How the birth and death of shear layers determine confinement evolution: from the L → H transition to the density limit.

Electric field profile structure-especially its shear-is a natural order parameter for the edge plasma, and characterizes confinement regimes ranging from the H-mode (Wagner et al. 1982 Phys. Rev. Lett. 49, 1408-1412 (doi:10.1103/PhysRevLett.49.1408)) to the density limit (DL) (Greenwald et al. 1988 Nucl. Fusion 28, 2199-2207 (doi:10.1088/0029-5515/28/12/009)). The theoretical developments and lessons learned during 40 years of H-mode studies (Connor & Wilson 1999 Plasma Phys. Control. Fusion 42, R1-R74 (doi:10.1088/0741-3335/42/1/201); Wagner 2007 Plasma Phys. Control. Fusion 49, B1-B33 (doi:10.1088/0741-3335/49/12b/s01)) are applied to the shear layer collapse paradigm (Hong et al. 2017 Nucl. Fusion 58, 016041 (doi:10.1088/1741-4326/aa9626)) for the onset of DL phenomena. Results from recent experiments on edge shear layers and DL phenomenology are summarized and discussed in the light of L [Formula: see text] H transition physics. The theory of shear layer collapse is then developed. We demonstrate that shear layer physics captures both the well known current (Greenwald) scaling of the DL (Greenwald 2002 Plasma Phys. Control. Fusion 44, R27-R53 (doi:10.1088/0741-3335/44/8/201); Greenwald et al. 2014 Phys. Plasmas 21, 110501 (doi:10.1063/1.4901920)), as well as the emerging power scaling (Zanca, Sattin, JET Contributors 2019 Nucl. Fusion 59, 126011 (doi:10.1088/1741-4326/ab3b31)). The derivation of the power scaling theory exploits an existing model, originally developed for the L [Formula: see text] H transition (Diamond, Liang, Carreras, Terry 1994 Phys. Rev. Lett. 72, 2565-2568 (doi:10.1103/PhysRevLett.72.2565); Kim & Diamond 2003 Phys. Rev. Lett. 90, 185006 (doi:10.1103/PhysRevLett.90.185006)). We describe the enhanced particle transport events that occur following shear layer collapse. Open problems and future directions are discussed. This article is part of a discussion meeting issue 'H-mode transition and pedestal studies in fusion plasmas'.

LINC02875 Upregulation Contributed to Poor Prognosis for the Hepatocellular Carcinoma and Progression for the Cancerous Cells.

The prognostic implications and physiological effect of LINC02875 are unknown in hepatocellular carcinoma (HCC). We sought to examine the prognostic value of LINC02875 in HCC and assessed its role in HCC cellular function. LINC02875 expression was evaluated by RT-qPCR in HCC specimens and cell lines. LINC02875 expression was subjected to assess the correlation with clinical parameters by Chi-squared test and overall survival by Kaplan - Meier curve and Cox regression analysis. The effects of LINC02875 on the biological characteristics of HCC cells were studied by MTS and Transwell assay. LINC02875 was high-expressed in HCC, and this was associated with unfavorable clinical features and poor prognosis of HCC, especially HBV-related HCC. Knockdown of LINC02875 inhibited the proliferation, migration, and invasion of HCC cells. miR-485-5p was a downstream microRNA of LINC02875. LINC02875 affects the prognosis of HCC patients, especially HBV-related ones. LINC02875 represents a suitable therapeutic target for HCC.

Diagnostic accuracy and potential covariates of artificial intelligence for diagnosing orthopedic fractures: a systematic literature review and meta-analysis.

