Doccol is a biotech company that started from solving real problems in biological research. In 2004, Doccol identified one of the key problems in experimental stroke research is the inconsistent quality of stroke models, and thence provided a solution for this by offerring standardized occluders, the silicone rubber-coated monofilaments, for middle cerebral artery occlusion (MCAO). Those MCAO occluders were liked very much by stroke reaearchers and given the name "MCAO sutures". Our delicate silicone rubber-coated monofilaments are specially designed and manufactured for inducing the intraluminal filament model of MCAO, which has been widely used for in vivo experimental stroke studies. Using Doccol MCAO sutures for inducing stroke models will improve your model quality by reducing the occurrence of both the incomplete occlusion and the intracranial bleeding. With Doccol MCAO sutures, you will be able to achieve a highly consistent infarct as well as a low mortality rate. In addition to the super product quality, Doccol provides MCAO sutures with a great variety that was designed to meet the diverse demand from stroke investigators. For many years our MCAO sutures have been preferably selected by stroke investigators for inducing stroke models. Using Doccol MCAO sutures for inducing MCAO models has been reported to be able to reduce the standard deviation to 5% of its corresponding mean value as for infarction volume; and this modeling method is becoming a methodological new standard for ensuring the highest quality of MCAO models. For more information please read Doccol Made a Difference in Stroke Modeling.
In 2010, Doccol noticed that microvascular catheterization procedures performed in most laboratories are inconvinient for both blood testing and drug delivery. Those "microcatheters" have a transition tubing requiring a needle connection, which may break when pressure is high, and may accidentally puncture into the operator's finger, before it can be connected to a synringe. These catheters also have a large inner volume that has to be dealt with for drug delivery. Doccol offerred specially designed microcatheters for improving performance, quality and productivity in rodent blood sampling, drug delivery, small flow rate liquid transferring, and physiological monitoring, in which invasive vascular access is necessary. Our microcatheters are permanently connected to an industrial standard Luer lock or stopcock, therefore, eliminated the transitional tubing and needle connection and also dramatically reduced inner volume. Doccol provides sufficient choices of micro catheters for vascular cannulation in all common locations, such as the tail, femoral, carotid, and brachial veins and arteries, and also the jugular veins.
During years of our dedicated services in stroke research, Doccol also started to provide our carefully-selected essential microsurgical tools and devices, and in 2019 Doccol developed its unique Arduino-based PID temperature controllers. These essential tools and devices ensure your experimental stroke research with high quality and high productivity.
Now, we are proud to say that our customers are top-ranked universities, highly prestigious research institutes, and world-leading pharmaceutical companies from the United States, Canada, most European countries, Australia, Japan, South Korea, and India.
In recent years, there are many video articles on MCAO models published, which are helpful resources for stroke researchers to improve stroke model quality. The following video articles cite Doccol products, you may click on the authors to access these articles:
Larpthaveesarp, A., Gonzalez, F. F. Transient Middle Cerebral Artery Occlusion Model of Neonatal Stroke in P10 Rats. J. Vis. Exp. (122), e54830, doi:10.3791/54830 (2017).
Bertrand, L., Dygert, L., Toborek, M. Induction of Ischemic Stroke and Ischemia-reperfusion in Mice Using the Middle Artery Occlusion Technique and Visualization of Infarct Area. J. Vis. Exp. (120), e54805, doi:10.3791/54805 (2017).
Vital, S. A., Gavins, F. N. Surgical Approach for Middle Cerebral Artery Occlusion and Reperfusion Induced Stroke in Mice. J. Vis. Exp. (116), e54302, doi:10.3791/54302 (2016).
Rousselet, E., Kriz, J., Seidah, N. G. Mouse Model of Intraluminal MCAO: Cerebral Infarct Evaluation by Cresyl Violet Staining. J. Vis. Exp. (69), e4038, doi:10.3791/4038 (2012).
Uluç K, Miranpuri A, Kujoth GC, Aktüre E, Ba?kaya MK. Focal cerebral ischemia model by endovascular suture occlusion of the middle cerebral artery in the rat. J Vis Exp. 2011 Feb 5;(48). pii: 1978. doi: 10.3791/1978. PMID: 21339721
A Comparative Study of Variables Influencing Ischemic Injury in the Longa and Koizumi Methods of Intraluminal Filament Middle Cerebral Artery Occlusion in Mice. PLoS One. 2016 Feb 12;11(2):e0148503. doi: 10.1371/journal.pone.0148503. PMID: 26870954
Popp A, Jaenisch N, Witte OW, Frahm C. Identification of ischemic regions in a rat model of stroke. PLoS One. 2009;4(3):e4764. Epub 2009 Mar 10. PMID: 19274095
Hoda MN, Singh I, Singh AK, Khan M. Reduction of lipoxidative load by secretory phospholipase A2 inhibition protects against neurovascular injury following experimental stroke in rat. J Neuroinflammation. 2009 Aug 13;6:21. PMID: 19678934
Liu F, Schafer DP, McCullough LD. TTC, fluoro-Jade B and NeuN staining confirm evolving phases of infarction induced by middle cerebral artery occlusion. J Neurosci Methods. 2009 Apr 30;179(1):1-8. Epub 2009 Jan 9. PMID: 19167427
Kim E, Tolhurst AT, Qin LY, Chen XY, Febbraio M, Cho S. CD36/fatty acid translocase, an inflammatory mediator, is involved in hyperlipidemia-induced exacerbation in ischemic brain injury. J Neurosci. 2008 Apr 30;28(18):4661-70.
Maysami S, Lan JQ, Minami M, Simon RP. Proliferating progenitor cells: a required cellular element for induction of ischemic tolerance in the brain. J Cereb Blood Flow Metab. 2008 Jun;28(6):1104-13.
Zhang Z, Yang X, Zhang S, Ma X, Kong J. BNIP3 upregulation and EndoG translocation in delayed neuronal death in stroke and in hypoxia.Stroke. 2007 May;38(5):1606-13.
Sayeed I, Wali B, Stein DG. Progesterone inhibits ischemic brain injury in a rat model of permanent middle cerebral artery occlusion. Restor Neurol Neurosci. 2007;25(2):151-9.
Pignataro G, Simon RP, Xiong ZG. Prolonged activation of ASIC1a and the time window for neuroprotection in cerebral ischaemia. Brain. 2007 Jan;130(Pt 1):151-8.
Pignataro G, Simon RP, Boison D. Transgenic overexpression of adenosine kinase aggravates cell death in ischemia. J Cereb Blood Flow Metab. 2007 Jan;27(1):1-5.
Solaroglu I, Tsubokawa T, Cahill J, Zhang JH. Anti-apoptotic effect of granulocyte-colony stimulating factor after focal cerebral ischemia in the rat. Neuroscience. 2006 Dec 28;143(4):965-74.
Liu S, Liu W, Ding W, Miyake M, Rosenberg GA, Liu KJ. Electron paramagnetic resonance-guided normobaric hyperoxia treatment protects the brain by maintaining penumbral oxygenation in a rat model of transient focal cerebral ischemia. J Cereb Blood Flow Metab. 2006 Oct;26(10):1274-84.