- Overview
- Data/Specifications
- Literature/Support
- How It Works
Overview
IgE is the least abundant isotype but has the capability of triggering powerful immune responses by binding to Fc receptors on the surface of cells such as mast cells, basophils, eosinophils, monocytes, macrophages and platelets.
IgE is well known for its involvement in eliciting an allergic or asthmatic response.Ovalbumin (OVA) is widely used for inducing an allergic response in mouse models of allergic asthma. Through T and B cell signalling, IgE production is stimulated and released into the bloodstream where it attaches to receptors on cells such as mast cells and basophils. These cells are then activated upon cross-linking of the IgE with the antigen initiating the allergic cascade.
Data/Specifications
Species:mouse
Sample Type :cell culture supernate, serum
Sample Preparation:dilute 1:10, adjust as needed
Test Volume:100 uL
Length:2 hours 15 min
Range:7.8-500ng/mL
Sensitivity:< 3.8 ng/mL
Literature/Support
Product Insert:
Mouse OVA-IgE ELISA Insert (PDF, 276 KB)
Articles/Troublshooting:
ELISA Troubleshooting Guide
ELISA Data Reduction Guide
IgE mediated immune response in allergic asthma (blog post)
Youngblood, B. A., Brock, E. C., Leung, J., Falahati, R., Bochner, B. S., Rasmussen, H. S., ... & Tomasevic, N. (2019). Siglec-8 antibody reduces eosinophils and mast cells in a transgenic mouse model of eosinophilic gastroenteritis. JCI insight, 4(19).
Seo, M. Y., Kim, K. R., Lee, J. J., Ryu, G., Lee, S. H., Hong, S. D., ... & Kim, H. Y. (2019). Therapeutic effect of topical administration of red onion extract in a murine model of allergic rhinitis.Scientific reports,9(1), 2883.
Aliu, H., Rask, C., Brimnes, J., & Andresen, T. L. (2017). Enhanced efficacy of sublingual immunotherapy by liposome-mediated delivery of allergen.International journal of nanomedicine,12, 8377.
Sjöberg, L. C., Nilsson, A. Z., Lei, Y., Gregory, J. A., Adner, M., & Nilsson, G. P. (2017). Interleukin 33 exacerbates antigen driven airway hyperresponsiveness, inflammation and remodeling in a mouse model of asthma.Scientific reports,7(1), 1-10.
Kuo, C. H., Collins, A. M., Boettner, D. R., Yang, Y., & Ono, S. J. (2017). Role of CCL7 in type I hypersensitivity reactions in murine experimental allergic conjunctivitis.The Journal of Immunology,198(2), 645-656.
Liu, B., Lee, J. B., Chen, C. Y., Hershey, G. K. K., & Wang, Y. H. (2015). Collaborative Interactions between Type 2 Innate Lymphoid Cells and Antigen-Specific CD4+ Th2 Cells Exacerbate Murine Allergic Airway Diseases with Prominent Eosinophilia. The Journal of Immunology, 194(8), 3583-3593.
Aven, L., Paez-Cortez, J., Achey, R., Krishnan, R., Ram-Mohan, S., Cruikshank, W. W., & Ai, X. (2014). An NT4/TrkB-dependent increase in innervation links early-life allergen exposure to persistent airway hyperreactivity. The FASEB Journal, 28(2), 897-907.
Arakawa, T., Deguchi, T., Sakazaki, F., Ogino, H., Okuno, T., & Ueno, H. (2013). Supplementary seleno-L-methionine suppresses active cutaneous anaphylaxis reaction. Biological and Pharmaceutical Bulletin, 36(12), 1969-1974.
Reddy, A. T., Lakshmi, S. P., Dornadula, S., Pinni, S., Rampa, D. R., & Reddy, R. C. (2013). The nitrated fatty acid 10-nitro-oleate attenuates allergic airway disease. The Journal of Immunology, 191(5), 2053-2063.
Paez-Cortez, J., Krishnan, R., Arno, A., Aven, L., Ram-Mohan, S., Patel, K. R., & Fine, A. (2013). A new approach for the study of lung smooth muscle phenotypes and its application in a murine model of allergic airway inflammation.
