2.Acupuncture and massage therapy for 23 cases of pharyngitis caused by cervical vertebra disease.
Xiang-Qian LIN ; Hong-Yi ZHAO ; Qing SUN
Chinese Acupuncture & Moxibustion 2012;32(2):166-166
Acupuncture Therapy
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Adult
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Cervical Vertebrae
;
injuries
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Combined Modality Therapy
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Female
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Humans
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Male
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Massage
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Middle Aged
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Pharyngitis
;
etiology
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therapy
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Spinal Diseases
;
complications
;
Young Adult
3.Leiomyosarcoma of the parotid gland: a case report.
Guo-lin XIANG ; Xing LONG ; Qian-chao HAN
Chinese Journal of Otorhinolaryngology Head and Neck Surgery 2012;47(1):72-73
Aged
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Female
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Humans
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Leiomyosarcoma
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pathology
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Parotid Gland
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pathology
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Parotid Neoplasms
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pathology
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Retrospective Studies
4.Progress in monoclonal antibody humanization based on complementarity-determining region grafting
xiao-lin, ZHU ; feng, CHENG ; guan-xiang, QIAN
Journal of Shanghai Jiaotong University(Medical Science) 2006;0(11):-
Humanized monoclonal antibodies(mAbs) are increasingly widely used in targeted therapy for cancer and some other major diseases.Complementarity-determining region(CDR) grafting makes quantities of humanized mAbs available.Herein,we provide an overview on the strategy and progress of CDR grafting.
5.Expression of pro-opiomelanocortin mRNA in the hypothalamic arcuate nucleus in young and senile rats
Zhenghua XIANG ; Lin MENG ; Ling JIANG ; Guozhen QIAN
Academic Journal of Second Military Medical University 2001;22(5):481-483
Objective: To observe the level of pro-opiomelanocortin (POMC) mRNA expression in the hypothalamic arcuate nucleus in young and senile rats. Methods: POMC mRNA was determined with in situ hybridization, the hybridization signals and areas of POMC mRNA-positive cells were measured with computer image analysis system. Results: Compared with young rats, average gray values of POMC mRNA-positive neurons in the hypothalalmic arcuate nucleus and near region in the senile rats decreased, but the numbers of POMC mRNA-positive neurons did not change significantly. Conclusion: The decrease of POMC mRNA expression level in individual neurons in hypothalamic arcuate nucleus of senile rats is one of the causes that decrease the expression of peptides-derived from POMC gene.
6.PID1 based connection of insulin resistance to hepatocellular carcinogenesis
Ming XIANG ; Qian-Qian XU ; Sen-Lin LI ; Bao-Tian WANG ; Ya-Li TUO
Chinese Journal of Pharmacology and Toxicology 2018;32(4):316-316
OBJECTIVE To investigate the effect of phosphotyrosine interaction domain containing 1 (PID1, NYGGF4) onpromotion of IR and HCC, and explore its underlying mechanisms. METHODS Lentivirus were used to mediate the knockdown of PID1 in HFD induced IR mouse model as well as ob/ob mice. Intraperitoneal glucose and insulin tolerance were performed 4 weeks after lentivirus injection. Hydrodynamics-based transfection was applied to induce the liver specific overexpression of PID1. Flow cytometry was exerted to detect the proportion and function of immune cells.qRT-PCR and Western blot were used to detect the expression of downstream pathways of PID1. Liquid chromatography-mass spectrometry (LC-MS) and co-immunoprecipitation (Co-IP) were conducted to identify proteins interacting with PID1.Chromatin immunoprecipitation(ChIP)was operated to measure the modification of H3K4me3 of PID1 promoter.RESULTS PID1 restriction improved insulin resistance,hyperglycemia and fatty liver. Conversely, hepatic knockdown of PID1 attenuated liver xenografted tumor growth. Moreover,PID1 liver-specific protooncogenes via hydrodynamics-based transfection established a primary hepatocellular carcinoma mouse model,induced an immunosuppressive environment,with the reduction of CD3+,CD4+,CD8+T cells,retarded maturation of dendritic cells(DCs),pronounced differentiation of regulatory T cells(Tregs),and recruitment of MDSC.In addition,PID1 overexpression activated prolifer-ation related genes, promoted anti-inflammatory genes, suppressed pro-inflammatory genes, induced glycolysis and lipid metabolism genes to facilitate tumorigenesis in liver. Importantly, PID1 exerted its tumor-promoting function through binding to epidermal growth factor receptor(EGFR)and activation of downstream KRAS/ERK pathway.As such,PID1 exist trimethylation of histone H3 at lysine 4(H3K4me3) modification and IR up-regulated the expression of PID1 by activation the H3K4me3 modification. CONCLUSION PID1 is a new gene that exerts both liver cancer-promoting and insulin resistance inducing function.IR accelerates liver cancer development and progression partially dependent on the activation of PID1.
