121 results on '"Fangfang Bi"'
Search Results
102. A new magnetic-field modulated machine with compound-structure magnets of spoke PMs and Halbach PMs
- Author
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Fangfang Bian, Caifei Ke, Jie Su, and Miao Li
- Subjects
Physics ,QC1-999 - Abstract
To increase the airgap flux density, this paper proposes a new magnetic-field-modulated permanent magnet (FMPM) machine. The proposed FMPM machine has the compound magnets in the rotor, which is composited by the spoke PMs (SPM) and Halbach PMs (HPM). The proposed SH-FMPM machine facilitates better use of space for armature winding and PMs and combines the benefits of high torque density and high torque/loss. The formation process, operation principle, and electromagnetic performance of the SH-FMPM machine are introduced. It is demonstrated that the SH-FMPM machine has the high torque density and low torque ripple compared to the S-FMPM machine and the H-FMPM machine.
- Published
- 2023
- Full Text
- View/download PDF
103. Evaluation of the efficacy of laparoscopic resection for the management of exogenous cesarean scar pregnancy
- Author
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Fangfang Bi, Lili Yin, Guangwei Wang, Dandan Wang, Rina Sa, Xiaofei Liu, and Qing Yang
- Subjects
Laparoscopic surgery ,Adult ,medicine.medical_specialty ,Absorption time ,medicine.medical_treatment ,Cesarean Scar Pregnancy ,Cicatrix ,Young Adult ,Blood loss ,Pregnancy ,medicine ,Humans ,Laparoscopic resection ,Laparoscopy ,Retrospective Studies ,medicine.diagnostic_test ,business.industry ,Cesarean Section ,Obstetrics and Gynecology ,Disease Management ,Surgery ,medicine.anatomical_structure ,Treatment Outcome ,Reproductive Medicine ,Hysteroscopy ,Feasibility Studies ,Female ,Uterine cavity ,business ,Follow-Up Studies - Abstract
Objective To retrospectively analyze the clinical data of 71 patients with exogenous cesarean scar pregnancy (CSP) treated in our hospital in the past 2 years, to compare the outcomes of exogenous CSP treated with different methods, and to evaluate the safety and feasibility of laparoscopic resection of exogenous CSP. Design Comparative observational study. Setting Tertiary medical centers. Patient(s) 71 women with exogenous cesarean scar pregnancy. Intervention(s) Hysteroscopic resection of CSP, and laparoscopic resection of CSP. Main Outcome Measure(s) Operation time, intraoperative blood loss, postoperative drainage of the uterine cavity, postoperative days in hospital, time for β-human chorionic gonadotropin (β-hCG) to return to normal levels, absorption time of the mass. Result(s) For the laparoscopic group, the time for serum β-hCG to return normal levels and the postoperative drainage of the uterine cavity were significantly lower than in the patients who had undergone hysteroscopic resection. We found no statistically significant difference in the intraoperative blood loss and postoperative days in hospital between the two groups, but the operation time was longer in laparoscopic group. Conclusion(s) Laparoscopic surgery for a cesarean scar pregnancy has the advantages of a high success rate, fewer complications, and a shorter time for β-hCG levels to normalize. This procedure is especially suitable for the treatment of exogenous CSP.
