Journal of neuropathology and experimental neurology
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J. Neuropathol. Exp. Neurol. · May 1995
Overexpression of TGF-beta 1 in the central nervous system of transgenic mice results in hydrocephalus.
Transforming growth factor beta (TGF-beta) has been proposed to play a number of roles in central nervous system (CNS) development and response to injury. To test these proposals, transgenic mice were generated which overproduce TGF-beta 1 in the CNS. ⋯ Ovary transplantation from an affected female founder has permitted perpetuation of one of the lines as a hydrocephalus model whose genetic defect is known. These results also demonstrate that the developing CNS is highly sensitive to TGF-beta, and suggest a role for aberrant expression of TGF-beta in the pathogenesis of developmental disease of the CNS.
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In rat sciatic nerve, relative neural toxicity and relative motor nerve conduction blockade were assessed for two amide-linked local anesthetics (etidocaine and lidocaine) and two ester-linked local anesthetics (chloroprocaine and procaine). As measures of neural toxicity, nerve fiber injury and edema were assayed by light microscopic examination of nerve tissue sampled 2 days after perineural (next to the sciatic nerve) injection of various concentrations of the local anesthetics. Both nerve injury and edema increased with concentration of local anesthetics, but injury was frequently present in nerve fascicles with little or no edema. ⋯ The resulting log concentration-response curves were analyzed for differences in potency. Both for injury and for conduction block, the order of decreasing potency was: etidocaine, lidocaine, chloroprocaine, procaine. These results are not consistent with the proposal that ester-linked agents are more likely than other local anesthetic agents to cause nerve injury.
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J. Neuropathol. Exp. Neurol. · Sep 1986
The role of 2-chloroprocaine and sodium bisulfite in rat sciatic nerve edema.
In order to evaluate the possible mechanisms of local anesthetic toxicity, the rat sciatic nerve was exposed to various solutions including Nesacaine (containing the antioxidant sodium bisulfite), 2-chloroprocaine in the Nesacaine vehicle (0.2% sodium chloride), 0.2% sodium bisulfite in 0.2% sodium chloride, or 0.2% sodium chloride alone. All solutions were pH balanced between 2.9 and 3.2. ⋯ Intrafascicular administration of five to ten microliter volumes of these solutions produced edema at 48 h in all cases, but the highest levels were observed with Nesacaine and the lowest levels with 0.2% bisulfite. The results of this study implicate the local anesthetic 2-chloroprocaine in the production of nerve edema, which is inconsistent with other reports that the toxicity of Nesacaine-CE can be attributed to the antioxidant bisulfite.
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J. Neuropathol. Exp. Neurol. · Nov 1976
Preclinical lesions and their progression in the experimental spongiform encephalopathies (kuru and Creutzfeldt-Jakob disease) in primates.
Creutzfeldt-Jakob disease and kuru were studied in experimental primates. Eight animals with clinical disease lasting from 1/2 to 12 1/2 months were evaluated for histological evidence of progression of the pathological triad of neuronal vacuolation, neuronal loss and fibrous astrocytosis. The first change to appear was neuronal vacuolation, in both the body of neurones and in the neuropil. ⋯ Neuronal loss was apparent when clinical signs were present. As the clinical disease progressed, so did the severity of neuronal loss and astrocytosis. Five animals, 1 1/2-10 1/2 months after intracerebral inoculation, before they had shown any signs of clinical disease, had histological evidence of neuronal vacuolation and astrocytosis.
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J. Neuropathol. Exp. Neurol. · Jul 1975
Comparative StudyThe neuropathological findings in irreversible coma. A critque of the "respirator".
1. Postmortem examinations were made on 240 of the 459 cases succumbing (52 percent of the deaths) in the Collaborative Study on Cerebral Survival; the central nervous system was examined in 226 cases. 2. The autopsy was performed on an average of 15.3 hours after death. 3. ⋯ The role of cardiac output in the production of a respirator brain 8. Since a respirator brain is an imperfectly defined entity, an exact correlation with any combination of clinical and EEG findings could not be expected. The use of a standardized measurement of CBF seems a logical and promising confirmatory test for respirator brain.