Cloots, R. H., Sankaranarayanan, S., de Theije, C. C., Poynter, M. E., Terwindt, E., van Dijk, P., & Koehler, S. E. (2013). Ablation of Arg1 in hematopoietic cells improves respiratory function of lung parenchyma, but not that of larger airways or inflammation in asthmatic mice. American Journal of Physiology-Lung Cellular and Molecular Physiology, 305(5), L364-L376.
Knolle, M. D., Nakajima, T., Hergrueter, A., Gupta, K., Polverino, F., Craig, V. J., & Owen, C. A. (2013). Adam8 limits the development of allergic airway inflammation in mice. The Journal of Immunology, 190(12), 6434-6449.
Mays, L. E., Ammon-Treiber, S., Mothes, B., Alkhaled, M., Rottenberger, J., Müller-Hermelink, E. S., & Kormann, M. S. (2013). Modified Foxp3 mRNA protects against asthma through an IL-10–dependent mechanism. The Journal of clinical investigation, 123(3), 1216.
McKee, A. S., Burchill, M. A., Munks, M. W., Jin, L., Kappler, J. W., Friedman, R. S., & Marrack, P. (2013). Host DNA released in response to aluminum adjuvant enhances MHC class II-mediated antigen presentation and prolongs CD4 T-cell interactions with dendritic cells. Proceedings of the National Academy of Sciences, 110(12), E1122-E1131.
Asosingh, K., Cheng, G., Xu, W., Savasky, B. M., Aronica, M. A., Li, X., & Erzurum, S. C. (2013). Nascent endothelium initiates Th2 polarization of asthma. The Journal of Immunology, 190(7), 3458-3465.
Lombardi, V., Speak, A. O., Kerzerho, J., Szely, N., & Akbari, O. (2012). CD8α+ β− and CD8α+ β+ plasmacytoid dendritic cells induce Foxp3+ regulatory T cells and prevent the induction of airway hyper-reactivity. Mucosal immunology, 5(4), 432-443.
Nkyimbeng-Takwi, E. H., Shanks, K., Smith, E., Iyer, A., Lipsky, M. M., Detolla, L. J., & Chapoval, S. P. (2012). Neuroimmune semaphorin 4A downregulates the severity of allergic response. Mucosal immunology, 5(4), 409-419.
MacSharry, J., O"Mahony, C., Shalaby, K. H., Sheil, B., Karmouty-Quintana, H., Shanahan, F., & Martin, J. G. (2012). Immunomodulatory effects of feeding with Bifidobacterium longum on allergen-induced lung inflammation in the mouse. Pulmonary pharmacology & therapeutics, 25(4), 325-334.
Kim, S. R., Lee, K. S., Lee, K. B., & Lee, Y. C. (2012). Recombinant IGFBP‐3 inhibits allergic lung inflammation, VEGF production, and vascular leak in a mouse model of asthma. Allergy, 67(7), 869-877.
Emo, J., Meednu, N., Chapman, T. J., Rezaee, F., Balys, M., Randall, T., ... & Georas, S. N. (2012). Lpa2 is a negative regulator of both dendritic cell activation and murine models of allergic lung inflammation. The Journal of Immunology, 188(8), 3784-3790.
Diesner, S. C., Olivera, A., Dillahunt, S., Schultz, C., Watzlawek, T., Förster-Waldl, E., ... & Rivera, J. (2012). Sphingosine-kinase 1 and 2 contribute to oral sensitization and effector phase in a mouse model of food allergy. Immunology letters, 141(2), 210-219.
Carr, V. M., Robinson, A. M., & Kern, R. C. (2012). Tissue-specific effects of allergic rhinitis in mouse nasal epithelia. Chemical senses, bjs048.
Singh, S. P., Gundavarapu, S., Peña-Philippides, J. C., Mishra, N. C., Wilder, J. A., Langley, R. J., ... & Sopori, M. L. (2011). Prenatal secondhand cigarette smoke promotes Th2 polarization and impairs goblet cell differentiation and airway mucus formation. The Journal of Immunology, 187(9), 4542-4552.
Reisacher, W. R., Liotta, D., Yazdi, S., & Putnam, D. (2011, September). Desensitizing mice to ovalbumin through subcutaneous microsphere immunotherapy (SMITH). In International forum of allergy & rhinology (Vol. 1, No. 5, pp. 390-395). Wiley Subscription Services, Inc., A Wiley Company.