- Published
- 2013
104. Reactive astrocytes secrete lcn2 to promote neuron death
- Author
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Zuoshang Xu, Robert Bowser, Guang Qiu, Qinxue Wu, Bo Huang, Fangfang Bi, Jianbin Tong, Cao Huang, Xu-Gang Xia, Fang Li, and Hongxia Zhou
- Subjects
Programmed cell death ,DNA, Complementary ,Neurotoxins ,Superoxide dismutase ,Animals, Genetically Modified ,Slice preparation ,Superoxide Dismutase-1 ,Lipocalin-2 ,medicine ,Animals ,Humans ,Neurons ,Multidisciplinary ,Microglia ,biology ,Base Sequence ,Cell Death ,Superoxide Dismutase ,Neurodegeneration ,Neurotoxicity ,Biological Sciences ,medicine.disease ,Molecular biology ,Lipocalins ,Recombinant Proteins ,Rats ,DNA-Binding Proteins ,medicine.anatomical_structure ,Astrocytes ,Culture Media, Conditioned ,Nerve Degeneration ,biology.protein ,RNA-Binding Protein FUS ,Frontotemporal Lobar Degeneration ,Neuron death - Abstract
Glial reaction is a common feature of neurodegenerative diseases. Recent studies have suggested that reactive astrocytes gain neurotoxic properties, but exactly how reactive astrocytes contribute to neurotoxicity remains to be determined. Here, we identify lipocalin 2 (lcn2) as an inducible factor that is secreted by reactive astrocytes and that is selectively toxic to neurons. We show that lcn2 is induced in reactive astrocytes in transgenic rats with neuronal expression of mutant human TAR DNA-binding protein 43 (TDP-43) or RNA-binding protein fused in sarcoma (FUS). Therefore, lcn2 is induced in activated astrocytes in response to neurodegeneration, but its induction is independent of TDP-43 or FUS expression in astrocytes. We found that synthetic lcn2 is cytotoxic to primary neurons in a dose-dependent manner, but is innocuous to astrocytes, microglia, and oligodendrocytes. Lcn2 toxicity is increased in neurons that express a disease gene, such as mutant FUS or TDP-43. Conditioned medium from rat brain slice cultures with neuronal expression of mutant TDP-43 contains abundant lcn2 and is toxic to primary neurons as well as neurons in cultured brain slice from WT rats. Partial depletion of lcn2 by immunoprecipitation reduced conditioned medium-mediated neurotoxicity. Our data indicate that reactive astrocytes secrete lcn2, which is a potent neurotoxic mediator.
- Published
- 2013
105. Expression of ALS-linked TDP-43 mutant in astrocytes causes non-cell-autonomous motor neuron death in rats
- Author
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Jianbin Tong, Xu-Gang Xia, Hongxia Zhou, Xionghao Liu, Qinxue Wu, Cao Huang, Fangfang Bi, Fang Li, and Bo Huang
- Subjects
Programmed cell death ,Mutant ,Blotting, Western ,Fluorescent Antibody Technique ,Biology ,Neuroprotection ,General Biochemistry, Genetics and Molecular Biology ,Article ,Immunoenzyme Techniques ,Lipocalin-2 ,mental disorders ,medicine ,Animals ,Humans ,Paralysis ,Amyotrophic lateral sclerosis ,Molecular Biology ,Denervation ,Motor Neurons ,General Immunology and Microbiology ,Microglia ,Behavior, Animal ,Cell Death ,General Neuroscience ,Amyotrophic Lateral Sclerosis ,nutritional and metabolic diseases ,Motor neuron ,medicine.disease ,Lipocalins ,Muscle Denervation ,Cell biology ,nervous system diseases ,Rats ,DNA-Binding Proteins ,Excitatory Amino Acid Transporter 1 ,Disease Models, Animal ,Muscular Atrophy ,medicine.anatomical_structure ,Biochemistry ,Excitatory Amino Acid Transporter 2 ,Spinal Cord ,Astrocytes ,Mutation ,Neuron ,Rats, Transgenic - Abstract
Mutation of Tar DNA-binding protein 43 (TDP-43) is linked to amyotrophic lateral sclerosis. Although astrocytes have important roles in neuron function and survival, their potential contribution to TDP-43 pathogenesis is unclear. Here, we created novel lines of transgenic rats that express a mutant form of human TDP-43 (M337V substitution) restricted to astrocytes. Selective expression of mutant TDP-43 in astrocytes caused a progressive loss of motor neurons and the denervation atrophy of skeletal muscles, resulting in progressive paralysis. The spinal cord of transgenic rats also exhibited a progressive depletion of the astroglial glutamate transporters GLT-1 and GLAST. Astrocytic expression of mutant TDP-43 led to activation of astrocytes and microglia, with an induction of the neurotoxic factor Lcn2 in reactive astrocytes that was independent of TDP-43 expression. These results indicate that mutant TDP-43 in astrocytes is sufficient to cause non-cell-autonomous death of motor neurons. This motor neuron death likely involves deficiency in neuroprotective genes and induction of neurotoxic genes in astrocytes.
