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STATIC WEIGHT BEARING TOUCH:
INCAPACITANCE TEST
(Model: BIO-SWB-TOUCH-M - For mice)
An easy and non pain-inducing solution for assessing the level of discomfort (incapacitance) in the injured paw of a small animal like a rat or a mouse by measuring the Postural Equilibrium – independently of the operator. The static weight bearing instrument is ideal for your research on analagesia and nociception involving rodents: osteo arthrisis, cartilage degeneration, inflammation models, nerve injury models, and much more... Discover the SWB-Touch: now with a brand new touch-screen console!

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  • PARATEK PHARMACEUTICALS INC. Boston, Etats-Unis
  • CEREP Paris, France
  • INSERM BORDEAUX, France
  • FACULTE DE MEDECINE RANGUEIL, CICT Toulouse, France
  • UNIVERSITE VICTOR SEGALEN BORDEAUX, France
  • FACULTE DE MEDECINE PHARMACOLOGIE VANDOEUVRE LES NANCY, France
  • BIOCODEX Compiegne, France
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! NEW RESEARCH WORK ! A recent publication by Cedo M. Bagi,corresponding author Edwin Berryman, David E. Zakur, Dean Wilkie, and Catharine J. Andresen in "Arthritis Res Ther. " highlights the merits of using Bioseb's Static Weight Bearing Touch: Incapacitance Test: Antiresorptive and Anabolic Bone Therapy Does not Improve Weight Bearing Capacity and Bone Strength in OA Rats

Antiresorptive and Anabolic Bone Therapy Does not Improve Weight Bearing Capacity and Bone Strength in OA Rats
Cedo M. Bagi,corresponding author Edwin Berryman, David E. Zakur, Dean Wilkie, and Catharine J. Andresen
Comparative Medicine, Global Science and Technology, Pfizer Global Research and Development, Pfizer Inc., 100 Eastern Point Road, Groton, CT 06340 USA
Published in "Arthritis Res Ther. " (2016-11-06)


Osteoarthritis (OA) is a leading cause of disability, but despite the high unmet clinical need and extensive research seeking dependable therapeutic interventions, no proven disease-modifying treatment for OA is currently available. Due to the close interaction and interplay between the articular cartilage and the subchondral bone plate, it has been hypothesized that antiresorptive drugs can also reduce cartilage degradation, inhibit excessive turnover of the subchondral bone plate, prevent osteophyte formation, and/or that bone anabolic drugs might also stimulate cartilage synthesis by chondrocytes and preserve cartilage integrity. The benefit of intensive zoledronate (Zol) and parathyroid hormone (PTH) therapy for bone and cartilage metabolism was evaluated in a rat model of OA.
Presentation

Overview of Bioseb's new Centor Touch Console
Bioseb's Incapacitance Test
(Static Weight Bearing):
The New Centor Touch Console
While normal rats and mice distribute weight equally on both paws, the ratio of weight distribution between injured and non injured paw is a natural measurement of the level of discomfort in the injured paw of a rodent, which correlates with the Paw Pressure Analgesia Meter (Randall and Sellito test). Bioseb Incapacitance Test or Static Weight Bearing (SWB Touch) Test allows you to measure this weight distribution and thus to easily and accurately estimate the level of discomfort.

By continuously measuring the weight borne by each paw, Bioseb's Static Weight Bearing Incapacitance Test allows the objective measurement of spontaneous pain by assessing the postural equilibrium, thus opening research fields not available when using traditional methods (like the Randall & Selitto test), which can only measure nociceptive thresholds and pain sensitivity using experimental nociceptive stimuli.

Research applications for Bioseb's Static Weight Bearing Incapacitance Test include nerve or tissue injury, Neuropathy, Carrageenin, Incision recovery, osteo-arthrisis, cartilage degeneration, inflammation models (CFA), peripheric nerve injury models, mechanical hyperalgia models, bone cancer pain models, and much more...

Operating principle

During the static weight bearing test, the rodent (rat or mouse) is placed into a holder holder where the animal is comfortably maintained while his hind paws rest on two separate sensor plates. The animal stands and makes a natural adjustment to the degree of pain by adapting weight distribution on both rear paws.

The spontaneous value of the weight applied on each sensor is displayed on the LCD screen of the control unit, which can also show statistical calculations. Now with a brand new touch-screen console! Using the optional remote foot-switch, the operator can start/stop the test hands-free. No PC is required during the experiment, but you have the option to send data to a software through the integrated RS-232 interface.

Main functionalities

Bioseb Incapacitance Test (Static Weight Bearing) offers numerous unique and innovative features for facilitating your research on nociception and analgesia :

A non pain-inducing method to measure discomfort: The animal stands and makes a natural adjustment to the degree of pain by adapting weight distribution on both rear paws.