OBJECTIVES: To systematically quantify the diagnostic accuracy and identify potential covariates affecting the performance of artificial intelligence (AI) in diagnosing orthopedic fractures. METHODS: PubMed, Embase, Web of Science, and Cochrane Library were systematically searched for studies on AI applications in diagnosing orthopedic fractures from inception to September 29, 2021. Pooled sensitivity and specificity and the area under the receiver operating characteristic curves (AUC) were obtained. This study was registered in the PROSPERO database prior to initiation (CRD 42021254618). RESULTS: Thirty-nine were eligible for quantitative analysis. The overall pooled AUC, sensitivity, and specificity were 0.96 (95% CI 0.94-0.98), 90% (95% CI 87-92%), and 92% (95% CI 90-94%), respectively. In subgroup analyses, multicenter designed studies yielded higher sensitivity (92% vs. 88%) and specificity (94% vs. 91%) than single-center studies. AI demonstrated higher sensitivity with transfer learning (with vs. without: 92% vs. 87%) or data augmentation (with vs. without: 92% vs. 87%), compared to those without. Utilizing plain X-rays as input images for AI achieved results comparable to CT (AUC 0.96 vs. 0.96). Moreover, AI achieved comparable results to humans (AUC 0.97 vs. 0.97) and better results than non-expert human readers (AUC 0.98 vs. 0.96; sensitivity 95% vs. 88%). CONCLUSIONS: AI demonstrated high accuracy in diagnosing orthopedic fractures from medical images. Larger-scale studies with higher design quality are needed to validate our findings. KEY POINTS: • Multicenter study design, application of transfer learning, and data augmentation are closely related to improving the performance of artificial intelligence models in diagnosing orthopedic fractures. • Utilizing plain X-rays as input images for AI to diagnose fractures achieved results comparable to CT (AUC 0.96 vs. 0.96). • AI achieved comparable results to humans (AUC 0.97 vs. 0.97) but was superior to non-expert human readers (AUC 0.98 vs. 0.96, sensitivity 95% vs. 88%) in diagnosing fractures.

miR-517b-3p promotes the progression of portal vein tumor thrombus via activating Wnt/ß-catenin signaling pathway in hepatocellular carcinoma.

AIMS: This study was aimed to investigate the expression patterns and prognostic value of microRNA-517b-3p (miR-517b-3p) in hepatocellular carcinoma (HCC) patients with portal vein tumor thrombus (PVTT). METHODS: The expression of miR-517b-3p in PVTT tissues and cells was estimated using qRT-PCR. Through Kaplan-Meier survival analysis, Cox regression assay and ROC analysis, the significance of miR-517b-3p was explored. In addition, cell experiments were performed to examine the functional role of miR-517b-3p during progression of PVTT. Moreover, the biological process and biological pathway analysis analyses were conducted through GSEA and FunRich. Besides, the protein-protein interaction (PPI) network of the DEGs was established through cBioPortal website. RESULTS: Compared with the controls, the miR-517b-3p was upregulated in both PVTT tissues and cells. The upregulated miR-517b-3p, which served as a potential diagnostic biomarker to distinguish PVTT from PT and controls, was associated with poor overall survival and acted as an independent prognostic factor. The cell proliferation, migration and invasion were proved to be enhanced by overexpression of miR-517b-3p. Furthermore, Wnt/ß-catenin signaling was suppressed by miR-517b-3p knockdown and might be involved in the progression of PVTT. CONCLUSION: miR-517b-3p may promote PVTT cell proliferation, migration and invasion via activation of Wnt/ß-catenin signaling pathway. Meanwhile, miR-517b-3p has overexpression in PVTT samples, and serves as a candidate diagnostic and prognostic biomarker in HCC patients with PVTT.

Discovery of Novel Pimprinine and Streptochlorin Derivatives as Potential Antifungal Agents.

Pimprinine and streptochlorin are indole alkaloids derived from marine or soil microorganisms. In our previous study, they were promising lead compounds due to their potent bioactivity in preventing many phytopathogens, but further structural modifications are required to improve their antifungal activity. In this study, pimprinine and streptochlorin were used as parent structures with the combination strategy of their structural features. Three series of target compounds were designed and synthesized. Subsequent evaluation for antifungal activity against six common phytopathogenic fungi showed that some of thee compounds possessed excellent effects, and this is highlighted by compounds 4a and 5a, displaying 99.9% growth inhibition against Gibberella zeae and Alternaria Leaf Spot under 50 µg/mL, respectively. EC50 values indicated that compounds 4a, 5a, 8c, and 8d were even more active than Azoxystrobin and Boscalid. SAR analysis revealed the relationship between 5-(3'-indolyl)oxazole scaffold and antifungal activity, which provides useful insight into the development of new target molecules. Molecular docking models indicate that compound 4a binds with leucyl-tRNA synthetase in a similar mode as AN2690, offering a perspective on the mode of action for the study of its antifungal activity. These results suggest that compounds 4a and 5a could be regarded as novel and promising antifungal agents against phytopathogens due to their valuable potency.

miR-181b-5p Promotes the Progression of Cholangiocarcinoma by Targeting PARK2 via PTEN/PI3K/AKT Signaling Pathway.