- Published
- 2012
106. Pathogenic mutation in VPS35 impairs its protection against MPP(+) cytotoxicity
- Author
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Cao Huang, Fang Li, Fangfang Bi, and Hongxia Zhou
- Subjects
1-Methyl-4-phenylpyridinium ,Parkinson's disease ,Genetic Vectors ,Immunoblotting ,Mutation, Missense ,Vesicular Transport Proteins ,Fluorescent Antibody Technique ,Substantia nigra ,Biology ,Applied Microbiology and Biotechnology ,Neuroprotection ,03 medical and health sciences ,VPS35 ,Open Reading Frames ,0302 clinical medicine ,vacuolar protein sorting 35 ,Dopaminergic Cell ,medicine ,MPP+ ,Missense mutation ,Humans ,Cloning, Molecular ,Molecular Biology ,Ecology, Evolution, Behavior and Systematics ,030304 developmental biology ,Regulation of gene expression ,0303 health sciences ,Dopaminergic Neurons ,Dopaminergic ,Parkinson Disease ,Cell Biology ,medicine.disease ,Molecular biology ,3. Good health ,Gene Expression Regulation ,Microscopy, Fluorescence ,Mutagenesis ,Cancer research ,030217 neurology & neurosurgery ,Developmental Biology ,Research Paper - Abstract
Parkinson's disease primarily results from progressive degeneration of dopaminergic neurons in the substantia nigra. Both neuronal toxicants and genetic factors are suggested to be involved in the disease pathogenesis. The mitochondrial toxicant 1-methyl-4-phenylpyridinium (MPP(+)) shows a highly selective toxicity to dopaminergic neurons. Recent studies indicate that mutation in the vacuolar protein sorting 35 (vps35) gene segregates with Parkinson's disease in some families, but how mutation in the vps35 gene causes dopaminergic cell death is not known. Here, we report that enhanced VPS35 expression protected dopaminergic cells against MPP(+) toxicity and that this neuroprotection was compromised by pathogenic mutation in the gene. A loss of neuroprotective functions contributes to the pathogenesis of VPS35 mutation in Parkinson's disease.
- Published
- 2012
107. Entorhinal cortical neurons are the primary targets of FUS mislocalization and ubiquitin aggregation in FUS transgenic rats
- Author
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Cao Huang, Hongxia Zhou, Qinxue Wu, Bo Huang, Xu-Gang Xia, Fangfang Bi, and Jianbin Tong
- Subjects
Dendritic spine ,Dendritic Spines ,Golgi Apparatus ,Rosiglitazone ,Prosencephalon ,Ubiquitin ,mental disorders ,Genetics ,medicine ,Animals ,Entorhinal Cortex ,Humans ,Amyotrophic lateral sclerosis ,Molecular Biology ,Genetics (clinical) ,Memory Disorders ,biology ,General Medicine ,Frontotemporal lobar degeneration ,Articles ,Motor neuron ,medicine.disease ,Entorhinal cortex ,Cell biology ,Mitochondria ,Rats ,DNA-Binding Proteins ,PPAR gamma ,Disease Models, Animal ,medicine.anatomical_structure ,Gene Expression Regulation ,Mutation ,biology.protein ,Cancer research ,RNA-Binding Protein FUS ,Thiazolidinediones ,Frontotemporal Lobar Degeneration ,Rats, Transgenic ,Frontotemporal dementia - Abstract
Ubiquitin-positive inclusion containing Fused in Sarcoma (FUS) defines a new subtype of frontotemporal lobar degeneration (FTLD). FTLD is characterized by progressive alteration in cognitions and it preferentially affects the superficial layers of frontotemporal cortex. Mutation of FUS is linked to amyotrophic lateral sclerosis and to motor neuron disease with FTLD. To examine FUS pathology in FTLD, we developed the first mammalian animal model expressing human FUS with pathogenic mutation and developing progressive loss of memory. In FUS transgenic rats, ubiquitin aggregation and FUS mislocalization were developed primarily in the entorhinal cortex of temporal lobe, particularly in the superficial layers of affected cortex. Overexpression of mutant FUS led to Golgi fragmentation and mitochondrion aggregation. Intriguingly, aggregated ubiquitin was not colocalized with either fragmented Golgi or aggregated mitochondria, and neurons with ubiquitin aggregates were deprived of endogenous TDP-43. Agonists of peroxisome proliferator-activated receptor gamma (PPAR-γ) possess anti-glial inflammation effects and are also shown to preserve the dendrite and dendritic spines of cortical neurons in culture. Here we show that rosiglitazone, a PPAR-γ agonist, rescued the dendrites and dendritic spines of neurons from FUS toxicity and preserved rats' spatial memory. Our FUS transgenic rats would be useful to the mechanistic study of cortical dementia in FTLD. As rosiglitazone is clinically used to treat diabetes, our results would encourage immediate application of PPAR-γ agonists in treating patients with cortical dementia.
