全身体积描记系统(兔、犬)
产品名称: 全身体积描记系统(兔、犬)
英文名称:
产品编号: WBP-T
产品价格: 0
产品产地: 上海
品牌商标: 塔望
更新时间: null
使用范围: null
- 联系人 :
- 地址 : 上海市松江区泗泾镇泗砖路351号6幢
- 邮编 : 201601
- 所在区域 : 上海
- 电话 : 152****5464 点击查看
- 传真 : 点击查看
- 邮箱 : shitan@tow-int.net
产品描述
无约束全身体积描记法(whole-bodyplethysmograph,WBP)可以对清醒自由活动的大动物进行肺功能及气道反应相关的测试,避免了创伤性气管切开术及麻醉的影响,使实验过程简便快捷,并适合长期跟踪研究。
塔望科技开发的全身体积描记系统,除了做小鼠、大鼠/豚鼠外,另外还提供大动物的测试舱,如兔子、犬、猴等。
产品特点
· 适用动物:兔子、犬
· 不需要做手术,操作简单
· 可在动物在自然状态下呼吸的研究以及长期跟踪实验,适合进行药物初筛
· 具有药物气溶胶雾化模块
· 具有自动标定功能
· 可提供食槽,进行长期连续监测
· 可选配测量心电、血压、体温、心率等指标,可与植入式遥测设备联合使用
· 具有分析软件,数据可保存至excel或txt格式
检测参数
Ti:吸气时间(s)
Te:呼气时间(s)
PIF:最大吸气流速(ml/s)
PEF:最大呼气流速(ml/s)
Volbal:吸气时间/呼气时间
F:呼吸频率(次/min)
Vt:潮气量(ml)
Mv:分钟通气量(ml)
AV:累积体积(ml)
EF50:呼出50%气量时对应的呼气流速(ml/s)
EIP:吸气峰值压力(仅在侵入式法测量时有效)
EEP:呼气峰值压力(仅在侵入式法测量时有效)
TR:松弛时间
PenH:增强呼气间歇(enhanced pause)
Rpef:相对时间
适用领域
各种呼吸疾病研究,如:哮喘、肺纤维化、肺损伤、ARDS、肺癌等
安全药理:药物对呼吸系统的影响
睡眠呼吸:监测动物低通气、阻塞性呼吸暂停等
环境毒理:环境污染物对动物呼吸的影响
吸入式毒理:染毒物质对呼吸系统的毒性影响
高原医学:高原环境对呼吸系统的影响
其它需要对呼吸参数评价的场合
型号说明
名称 | 型号 | 说明 | 单位 |
大动物全身体积描记系统 | WBP-P | 适用于猕猴、食蟹猴 | 套 |
大动物全身体积描记系统 | WBP-T | 适用于兔子 | 套 |
参考文献
[1]Tang Deng, Qifeng Huang, Kaiwen Lin, Jin Qian, Qi Li,Lihua Li, Shuangqin Xu, Hongfang Yun, Hangfei Wang, Xinxin Wu, Heng Liu, Guiyun Jin, Xiaoran Liu. “Midkine-Notch2 Pathway Mediates Excessive Proliferation of Airway Smooth Muscle Cells in Chronic Obstructive Lung Disease”[J]. Frontiers in Pharmacology. doi: 10.3389/fphar.2022.794952
[2]Tianxiao Sun, Haihua Li, Yan Zhang, Guixin Xiong, Yuerun Liang, Fang Lu, Rong Zheng, Qi Zou, Jiejie Hao. “Inhibitory Effects of 3-Cyclopropylmethoxy-4-(diflfluoromethoxy) Benzoic Acid on TGF-β1-Induced Epithelial-Mesenchymal Transformation of In Vitro and Bleomycin-Induced Pulmonary Fibrosis In Vivo”
[J]. Pulmonary Fibrosis In Vivo. Int. J. Mol. Sci. 2023, 24, 6172.
