Academic literature on the topic 'Hu huan xing'
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Journal articles on the topic "Hu huan xing"
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Unschuld, Paul U. "Yin-Yang Theory, the Human Organism, and the Bai hu tong: A Need for Pairing and Explaining." Asian Medicine 5, no. 1 (2009): 19–38. http://dx.doi.org/10.1163/157342109x568928.
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AbstractThis paper discusses some terminological consequences of the acceptance of a seemingly all-pervasive yin yang dualism by ancient Chinese naturalists, with a focus on the origin of certain technical terms introduced to designate morphological and functional items in the emerging Chinese medicine. These terms were selected from words not originally linked to morphological and physiological notions. They served as metaphors to illustrate both function and the yin yang nature of the items they were chosen to designate. How to translate these terms into Western languages is a complex issue not sufficiently discussed among philologists.In 79 CE, the historian Ban Gu (32‐92) published the Bai hu tong , based on contributions by an unknown number of participants in one of the first documented meetings of intellectuals in antiquity. Chapter 8 offers a discourse on the meaning of qing , ‘emotion’, and xing , ‘moral disposition’. Two terms were available that had been in long use in this arena of meanings, albeit without a clear-cut distinction along the lines of a Yin-Yang categorisation. No metaphors were required here. Rather, a redefinition of qing and xing was required to assign a yang nature to the former and a yin nature to the latter.The Bai hu tong is a telling example of a continuing heterogeneity of explanatory models in early Chinese life sciences. The following discussion offers an impression of the merger of what may originally have been a neutral attempt at a dualistic categorisation of all phenomena in terms of two natural categories of yin and yang with another doctrine. The second clearly valued yang phenomena more highly than yin phenomena and applied this distinction to more and less desirable moral categories. Also, the Bai hu tong offers evidence of different metaphorical usages of the term fu in physiological theory from as early as Han times. To the older meaning: ‘short-term storage facility’ a second meaning of ‘palace’ was added. The question of an adequate translation of such terms in modern languages is worth further thought.1
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Pennisi, Angela, Xin Li, Bart Barlogie, John Shaughnessy PhD, and Shmuel Yaccoby. "Consequences of Intermittent PTH Treatment on Myeloma Growth, Bone Disease and Molecular Profiling of Whole Myelomatous Bone." Blood 116, no. 21 (November 19, 2010): 4063. http://dx.doi.org/10.1182/blood.v116.21.4063.4063.
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Abstract Abstract 4063 Intermittent PTH (iPTH) treatment is bone anabolic and has been successfully used for treatment of osteoporosis. The aims of the study were to investigate the effects of iPTH-induced bone formation on myeloma progression and unravel molecular mechanisms associated with these effects, using the SCID-rab and SCID-hu models. Using our reported procedure (Xin et al., BJH 2007), we established a novel myeloma cell line, Hg, capable of sequential passaging in experimental models. Hg cells have similar gene expression profiling (GEP) as the original patient's plasma cells, are classified in the MMSET subtype and express DKK1. SCID-hu or SCID-rab (8-10 hosts/group in each model) mice engrafted with Hg myeloma cells were subcutaneously treated with saline or iPTH (80 ug/kg/day) for 4 weeks. Overall, whereas BMD of the myelomatous bones in saline-treated hosts was similarly reduced in SCID-rab and SCID-hu mice by 14±5%, it was increased by 10±2% in iPTH-treated hosts (p<0.002 saline vs. iPTH-treated hosts). Histologic and histomorphometric analyses revealed increased bone formation parameters and no effect on number of osteoclasts. The bone anabolic effect of iPTH was associated with reduced myeloma growth by >50% (p<0.03) assessed by measurement of human immunoglobulin level in mice sera and histologically. Treatment with iPTH also increased BMD and attenuated myeloma growth in SCID-rab mice engrafted with myeloma cells from 10 patients. We found by qRT-PCR that type-1 PTH receptor was not expressed by myeloma