A novel mutation in GPR68 causes hypomaturation amelogenesis imperfecta.

OBJECTIVES: To identify the genetic cause of a Chinese family with hypomaturation amelogenesis imperfecta (AI) and to characterize the structure of GPR68 mutated enamel in order to develop a deeper understanding of the role of the GPR68 protein during the intricate process of amelogenesis. DESIGN: One Chinese family with generalized hypomaturation AI was recruited. Two of the third molars from the proband were subjected to scanning electron microscopy (SEM) and energy dispersive X-ray spectroscopy (EDX). Whole exome sequencing (WES) was performed, and the identified mutation was confirmed by Sanger sequencing. Bioinformatics studies were further conducted to analyze the potential deleterious effects of the mutation. RESULTS: The proband presented with a hypomaturation AI phenotype, characterized by fragile and discolored enamel surface. The AI enamel showed prismatic structure, which was sporadically obscured by areas of amorphous material and porous structure. EDX analysis showed the proband's enamel demonstrated a significant decrease in calcium and phosphorus content and a significant increase in oxygen compared with normal enamel. A novel homozygous mutation of G protein-coupled receptor 68 (GPR68) (c .149 T > A, p.Ile50Asn) was identified in the proband. Bioinformatics analysis indicated that the mutation site displayed a high level of evolutionary conservation among species, and the mutation might impact the stability and conformation of the protein. CONCLUSION: The novel homozygous GPR68 mutation resulted in hypomaturation AI. We first described the effect of GPR68 mutation on enamel structure. Our results provide new genetic evidence that mutations involved in GPR68 contribute to hypomaturation AI.

The mechanisms related to fibroblasts in burn surface.

PURPOSE: Mesenchymal stem cells (MSCs) can promote burn wound healing, skin appearance, and function recovery by promoting the differentiation and migration of fibroblasts of a wound. The burn environment can activate the autophagy of MSCs. However, it is not clear whether this autophagy can affect the proliferation and migration of fibroblasts. METHODS: In this study, pretreated MSCs with rapamycin and 3-methyladenine modulated autophagy and co-cultured with fibroblasts of burn. Cell migration was detected by immunofluorescence chemical staining. Western blot analysis and enzyme-linked immunosorbent assay were performed to detect 2,3-Dioxygenase (IDO), cytokine synthesis inhibitory factor 10 (IL-10), cytokine synthesis inhibitory factor 6 (IL-6), prostaglandin E2 (PGE2), transforming growth factor beta 1 (TGF-ß1) proteins levels, and the autophagy proteins p62 and microtubule-associated protein LC3-II/I. RESULTS: We demonstrated that autophagy regulates MSCs survival and proliferation in burn wound transplants and found that autophagy inhibition with 3-methyladenine reduced MSCs-mediated, fibroblast proliferation and migration in burn environment. However, rapamycin-induced autophagy had the opposite effect and increased the TGF-ß1 expression. Therefore, we speculate that MSCs may promote fibroblast proliferation and migration by secreting TGF-ß1 via the AKT/mTOR (RAC-alpha serine/threonine-protein kinase/mammalian target of rapamycin) pathway. CONCLUSION: Autophagy of MSCs regulates burn wound fibroblast proliferation and migration by affecting TGF-ß1 and prostaglandin E2 production adjacent to MSCs transplanted on the burn wound. The results of this study provide a potential strategy for promoting MSCs treatment of burns.

The effect of the root dilaceration on the treatment duration and prognosis of unilateral impacted immature maxillary central incisors.

INTRODUCTION: This study aimed to investigate the effect of root dilaceration on the closed-eruption technique treatment and prognosis on impacted immature maxillary central incisors. METHODS: In this retrospective study, we compared the age at the beginning of the treatment, the treatment duration, root development, and alveolar bone mass after the closed-eruption technique between the impacted immature maxillary central incisors with dilacerated roots (group 1) and those with straight roots (group 2). RESULTS: The mean age at the time of the surgery of group 1 was 0.9 years younger than that of group 2 (P = 0.008). The mean traction time was greater in group 1 (8.0 ± 1.8 months), with a difference of 1.4 months than in group 2 (6.6 ± 2.1 months) (P = 0.042). The measurements of lingual bone thickness at the alveolar crest (C) showed significant differences between the 2 groups (P = 0.025). No significant differences were found in other treatment duration or measurements of root development and alveolar bone mass between the 2 groups. CONCLUSIONS: Patients with impacted immature incisors with dilacerated roots were younger at the beginning of the closed-eruption treatment and had a longer traction time than those with impacted immature incisors having straight roots. The root dilaceration had little or no effect on root development and alveolar bone mass after the closed-eruption treatment. The closed-eruption treatment of impacted immature incisors with root dilaceration is suggested to commence as early as possible.

