To study the effects of polyphenols on the Na(+)/glucose cotransporter (SGLT1) response, SGLT1 was expressed in Xenopus oocytes by injecting cRNA synthesized from the cloned cDNA of the small intestine cotransporter of rats, and the electrical response elicited by glucose or galactose was measured by a voltage clamping method. Most phenol derivatives had no effect on the response. However, the polyphenols (+)-catechin, (-)-epicatechin gallate (ECg), and (-)-epigallocatechin gallate (EGCg), which are components of green tea, caused an inhibition of the response, which was almost independent of glucose concentration. The inhibition constants were estimated to be 2.3 mM for (+)-catechin and 0.45 mM for both ECg and EGCg, assuming the noncompetitive inhibition mechanism. Saponin prepared from tea seeds also inhibited the response significantly. Tannic acid and aqueous extracts of teas induced nonspecific electrical responses in both cRNA-injected and noninjected oocytes at lower concentrations than those that caused an inhibition of the SGLT1 response when their dose-dependent effects were examined. These results are possibly helpful in the development of a dietary supplement for diabetic patients.
P19 embryonic carcinoma (EC) cells are one of the simplest systems for analyzing the neuronal differentiation. To identify the membrane-associated molecules on the neuronal cells involved in the early neuronal differentiation in mice, we generated two monoclonal antibodies, SKY-1 and SKY-2, by immunizing rats with a membrane fraction of the neuronally committed P19 EC cells as an antigen. SKY-1 and SKY-2 recognized the carbohydrate moiety of a 90 kDa protein (RANDAM-1) and the polypeptide core of a 40 kDa protein (RANDAM-2), respectively. In the P19 EC cells, the expression of RANDAM-1 was colocalized to a part of Nestin-positive cells, whereas that of RANDAM-2 was observed in most Nestin-positive cells as well as -III-tubulin positive neurons. In the embryonic and adult brain of mice, RANDAM-1 was expressed at embryonic day 8.5 (E8.5), and the localization of antigen was restricted on the neuroepithelium and choroid plexus. The RANDAM-2 expression commenced at E6.0, and the antigen was distributed not only on the neuroepithelium of embryonic brain but on the neurons of adult brain. Collectively, it was concluded that RANDAM-1 is a stage specific antigen to express on the neural stem cells, and RANDAM-2 is constitutively expressed on both the neural stem cells and differentiated neuronal cells in mouse central nervous system (CNS).
The patient was a Japanese woman who experienced a decrease in activity and gait disturbance as the initial symptoms at the age of 86, followed by disorientation and memory dysfunction. Magnetic resonance imaging showed extensive cortical regions with hyperintensity in diffusion-weighted images, and these regions showed swelling in T2-weighted and fluid-attenuated inversion recovery (FLAIR) images. The medial occipital cortex and striatum showed no apparent hyperintensity on diffusion-weighted imaging (DWI). Mild myoclonus was detected, and the patient died 10 months after the onset of symptoms; she did not enter the akinetic mutism state. The patient's brain weighed 1050 g, and neuropathological examination showed extensive characteristic various-sized and non-confluent (VaSNoC) vacuoles in the cerebral cortex. These vacuoles were observable macroscopically by loupe on images of hematoxylin and eosin-stained tissue. Gliosis, hypertrophic astrocytosis, and neuron loss were generally mild in character. Prion protein (PrP) immunostaining showed very mild diffuse-synaptic-type PrP deposition in the cerebral gray matter. These clinicopathological findings led us to several conclusions relative to the early disease pathology of V180I genetic Creutzfeldt-Jakob disease: (i) spongiform change was not found in the medial occipital cortex, which corresponds to the results of DWI; (ii) VaSNoC-type spongiform changes, extensively recognized in the cerebral cortex, corresponded to the DWI findings showing continued hyperintensity with higher brightness, and T2-weighted and FLAIR images findings showing a swelling; and (iii) spongiform changes first appear in the deeper layer and subsequently in the superficial layer in the cerebral cortex.
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