[3]Richeldi, L.; Collard, H.R.; Jones, M.G. Idiopathic pulmonary fibrosis. Lancet 2017, 389, 1941–1952. [CrossRef] [PubMed]
[4]Cheresh, P.; Kim, S.J.; Tulasiram, S.; Kamp, D.W. Oxidative stress and pulmonary fibrosis. Biochim. Biophys. Acta 2013, 1832,1028–1040. [CrossRef] [PubMed]
[5]Gross, J.T.; Hunninghake, W.G. Idiopathic pulmonary fibrosis. N. Engl. J. Med. 2001, 345, 517–525. [CrossRef] [PubMed]
[6]Raghu, G.; Collard, H.R.; Egan, J.J.; Martinez, F.J.; Behr, J.; Brown, K.K.; Colby, T.V.; Cordier, J.F.; Flaherty, K.R.; Lasky, J.A.; et al.An official ATS/ERS/JRS/ALAT statement: Idiopathic pulmonary fibrosis: Evidence-based guidelines for diagnosis and management. Am. J. Respir. Crit. Care Med. 2011, 183, 788–824. [CrossRef]
[7]Ley, B.; Collard, H.R. Epidemiology of idiopathic pulmonary fibrosis. Clin. Epidemiol. 2013, 5, 483–492. [CrossRef] [PubMed]
[8]Ley, B.; Collard, H.R.; King, T.E., Jr. Clinical course and prediction of survival in idiopathic pulmonary fibrosis. Am. J. Respir. Crit.Care Med. 2011, 183, 431–440. [CrossRef]
[9]Hutchinson, J.; Fogarty, A.; Hubbard, R.; McKeever, T. Global incidence and mortality of idiopathic pulmonary fibrosis:A systematic review. Eur. Respir. J. 2015, 46, 795–806. [CrossRef]
[10]Karimi-Shah, A.B.; Chowdhury, A.B. Forced Vital Capacity in Idiopathic Pulmonary Fibrosis—FDA Review of Pirfenidone and Nintedanib. N. Engl. J. Med. 2015, 372, 1187–1191. [CrossRef]
[11]Kalafatis, D.; Löfdahl, A.; Näsman, P.; Dellgren, G.; Wheelock, Å.M.; Elowsson Rendin, L.; Sköld, M.; Westergren-Thorsson,G. Distal Lung Microenvironment Triggers Release of Mediators Recognized as Potential Systemic Biomarkers for Idiopathic Pulmonary Fibrosis. Int. J. Mol. Sci. 2021, 22, 13421. [CrossRef]
[12]Salton, F.; Ruaro, B.; Confalonieri, P.; Confalonieri, M. Epithelial-Mesenchymal Transition: A Major Pathogenic Driver in Idiopathic Pulmonary Fibrosis? Medicina 2020, 56, 608. [CrossRef]
[13]Jolly, M.K.; Ward, C.; Eapen, M.S.; Myers, S.; Hallgren, O.; Levine, H.; Sohal, S.S. Epithelial-mesenchymal transition, a spectrum of states: Role in lung development, homeostasis, and disease. Dev. Dyn. 2018, 247, 346–358. [CrossRef] [PubMed]
[14]Frangogiannis, G.N. Transforming growth factor-beta in tissue fibrosis. J. Exp. Med. 2020, 217, e20190103. [CrossRef] [PubMed]
[15]Gauldie, J.; Kolb, M.; Sime, J.P. A new direction in the pathogenesis of idiopathic pulmonary fibrosis? Respir. Res. 2002, 3, 1.[CrossRef]
[16]Ruaro, B.; Soldano, S.; Smith, V.; Paolino, S.; Contini, P.; Montagna, P.; Pizzorni, C.; Casabella, A.; Tardito, S.; Sulli, A.; et al.Correlation between circulating fibrocytes and dermal thickness in limited cutaneous systemic sclerosis patients: A pilot study.Rheumatol. Int. 2019, 39, 1369–1376. [CrossRef]
[17]Kelly, M.; Kolb, M.; Bonniaud, P.; Gauldie, J. Re-evaluation of Fibrogenic Cytokines in Lung Fibrosis. Curr. Pharm. Des. 2003, 9,39–49. [CrossRef]
[18]Willis, B.C.; Borok, Z. TGF-beta-induced EMT: Mechanisms and implications for fibrotic lung disease. Am. J. Physiol. Lung Cell Mol. Physiol. 2007, 293, L525–L534. [CrossRef]