cells and that PTH had no direct effect on in vitro growth of myeloma cells indicating that PTH anti-myeloma effect is indirectly mediated through modulation of the BM microenvironment. To shed light on molecular mechanisms associated with iPTH effects, human GEP and qRT-PCR validation of selected genes were preformed on whole myelomatous human bones from Hg-bearing SCID-hu mice treated with saline or iPTH for 4 weeks (5 hosts/group). Mice were sacrificed 2 hours after the last injection. Treatment with iPTH upregulated 343 genes and downregulated 410 genes ('2 folds, p<0.05) in myelomatous bones. There was a remarkable alteration in expression of genes associated with cAMP (e.g. RGS1/2 upregulation) and Wnt (e.g. LRP4 upregulation; DKK1 downregulation) signaling, upregulation of growth factors and receptors involved in bone remodeling (e.g. FGFR1/2, FDGFA, FDGFRA, TGFB, TGFBR1), and increased expression of osteoblast markers (e.g. osteocalcin, RUNX2). Interestingly, although iPTH induced upregulation of RANKL there was a reduction in expression of osteoclastic genes (e.g. ACP5/TRAP, NFATC1), probably due to increased osteoblast numbers, downregulation of inflammatory genes (e.g. AIF1) and upregulation of anti-inflammatory genes (e.g. TNFAIP6, CXCL14). Moreover, iPTH reduced expression of typical myeloma associated genes (e.g. CD38, WHSC1, IRF4) and had no effect on expression of myeloma growth factors such as IL6 and IGF1. Expression of certain documented anti-myeloma factors was upregulated by iPTH (e.g. decorin). We conclude that iPTH-induced bone formation in myelomatous bones is mediated by activation of multiple signaling pathways involved in osteoblastogenesis, and attenuated bone resorption and myeloma growth through mechanisms involving increased production of anti-myeloma factors by osteoblasts and minimizing inflammatory conditions induced by myeloma. Treatment with iPTH may be a promising approach for myeloma bone disease and tumor progression. Disclosures: No relevant conflicts of interest to declare.
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Li, Naren, Liang Hu, Qinfang Liu, Yulan Xiong, and Jianzhong Yu. "Abstract 866: Translational repression by a novel partner of human cytoplasmic poly(A) binding protein." Cancer Research 82, no. 12_Supplement (June 15, 2022): 866. http://dx.doi.org/10.1158/1538-7445.am2022-866.
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Abstract In higher eukaryotes, post-transcriptional regulation of gene expression, which is accomplished by an ensemble of RNA-binding proteins (RBPs), is critical for cellular homeostasis. Unkempt (UNK) is an evolutionarily conserved Zinc Finger/RING domain RNA-binding protein that was originally identified as a developmental regulator in Drosophila. Recent studies suggest that UNK targets specific mRNAs through its two compact zinc finger clusters and regulates their translation. However, the underlying molecular mechanisms by which UNK represses translation remain unclear. To examine UNK interactions, we purified Flag-tagged UNK and subjected the preparations to Mass spectrometry (MS) and identified an enriched protein Cytoplasmic poly(A)-binding protein(PABPC1), a key component of the translation machinery that binds to the poly(A) tail of mRNAs to promote translation and mRNA turnover. GST Pull down assay and reciprocal immunoprecipitations in HEK293 cells further confirmed the strong interaction between UNK and PABPC1 and showed that the interaction is RNA-dependent. Notably, the structural analysis, along with mutational studies proved that the interaction is mediated by the C-terminal MLLE domain of PABPC1 and the C-terminal Domain of UNK both in vitro and in vivo. Further MS2 tethering assay indicated that UNK inhibits PABPC1-stimulated translation activity. Our studies identified Unkempt as a novel partner of PABPC1 that functions to represses PABPC1-stimulated translation. The findings provide novel insight into the molecular function of Unkempt and PABPC1-mediated translational machinery. Citation Format: Naren Li, Liang Hu, Qinfang Liu, Yulan Xiong, Jianzhong Yu. Translational repression by a novel partner of human cytoplasmic poly(A) binding protein [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 866.
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Keightley, David N. "Neolithic and Shang Periods." Journal of Asian Studies 54, no. 1 (February 1995): 128–45. http://dx.doi.org/10.1017/s0021911800021604.