MacNeil, A. J., Yang, Y. J., & Lin, T. J. (2011). MAPK Kinase 3 Specifically Regulates FcεRI-Mediated IL-4 Production by Mast Cells. The Journal of Immunology, 187(6), 3374-3382.
Stemmy, E. J., Balsley, M. A., Jurjus, R. A., Damsker, J. M., Bukrinsky, M. I., & Constant, S. L. (2011). Blocking cyclophilins in the chronic phase of asthma reduces the persistence of leukocytes and disease reactivation. American journal of respiratory cell and molecular biology, 45(5), 991-998.
Kim, S. R., Lee, K. S., Park, S. J., Min, K. H., Lee, M. H., Lee, K. A., & Lee, Y. C. (2011). A novel dithiol amide CB3 attenuates allergic airway disease through negative regulation of p38 mitogen-activated protein kinase. American journal of respiratory and critical care medicine, 183(8), 1015-1024.
Wang, W., Zhu, Z., Zhu, B., & Ma, Z. (2011). Peroxisome Proliferator-Activated Receptor–γ Agonist Induces Regulatory T Cells in a Murine Model of Allergic Rhinitis. Otolaryngology--Head and Neck Surgery, 144(4), 506-513.
Balsley, M. A., Malesevic, M., Stemmy, E. J., Gigley, J., Jurjus, R. A., Herzog, D., & Constant, S. L. (2010). A cell-impermeable cyclosporine A derivative reduces pathology in a mouse model of allergic lung inflammation. The Journal of Immunology, 185(12), 7663-7670.
Lauenstein, H. D., Quarcoo, D., Plappert, L., Schleh, C., Nassimi, M., Pilzner, C. & Groneberg, D. A. (2011). Pituitary adenylate cyclase‐activating peptide receptor 1 mediates anti‐inflammatory effects in allergic airway inflammation in mice. Clinical & Experimental Allergy, 41(4), 592-601.
Kim, S. R., Lee, K. S., Park, S. J., Min, K. H., Lee, M. H., Lee, K. A., ... & Lee, Y. C. (2011). A novel dithiol amide CB3 attenuates allergic airway disease through negative regulation of p38 mitogen-activated protein kinase. American journal of respiratory and critical care medicine, 183(8), 1015-1024.
Lyons, A., O"Mahony, D., O"Brien, F., MacSharry, J., Sheil, B., Ceddia, M., & O"Mahony, L. (2010). Bacterial strain‐specific induction of Foxp3+ T regulatory cells is protective in murine allergy models. Clinical & Experimental Allergy, 40(5), 811-819.
Wang, W., Zhu, Z., Zhu, B., & Ma, Z. (2011). Peroxisome Proliferator-Activated Receptor–γ Agonist Induces Regulatory T Cells in a Murine Model of Allergic Rhinitis. Otolaryngology--Head and Neck Surgery, 144(4), 506-513.
Breslow, R. G., Rao, J. J., Xing, W., Hong, D. I., Barrett, N. A., & Katz, H. R. (2010). Inhibition of Th2 adaptive immune responses and pulmonary inflammation by leukocyte Ig-like receptor B4 on dendritic cells. The journal of immunology, 184(2), 1003-1013.
Yadav, U. C., Naura, A. S., Aguilera-Aguirre, L., Ramana, K. V., Boldogh, I., Sur, S., & Srivastava, S. K. (2009). Aldose reductase inhibition suppresses the expression of Th2 cytokines and airway inflammation in ovalbumin-induced asthma in mice. The Journal of Immunology, 183(7), 4723-4732.
Park, S. J., Lee, K. S., Kim, S. R., Min, K. H., Choe, Y. H., Moon, H., ... & Lee, Y. C. (2009). Peroxisome proliferator-activated receptor γ agonist down-regulates IL-17 expression in a murine model of allergic airway inflammation. The Journal of Immunology, 183(5), 3259-3267.
Larsen, S. T., Roursgaard, M., Jensen, K. A., & Nielsen, G. D. (2010). Nano titanium dioxide particles promote allergic sensitization and lung inflammation in mice. Basic & clinical pharmacology & toxicology, 106(2), 114-117.
