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)

Interaction of chlorotetracycline (CTC) with bovine serum albumin (BSA) was investigated under simulated physiological conditions by spectroscopy with the aid of multivariate curve resolution-alternating least squares (MCR-ALS). Eosin Y was selected as an alternative site I marker on the BSA to study the above molecular interaction. The binding of Eosin Y and CTC to BSA showed that CTC was displaced from CTC-BSA complex by Eosin Y, and Eosin Y-BSA complex was formed. However, the recorded fluorescence spectra of Eosin Y and Eosin Y-BSA overlapped and MCR-ALS was applied to resolve the two-way fluorescence spectra. From the resolved equilibrium concentration profiles, it was observed that Eosin Y competed with CTC in the binding process with BSA; it was also shown that the binding site of CTC on BSA was site I, and this was further confirmed by the fluorescence polarization method. Compared with some common site I markers for BSA, the fluorescence and UV-vis spectral shapes of the Eosin Y-BSA complex were quite different from that of Eosin Y, and this feature facilitated the investigation of the small molecule-BSA interaction.
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PMID:Spectrophotometric study of the interaction between chlorotetracycline and bovine serum albumin using Eosin Y as site marker with the aid of chemometrics. 2116 87

Peripherin is a type III intermediate filament protein expressed with low levels in spinal motor neurons. Amyotrophic lateral sclerosis (ALS) is characterized by the presence of Bunina bodies, skein-like inclusions, and Lewy body-like inclusions (LBLIs) in the remaining anterior horn cells, where the first and third structures are detected by Hematoxylin-Eosin (H & E) staining. We examined paraffin sections of lumbar spinal cords from six ALS patients, using H & E staining and immunostaining for human peripherin. The results demonstrated that there were a total of 73 anterior horn cells containing one or more Bunina bodies, and that twelve of these cells (approximately 16.4%) demonstrated peripherin-positive Bunina bodies. In fact, some part of chain-like Bunina bodies showed peripherin-positive reaction, although there were a much higher number of non-immunoreacitive Bunina bodies in each neuron. LBLIs were clearly immunostained for peripherin corresponding to the core, while some of them showed different types of immunoreactivities due to oblique cutting of inclusions. Our findings suggest that although the mechanisms underlying peripherin co-localization in Bunina bodies are unknown, peripherin could be involved in forming these inclusions. Furthermore, following cystatin C and transferrin, peripherin is the third most prevalent protein that partially localizes in Bunina bodies.
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PMID:Peripherin partially localizes in Bunina bodies in amyotrophic lateral sclerosis. 2124 94

Aluminum is a light weight and toxic metal present ubiquitously on earth, which has gained considerable attention due to its neurotoxic effects. It also has been linked ecologically and epidemiologically to several neurological disorders, including Alzheimer's disease (AD), Parkinson's disease (PD), Guamanian-Parkinsonian complex and Amyotrophic lateral sclerosis (ALS). The mechanism of aluminum neurotoxicity is poorly understood, but it is well documented that aluminum generates reactive oxygen species (ROS). Enhanced ROS production leads to disruption of cellular antioxidant defense systems and release of cytochrome c (cyt-c) from mitochondria to cytosol resulting in apoptotic cell death. Quercetin (a natural flavonoid) protects it from oxidative damage and has been shown to decrease mitochondrial damage in various animal models of oxidative stress. We hypothesized that if oxidative damage to mitochondria does play a significant role in aluminum-induced neurodegeneration, and then quercetin should ameliorate neuronal apoptosis. Administration of quercetin (10 mg/kg body wt/day) reduced aluminum (10 mg/kg body wt/day)-induced oxidative stress (decreased ROS production, increased mitochondrial superoxide dismutase (MnSOD) activity). In addition, quercetin also prevents aluminum-induced translocation of cyt-c, and up-regulates Bcl-2, down-regulates Bax, p53, caspase-3 activation and reduces DNA fragmentation. Quercetin also obstructs aluminum-induced neurodegenerative changes in aluminum-treated rats as seen by Hematoxylin and Eosin (H&E) staining. Further electron microscopic studies revealed that quercetin attenuates aluminum-induced mitochondrial swelling, loss of cristae and chromatin condensation. These results indicate that treatment with quercetin may represent a therapeutic strategy to attenuate the neuronal death against aluminum-induced neurodegeneration.
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PMID:Quercetin attenuates neuronal death against aluminum-induced neurodegeneration in the rat hippocampus. 2694 3