Implications of Two Different Types of Diffusion for Biological Membranes

AS it is not widely appreciated that diffusion within complex media can be strikingly and often qualitatively different from that in simple liquids such as water, there is confusion concerning transport processes across biological membranes^1,2. We would like to draw attention to some fundamental differences between the diffusion process in simple liquids and that in more complex media-non-porous networks of hydrophobic polymers and biological membranes.     

Genetic and morphological variation in a partially isolated population of Caucasian shrew <Emphasis Type="Italic">Sorex satunini</Emphasis> (Mammalia)

Morphological and genetic variation at microsatellite loci of Caucasian shrew Sorex satunini Ogn. is examined and compared with that of the common shrew S. araneus L. Genetic distance at microsatellite loci between the common shrew and Caucasian shrew proved to be threefold higher than between chromosome races of the common shrew. The Caucasian shrew manifested low polymorphism in studies of both microsatellites and morphometric mandibular traits. The heterozygote deficit was also typical. These properties may be a consequence of partial isolation of the population and gene drift.     

Passive and active reactions of embryonic tissues to the action of dosed mechanical forces

With the help of a suction manometric device, the relation between the deformation of Xenonus laevis embryo at the gastrula and neurula stages and the value of the applied force has been studied. Stiffness modules of embryonic tissues were in the order of several dozens of Pascal and they were inversely proportional during deformation from 40 to 20%. At the gastrula stage, a uniform or an increasing rate of expansion of the embryo body in the suction capillary with the diameter of approximately half that of the embryo was observed for 30 min after the action of the suction forces. The length of the stretched portion of the embryo correlates with the value of its deformation at the first minute. As a result of the expansion, the total body surface area of the deformed embryo increases more than twice compared to intact embryos. After expelling the embryo from the capillary, its surface reduced and the deformation became smoothened within 5 min, which indicates the existence of tensional force in the expanded embryo. These data confirm that, at the embryo gastrula stage, external mechanical forces do not only passively deform the embryo but also initiate the active expansion of the embryo which takes place at zero external force and overcomes the tensional resistance of tissues. The mechanism of active expansion and its link with the processes of normal morphogenesis are discussed.     

Synthesis of positively charged galactose-bearing surfactants

An approach to the synthesis of cationic carbohydrate surfactants with potential antimicrobial and transfecting activities is proposed.     

Electron beam relaxation in nonuniform plasma of a steady-state beam-plasma discharge at moderately low gas pressures

Electron beam relaxation in plasma under conditions typical of laboratory plasma devices based on a steady-state beam-plasma discharge was investigated. It is shown that the measured dependences of the beam loss factor in a discharge operating at a moderately low gas pressure disagree with theoretical dependences calculated for a longitudinally uniform plasma. Analytic dependences obtained in the framework of quasilinear theory with allowance for longitudinal plasma inhomogeneity agree with experimental data. Some effects caused by the influence of the main discharge parameters on electron beam relaxation are analyzed.     

Changes in the size of the myocardial damaged area in postischemic reperfusion

The changes in the size of the myocardial injury area during reperfusion after the coronary occlusion-induced ischemia lasting 30 minutes are phasic in nature. Until 3.5 h the injured area increases and after 23.5 h relatively diminishes. After a more prolonged ischemia such manifestations are either unmarked or absent. Ischemia lasting from 30 min to 4 hours followed by reperfusion, as compared with ischemia of the same duration without reperfusion, normally gives rise to the formation of an area of injury, which is less or occasionally equal in size. The data obtained and reported indicate that in the area of coronary occlusion there are groups of cardiomyocytes that differ as regards the resistance to ischemia.     

Deadly liaisons: fatal attraction between CCN matricellular proteins and the tumor necrosis factor family of cytokines

Recent studies have revealed an unexpected synergism between two seemingly unrelated protein families: CCN matricellular proteins and the tumor necrosis factor (TNF) family of cytokines. CCN proteins are dynamically expressed at sites of injury repair and inflammation, where TNF cytokines are also expressed. Although TNFα is an apoptotic inducer in some cancer cells, it activates NFκB to promote survival and proliferation in normal cells, and its cytotoxicity requires inhibition of de novo protein synthesis or NFκB signaling. The presence of CCN1, CCN2, or CCN3 overrides this requirement and unmasks the apoptotic potential of TNFα, thus converting TNFα from a proliferation-promoting protein into an apoptotic inducer. These CCN proteins also enhance the cytotoxicity of other TNF cytokines, including LTα, FasL, and TRAIL. Mechanistically, CCNs function through integrin α₆β₁ and the heparan sulfate proteoglycan (HSPG) syndecan-4 to induce reactive oxygen species (ROS) accumulation, which is essential for apoptotic synergism. Mutant CCN1 proteins defective for binding α₆β₁-HSPGs are unable to induce ROS or apoptotic synergism with TNF cytokines. Further, knockin mice that express an α₆β₁-HSPG-binding defective CCN1 are blunted in TNFα- and Fas-mediated apoptosis, indicating that CCN1 is a physiologic regulator of these processes. These findings implicate CCN proteins as contextual regulators of the inflammatory response by dictating or enhancing the cytotoxicity of TNFα and related cytokines.