A Novel lncRNA Mediates the Delayed Tooth Eruption of Cleidocranial Dysplasia.

Delayed eruption of permanent teeth is a common symptom of cleidocranial dysplasia (CCD). Previous studies have focused on the anomaly of osteogenesis resulting from mutations in the Runt-related transcription factor-2 gene (RUNX2). However, deficiencies in osteoclastogenesis and bone resorption, and the epigenetic regulation mediated by long non-coding (lnc)RNAs in CCD remain to be elucidated. Here, a novel osteoclast-specific lncRNA (OC-lncRNA) was identified during the osteoclast differentiation of RAW 264.7 cells transfected with a RUNX2 mutation expression cassette. We further confirmed that OC-lncRNA positively regulated osteoclastogenesis and bone resorption. The OC-lncRNA promoted the expression of CXC chemokine receptor type 3 (CXCR3) by competitively binding to microRNA (miR)-221-5p. The CXCR3-CXC-motif chemokine ligand 10 (CXCL10) interaction and nuclear factor-κB constituted a positive feedback that positively regulated osteoclastogenesis and bone resorption. These results demonstrate that OC-lncRNA-mediated osteoclast dysfunction via the OC-lncRNA-miR-221-5p-CXCR3 axis, which is involved in the process of delayed tooth eruption of CCD.

Orrella daihaiensis sp. nov., a bacterium isolated from Daihai Lake in Inner Mongolia.

A novel aerobic, Gram-staining-negative, non-motile, short-rod-shaped strain, designated f23T, was obtained from Daihai Lake, Inner Mongolia, Republic of China. 16S rRNA gene sequences analysis showed that f23T belongs to the genus Orrella and is most closely related to Orrella marina H-Z20T with 98.35% sequence similarity. The strain was oxidase positive, catalase positive and had well growth at pH 6.5-8.5, at temperature 28-40 °C and at 0-4.5% (w/v) NaCl. Colonies incubated at 37 °C on marine 2216 agar for 3 days were white, smooth, transparent, circular and less than 1.0 mm in diameter. The total genome size of f23T was 2,803,849 bp with a G + C content of 52.79%. The average nucleotide identity (ANI) and digital DNA-DNA hybridization (dDDH) values between strain f23T and O. marina H-Z20T were 69.62% and 20.5%, which both below the species delineation threshold. Chemotaxonomic analysis showed that C16:0, cyclo-C17:0, C18:0, Sum Feature 3 (C16:1ω7c and/or C16:1ω6c) and Sum Feature 8 (C18:1ω6c and C18:1ω7c) as the major fatty acids, ubiquinone-8 as the major isoprenoid quinone, phosphatidylethanolamine as the major cellular polar lipids. Based on the polyphasic analysis, f23T represents a novel species within the genus Orrella, for which the name Orrella daihaiensis sp. nov. is proposed. The type strain is f23T (= CGMCC 1.18761 T = KCTC 82425 T).

Morphological and molecular characterization of Geocenamus persici n. sp. (Nematoda: Merliniinae) from China.

A new stunt nematode species, Geocenamus persici n. sp. was recovered from the rhizosphere of peach (Prunus persica) in Zhejiang Province, China. This species is characterized by a dome-shaped labial region with six bulging sectors. The lip region is slightly offset from the rest of the body with five annuli; cuticle with over 30 longitudinal striae; stylet slender, 19 to 21 m long; excretory pore at the anterior region of the basal pharyngeal bulb; tail cylindrical, 55 to 79 m long with striated terminus. Males are common. Morphologically, the species is close to G. brevicaudatus, G. chengi, G. conicaudatus, G. quadrifer, G. rugosus, and G. tartuensis. Phylogenetic relationships of the new species placed G. persici n. sp. with other species of subfamily Merliniinae. However, it has a sister relationship with G. chengi. Since the new species is found in the peach plantations, our study will lay a foundation to initiate investigations on the occurrence of stunt nematodes in peach growing areas and will aid the researchers to determine whether this group of nematodes cause peach plantation diseases.

