Absorption by the bovine retina of physiological concentration of PLP-GABA increase clearing 2-32 minutes of incubation in difference of GABA and its non metabolic preparations, which store up as much as possible in first minutes: picamilon > PLP-GABA > GABA > panthogam > biotinil-GABA. Kinetics of transport of GABA and its preparations into retina has a complex character. By the growth of concentration from 33 mM to 528 mM, it is linear for picamilion, showing diffusion, and not linear for GABA, PLP-GABA and panthogam, showing differently systems of its transport. And only GABA transport is activated by Na-ions.
Americium-241 (²4¹Am) is the second most significant radiation hazard after ²³?Pu at some of the Mayak Production Association facilities. This study summarizes current data on the accumulation, distribution, and excretion of americium compared with plutonium in different organs from former Mayak PA workers. Americium and plutonium were measured in autopsy and bioassay samples and correlated with the presence or absence of chronic disease and with biological transportability of the aerosols encountered at different workplaces. The relative accumulation of ²4¹Am was found to be increasing in the workers over time. This is likely from ²4¹Pu that increases with time in reprocessed fuel and from the increased concentrations of ²4¹Am and ²4¹Pu in inhaled alpha-active aerosols. While differences were observed in lung retention with exposures to different industrial compounds with different transportabilities (i.e., dioxide and nitrates), there were no significant differences in lung retention between americium and plutonium within each transportability group. In the non-pulmonary organs, the highest ratios of ²4¹Am/²4¹Am + SPu were observed in the skeleton. The relative ratios of americium in the skeleton versus liver were significantly greater than for plutonium. The relative amounts of americium and plutonium found in the skeleton compared with the liver were even greater in workers with documented chronic liver diseases. Excretion rates of ²4¹Am in ‘‘healthy’’ workers were estimated using bioassay and autopsy data. The data suggest that impaired liver function leads to reduced hepatic ²4¹Am retention, leading to increased ²4¹Am excretion.
Human plasminogen isolated from the placenta serum fraction by means of affinity chromatography was activated by trypsin being in covalent bond with sepharose. The activation is studied as dependent on pH, temperature and the proenzyme-activator ratio in the presence of 25% glycerol as a stabilizing agent and without it. Utilization of the immobilized trypsin as a plasminogen activator makes it possible to transform completely the proenzyme to plasmin varying the plasminogen-trypsin ratio and time of activation when it is conducted under optimal conditions: in the presence of 25% glycerol at pH 7.0-7.1 and the temperature of 30 degrees C.
Polar fishes are known to have serum proteins and glycoproteins that protect them from freezing, by a noncolligative process. Measurements of antifreeze concentrations in ice and scanning electron micrographs of freeze-dried antifreeze solutions indicate that the antifreezes are incorporated in ice during freezing. The antifreezes also have a pronounced effect on the crystal habit of ice grown in their presence. Each of four antifreezes investigated caused ice to grow in long needles whose axes were parallel to the ice c axis. Together these results indicate the antifreezes adsorb to ice surfaces and inhibit their growth. A model in which adsorbed antifreezes raise the curvature of growth steps on the ice surface is proposed to account for the observed depression of the temperature at which freezing occurs and agrees well with experimental observations. The model is similar to one previously proposed for other cases of crystal growth inhibition.
Normal aging of the rodent heart results in prominent prolongation of the twitch. We tested the hypothesis that increased expression of beta-myosin heavy chain (MHC), as occurs in the normal aging process in the rodent heart, contributes to the prolongation of the twitch by depressing the kinetics of cross-bridge interaction. Using 3-, 9-, 21-, and 33-mo-old male Fischer 344 x Brown Norway F1 hybrid rats, we examined both the rate of tension development (kCa) and unloaded shortening velocity in chemically skinned myocardium. Although kCa in all four age groups was dependent on the level of Ca2+ activation, both submaximal and maximal kCa were significantly slower in 9-, 21-, and 33-mo-old rats relative to 3-mo-old rats. Furthermore, unloaded shortening velocity was significantly reduced in 9-, 21-, and 33-mo-old rats compared with 3-mo-old rats. Collectively, these data strongly suggest that the aging-related increase in beta-MHC expression results in a progressive slowing of cross-bridge interaction kinetics in skinned myocardium, which most likely contributes to the overall aging-dependent reduction in myocardial functional capacity.
