• Progress in Medical Physics
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• v.13 no.3
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• pp.120-128
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• 2002

To investigate differences between the metabolic ratios of normal controls and brain tumors such as astrocytomas and glioblastoma multiforme (GM) by proton MR spectroscopy (MRS) at 37 high field system. Using 3T MRI/MRS system, localized water-suppressed single-voxel technique in patients with brain tumors was employed to evaluate spectra with peaks of N-acetyl aspartate (NAA), choline-containing compounds (Cho), creatine/phosphocreatine (Cr) and lactate. On the basis of Cr, these peak areas were quantificated as a relative ratio. The variation of metabolites measurements of the designated region in 10 normal volunteers was less than 10%. Normal ranges of NAA/Cr and Cho/Cr ratios were 1.67$\pm$018 and 1.16$\pm$0.15, respectively. NAA/Cr ratio of all tumor tissues was significantly lower than that of the normal tissues (P=0.005). Cho/Cr ratio of glioblastoma multiforme was significantly higher than that of astrocytomas (P=0.001). Lactate was observed in all tumor cases. The present study demonstrated that the neuronal degradation or loss was observed in all tumor tissues. Higher grade of brain tumors was correlated with higher Cho/Cr ratio, indicating a significant dependence of Cho levels on malignancy of gliomas. This results suggest that clinical proton MR spectroscopy could be useful to predict tumor malignancy.

• Investigative Magnetic Resonance Imaging
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• v.2 no.1
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• pp.14-30
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• 1998

Manganese is an essential element in the body. It is mainly deposited in the liver and to a lesser degree in the basal ganglia of the brain and eliminated through the bile duct. Rapid turnover of managanese in the body makes it difficult to evaluate the manganese exposure in workers, esecially in those with irregular or intermittent exposure, like welders. Therefore, conventional biomarkers, including blood and urine manganese can provide only a limited information about the long-tern or cumulative exposure to manganese. Introduction of magnetic resonance imaging (MRI) made a progress in the assessment of manganese exposure in the medical conditions related to manganese accumulation, e. g. hepatic failure and long-term total parenteral nutrition. Manganese shortens spin-lattice(T1) relaxation time on MRI due to its paramagnetic property, resulting in high signal intensity (HSI) on T1-weighted image(T1W1) of MRI. Manganese deposition in the brain, therefore, can be visualizedas an HSI in the globus pallidus, the substantia nigra, the putamen and the pituitary. clinical and epidemiologic studies regarding the MRI findings in the cases of occupational and non-occupational manganese exposure were reviewed. relationships between HSI on T1W1 of MRI and age, gender, occupational manganese exposure, and neurological dysfunction were analysed. Relationships betwen biological exposure indices and HSI on MRE werealso reviewed. Literatures were reviewed to establish the relationships between HSI, Manganese deposition in the brain, pathologic findings, and neurological dysfunction. HSI on T1W1 of MRI reflects regional manganese deposition in the brain. This relationship enables an estimation of regional manganese deposition in the brain by analysing MR signal intensity. Manganese deposition in the brain can induce a neuronal loss in the basal ganglia but functional abnormality is supposed to be related to the cumulative exposure of manganese in the brain, use of brain MRI for the assessment of exposure in a group of workers seems to be hardly rationalized, while ti can be a useful adjunct for the evaluation of manganese exposure int he cases with suspected manganese-related health problems.

• Journal of Life Science
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• v.29 no.6
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• pp.747-753
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• 2019

Cognitive decline is characterized by reduced long-/short-term memory and attention span, and increased depression and anxiety. Such decline is associated with various degenerative brain disorders, especially Alzheimer's disease (AD) and Parkinson's disease (PD). The increases in elderly populations suffering from cognitive decline create social problems and impose economic burdens, and also pose safety threats; all of these problems have been extensively researched over the past several decades. Possible causes of cognitive decline include metabolic and hormone imbalance, infection, medication abuse, and neuronal changes associated with aging. However, no treatment for cognitive decline is available. In neurodegenerative diseases, changes in the gut microbiota and gut metabolites can alter molecular expression and neurobehavioral symptoms. Changes in the gut microbiota affect memory loss in AD via the downregulation of NMDA receptor expression and increased glutamate levels. Furthermore, the use of probiotics resulted in neurological improvement in an AD model. PD and gut microbiota dysbiosis are linked directly. This interrelationship affected the development of constipation, a secondary symptom in PD. In a PD model, the administration of probiotics prevented neuron death by increasing butyrate levels. Dysfunction of the blood-brain barrier (BBB) has been identified in AD and PD. Increased BBB permeability is also associated with gut microbiota dysbiosis, which led to the destruction of microtubules via systemic inflammation. Notably, metabolites of the gut microbiota may trigger either the development or attenuation of neurodegenerative disease. Here, we discuss the correlation between cognitive decline and the gut microbiota.