[19]Chen, Y.L.; Zhang, X.; Bai, J.; Gai, L.; Ye, X.L.; Zhang, L.; Xu, Q.; Zhang, Y.X.; Xu, L.; Li, H.P.; et al. Sorafenib ameliorates bleomycin-induced pulmonary fibrosis: Potential roles in the inhibition of epithelial-mesenchymal transition and fibroblast activation. Cell Death Dis. 2013, 4, e665. [CrossRef]
[20]Kalluri, R.; Neilson, E.G. Epithelial-mesenchymal transition and its implications for fibrosis. J. Clin. Investig. 2003, 112, 1776–1784.[CrossRef]
[21]Liu, Y. Epithelial to mesenchymal transition in renal fibrogenesis: Pathologic significance, molecular mechanism, and therapeutic intervention. J. Am. Soc. Nephrol. 2004, 15, 1–12. [CrossRef]
[22]Desmouliere, A.; Darby, I.A.; Gabbiani, G. Normal and pathologic soft tissue remodeling: Role of the myofibroblast, with special emphasis on liver and kidney fibrosis. Lab. Investig. 2003, 83, 1689–1707. [CrossRef] [PubMed]
[23]Desmouliere, A. Factors influencing myofibroblast differentiation during wound healing and fibrosis. Cell Biol. Int. 1995, 19,471–476. [CrossRef] [PubMed]
[24]Nightingale, J.; Patel, S.; Suzuki, N.; Buxton, R.; Takagi, K.I.; Suzuki, J.; Sumi, Y.; Imaizumi, A.; Mason, R.M.; Zhang, Z. Oncostatin M, a cytokine released by activated mononuclear cells, induces epithelial cell-myofibroblast transdifferentiation via Jak/Stat pathway activation. J. Am. Soc. Nephrol. 2004, 15, 21–32. [CrossRef] [PubMed]
[25]Li, X.; Ma, L.; Huang, K.; Wei, Y.; Long, S.; Liu, Q.; Zhang, D.; Wu, S.; Wang, W.; Yang, G.; et al. Regorafenib-Attenuated,Bleomycin-Induced Pulmonary Fibrosis by Inhibiting the TGF-β1 Signaling Pathway. Int. J. Mol. Sci. 2021, 22, 1985. [CrossRef][PubMed]
[26]Miyazono, K. TGF-beta signaling by Smad proteins. Cytokine Growth Factor Rev. 2000, 11, 15–22. [CrossRef] [PubMed]
[27]Ma, J.; Sanchez-Duffhues, G.; Goumans, M.J.; Ten Dijke, P. TGF-beta-Induced Endothelial to Mesenchymal Transition in Disease and Tissue Engineering. Front. Cell Dev. Biol. 2020, 8, 260. [CrossRef]
[28]Heldin, H.C.; Miyazono, K.; Dijke, T.P. TGF-beta signalling from cell membrane to nucleus through SMAD proteins. Nature 1997,390, 465–471. [CrossRef]
[29]Noble, P.W. Epithelial fibroblast triggering and interactions in pulmonary fibrosis. Eur. Respir. Rev. 2008, 17, 123–129. [CrossRef]
[30]Aschner, Y.; Downey, G.P. Transforming Growth Factor-beta: Master Regulator of the Respiratory System in Health and Disease.Am. J. Respir. Cell Mol. Biol. 2016, 54, 647–655. [CrossRef]
[31]Guillot, L.; Nathan, N.; Tabary, O.; Thouvenin, G.; Le Rouzic, P.; Corvol, H.; Amselem, S.; Clement, A. Alveolar epithelial cells:Master regulators of lung homeostasis. Int. J. Biochem. Cell Biol. 2013, 45, 2568–2573. [CrossRef]
[32]Winters, N.I.; Burman, A.; Kropski, J.A.; Blackwell, T.S. Epithelial Injury and Dysfunction in the Pathogenesis of Idiopathic PulmonaryFibrosis. Am. J. Med. Sci. 2019, 357, 374–378. [CrossRef] [PubMed]
[33]Fernandez, I.E.; Eickelberg, O. The impact of TGF-beta on lung fibrosis: From targeting to biomarkers. Proc. Am. Thorac. Soc.2012, 9, 111–116. [CrossRef] [PubMed]
[34]Kasai, H.; Allen, J.T.; Mason, R.M.; Kamimura, T.; Zhang, Z. TGF-beta1 induces human alveolar epithelial to mesenchymal cell transition (EMT). Respir. Res. 2005, 6, 56. [CrossRef] [PubMed]