An objective spontaneous pain measurement solution: Dual channel scale based measurement is done independently of the operator’s reaction time or subjective judgment about the animal’s flinching.

An easy and precise instrument: No restraint requirements, a footswitch to tare scales, direct display of the average value on the LCD for each of the back paws.

A stand alone instrument: No PC is required for running the incapacitance test, although you have the possibility to send collected data from the instrument to a PC through the integrated RS232 interface. It can also be run on battery.

• The Incapacitance (Static Weight Bearing) Test allows the user to compute and display statistics (mean, sd) for groups of rodents (rats or mice) during the measurement process.

Units are selected by the user in grams, Newtons or oz/lbs.

• The Instrument has an internal memory of up to 200 individual values (ie 1 animal, 2 paws) or up to 200 groups when the statistics are used. Those values are available for editing directly on the sceen, or to be printed out or transferred to a PC, later on. Transfert includes date and time for glp protocols.

Independent platform and control unit: a 1 meter cable allows some distance between the animal and the operator, reducing the placement time.

Bioseb's new Centor Touch Console : Screenshot
Bioseb's new Centor Touch Console : Screenshot
Dedicated software

An embedded statistical computation has been included in the electronic device. This is a very useful feature that as been very well received and used by users of large numbers of tests. The display shows in real time the mean, standard deviation and variation coefficient from groups of animals.

The optional Bioseb’s BIO-CIS software sends datas acquired via the Static Weight Bearing Test into a MS Excel sheet using the RS232 port. Easy to set up, this soft interface uses the full power of MS Excel functions, to let you create statistical tables and graphics.

Domains of application

• Osteo arthrisis and cartilage degeneration
• Inflammation and nerve injury models
• Bone cancer pain models
• Post-operative pain

Supplied with

• 1 animal holder/restrainer (rat or mouse)
• 1 control unit
• 1 platform with sensors.
• Footswitch to start/stop experiment hands free
Optional: Cable and software for data transfer.


Publications (Click on an article to show details and read the abstract)

PAIN
- Mechanical allodynia & hyperlagesia -
Polyamine deficient diet to relieve pain hypersensitivity. (2008)
Polyamine deficient diet to relieve pain hypersensitivity.
C. Rivat, P. Richebé, E. Laboureyras, J.-P. Laulin, R. Havouis et al.
UMR CNRS 5227, “Mouvement-Adaptation-Cognition”, Team “Homéostasie-Allostasie-Pathologie-Réhabilitation”, Bordeaux, France.
Published in "Pain" (2008-06-30)

There is a compelling body of evidence that N-methyl-d-aspartate receptors (NMDA-R) play a critical role in the development and maintenance of pain hypersensitivity. However, long-term treatments with NMDA-R antagonists are limited by unacceptable side effects. Since polyamines modulate the functioning of NMDA-R and mainly originate from normal dietary intake and bacterial metabolism in the gut, we developed a nutritional therapy based on dietary polyamine deficiency. Here, we reported that a polyamine deficient diet (PD diet) for 7 days prevented the enhancement of tyrosine phosphorylation of the spinal NR2B subunit-containing NMDA-R associated with inflammation in rats. Based on these data, we studied the ability of PD diet to prevent long-lasting pain hypersensitivity associated with tissue injury on one hind paw by evaluating long-lasting changes in both mechanical nociceptive threshold and weight bearing. A PD diet strongly reduced long-lasting hyperalgesia induced by inflammation or incision, especially in fentanyl-treated rats. Moreover a PD diet also prevented the exaggerated hyperalgesia induced by a second inflammation performed 7 days after the first one. A PD diet also opposed paradoxical hyperalgesia induced by non-nociceptive environmental stress in rats with pain and opioid experiences. A PD diet reversed pain hypersensitivity associated with monoarthritis or neuropathy and restored the analgesic effect of morphine. Since PD diet was devoid of any noticeable side effects, this nutritional therapy could be part of an effective and safe strategy for pre-emptive analgesia and for reducing the transition from acute to chronic pain and its outcomes in various pain syndromes.

- Neuropathic pain -
GABAergic pathway in a rat model of chronic neuropathic pain: Modulation after intrathecal transplantation of a human neuronal cell line. (2011)
GABAergic pathway in a rat model of chronic neuropathic pain: Modulation after intrathecal transplantation of a human neuronal cell line.
L. Vaysse, J.C. Sol, Y. Lazorthes, M. Courtade-Saidi, M.J. Eaton et al.
Laboratory of Approches expérimentales et Thérapeutiques des Douleurs Neuropathiques, Toulouse, France.
Published in "Neuroscience Research" (2011-02-21)