Lee, C. G., Hartl, D., Lee, G. R., Koller, B., Matsuura, H., Da Silva, C. A., ... & Elias, J. A. (2009). Role of breast regression protein 39 (BRP-39)/chitinase 3-like-1 in Th2 and IL-13–induced tissue responses and apoptosis. The Journal of experimental medicine, 206(5), 1149-1166.
Beigelman, A., Gunsten, S., Mikols, C. L., Vidavsky, I., Cannon, C. L., Brody, S. L., & Walter, M. J. (2009). Azithromycin attenuates airway inflammation in a noninfectious mouse model of allergic asthma. CHEST Journal, 136(2), 498-506.
| References/Citations: | Application: |
| Tissue-specific effects of allergic rhinitis in mouse nasal epithelia Carr, V.M. et al., Chem Senses, Sep 2012; 37: 655 - 668. | Serum from individual animals was analyzed for the presence ofOVA-specific IgE using an ELISA kit purchased from MD Bioproducts. |
| Lpa2 is a negative regulator of both dendritic cell activation and murine models of allergic lung inflammation Emo, J et al., J. Immunol., Apr 2012; 188: 3784 - 3790 | Serum from individual animals was analyzed for the presence of OVA-specific IgE using an ELISA kit purchasedfrom MD Bioproducts. |
| Peroxisome Proliferator-Activated Receptor–γ Agonist Induces Regulatory T Cells in a Murine Model of Allergic Rhinitis Wang, W. et al., Otolaryngology -- Head and Neck Surgery, Feb 2011 | Measure concentration of OVA-IgE from Balb/c mice with either PPAR-γ agonist pioglitazone (30 mg/kg/d) or pioglitazone plus PPAR-γ antagonist GW9662 (0.5 mg/d). |
| A Cell-Impermeable Cyclosporine A Derivative Reduces Pathology in a Mouse Model of Allergic Lung Inflammation Balsley, M et al., J. Immunol., Dec 2010; 185: 7663 | Serum from individual animals was analyzed for the presence of OVA-specific IgE using an ELISA kit purchasedfrom MD Bioproducts. |
| Inhibition of Th2 Adaptive Immune Responses and Pulmonary Inflammation by Leukocyte Ig-Like Receptor B4 on Dendritic Cells Breslow, R et al., J. Immunol., Jan 2010; 184: 1003 - 1013. | Measure the concentration of serum IgE in genetically modified female mice of the BALB/c background (6-12 weeks old). |
| A Novel Dithiol Amide CB3 attenuates allergic airway disease through negative regulation of p38 MAPKKim SR, et al. Am. J. Respir. Crit. Care Med. April 2010 | Serum from individual animals was analyzed for the presence ofOVA-specific IgE using an ELISA kit purchased from MD Bioproducts. |
| Aldose Reductase Inhibition Suppresses the Expression of Th2 Cytokines and Airway Inflammation in Ovalbumin-Induced Asthma in Mice Umesh C. S. Yadav et al.,J. Immunol., Oct 2009; 183: 4723 - 4732. | Measure the concentration of OVA-IgE in broncheoalveolar lavage (BAL) fluid from C57BL/6 mice. |
Role of breast regression protein 39 (BRP-39)/chitinase 3-like-1 in Th2 and IL-13–induced tissue responses and apoptosis Chun Geun Lee et al.,J. Exp. Med., May 2009; 206: 1149 - 1166. | Measure the concentration of OVA-IgE in splenocytes isolated from BALB/c WT and mutant mice. |
| Peroxisome Proliferator-Activated Receptor Agonist Down-Regulates IL-17 Expression in a Murine Model of Allergic Airway Inflammation Seoung Ju Park et al,J. Immunol., Sep 2009; 183: 3259 - 3267. | |
| Azithromycin Attenuates Airway Inflammation in a Noninfectious Mouse Model of Allergic Asthma Avraham Beigelman et al.,Chest, Aug 2009; 136: 498 - 506. | Measure the concentration of serum specific OVA-IgE in 7-week oldBALB/cJ female mice. |
How It Works
ELISA or Enzyme-linked Immunosorbent Assay is a colorimetric based immunoassay utilizing a capture antibodyand a detection antibody to provide a unique and powerful assay system. Antibody/antigen reactionstake place on the suface of microplate wells that have been previously coated with a monoclonal antibodyto mouse IgE heavy chain. Biotinylated ovalbumin and streptavidin-peroxidase, in the presence of substrate quantifies theanalyte bound.
