Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0002736 (amyotrophic lateral sclerosis)
 19,048 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Somatosensory evoked potentials (SEPs) were studied in 115 patients with spinal cord diseases (multiple sclerosis, amyotrophic lateral sclerosis, cervical myelopathy, subacute combined degeneration, myelitis, spinal cord injury, tumours). The SEPs were recorded at three levels: parietal, spinal (cervical or lumbar), and at the Erb point. The central conduction time was also estimated (N9-N13 and lumbar potential (LP): LP-P37). The most sensitive test (95% abnormalities) was represented by the cortical recording of the SEPs when the tibial nerve was stimulated. The interval LP-P37 was increased, the SEPs being delayed or unrecordable and desynchronized (in cases of polyneuropathies only the latency was increased whereas the waveform was normal). In 50 patients with definite form of multiple sclerosis (MS) abnormalities of the cervical potential N13 were obtained in 96% of cases. The cortical SEPs to the median nerve stimulation were abnormal in 64% of cases only (32 patients). Of 10 patients with amyotrophic lateral sclerosis (ALS), cortical SEPs to the lower limb stimulation were abnormal in 6 patients (20%) and only 2 patients had also abnormal N13 and N20. Of 15 patients with cervical myelopathy, SEPs to the tibial nerve stimulation were abnormal and N9-N13 delayed in all but 2 patients. All the 5 patients with subacute combined degeneration had abnormal SEPs to the tibial nerve stimulation. In all the 15 patients with inflammatory spinal cord diseases, the SEPs were abnormal and the central conduction time was delayed. In 5 cases with spinal cord injury the SEPs were absent above the lesion. In 15 patients with tumoral compression SEPs to the stimulation of the nerve dependent on the sensitive root compressed as well as the lower limb SEPs were abnormal.
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PMID:Somatosensory evoked potentials in spinal cord diseases. 258 29

Although it was first described over a century ago (by Charcot in 1865; by Erb in 1875), the concept of primary lateral sclerosis (PLS) is still not universally accepted. Despite this skepticism, several well-documented cases of isolated degeneration with varying degrees of involvement of corticospinal pyramidal pathways have been reported in the literature. The clinical manifestations in these cases can take one of two forms, ie, isolated spasmodic paraplegia or tetraplegia on the one hand or spasmodic tetraplegia associated with a pseudobulbar syndrome featuring severe spastic dysarthria (chronic progressive bilateral spinobulbar spasticity) on the other hand. Obviously, without firm pathologic data, PLS is a hazardous diagnosis for isolated paraplegia or tetraplegia. Conversely, for bilateral spinobulbar spasticity, it would appear to be the only diagnosis possible once investigate findings have eliminated the other possibilities, such as a pyramidal form of amyotrophic lateral sclerosis or a spinal form of multiple sclerosis. To underscore this point, in this report, five cases of chronic progressive bilateral spinobulbar spasticity developed over 5, 10, 12, 10, and 28 years, respectively, for which the only possible diagnosis was PLS. It was concluded that there are three forms of degenerative diseases of the principal motor pathways: one involving both central and peripheral neurons, ie, amyotrophic lateral sclerosis; one involving only peripheral neurons, ie, spinal amyotrophy; and one involving only central motor neurons, ie, PLS.
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PMID:Chronic progressive spinobulbar spasticity. A rare form of primary lateral sclerosis. 335 2

The sensory symptoms and the involvement of the sensory tracts in amyotrophic lateral sclerosis (ALS) were much debated by various authors. The SEPs were studied in 10 patients with ALS by percutaneous stimulation of the median and tibial nerves. The SEPs were recorded at: Erb's point, cervical level (CII), lumbar level (L1) and parietal level. The peripheral sensory and motor nerve conduction were normal, excluding the spondylotic origin of altered SEPs found in these patients. There were 9 patients with abnormal parietal SEPs to the tibial nerve stimulation, usually bilateral. Abnormal cervical potential (N13) to the median stimulation was noted in 7 cases of whom 3 had also abnormal parietal SEPs. The most severe abnormalities were obtained in the 5 patients with fast advancing ALS and notably to the tibial nerve stimulation. Our results confirm the findings of other authors and reflect physiological dysfunction in the sensory system in a disease considered so far as restricted to the motor system.
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PMID:Abnormal somatosensory evoked potentials in amyotrophic lateral sclerosis. 801 89

BACKGROUND The network pharmacological approach was used to identity the anti-colorectal cancer (CRC) targets of formononetin (FN) and the molecular mechanisms of FN against CRC. MATERIAL AND METHODS A tool of the DisGeNET database was used for collection of CRC-based targets. Other tools of SuperPred, herbal ingredients target (HIT), and SwissTargetPrediction databases were applied in prediction of pharmacological targets of FN against cancer. A protein-protein interaction (PPI) network of FN against CRC was obtained by using a STRING database. All top biological functional processes and signaling pathways of FN against CRC were identified by using Database for Annotation, Visualization and Integrated Discovery (DAVID) software and Omicshare cloud platform. RESULTS The most key anti-CRC targets of FN were identified as tumor protein p53 (TP53), cytochrome P450 3A4 (CYP3A4), ATP binding cassette subfamily G member 2 (ABCG2), tumor necrosis factor (TNF), epidermal growth factor receptor (EGFR), Erb-B2 receptor tyrosine kinase 2 (ERBB2), and cytochrome P450 1A1 (CYP1A1). In further assays, the treatment of CRC by FN was mainly involved in biological functional processes of reactive oxygen species metabolic process, positive regulation of transcription, DNA-templated, positive regulation of nucleic acid-templated transcription, and positive regulation of RNA metabolic process. anti-CRC by FN of signaling pathways were associated with amyotrophic lateral sclerosis (ALS), allograft rejection, cytokine-cytokine receptor interaction, asthma, mitogen-activated protein kinase (MAPK) signaling pathways, and others. CONCLUSIONS The anti-CRC molecular mechanisms of FN are implicated in suppression of cellular proliferation and regulation of cancer-related metabolic pathways. Interestingly, 8 optimal biological targets may be used as potential molecular markers for predicting and treating CRC.
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PMID:Anti-Colorectal Cancer Mechanisms of Formononetin Identified by Network Pharmacological Approach. 3160 99