Environmental exposure during pregnancy may have lifelong health consequences for the offspring and some studies have association between maternal exposure to air pollution during pregnancy and offspring's birth weight. However, many of these studies do not take into account small-scale variations in exposure, residential mobility, and work addresses during pregnancy. We used information from the National Birth Registry of Norway to examine associations between ambient environmental exposure such as air pollution and temperature, and offspring's birth weight taking advantage of information on migration history and work address in a large population-based cohort. A dispersion model was used to estimate ambient air pollution levels at all residential addresses and work addresses for a total of 25,229 pregnancies between 1999 and 2002 in Oslo, Norway. Ambient exposure to traffic pollution for the entire pregnancy was associated with a reduction in term birth weight in crude analyzes when comparing children of the highest and lowest exposed mothers. No evidence for an association between exposure to traffic pollution at home and work addresses and term birth weight after adjustment for covariates known to influence birth weight during pregnancy. After stratification, small statistically non-significant reductions were present but only for multiparious mothers. This group also had less residential mobility and less employment during pregnancy. The overall findings suggest no clear association between term birth weight and traffic pollution exposure during pregnancy. However, mobility patterns could introduce possible confounding when examining small-scale variations in exposure by using addresses. This could be of importance in future studies.
Substrate properties of various morpholinonucleoside triphosphates in the reaction of DNA elongation catalyzed by DNA polymerase beta, reverse transcriptase of human immunodeficiency virus (HIV-1 RT), and reverse transcriptase of Moloney murine leukemia virus (M-MuLV RT) were compared. Morpholinonucleoside triphosphates were utilized by DNA polymerase beta and HIV-1 reverse transcriptase as substrates, which terminated further synthesis of DNA, but were virtually not utilized by M-MuLV reverse transcriptase. The kinetic parameters of morpholinoderivatives of cytosine (MorC) and uridine (MorU) were determined in the reaction of primer elongation catalyzed by DNA polymerase beta and HIV-1 reverse transcriptase. MorC was a more effective substrate of HIV-1 reverse transcriptase and significantly less effective substrate of DNA polymerase beta than MorU. The possible use of morpholinonucleoside triphosphates as selective inhibitors of HIV-1 reverse transcriptase is discussed.
Human genetics link Alzheimer's disease pathogenesis to excessive accumulation of amyloid-beta (Abeta) in brain, but the symptoms do not correlate with senile plaque burden. Since soluble Abeta aggregates can cause synaptic dysfunctions and memory deficits, these species could contribute to neuronal dysfunction and dementia. Here we explored selective targeting of large soluble aggregates, Abeta protofibrils, as a new immunotherapeutic strategy. The highly protofibril-selective monoclonal antibody mAb158 inhibited in vitro fibril formation and protected cells from Abeta protofibril-induced toxicity. When the mAb158 antibody was administered for 4 months to plaque-bearing transgenic mice with both the Arctic and Swedish mutations (tg-ArcSwe), Abeta protofibril levels were lowered while measures of insoluble Abeta were unaffected. In contrast, when treatment began before the appearance of senile plaques, amyloid deposition was prevented and Abeta protofibril levels diminished. Therapeutic intervention with mAb158 was however not proven functionally beneficial, since place learning depended neither on treatment nor transgenicity. Our findings suggest that Abeta protofibrils can be selectively cleared with immunotherapy in an animal model that display highly insoluble Abeta deposits, similar to those of Alzheimer's disease brain.