Podocan promoting skeletal muscle post-injury regeneration by inhibiting TGF-ß signaling pathway.

Podocan, the fifth member of Small Leucine-Rich Proteoglycan (SLRP) family of extracellular matrix components, is poorly known in muscle development. Previous studies have shown that Podocan promotes C2C12 differentiation in mice. In this study, we elucidated the effect of Podocan on skeletal muscle post-injury regeneration and its underlying mechanism. Injection of Podocan protein promoted the process of mice skeletal muscle post-injury regeneration. This effect seemed to be from the acceleration of muscle satellite cell differentiation in vivo. Meanwhile, Podocan promoted myogenic differentiation in vitro by binding with TGF-ß1 to inhibit the activity of the TGF-ß signaling pathway. These results indicated that Podocan had the potential roles to enhance skeletal muscle post-injury regeneration. Its mechanism is likely the regulation of the expression of p-Smad2 and p-Smad4 related to the TGF-ß signaling pathway by interacting with TGF-ß1.

Wi-Fi-Based Indoor Localization and Navigation: A Robot-Aided Hybrid Deep Learning Approach.

Indoor localization and navigation have become an increasingly important problem in both industry and academia with the widespread use of mobile smart devices and the development of network techniques. The Wi-Fi-based technology shows great potential for applications due to the ubiquitous Wi-Fi infrastructure in public indoor environments. Most existing approaches use trilateration or machine learning methods to predict locations from a set of annotated Wi-Fi observations. However, annotated data are not always readily available. In this paper, we propose a robot-aided data collection strategy to obtain the limited but high-quality labeled data and a large amount of unlabeled data. Furthermore, we design two deep learning models based on a variational autoencoder for the localization and navigation tasks, respectively. To make full use of the collected data, a hybrid learning approach is developed to train the models by combining supervised, unsupervised and semi-supervised learning strategies. Extensive experiments suggest that our approach enables the models to learn effective knowledge from unlabeled data with incremental improvements, and it can achieve promising localization and navigation performance in a complex indoor environment with obstacles.

A Double-Layer Vehicle Speed Prediction Based on BPNN-LSTM for Off-Road Vehicles.

The accurate prediction of vehicle speed is crucial for the energy management of vehicles. The existing vehicle speed prediction (VSP) methods mainly focus on road vehicles and rarely on off-road vehicles. In this paper, a double-layer VSP method based on backpropagation neural network (BPNN) and long short-term memory (LSTM) for off-road vehicles is proposed. First of all, considering the motion characteristics of off-road vehicles, the VSP problem is established and the relationship between the variables in the problem is carefully analyzed. Then, the double-layer VSP framework is presented, which consists of speed prediction and information update layers. The speed prediction layer established by using LSTM is to predict vehicle speed in the horizon, and the information update layer built by BPNN is to update the prediction information. Finally, with the help of mining truck and loader operation scenarios, the proposed VSP method is compared with the analytical method, BPNN prediction method, and recurrent neural network (RNN) prediction method in terms of speed prediction accuracy. The results show that, under the premise of ensuring the real-time prediction performance, the average prediction error of the proposed BPNN-LSTM prediction method under two operation scenarios reduces by 48.14%, 35.82% and 30.09% compared with the other three methods, respectively. The proposed speed prediction method provides a new solution for predicting the speed of off-road vehicles, effectively improving the speed prediction accuracy.

A Unified Multimodal De- and Re-Coupling Framework for RGB-D Motion Recognition.