7.Relationship between MTA1 expression and invasive and metastatic ability of cervical cancer cell
Xiaoyan HAN ; Haili QIAN ; Junjun YANG ; Xueyan ZHANG ; Ming FU ; Xiao LIANG ; Chen LIN ; Yang XIANG
Chinese Journal of Obstetrics and Gynecology 2011;46(9):678-683
ObjectiveTo investigate the relationship between metastasis-associated gene 1 ( MTA1 )expression and invasive and metastatic ability of cervical cancer cell. MethodsThree kinds of plasmids pcDNA3( control group), pcDNA3-MTA1 ( MTA1 group) and pSilencer3. 1-MTA1-siRNA ( MTA1-siRNAgroup) were transfected into human cervical cancer cell line CaSki cells. Reverse transcription (RT)-PCR and western blot were used to detected MTA1 mRNA and protein expressions. The effects of MTA1 expression on CaSki cell growth and proliferation, cell migration, adhesion and invasion, and cell cycles were tested by methyl thiazolyl tetrazolium (MTT), clone formation experiment, wound-healing assay, transwell assay, adhesion assay and flow cytometry, respectively. In animal experiment, three groups of cells were inoculated to BALB/c nude mouse subcutaneously to observe tumor formation ability. ResultsCompared with control group, MTA1 mRNA and protein were significantly overexpressed in MTA1 group, while MTA1-siRNA group showed lower MTA1 expression. Compared with control group, MTA1 group showed significantly accelerated cell growth; while MTA1-siRNA group showed decreased cell growth since the second day (P<0. 05). Clone formation number in control, MTA1 and MTA1-siRNA group were 133 ±6, 169 ± 10 and 57 ±5,respectively. MTA1 group showed accelerated cell formation, while MTA1-siRNA group showed the reverse effect compared with that in control group(P < 0. 05 ). At 24, 48 and 72 hours after wounding, the healing ability of MTA1-siRNA group significantly lagged behind that in the control group, while MTA1 group showed accelerated cell healing ability. The adhesion rate of control, MTA1 and MTA1-siRNA group were (69. 3 ± 3. 6) %, ( 80. 4 ± 5. 6 ) % and ( 39. 2 ± 7.4 ) % separately at 90 minutes after cell seeding. In contrast with control group, MTA1 group promoted the adhesion of CaSki cell to matrigel matrix, while MTA1-siRNA group inhibited the adhesion process (P <0. 05 ). In the migration assay, the number of cells migrated to the bottom side of the membrane in control,MTA1 and MTA1-siRNA group were 153 ± 17,247 ± 38 and 82 ± 10, respectively. The number of cells in the invasion assay were 231 ± 19,354 ± 36 and 76 ± 7, respectively. Compared with the control group, MTA1 group significantly increased the migration and invasion ability, while MTA 1-siRNA group showed lower cell migration and invasion ability (P < 0. 05 ). In cell cycle experiment, no significant differences of cell proportions including G1, S and G2 stage were found among three groups (P > 0.05).In animal experiment, compared with control group,MTA1 group showed accelersted tumor formation and growth,whilethe MTA1-siRNA group showed the reverse effect ( P < 0. 05 ). ConclusionsMTA1 may play its roles to promote cervical cancer cell invasion, migration, adhesion, as well as cell growth and colony formation, while RNA interference against MTA1 may decrease the malignant phenotypes. This study shows that it will be an effective beginning to explore metastasis mechanisms and cancer gene therapy strategy targeting MTA1 in cervical cancer.