This study combined with bioinformatics analysis and investigated the expression pattern of miR-181b-5p, as well as explored its role and mechanism in cholangiocarcinoma (CCA or CHOL). Several bioinformatics databases were used to analyze the expression of miR-181b and the enrichment of miR-181b in biological activities and biological pathways in CCA. The RT-qPCR analysis was used to examine the expression levels of miR-181b-5p. A receiver operation characteristics (ROC) curve analysis and the Kaplan-Meier survival assay were conducted to validate the diagnostic and prognostic implication of miR-181b-5p. Cell experiments were used to explore the possible functional role of miR-181b-5p in CCA progression. The bioinformatics assay was used to predict the target gene of miR-181b-5p and Western blot was used to confirm the related signaling pathway. The bioinformatics analysis results suggest that miR-181b-5p was highly expressed in cholangiocarcinoma and its expression was negatively related to PARK2 expression in CCA tissues. miR-181b-5p expression in the serum and tissues was upregulated and associated with lymph node metastasis and TNM stage. Increased expression of miR-181b-5p had relatively high diagnostic accuracy and showed poor prognosis in CCA patients. In addition, miR-181b-5p overexpression enhanced cell proliferation, migration, and invasion by targeting PARK2. Overexpression of miR-181b-5p activated the PI3K/AKT signaling pathway, while knockdown of miR-181b-5p suppressed the signaling pathway. Increased expression of miR-181b-5p in CCA may be a potential diagnostic or/and prognostic indicator for CCA patients. The present data indicated miR-181b-5p acted as an oncogene in CCA through promoting tumor cell proliferation, migration, and invasion of CCA via the PTEN/PI3K/AKT signaling pathway by targeting PARK2, which might be a promising therapeutic target or biomarker for CCA.

Multivariate analysis of factors associated with spinal cord area in single-door cervical laminoplasty with miniplate fixation.

OBJECTIVES: To explore the factors associated with the increased spinal cord area in single-door cervical laminoplasty (SDCL) with miniplate fixation. METHODS: A retrospective study enrolled 83 patients underwent SDCL with miniplate fixation and the patient characteristics such as age, gender, tobacco use, alcohol use, diabetes mellitus, hypertension, diagnosis, operative level, etc., were obtained. The opening angle, door shaft position and spinal canal area of the patients were measured after surgery. The sagittal canal diameter (SCD), the C2-7 Cobb angle, the cervical curvature index (CCI), the range of motion (ROM) and the spinal canal area were measured before and after operation. The increased cervical spinal cord area was also measured before and after surgery, and the correlation between the above indicators and the increased cervical spinal cord area was studied through Pearson's correlation analysis and multivariate logistic regression analysis. RESULTS: There were 34 patients in small spinal cord area increment group (SAI group), 29 patients in middle spinal cord area increment group (MAI group) and 20 patients in large spinal cord area increment group (LAI group). The preoperative diagnosis(P = 0.001), door shaft position (P = 0.008), preoperative spinal canal area (P = 0.004) and postoperative spinal canal area (P = 0.015) were significant different among the 3 groups. The multivariate analysis showed that the preoperative diagnosis (OR = 2.076, P = 0.035), door shaft position (OR = 3.425, P = 0.020) and preoperative spinal canal area (OR = 10.217, P = 0.009) were related to increased spinal cord area. CONCLUSIONS: The preoperative diagnosis, door shaft position and preoperative spinal canal area might be associated with increased spinal cord area after cervical laminoplasty with miniplate fixation. Preoperative symptoms are mostly caused by compression of the spinal cord, so spinal cord area enlargement can bring a better recovery in patients alongside long-term. Spine surgeons should pay more attention to the accuracy of the preoperative diagnosis, the preoperative measurement of spinal canal area and the door shaft position during the operation.

Activation of peroxisome proliferation-activated receptor-γ inhibits transforming growth factor-ß1-induced airway smooth muscle cell proliferation by suppressing Smad-miR-21 signaling.