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The common occurrence of cults of the dead in Neolithic and early Bronze Age societies around the world raises at least one major question about early Chinese religion: what factors account for the elaboration of ancestor worship in China and for the degree to which—compared to its role in other cultures—it endured? The study of Chinese religion in the Neolithic and Shang periods (ca. 4000–1050 B.C.E.) can contribute to our understanding of such matters, but the bulk of recent scholarship is inevitably and properly focused on technical analyses of sites, artifacts, rituals, and spiritual Powers. Many studies address problems of definition, such as the nature of Ti, the high god of the Shang, and his cult (Akatsuka 1977:471–537; Ikeda 1981:25–39; Eno 1990); images of T'ien (Heaven, Sky) (Hayashi 1989a); the nature of the Earth Power and its associated altar of the soil (Tai Chia-hsiang 1986); the role of sun, bird, and other totems in Neolithic and Shang belief (Hu Hou-hsüan 1977; Allan 1981; Tu Chin-p'eng 1992; Wu Hung 1985; Paper 1986; Ch'ien Chihch'iang 1988; Juyü 1991; Wang Chi-huai 1992; Xiong Chuanxin 1992; Chang Teshui 1993; Chang Wen 1994; Wang Lu-ch'ang 1994); methods and objects of sacrifice (Ikeda 1980; Ch'iu Hsi-kuei 1985; Childs-Johnson 1987; Lien Shao-ming 1989; Itō 1990; Hao Pen-hsing 1992); the religious dimensions of illness (Takashima 1980) and of settlement building (Akatsuka 1977:494–99).
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Cheng, Shan, Jinghua Yang, Miao Su, Jicheng Sun, Kaiwen Xiong, Jin Ma, and Wendong Hu. "Postural Stability Change Under Sleep Deprivation and Mental Fatigue Status." Aerospace Medicine and Human Performance 92, no. 8 (August 1, 2021): 627–32. http://dx.doi.org/10.3357/amhp.5755.2021.
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AbstractBACKGROUND: Based on posturography parameters during sleep deprivation (SD), a mental fatigue index (MFI) was constructed for healthy male cadets.METHODS: There were 37 young male subjects who volunteered for two successive days of SD. Their posturography balance, profile of mood status (POMS), and heart rate variability (HRV) were measured at four different times (10:00 and 22:00 of day 1, 10:00 and 22:00 of day 2). According to the methods used in our previous research, similar MFIs based on posturography parameters were computed. Then, correlations of MFIs with POMS scores and HRV values were evaluated by linear and nonlinear methods including quadratic, S-curve, growth, and exponential analyses.RESULTS: MFI continued to increase during SD and MFI as the independent variable had quadratic relationships with fluster (R2 0.057), depression (R2 0.067), and anger (R2 0.05) scores of POMS. A linear correlation was found between MFI and the depression score (R2 0.045) and MFI correlated linearly (R2 0.029) and nonlinearly (R2 0.03) with heart rate. Similarly, MFI reflected changes in the time and frequency domain parameters of HRV, with linear (R2range: 0.0290.082) or nonlinear (R2range: 0.0300.082) relationships.DISCUSSION: The increase of MFI was linked with amplification of personal negative moods and an imbalance of autonomic nervous system activity. The findings suggest that MFI might be a potential indicator of mental fatigue and provide a method to prevent driving fatigue and human errors.Cheng S, Yang J, Su M, Sun J, Xiong K, Ma J, Hu W. Postural stability change under sleep deprivation and mental fatigue status. Aerosp Med Hum Perform. 2021; 92(8):627632.
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Bi, Siling, Liang Xu, Shouqiang Chen, Shuai Bu, and Yunsheng Xu. "Detection of Herbal Combinations and Pharmacological Mechanisms of Clinical Prescriptions for Coronary Heart Disease Using Data Mining and Network Pharmacology." Evidence-Based Complementary and Alternative Medicine 2021 (October 23, 2021): 1–20. http://dx.doi.org/10.1155/2021/9234984.