8.A case-control study on high-risk factors for newborn hearing loss in seven cities of Shandong province.
Wenying, NIE ; Hanrong, WU ; Yisheng, QI ; Qian, LIN ; Lili, XIANG ; Hui, LI ; Yinghui, LI
Journal of Huazhong University of Science and Technology (Medical Sciences) 2007;27(2):217-20
To investigate the high-risk factors for newborn hearing loss and to provide information for preventing the development of hearing loss and delaying its progression, from May 2003 to June 2006, neonates who failed to pass the universal newborn hearing screening (UNHS) were referred to Jinan Newborn Hearing Screening and Rehabilitation Center from 7 newborn hearing screening centers in seven cities of Shandong province. One-to-one pair-matched case-control method was employed for statistical analysis of the basic features of definitely identified cases. High-risk factors relating to the bilateral hearing loss were evaluated by univariate and multivariate Logistic regression analysis. Our results revealed that 721 transferred newborns who didn't pass the hearing screening received audiological and medical evaluation and 367 were confirmed to have hearing loss. Of them, 177 neonates with hearing loss who met the matching requirements were included in the study as subjects. Univariate analysis showed that high-risk factors related to hearing loss incuded age of father, education backgrounds of parents, parity, birth weight, gestational weeks, craniofacial deformity, history of receiving treatment in neonatal intensive care unit (NICU), neonatal disease, family history of otopathy and family history of congenital hearing loss. Multivariate Logistic regression analysis revealed that 4 independent risk factors were related to bilateral hearing loss, including parity (OR=16.285, 95% CI 3.379-78.481), neonatal disease (OR=34.968, 95% CI 2.720-449.534), family history of congenital hearing loss (OR=69.488, 95% CI 4.417-1093.300) and birth weight (OR=0.241, 95% CI 0.090-0.648). It is concluded that parity, neonatal disease and family history of hearing loss are the promoting factors of bilateral hearing loss in neonates and appropriate intervention measures should be taken to deal with the risk factors.
10.Intracerebroventricular administrations of angiotensin IV (Ang IV) ameliorate cognitive disorder in diabetic rats
Hui-Min Du ; -Lin Niu MM ; Ke-Xiang Zhao ; Juan Li MMS ; Qian Xiao
Neurology Asia 2013;18(2):195-202
Cognitive impairment is a common complication of diabetes. Hippocampus plays an important role
in cognitive function. In hyperglycemia, synaptophysin, a crucial synaptic vesicle membrane protein
in hippocampus neuron is found to be down-regulated. Recent evidences have shown that angiotensin
IV can facilitate memory acquisition and recovery. However, whether it can also improve cognitive
functions of diabetic rats with cognitive disorder, and the possible mechanisms are uncertain. Hence,
the objectives of this study. Forty fi ve Sprague Dawley male rats were randomly divided into three
groups: Control, diabetic group and diabetes with angiotensin IV treatment group. The cognitive
functions, mainly learning and memory of the rats were evaluated using Morris water maze task. The
synapses ultrastructure, relative mRNA concentrations and protein expression levels of synaptophysin
in hippocampus CA1 area were estimated using transmission electron microscope, RT-PCR,
immunohistochemistry and western blotting, respectively. Our study showed that in the diabetic rats with
angiotensin IV treatment, the cognitive impairment as measured by Morris water maze task improved,
the ultrastructure of synapses in hippocampus reversed, the relative mRNA concentrations and protein
levels of synaptophysin in hippocampus signifi cantly increased, when compared with diabetic rats.
We conclude that angiotensin IV plays an important role in improving cognitive function of diabetic
rats. The possible mechanisms are up-regulating the expression of synaptophysin and normalizing the
ultrastructure of synapses in hippocampus.