ObjectGraphene possesses unique electrical, physical, and chemical properties that may offer significant potential as a bioscaffold for neuronal regeneration after spinal cord injury. The purpose of this investigation was to establish the in vitro biocompatibility of pristine graphene for interface with primary rat cortical neurons.MethodsGraphene films were prepared by chemical vapor deposition on a copper foil catalytic substrate and subsequent apposition on bare Permanox plastic polymer dishes. Rat neuronal cell culture was grown on graphene-coated surfaces, and cell growth and attachment were compared with those on uncoated and poly-d-lysine (PDL)-coated controls; the latter surface is highly favorable for neuronal attachment and growth. Live/dead cell analysis was conducted with flow cytometry using ethidium homodimer-1 and calcein AM dyes. Lactate dehydrogenase (LDH) levels—indicative of cytotoxicity—were measured as markers of cell death. Phase contrast microscopy of active cell culture was conducted to assess neuronal attachment and morphology.ResultsStatistically significant differences in the percentage of live or dead neurons were noted between graphene and PDL surfaces, as well as between the PDL-coated and bare surfaces, but there was little difference in cell viability between graphene-coated and bare surfaces. There were significantly lower LDH levels in the graphene-coated samples compared with the uncoated ones, indicating that graphene was not more cytotoxic than the bare control surface. According to phase contrast microscopy, neurons attached to the graphene-coated surface and were able to elaborate long, neuritic processes suggestive of normal neuronal metabolism and morphology.ConclusionsFurther use of graphene as a bioscaffold will require surface modification that enhances hydrophilicity to increase cellular attachment and growth. Graphene is a nanomaterial that is biocompatible with neurons and may have significant biomedical applications.
Long-term outcomes in poor grade patients who improve after EVD placement are similar to patients with lower grade hemorrhages. When an EVD is placed preoperatively in a poor grade aSAH patient, the neurological status after EVD determines the clinical grade.
The ventriculoperitoneal shunt is the mainstay of treatment for hydrocephalus. Despite its widespread use and safety record, it often malfunctions due to complications such as obstruction, breakage, migration and infection. This necessitates a systematic approach to diagnosing the etiology of shunt failure. Any evaluation should begin with an appraisal of the patient's symptoms. In acute malfunction, nausea, vomiting, irritability, seizures, headache, lethargy, coma and stupor are seen. In chronic malfunction, neuropsychological signs, feeding pattern changes, developmental delay, decline in school performance, headaches and increased head size are often seen. The next step in evaluation is a CT scan of the head to evaluate ventricular size. Prior imaging studies should be obtained for comparison; if the ventricles have enlarged over time, shunt malfunction is likely. If there is no such increase or dilation in the first place, other diagnoses are possible. However, "slit ventricle syndrome" should also be considered. When prior imaging is not available, pumping the reservoir, a radionuclide shuntogram, a shunt tap or even surgical exploration are options. The goals of this paper are to provide an algorithm for evaluating shunt malfunction and to illustrate the radiographic findings associated with shunt failure.
Based on MRI assessment, these devices, at more than 2-year follow-up, did not indicate any local chronic inflammation or swelling resulting from their degradation. Clinical symptoms of dysphagia or dysarthria, a common reported problem following anterior cervical spine procedures, were not observed in any patient.
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