- Published
- 2012
108. Mutant TDP-43 in motor neurons promotes the onset and progression of ALS in rats
- Author
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Hongxia Zhou, Fangfang Bi, Xu-Gang Xia, Cao Huang, and Jianbin Tong
- Subjects
Pathology ,medicine.medical_specialty ,Transgene ,Mutant ,Biology ,Atrophy ,Paralysis ,medicine ,Myocyte ,Animals ,Humans ,Amyotrophic lateral sclerosis ,DNA Primers ,Denervation ,Motor Neurons ,Base Sequence ,Amyotrophic Lateral Sclerosis ,Skeletal muscle ,General Medicine ,medicine.disease ,Recombinant Proteins ,Cell biology ,Rats ,DNA-Binding Proteins ,Disease Models, Animal ,medicine.anatomical_structure ,Doxycycline ,TDP-43 Proteinopathies ,Nerve Degeneration ,Disease Progression ,Mutant Proteins ,medicine.symptom ,Rats, Transgenic ,Research Article - Abstract
Amyotrophic lateral sclerosis (ALS) is characterized by progressive motor neuron degeneration, which ultimately leads to paralysis and death. Mutation of TAR DNA binding protein 43 (TDP-43) has been linked to the development of an inherited form of ALS. Existing TDP-43 transgenic animals develop a limited loss of motor neurons and therefore do not faithfully reproduce the core phenotype of ALS. Here, we report the creation of multiple lines of transgenic rats in which expression of ALS-associated mutant human TDP-43 is restricted to either motor neurons or other types of neurons and skeletal muscle and can be switched on and off. All of these rats developed progressive paralysis reminiscent of ALS when the transgene was switched on. Rats expressing mutant TDP-43 in motor neurons alone lost more spinal motor neurons than rats expressing the disease gene in varying neurons and muscle cells, although these rats all developed remarkable denervation atrophy of skeletal muscles. Intriguingly, progression of the disease was halted after transgene expression was switched off; in rats with limited loss of motor neurons, we observed a dramatic recovery of motor function, but in rats with profound loss of motor neurons, we only observed a moderate recovery of motor function. Our finding suggests that mutant TDP-43 in motor neurons is sufficient to promote the onset and progression of ALS and that motor neuron degeneration is partially reversible, at least in mutant TDP-43 transgenic rats.
- Published
- 2011
109. Selective loss and axonal sprouting of GABAergic interneurons in the sclerotic hippocampus induced by LiCl-pilocarpine
- Author
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Lili Long, M. Abuhamed Mutasem, Li Feng, Fangfang Bi, Bo Xiao, Shu-yu Li, Yi Li, Fang Yi, Si Chen, and Guoliang Li
- Subjects
Male ,genetic structures ,Hippocampus ,Status epilepticus ,Inhibitory postsynaptic potential ,Rats, Sprague-Dawley ,Status Epilepticus ,Interneurons ,medicine ,Animals ,Neuropeptide Y ,gamma-Aminobutyric Acid ,Sclerosis ,biology ,musculoskeletal, neural, and ocular physiology ,General Neuroscience ,Pilocarpine ,General Medicine ,Neuropeptide Y receptor ,Axons ,Rats ,Disease Models, Animal ,Somatostatin ,Parvalbumins ,nervous system ,Nerve Degeneration ,biology.protein ,GABAergic ,medicine.symptom ,Lithium Chloride ,Neuroscience ,Parvalbumin ,medicine.drug - Abstract
In this study, we performed immunohistochemistry for somatostatin (SS), neuropeptide Y (NPY), and parvalbumin (PV) in LiCl-pilocarpine-treated rats to observe quantitative changes and axonal sprouting of GABAergic interneurons in the hippocampus, especially in the sclerotic hippocampus. Fluoro-Jade B (FJB) was performed to detect the specific degeneration of GABAergic interneurons. Compared with age-matched control rats, there were fewer SS/NPY/PV-immunoreactive (IR) interneurons in the hilus of the sclerotic hippocampus in pilocarpine-treated rats; hilar dentritic inhibitory interneurons were most vulnerable. FJB stain revealed degeneration was evident at 2 months after status epilepticus. Some SS-IR and NPY-IR interneurons were also stained for FJB, but there was no evidence of degeneration of PV-IR interneurons. Axonal sprouting of GABAergic interneurons was present in the hippocampus of epileptic rats, and a dramatic increase of SS-IR fibers was observed throughout all layers of CA1 region in the sclerotic hippocampus. These results confirm selective loss and degeneration of a specific subset of GABAergic interneurons in specific subfields of the hippocampus. Axonal sprouting of inhibitory GABAergic interneurons, especially numerous increase of SS-IR neutrophils within CA1 region of the sclerotic hippocampus, may constitute the aberrant inhibitory circum and play a significant role in the generation and compensation of temporal lobe epilepsy.
