BackgroundLead is a heavy metal and important environmental toxicant and nerve poison that can destruction many functions of the nervous system. Lead poisoning is a medical condition caused by increased levels of lead in the body. Lead interferes with a variety of body processes and is toxic to many organs and issues, including the central nervous system. It interferes with the development of the nervous system, and is therefore particularly toxic to children, causing potentially permanent neural and cognitive impairments. In this study, we investigated the relationship between lead poisoning and the intellectual and neurobehavioral capabilities of children.MethodsThe background characteristics of the research subjects were collected by questionnaire survey. Blood lead levels were detected by differential potentiometric stripping analysis (DPSA). Intelligence was assessed using the Gesell Developmental Scale. The Achenbach Child Behavior Checklist (CBCL) was used to evaluate each child’s behavior.ResultsBlood lead levels were significantly negatively correlated with the developmental quotients of adaptive behavior, gross motor performance, fine motor performance, language development, and individual social behavior (P < 0.01). Compared with healthy children, more children with lead poisoning had abnormal behaviors, especially social withdrawal, depression, and atypical body movements, aggressions and destruction.ConclusionLead poisoning has adverse effects on the behavior and mental development of 2–4-year-old children, prescribing positive and effective precautionary measures.

Background: Nutritional status, systemic inflammation, and coagulation mechanism are closely related to tumor progression. Herein, we examined the role of fibrinogen-to-albumin ratio index (FARI) in the prognosis of gastrointestinal stromal tumors (GISTs) and developed a novel nomogram predicting recurrence-free survival (RFS). Methods: We retrospectively analyzed data from 357 GIST patients admitted at the gastrointestinal surgery of the Beijing Hospital from January 2008 to January 2018 and underwent curative resection. FARI was calculated as fibrinogen level (g/L) /albumin level (g/L). The cutoff point of FARI was set using the point with the largest Youden index on the receiver operating characteristic curve with the 5-years recurrence-free survival as an endpoint. We used the Kaplan-Meier approach and multivariable Cox regression model to study the impact of FARI on recurrence-free survival. Finally, we developed a nomogram based on tumor size, location, mitotic index, and FARI to predict RFS. The nomogram was assessed by calculating concordance probabilities and testing calibration of predicted RFS with observed RFS. Concordance probabilities were also compared with the National Institute of Health (NIH) risk classification system. Results: The ROC curve revealed that the best cutoff point of the FARI was set as 0.08. The patients were classified into the FARI-high (≥0.08) and FARI-low (<0.08) groups. FARI was significantly associated with age, size of the tumor, NIH risk category, and Mitotic Index (all P < 0.05). FARI was weakly associated with NLR and PLR. FARI and PNI had a weak negative association. Multivariate analysis showed that the NIH risk category and FARI were independent prognostic predictors for worse outcomes concerning RFS in GIST patients. In the high-risk subgroup, patients with low FARI also had a more prolonged RFS than patients with high FARI (P <0.05). The nomogram had a concordance probability of 0.802 (SE 0.025). Nomogram predictions were well-calibrated. Concordance probabilities of the nomogram were better than NIH risk classification system [0.802 [0.025] vs. 0.737 [0.024], p < 0.01].

Abstract. The aim of this study was to determine the expression and function of epithelial membrane protein 1 (EMP1) in gastric carcinoma. Gastric samples were taken from cancer lesions and adjacent normal tissue in gastric cancer patients immediately after endoscopic biopsy. A portion of the sample was either fixed in 4% paraformaldehyde and embedded in paraffin for immunohistochemistry or stored in liquid nitrogen for western blotting. In order to determine protein expression of EMP1 in gastric cancer (n=65) and normal tissue (n=27), semi-quantitative immunohistochemistry and western blotting were utilized. For in vitro studies, the human gastric cancer cell line SGC-7901 was maintained in RPMI-1640 medium supplemented with 10% fetal bovine serum. Recombinant lentivirus mediated overexpression of EMP1 in SGC-7901 cells was quantified with quantitative polymerase chain reaction (qPCR) and western blotting. Control SGC-7901 cells were transfected with an empty vector. To further study the effect of EMP1 overexpression in SGC-7901 cells, cell proliferation, cell apoptosis and migration and invasion assays were conducted. The expression of EMP1 was significantly lower in gastric cancer tissue compared to normal tissue using both immunohistochemistry (41.5