[35]Yu, H.; Shen, Y.; Hong, J.; Xia, Q.; Zhou, F.; Liu, X. The contribution of TGF-beta in Epithelial-Mesenchymal Transition (EMT):Down-regulation of E-cadherin via snail. Neoplasma 2015, 62, 1–15. [CrossRef] [PubMed]
[36]Zhou, E.; Fu, Y.; Wei, Z.; Yu, Y.; Zhang, X.; Yang, Z. Thymol attenuates allergic airway inflammation in ovalbumin (OVA)-induced mouse asthma. Fitoterapia 2014, 96, 131–137. [CrossRef] [PubMed]
[37]Chacko, B.M.; Qin, B.Y.; Tiwari, A.; Shi, G.; Lam, S.; Hayward, L.J.; de Caestecker, M.; Lin, K. Structural Basis of Heteromeric Smad Protein Assembly in TGF-β Signaling. Mol. Cell 2004, 15, 813–823. [CrossRef] [PubMed]
[38]DeMaio, L.; Buckley, S.T.; Krishnaveni, M.S.; Flodby, P.; Dubourd, M.; Banfalvi, A.; Xing, Y.; Ehrhardt, C.; Minoo, P.; Zhou, B.; et al. Ligand-independent transforming growth factor-β type I receptor signalling mediates type I collagen-induced epithelialmesenchymal transition. J. Pathol. 2012, 226, 633–644. [CrossRef]
[39]Liu, T.; De Los Santos, F.G.; Phan, S.H. The Bleomycin Model of Pulmonary Fibrosis. Methods Mol. Biol. 2017, 1627, 27–42.
[40]Shimbori, C.; Upagupta, C.; Bellaye, P.S.; Ayaub, E.A.; Sato, S.; Yanagihara, T.; Zhou, Q.; Ognjanovic, A.; Ask, K.; Gauldie, J.; et al.Mechanical stress-induced mast cell degranulation activates TGF-beta1 signalling pathway in pulmonary fibrosis. Thorax 2019,74, 455–465. [CrossRef]
[41]Lu, Y.; Zhang, T.; Shan, S.; Wang, S.; Bian, W.; Ren, T.; Yang, D. MiR-124 regulates transforming growth factor-beta1 induced differentiation of lung resident mesenchymal stem cells to myofibroblast by repressing Wnt/beta-catenin signaling. Dev. Biol.2019, 449, 115–121. [CrossRef]
[42]Hou, J.; Ma, T.; Cao, H.; Chen, Y.; Wang, C.; Chen, X.; Xiang, Z.; Han, X. TNF-alpha-induced NF-kappaB activation promotes myofibroblast differentiation of LR-MSCs and exacerbates bleomycin-induced pulmonary fibrosis. J. Cell Physiol. 2018, 233,2409–2419. [CrossRef] [PubMed]
[43]Mouratis, M.A.; Aidinis, V. Modeling pulmonary fibrosis with bleomycin. Curr. Opin. Pulm. Med. 2011, 17, 355–361. [CrossRef][PubMed]
[44]Kolb, P.; Upagupta, C.; Vierhout, M.; Ayaub, E.; Bellaye, P.S.; Gauldie, J.; Shimbori, C.; Inman, M.; Ask, K.; Kolb, M.R.J. The importance of interventional timing in the bleomycin model of pulmonary fibrosis. Eur. Respir. J. 2020, 11, 55. [CrossRef][PubMed]
[45]Wynn, T.A. Integrating mechanisms of pulmonary fibrosis. J. Exp. Med. 2011, 208, 1339–1350. [CrossRef]
[46]Chen, H.; Qu, J.; Huang, X.; Kurundkar, A.; Zhu, L.; Yang, N.; Venado, A.; Ding, Q.; Liu, G.; Antony, V.B.; et al. Mechanosensing by the alpha6-integrin confers an invasive fibroblast phenotype and mediates lung fibrosis. Nat. Commun. 2016, 7, 12564. [CrossRef]
[47]Engelmann, T.A.; Knudsen, L.; Leitz, D.H.W.; Duerr, J.; Beers, M.F.; Mall, M.A.; Ochs, M. Linking Fibrotic Remodeling and Ultrastructural Alterations of Alveolar Epithelial Cells after Deletion of Nedd4-2. Int. J. Mol. Sci. 2021, 22, 7607. [CrossRef] [PubMed]
*我公司可以根据客户的特殊应用、特殊需求提供功能定制服务,也可以提供相关的实验服务,详情请来电咨询。