A Two-Year Randomized Trial of Interventions to Decrease Stress Hormone Vasopressin Production in Patients with Meniere’s Disease—A Pilot Study by Tadashi Kitahara (702040)

“…Because mental/physical stress and subsequent increase in the stress hormone vasopressin supposedly trigger Meniere's disease, we set a pilot study to seek new therapeutic interventions, namely management of vasopressin secretion, to treat this disease. …”

Glycine is able to induce both a motility speed in- and decrease during zebrafish neuronal migration by Ulrike Theisen (4734555)

Mean ± SD values of unipedal stance parameters evaluated at the different time points of the postural training session. by Cristina Dolciotti (16317330)

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Mean ± SD of the different parameters relative to bipedal stance on soft support with the eyes open recorded in the Chewing and Hand Grip groups. by Cristina Dolciotti (16317330)

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Time course of Path Length, LFS and Velocity during postural training. by Cristina Dolciotti (16317330)

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Relation of the changes in Y Sway Amplitude and LFS induced by postural training with those in 95% Area. by Cristina Dolciotti (16317330)

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Training-induced changes in bipedal stance. by Cristina Dolciotti (16317330)

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Between-group differences in 95% Area, Y Sway Amplitude and LFS during postural training. by Cristina Dolciotti (16317330)

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Relation between training-related changes in unipedal and bipedal stance. by Cristina Dolciotti (16317330)

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Consolidation of training-induced changes in unipedal stance: 95% Area, Y Sway Amplitude and LFS. by Cristina Dolciotti (16317330)

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Consolidation of training-induced changes in unipedal stance: Path Length, X Sway Amplitude and Velocity. by Cristina Dolciotti (16317330)

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Time course of 95% Area, X and Y Amplitude Sway during postural training. by Cristina Dolciotti (16317330)

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Correlations between unipedal and bipedal stance parameters recorded at the beginning of the training and of the control session. by Cristina Dolciotti (16317330)

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Flow diagram. by Cristina Dolciotti (16317330)

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Image_3_A decrease in Fkbp52 alters autophagosome maturation and A152T-tau clearance in vivo.TIF by Emilie Lesport (19214344)

“…<p>The failure of the autophagy-lysosomal pathway to clear the pathogenic forms of Tau exacerbates the pathogenesis of tauopathies. We have previously shown that the immunophilin FKBP52 interacts both physically and functionally with Tau, and that a decrease in FKBP52 protein levels is associated with Tau deposition in affected human brains. …”

Table_1_A decrease in Fkbp52 alters autophagosome maturation and A152T-tau clearance in vivo.DOCX by Emilie Lesport (19214344)

“…<p>The failure of the autophagy-lysosomal pathway to clear the pathogenic forms of Tau exacerbates the pathogenesis of tauopathies. We have previously shown that the immunophilin FKBP52 interacts both physically and functionally with Tau, and that a decrease in FKBP52 protein levels is associated with Tau deposition in affected human brains. …”

Image_2_A decrease in Fkbp52 alters autophagosome maturation and A152T-tau clearance in vivo.TIF by Emilie Lesport (19214344)

“…<p>The failure of the autophagy-lysosomal pathway to clear the pathogenic forms of Tau exacerbates the pathogenesis of tauopathies. We have previously shown that the immunophilin FKBP52 interacts both physically and functionally with Tau, and that a decrease in FKBP52 protein levels is associated with Tau deposition in affected human brains. …”

Video_2_A decrease in Fkbp52 alters autophagosome maturation and A152T-tau clearance in vivo.AVI by Emilie Lesport (19214344)

“…<p>The failure of the autophagy-lysosomal pathway to clear the pathogenic forms of Tau exacerbates the pathogenesis of tauopathies. We have previously shown that the immunophilin FKBP52 interacts both physically and functionally with Tau, and that a decrease in FKBP52 protein levels is associated with Tau deposition in affected human brains. …”

Video_3_A decrease in Fkbp52 alters autophagosome maturation and A152T-tau clearance in vivo.AVI by Emilie Lesport (19214344)

“…<p>The failure of the autophagy-lysosomal pathway to clear the pathogenic forms of Tau exacerbates the pathogenesis of tauopathies. We have previously shown that the immunophilin FKBP52 interacts both physically and functionally with Tau, and that a decrease in FKBP52 protein levels is associated with Tau deposition in affected human brains. …”

Image_1_A decrease in Fkbp52 alters autophagosome maturation and A152T-tau clearance in vivo.TIF by Emilie Lesport (19214344)

“…<p>The failure of the autophagy-lysosomal pathway to clear the pathogenic forms of Tau exacerbates the pathogenesis of tauopathies. We have previously shown that the immunophilin FKBP52 interacts both physically and functionally with Tau, and that a decrease in FKBP52 protein levels is associated with Tau deposition in affected human brains. …”