Patterning of dielectric nanoparticles using dielectrophoretic forces generated by ferroelectric polydomain films

A theoretical study of a dielectrophoretic force, i.e. the force acting on an electrically neutral particle in the inhomogeneous electric field, which is produced by a ferroelectric domain pattern, is presented. It has been shown by several researchers that artificially prepared domain patterns with given geometry in ferroelectric single crystals represent an easy and flexible method for patterning dielectric nanoobjects using dielectrophoretic forces. The source of the dielectrophoretic force is a strong and highly inhomogeneous (stray) electric field, which exists in the vicinity of the ferroelectric domain walls at the surface of the ferroelectric film. We analyzed dielectrophoretic forces in the model of a ferroelectric film of a given thickness with a lamellar 180${}^\circ$ domain pattern. The analytical formula for the spatial distribution of the stray field in the ionic liquid above the top surface of the film is calculated including the effect of free charge screening. The spatial distribution of the dielectrophoretic force produced by the domain pattern is presented. The numerical simulations indicate that the intersection of the ferroelectric domain wall and the surface of the ferroelectric film represents a trap for dielectric nanoparticles in the case of so called positive dielectrophoresis. The effects of electrical neutrality of dielectric nanoparticles, free charge screening due to the ionic nature of the liquid, domain pattern geometry, and the Brownian motion on the mechanism of nanoparticle deposition and the stability of the deposited pattern are discussed.Comment: Accepted in the Journal of Applied Physics, 10 pages, 5 figure

Pressure on charged domain walls and additional imprint mechanism in ferroelectrics

The impact of free charges on the local pressure on a charged ferroelectric domain wall produced by an electric field has been analyzed. A general formula for the local pressure on a charged domain wall is derived considering full or partial compensation of bound polarization charges by free charges. It is shown that the compensation can lead to a very strong reduction of the pressure imposed on the wall from the electric field. In some cases this pressure can be governed by small nonlinear effects. It is concluded that the free charge compensation of bound polarization charges can lead to substantial reduction of the domain wall mobility even in the case when the mobility of free charge carriers is high. This mobility reduction gives rise to an additional imprint mechanism which may play essential role in switching properties of ferroelectric materials. The effect of the pressure reduction on the compensated charged domain walls is illustrated for the case of 180-degree ferroelectric domain walls and of 90-degree ferroelectric domain walls with the head-to-head configuration of the spontaneous polarization vectors.Comment: subm. to PRB. This verion is extended by appendi

Human Prominin-1 (CD133) Is Detected in Both Neoplastic and Non-Neoplastic Salivary Gland Diseases and Released into Saliva in a Ubiquitinated Form.

Prominin-1 (CD133) is physiologically expressed at the apical membranes of secretory (serous and mucous) and duct cells of major salivary glands. We investigated its expression in various human salivary gland lesions using two distinct anti-prominin-1 monoclonal antibodies (80B258 and AC133) applied on paraffin-embedded sections and characterized its occurrence in saliva. The 80B258 epitope was extensively expressed in adenoid cystic carcinoma, in lesser extent in acinic cell carcinoma and pleomorphic adenoma, and rarely in mucoepidermoid carcinoma. The 80B258 immunoreactivity was predominately detected at the apical membrane of tumor cells showing acinar or intercalated duct cell differentiation, which lined duct- or cyst-like structures, and in luminal secretions. It was observed on the whole cell membrane in non-luminal structures present in the vicinity of thin-walled blood vessels and hemorrhagic areas in adenoid cystic carcinoma. Of note, AC133 labeled only a subset of 80B258-positive structures. In peritumoral salivary gland tissues as well as in obstructive sialadenitis, an up-regulation of prominin-1 (both 80B258 and AC133 immunoreactivities) was observed in intercalated duct cells. In most tissues, prominin-1 was partially co-expressed with two cancer markers: carcinoembryonic antigen (CEA) and mucin-1 (MUC1). Differential centrifugation of saliva followed by immunoblotting indicated that all three markers were released in association with small membrane vesicles. Immuno-isolated prominin-1-positive vesicles contained CEA and MUC1, but also exosome-related proteins CD63, flotillin-1, flotillin-2 and the adaptor protein syntenin-1. The latter protein was shown to interact with prominin-1 as demonstrated by its co-immunoisolation. A fraction of saliva-associated prominin-1 appeared to be ubiquitinated. Collectively, our findings bring new insights into the biochemistry and trafficking of prominin-1 as well as its immunohistochemical profile in certain types of salivary gland tumors and inflammatory diseases