Assay Principle:
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RCF = 1.119 x 10-5 x (rpm)2 x r
其中r 表示离心机转轴中心与离心管中心的距离，单位为cm。由于离心管的位置由转子（rotor）决定，因此r 必须由查阅相关转子的参数而得。
医用细胞涂片离心机
医用细胞离心涂片机
医用细胞离心涂片机是第一款使用精密控制的离心技术对细胞进行分离，形成薄层同时还能保持细胞完整的设备。它采用离心原理，将细胞
转移到诊断载玻片的固定区域，样品残液则被过滤卡吸收。通过离心力的作用，细胞结构趋向扁平，故细胞核表达尤为清晰。各种细胞在离
心过程中机会均等，不存在某些细胞或成份被人为过滤的情况，故最能反映细胞的真实环境状态。医用细胞离心涂片机特殊的倾斜结构设计还可避免细
胞在制备过程中丢失
医用细胞离心涂片机的主要特点
●医用细胞离心涂片适用于所有液基样本，尤其是细胞含量低的液基样本，如脑脊液、尿液
●医用细胞离心涂片同时处理12份样本
●医用细胞离心涂片优化的盖门开关，方便人员单手操作
●医用细胞离心涂片医用细胞离心涂片带自锁功能的塑料外盖，且仅有在盖门上锁的情况下，仪器方能进入运行状态
●医用细胞离心涂片标配一个密封舱，可高温高压消毒
●医用细胞离心涂片3级加速控制，保护脆性样品
●符合ICE61010的离心安全标准
●样本安全警报：结束后每分钟报警一次，提醒客户及时取出样本，防止风干
●可选择一次性使用耗材或反复多次使用耗材
医用细胞离心涂片适用于医院临床检验、生物、化学实验室和血站、血浆站对血液等样品的分离，是最新一代具有专门功能的产品。由微机控制，变频电机驱动，无碳刷粉尘污染，内腔由优质不锈钢制成，快速升降，操作简便，噪声低，振动小。
该系列离心机广泛适用于免疫血液学实验室、检验室、研究室，可进行红细胞血清学实验，做抗原、抗体的鉴定及库姆式实验的结果判断等，是各类医院血库，实验室，血站，医学院校和医学研究机构的必备设备。
医用细胞涂片离心机http://www.fameinstrument.cn/
自动脱帽离心机的工作原理是什么?自动脱帽离心机的使用守则是什么?该产品具有运行平稳，体积小、噪音低、造型美观、温升小，配有安全门锁装置，自动调节平衡，整机采用微电脑控制系统的一系列性能特征，自动脱帽离心机的工作原理是什么?自动脱帽离心机的使用守则是什么大家也明白吗?那迈克尔离心机小编给大家做个解释。
工作原理
自动脱帽离心机亦称脱盖离心机、真空采血管专用脱帽离心机、脱帽离心机。是指在离心的过程中，利用离心力，完成脱帽，集自动脱帽、离心一次完成，彻底解决医院在分离真空采血管中脱帽的难题，提高了工作效率。
使用守则
一.脱帽离心机在离心结束后取出转头要倒置于实验台上，擦干腔内余水，离心机盖处于打开状态。
二.转头盖摆放在离心机的平台上，或摆放在实验台上，千万不可不拧紧浮放在转头上，因为一旦误启动，转头盖就会飞出，造成事故!