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Though widely used in the treatment of coronary heart disease (CHD), the mechanism of traditional Chinese medicine (TCM) is still unclear because of its complex prescription rules. This study prospectively collected 715 prescriptions of TCM for the treatment of CHD. The characteristics of TCM in prescriptions were described and analyzed, and the rules of prescriptions were analyzed by using association rules. Frequency statistics showed that the high-frequency herbs with a frequency of more than 60% were Gan-cao, Huang-qi, Dang-gui, Chuan-xiong, Yan-hu-suo, and San-qi. The high-frequency herb combinations were summarized by using association rules. By using the method of the “Top N groups” to excavate the empirical prescriptions, the basic prescriptions for treating CHD were summarized. We named the intersection herbs of the basic prescriptions and the high frequency herbs as the core herbal prescription. To explore the possible mechanisms underlying the anti-CHD effect of the core herbal prescription, the bioactive components of core herbal prescription and their targets were screened out by using network pharmacology. Molecular docking was performed between the bioactive components and core targets. A total of 28 potential active ingredients and 5 core targets were identified for the treatment of CHD with core herbal prescription. The enrichment analysis results indicated that the mechanism of action mainly involved neuroactive ligand-receptor interaction and calcium signaling pathway. The commonly used herbal pairs for CHD with qi deficiency and blood stasis syndrome were Huang-qi and Dang-gui. The mechanism of action of common herbal pairs was also studied by network pharmacology. This study summarized the prescription rule of TCM in the treatment of CHD and may provide a new idea for the treatment of CHD.
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Li, Xin, Feng Zhu, Chengfei Jiang, Yongmei Zhao, Bao Tran, Donna Butcher, Xiaolin Wu, Tross Debra, and Yinling Hu. "Abstract 926: IIKKa deletion amplifies renal transitional epithelial stem cells and initiates lethal invasive papillary urothelial cell carcinoma development." Cancer Research 82, no. 12_Supplement (June 15, 2022): 926. http://dx.doi.org/10.1158/1538-7445.am2022-926.
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Abstract Urothelial cell carcinoma is the most common cancer of the renal pelvis or ureter in humans. Due to a lack of animal models, its pathogenic causes remain elusive. Here, we generated IkkαΔKsp mice lacking Ikkα specifically in epithelial cells of the developing kidney and genitourinary tract as well as renal tubules. The mutant mice developed invasive papillary urothelial cell carcinomas initiated from the pelvis, leading to hydronephrosis, and the animals eventually died. Depleting neutrophils or antibiotic treatment slowed down the development of phenotypes but did not rescue them, suggesting that epithelial-cell-autonomous aberrant alterations induced by Ikkα loss are critical for the initiation of urothelial cancer. Moreover, We found that the urothelial cell carcinomas in the mutant mice highly expressed cancer stem-cell markers such as Sox2, K15, p63, Nanog, and CD44, as well as FGFR3 and osteopontin (OPN). Thus, we hypothesize that Ikkα ablation-mediated OPN and FGFR3 overexpression regulates and amplifies CD44+ renal cancer-stem cells for tumor initiation. These alterations are shared with human papillary urothelial cell carcinomas. Citation Format: Xin Li, Feng Zhu, Chengfei Jiang, Yongmei Zhao, Bao Tran, Donna Butcher, Xiaolin Wu, Tross Debra, Yinling Hu. IIKKa deletion amplifies renal transitional epithelial stem cells and initiates lethal invasive papillary urothelial cell carcinoma development [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 926.
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Ouyang, Quchang, Huihua Xiong, Min Yan, Jincai Zhong, Li Ran, Ting Luo, Liping Liu, et al. "Abstract P2-13-32: Pyrotinib in combination with letrozole for estrogen receptor (ER)-positive, human epidermal growth factor receptor 2 (HER2)-positive metastatic breast cancer: A multicenter, single-arm, phase II trial." Cancer Research 82, no. 4_Supplement (February 15, 2022): P2–13–32—P2–13–32. http://dx.doi.org/10.1158/1538-7445.sabcs21-p2-13-32.