Motion recognition is a promising direction in computer vision, but the training of video classification models is much harder than images due to insufficient data and considerable parameters. To get around this, some works strive to explore multimodal cues from RGB-D data. Although improving motion recognition to some extent, these methods still face sub-optimal situations in the following aspects: (i) Data augmentation, i.e., the scale of the RGB-D datasets is still limited, and few efforts have been made to explore novel data augmentation strategies for videos; (ii) Optimization mechanism, i.e., the tightly space-time-entangled network structure brings more challenges to spatiotemporal information modeling; And (iii) cross-modal knowledge fusion, i.e., the high similarity between multimodal representations leads to insufficient late fusion. To alleviate these drawbacks, we propose to improve RGB-D-based motion recognition both from data and algorithm perspectives in this article. In more detail, firstly, we introduce a novel video data augmentation method dubbed ShuffleMix, which acts as a supplement to MixUp, to provide additional temporal regularization for motion recognition. Secondly, a Unified Multimodal De-coupling and multi-stage Re-coupling framework, termed UMDR, is proposed for video representation learning. Finally, a novel cross-modal Complement Feature Catcher (CFCer) is explored to mine potential commonalities features in multimodal information as the auxiliary fusion stream, to improve the late fusion results. The seamless combination of these novel designs forms a robust spatiotemporal representation and achieves better performance than state-of-the-art methods on four public motion datasets. Specifically, UMDR achieves unprecedented improvements of ↑ 4.5% on the Chalearn IsoGD dataset.

Transformer-based multi-task learning for classification and segmentation of gastrointestinal tract endoscopic images.

Despite being widely utilized to help endoscopists identify gastrointestinal (GI) tract diseases using classification and segmentation, models based on convolutional neural network (CNN) have difficulties in distinguishing the similarities among some ambiguous types of lesions presented in endoscopic images, and in the training when lacking labeled datasets. Those will prevent CNN from further improving the accuracy of diagnosis. To address these challenges, we first proposed a Multi-task Network (TransMT-Net) capable of simultaneously learning two tasks (classification and segmentation), which has the transformer designed to learn global features and can combine the advantages of CNN in learning local features so that to achieve a more accurate prediction in identifying the lesion types and regions in GI tract endoscopic images. We further adopted the active learning in TransMT-Net to tackle the labeled image-hungry problem. A dataset was created from the CVC-ClinicDB dataset, Macau Kiang Wu Hospital, and Zhongshan Hospital to evaluate the model performance. Then, the experimental results show that our model not only achieved 96.94% accuracy in the classification task and 77.76% Dice Similarity Coefficient in the segmentation task but also outperformed those of other models on our test set. Meanwhile, active learning also produced positive results for the performance of our model with a small-scale initial training set, and even its performance with 30% of the initial training set was comparable to that of most comparable models with the full training set. Consequently, the proposed TransMT-Net has demonstrated its potential performance in GI tract endoscopic images and it through active learning can alleviate the shortage of labeled images.

SD-HRNet: Slimming and Distilling High-Resolution Network for Efficient Face Alignment.

Face alignment is widely used in high-level face analysis applications, such as human activity recognition and human-computer interaction. However, most existing models involve a large number of parameters and are computationally inefficient in practical applications. In this paper, we aim to build a lightweight facial landmark detector by proposing a network-level architecture-slimming method. Concretely, we introduce a selective feature fusion mechanism to quantify and prune redundant transformation and aggregation operations in a high-resolution supernetwork. Moreover, we develop a triple knowledge distillation scheme to further refine a slimmed network, where two peer student networks could learn the implicit landmark distributions from each other while absorbing the knowledge from a teacher network. Extensive experiments on challenging benchmarks, including 300W, COFW, and WFLW, demonstrate that our approach achieves competitive performance with a better trade-off between the number of parameters (0.98 M-1.32 M) and the number of floating-point operations (0.59 G-0.6 G) when compared to recent state-of-the-art methods.

PRDX6 inhibits hepatic stellate cells activation and fibrosis via promoting MANF secretion.

