Electrophoretic Mobility of a Water-in-Oil Droplet Separately Affected by the Net Charge and Surface Charge Density.

Water-in-oil emulsions and droplets exhibit physicochemical properties completely different from those of oil-in-water emulsions and droplets. Thus, directly applying a standard theoretical model to water-in-oil systems cannot describe these anomalous properties. Here, the electrophoretic mobility of a water-in-oil droplet is analytically investigated using Debye-Hückel linearization and neglecting the Marangoni effect. The resulting electrophoretic mobility is shown to be separately dependent on the net charge of the droplet and the surface charge density at the droplet interface. Furthermore, when the net charge is negligible, the electrophoretic mobility is proportional to the surface charge density with a negative coefficient. This indicates that the internal electric double layer inversely contributes to the electrophoresis. This theory is applied to experimental data of water-in-oil emulsions and droplets in the literature, and qualitative and quantitative verification of the theory is discussed.

Thyroid-related ophthalmopathy development in concurrence with growth hormone administration.

BACKGROUND: Thyroid stimulating hormone (TSH) receptor and local infiltrate lymphocytes have been considered as major pathological factors for developing thyroid-related ophthalmopathy. Overexpression of insulin-like growth factor-I (IGF-I) receptor has emerged as a promising therapeutic target for refractory patients. However, the relationship between activation of growth hormone (GH)/IGF-I receptor signaling and development or exacerbation of thyroid ophthalmopathy has not been elucidated. Herein we describe a case that provides further clarification into the association between thyroid-related ophthalmopathy and GH/IGF-I receptor signaling. CASE PRESENTATION: A 62-year-old Japanese female diagnosed with thyroid-related ophthalmopathy was admitted to Kurume University Hospital. She had received daily administration of GH subcutaneously for severe GH deficiency; however, serum IGF-I levels were greater than + 2 standard deviation based on her age and sex. She exhibited mild thyrotoxicosis and elevation in levels of TSH-stimulating antibody. Discontinuation of GH administration attenuated the clinical activity scores of her thyroid-related ophthalmopathy. Additionally, concomitant use of glucocorticoid and radiation therapies resulted in further improvement of thyroid-related ophthalmopathy. The glucocorticoid administration was reduced sequentially, followed by successful termination. Thereafter, the patient did not undergo recurrence of thyroid-related ophthalmopathy and maintained serum IGF-I levels within normal physiological levels. CONCLUSIONS: We describe here a case in which development of thyroid-related ophthalmopathy occurred upon initiation of GH administration. GH/IGF-I signaling was highlighted as a risk factor of developing thyroid-related ophthalmopathy. Additionally, aberrant TSH receptor expression was suggested to be a primary pathophysiological mechanism within the development of thyroid-related ophthalmopathy. Physicians should be aware of the risks incurred via GH administration, especially for patients of advanced age, for induction of thyroid-related ophthalmopathy.

Remarks on muscle contraction mechanism II. Isometric tension transient and isotonic velocity transient.

Mitsui and Ohshima (2008) criticized the power-stroke model for muscle contraction and proposed a new model. In the new model, about 41% of the myosin heads are bound to actin filaments, and each bound head forms a complex MA(3) with three actin molecules A1, A2 and A3 forming the crossbridge. The complex translates along the actin filament cooperating with each other. The new model well explained the experimental data on the steady filament sliding. As an extension of the study, the isometric tension transient and isotonic velocity transient are investigated. Statistical ensemble of crossbridges is introduced, and variation of the binding probability of myosin head to A1 is considered. When the binding probability to A1 is zero, the Hill-type force-velocity relation is resulted in. When the binding probability to A1 becomes finite, the deviation from the Hill-type force-velocity relation takes place, as observed by Edman (1988). The characteristics of the isometric tension transient observed by Ford, Huxley and Simmons (1977) and of the isotonic velocity transient observed by Civan and Podolsky (1966) are theoretically reproduced. Ratios of the extensibility are estimated as 0.22 for the crossbridge, 0.26 for the myosin filament and 0.52 for the actin filament, in consistency with the values determined by X-ray diffraction by Wakabayashi et al. (1994).

