Tbi 0310

Manufactured by Precision Systems and Instrumentation

Sourced in United States

The TBI-0310 is a precision temperature and humidity controller designed for laboratory applications. It features a digital display, adjustable temperature and humidity set points, and a range of monitoring capabilities. The device is suitable for use in a variety of controlled environment settings, but a more detailed description of its intended use is not provided.

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Lab products found in correlation

Surgicel, by Johnson & Johnson (2 mentions) Xylazine, by Troy Laboratories (2 mentions) Lsm800 confocal microscope, by Zeiss (2 mentions) Stereotaxic frame, by World Precision Instruments (1 mentions) Zoletil 100, by Virbac (1 mentions) Ilium xylazil 100, by Troy Laboratories (1 mentions) Zoletil 50, by Virbac (1 mentions) 500 mhz nmr spectrometer, by Agilent Technologies (1 mentions) Agilent 1100 hplc system, by Thermo Fisher Scientific (1 mentions) Kta pure system, by GE Healthcare (1 mentions) Hypersil ods c18 column, by Thermo Fisher Scientific (1 mentions) Pearl imaging system, by LI COR (1 mentions) Superdex 200 increase column 10 300 gl, by Wyatt Technology (1 mentions) Tiletamine zolazepam, by Virbac (1 mentions)

28 protocols using tbi 0310

Controlled Cortical Impact Injury Model

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Seven to nine week-old male mice were anesthetized using 5% inhaled isoflurane, their heads were shaved and placed in a Kopf stereotaxic head frame where they were maintained under anesthesia using 2% isoflurane. A 4-mm craniotomy was performed midway between lambda and bregma on the left side. The exposed dura was then impacted using a Precision Systems and Instrumentation TBI-0310 (Fairfax Station, VA, USA) at a speed of 3.5 m/s with a 200 ms dwell time. This procedure was similar to previous reports (Mattson and Scheff, 1994 (link); Smith et al., 1995 (link)). Injury depths of 0.5 and 1.0 mm were used to simulate moderate and severe injuries, respectively. After injury, Surgicel (Johnson and Johnson, Dallas, TX, USA) was placed over the injury site, the removed skull was adhered back to its original place with dental cement and the wound closed with wound clips. 0.5% bupivacaine with 1:200,000 epinephrine was used as an analgesic. Naïve animals were not exposed to injury, craniotomy or anesthesia.

Harrison E.B., Emanuel K., Lamberty B.G., Morsey B.M., Li M., Kelso M.L., Yelamanchili S.V, & Fox H.S. (2017). Induction of miR-155 after Brain Injury Promotes Type 1 Interferon and has a Neuroprotective Effect. Frontiers in Molecular Neuroscience, 10, 228.

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Controlled Cortical Impact: Rat TBI Model

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Male Sprague-Dawley rats (280–320 g) were purchased from Shanghai SLAC Laboratory Animal Co. Ltd., Shanghai, China. Animals were housed under 12-h light/dark cycle in a temperature- and humidity-controlled animal facility. All animal experiments were approved by the Institutional Animal Care and Use Committee of Fudan University and performed in accordance with the NIH Guide for the Care and Use of Laboratory Animals.
Rats were subjected to unilateral controlled cortical impact injury (CCI) as described previously with slight modification [22 (link)]. General anesthesia was induced with 4% isoflurane and maintained with 1.5–2.5% isofluorane during surgery. Animals were fixed on a stereotaxic frame. A right parietal craniotomy (2.7 mm frontal and 2.7 mm lateral to the bregma, diameter 5.4 mm) was made with a drill under aseptic conditions. CCI was produced using a pneumatically-driven cortical impact device (TBI 0310, Precision Systems and Instrumentation, Fairfax Station, VA) with a 5 mm diameter flat-tipped impactor which compressed the exposed dura mater and underlying brain to a depth of 3.2 mm for 0.5 s at 4.0 m/s velocity. Temperature was maintained at 36.5–37.5°C throughout the experiment. Sham controls were anesthetized and only the right parietal craniotomy was conducted. All outcome assessments were done by investigators blinded to treatment assignments.

Shi H., Wang H., Pu H., Shi Y., Zhang J., Zhang W., Wang G., Hu X., Leak R.K., Chen J, & Gao Y. (2014). Ethyl Pyruvate Protects against Blood–Brain Barrier Damage and Improves Long‐term Neurological Outcomes in a Rat Model of Traumatic Brain Injury. CNS Neuroscience & Therapeutics, 21(4), 374-384.