Hepatic fibrosis is a chronic inflammatory process with hepatic stellate cells (HSCs) activation. Peroxiredoxin 6 (PRDX6), a multifunctional protein, was reported to protect against liver injury induced by ischemia/reperfusion and high-fat diet. However, the effect of PRDX6 on hepatic fibrosis remains unclear. Male Sprague-Dawley rats were treated with carbon tetrachloride (CCl4) for 4-8 weeks to induce hepatic fibrosis. Here, we found that PRDX6 was mainly expressed in hepatocytes and significantly upregulated in CCl4-induced liver fibrosis. To clarify the impact of PRDX6 in hepatic fibrosis, we constructed a PRDX6 knockout (PRDX6-/-) rat model by using CRISPR/Cas9 method. We found that PRDX6 deficiency accelerated CCl4-induced liver fibrosis. Furthermore, we found that PRDX6 knockout promoted α-SMA expression in normal and fibrotic conditions, especially in hepatic fibrosis. PRDX6 knockout significantly upregulated Col1α1 and Col3α1 in fibrotic tissues. To explore the underlying mechanisms, we identified mesencephalic astrocyte-derived neurotrophic factor (MANF), a suppressor for hepatic fibrosis and NF-κB pathway, as an interacting protein of PRDX6. PRDX6 promoted MANF secretion by binding to the C-terminus of MANF, which did not depend on its peroxidase and PLA2 activities. Similarly, MANF increased PRDX6 protein level and promoted its secretion. Additionally, PRDX6 knockout increased p65 level either in cytoplasm or nuclei in HSCs under fibrotic condition. In conclusion, PRDX6 is an effective inhibitor for hepatic fibrosis through a non-enzymic dependent interacting with MANF, which will offer a potential target for hepatic fibrosis therapy.

RVFace: Reliable Vector Guided Softmax Loss for Face Recognition.

Face recognition has witnessed significant progress with the advances of deep convolutional neural networks (CNNs), and the central task of which is how to improve the feature discrimination. To this end, several margin-based (e.g., angular, additive and additive angular margins) softmax loss functions have been proposed to increase the feature margin between different classes. However, despite great achievements have been made, they mainly suffer from four issues: 1) They are based on the assumption of well-cleaned training sets, without considering the consequence of noisy labels inherently existing in most of face recognition datasets; 2) They ignore the importance of informative (e.g., semi-hard) features mining for discriminative learning; 3) They encourage the feature margin only from the perspective of ground truth class, without realizing the discriminability from other non-ground truth classes; and 4) They set the feature margin between different classes to be same and fixed, which may not adapt the situation of unbalanced data in different classes very well. To cope with these issues, this paper develops a novel loss function, which explicitly estimates the noisy labels to drop them and adaptively emphasizes the semi-hard feature vectors from the remaining reliable ones to guide the discriminative feature learning. Thus we can address all the above issues and achieve more discriminative features for face recognition. To the best of our knowledge, this is the first attempt to inherit the advantages of feature-based noisy labels detection, feature mining and feature margin into a unified loss function. Extensive experimental results on a variety of face recognition benchmarks have demonstrated the effectiveness of our method over state-of-the-art alternatives. Our source code is available at http://www.cbsr.ia.ac.cn/users/xiaobowang/.

Phosphorylated STYK1 restrains the inhibitory role of EGFR in autophagy initiation and EGFR-TKIs sensitivity.

Epidermal growth factor receptor (EGFR) plays critical roles in cell proliferation and tumorigenesis. Autophagy has emerged as a potential mechanism involved in the acquired resistance to anti-EGFR treatments, however, the molecular mechanisms has not been fully addressed. In this study, we identified EGFR interacts with STYK1, a positive autophagy regulator, in EGFR kinase activity dependent manner. We found that EGFR phosphorylates STYK1 at Y356 site and STYK1 inhibits activated EGFR mediated Beclin1 tyrosine phosphorylation and interaction between Bcl2 and Beclin1, thus enhances PtdIns3K-C1 complex assembly and autophagy initiation. We also demonstrated that STYK1 depletion increased the sensitivity of NSCLC cells to EGFR-TKIs in vitro and in vivo. Moreover, EGFR-TKIs induced activation of AMPK phosphorylates STYK1 at S304 site. STYK1 S304 collaborated with Y356 phosphorylation to enhance the EGFR-STYK1 interaction and reverse the inhibitory effects of EGFR to autophagy flux. Collectively, these data revealed new roles and cross-talk between STYK1 and EGFR in autophagy regulation and EGFR-TKIs sensitivity in NSCLC.

Analysis of Antimicrobial Resistance and Genetic Correlations of Escherichia Coli in Dairy Cow Mastitis.