Surface potential of phosphoinositide membranes: comparison between theory and experiment.

Surface potential of lipid membranes made of phosphatidylcholine (PC) and one of the phosphoinositides (PPI); PI, PIP or PIP(2), was studied by using the electrophoretic mobility of these lipid membrane vesicles, and a theoretical model of the surface potential developed for these membranes containing PPIs. By using the measured zeta-potential for the PI/PC membranes and a well-known surface potential theory, the inositol ring of the PI molecule was found to extend into the aqueous phase approximately normal to the membrane surface for various PI/PC ratios investigated. The outer edge of the inositol ring is located at about 5.2A from the phosphate group conjugated with the glycerol of the phospholipids. The inositol group was slightly tilted from the membrane normal direction. For both PIP/PC and PIP(2)/PC membranes, the analyses of surface potential using the measured zeta-potential values and the surface potential theory which was developed for these membranes gave consistent results with respect to the slipping layer distance from the second surface charge layer. The conclusion is that the experimental data can be fairly well resolved by using a linearized Poisson-Boltzmann surface potential equation set up for a PPI/PC membrane model up to a certain concentration of PPI in PC membranes. Our theoretical model made for these membrane surface potentials seems to be reasonable for analysis of electrical surface phenomena for these PPI/PC membranes containing small concentrations of PPI molecules.

Proposed model for the flagellar rotary motor.

Flagellated bacteria swim by rotating helical filaments driven by motors embedded in the cell wall and cytoplasmic membrane. A model is proposed to explain the mechanism of the motor. The protons passing through the channels induce a strong electric field in Mot molecules. This field originates an impulse force to cause the flagellar rotation if the following conditions are fulfilled: (a) Mot molecules have a spontaneous electric polarization. (b) The lipid bilayers are viscoelastic. (c) There is a delay of deformation in response to stress in Mot molecules. The conclusions driven from the model are in agreement with the following experimental observations, denoting the flagellar rotation velocity as omega. (1) The torque is practically constant independent of omega from 0 to a critical value omega(cr) and then decreases sharply. (2) When omega is smaller than omega(cr), the torque varies little with temperature. (3) The critical velocity omega(cr) shifts to lower speed at lower temperatures. (4) Where omega is larger than omega(cr), declining of the torque steepens at lower temperatures. (5) When omega is smaller than omega(cr), one revolution of the flagellar rotation consists of a constant number of steps. (6) When omega is smaller than omega(cr), omega is proportional to the transmembrane potential difference. (7) The stator produces constant torque even when the stator is rotated relative to the rotor by external forces. (8) How the flagellar rotation velocity changes when the direction of the proton passage is reversed. (9) The motor has a switch that reverses the sense of the flagelllar rotation with the same absolute value of torque.

Therapeutic effect of in vivo sustained estradiol release from poly (lactide-co-glycolide) microspheres on bone mineral density of osteoporosis rats.

Poly (lactide-co-glycolide or PLGA) microspheres containing 0.3% (w/w) of estradiol were prepared by a solvent evaporation method. These PLGA microspheres had a wide particle distribution between 0.5 and more than 100 microm. The average size was 76 microm. Physicochemical properties of the microspheres were characterized by X-ray diffraction patterns, FT-IR spectra and DSC. In vitro estradiol release was maintained at a constant rate from these PLGA microspheres for 1 month. The loaded drug was totally recovered in the collection buffer within this time period. In vivo experiments were performed on Wistar rats that had received ovariectomy. These rats were fed with a vitamin D-deficient and Ca-deficient diet. The combination of ovariectomy and diet induced osteoporosis. PLGA microspheres containing either 50, 100, or 200 microg estradiol were injected into these rats. The plasma estradiol in each rat was monitored for 50 days. These in vivo drug release patterns were found to be different from the one obtained from in vitro release. The Ca-AUC was not significant different among various dosages administered. However, bone mineral density for rats after the injection of estradiol loaded microspheres was higher than that obtained for the control. This suggested that all estradiol microspheres administration induced bone generation in osteoporosis rats.