Solitary Median Maxillary Central Incisor Syndrome: An Exploration of the Pathogenic Mechanism.

This study aimed to identify the genetic cause of one Chinese family with solitary median maxillary central incisor (SMMCI) and explore the relationship between genotype and its phenotype. One Chinese family with clinical diagnosis of SMMCI was collected. Single Nucleotide Polymorphism (SNP) array was performed and identified variation was confirmed by whole-genome sequencing (WGS). The reported chromosomal abnormalities and pathogenic genes in patients with SMMCI in literature were reviewed and summarized. The proband was an 8-year-old boy presenting a typical solitary median maxillary central incisor with a range of other phenotypic anomalies, including ptosis. SNP array revealed a 14.3 Mbp heterozygous deletion at chromosome 18p11.32-p11.21 in the proband but not in the unaffected parents. WGS further confirmed the identified deletion. 194 genes were involved in the chromosome region. Among them, 12 genes had been shown to be associated with diseases, including TGIF1, a reported SMMCI gene. The de novo 18p deletion resulted in SMMCI in the present study. Our results provide new genetic evidence that structural abnormality in chromosome 18p contributes to solitary median maxillary central incisor.

A novel ENAM mutation causes hypoplastic amelogenesis imperfecta.

OBJECTIVES: To identify the genetic cause of one Chinese family with hypoplastic amelogenesis imperfecta (AI) and explore the relationship between genotype and its phenotype. MATERIAL AND METHODS: One Chinese family with generalized hypoplastic AI was recruited. One deciduous tooth from the proband was subjected to scanning electron microscopy. Whole-exome sequencing was performed and identified mutation was confirmed by Sanger sequencing. Bioinformatics studies were further conducted to analyze potential deleterious effects of the mutation. RESULTS: The proband presented a typical hypoplastic AI phenotype whose teeth in deciduous and permanent dentitions showed thin, yellow, and hard enamel surface. The affected enamel in deciduous tooth showed irregular, broken, and collapsing enamel rods with borders of the enamel prisms undulated and structural shapes of prisms irregular. A novel homozygous nonsense mutation in the last exon of the enamelin (ENAM) gene (NM_031889.3; c.2078C>G) was identified in the proband, which was predicted to produce a highly truncated protein (NP_114095.2; p.(Ser693*)). This mutation was also identified in the proband's parents in heterozygous form. Surprisingly, the clinical phenotype of the heterozygous parents varied from a lack of penetrance to mild enamel defects. Additional bioinformatics studies demonstrated that the detected mutation could change the 3D structure of the ENAM protein and severely damaged the function of ENAM. CONCLUSION: The novel homozygous ENAM mutation resulted in hypoplastic AI in the present study. Our results provide new genetic evidence that mutations involved in ENAM contribute to hypoplastic AI.

CircRNA circ_0006892 regulates miR-24/PHLPP2 axis to mitigate cigarette smoke extract-induced bronchial epithelial cell injury.