Introduction: Escherichia coli is a widespread environmental pathogen frequently causing dairy cow mastitis. This bacterium is particularly capable of acquiring antimicrobial resistance, which can have severe impacts on animal food safety and human health. The objective of the study was to investigate antimicrobial resistance and genetic correlations of E. coli from dairy cow mastitis cases in northern China. Material and Methods: Forty strains of E. coli from 196 mastitis milk samples were collected, susceptibility to 13 common antibiotics and the prevalence of resistance genes were tested in these strains, and the genetic characteristics were identified by multilocus sequence typing. Results: The results showed that most isolates were multidrug resistant (MDR) (75%), and the resistance rates to cefazolin, trimethoprim-sulfamethoxazole and ampicillin were 77.5%, 55.0%, and 52.5%, respectively. The representative genes of the isolates were aadA (62.5%) and tet(B) (60.0%). Multilocus sequence typing showed 19 different sequence types (STs) and 5 clonal complexes (CCs) in the 40 isolates, mainly represented by ST10 and CC10. The strains of the same ST or CC showed a high level of genetic relatedness, but the characteristics of their antimicrobial resistance were markedly different. Conclusion: Most E. coli isolates in the study were MDR strains. Some strains of the same ST or CC showed diverse resistance characteristics to common antimicrobials. Therefore, E. coli from dairy cow mastitis in northern China should be investigated to elucidate its antimicrobial resistance and genotypes.

Urotensin II Induces Cardiac Fibrosis through the TGF-ß/Smad Signaling Pathway during the Development of Cardiac Hypertrophy.

Myocardial fibrosis is an important pathological phenomenon of cardiac remodeling that is induced by hypertension, myocardial ischemia, valvular heart disease, hypertrophic cardiomyopathy, and other heart diseases and can progress to heart failure. Urotensin II (UII) is regarded as a cardiovascular autacoid/hormone that is not only the most potent vasoconstrictor in mammals but also involved in cardiac remodeling. However, the molecular mechanisms responsible for UII-induced cardiac fibrosis have not yet been fully elucidated. Therefore, we aimed to investigate the effect of UII on myocardial fibrosis in cardiac hypertrophy and the mechanism of UII-induced cardiac fibrosis. Cardiac tissue from mice subjected to Transverse aortic constriction (TAC) was collected. Cardiac hypertrophy, myocardial fibrosis, and the expression of UII protein were assessed using echocardiography and pathological and molecular biological analyses. The effect of UII on fibrosis was evaluated in UII-treated mice and isolated rat primary cardiac fibroblasts, and the results indicated that UII induced significant myocardial fibrosis and increases in the proliferation and fibrotic responses both in mice and cultured fibroblasts. Mechanistically, UII treatment induced activation of the TGF-ß/Smad signaling pathway, which was suppressed by the UII receptor antagonist. In conclusion, UII plays critical roles in cardiac fibrosis by modulating the TGF-ß/Smads signaling pathway, which may be a promising therapeutic target in hypertrophic cardiomyopathy and related problems, such as cardiac remodeling and heart failure.

Intraocular Foreign Bodies: Clinical Characteristics and Factors Affecting Visual Outcome.

OBJECTIVE: To investigate the clinical characteristics and factors affecting visual outcome in patients with intraocular foreign bodies (IOFBs) and determine the risk factors for the development of endophthalmitis. Study Design. A retrospective case-series study design was adopted. SUBJECTS: In total, 242 patients (242 eyes) who were hospitalized and underwent surgical treatment for IOFB at the Second Hospital of Hebei Medical University between January 1, 2008, and December 31, 2019, were included. METHODS: The demographic data, cause of injury, characteristics of IOFBs, postinjury ocular manifestations, and surgical details of the subjects were collected, and the factors affecting visual outcome and endophthalmitis development were analyzed. RESULTS: The most common cause of IOFBs was the propulsion of foreign bodies into the eye due to hammering (149 cases, 61.57%), followed by foreign body penetration (57 cases, 23.55%). Most of the subjects were young adult men who sustained injuries in the work environment. Poorer visual outcomes were found in subjects with initial presenting symptoms visual acuity (PVA) < 0.1, largest IOFB diameter ≥ 3 mm, IOFBs located in the posterior segment, wound length > 5 mm, entrance wound length larger than the largest IOFB diameter, concomitant retinal detachment, concomitant vitreous hemorrhage, concomitant endophthalmitis, and concomitant proliferative vitreoretinopathy (PVR). Factors related to the development of endophthalmitis included lens capsule rupture, time of stage 1 repair surgery ≥ 24 h after trauma, removal of IOFBs ≥ 24 h after trauma, and nonadministration of intravitreal antibiotic injection. CONCLUSION: Among patients with IOFBs, initial PVA < 0.1, entrance wound length larger than the largest IOFB diameter, concomitant endophthalmitis, and concomitant PVR were risk factors for poor visual outcomes. Lens capsule rupture was a risk factor for endophthalmitis development, and the administration of intravitreal antibiotic injection was a protective factor against endophthalmitis development.