Ultrashort Bradycardic Effect of Newly Synthesized Compounds

Changes in the heart rate induced by four different doses of two newly synthesized potential ultrashort-action antagonists of beta adrenergic receptors were tested in 90 male laboratory Wistar rats. The isoprenaline-induced tachycardia model was used. Their effects were compared with those of esmolol. In the second part of the study, approximate electro-physiological measurements were made in vitro to assess the influence of the compounds tested on ion membrane currents in isolated ventricular cardiomyocytes. Both compounds demonstrated significant bradycardic effects in all concentrations tested compared with the control group, but they differed in the time of the onset of their action. Both newly synthesized compounds induced blockade of the fast sodium current (INa) and potassium currents (Ito, IK1, IK,end)

Pharmacologic modulation of experimentally induced allergic asthma

Allergic asthma is the most frequent disease of the respiratory tract. The aim of the current experimental and clinical studies was to find new sources of drugs able to control asthmatic inflammation and airway hyperresponsiveness. Our experimental studies were focused on efficiency evaluation of substances able to influence activities of ion channels, phosphodiesterase (PDE) isoforms, substances from the group of polyphenols and NO metabolism modulators during experimentally induced allergic asthma

The Neurotoxicity of DOPAL: Behavioral and Stereological Evidence for Its Role in Parkinson Disease Pathogenesis

BACKGROUND: The etiology of Parkinson disease (PD) has yet to be fully elucidated. We examined the consequences of injections of 3,4-dihydroxyphenylacetaldehyde (DOPAL), a toxic metabolite of dopamine, into the substantia nigra of rats on motor behavior and neuronal survival. METHODS/PRINCIPAL FINDINGS: A total of 800 nl/rat of DOPAL (1 µg/200 nl) was injected stereotaxically into the substantia nigra over three sites while control animals received similar injections of phosphate buffered saline. Rotational behavior of these rats was analyzed, optical density of striatal tyrosine hydroxylase was calculated, and unbiased stereological counts of the substantia nigra were made. The rats showed significant rotational asymmetry ipsilateral to the lesion, supporting disruption of dopaminergic nigrostriatal projections. Such disruption was verified since the density of striatal tyrosine hydroxylase decreased significantly (p<0.001) on the side ipsilateral to the DOPAL injections when compared to the non-injected side. Stereological counts of neurons stained for Nissl in pars compacta of the substantia nigra significantly decreased (p<0.001) from control values, while counts of those in pars reticulata were unchanged after DOPAL injections. Counts of neurons immunostained for tyrosine hydroxylase also showed a significant (p=0.032) loss of dopaminergic neurons. In spite of significant loss of dopaminergic neurons, DOPAL injections did not induce significant glial reaction in the substantia nigra. CONCLUSIONS: The present study provides the first in vivo quantification of substantia nigra pars compacta neuronal loss after injection of the endogenous toxin DOPAL. The results demonstrate that injections of DOPAL selectively kills SN DA neurons, suggests loss of striatal DA terminals, spares non-dopaminergic neurons of the pars reticulata, and triggers a behavioral phenotype (rotational asymmetry) consistent with other PD animal models. This study supports the "catecholaldehyde hypothesis" as an important link for the etiology of sporadic PD