Chronic obstructive pulmonary disease (COPD) is a chronic airway disorder mainly resulted from cigarette smoke exposure. The dysregulated circular RNAs (circRNAs) are relevant to the pathogenesis of COPD. This study aims to explore the function and mechanism of circRNA hsa_circ_0006892 (circ_0006892) in cigarette smoke extract (CSE)-induced bronchial epithelial injury. The lung tissues were collected from 17 nonsmokers and 23 smokers with COPD. The bronchial epithelial cells (BEAS-2B and 16HBE) were stimulated via CSE. Circ_0006892, microRNA-24 (miR-24), and PH domain and leucine-rich repeat protein phosphatase 2 (PHLPP2) abundances were examined via a quantitative reverse transcription polymerase chain reaction or Western blot. Cell viability, apoptosis, and inflammatory response were assessed via cell counting kit-8 (CCK-8), flow cytometry, and enzyme-linked immunosorbent assay (ELISA). The target relationship of miR-24 and circ_0006892 or PHLPP2 was tested via dual-luciferase reporter analysis, RNA immunoprecipitation, and RNA pull-down. Circ_0006892 expression was reduced in lung tissues of smokers with COPD and CSE-stimulated bronchial epithelial cells. Circ_0006892 overexpression alleviated CSE-induced viability reduction and promotion of apoptosis and inflammatory response. MiR-24 was bound via circ_0006892, and miR-24 overexpression reversed the effect of circ_0006892 on CSE-induced injury. PHLPP2 was targeted via miR-24, and miR-24 knockdown mitigated CSE-induced viability reduction and promotion of apoptosis and inflammatory response via regulating PHLPP2. Circ_0006892 could promote PHLPP2 expression via regulating miR-24. Circ_0006892 attenuated CSE-induced bronchial epithelial cell apoptosis and inflammatory response via regulating miR-24/PHLPP2 axis.

Identification and experimental validation of key m6A modification regulators as potential biomarkers of osteoporosis.

Osteoporosis (OP) is a severe systemic bone metabolic disease that occurs worldwide. During the coronavirus pandemic, prioritization of urgent services and delay of elective care attenuated routine screening and monitoring of OP patients. There is an urgent need for novel and effective screening diagnostic biomarkers that require minimal technical and time investments. Several studies have indicated that N6-methyladenosine (m6A) regulators play essential roles in metabolic diseases, including OP. The aim of this study was to identify key m6A regulators as biomarkers of OP through gene expression data analysis and experimental verification. GSE56815 dataset was served as the training dataset for 40 women with high bone mineral density (BMD) and 40 women with low BMD. The expression levels of 14 major m6A regulators were analyzed to screen for differentially expressed m6A regulators in the two groups. The impact of m6A modification on bone metabolism microenvironment characteristics was explored, including osteoblast-related and osteoclast-related gene sets. Most m6A regulators and bone metabolism-related gene sets were dysregulated in the low-BMD samples, and their relationship was also tightly linked. In addition, consensus cluster analysis was performed, and two distinct m6A modification patterns were identified in the low-BMD samples. Subsequently, by univariate and multivariate logistic regression analyses, we identified four key m6A regulators, namely, METTL16, CBLL1, FTO, and YTHDF2. We built a diagnostic model based on the four m6A regulators. CBLL1 and YTHDF2 were protective factors, whereas METTL16 and FTO were risk factors, and the ROC curve and test dataset validated that this model had moderate accuracy in distinguishing high- and low-BMD samples. Furthermore, a regulatory network was constructed of the four hub m6A regulators and 26 m6A target bone metabolism-related genes, which enhanced our understanding of the regulatory mechanisms of m6A modification in OP. Finally, the expression of the four key m6A regulators was validated in vivo and in vitro, which is consistent with the bioinformatic analysis results. Our findings identified four key m6A regulators that are essential for bone metabolism and have specific diagnostic value in OP. These modules could be used as biomarkers of OP in the future.

An Exploration of Mutagenesis in a Family with Cleidocranial Dysplasia without RUNX2 Mutation.

Cleidocranial dysplasia (CCD) is an autosomal dominant inheritable skeletal disorder characterized by cranial dysplasia, clavicle hypoplasia, and dental abnormalities. Mutations involving Runt-related transcription factor 2 (RUNX2) are currently the only known molecular etiology for CCD but are not identified in all CCD patients. No RUNX2 abnormality can be detected in about 20-30% of patients, and the molecular cause remains unknown. The present study includes a family case with typical features of CCD. RUNX2 mutation was first screened by sequencing analysis, and no mutation was detected. Copy number alterations of the RUNX2 gene were then measured by quantitative PCR and multiplex ligation-dependent probe amplification (MLPA). No copy number variation in RUNX2 could be detected. We performed whole-exome sequencing (WES) to identify the underlying genetic mutations. Unexpectedly, no abnormalities could be detected in genes related to the RUNX2 signaling pathway. Therefore, it was supposed that other new unknown gene variations might contribute to the CCD phenotype. We focused on Immunoglobulin superfamily member 10 (IGSF10), a gene related to bone development. An IGSF10 frameshift mutation (c.6001_6002delCT, p.Leu2001Valfs*24) was detected by WES. Sanger sequencing verified that this mutation was only detected in the patient and her affected mother but not in her unaffected father. Bioinformatics studies demonstrated that this mutation could change the 3D structure of the IGSF10 protein and severely damage its function. In addition, alkaline phosphatase (ALP) activity and the ability to form mineralized nodules were inhibited by IGSF10 knockdown compared with normal controls. The expression of bone sialoprotein (BSP) was significantly reduced by IGSF10 knockdown, but not that of other osteogenic markers. Our results provide new genetic evidence that IGSF10 mutation might contribute to CCD.