- Published
- 2010
110. OVCA1 expression and its correlation with the expression levels of cyclin D1 and p16 in cervical cancer and intraepithelial neoplasia.
- Author
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RUI TONG, QING YANG, CHUNYAN WANG, FANGFANG BI, and BING JIANG
- Subjects
GENE expression ,PROTEIN expression ,MESSENGER RNA ,OVARIAN cancer ,CANCER genetics ,CYCLIN genetics ,CERVICAL cancer ,CERVICAL intraepithelial neoplasia ,GENETICS - Abstract
The present study aimed to examine the associations between the protein and mRNA expression levels of ovarian cancer gene 1 (OVCA1), cyclin D1 and p16 and high-risk human papillomavirus (HR-HPV) infection in cervical lesions. The protein expression levels of OVCA1, cyclin D1 and p16 in 66 cases of cervical cancer, 64 cases of cervical intraepithelial neoplasia (CIN) and 34 normal cervix tissues were detected using immunohistochemistry. The mRNA expression levels of OVCA1, cyclin D1 and p16 in cervical cancer and normal cervix cells were detected using real-time polymerase chain reaction. The results revealed that the protein expression levels of OVCA1 increased gradually, whereas its mRNA expression levels decreased gradually, in the progression from normal cervix tissue to CIN and cervical cancer (P<0.01). In addition, significant differences in the protein expression levels of OVCA1 between low-and high-level CIN, as well as between the early and advanced stages of cervical cancer, were observed (P<0.05). No significant associations were detected between the protein and mRNA expression levels of OVCA1 and the pathological type of cervical cancer or the presence of lymph node metastasis (P>0.05). The expression levels of OVCA1 mRNA and protein were positively correlated with the levels of p16 expression (P<0.01). Significant differences were also observed in the OVCA1 protein and mRNA expression levels between the HR-HPV (+) and HR-HPV (-) groups (P<0.05). Therefore, aberrant expression of OVCA1 protein and mRNA may be important during the development of cervical lesions, particularly in the early stages. In addition, the mechanisms underlying the effects of OVCA1 during cervical cancer development may involve p16 and HPV, as the levels of OVCA1 in cervical lesions were correlated with abnormal expression of p16 and HR-HPV infection. [ABSTRACT FROM AUTHOR]
- Published
- 2017
- Full Text
- View/download PDF
111. α- and β-Naphthoflavone synergistically attenuate H2O2-induced neuron SH-SY5Y cell damage.