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Unilateral Focal Cortical Contusion Injury in Mice

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Mice were administered a unilateral, focal contusion injury using CCI as previously reported (Scheff et al., 1997 (link); Hunt et al., 2009 (link), 2010 (link), 2011 (link), 2012 (link)). Briefly, animals were anesthetized using 2% isoflurane and placed in a stereotaxic frame. A midline incision was made to reveal the skull and a 5 mm craniotomy was performed lateral to the sagittal suture and centered between bregma and lambda. The skull cap was removed without damage to the underlying dura. A computer controlled, pneumatically driven impactor fitted with a 3 mm stainless-steel beveled tip (TBI-0310; Precision Systems and Instrumentation, Fairfax Station, VA, United States) was used to compress the cortex without breaking the dura mater. Impact parameters were set to 1.0 mm depth (hard stop), 3.5 m/s velocity, and 500 ms duration. For sham-injured controls, craniotomy was performed but no impact was administered to the brain. The incision was sutured and the animals were allowed to recover. All mice given CCI survived and remained otherwise healthy until experimentation. These parameters result in a well-characterized injury that predisposes mice to development of posttraumatic epilepsy by 8–12 weeks post-injury (Hunt et al., 2009 (link), 2010 (link), 2011 (link), 2012 (link)).

Boychuk J.A., Butler C.R., Smith K.C., Halmos M.B, & Smith B.N. (2022). Zolpidem Profoundly Augments Spared Tonic GABAAR Signaling in Dentate Granule Cells Ipsilateral to Controlled Cortical Impact Brain Injury in Mice. Frontiers in Systems Neuroscience, 16, 867323.

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Controlled Cortical Impact Traumatic Brain Injury in Rats

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For inducing the CCI model, rats were first anesthetised with isoflurane (5% for induction, 1–2% for maintenance) in 40% oxygen and placed in a stereotaxic frame. After incision of the scalp, a 5 mm diameter craniotomy was performed over the right hemisphere (centred at 3 mm posterior to the Bregma and 3 mm left lateral to the midline), without damaging the underlying dura. The CCI injury was applied in the TBI animals using an impactor (TBI 0310; Precision Systems and Instrumentation, USA) with a cylindrical piston tip 4 mm in diameter, operating at a velocity of 5 m/sec, and penetrating to a depth of 2 mm with a dwell time of 200 ms. After injury, the bone plug from the craniotomy was replaced and the scalp was sutured. Sham rats underwent the same procedure, but with omission of the impact. Rats showed no conspicuous signs of motor disability during monitored recovery.

Mohamed A.Z., Cumming P, & Nasrallah F.A. (2021). Traumatic brain injury augurs ill for prolonged deficits in the brain’s structural and functional integrity following controlled cortical impact injury. Scientific Reports, 11, 21559.

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Controlled Cortical Impact-Induced TBI in Mice

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A standard protocol and a controlled cortical impact (CCI) device (TBI-0310, Precision Systems and Instrumentation, Fair fax, VA, USA) were utilized to induce brain injuries as described previously [10 (link)]. Briefly, after anaesthetization, a circular craniotomy (3 mm in diameter) was performed (1 mm posterior to bregma and 1 mm lateral to the sagittal suture over the right parietal cortex). Following the craniotomy, the CCI model was established with a TBI-0310 TBI model system with the following impact parameters: velocity, 5.0 m/s; depth, 2.0 mm; and dwelling time, 100 ms. As a result, a moderately severe contusion was induced in the right sensorimotor cortex underlying the hippocampus. The mice exhibited pronounced behavioural deficits but none died [26 (link)]. Mice in the Sham group underwent identical surgical procedures but without impact. Following the injury, the hole was sealed with bone wax, and the skin incision was sutured. Finally, the mice were kept on an electric blanket to maintain their normal body temperature until the completely awakened.

Zhang Y., Wang L., Pan Q., Yang X., Cao Y., Yan J., Wang Y., Tao Y., Fan R., Sun X, & Li L. (2022). Selective sphingosine-1-phosphate receptor 1 modulator attenuates blood–brain barrier disruption following traumatic brain injury by inhibiting vesicular transcytosis. Fluids and Barriers of the CNS, 19, 57.

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Controlled Cortical Impact Induces Moderate Traumatic Brain Injury in Mice

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TBI was induced in mice using a controlled cortical impact (CCI) device TBI-0310 (Precision Systems and Instrumentation, Fairfax, VA, USA), as described previously (43 (link)). Mice were anesthetized with 3% isoflurane in 67% N₂O/30% O₂ until they were nonresponsive to the tail-pinch test. Then, 1.5% isoflurane was used to maintain anesthesia. The diameter of the impactor was 3 mm. The machine was set at a velocity of 5.0 m/s, a depth of 2.0 mm, and a dwell time of 100 ms, which produced a moderate contusion in the right cortex and underlying hippocampus, with pronounced behavioral deficits but virtually no mortality, thereby mimicking moderate TBI in humans. Mice were maintained at 36° to 37°C throughout the procedure. At 24 hours after CCI, mice were sacrificed under deep anesthesia, and the brain tissues around the injury site were subsequently harvested for Western blotting.

Yang Y., Tian X., Xu D., Zheng F., Lu X., Zhang Y., Ma Y., Li Y., Xu X., Zhu B, & Wang X. (2018). GPR40 modulates epileptic seizure and NMDA receptor function. Science Advances, 4(10), eaau2357.