Effects of GATA6-AS/MMP9 on malignant progression of endometrial carcinoma.

PURPOSE: Previous studies have shown that long non-coding RNA (lncRNA) GATA6-AS is a tumor suppressor gene. However, the role of GATA6-AS in endometrial cancer (EC) has not been reported. We aimed at investigating the expression characteristics of GATA6-AS in EC tissues and cell lines, and explored whether it inhibits the malignant progression of EC through modulating matrix metalloproteinase-9 (MMP9). METHODS: GATA6-AS expression in 17 pairs of EC tissues and adjacent ones was studied by quantitative real-time polymerase chain reaction (qRT-PCR) analysis. Meanwhile, GATA6-AS expression levels in EC cell lines were also evaluated by qRT-PCR assay. In addition, GATA6-AS overexpression model was constructed using lentivirus in EC cell lines KLE and HEC-1B. The impacts of GATA6-AS overexpression model was constructed using lentivirus in EC cell lines KLE and HEC-1B on the proliferation capacity and apoptosis of EC cells were assessed by cell counting kit-8 (CCK-8), 5-Ethynyl-2'- deoxyuridine (EdU), and flow cytometry experiments. Furthermore, we explored the interaction between GATA6-AS and MMP9 in EC cells via performing luciferase assay and cell reverse experiments. RESULTS: Our data showed that GATA6-AS expression in EC tissue specimens was remarkably lower than that in adjacent ones. In vitro cell experiments revealed that overexpression of GATA6-AS markedly attenuated the proliferation ability of EC cells while elevated their apoptosis. Meanwhile, luciferase assay confirmed the binding relationship between GATA6-AS and MMP9. In addition, cell reverse experiments further demonstrated the mutual regulation between GATA6-AS and MMP9, which was, overexpression of MMP9 reversed the inhibitory influence of upregulation of GATA6-AS on the malignant progression of EC. CONCLUSIONS: lncRNA GATA6-AS, lowly expressed in EC tissue samples. Additionally, lncRNA GATA6-AS may suppress the malignant progression of EC through the modulation of regulating MMP9.

Boosting the Electrochemical Performance of Li- and Mn-Rich Cathodes by a Three-in-One Strategy.

There are plenty of issues need to be solved before the practical application of Li- and Mn-rich cathodes, including the detrimental voltage decay and mediocre rate capability, etc. Element doping can effectively solve the above problems, but cause the loss of capacity. The introduction of appropriate defects can compensate the capacity loss; however, it will lead to structural mismatch and stress accumulation. Herein, a three-in-one method that combines cation-polyanion co-doping, defect construction, and stress engineering is proposed. The co-doped Na+/SO42- can stabilize the layer framework and enhance the capacity and voltage stability. The induced defects would activate more reaction sites and promote the electrochemical performance. Meanwhile, the unique alternately distributed defect bands and crystal bands structure can alleviate the stress accumulation caused by changes of cell parameters upon cycling. Consequently, the modified sample retains a capacity of 273 mAh g-1 with a high-capacity retention of 94.1% after 100 cycles at 0.2 C, and 152 mAh g-1 after 1000 cycles at 2 C, the corresponding voltage attenuation is less than 0.907 mV per cycle.

Energy Loss and Radial Force Variation Caused by Impeller Trimming in a Double-Suction Centrifugal Pump.

