Self-assembly and salt-induced thermoresponsive properties of amphiphilic PEG/cation random terpolymers in water

Herein, we report the self-assembly and salt-induced thermoresponsive properties of amphiphilic random terpolymers consisting of hydrophilic poly(ethylene glycol) (PEG) and quaternary ammonium cations, and hydrophobic dodecyl groups in water. The random terpolymers self-assembled into size-controlled multichain micelles in pure water or in water containing NaCl. The micelle size increased upon increasing the content of the cationic groups in the total hydrophilic monomer units (∼50 mol%) and turned larger in the presence of NaCl than that in pure water. More uniquely, the random terpolymer micelles showed lower critical solution temperature-type solubility in water containing salts such as NaCl, while the solutions of the polymer micelles in pure water were transparent even upon heating to over 90 °C. The cloud point (Cp) temperature of the aqueous polymer micelle solution was controlled by the concentration of NaCl or the composition of the terpolymers. The critical concentration of NaCl for thermoresponsive solubility depended on the PEG/cation composition of the terpolymers. For example, a PEG/cation/dodecyl (1/1/2) random terpolymer micelle exhibited thermoresponse in water containing more than 0.5 M NaCl; the Cp of the aqueous solution decreased from 86 °C to 59 °C upon increasing the concentration of NaCl from 0.5 M to 2.0 M. The Cp of their terpolymers increased upon increasing the content of quaternary ammonium cations

Glaucomatous vertical vessel density asymmetry of the temporal raphe detected with optical coherence tomography angiography.

Changes in retinal vasculature and ocular circulation may play an important role in the glaucoma development and progression. We evaluated the vertical asymmetry across the temporal raphe of the deep retinal layer vessel density, using swept-source optical coherence tomography angiography (SS-OCTA), and its relationship with the central visual field (VF) loss. Thirty-four eyes of 27 patients with open-angle glaucoma were included. SS-OCTA macular scanning was performed within a 3 × 3 mm (300 × 300 pixels) volume, centred on the fovea. The relationships between the vertical asymmetrical deep retinal vessel density reduction (ADRVD) across the temporal raphe and various ocular parameters were analysed. Twenty-two glaucomatous eyes with ADRVDs had central VF loss. Contrarily, ADRVDs were not found in any of the 12 eyes without central VF loss. Thirteen eyes (59.1%) with central VF loss had ADRVDs topographically corresponding to the central VF loss and macular ganglion cell complex thinning. The glaucomatous eyes with ADRVDs exhibited inferior rather than superior central VF loss (P = 0.032). Thus, ADRVD specifically indicates the glaucomatous central visual loss. Further analysis of ADRVD may improve our understanding on glaucoma pathogenesis, offering new treatment insights

Effect of chemical treatment on mineralization of C and N in Andosols rich in Al-humus complexes

Poster Sessio

Brain-specific gene expression by immortalized microglial cell-mediated gene transfer in the mammalian brain

AbstractThe intra-arterial injection of immortalized microglia transfected with the lacZ gene, resulted in the expression of β-galactosidase in the rat brain at 48 h and the activity of β-galactosidase was detected for up to 3 weeks post-injection. More than 30-fold higher activity of β-galactosidase was detected in the brain than in the liver, lung or spleen at 48 h post-injection. This method allows us to easily deliver the gene of interest to the brain without influencing other organs. Our brain-targeting gene delivery system can facilitate gene therapy of several brain disorders, including brain tumor, metabolic disorders, and degenerative disorders, as well as investigation into the roles of particular genes in brain function and development

Distant organ injury following unilateral renal ischemia-reperfusion in hypertensive Dahl salt-sensitive rats and the ameliorating effect of rosuvastatin pretreatment

博士（医学）福島県立医科大

Phorbol ester impairs electrical excitation of rat pancreatic beta-cells through PKC-independent activation of K(ATP) channels