The aims of the current study were to examine the signaling mechanisms for transforming growth factor-ß1 (TGF-ß1)-induced rat airway smooth muscle cell (ASMC) proliferation and to determine the effect of activation of peroxisome proliferation-activated receptor-γ (PPAR-γ) on TGF-ß1-induced rat ASMC proliferation and its underlying mechanisms. TGF-ß1 upregulated microRNA 21 (miR-21) expression by activating Smad2/3, and this in turn downregulated forkhead box O1 (FOXO1) mRNA expression. In addition, TGF-ß1-Smad-miR-21 signaling also downregulated phosphatase and tensin homolog deleted on chromosome ten (PTEN) expression and thus de-repressed the PI3K-Akt pathway. Depletion of PTEN reduced the nuclear FOXO1 protein level without affecting its mRNA level. Inhibition of the PI3K-Akt pathway or proteasome function reversed PTEN knockdown-induced nuclear FOXO1 protein reduction. Our study further showed that loss of FOXO1 increased cyclin D1 expression, leading to rat ASMC proliferation. Preincubation of rat ASMCs with pioglitazone, a PPAR-γ activator, blocked TGF-ß1-induced activation of Smad2/3 and its downstream targets changes of miR-21, PTEN, Akt, FOXO1, and cyclin D1, resulting in the inhibition of rat ASMC proliferation. Our study suggests that the activation of PPAR-γ inhibits rat ASMC proliferation by suppressing Smad-miR-21 signaling and therefore has a potential value in the prevention and treatment of asthma by negatively modulating airway remodeling.

iTRAQ-Based Differential Proteomic Analysis Reveals the Pathways Associated with Tigecycline Resistance in Acinetobacter baumannii.

BACKGROUND/AIMS: Acinetobacter baumannii is an aerobic and Gram-negative bacterial pathogen with high morbidity and mortality. It remains a serious public health problem arising from its multidrug-resistant and extensive antibiotic resistance spectrum. METHODS: In the present study, iTRAQ coupled with 2D LC-MS/MS was used to evaluate the proteome in standard Acinetobacter baumannii standard strains and tigecycline-resistant strains. RESULTS: A total of 3639 proteins were identified and 961 proteins were identified to be differentially expressed in tigecycline-resistant Acinetobacter baumannii strains compared to the standard strains. 506 (52.6%) proteins were up-regulated and 455 (47.4%) proteins were down-regulated. Based on the GO enrichment analysis and KEGG pathway analysis, we concluded that most differentially expressed proteins were associated with stress responses, cellular component organization, proteins synthesis, degradation and function. Moreover, ß-lactam resistance, the longevity regulating pathway and other related pathways were also involved in the regulation of tigecycline-resistant Acinetobacter baumannii. The differential expression of key proteins were evaluated by transcript analysis using quantitative RT-PCR. CONCLUSION: These results may provide new insights into the mechanisms of drug resistance in Acinetobacter baumannii.

Association between psoriasis and asthma risk: A meta-analysis.

BACKGROUND: Psoriasis has been shown to be related to an increased risk of asthma, although the results remain inconclusive. Therefore, we performed a meta-analysis to determine whether psoriasis increases the risk of asthma. METHODS: A comprehensive search of medical literature data bases was conducted through May 2017. The pooled odds ratios (OR) and corresponding 95% confidence intervals (CI) were calculated. RESULTS: A total of six studies with 66,772 psoriasis cases and 577,415 controls were included. Our meta-analysis showed that psoriasis was significantly associated with the increased risk of asthma (OR 1.32 [95% CI, 1.20-1.46]). The older age patients with psoriasis (≥50 years) (OR 1.64 [95% CI, 1.44-1.88]) had a higher risk of asthma susceptibility compared with the younger patients (20-49 years old) (OR 1.25 [95% CI 1.09-1.44]). Subgroup analysis by ethnicity indicated a significant increase in asthma risk in both Asian populations (OR 1.35 [95% CI, 1.18-1.54]) and white populations (OR 1.27 [95% CI, 1.05-1.54]) with psoriasis compared with those without psoriasis. CONCLUSION: Results of this meta-analysis indicated that the patients with psoriasis had a higher risk of asthma susceptibility, especially among the older patients with psoriasis.

[Clinical effect and mechanism of hemoperfusion in treatment of children with severe abdominal Henoch-Schönlein purpura].