Current understanding of chronic pain points a decrease in level of the inhibitory neurotransmitter GABA, in the spinal dorsal horn, leading to an imbalance between excitatory and inhibitory pathways. A subcloned derivative of the human NT2 cell line (hNT2.17) which, after neuronal differentiation, secretes different inhibitory neurotransmitters such as GABA and glycine has been recently isolated. In this study, we have investigated the effect of this new cell line on peripheral nerve injury induced by chronic constriction (CCI) and notably the effect on the cellular GABAergic pathway. Our data show that the decrease in GABA expression in the spinal dorsal horn of injured animals is concomitant with a decline of its synthetic enzyme GAD67-Ir and mRNA but not GAD65. Interestingly, in transplanted animals we observed a strong induction of GAD67 mRNA with one week after graft, which is followed by a recovery of GAD67 and GABA Ir. This effect paralleled a reduction of hindpaw hypersensitivity and thermal hyperalgesia induced by CCI. These results suggest that hNT2.17 GABA cells can modulate neuropathic pain after CCI certainly by minimizing the imbalance and restoring the cellular GABAergic pathway.

- Chronic pain -
GABAergic pathway in a rat model of chronic neuropathic pain: Modulation after intrathecal transplantation of a human neuronal cell line. (2011)
GABAergic pathway in a rat model of chronic neuropathic pain: Modulation after intrathecal transplantation of a human neuronal cell line.
L. Vaysse, J.C. Sol, Y. Lazorthes, M. Courtade-Saidi, M.J. Eaton et al.
Laboratory of Approches expérimentales et Thérapeutiques des Douleurs Neuropathiques, Toulouse, France.
Published in "Neuroscience Research" (2011-02-21)

Current understanding of chronic pain points a decrease in level of the inhibitory neurotransmitter GABA, in the spinal dorsal horn, leading to an imbalance between excitatory and inhibitory pathways. A subcloned derivative of the human NT2 cell line (hNT2.17) which, after neuronal differentiation, secretes different inhibitory neurotransmitters such as GABA and glycine has been recently isolated. In this study, we have investigated the effect of this new cell line on peripheral nerve injury induced by chronic constriction (CCI) and notably the effect on the cellular GABAergic pathway. Our data show that the decrease in GABA expression in the spinal dorsal horn of injured animals is concomitant with a decline of its synthetic enzyme GAD67-Ir and mRNA but not GAD65. Interestingly, in transplanted animals we observed a strong induction of GAD67 mRNA with one week after graft, which is followed by a recovery of GAD67 and GABA Ir. This effect paralleled a reduction of hindpaw hypersensitivity and thermal hyperalgesia induced by CCI. These results suggest that hNT2.17 GABA cells can modulate neuropathic pain after CCI certainly by minimizing the imbalance and restoring the cellular GABAergic pathway.

- Postoperative pain -
Long-Term Pain Vulnerability After Surgery in Rats: Prevention by Nefopam, an Analgesic with Antihyperalgesic Properties. (2009)
Long-Term Pain Vulnerability After Surgery in Rats: Prevention by Nefopam, an Analgesic with Antihyperalgesic Properties.
E. Laboureyras, J. Chateauraynaud, P. Richebé, G. Simonnet.
Université Bordeaux 2, Université Bordeaux 1, CNRS UMR 5227, Bordeaux, France.
Published in "Anesthesia and Analgesia" (2009-08-30)

BACKGROUND: Tissue damage associated with surgery often produces peripheral and central sensitization that may outlast the stimuli, leading to exaggerated postoperative pain. Paradoxically, the use of opioid analgesia, which is essential for surgical pain management may induce pain sensitization leading to enhanced postoperative pain and an increased risk of developing chronic pain. We studied whether a surgical incision in the rat hindpaw may favor the development of long-term pain vulnerability by estimating hyperalgesia induced by an inflammatory stimulation of the unlesioned contralateral hindpaw 3 wk later. We also evaluated the ability of nefopam, an analgesic drug commonly used in postoperative pain management, to prevent not only exaggerated postoperative pain but also long-term pain vulnerability. The efficacy of morphine was assessed 1 day after surgical incision. METHODS: On Day 0, a surgical plantar incision was performed in one hindpaw of rats treated or untreated with fentanyl (4 _ 100 _g/kg, one injection every 15 min). Nefopam (10 mg/kg) or saline was subcutaneously injected 30 min before injury. Three weeks later, once pain measures had returned to basal values, a subsequent nociceptive stimulus, specifically intraplantar carrageenan injection, was performed to evaluate pain sensitivity in incision- and fentanyl-experienced rats. Pain was measured by the paw-pressure vocalization test and the weight bearing test. RESULTS: Surgical incision in rats induced latent and long-term pain hypersensitivity, which was manifested by exaggerated hyperalgesia on carrageenan injection. Administering fentanyl in association with the surgical incision induced exaggerated postoperative pain. When injected before incision, nefopam reduced the exaggerated postoperative pain induced by perioperative fentanyl treatment and prevented the development of long-term pain hypersensitivity. Preoperative nefopam administration also improved morphine analgesic efficacy in the context of fentanyl-induced postoperative hyperalgesia. CONCLUSIONS: Given preemptively, nefopam may be effective at improving postoperative pain management and at reducing the risk of developing postoperative chronic pain, because the drug has both analgesic and antihyperalgesic properties.