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Abstract Background: HER2-targeted agents combined with endocrine therapy (ET) has been recommended as an optional therapeutic strategy for hormone receptor (HR)/human epidermal growth factor receptor 2 (HER2) co-positive metastatic breast cancer (MBC). Pyrotinib is an oral irreversible pan-ErbB receptor tyrosine kinase inhibitor targeting EGFR, HER2 and HER4, with proven efficacy in combination with chemotherapy in HER2-positive MBC. This multicenter, single-arm phase 2 trial aimed to investigate the efficacy and safety of pyrotinib plus letrozole in patients with estrogen receptor (ER)-positive, HER2-positive MBC (NCT04407988). Methods: Pre-/perimenopausal or postmenopausal women with histologically confirmed HER2-positive (immunohistochemistry [IHC] 3+ or 2+ with fluorescence in situ hybridization positive) and ER-positive (the percentage of ER+ cells ≥ 10% by IHC) MBC were enrolled. Prior treatment for metastatic disease was not allowed. Eligible patients received pyrotinib (400 mg, po, qd) plus letrozole (2.5 mg, po, qd) until disease progression or unacceptable toxicity. For pre-/perimenopausal patients, additional treatment with ovarian function suppression (OFS) was required. The primary endpoint was clinical benefit rate (CBR), defined as the rate of patients with complete response (CR), partial response (PR), or stable disease (SD) for at least 24 weeks per RECIST 1.1. Secondary endpoints included objective response rate (ORR), progression-free survival (PFS), overall survival (OS), and safety. Results: Between December 3, 2019 and April 2, 2021, 26 patients were enrolled. As of July 5, 2021, CBR was 76.9% (20 of 26; 95% CI 56.4% to 91.0%) and ORR was 57.7% (15 of 26; 95% CI 36.9% to 76.6%). One of the 26 patients (3.8%) had CR, 14 (53.8%) had PR, 5 (19.2%) had SD, 5 (19.2%) had progressive disease, and 1 (3.8%) had not evaluable disease. The benefits in CBR and ORR were observed across all subgroups. The most common any grade AEs were diarrhea (25 of 26, 96.2%), vomiting (8 of 26, 30.8%), nausea (6 of 26, 23.1%), and oral ulceration (6 of 26, 23.1%). Diarrhea was the only reported grade 3 AE that occurred in 5 patients (19.2%). No grade 4 or 5 AEs occurred during this study. Conclusions: Pyrotinib combined with letrozole showed an encouraging antitumor activity with good tolerance in patients with ER/HER2 co-positive MBC, promising as an alternative treatment option for this disease. The study is ongoing. Citation Format: Quchang Ouyang, Huihua Xiong, Min Yan, Jincai Zhong, Li Ran, Ting Luo, Liping Liu, Jing Li, Xiaohong Yang, Huawu Xiao, Ning Xie, Hui Wu, Jianxiang Gao, Jun Lu, Xuming Hu, Zheyu Hu, Can Tian, Zhengrong Shui, Min Cao. Pyrotinib in combination with letrozole for estrogen receptor (ER)-positive, human epidermal growth factor receptor 2 (HER2)-positive metastatic breast cancer: A multicenter, single-arm, phase II trial [abstract]. In: Proceedings of the 2021 San Antonio Breast Cancer Symposium; 2021 Dec 7-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2022;82(4 Suppl):Abstract nr P2-13-32.
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Chen, Li, Yi-Zhou Jiang, Songyang Wu, Jiong Wu, Genhong Di, Guangyu Liu, Keda Yu, et al. "Abstract P2-14-04: Updated data from FUTURE-C-PLUS: Combination of famitinib with camrelizumab plus nab-paclitaxel as first-line treatment for advanced, immunomodulatory triple-negative breast cancer, an open-label, single-arm, phase 2 trial." Cancer Research 82, no. 4_Supplement (February 15, 2022): P2–14–04—P2–14–04. http://dx.doi.org/10.1158/1538-7445.sabcs21-p2-14-04.
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Abstract Background Camrelizumab and nab-paclitaxel demonstrated promising anti-tumour activity in refractory metastatic immunomodulatory triple-negative breast cancer (TNBC) in FUTURE trial. Anti-angiogenic agents have been reported to facilitate immune infiltration. Famitinib is a tyrosine kinase inhibitor targeting VEGFR-2, PDGFR and c-kit. The FUTURE-C-PLUS trial (NCT04129996) which added famitinib to camrelizumab and nab-paclitaxel is a single-arm, phase 2 trial evaluating this novel triplet combinatorial strategy in patients with advanced immunomodulatory TNBC. Study design and the primary endpoint ORR has been reported previously (Zhi-ming Shao, et al. ASCO 2021, Abstract 1007). Here, we reported the updated results of this trial. Method Briefly, this study enrolled women aged 18-70 years, with previously untreated, histologically confirmed, unresectable, locally advanced, recurrent or metastatic immunomodulatory TNBC. Immunomodulatory TNBC was defined as CD8 expression on at least 10% of cells using immunohistochemistry analysis. Eligible patients received the triple therapy. Study design has been reported previously in ASCO 2021. Results Between Oct 2019 and Oct 2020, 48 patients were enrolled and treated. 