OBJECTIVE: To study the clinical effect and mechanism of hemoperfusion (HP) in the treatment of children with severe abdominal Henoch-Schönlein purpura (HSP). METHODS: A total of 24 children with severe abdominal HSP were divided into two groups: conventional treatment and HP (n=12 each). Ten healthy children who underwent physical examination were enrolled as the control group. Before and after treatment, chemiluminescence was used to measure the serum levels of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α); thiobarbituric acid colorimetry was used to measure the plasma level of malondialdehyde (MDA); the hydroxylamine method was used to measure the plasma level of superoxide dismutase (SOD); chemical colorimetry was used to measure the plasma level of total anti-oxidant capability (T-AOC). RESULTS: Compared with the control group, the conventional treatment and HP groups had significantly higher IL-6, TNF-α, and MDA levels and significantly lower SOD and T-AOC levels before treatment (P<0.05), but there were no significant differences between the conventional treatment and HP groups (P>0.05). After treatment, the conventional treatment and HP groups had significant reductions in IL-6, TNF-α, and MDA levels and significant increases in SOD and T-AOC levels (P<0.05). The HP group had significantly greater changes than the conventional treatment group; however, there were still significant differences in these indices between the HP and control groups (P<0.05). Compared with the HP group, the conventional treatment group had a significantly lower percentage of children with disappearance of digestive tract symptoms at 4 days after treatment and significantly longer time to disappearance of rash and digestive tract symptoms (P<0.05). Compared with the conventional treatment group, the HP group had a significantly lower amount of glucocorticoid used during treatment and a significantly lower percentage of children who experienced hematuria and/or proteinuria within 6 months of the disease course (P<0.05). There were no significant differences between the two groups in length of hospital stay and recurrence rates of rash and abdominal pain within 6 months of the disease course. CONCLUSIONS: HP can reduce the amount of glucocorticoid used during treatment and the incidence rate of kidney injury in children with severe abdominal HSP, possibly by eliminating IL-6, TNF-α, and MDA.

Interleukin-12B gene polymorphisms and bronchial asthma risk: A meta-analysis.

OBJECTIVE: This meta-analysis aims to investigate whether interleukin-12B (IL-12B) -1188A/C or the promoter polymorphisms may be a risk factor for asthma. DATA SOURCES: Web of Science, PubMed, China National Knowledge Infrastructure (CNKI) and Wanfang databases were searched (updated August 20, 2015). STUDY SELECTIONS: Articles evaluating the association between IL-12B genetic polymorphisms and asthma risk were selected. RESULTS: 13 eligible studies with a total of 5092 subjects were finally included in this meta-analysis. For IL-12B -1188A/C, analysis by ethnicity indicated that there was a markedly reduced risk for asthma in East Asian (CC + AC vs. AA: OR = 0.64, 95% CI = 0.50-0.81, P < 0.001). For IL-12B promoter, analysis by ethnicity indicated there was a markedly increased risk in East Asian (MM vs. WM + WW: OR = 1.57, 95% CI = 1.18-2.10, P = 0.002). Analysis by allergic state revealed the similar results in atopic subgroup. CONCLUSIONS: IL-12B -1188 C allele may be a protective factor against asthma in East Asian. In addition, promoter MM genotype may be a risk factor for asthma in East Asian and allergic people.

Knockdown of AMPKα2 Promotes Pulmonary Arterial Smooth Muscle Cells Proliferation via mTOR/Skp2/p27(Kip1) Signaling Pathway.

It has been shown that activation of adenosine monophosphate-activated protein kinase (AMPK) suppresses proliferation of a variety of tumor cells as well as nonmalignant cells. In this study, we used post-transcriptional gene silencing with small interfering RNA (siRNA) to specifically examine the effect of AMPK on pulmonary arterial smooth muscle cells (PASMCs) proliferation and to further elucidate its underlying molecular mechanisms. Our results showed that knockdown of AMPKα2 promoted primary cultured PASMCs proliferation; this was accompanied with the elevation of phosphorylation of mammalian target of rapamycin (mTOR) and S-phase kinase-associated protein 2 (Skp2) protein level and reduction of p27(Kip1). Importantly, prior silencing of mTOR with siRNA abolished AMPKα2 knockdown-induced Skp2 upregulation, p27(Kip1) reduction as well as PASMCs proliferation. Furthermore, pre-depletion of Skp2 by siRNA also eliminated p27(Kip1) downregulation and PASMCs proliferation caused by AMPKα2 knockdown. Taken together, our study indicates that AMPKα2 isoform plays an important role in regulation of PASMCs proliferation by modulating mTOR/Skp2/p27(Kip1) axis, and suggests that activation of AMPKα2 might have potential value in the prevention and treatment of pulmonary arterial hypertension.