Urotensin II induces activation of NLRP3 and pyroptosis through calcineurin in cardiomyocytes.

Cell pyroptosis, a new type of programmed cell death, has been recently reported to play important roles in the development of cardiac remodeling. How cardiomyocyte pyroptosis is induced remains to be elucidated. Urotensin II (UII) has been known closely related to cardiac remodeling and the development of heart failure. Inhibition of UII receptors has been shown to be effective in the treatment of cardiac hypertrophy and remodeling. However, it is not clear whether UII might induce cardiomyocyte pyroptosis. We here examined the effect of UII treatment on pyroptosis in cultured cardiomyocytes. Treatment of cardiomyocyes of neonatal rats with UII (500 nmol/l) for 48 hours induced a significant pyroptosis as evidenced by not only increased cell death but also upregulated expression levels of NLR family pyrin domain containing 3 (NLRP3), caspase-1, IL-1ß, IL-18 and gasdermin D (GMDSD)-N which are important markers for the identification of cell pyroptosis. All these pyroptosis responses induced by UII were abrogated by an inhibitor of NLRP3. Moreover, the antagonist of UII receptor, Urantide abolished UII- induced cardiomyocyte pyroptosis. Additionally, inhibition of calcineurin by cyclosporin A rather than that of CaMKII by KN93 suppressed the UII-upregulated expression levels of those pyroptosis markers. We therefore demonstrate that UII might induce cardiomyocyte pyroptosis through calcineurin.

Sp1 Targeted PARP1 Inhibition Protects Cardiomyocytes From Myocardial Ischemia-Reperfusion Injury via Downregulation of Autophagy.

Myocardial ischemia-reperfusion injury (MIRI), characterized by post-ischemic cardiomyocytes death and reperfusion myocardial damage, is a lethal yet unresolved complication in the treatment of acute myocardial infarction (AMI). Previous studies have demonstrated that poly(ADP-ribose) polymerase-1 (PARP1) participates in the progression of various cardiovascular diseases, and various reports have proved that PARP1 can be a therapeutic target in these diseases, but whether it plays a role in MIRI is still unknown. Therefore, in this study, we aimed to explore the role and mechanism of PARP1 in the development of MIRI. Firstly, we demonstrated that PARP1 was activated during MIRI-induced myocardial autophagy in vitro. Moreover, PARP1 inhibition protected cardiomyocytes from MIRI through the inhibition of autophagy. Next, we discovered that specificity protein1 (Sp1), as a transcription factor of PARP1, regulates its target gene PARP1 through binding to its target gene promoter during transcription. Furthermore, silencing Sp1 protected cardiomyocytes from MIRI via the inhibition of PARP1. Finally, the functions and mechanisms of PARP1 in the development of MIRI were also verified in vivo with SD rats model. Based on these findings, we concluded that PARP1 inhibition protects cardiomyocytes from MIRI through the inhibition of autophagy, which is targeted by Sp1 suppression. Therefore, the utilization of PARP1 exhibits great therapeutic potential for MIRI treatment in future.

TSPAN1 promotes autophagy flux and mediates cooperation between WNT-CTNNB1 signaling and autophagy via the MIR454-FAM83A-TSPAN1 axis in pancreatic cancer.

