Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.3.16 (calcineurin)
 17,112 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Calcineurin is one of the calmodulin binding proteins and a Ca2+-dependent and calmodulin-stimulated phosphoprotein phosphatase. We used antisera to the calcineurin as a cell-type-specific marker in order to identify neuronal cells in the rat brain and human neoplasms. In normal rat brain slices, basal ganglia were stained macroscopically, and other areas such as cerebral cortex, corpus callosum, cerebellar cortex, granular layer and pyramidal tract of the spinal cord were lightly identified as well. Under the light microscope, it was found that only the neuronal cells were stained, and astrocytes, oligodendrocytes, ependymal cells and vessels were not. Intracellular distribution of the staining showed various patterns and staining intensity of varying degree. Using the PAP method, localization of the calcineurin in formalin-fixed, paraffin-embedded tissues were studied in 65 human intracranial neoplasms, and in 11 human extracranial neoplasms. The neuronal elements of neuroblastoma, ganglioglioma, ganglioneuroma and retinoblastoma were clearly stained. In contrast, glioblastoma, astrocytoma, oligodendroglioma, ependymoma, meningioma, neurinoma, pituitary adenoma, craniopharyngioma, hemangioblastoma, hamartoma, lymphoma and mesenchymal tumor were all negative. Two cases out of 5 medulloblastomas were stained, but others were not. Although positive tumors disclosed various staining patterns and intensities, these results indicated that calcineurin could be a new neuronal marker in human brain tumors.
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PMID:Calcineurin as a neuronal marker of human brain tumors. 242 51

Renal transplantation is method of choice for treatment of patients with end-stage renal disease without contraindications for immunosuppressive therapy. Neurological complications occur frequently in renal transplant recipients. They may be the consequence of immunosuppressive treatment, but more often evolve as the consequence of previous disturbances which developed during the state of uraemia and treatment with dialysis. The most pronounced neurotoxic effect has calcineurin inhibitors tacrolimus and cyclosporine. The spectrum of neurological disturbances caused by calcineurin inhibitors range from very mild symptoms as paraesthesiae, tremor, headache or flushing, to severe changes that may cause lethal outcome. Peripheral neuropathies in renal transplant recipients may occur in the form of mononeuropathy or polyneuropathy. Cerebrovascular diseases are consequence of changes on blood vessels caused by uraemia, dialysis and side effects of immunosuppressive drugs. They cause death in 8% of renal transplant recipients. Central nervous system (CNS) infections usually occur during the first posttransplant year. Unclear symptomatology frequently postpones the diagnosis. Diagnostic evaluation should include magnetic resonance imaging for localization of the process, as well as lumbal puncture in cases without contraindications for the procedure, in order to determine the causative agent. Regarding the ominous prognosis of CNS infections in the immunocompromised host, only timely diagnosis may improve survival. The most common causative agents are Cryptococcus neoformans, Listeria monocytogenes and Aspergillus funigatus. Viral infections also occur, and are commonly caused by herpes virideae, varicella-zoster virus and papova virus. CNS infections clinically present as meningitis, progressive dementia or focal neurological defect. The most common primary brain tumors are B-cell lymphomas, but glioblastoma, hemangioblastoma, leiomyosarcoma or glioma may also occur. In cases of neurological posttransplant complications, optimal treatment should be guided by neurologist, nephrologist and infectologist, in some cases also by neurosurgeons.
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PMID:[Neurological complications in renal transplant recipients]. 1857 36