Deficiencies in the National Institute of Health's Guidelines for the Care and Protection of Laboratory Animals

Stephenson, Wendell Holmes

doi:10.1093/jmp/18.4.375

Cited by 27 publications

(8 citation statements)

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“…They were kept for 1 week under these conditions before surgery. All procedures were performed in accordance with the Guidance Suggestions for the Care and Use of Laboratory Animals, formulated by the Ministry of Science and Technology of China [ 12 ]. To produce persistent neuropathic pain, SNL was performed according to our previous protocols.…”

Section: Methodsmentioning

confidence: 99%

Intrathecal injection of fluorocitric acid inhibits the activation of glial cells causing reduced mirror pain in rats

Cao

Zhang

et al. 2014

BMC Anesthesiol

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BackgroundGrowing evidence has shown that unilateral nerve injury results in pain hypersensitivity in the ipsilateral and contralateral sides respective to the injury site. This phenomenon is known as mirror image pain (MIP). Glial cells have been indicated in the mechanism of MIP; however, it is not clear how glial cells are involved in MIP.MethodsTo observe phenomenon MIP and the following mechanism, 20 adult male Sprague–Dawley rats (weighing 180–220 g) were separated into two groups: Sham Group (n = 10) and left L5 spinal nerve ligated and sectioned (SNL) group (n = 10). Thermal hyperalgesia and mechanical hypersensitivity were measured for both groups to determine if the SNL model had Mirror image of Pain (MIP). Nav1.7 protein expression in DRG was analyzed using immunohistochemistry and western-blotting. And then to observe the effect of fluorocitrate on MIP, 15 rats were separated into three Groups: Sham Group (n = 5); SNL + FC group: intrathecal injection of Fluorocitric acid(FC) 1 nmol/10 μL (n = 5); SNL + NS group: intrathecal injection of 0.9% Normal Saline (n = 5). Behavior testing, immunocytochemistry, and western-blotting using dorsal root ganglion (DRG) from both sides were then conducted.ResultsThe results showed pain hypersensitivity in both hind-paws of the SNL animals, Mechanical tests showed the paw withdrawal threshold dropped from 13.30 ± 1.204 g to 2.57 ± 1.963 g at 14 d as will as the ipsilateral paw thermal withdrawal threshold dropped from 16.5 ± 2.236 s to 4.38 ± 2.544 s at 14d. Mechanical tests showed the contralateral paw withdrawal threshold dropped from 14.01 ± 1.412 to 4.2 ± 1.789 g at 7d will the thermal withdrawal threshold dropped from 16.8 ± 2.176 s to 7.6 ± 1.517 s at 7d. Nav1.7 expression increased and glial cells actived in bilateral side DRG after SNL compared with sham group. After intrathecal injection of fluorocitrate, the glial cell in bilatral DRG were inhibited and the pain behavior were reversed in both hindpaws too.ConclusionsFluorocitrate can inhibit the activation of glial cells in spinal cord and DRG, and reduce MIP.

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Section: Methodsmentioning

confidence: 99%

Intrathecal injection of fluorocitric acid inhibits the activation of glial cells causing reduced mirror pain in rats

Cao

Zhang

et al. 2014

BMC Anesthesiol

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“…The rats had free access to standard laboratory diet and water, and were maintained according to the recommendations of the National Institute of Health's guidelines for the care and use of laboratory animals [9].…”

Section: Experimental Designmentioning

confidence: 99%

Sepsis induces early phrenic nerve neuropathy in rats

Naycı

Atış²,

Çömelekoğlu³

et al. 2005

Eur Respir J

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The aim of the present study was to investigate the electrophysiology of the phrenic nerve and the diaphragm muscle during sepsis.In total, 26 rats underwent either sham laparotomy or caecal ligation and puncture (CLP). Electrophysiology was evaluated via a phrenic nerve conduction study and needle electromyography of the diaphragm, prior to CLP, 6 and 24 h post-CLP and on day 7. The histopathology of the diaphragm muscle and phrenic nerve was also examined on day 7.In the sepsis group, the phrenic nerve conduction study showed decreased amplitude of compound action potential (CMAP), and prolongation in the duration and the latency of CMAP. The diaphragmatic needle electromyography showed decreased amplitude and frequency of the motor unit action potential (MUP), and prolongation in the duration of MUP, at all time points, compared with the pre-CLP values. The electrophysiological abnormalities were consistent with axonal and demyelinating phrenic nerve neuropathy. Electrophysiological abnormalities were present at 6 h with worsening at 24 h and on day 7. Histopathological examination showed normal muscular fibres and focally slight myelin degenerations of the phrenic nerve fibres.In conclusion, sepsis induced phrenic nerve neuropathy as early as the 6th h in rats.

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“…The mice were housed in a pathogen-free central animal facility (temperature, 20~26°C; relative humidity, 40~70%; light-dark alternate time, 12/12 h; food and water were disinfected and sterilized, the mice had continuous access to the food and water) at the Bengbu Medical College. The animal experiments were performed based on the recommendations provided in the National Institutes of Health Laboratory Animal Care and Use Guidelines (15). LLC cells were washed twice with PBS and filtered through a 40 µm filter membrane prior to being resuspended at a density of 2×10 7 cells/ml and subcutaneously injected into the left forelimbs of these mice.…”

Section: Methodsmentioning

confidence: 99%

Effect of inhibiting ACAT‑1 expression on the growth and metastasis of Lewis lung carcinoma

Qiao

Zhang

et al. 2019

Oncol Lett

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Accumulating evidence suggests that acetyl-CoA acetryltransferase 1 (ACAT-1) may mediate tumor development and metastasis. However, the specific function served by ACAT-1 in lung cancer is not well understood. Therefore, the present study initially verified that ACAT-1 was overexpressed in Lewis lung carcinoma (LLC) tissues compared with non-LLC mice and that this overexpression promoted the proliferation, invasion and metastasis of these LLC samples. Western blotting, immunofluorescence microscopy and flow cytometry allowed the present study to determine that the ACAT-1 inhibitor avasimibe significantly reduced the expression of ACAT-1 in LLC compared with LLC cells that are not treated with avasimibe (P<0.05). A combination of Cell Counting Kit-8 and wound healing assays demonstrated that downregulating ACAT-1 expression sufficiently inhibited the proliferation of LLC cells. Avasimibe promoted LLC cell apoptosis as assessed by a Annexin V/propidium iodide double staining assay. Furthermore, avasimibe inhibited tumor growth in vivo and improved immune responses, with tissue biopsies from LLC model mice exhibiting higher levels of ACAT-1 compared with in healthy controls. Altogether, the results of the present study reveal that avasimibe may inhibit the progression of LLC by downregulating the expression of ACAT-1, which may thus be a potential novel therapeutic target for lung cancer treatment.

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Deficiencies in the National Institute of Health's Guidelines for the Care and Protection of Laboratory Animals

Cited by 27 publications

References 0 publications

Intrathecal injection of fluorocitric acid inhibits the activation of glial cells causing reduced mirror pain in rats

Intrathecal injection of fluorocitric acid inhibits the activation of glial cells causing reduced mirror pain in rats

Sepsis induces early phrenic nerve neuropathy in rats

Effect of inhibiting ACAT‑1 expression on the growth and metastasis of Lewis lung carcinoma

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