BACKGROUND: Phorbol 12-myristate 13-acetate (PMA) is often used as an activating phorbol ester of protein kinase C (PKC) to investigate the roles of the kinase in cellular functions. Accumulating lines of evidence indicate that in addition to activating PKC, PMA also produces some regulatory effects in a PKC-independent manner. In this study, we investigated the non-PKC effects of PMA on electrical excitability of rat pancreatic β-cells by using patch-clamp techniques. RESULTS: In current-clamp recording, PMA (80 nM) reversibly inhibited 15 mM glucose-induced action potential spikes superimposed on a slow membrane depolarization and this inhibition can not be prevented by pre-treatment of the cell with a specific PKC inhibitor, bisindolylmaleimide (BIM, 1 μM). In the presence of a subthreshold concentration (5.5 mM) of glucose, PMA hyperpolarized β-cells in a concentration-dependent manner (0.8–240 nM), even in the presence of BIM. Based on cell-attached single channel recordings, PMA increased ATP-sensitive K(+) channel (K(ATP)) activity. Based on inside-out patch-clamp recordings, PMA had little effect on K(ATP) activity if no ATP was in the bath, while PMA restored K(ATP) activity that was suppressed by 10 μM ATP in the bath. In voltage-clamp recording, PMA enhanced tolbutamide-sensitive membrane currents elicited by repetitive ramp pulses from -90 to -50 mV in a concentration-dependent manner, and this potentiation could not be prevented by pre-treatment of cell with BIM. 4α-phorbol 12,13-didecanoate (4α-PDD), a non-PKC-activating phorbol ester, mimicked the effect of PMA on both current-clamp and voltage-clamp recording configurations. With either 5.5 or 16.6 mM glucose in the extracellular solution, PMA (80 nM) increased insulin secretion from rat islets. However, in islets pretreated with BIM (1 μM), PMA did not increase, but rather reduced insulin secretion. CONCLUSION: In rat pancreatic β-cells, PMA modulates insulin secretion through a mixed mechanism: increases insulin secretion by activation of PKC, and meanwhile decrease insulin secretion by impairing β-cell excitability in a PKC-independent manner. The enhancement of K(ATP) activity by reducing sensitivity of K(ATP) to ATP seems to underlie the PMA-induced impairment of β-cells electrical excitation in response to glucose stimulation

Cognitive Profile of Idiopathic Normal Pressure Hydrocephalus

Background/Aims: Frontal lobe dysfunction is believed to be a primary cognitive symptom in idiopathic normal pressure hydrocephalus (iNPH); however, the neuropsychology of this disorder remains to be fully investigated. The objective of this study was to delineate a comprehensive profile of cognitive dysfunction in iNPH and evaluate the effects of cerebrospinal fluid (CSF) shunt surgery on cognitive dysfunction. Methods: A total of 32 iNPH patients underwent neuropsychological testing of memory, attention, language, executive function, and visuoperceptual and visuospatial abilities. Of these 32 patients, 26 were reevaluated approximately 1 year following CSF shunt surgery. The same battery of tests was performed on 32 patients with Alzheimer’s disease (AD) and 30 healthy elderly controls. Results: The iNPH patients displayed baseline deficits in attention, executive function, memory, and visuoperceptual and visuospatial functions. Impairments of attention, executive function, and visuoperceptual and visuospatial abilities in iNPH patients were more severe than in those with AD, whereas the degree of memory impairment was comparable to that in AD patients. A significant improvement in executive function was observed following shunt surgery. Conclusion: Patients with iNPH are impaired in various aspects of cognition involving both ‘frontal’ executive functions and ‘posterior cortical’ functions. Shunt treatment can ameliorate executive dysfunction

Yeast Eps15-like endocytic protein Pan1p regulates the interaction between endocytic vesicles, endosomes and the actin cytoskeleton

The actin cytoskeleton plays important roles in the formation and internalization of endocytic vesicles. In yeast, endocytic vesicles move towards early endosomes along actin cables, however, the molecular machinery regulating interaction between endocytic vesicles and actin cables is poorly understood. The Eps15-like protein Pan1p plays a key role in actin-mediated endocytosis and is negatively regulated by Ark1 and Prk1 kinases. Here we show that pan1 mutated to prevent phosphorylation at all 18 threonines, pan1-18TA, displayed almost the same endocytic defect as ark1Δ prk1Δ cells, and contained abnormal actin concentrations including several endocytic compartments. Early endosomes were highly localized in the actin concentrations and displayed movement along actin cables. The dephosphorylated form of Pan1p also caused stable associations between endocytic vesicles and actin cables, and between endocytic vesicles and endosomes. Thus Pan1 phosphorylation is part of a novel mechanism that regulates endocytic compartment interactions with each other and with actin cables