Combination of Microsurgery and Gene Therapy for Spinal Dorsal Root Injury Repair. (2009)
Combination of Microsurgery and Gene Therapy for Spinal Dorsal Root Injury Repair.
S. Liu, D. Bohl, S. Blanchard, J. Bacci, G. Saïd et al.
Institut Pasteur, Department of Neuroscience, Unité Rétrovirus et Transfert Génétique, INSERM U622, Paris, France.
Published in "Molecular Therapy" (2009-06-30)

Brachial plexus injury is frequent after traffic accident in adults or shoulder dystocia in newborns. Whereas surgery can restore arm movements, therapeutic options are missing for sensory defects. Dorsal root (DR) ganglion neurons convey sensory information to the central nervous system (CNS) through a peripheral and a central axon. Central axons severed through DR section or avulsion during brachial plexus injury inefficiently regenerate and do not reenter the spinal cord. We show that a combination of microsurgery and gene therapy circumvented the functional barrier to axonal regrowth at the peripheral and CNS interface. After cervical DR section in rats, microsurgery restored anatomical continuity through a nerve graft that laterally connected the injured DR to an intact DR. Gene transfer to cells in the nerve graft induced the local release of neurotrophin-3 (NT-3) and glial cell line–derived neurotrophic factor (GDNF) and stimulated axonal regrowth. Central DR ganglion axons efficiently regenerated and invaded appropriate areas of the spinal cord dorsal horn, leading to partial recovery of nociception and proprioception. Microsurgery created conditions for functional restoration of DR ganglion central axons, which were improved in combination with gene therapy. This combination treatment provides means to reduce disability due to somatosensory defects after brachial plexus injury.

CENTRAL NERVOUS SYSTEM (CNS)
- Spinal Cord -
Combination of Microsurgery and Gene Therapy for Spinal Dorsal Root Injury Repair. (2009)
Combination of Microsurgery and Gene Therapy for Spinal Dorsal Root Injury Repair.
S. Liu, D. Bohl, S. Blanchard, J. Bacci, G. Saïd et al.
Institut Pasteur, Department of Neuroscience, Unité Rétrovirus et Transfert Génétique, INSERM U622, Paris, France.
Published in "Molecular Therapy" (2009-06-30)

Brachial plexus injury is frequent after traffic accident in adults or shoulder dystocia in newborns. Whereas surgery can restore arm movements, therapeutic options are missing for sensory defects. Dorsal root (DR) ganglion neurons convey sensory information to the central nervous system (CNS) through a peripheral and a central axon. Central axons severed through DR section or avulsion during brachial plexus injury inefficiently regenerate and do not reenter the spinal cord. We show that a combination of microsurgery and gene therapy circumvented the functional barrier to axonal regrowth at the peripheral and CNS interface. After cervical DR section in rats, microsurgery restored anatomical continuity through a nerve graft that laterally connected the injured DR to an intact DR. Gene transfer to cells in the nerve graft induced the local release of neurotrophin-3 (NT-3) and glial cell line–derived neurotrophic factor (GDNF) and stimulated axonal regrowth. Central DR ganglion axons efficiently regenerated and invaded appropriate areas of the spinal cord dorsal horn, leading to partial recovery of nociception and proprioception. Microsurgery created conditions for functional restoration of DR ganglion central axons, which were improved in combination with gene therapy. This combination treatment provides means to reduce disability due to somatosensory defects after brachial plexus injury.



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Measurement range 0-2000g for Mouse or Rat
Resolution 0, 2g
Accuracy 0.1% of full Scale
Measurement time User-defined : from 1 to 99 seconds
Display Average value for each paw on the display
Special feature Touch screen
Direct calculation of MEAN and SD per Group
Real-time display of force curve for both paw
Output RS232 for BIO-CIS software
Internal memory Up to 200 individual values
Animals Rats, mice
Other animals : contact us
Platform Dimensions 200 x 100 x 40 mm - without restrainer
Operation Battery operated (6 to 8 hours) and/or on the mains
Options BIO-CIS data transfer software

Model:
BIO-SWB-TOUCH-M
Static Weight Bearing Touch: Incapacitance Test (Modif.)
For mice Contact us

Accessories :
BIO-CIS
Contact us

Accessories :
- RSIC Software: Direct transfert of RS232 Data to MS Excel
- Rat Restrainer
- Mice Restrainer
Print version

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Phone worldwide : +33 442 344 360 - USA/Canada : (727) 521-1808
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