Motion control and positioning system of multi-sensor tunnel defect inspection robot: from methodology to application.

As the mileage of subway is increasing rapidly, there is an urgent need for automatic subway tunnel inspection equipment to ensure the efficiency and frequency of daily tunnel inspection. The subway tunnel environment is complex, it cannot receive GPS and other satellite signals, a variety of positioning sensors cannot be used. Besides, there are random interference, wheel and rail idling and creep. All the above results in poor performance of conventional speed tracking and positioning methods. In this paper, a multi-sensor motion control system is proposed for the subway tunnel inspection robot. At the same time, a trapezoidal speed planning and a speed tracking algorithm based on MPC (Model Predictive Control) are proposed, which simplify longitudinal dynamics model to overcome the complex and variable nonlinear problems in the operation of the maintenance robot. The optimal function of speed, acceleration and jerk constraint is designed to make the tunnel inspection robot achieve efficient and stable speed control in the subway tunnel environment. In this paper, the "INS (inertial navigation system) + Odometer" positioning method is proposed. The difference between the displacement measured by the inertial navigation system and the displacement calculated by the odometer is taken as the measurement value, which reduces the dimension of the conventional algorithm. The closed-loop Kalman filter is used to establish the combined positioning model, and the system error can be corrected in real time with higher accuracy. The algorithms were verified on the test line. The displacement target was set to be 1 km and the limit speed was 60 km/h. The overshooting error of the speed tracking algorithm based on trapezoidal velocity planning and MPC was 0.89%, and the stability error was 0.32%. It improved the accuracy and stability of the speed following, and was much better than the PID speed tracking algorithm. At the speed of 40 km/h, the maximum positioning error of the robot within 2 km is 0.15%, and the average error is 0.08%. It is verified that the multi-sensor fusion positioning algorithm has significantly improved the accuracy compared with the single-odometer positioning algorithm, and can effectively make up for the position error caused by wheel-rail creep and sensor error.

Association of Rare PTGIS Variants With Susceptibility and Pulmonary Vascular Response in Patients With Idiopathic Pulmonary Arterial Hypertension.

Importance: Idiopathic pulmonary arterial hypertension (IPAH) is a fatal disease with high heritability; however, the bone morphogenetic protein receptor 2 (BMPR2) gene only accounts for 17% of IPAH. The genetic basis of IPAH needs further investigation. Objective: To identify novel IPAH susceptibility genes other than BMPR2. Design, Setting, and Participants: This 2-stage, case-control genetic association study enrolled 230 patients with IPAH from 2 referral pulmonary hypertension centers in China. Eligible patients had no BMPR2 variants and were compared with 968 healthy control participants. Data were collected from January 1, 2000, to July 31, 2015, and analyzed from August 1, 2015, to May 30, 2018. Exposures: PTGIS rare variants. Main Outcomes and Measures: Whole-genome sequencing was performed to identify putative IPAH genes in a discovery cohort, with validation in an independent referral cohort. Correlation of genotype and hemodynamic characteristics was then evaluated at baseline and after pulmonary vasodilator testing. Functional assessments were conducted to analyze the effects of identified genetic variants on transcript splicing, enzymatic activity, and endothelial cell phenotypes. Results: Among 230 patients with IPAH (164 female [71.3%]; mean [SD] age, 34 [18] years), an enrichment of rare variants in a gene encoding prostacyclin synthase (PTGIS) was identified in the discovery cohort. The association of PTGIS rare variants with IPAH was confirmed in the replication cohort. In the combined data set, PTGIS rare variants were found in 14 of 230 cases (6.1%) and 8 of 968 controls (0.8%) (odds ratio, 7.8; 95% CI, 3.2-18.8; P = 5 × 10-6, logistic regression). Compared with patients without PTGIS variants, inhaled iloprost induced a more significant decrease of pulmonary vascular resistance (difference in the least square mean, -21.7%; 95% CI, -31.4% to -12.0%; P < .001, linear regression model) and an increase of cardiac index (difference in the least square mean, 18.3%; 95% CI, 8.8%-27.8%; P < .001, linear regression model) in patients with PTGIS variants. The minigene assay indicated that the c.521 + 1G>A variant resulted in aberrant messenger RNA transcripts. The functional studies showed that the 2 missense rare variants (R252Q and A447T) resulted in a decrease in prostacyclin production and increased cell death of pulmonary microvascular endothelial cells. Conclusions and Relevance: This study identified 3 rare loss-of-function variants in the PTGIS gene from 2 independent cohorts with IPAH. The genetic variants of PTGIS predispose pulmonary vascular responses to the iloprost stimulation. These findings suggest that PTGIS variants may be involved in the pathogenesis of IPAH.

A novel phenotype with splicing mutation identified in a Chinese family with desminopathy.