Pancreatic cancer is one of the most aggressive tumors associated with a poor clinical prognosis, weakly effective therapeutic options. Therefore, there is a strong impetus to discover new therapeutic targets in pancreatic cancer. In the present study, we first demonstrated that TSPAN1 is upregulated in pancreatic cancer and that TSPAN1 depletion decreases pancreatic cancer cell proliferation in vitro and in vivo. TSPAN1 expression was correlated with poor overall survival of pancreatic cancer patients. Moreover, we demonstrated that TSPAN1 is a novel positive regulator of macroautophagy/autophagy characterized by decreased LC3-II and SQSTM1/p62 expressions, inhibited puncta formation of GFP-LC3 and autophagic vacuoles. We also demonstrated that tspan1 mutation impaired autophagy in the zebrafish model. Furthermore, we showed that TSPAN1 promoted autophagy maturation via direct binding to LC3 by two conserved LIR motifs. Mutations in the LIR motifs of TSPAN1 resulted in a loss of the ability to induce autophagy and promote pancreatic cancer proliferation. Second, we discovered two conservative TCF/LEF binding elements present in the promoter region of the TSPAN1 gene, which was further verified through luciferase activity and ChIP assays. Furthermore, TSPAN1 was upregulated by FAM83A through the canonical WNT-CTNNB1 signaling pathway. We further demonstrated that both TSPAN1 and FAM83A are both direct targets of MIR454 (microRNA 454). Additionally, we revealed the role of MIR454-FAM83A-TSPAN1 in the proliferation of pancreatic cancer cells in vitro and in vivo. Our findings suggest that components of the MIR454-FAM83A-TSPAN1 axis may be valuable prognosis markers or therapeutic targets for pancreatic cancer.Abbreviations: AMPK: adenosine 5'-monophosphate (AMP)-activated protein kinase; APC: APC regulator of WNT signaling pathway; ATG: autophagy related; AXIN2: axin 2; BECN1: beclin 1; CCND1: cyclin D1; CSNK1A1/CK1α: casein kinase 1 alpha 1; CTNNB1/ß-catenin: catenin beta 1; DAPI: 4'6-diamino-2-phenylindole; EBSS: Earle's balanced salt solution; EdU: 5-ethynyl-20-deoxyuridine; FAM83A: family with sequence similarity 83 member A; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; GFP: green fluorescent protein; GSEA: gene set enrichment analysis; GSK3B: glycogen synthase kinase 3 beta; IHC: immunohistochemical; LAMP1: lysosomal associated membrane protein 1; LIR: LC3-interacting region; MAP1LC3/LC3, microtubule associated protein 1 light chain 3; MIR454: microRNA 454; miRNA: microRNA; MKI67: antigen identified by monoclonal antibody Ki 67; MTOR: mechanistic target of rapamycin kinase; MTT: 3-(4,5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide; MYC: MYC proto-oncogene, bHLH transcription factor; OS: overall survival; PDAC: pancreatic ductal adenocarcinoma; RAB7A: RAB7A, member RAS oncogene family; shRNA: short hairpin RNA; SQSTM1: sequestosome 1; TBE: TCF/LEF binding element; TCGA: The Cancer Genome Atlas; TCF/LEF: transcription factor/lymphoid enhancer binding factor; TCF4: transcription factor 4; TSPAN1: tetraspanin 1; TUNEL: terminal deoxynucleotidyl transferase mediated dUTP nick end labeling; UTR: untranslated region; WT: wild type.

[Construction and optimization of ecological network in Xi'an based on landscape analysis]. / 基于景观分析的西安市生态网络构建与优化.

Ecological network can connect fragmented habitat patches to increase the connectivity among landscapes, which plays an important role to landscapes and ecological problems caused by urbanization. In this study, the ecological networks of Xi'an City were constructed using landscape pattern index and morphological spatial pattern analysis to reveal landscape pattern features. The performance of the network was evaluated with the gravity model to provide an optimization strategy. The landscape richness index was relatively high, with significant differences of landscape patterns between north and south parts. The ecological sources were predominated in the south and east areas, while a higher comprehensive resistance with low connectivity was found in the north and central areas. The ecological corridors were unevenly distributed, with the radiation channels derived from hydrological analysis providing a supplementary role. Furthermore, ecological networks could be optimized by introducing other ecological sources, supplementing stepping stones, and repairing fracture points, to reduce the problems of uneven distribution of ecological sources, the excessively long ecological corridors in local regions, and the obstruction of road networks. Our optimization method provided an optional way to assist urban planning of Xi'an City.