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Controlled Cortical Impact Injury in Mice

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Mice (FVB/NJ) weighing 25–30 g were anaesthetized and placed in a Kopf stereotaxic head frame (David Kopf Instruments). By using a dental drill, a 5-mm craniotomy was performed over the left parietal cortex between the bregma and lambda. The bone flap was removed and injury was made using a Precision Systems and Instrumentation TBI-0310 (Fairfax Station, VA) that administered a 1 mm cortical compression (3 mm impactor diameter, 2.5 m/s velocity, 150 ms duration dwell time) [13] (link). Sham animals were anesthetized but no CCI. Body temperature was monitored throughout the surgery by a rectal probe; temperature was maintained at 37.0±0.5 °C using a heated pad.

Chuang J.Y., Kao T.J., Lin S.H., Wu A.C., Lee P.T., Su T.P., Yeh S.H., Lee Y.C., Wu C.C, & Chang W.C. (2016). Specificity protein 1-zinc finger protein 179 pathway is involved in the attenuation of oxidative stress following brain injury. Redox Biology, 11, 135-143.

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Controlled Cortical Impact Injury Model

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The rats were anesthetized with 3% pentobarbital sodium (50 mg/kg), and the rats were mounted in a stereotaxic frame. Following a midline incision, the skin and temporal muscles were reflected to expose the skull. A craniotomy, with the diameter of 4.0 mm, was performed using dental bur at the left. Briefly, a controlled cortical impact (CCI) device (TBI0310, precision systems and instrumentation, Fairfax Station, VA) was used to impact the brain (tip diameter, 4.0 mm; cortical contusion depth, 5.0 mm; impact velocity, 6.0 m/s; dwell time, 50.0 ms). After injury, the skin incision was closed with nylon sutures. The sham group was only subject to craniotomy. The rats were placed on a heating pad during surgery. At the end of the procedure, the animals were removed from the stereotaxic frame, went back to their cages and were closely monitored until the recovery from anesthesia was complete.

Yang Z., Fan R., Sun P., Cui H., Peng W., Luo J., Zhang C., Xiong X., Huang W, & Liu W. (2018). Rhubarb attenuates cerebral edema via inhibition of the extracellular signal-regulated kinase pathway following traumatic brain injury in rats. Pharmacognosy Magazine, 14(53), 134-139.

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Cortical Contusion Injury in Mice

Cited 3 times

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Mice were subjected to severe unilateral, cortical contusion injury by CCI, as described previously (Dixon et al., 1991 (link); Scheff et al., 1997 (link); Hall et al., 2005 (link); Hunt et al., 2009 (link); Guo et al., 2013 (link); Butler et al., 2015 (link)). Briefly, mice were anesthetized by 2% isoflurane inhalation and placed in a stereotaxic frame. The skull was exposed by midline incision, and ∼5 mm craniotomy was made lateral to the sagittal suture, centered between bregma and lambda. The skull cap was carefully removed, avoiding damage to the exposed underlying dura. The contusion device consisted of a computer-controlled, pneumatically driven impactor fitted with a beveled stainless-steel tip 3 mm in diameter (TBI-0310, Precision Systems and Instrumentation). A focal, nonpenetrating brain injury was delivered to compress the cortex 1.0 mm in depth (hard stop) at a velocity of 3.5 m/s and 500 ms duration. A qualitative postoperative health assessment was performed daily for 4 d after CCI and periodically thereafter.

Butler C.R., Boychuk J.A, & Smith B.N. (2017). Brain Injury-Induced Synaptic Reorganization in Hilar Inhibitory Neurons Is Differentially Suppressed by Rapamycin. eNeuro, 4(5), ENEURO.0134-17.2017.

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Controlled Cortical Impact Injury in Mice

Cited 3 times

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Mice were subjected to severe unilateral, cortical contusion injury by controlled cortical impact (CCI), as previously described (Hunt et al., 2012 (link); Hunt et al., 2009 (link), 2010 (link), 2011 (link)). Briefly, mice were anesthetized by 2% isoflourane inhalation and placed in a stereotaxic frame. The skull was exposed by midline incision, and a ∼5 mm diameter craniotomy was made lateral to the sagittal suture and centered between bregma and lambda. The skull cap was removed without damage to the exposed underlying dura. The contusion device consisted of a computer-controlled, pneumatically driven impactor fitted with a beveled stainless-steel tip 3 mm in diameter (TBI-0310; Precision Systems and Instrumentation, Fairfax, VA). Brain injury was delivered using this device to compress the cortex to a depth of 1.0 mm (hard stop) at a velocity of 3.5 m/sec and 500 msec duration. A qualitative postoperative health assessment was performed daily for 4 days after CCI and periodically thereafter.

Butler C.R., Boychuk J.A, & Smith B.N. (2016). Differential effects of rapamycin treatment on tonic and phasic GABAergic inhibition in dentate granule cells after focal brain injury in mice. Experimental neurology, 280, 30-40.

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