- Author
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YONG ZHU, FANGFANG BI, YANCHUN LI, HUIMING YIN, NA DENG, HAIQUAN PAN, DONGFANG LI, and BO XIAO
- Subjects
- *
OXIDATIVE stress , *FLAVONOIDS , *FLAVONES , *APOPTOSIS , *CELL survival - Abstract
Previous studies have demonstrated an association between neurological diseases and oxidative stress (OS). Naphthoflavone is a synthetic derivative of naturally occurring flavonoids that serves an important role in the treatment and prevention of OS-related diseases. The current study was designed to apply α- and β-Naphthoflavone individually and in combination to counteract the detrimental effects of OS on neurons in vitro. Neuronal SH-SY5Y cells were subjected to 20 μM H2O2, followed by exposure to 20 μM α-Naphthoflavone and/or 10 μM β-Naphthoflavone. Results indicated that α- and β-Naphthoflavone effectively antagonized the apoptosis-promoting effect of H2O2 on neuronal SH-SY5Y cells, and that β-Naphthoflavone significantly (P<0.05) reversed H2O2-inhibited cell viability. Notably, co-treatment of α- and β-Naphthoflavone reversed the H2O2-induced apoptosis rate elevation and cell viability reduction. Further analysis demonstrated that H2O2 inhibited the activities of antioxidant enzymes including catalase, superoxide dismutase and glutathione peroxidase, but this was reversed by the co-treatment with α- and β-Naphthoflavone and selectively enhanced by the treatment with α- or β-Naphthoflavone. H2O2-stimulated p38 mitogen-activated protein kinase activation was repressed following treatment with α- and/or β-Naphthoflavone, along with a decreased expression of the apoptosis-related factors and inhibited caspase-3 activation. In conclusion, co-treatment with α- and β-Naphthoflavone minimized H2O2-led neuron damage compared with treatment with α- or β-Naphthoflavone, suggesting a synergetic effect between α- and β-Naphthoflavone. This indicates that utilizing α- and β-Naphthoflavone together in the clinical setting may provide a novel therapeutic for neurological disease. [ABSTRACT FROM AUTHOR]
- Published
- 2017
- Full Text
- View/download PDF
112. DEK protein overexpression predicts poor prognosis in pancreatic ductal adenocarcinoma.
- Author
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JIE SUN, FANGFANG BI, YANG YANG, YUAN ZHANG, AIHUA JIN, JINZI LI, and ZHENHUA LIN
- Published
- 2017
- Full Text
- View/download PDF
113. Reactive astrocytes secrete lcn2 to promote neuron death.
- Author
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Fangfang Bi, Cao Huang, Jianbin Tong, Guang Qiu, Bo Huang, Qinxue Wu, Fang Li, Zuoshang Xu, Robert Bowser, Xu-Gang Xia, and Hongxia Zhou
- Subjects
- *
NEUROGLIA , *NEURODEGENERATION , *ASTROCYTES , *NEUROTOXICOLOGY , *LIPOCALIN-1 , *AMYOTROPHIC lateral sclerosis - Abstract
Glial reaction is a common feature of neurodegenerative diseases. Recent studies have suggested that reactive astrocytes gain neurotoxic properties, but exactly how reactive astrocytes contribute to neurotoxicity remains to be determined. Here, we identify lipocalin 2 (lcn2) as an inducible factor that is secreted by reactive astrocytes and that is selectively toxic to neurons. We show that lcn2 is induced in reactive astrocytes in transgenic rats with neuronal expression of mutant human TAR DNA-binding protein 43 (TDP-43) or RNA-binding protein fused in sarcoma (FUS). Therefore, lcn2 is induced in activated astrocytes in response to neurodegeneration, but its induction is independent of TDP-43 or FUS expression in astrocytes. We found that synthetic lcn2 is cytotoxic to primary neurons in a dose-dependent manner, but is innocuous to astrocytes, microglia, and oligodendrocytes. Lcn2 toxicity is increased in neurons that express a disease gene, such as mutant FUS or TDP-43. Conditioned medium from rat brain slice cultures with neuronal expression of mutant TDP-43 contains abundant lcn2 and is toxic to primary neurons as well as neurons in cultured brain slice from WT rats. Partial depletion of lcn2 by immunoprecipitation reduced conditioned medium-mediated neurotoxicity. Our data indicate that reactive astrocytes secrete lcn2, which is a potent neurotoxic mediator. [ABSTRACT FROM AUTHOR]
- Published
- 2013
- Full Text
- View/download PDF
114. Morphological Characteristics and Comparative Transcriptome Analysis of Three Different Phenotypes of Pristella maxillaris
- Author
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Fangfang Bian, Xuefen Yang, Zhijie Ou, Junzhi Luo, Bozhen Tan, Mingrui Yuan, Tiansheng Chen, and Ruibin Yang
- Subjects
Pristella maxillaris ,RNA-seq ,melanophores ,iridophores ,molecular mechanism ,Genetics ,QH426-470 - Abstract
Pristella maxillaris is known as the X-ray fish based on its translucent body. However, the morphological characteristics and the molecular regulatory mechanisms of these translucent bodies are still unknown. In this study, the following three phenotypes, a black-and-gray body color or wild-type (WT), a silvery-white body color defined as mutant I (MU1), and a fully transparent body with a visible visceral mass named as mutant II (MU2), were investigated to analyze their chromatophores and molecular mechanisms. The variety and distribution of pigment cells in the three phenotypes of P. maxillaris significantly differed by histological assessment. Three types of chromatophores (melanophores, iridophores, and xanthophores) were observed in the WT, whereas MU1 fish were deficient in melanophores, and MU2 fish lacked melanophores and iridophores. Transcriptome sequencing of the skin and peritoneal tissues of P. maxillaris identified a total of 166,089 unigenes. After comparing intergroup gene expression levels, more than 3,000 unigenes with significantly differential expression levels were identified among three strains. Functional annotation and Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses of the differentially expressed genes (DEGs) identified a number of candidates melanophores and iridophores genes that influence body color. Some DEGs that were identified using transcriptome analysis were confirmed by quantitative real-time PCR. This study serves as a global survey of the morphological characteristics and molecular mechanism of different body colors observed in P. maxillaris and thus provides a valuable theoretical foundation for the molecular regulation of the transparent phenotype.