三.转头盖在拧紧后一定要用手指触摸转头与转盖之间有无缝隙，如有缝隙要拧开重新拧紧，直至确认无缝隙方可启动离心机。
四.在离心过程中，操作人员不得离开离心机室，一旦发生异常情况操作人员不能关电源(POWER)，要按STOP
五.不得使用伪劣的离心使管，不得用老化、变形、有裂纹、质量不合格的离心管。
六.在节假日和晚间最后一个使用离心机的工作人员必须例行安全检查后方能离去。
七.在仪器使用过程中发生机器故障，部件损坏情况时要及时与厂家。
自动脱帽离心机的工作原理是什么?自动脱帽离心机的使用守则是什么迈克尔离心机小编介绍了这么多，希望可以帮到大家。谢谢关注。
更多资讯请咨询离心机http://www.mekeerlxj.com/
本人和同学是刚刚参与临床试验的小白，主要参与样品处理部分。
实验室离心机用的是赛默飞的HeraeusMultifugeX1R。
测转速的仪器为testo470-精密型光学/机械转速测量仪，在离心机中心轴的位置贴上反射贴，测量时将仪器红色光速对准反射贴就可以测量。
然后，4月初，老板说想要自己做温度校准。
发现实验室自己做温度校准非常少。方法也都写的不全，咨询了离心机厂家，学习到了一些：
1.使用离心机前应该提前做预冷，2000rpm，转30min。
2.低温离心机的设定温度如4℃，是腔体温度，所以当离心机屏幕显示温度降到4℃时其中的离心样品不一定是4℃。
有两种自己可以做的温度校准。
1：用连有探头的热敏电阻温度计测量腔体温度。预冷后，将温度计探头放入离心机内盖上盖子测量温度即可。但是离心机内不同位置温度稍有不同，若探头贴在金属壁上温度会过低。另外，一定不能在离心机运转时测量！
2：测量样品温度。用甘油代替样品，配平后，2000rpm，转2h。没错，是两小时，甘油降温非常慢。之后，拿出离心管用快速插入式温度计测量甘油温度。我们购买了testo905-T1-刺入式温度计，还在试用中。（如果不用甘油而用水的话，拿出来测到的温度在4.6~5.8摄氏度左右。）
因为2h实在是太久了，实验室正好有5℃左右的冰箱，准备周四的时候试一试先把甘油放在冰箱，再放入预冷后的离心机离心一段时间，看看能减少多久时间。
如果有更好的方法请各位大大指导。
靠转筒高速旋转，令里面的液体产生离心力分离或附在筒壁上。常用的衣服脱水机就可以看成是一种离心机。
一般用于煤焦油等脱水脱渣的设备，根据液体中介质的密度不同旋转后产生分层，从而起到分离的效果
离心机机械分离过程主要是物理过程，分离机械分离性能的优劣，与被分离物料的物理性能有极大的关系。如利用沉降原理进行分离的重力沉降或沉降式离心机与固相颗粒的粒径分布、固相密度、颗粒形状以及液相的密度、粘度和表面张力等均密切相关。各种沉降式分离机械的适应范围也依据物料的性质来划分。
步骤/方法1、机器裸露部分涂有防锈油脂，安装前应清除之。待安装完毕，重新涂上润滑油。然后将机器安装在混凝土基础或钢架上。安装过滤机时以两横梁为基础校正水平。
2、然后灌浇混凝土。机器周围要留有余地.考虑安装、拆卸管道以及出滤饼和检修等的方便。按要求接入管道、阀门等。根据您的机型和工艺需要配好管路。
3、按线路容量选好橡套软电缆，外套金属软管，分别接入L1、L2、L3和PEN。试运转；观察油泵电机（风叶从上端往下看）应顺时针旋转。
4、先安装压滤机的滤布，然后再安装滤板，这是比较正常的流程。关于滤布的选择：最好是根据悬浮液的性质对滤饼的要求选择滤布。
5、滤布的性能决定着过滤效果和滤布的使用寿命。滤布的结构：本机型滤布的结构为袖套式滤布。
6、压滤机的头板已被安装固定在压滤机的止推板上；尾板安装固定在压滤机的压紧板上。按要求品质的液压油，经20μm的滤网孔过滤后加入油箱内至视镜上限。
7、启动油泵将油压入液压缸，此时液位应位于视镜中线位。查看过滤机的压力表。表示数值应≤相应款式压滤机插页中所规定的液压工作压力的Mpa数。
8、如查证液压泵系统正常、压力表无误、压力不符合插页规定数值时，可调节压力。调节压力：使泄压压力大于液压工作压力约1Mpa。
9、电接点压力表上限调整至液压工作压力值，下限为液压工作压力减去2Mpa。检查并调整自动型压滤机的传动部分和拉板盒的正确位置。