Post-exercise cardiac troponin release has been extensively described in athletic groups but little attention has been given to any role of sex in mediating this phenomenon. OBJECTIVE: We compared the release of cardiac troponin T (cTnT) after endurance running in training-experience, biological-age and maturity-matched young male and female runners. MATERIALS AND METHODS: Nineteen male (training history: 2.3±1.0 yr; mean age: 16.1±1.2 yr; Tanner stage: 3.7±0.6) and 19 female (training history: 2.2±1.0 yr; mean age: 15.9±1.4 yr; Tanner stage: 4.0±0.4) runners performed a 21 km run with "all-out" effort. Serum cTnT levels were assessed at pre-exercise (Pre-ex) and at 4 h post-exercise (Post-ex). RESULTS: At Pre-ex, cTnT concentrations were below the 99th percentile value (10 ng.l-1) in 32/38 runners. Postex cTnT increased in all subjects but the response was substantially higher (P<0.05) in males [median (range): 210 (20-1360) ng.l-1 ] than females [median (range): 80 (10-550) ng.l-1 ]. At Post-ex, 95% (95% confidence interval: 75-99%) of males and 63% (95% confidence interval: 41-81%) of females (P<0.05) had cTnT concentrations above the cutoff for acute myocardial infarction. CONCLUSIONS: The present data suggest that post-exercise cTnT elevation occurs in all runners but is augmented in young male compared to female athletes.

The prognostic nutritional index (PNI) has been correlated with long-term outcomes in cancer patients. However, the relationship between PNI, the postoperative complications, and long-term outcomes in patients with colorectal cancer (CRC) undergoing curative laparoscopic surgery has not been fully investigated. This retrospective study was conducted in the Beijing Hospital between January 2009 and January 2012. A total of 228 patients diagnosed with primary CRC undergoing curative laparoscopic surgery in the center were analyzed. The last follow-up date was December 2015. The associations of the PNI status with postoperative outcomes were examined using univariate and multivariate analyses. The optimal cutoff value of the preoperative PNI was set at 44.55 using the receiver operating characteristic curve. The patients were classified into PNI-high (≥44.55) and PNI-low groups (<44.55). The patients in the PNI-low group were more likely to have increased levels of tumor markers such as carcinoembryonic antigen and carbohydrate antigen 19-9, aggressive histological features, advanced tumor-nodes-metastasis (TNM) stages (all P < 0.05). Multivariate analyses revealed PNI<44.55 as an independent factor associated with the incidence of severe postoperative complications and overall survival. In conclusion, for patients with CRC undergoing curative laparoscopic surgery, PNI is a valuable biomarker in preoperative estimation as well as prognosis prediction.

Prostate cancer is closely associated with constitutive transactivation of the androgen receptor (AR) signaling pathway. After treatment with androgen-deprivation therapy (ADT), the majority of patients develop castration-resistant prostate cancer within months or years. In order to investigate potential novel therapeutic targets in addition to ADT, the present study examined the regulatory mechanisms of the AR signaling pathway. In the present study, LNCaP cells were metabolically-labeled with Alk-C16, a palmitate probe. In addition, cells were treated with R1881, an androgen, or DMSO. Subsequently, click-chemistry-based palmitoylome profiling was performed in LNCaP cells and palmitoylated proteins were compared between cells treated with androgen and untreated cells. Androgen treatment was revealed to significantly increase the palmitoylation level of α-tubulin. In addition, the palmitoylation level of Ras-related protein Rab-7a (Rab7a) was enhanced by androgen treatment. Palmitoylation of α-tubulin and Rab7a were essential for cell proliferation. Notably, in the supernatant of LNCaP cells, the palmitoylation level of α-tubulin was also increased following androgen treatment. Palmitoylation of α-tubulin may provide a new potential target for the treatment of prostate cancer. In addition, the high level of α-tubulin palmitoylation in the supernatant may represent a biomarker for early-stage prostate cancer.

Purpose: To investigate the role of integrin-linked kinase (ILK) in endothelial cell migration, proliferation and tube formation in vitro. Materials and Methods: Cultured RF/6A cells were knocked down for ILK using small interfering RNA (siRNA). Cellular ILK expression was quantified by real-time quantitative PCR and Western blot analysis. Cell migration was measured by cell counting in modified Boyden chambers, while microfilament dynamics were assessed by immunofluorescence analysis. Cell cycling was determined using a FACS Calibur flow cytometer, and the expression of cyclin D₁ was also measured by the Western blot assay. The secretion of vascular endothelial growth factor (VEGF) in culture medium samples was assessed by ELISA, and capillary/tube-like network formation assays were performed using matrigel. Results: Both ILK mRNA and protein levels were vir- tually undetectable after transfection with ILK siRNA. In addition, there was a significant accumulation of cells in the G₀–G₁ phase and a marked decrease in cell numbers in the S phase in ILK-specific siRNA-transfected cells, and the expression of cyclin D₁ was decreased after transfection. The knockdown of ILK significantly inhibited cell migration ability by disturbing F actin assembly, and VEGF secretion in conditioned medium was also reduced by 33%. Furthermore, treatment with ILK siRNA suppressed tube formation in RF/6A cells and significantly reduced the overall length of the tubes. Conclusions: Knockdown of ILK with siRNA effectively inhibits endothelial cell migration, proliferation and tube formation in vitro.

Targeting ILK with siRNA suppresses the growth of gastric cancer cells both in vitro and in vivo. ILK plays an important role in gastric cancer progression.