Impeller trimming is an economical method for broadening the range of application of a given pump, but it can destroy operational stability and efficiency. In this study, entropy production theory was utilized to analyze the variation of energy loss caused by impeller trimming based on computational fluid dynamics. Experiments and numerical simulations were conducted to investigate the energy loss and fluid-induced radial forces. The pump's performance seriously deteriorated after impeller trimming, especially under overload conditions. Energy loss in the volute decreased after trimming under part-load conditions but increased under overload conditions, and this phenomenon made the pump head unable to be accurately predicted by empirical equations. With the help of entropy production theory, high-energy dissipation regions were mainly located in the volute discharge diffuser under overload conditions because of the flow separation and the mixing of the main flow and the stalled fluid. The increased incidence angle at the volute's tongue after impeller trimming resulted in more serious flow separation and higher energy loss. Furthermore, the radial forces and their fluctuation amplitudes decreased under all the investigated conditions. The horizontal components of the radial forces in all cases were much higher than the vertical components.

A Universal Strategy toward the Precise Regulation of Initial Coulombic Efficiency of Li-Rich Mn-Based Cathode Materials.

Li-rich Mn-based cathode materials (LRMs) are potential cathode materials for high energy density lithium-ion batteries. However, low initial Coulombic efficiency (ICE) severely hinders the commercialization of LRM. Herein, a facile oleic acid-assisted interface engineering is put forward to precisely control the ICE, enhance reversible capacity and rate performance of LRM effectively. As a result, the ICE of LRM can be precisely adjusted from 84.1% to 100.7%, and a very high specific capacity of 330 mAh g-1 at 0.1 C, as well as outstanding rate capability with a fascinating specific capacity of 250 mAh g-1 at 5 C, are harvested. Theoretical calculations reveal that the introduced cation/anion double defects can reduce the diffusion barrier of Li+ ions, and in situ surface reconstruction layer can induce a self-built-in electric field to stabilize the surface lattice oxygen. Moreover, this facile interface engineering is universal and can enhance the ICEs of other kinds of LRM effectively. This work provides a valuable new idea for improving the comprehensive electrochemical performance of LRM through multistrategy collaborative interface engineering technology.

Optimization of the Radiation Dose of Digital Breast Tomosynthesis in Opportunistic Screening by Studying the Effect of Different Combinations of FFDM and DBT Views.

BACKGROUND: Full-field digital mammography (FFDM) and digital breast tomosynthesis (DBT) are used separately or in combination to identify small breast lesions. The dose of the examination depends on the density of the breast and the imaging (FFDM or DBT) performed. We have performed a retrospective review of FFDM and DBT in women with denser breasts in order to demonstrate how varying the combination of FFDM and DBT in CC and MLO views affects lesion detection and the average gland dose. METHODS: Eighty-one patients with dense breast received both full-field digital mammography (FFDM) and DBT bilateral screening. The recorded data included the display rates for small lesions or other positive lesions, the type of breast gland, the average gland dose (AGD), and the compression thickness of different collection methods. ANOVA was used to compare the AGD among different collection combinations, and t-test was used to perform pairwise comparison between groups with the same gland type. The relationship between AGD and compression thickness was analyzed by Pearson linear correlation, and the lesion display rates were compared using Chi-square test. RESULTS: We found that AGDs were significantly different among the 6 collection methods (F = 119.06, p<0.01), but were not obviously different between groups with the same gland type (F = 0.848, p>0.05). The types of dense glands were correlated with compression thickness, and the thickness was moderately to strongly correlated with AGD (r=0.596-0.736). The combination of single-view DBT(CC-DBT) and FFDM showed significantly higher mass display rates than the two-view FFDM (p<0.05), while the display rates for other positive lesions were similar (p>0.05). CONCLUSION: Our study showed that in opportunistic screening of patients with small breast masses that can be easily detected by ultrasound, MLO-FFDM+CC-DBT or CC-FFDM+MLO-DBT combinations can better balance the individual average gland dose and detection accuracy. The study result cannot be applied to the detection of non-mass lesions as the numbers are too small.

Evaluation on blood coagulation and C-reactive protein level among children with mycoplasma pneumoniae pneumonia by different chest imaging findings.