Inhibition of Notch3 prevents monocrotaline-induced pulmonary arterial hypertension.

It has been shown that activation of Notch3 signaling is involved in the development of pulmonary arterial hypertension (PAH) by stimulating pulmonary arteries remodeling, while the molecular mechanisms underlying this are still largely unknown. The aims of this study are to address these issues. Monocrotaline dramatically increased right ventricle systolic pressure to 39.0 ± 2.6 mmHg and right ventricle hypertrophy index to 53.4 ± 5.3% (P < 0.05 versus control) in rats, these were accompanied with significantly increased proliferation and reduced apoptosis of pulmonary vascular cells as well as pulmonary arteries remodeling. Treatment of PAH model with specific Notch inhibitor DAPT significantly reduced right ventricle systolic pressure to 26.6 ± 1.3 mmHg and right ventricle hypertrophy index to 33.5 ± 2.6% (P < 0.05 versus PAH), suppressed proliferation and enhanced apoptosis of pulmonary vascular cells as well as inhibited pulmonary arteries remodeling. Our results further indicated that level of Notch3 protein and NICD3 were increased in MCT-induced model of PAH, this was accompanied with elevation of Skp2 and Hes1 protein level and reduction of P27Kip1. Administration of rats with DAPT-prevented MCT induced these changes. Our results suggest that Notch3 signaling activation stimulated pulmonary vascular cells proliferation by Skp2-and Hes1-mediated P27Kip1 reduction, and Notch3 might be a new target to treat PAH.

Self-catalytic polymerization of a water-soluble selenium/polypyrrole nanocomposite and its nonlinear optical properties.

A facile one-step method for the synthesis of a water-soluble selenium/polypyrrole (Se/PPy) nanocomposite was developed. In the aqueous synthesis process, the pyrrole acted as a reductant for the reduction of H2SeO3, and then the elemental Se formed in situ acted as a catalyst for the polymerization of pyrrole. The characterization results show that the as-obtained composite (Se/PPy) is a spherical (Φ80 nm) product that is made up of amorphous Se particles coated by PPy layers. The formation mechanism and influence factors of the products were discussed, based on a series of experiments. It is proposed that remainder H2SeO3 adsorbed on the PPy chains increased the water-solubility and conductivity of the Se/PPy nanocomposite. Significantly, relying on the synergistic effect of photo-conductive Se nanoparticles and electric-conductive PPy molecules, the Se/PPy nanocomposite possesses a large two-photon absorption (2PA) cross-section and good optical limiting properties, which were demonstrated by the Z-scan technique using a femtosecond laser. We believe that this work should be an interesting strategy for developing polymer composites with excellent optoelectrical properties.

Activation of AMPK inhibits pulmonary arterial smooth muscle cells proliferation.

The aims of the present study were to examine the effect of AMPK activation on pulmonary arterial smooth muscle cells (PASMCs) proliferation and to address its potential mechanisms. ET-1 dose and time-dependently induced PASMCs proliferation, and this effect was suppressed by a selective AMPK activator metformin. The results of the study further indicated that the proliferation of PASMCs stimulated by ET-1 was associated with the increase of Skp2 and decrease of p27, and metformin reversed ET-1-induced Skp2 elevation and raised p27 protein level. Our study suggests that activation of AMPK suppresses PASMCs proliferation and has potential value in negatively modulating pulmonary vascular remodeling and therefore could prevent or treat the development of pulmonary arterial hypertension (PAH).

Growth of the skull in young children in Baotou, China.

BACKGROUND: There are some controversies about the optimal time to perform skull repair in very young Chinese children because of the rapid skull growth in this stage of life. The purpose of this current study is to describe the characteristics of skull growth and to discuss the optimal time for skull repair in young Chinese children with skull defects. METHODS: A total of 112 children born in the First Affiliated Hospital of Baotou Medical College were measured for six consecutive years starting in 2006. Cranial length (CL, linear distance between the eyebrows to the pillow tuberosity), cranial width (CW, double-sided linear distance of connection of external auditory canal), ear over the top line (EOTL), the eyebrows-the posterior tuberosity line (EPTL), and head circumference (HC) were measured to describe the skull growth. RESULTS: The most rapid period of skull growth occurs during the first year of life. The second and third most rapid periods are the second and third years, respectively. Then, the skull growth slowed and the values of the skull growth index of 6-year-old children were close to those of adults. CONCLUSION: Children 0-1 years old should not receive skull repair due to their rapid skull growth. The indexes of children 3 years old or older were close to those of the adult; therefore, 3 years old or older may receive skull repair.