- Published
- 2019
- Full Text
- View/download PDF
115. Design and analysis of a field modulated magnetic screw for artificial heart
- Author
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Zhijian Ling, Jinghua Ji, Fangqun Wang, and Fangfang Bian
- Subjects
Physics ,QC1-999 - Abstract
This paper proposes a new electromechanical energy conversion system, called Field Modulated Magnetic Screw (FMMS) as a high force density linear actuator for artificial heart. This device is based on the concept of magnetic screw and linear magnetic gear. The proposed FMMS consists of three parts with the outer and inner carrying the radially magnetized helically permanent-magnet (PM), and the intermediate having a set of helically ferromagnetic pole pieces, which modulate the magnetic fields produced by the PMs. The configuration of the newly designed FMMS is presented and its electromagnetic performances are analyzed by using the finite-element analysis, verifying the advantages of the proposed structure.
- Published
- 2017
- Full Text
- View/download PDF
116. A novel PM motor with hybrid PM excitation and asymmetric rotor structure for high torque performance
- Author
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Gaohong Xu, Guohai Liu, Xinxin Du, and Fangfang Bian
- Subjects
Physics ,QC1-999 - Abstract
This paper proposes a novel permanent magnet (PM) motor for high torque performance, in which hybrid PM material and asymmetric rotor design are applied. The hybrid PM material is adopted to reduce the consumption of rare-earth PM because ferrite PM is assisted to enhance the torque production. Meanwhile, the rotor structure is designed to be asymmetric by shifting the surface-insert PM (SPM), which is used to improve the torque performance, including average torque and torque ripple. Moreover, the reasons for improvement of the torque performance are explained by evaluation and analysis of the performances of the proposed motor. Compared with SPM motor and V-type motor, the merit of high utilization ratio of rare-earth PM is also confirmed, showing that the proposed motor can offer higher torque density and lower torque ripple simultaneously with less consumption of rare-earth PM.
- Published
- 2017
- Full Text
- View/download PDF
117. Eddy current loss analysis of open-slot fault-tolerant permanent-magnet machines based on conformal mapping method
- Author
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Jinghua Ji, Jianhua Luo, Qian Lei, and Fangfang Bian
- Subjects
Physics ,QC1-999 - Abstract
This paper proposed an analytical method, based on conformal mapping (CM) method, for the accurate evaluation of magnetic field and eddy current (EC) loss in fault-tolerant permanent-magnet (FTPM) machines. The aim of modulation function, applied in CM method, is to change the open-slot structure into fully closed-slot structure, whose air-gap flux density is easy to calculate analytically. Therefore, with the help of Matlab Schwarz-Christoffel (SC) Toolbox, both the magnetic flux density and EC density of FTPM machine are obtained accurately. Finally, time-stepped transient finite-element method (FEM) is used to verify the theoretical analysis, showing that the proposed method is able to predict the magnetic flux density and EC loss precisely.
- Published
- 2017
- Full Text
- View/download PDF
118. A high power factor fault-tolerant vernier permanent-magnet machine
- Author
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Xuhui Zhu, Wenxiang Zhao, Jian Zhu, and Fangfang Bian
- Subjects
Physics ,QC1-999 - Abstract
Vernier permanent-magnet (VPM) machine offers the advantage of high torque density. However, the existing VPM machines usually suffer from relatively low power factor. To solve the problem, this paper proposes a new high power factor fault-tolerant VPM machine. Compared with the existing one, the proposed VPM machine has higher power factor and higher torque density. Also, the fault-tolerant capability is provided. The electromagnetic characteristics of the proposed machine are analyzed by using the finite element method.