39 (81.3%, 95% CI 70.2-92.3) patients had a confirmed objective response which has been reported in ASCO 2021. At this updating data cutoff (June 30, 2021), the median progression-free survival was 11.9 months (95% CI, 7.3-16.5) with the median follow-up was 14.0 months. While overall survival data were not mature yet, a promising overall survival rate was observed at 12 months (84•2%, 95% CI 73.4-95.0) and 18 months (73.6%, 95% CI 52.0-95.2). In the 39 responders, median duration of response was also not mature. The disease control rate was 95.8% (46/48). The most common treatment-related grade 3 or 4 adverse events were neutropenia (16 [33.3%]), anemia (5 [10.4%]), febrile neutropenia (5 [10.4%]), and thrombocytopenia (4 [8.3%]). No treatment-related deaths were reported. Conclusions These data, combined with those from our previous reports, provide further evidence for the triplet combination of famitinib, camrelizumab and nab-paclitaxel as an active therapy in advanced Immunomodulatory TNBC. To our knowledge, this is the best objective response rate reached in first-line treatment of advanced TNBC. A randomized controlled FUTURE-Super trial (NCT04395989) is keeping recruiting patients to further validate those findings. Citation Format: Li Chen, Yi-Zhou Jiang, Songyang Wu, Jiong Wu, Genhong Di, Guangyu Liu, Keda Yu, Lei Fan, Junjie Li, Yifeng Hou, Zhen Hu, Canming Chen, Xiaoyan Huang, Ayong Cao, Xin Hu, Shen Zhao, Xiaoyan Ma, Xiaoyu Zhu, Jianjun Zou, Wentao Yang, Zhonghua Wang, Zhi-ming Shao. Updated data from FUTURE-C-PLUS: Combination of famitinib with camrelizumab plus nab-paclitaxel as first-line treatment for advanced, immunomodulatory triple-negative breast cancer, an open-label, single-arm, phase 2 trial [abstract]. In: Proceedings of the 2021 San Antonio Breast Cancer Symposium; 2021 Dec 7-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2022;82(4 Suppl):Abstract nr P2-14-04.
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Merlin, Lisa R. "The Fragile X Mental Retardation Protein: A Valuable Partner in the Battle against Epileptogenesis." Epilepsy Currents 9, no. 4 (July 2009): 116–18. http://dx.doi.org/10.1111/j.1535-7511.2009.01311.x.
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Correction of Fragile X Syndrome in Mice. Dölen G, Osterweil E, Rao BSS, Smith GB, Auerbach BD, Chattarji S, Bear MF. Neuron 2007;56:955–962. Fragile X syndrome (FXS) is the most common form of heritable mental retardation and the leading identified cause of autism. FXS is caused by transcriptional silencing of the FMR1 gene that encodes the fragile X mental retardation protein (FMRP), but the pathogenesis of the disease is unknown. According to one proposal, many psychiatric and neurological symptoms of FXS result from unchecked activation of mGluR5, a metabotropic glutamate receptor. To test this idea we generated Fmr1 mutant mice with a 50% reduction in mGluR5 expression and studied a range of phenotypes with relevance to the human disorder. Our results demonstrate that mGluR5 contributes significantly to the pathogenesis of the disease, a finding that has significant therapeutic implications for fragile X and related developmental disorders. Limbic Epileptogenesis in a Mouse Model of Fragile X Syndrome. Qiu LF, Lu TJ, Hu XL, Yi YH, Liao WP, Xiong ZQ. Cereb Cortex 2009 in press. (doi:10.1093/cercor/bhn163) Fragile X syndrome (FXS), caused by silencing of the Fmr1 gene, is the most common form of inherited mental retardation. Epilepsy is reported to occur in 20–25% of individuals with FXS. However, no overall increased excitability has been reported in Fmr1 knockout (KO) mice, except for increased sensitivity to auditory stimulation. Here, we report that kindling increased the expressions of Fmr1 mRNA and protein in the forebrain of wild-type (WT) mice. Kindling development was dramatically accelerated in Fmr1 KO mice, and Fmr1 KO mice also displayed prolonged electrographic seizures during kindling and more severe mossy fiber sprouting after kindling. The accelerated rate of kindling was partially repressed by inhibiting N-methyl-D-aspartic acid receptor (NMDAR) with MK-801 or mGluR5 receptor with 2-methyl-6-(phenylethynyl)-pyridine (MPEP). The rate of kindling development in WT was not effected by MPEP, however, suggesting that FMRP normally suppresses epileptogenic signaling downstream of metabotropic glutamate receptors. Our findings reveal that FMRP plays a critical role in suppressing limbic epileptogenesis and predict that the enhanced susceptibility of patients with FXS to epilepsy is a direct consequence of the loss of an important homeostatic factor that mitigates vulnerability to excessive neuronal excitation.