ABSTRACT: Mycoplasma pneumoniae infection may induce a systemic hypercoagulable abnormality, like organ embolism and infarction. Indexes of blood coagulation and C-reactive protein (CRP) have been reported different between healthy people and mycoplasma pneumoniae pneumonia (MPP) patients, but this difference in MPP patients with different chest imaging findings has rarely been reported.We performed a retrospective study of 101 children with MPP and 119 controls, combined with radiological examination and blood tests, to compare the blood coagulation and CRP level among MPP children with different chest imaging findings.For the MPP children with different chest imaging findings, there were significant differences in CRP, fibrinogen (FIB) and D-dimer (D-D) levels among subgroups (P = .004, P = .008 and P < .001 respectively). The CRP level in group of interstitial pneumonia was significantly higher than that in groups of bronchopneumonia and hilar shadow thickening (P = .003 and P = .001 respectively). And the FIB and D-D values in group of lung consolidation were significantly higher than that in the other 3 groups (all P < .05). When compared with controls, the white blood cell, CRP, FIB, and D-D levels in MPP children were significantly higher, and the activated partial thromboplastin time and thrombin time levels were significantly lower (all P < .05).Our results showed that CRP level changed most significantly in group of interstitial pneumonia, whereas FIB, D-D levels changed most significantly in the lung consolidation group.

Differentiating atypical hemangiomas and vertebral metastases: a field-of-view (FOV) and FOCUS intravoxel incoherent motion (IVIM) diffusion-weighted imaging (DWI) study.

PURPOSE: Some atypical vertebral hemangiomas (VHs) may mimic metastases on routine MRI and can result in misdiagnosis and ultimately to additional imaging, biopsy and unnecessary costs. The purpose of this study is to assess the utility of intravoxel incoherent motion (IVIM) diffusion-weighted imaging (DWI) on account of field-of-view optimized and constrained undistorted single shot (FOCUS) in distinguishing atypical VHs and vertebral metastases. METHODS: A total of 25 patients with vertebral metastases and 25 patients with atypical VHs were confirmed by clinical follow-up or pathology. IVIM-DWI imaging was performed at different b values (0, 30, 50, 100, 150, 200, 400, 600, 800, 1000 mm2/s). IVIM parameters [the true diffusion coefficient (D), pseudodiffusion coefficient (D*), standard apparent diffusion coefficient (ADC), and perfusion fraction (f)] were calculated and compared between two groups by using Student's t test. A receiver operating characteristic analysis was performed. RESULTS: Quantitative analysis of standard ADC and D parameters showed significantly lower values in vertebral metastases when compared to atypical hemangiomas [ADC value: (0.70 ± 0.12) × 10-3 mm2/s vs (1.14 ± 0.28) × 10-3 mm2/s; D value: (0.47 ± 0.07) × 10-3 mm2/s vs (0.76 ± 0.14) × 10-3 mm2/s, all P < 0.01]. The sensitivity and specificity of D value were 93.8% and 92.3%, respectively. CONCLUSION: The standard ADC value and D value may be used as an indicator to distinguish vertebral metastases from atypical VHs. FOCUS IVIM-derived parameters provide potential value in the quantitatively differentiating vertebral metastases from vertebral atypical hemangiomas.

Manipulating External Electric Field and Tensile Strain toward High Energy Density Stability in Fast-Charging Li-Rich Cathode Materials.

Li-rich layered oxides (LLOs) are promising cathodes for lithium-ion batteries because of their high energy density provided by anionic redox. Although great improvements have been achieved in electrochemical performance, little attention has been paid to the energy density stability during fast charging. Indeed, LLOs have severe capacity fading and voltage decay especially at a high state of charge (SOC), disabling the application of the frequently used constant-current-constant-voltage mode for fast charging. Herein, we address this problem by manipulating the external electric field and tensile strain induced by lattice expansion effect in nanomaterials under the guidance of theoretical calculations, which indicate that LLOs at high SOC have almost a zero band gap and a low oxygen formation energy. This strategy will weaken polarization, stabilize lattice oxygen, and restrict phase transition simultaneously. Thus, the energy density during fast charging can be highly stabilized. Therefore, it may be of great value for the practical application of layered cathodes.