A case report of lineage switch from T-cell acute leukemia to B-cell acute leukemia.

RATIONALE: ALL is the most common form of leukemia (75% to 80%), it is characterized by clonal expansion of the lymphoid blasts in bone marrow, blood, and other tissues, which can be divided into T lineage and B lineage. Although relapse of acute leukemia is common, a change of immunophenotype at relapse only occurs rarely. Some of these cases have been labeled "lineage switch". PATIENT CONCERNS: A 31-year-old man had multiple lymph nodes in the neck, and the lymph nodes on the right side adhered to the surrounding tissues. His lymphocytes ratio in blood was up to 86.3%. Flow cytometry of the bone marrow aspirate showed positive results for CD2, CD5, CD7, cCD3, TDT, CD4, CD8, and CD10, negative results for CD34, CD117, CD33, HLA-DR, CD19, and CD20. Twenty six months later, the patient felt pain in the neck and shoulder after touching. His lymphocytes of blood were 109.9×109 /L. 43 fusion genes and positive BCR/ABL was detected. Flow cytometry of the bone marrow aspirate showed pro B lymphocytes accounted for 85.54%, and positive expression of CD38, CD10, CD34, CD33, TDT, CD9, and HLA-DR. Moreover, the RT-PCR data showed the patient expressed high level of T cell and B cell development transcription factors. DIAGNOSES: Upon examination, the patient was initially diagnosed with T-lineage pro cell ALL. BM morphologic analysis presented complete remission (CR) after systemic chemotherapy. Twenty six months later, we discovered the patient was diagnosed with B-lineage acute lymphocytic leukemia. INTERVENTIONS: Systemic chemotherapy is first given when a patient was diagnosed with T-cell acute lymphoblastic leukemia. After the patient happened linage switch, we adjusted the treatment plan, and the patient was complete remission after 1 course of treatment. OUTCOMES: Our case provides information of lineage switch from T-ALL to B-ALL in this report, which is never seen in our knowledge. LESSONS: This lineage switch from T-ALL to B-ALL is never reported beforemoreover, the RT-PCR data showed the patient expressed high level of T cell and B cell development transcription factors. Its early recognition can let doctor provides appropriate therapy to patient.

Clobetasol Attenuates White Matter Injury by Promoting Oligodendrocyte Precursor Cell Differentiation.

INTRODUCTION: White matter injury (WMI) is the most common brain injury in preterm infants and can result in life-long neurological deficits. The main cause of WMI is damage to the oligodendrocyte precursor cells (OPC) in the brain that results in delayed myelin sheath formation, or the destruction of existing myelin sheaths. OPC undergo highly regulated and strictly timed developmental changes that result in their transformation to mature oligodendrocytes capable of myelin production. OBJECTIVE: Studies have shown that clobetasol strongly promotes differentiation of OPC into myelin sheaths. Therefore, we hypothesized that clobetasol may be a therapeutic option for the treatment of preterm WMI. METHODS: We induced a WMI rat model and observed white matter damage under an optical microscope. Rats subjected to WMI were injected intraperitoneally with clobetasol (2 or 5 mg/kg daily) from day 1 to day 5 in the early treatment groups, or from day 6 to day 10 in the late treatment groups. After 17 days, the rats were sacrificed and the expression of myelin basic protein (MBP) was visualized using immunofluorescence. In addition, we evaluated myelin sheath formation using electron microscopy. The rats were also subjected to the suspension test, ramp test, and open field test to evaluate neurobehavioral functions. RESULTS: A rat model of WMI was successfully induced. It was found that clobetasol significantly induced MBP expression and myelin sheath formation and improved neurobehavioral function in the rats subjected to WMI. CONCLUSIONS: Our results indicate that clobetasol attenuates WMI by promoting OPC differentiation, and it may be an effective therapeutic agent for the treatment of preterm WMI.