Dissertations / Theses on the topic "Hu huan xing"
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Zhang, Qiong. "Ambivalence & ambiguity Chinese-American literature beyond politics and ethnography = Mao dun qing jie yu yi shu mo hu xing : chao yue zheng zhi he zu yi de Meiguo Hua yi wen xue /." Shanghai : Fu dan da xue chu ban she, 2006. http://books.google.com/books?id=cQ1IAAAAMAAJ.
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Siu, Sai-yau, and 蕭世友. "The relationship between emperors and monks in the northwest region in the Sixteen Kingdoms period : theoretical model and data visualization = Wu Hu shi liu guo shi dai xi bei zheng quan zhi jun zhu yu seng ren guan xi yan jiu : sha lou li lun mo xing ji shi liao shi xiang hua." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2014. http://hdl.handle.net/10722/206681.
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The Sixteen Kingdoms was a period of political disintegration in medieval China. Foreign rulers of Wu Hu (“Five Barbarian Tribes”) captured the northern China during the 3rd – 5th centuries and established independent states through continuous military actions. This thesis aims at studying the relationship between the emperors and Buddhist monks in the Northwest empires in the Sixteen Kingdoms Period, including the Former Liang (320-376), the Western Qin (385-400; 409-431), the Later Liang (386-403), the Northern Liang (397-439) and the Xia (407-431), by developing a theoretical model called “Hourglass Model”.
The model provides a holistic framework for investigating not only the emperors’ changing attitudes towards Buddhism but also the dissemination of the Dharma by monks. In addition, the concept of “data visualization” is implemented to re-interpret various historical sources. The complex interaction among imperial clans and Buddhist practitioners is further analyzed with computer-aided historical research methods.
This thesis hopes to reveal the inspiring nature of the political religion in China’s early medieval age and expand the scope of Chinese Studies by rethinking about foreign rulers and Buddhist monks’ roles in reshaping and vitalizing the Chinese civilization. Moreover, this study develops alternative approaches to the research on the history of Chinese Buddhism, and attempts to shed new lights on theories and research methodology.published_or_final_version
Chinese
Master
Master of Philosophy
Books on the topic "Hu huan xing"
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London, Jack. Yeh xing di hu huan. Taibei Shi: Lin yü wen hua shi yeh yu xian gong si, 1997.
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1876-1916, London Jack, and Zhang Zhigang ill, eds. Yeh xing di hu huan. Tainan Shi: Da qian wen hua chu ban shi yeh gong si, 1992.
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London, Jack. Ye xing de hu huan. Nanjing shi: Feng huang chu ban chuan mei ji tuan, 2011.
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London, Jack. Yeh xing di hu huan. Taibei Shi: Tai-wan shang wu yin shu guan, 1998.
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London, Jack. Ye xing de hu huan. Taibei Shi: Xi dai shu ban gu fen you xian gong si, 2000.
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London, Jack. Yeh xing di hu huan. Taibei Xian: Shu hua chu ban shi yeh yu xian gong si, 1986.
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Ning, Yu, and Shi Yafang, eds. Ye xing de hu huan. Beijing: Shang wu yin shu guan, 2015.
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London, Jack. Ye xing de hu huan. Hang zhou: Zhe jiang shao nian er tong chu ban she, 2001.
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London, Jack. Ye xing de hu huan. 2nd ed. Taibei Shi: Ji tian wen hua shi ye you xian gong si, 2002.
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London, Jack. Ye xing de hu huan. 2nd ed. Yan ji: Yan bian ren min chu ban she, 2005.
Find full textBook chapters on the topic "Hu huan xing"
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"Optical Detection of Cancers / Xin-Hua Hu, Jun Qing Lu." In Encyclopedia of Biomaterials and Biomedical Engineering, 2041–50. CRC Press, 2008. http://dx.doi.org/10.1201/9780429154065-193.
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