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In order to solve the traditional A* algorithm is not taken into account when planning path obstacle distribution on the influence of the path selection,this paper puts forward an improved A* algorithm,the artificial potential field of thought and the traditional A* algorithm,the combination of the obstacles in grid map gives repulsive force function and the repulsive force around the grid size calculation,in order to improve the searching ability of A* algorithm,the repulsive force of the grid is introduced into the evaluation function of A* algorithm.The results of MATLAB simulation and Turtlebot experiments show that,compared with the traditional A* algorithm,the new improved algorithm combined with artificial potential field algorithm can plan a better path,improve the efficiency of path planning,and increase the search speed by 13.40%~29.68%.The path length is shortened by 10.56%~24.38%,and the number of path nodes is reduced by 6.89%~27.27%.The experimental results show that the improved A* algorithm has obvious optimization effect and is effective and feasible.

Purpose: Results from studies of extended capecitabine after the standard adjuvant chemotherapy in early stage triple-negative breast cancer (TNBC) were inconsistent, and only low-dose capecitabine from the SYSUCC-001 trial improved disease-free survival (DFS). Adjustment of the conventional adjuvant chemotherapy doses affect the prognosis and may affect the efficacy of subsequent treatments. This study investigated whether the survival benefit of the SYSUCC-001 trial was affected by dose adjustment of the standard adjuvant chemotherapy or not. Patients and Methods: We reviewed the adjuvant chemotherapy regimens before the extended capecitabine in the SYSUCC-001 trial. Patients were classified into "consistent" (standard acceptable dose) and "inconsistent" (doses lower than acceptable dose) dose based on the minimum acceptable dose range in the landmark clinical trials. Cox proportional hazards model was used to investigate the impact of dose on the survival outcomes. Results: All 434 patients in SYSUCC-001 trial were enrolled in this study. Most of patients administered the anthracycline-taxane regimen accounted for 88.94%. Among patients in the "inconsistent" dose, 60.8% and 47% received lower doses of anthracycline and taxane separately. In the observation group, the "inconsistent" dose of anthracycline and taxane did not affect DFS compared with the "consistent" dose. Moreover, in the capecitabine group, the "inconsistent" anthracycline dose did not affect DFS compared with the "consistent" dose. However, patients with "consistent" taxane doses benefited significantly from extended capecitabine (P=0.014). The sufficient dose of adjuvant taxane had a positive effect of extended capecitabine (hazard ratio [HR] 2.04; 95% confidence interval [CI] 1.02 to 4.06). Conclusion: This study found the dose reduction of adjuvant taxane might negatively impact the efficacy of capecitabine. Therefore, the reduction of anthracycline dose over paclitaxel should be given priority during conventional adjuvant chemotherapy, if patients need dose reduction and plan for extended capecitabine. [ABSTRACT FROM AUTHOR]

Lipotoxicity has been implicated in pancreatic β-cell dysfunction in type 2 diabetes, but the exact mechanisms remain unknown. The current study explored the role of the endoplasmic reticulum (ER) stress pathway in cholesterol-induced lipotoxicity. Two different insulinoma cell lines were treated with cholesterol with or without inhibitors. ER stress-associated proteins glucose-regulated protein (GRP) 78, activating transcription factor (ATF) 4 and C/EBP homologous protein (CHOP), as was phosphorylation of eukaryotic initiation factor (EIF) 2α, were all up-regulated by cholesterol. Cholesterol also up-regulated microtubule-associated protein 1 light chain 3 (LC3)-II and stimulated the formation of autophagic vacuoles and LC3-II aggregates. Cholesterol-induced autophagy and cell injuries were suppressed by pretreatment with the ER stress inhibitor 4-phenylbutyrate (4-PBA). Pretreatment with autophagy inhibitors E-64d/pepstatin A increased ER stress-induced cell injuries as indicated by increased cell apoptosis and decreased insulin secretion. These results suggest that cholesterol treatment induces apoptosis and dysfunction of β-cells, and enhances autophagy through activation of the ER stress pathway. More importantly, autophagy induced by cholesterol may protect β-cells against ER stress-associated cell damages. [ABSTRACT FROM AUTHOR]

Objective: To investigate the clinical features of mild encephalitis/encephalopathy with a reversible splenial lesion (MERS) in children., Methods: The clinical data of 8 children with MERS were retrospectively analyzed., Results: The mean age of onset was 5 years and 2 months (range 10 months to 12 years). The major clinical features included a history of prodromal infection, and among these children, 5 had pyrexia and 4 had vomiting. Of all the children, 6 were manifested as convulsion and 3 each were manifested as disturbance of consciousness and paroxysmal paropsia. Cranial diffusion-weighted magnetic resonance imaging (MRI) showed high signals in the splenium of the corpus callosum. Among these children, one child had symmetric and multiple long T1 and long T2 signals in the bilateral centrum semiovale and part of the temporal white matter. MRI reexamination performed after 5-30 days showed the disappearance of abnormal signals in all the children. The children were followed up for 3 months to 2 years, and no child experienced abnormal neurodevelopment., Conclusions: The development of MERS in children is closely associated with infection. MERS is characterized by high signals in the splenium of the corpus callosum on cranial diffusion-weighted MRI. Most children have good prognosis.

Objective: The pathogenesis of electrical status epilepticus during sleep (ESES) in children remains unknown. We undertook a retrospective study of epileptic children who presented with ESES to investigate the correlation factors of ESES., Methods: Thirty epileptic children with ESES (ESES group) and 30 age-and sex-matched epileptic children without ESES (control group) admitted to Maternal and Child Health Care Hospital of Tangshan between January 2000 and July 2006 were enrolled. The results of questionnaire and laboratory examinations were compared between the two groups., Results: Nine patients had a family history of epilepsy in the ESES group, but only 2 patients in the control group (<0.05). Language disorder was found in 11 patients in the ESES group, but only 2 patients in the control group (<0.05). Thirteen patients were confirmed with epileptic syndrome in the ESES group, but only 5 patients in the control group (<0.05). Twenty five patients in the ESES group showed mental retardation, but only 5 patients from the control group (<0.01)., Conclusions: ESES may be correlated with family history of epilepsy, epileptic syndrome, mental retardation and language disorder.

Aim: To investigate the inhibition of amyloid beta-protein 42 (Abeta42) production in M146L cells by gamma-schisandrin., Methods: M146L cells which can produce considerable Abeta42 in vitro were treated with gamma-schisandrin (1.67, 5.00 and 15.00 microg x mL(-1)), beta-secretase inhibitor (S4562, 100.00 microg x mL(-1)) and gamma-secretase inhibitor (S2188, 13.68 microg x mL(-1)), separately. Cell counting kit-8 (CCK-8) was used to assess cell viability. Enzyme-linked immunosorbent assay (ELISA) was carried out to determine the amount of Abeta42. Western blotting was used to examine C99, an intermediary product of APP cleaved by beta-secretase. beta-Secretase and gamma-secretase activities were assayed by commercial kits., Results: The CCK-8 assay indicated that different concentrations of gamma-schisandrin had no neurotoxicity on the cultured M146L. And the ELISA test showed that the amount of Abeta42 secreted by M146L cells treated with gamma-schisandrin (5.00 and 15.00 microg x mL(-1)) decreased obviously as compared with solvent control. The results of Western blotting test indicated that there was no change of C99 contents and beta-secretase activity in gamma-schisandrin treated cells, while gamma-secretase activity decreased obviously., Conclusion: gamma-Schisandrin inhibited production of Abeta42 in M146L cells through inhibiting gamma-secretase.