the peak in winter. Some children are found to have co-infections with rotavirus.


Assuntos
Gastroenterite , Norovirus , Infecções por Caliciviridae , Criança , China/epidemiologia , Fezes , Gastroenterite/epidemiologia , Genótipo , Humanos , Epidemiologia Molecular , Filogenia , RNA Viral , Análise de Sequência de DNA
19.
Free Radic Biol Med ; 134: 87-98, 2019 04.
Artigo em Inglês | MEDLINE | ID: mdl-30611867

RESUMO

Although insulin-like growth factor-1 receptor (IGF-1R) has been accepted as a major determinant of cancers, its biological roles and corresponding mechanisms in tumorigenesis have remained elusive. Herein, we demonstrate that IGF-1R plays pivotal roles in the regulation of mitochondrial respiratory chain and functions during colitis and tumorigenesis. Heterozygous knockout IGF-1R attenuated azoxymethane (AOM)/dextran sulfate sodium (DSS)-induced colitis and colitis associated cancer (CAC) in Igf1r+/- mice. Heterozygous knockout IGF-1R confers resistance to oxidative stress-induced damage on colorectal epithelial cells by protecting mitochondrial dynamics and structures. IGF-1R low expression improves the biological function of mitochondrial fusion under oxidative stress. Mechanically, an increase in respiratory coupling index (RCI) and oxidative phosphorylation index (ADP/O) was seen in colorectal epithelial cells of Igf1r+/- mice. Seahorse XFe-24 analyzer analysis of mitochondrial bioenergetics demonstrated an increase in oxygen consumption rate (OCR) and a decrease of extracellular acidification rate (ECAR) in Igf1r+/- cells. Further analysis suggests the protection mechanisms of Igf1r+/- cells from oxidative stress through the activation of the mitochondrial respiratory chain and LKB1/AMPK pathways. These results highlight the biological roles of IGF-1R at the nexus between oxidative damage and mitochondrial function and a connection between colitis and colorectal cancer.

20.
Am J Physiol Gastrointest Liver Physiol ; 316(3): G387-G396, 2019 Mar 01.
Artigo em Inglês | MEDLINE | ID: mdl-30629471

RESUMO

Tumor necrosis factor-α (TNF-α) is a highly pleiotropic cytokine executing biological functions as diverse as cell proliferation, metabolic activation, inflammatory responses, and cell death. TNF-α can induce multiple mechanisms to initiate apoptosis in hepatocytes leading to the subsequent liver injury. Since the phosphoinositide-3-kinase/protein kinase B (PI3K/Akt) pathway is known to have a protective role in death factor-mediated apoptosis, it is our hypothesis that activation of Akt may represent a therapeutic strategy to alleviate TNF-α-induced hepatocyte apoptosis and liver injury. We report here that the Akt activator SC79 protects hepatocytes from TNF-α-induced apoptosis and protects mice from d-galactosamine (d-Gal)/lipopolysaccharide (LPS)-induced TNF-α-mediated liver injury and damage. SC79 not only enhances the nuclear factor-κB (NF-κB) prosurvival signaling in response to TNF-α stimulation, but also increases the expression of cellular FLICE (FADD-like IL-1ß-converting enzyme)-inhibitory protein L and S (FLIPL/S), which consequently inhibits the activation of procaspase-8. Furthermore, pretreatment of the PI3K/Akt inhibitor LY294002 reverses all the SC79-induced hepatoprotective effects. These results strongly indicate that SC79 protects against TNF-α-induced hepatocyte apoptosis and suggests that SC79 is likely a promising therapeutic agent for ameliorating the development of liver injury. NEW & NOTEWORTHY SC79 protects hepatocytes from TNF-α-mediated apoptosis and mice from Gal/LPS-induced liver injury and damage. Cytoprotective effects of SC79 against TNF-α act through both AKT-mediated activation of NF-κB and upregulation of FLIPL/S.

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