注意事项（1）液相属易挥发性或易引起爆炸和易燃性物料时，不能用真空过滤，且要求密闭防爆。
（2）腐蚀性较强的物料，对分离机械材料的选择有特殊要求。
（3）固相颗粒硬度较大时，则要求所选分离机械材料的耐磨性好。
（4）被分离物料，无论是固相或液相，若属于贵重物料，则要求回收率高。
（5）固相物料为结晶产品时，要求分离时结晶的破损程度低。这对分离机械的结构及卸料方式、方法都有特殊要求。
1.冷凝器积垢：冷凝器换热管内表水质积垢(开式循环的冷却水系统最容易积垢)，而导致传热热阻增大，换热效果降低，使冷凝温度升高或蒸发温度降低，另外，由于水质未经处理和维护不善，同样造成换热管内表面沉积沙土、杂质、藻类等物，造成冷凝压力升高而导致离心机喘振发生。
2.制冷系统有空气：当离心机组运行时，由于蒸发器和低压管路都处于真空状态，所以连接处极容易渗入空气，另外空气属不凝性气体，绝热指数很高，为1.4，当空气凝积在冷凝器上部时，造成冷凝压力和冷凝温度升高，而导致离心机喘振发生。
3.冷却塔冷却水循环量不足，进水温度过高等。由于冷却塔冷却效果不佳而造成冷凝压力过高，而导致喘振发生。
4.蒸发器蒸发温度过低：由于系统制冷剂不足、制冷量负荷减小，球阀开启度过小，造成蒸发压力过低而喘振。
5.关机时未关小导叶角度和降低离心机排气口压力。当离心机停机时，由于增压突然消失，蜗壳及冷凝器中的高压制冷剂蒸气倒灌，容易喘振。
离心机喘振排除
1.冷凝器结垢：清除传热面的污垢和清洗冷却塔。
2.系统中空气排除：离心机采用K11制冷剂时，一般液体温度超过28℃ 时，表明系统中有空气存在。排除方法：启动抽气回收装置，将不凝性气体排出，一般将制冷剂R11的压力抽到稍低于制冷荆液体温度相对应的饱和压力，即28℃以下的对应压力：117．68KMP以下即可。
3.启动后发生喘振：进行反喘振调节。当能量调节大幅度减少时，造成吸气量不足，即蒸气不能均匀流入叶轮，导致排气压力陡然下降，压缩机处于不稳定工作区，而发生喘振。为了防止喘振，可将一部分被压缩后的蒸气，由排气管旁通到蒸发器，不但可防喘振．而且对离心机启动时也有益：减少蒸气密度和启动时的压力，可减小启动功率。
4.蒸发压力过低：检查蒸发压力过低原因，制冷剂不足添加制冷剂，制冷量负荷小，关闭能量调节叶片。
5.停机时喘振：停离心机时应注意主电机有无反转现象，并尽可能关小导叶角度，降低离心机排气口压力。
离心机操作过程中，应保持冷凝压力和蒸发压力的稳定，使离心机制冷量高于喘振点对应制冷量，以防喘振
GB 19815-2005 离心机安全要求
GB 6065-1985 TZ立式振动离心机
GB 12258-1990 医用低速离心机
JB/T 3263-2000 卧式振动离心机
JB/T 4064-2005 上悬式离心机
JB/T 5519-1991高速冷冻离心机
JB/T 6118-1992 TCL沉降过滤离心机
JB/T 53190-1999 三足式离心机 产品质量分等
JB 447-1985卧式活塞推料离心机技术条件
JB/T 502-2004 螺旋卸料沉降离心机
JB/T 5284-1991 防爆型刮刀卸料离心机 序号 标 准 代 号 标 准 名 称 1 GB/T 4774-2004 分离机械 名词术语 2 GB 7779-2005 离心机型号编制方法 3 GB 10901-2005 离心机 性能测试方法 4 GB/19815-2005 离心机 安全要求 5 GB/T10894-2004 分离机械 噪音测试方法 6 GB/T10895-2004 离心机 分离机 机械振动测试方法 7 JB/T 447-2004 活塞推料离心机 8 JB/T 10411-2004 离心机、分离机奥氏体钢锻件超声检测及质量评级 9 JB/T 8051-2006 离心机转鼓强度计算规范 10 JB/T 8865-2001 活塞推料离心机用滤网 11 JB/T 9095-1999 离心机、分离机锻焊件无损探伤技术规范 12 JB/T 7217-2006 分离机械涂装通用技术条件 13 JB/T 6418-2006 分离机械 清洁度测定方法向左转|向右转