Path-following control of wheeled planetary exploration robots moving on deformable rough terrain.

The control of planetary rovers, which are high performance mobile robots that move on deformable rough terrain, is a challenging problem. Taking lateral skid into account, this paper presents a rough terrain model and nonholonomic kinematics model for planetary rovers. An approach is proposed in which the reference path is generated according to the planned path by combining look-ahead distance and path updating distance on the basis of the carrot following method. A path-following strategy for wheeled planetary exploration robots incorporating slip compensation is designed. Simulation results of a four-wheeled robot on deformable rough terrain verify that it can be controlled to follow a planned path with good precision, despite the fact that the wheels will obviously skid and slip.

The effects of CoCl2 on HIF-1α protein under experimental conditions of autoprogressive hypoxia using mouse models.

It is well known that cobalt chloride (CoCl2) can enhance the stability of hypoxia-inducible factor (HIF)-1α. The aim of this study is to detect the effect of CoCl2 on the hypoxia tolerance of mice which were repeatedly exposed to autoprogressive hypoxia. Balb/c mice were randomly divided into groups of chemical pretreatment and normal saline (NS), respectively injected with CoCl2 and NS 3 h before exposure to hypoxia for 0 run (H0), 1 run (H1), and 4 runs (H4). Western Blot, electrophoretic mobility shift assay (EMSA), extracellular recordings population spikes in area cornus ammonis I (CA 1) of mouse hippocampal slices and real-time were used in this study. Our results demonstrated that the tolerance of mice to hypoxia, the changes of HIF-1α protein level and HIF-1 DNA binding activity in mice hippocampus, the mRNA level of erythropoietin (EPO) and vascular endothelial growth factor (VEGF), and the disappearance time of population spikes of hippocampal slices were substantially different between the control group and the CoCl2 group. Over-induction of HIF-1α by pretreatment with CoCl2 before hypoxia did not increase the hypoxia tolerance.

Addition of nimotuzumab to concurrent chemoradiotherapy after induction chemotherapy improves outcomes of patients with locally advanced nasopharyngeal carcinoma.

Purpose: To investigate the survival outcomes and toxicities associated with the addition of nimotuzumab to concurrent chemoradiotherapy (CCRT) in locally advanced nasopharyngeal carcinoma (LANPC) patients who received induction chemotherapy (IC). Methods: Patients with stage III-IVA nasopharyngeal carcinoma who received IC and CCRT between January 2017 and October 2021 were retrospectively included. We aimed to compare the locoregional recurrence-free survival (LRFS), distant metastasis-free survival (DMFS), disease-free survival (DFS), and overall survival (OS) between patients treated with CCRT+nimotuzumab and CCRT alone. Results: We included 411 patients in the analysis. Of these patients, 267 (65.0%) and 144 (35.0%) had CCRT+nimotuzumab and CCRT alone, respectively. Similar LRFS was found between those with and without nimotuzumab (92.9% vs. 92.6%, p = 0.855). The 3-year DMFS was 88.2% and 76.2% in those with and without nimotuzumab (p = 0.002). The 3-year DFS was 83.4% and 70.6% in those with and without nimotuzumab treatment (p = 0.003). The 3-year OS was 92.1% and 81.1% in those with and without nimotuzumab (p = 0.003). The multivariate Cox regression analysis indicated that the addition of nimotuzumab was independently associated with better DMFS (hazard ratio [HR] 0.606, p = 0.049), DFS (HR 0.613, p = 0.028), and OS (HR 0.497, p = 0.019). No significant differences in major toxicities were found between the two treatment arms, including hematologic toxicities, hepatoxicity, nephrotoxicity, gastrointestinal reactions, and mucositis (all p > 0.05). Conclusion: The addition of nimotuzumab to CCRT after IC in LANPC has shown promising results in improving treatment outcomes and acceptable toxicities.