BACKGROUND: Desminopathy, a hereditary myofibrillar myopathy, mainly results from the desmin gene (DES) mutations. Desminopathy involves various phenotypes, mainly including different cardiomyopathies, skeletal myopathy, and arrhythmia. Combined with genotype, it helps us precisely diagnose and treat for desminopathy. METHODS: Sanger sequencing was used to characterize DES variation, and then a minigene assay was used to verify the effect of splice-site mutation on pre-mRNA splicing. Phenotypes were analyzed based on clinical characteristics associated with desminopathy. RESULTS: A splicing mutation (c.735+1G>T) in DES was detected in the proband. A minigene assay revealed skipping of the whole exon 3 and transcription of abnormal pre-mRNA lacking 32 codons. Another affected family member who carried the identical mutation, was identified with a novel phenotype of desminopathy, non-compaction of ventricular myocardium. There were 2 different phenotypes varied in cardiomyopathy and skeletal myopathy among the 2 patients, but no significant correlation between genotype and phenotype was identified. CONCLUSIONS: We reported a novel phenotype with a splicing mutation in DES, enlarging the spectrum of phenotype in desminopathy. Molecular studies of desminopathy should promote our understanding of its pathogenesis and provide a precise molecular diagnosis of this disorder, facilitating clinical prevention and treatment at an early stage.

Hyperoside protects against hypoxia/reoxygenation induced injury in cardiomyocytes by suppressing the Bnip3 expression.

AIMS: Role of hyperoside in protecting cardiomyocytes from ischemia/reperfusion induced injury has been proved. However, possible protecting mechanisms remain unclear. To fix the problem, an essential pro-apoptotic protein Bnip3 was studied in our experiments. METHODS AND RESULTS: Neonatal rat cardiomyocytes were used and submitted to hypoxia for 8h followed by reoxygenation for 2h to simulate the ischemia/reperfusion injury. Hypoxia/reoxygenation(H/R) induced damage to cardiomyocytes and the protective effect of hyperoside were examined by means of MTT assay. H/R-induced apoptosis was assessed by Terminal-deoxynucleoitidyl Transferase Mediated Nick End Labeling(TUNEL) and DNA Ladder assay. mRNA expression of Bnip3 was determined by use of quantitative real-time reverse transcription polymerase chain reaction assay. Protein levels of Bnip3, Bax, Bcl-2 and cleaved caspase-3 were examined using western-blot assay. Our results showed that H/R caused great damage to cardiomyocytes, upregulated the protein expressions of Bnip3, Bax, cleaved caspase3, and decreased the expression of the anti-apoptotic protein of Bcl-2. Whereas, compared with the H/R group, a decrease in activities of Bnip3, Bax, cleaved caspase3, and a promoting expression of Bcl-2 were detected in the H/R goup pretreated with hyperoside. CONCLUSION: It was concluded in our study that H/R-induced apoptotic effect in cardiomyocytes could be attenuated by hyperoside, and the protective role of hyperoside, if not completely, could be partly through the suppression of the pro-apoptotic gene Bnip3.

[Treatment of acute myocardial infarction with autologous bone marrow stem cells mobilization combined with recombinant growth factor in rat].

OBJECTIVE: To observe the regeneration cardiomyocytes and neovascularization after mobilizing autologous bone marrow stem cells by granulocyte colony stimulating factor (G-CSF) alone or G-CSF combined with recombinant human growth hormone (rhGH) in Wistar rats with acute myocardial infarction (AMI). METHODS: AMI rat model was reproduced by liquid nitrogen cryoinjury. The rats were randomly divided into six groups: mobilization group (N group, n=8), sham operation group (SO group, n=6), myocardial infarction group (MI group, n=8), G-CSF group (G group, n=8), rhGH group (GH group, n=8) and G-CSF combined with rhGH group (GG group, n=8). White blood cell (WBC) count and mononuclear cells proportion (MNC%) in peripheral blood were determined with ABX blood cell analyzer to estimate bone marrow stem cells mobilization. Four weeks after intervention, the rats were sacrificed, their respective body and heart weight were obtained, and the hearts were harvested for hematoxylin and eosin (HE) and immunohistochemical examination. RESULTS: (1)Comparing with baseline values, after 6 days administration of G-CSF, the WBC and MNC% increased in N and G groups (both P<0.01); WBC increased (P<0.01) but no difference of MNC% in MI group (P>0.05); WBC and MNC% were significantly higher in G group than those in MI group (all P<0.05). (2)Body and heart weights in GH and GG groups were higher than those in SO, MI and G groups respectively (all P<0.05). The ratio of heart and body weight was higher in GC group than that in MI,G and SO groups (P<0.05). (3)There were no significant differences in infarct size among MI, G, GH, and GG groups (P>0.05). (4)The capillary densities were higher in G, GH and GG groups than those in MI and SO groups; the density in GG group was higher than that in G and GH groups (all P<0.01). (5)BrdU positively stained neonatal cells were observed in G, GH and GG groups. Of them some developed into the endothelial cells. BrdU and cTnI double positive stained cells were observed in G and GG groups, which implied these cells might have differentiated into cardiac myocyte like cells. CONCLUSION: (1)G-CSF can mobilize bone marrow stem cells into peripheral blood in normal and cardiac infarct rats. The mobilized stem cells may enter into the infarct zone and induce the regeneration of cardiac myocyte like cells and vascular endothelial cells. (2)rhGH may promote the regeneration of capillary in the zone of infarction, but does not induce regeneration of cardiac myocyte like cells. (3)The combination of G-CSF with rhGH might promote more capillary regeneration than either of them used alone.