- Published
- 2017
- Full Text
- View/download PDF
119. A new dual stator linear permanent-magnet vernier machine with reduced copper loss
- Author
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Fangfang Bian and Wenxiang Zhao
- Subjects
Physics ,QC1-999 - Abstract
In this paper, a new dual stator linear permanent-magnet (PM) vernier (LPMV) machine with toroidal winding is proposed and analyzed. The proposed machine enjoys the advantages of less copper usage and copper loss without sacrificing the thrust force performance. For a fair comparison, the proposed machine is designed with the same geometrical parameters based on the conventional dual stator LPMV machine with concentrated winding. Finally, the electromagnetic performances of the proposed machine and the conventional one are compared and analyzed by using finite element method, verifying that the proposed machine with the low copper loss can obtain high force density.
- Published
- 2017
- Full Text
- View/download PDF
120. Mutant TDP-43 in motor neurons promotes the onset and progression of ALS in rats.
- Author
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Cao Huang, Jianbin Tong, Fangfang Bi, Hongxia Zhou, and Xu-Gang Xia
- Subjects
- *
AMYOTROPHIC lateral sclerosis , *MOTOR neuron diseases , *NEURONS , *DNA-binding proteins , *GENES - Abstract
Amyotrophic lateral sclerosis (ALS) is characterized by progressive motor neuron degeneration, which ultimately leads to paralysis and death. Mutation of TAR DNA binding protein 43 (TDP-43) has been linked to the development of an inherited form of ALS. Existing TDP-43 transgenic animals develop a limited loss of motor neurons and therefore do not faithfully reproduce the core phenotype of ALS. Here, we report the creation of multiple lines of transgenic rats in which expression of ALS-associated mutant human TDP-43 is restricted to either motor neurons or other types of neurons and skeletal muscle and can be switched on and off. All of these rats developed progressive paralysis reminiscent of ALS when the transgene was switched on. Rats expressing mutant TDP-43 in motor neurons alone lost more spinal motor neurons than rats expressing the disease gene in varying neurons and muscle cells, although these rats all developed remarkable denervation atrophy of skeletal muscles. Intriguingly, progression of the disease was halted after transgene expression was switched off; in rats with limited loss of motor neurons, we observed a dramatic recovery of motor function, but in rats with profound loss of motor neurons, we only observed a moderate recovery of motor function. Our finding suggests that mutant TDP-43 in motor neurons is sufficient to promote the onset and progression of ALS and that motor neuron degeneration is partially reversible, at least in mutant TDP-43 transgenic rats. [ABSTRACT FROM AUTHOR]
- Published
- 2012
- Full Text
- View/download PDF
121. Comparison between solitary and multiple intracranial tuberculoma.
- Author
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Abuhamed MM, Bo X, Xiaoqin L, Fufeng Z, Long L, Fangfang B, and Jing L
- Abstract
Objective: To compare and analyze the clinical, radiological, and pathological features of solitary or/and multiple CNS tuberculomas (CNSTs)., Methods: The study was conducted at Central South University, First Xiangya Hospital, Changsha, Hunan, China between 1998-2008. Forty-two subjects with diagnosed CNSTs were compared and analyzed by multiple or solitary lesions seen on enhanced MRI. The final diagnosis of tuberculomas was confirmed by histopathology., Results: From the 42 subjects, 64.3% multiple CNSTs were observed, out of which, 55.6% were with meningitis and 44.4% without meningitis. Of the CNSTs, solitary lesions were present in 35.7%, 80% of which were without meningeal involvement, and 20% with meningeal involvement. In multiple CNSTs, 55.6% were noncaseating granulomas, and 74.1% caseating granulomas with a solid center, while in solitary CNSTs, 80% were caseating granulomas with a solid center. For multiple lesions, temporal lobe, frontal lobe, cerebella, and brain stem were predilection sites. While for solitary lesions, apical lobe, and cerebellum were predilection sites. The histopathological features were the same in all multiple and solitary lesions., Conclusion: Multiple CNSTs are more often associated with meningitis, while solitary CNSTs particularly occur with less or atypical clinical manifestation. Difference in the predilection sites between multiple and solitary CNSTs were observed.
- Published
- 2009
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