Radionuclides in the Kara sea bottom sediments

The contents and distribution of natural (214Pb, 214Bi, 228Ac, and 208Tl) and technogenic (90Sr, 137Cs, and 60Co) radionuclides in the Kara Sea bottom sediments was analyzed by using the materials collected by R/V "Pomor" (Murmansk Marine Biological Institute). In 1994, no high (critical) concentrations of technogenic radioisotopes were found in the sea sediments, while the spots (regions) of elevated 137Cs content found in 1984 were not confirmed in 1994. It was proposed that the main sources of entry of technogenic radionuclides in the sea sediments in the last years are the flow of the Ob'-Yenisei waters and container burials of radioactive waste in the sea, which appeared to have been markedly corroded. The latter is confirmed by detection in some places of 60Co, which was not previously found in the sediments.     

Native serotonin 5-HT3 receptors expressed in Xenopus oocytes differ from homopentameric 5-HT3 receptors

Efficacies of the 5-hydroxytryptamine (serotonin) 5-HT3 receptor (5-HT3R) agonists 2-methyl-5-HT, dopamine, and m-chlorophenylbiguanide on 5-HT3R native to N1E-115 cells and on homopentameric 5-HT3R expressed in Xenopus oocytes were determined relative to that of 5-HT. Efficacies of 2-methyl-5-HT and dopamine on 5-HT3R native to differentiated N1E-115 cells are high (54 and 36%) as compared with their efficacies on homopentameric 5-HT3R-A(L) and 5-HT3R-A(S) receptors expressed in oocytes (4-8%). m-Chlorophenylbiguanide does not distinguish between 5-HT3R in N1E-115 cells and in oocytes. The distinct pharmacological profile of 5-HT3R native to differentiated N1E-115 cells is conserved when poly(A)+ mRNA from these cells is expressed in oocytes. The results indicate that, apart from the known 5-HT3R subunits, N1E-115 cells express additional proteins involved in 5-HT3R function.     

Presidential reflections

Two direct methods for the diagnosis of trichinellosis were compared: trichinoscopy and artificial digestion. Muscles from 17 wistar rats, orally infected with 500 Trichinella spiralis encysted larvae were examined. From each of the following muscles: diaphragm, tongue, masseters, intercostals, triceps brachialis and cuadriceps femoralis, 648,440 larvae from 1 g samples were recovered. The linear correlation between trichinoscopy and artificial digestion was very high and significant (r = 0.94, p < 0.0001), showing that both methods for the detection of muscular larvae did not differ significantly. In both methods, significant differences were found in the distribution of larvae per gramme of muscle.     

A lysine to arginine substitution at position 146 of rabbit aldolase A changes the rate-determining step to Schiff base formation

Lys146 of rabbit aldolase A [D-fructose-1,6-bis(phosphate):D-glyceraldehyde-3-phosphate lyase, EC 4.1.2.13 [EC] ] was changedto arginine by site-directed mutagenesis. The k_cat of the resultingmutant protein, K146R, was 500 times slower than wild-type insteady-state kinetic assays for both cleavage and condensationof fructose-1,6-bis(phosphate), while the Km for this substratewas unchanged. Analysis of the rate of formation of catalyticintermediates showed K146R was significantly different fromthe wild-type enzyme and other enzymes mutated at this site.Single-turnover experiments using acid precipitation to trapthe Schiff base intermediate on the wild-type enzyme failedto show a build-up of this intermediate on K146R. However, K146Rretained the ability to form the Schiff base intermediate asshown by the significant amounts of Schiff base intermediatetrapped with NaBH₄. In the single-turnover experiments it appearedthat the Schiff base intermediate was converted to productsmore rapidly than it was produced. This suggested a maximalrate of Schiff base formation of 0.022 s^–1, which wasclose to the value of k_cat for this enzyme. This observationis strikingly different from the wild-type enzyme in which Schiffbase formation is >100 times faster than k_cat. For K146Rit appears that steps up to and including Schiff base formationare rate limiting for the catalytic reaction. The carbanionintermediate derived from either substrate or product, and theequilibrium concentrations of covalent enzyme-substrate intermediates,were much lower on K146R than on the wild-type enzyme. The greaterbulk of the guanidino moiety may destabilize the covalent enzyme-substrateintermediates, thereby slowing the rate of Schiff base formationsuch that it becomes rate limiting. The K146R mutant enzymeis significantly more active than other enzymes mutated at thissite, perhaps because it maintains a positively charged groupat an essential position in the active site or perhaps the Argfunctionally substitutes as a general acid/base catalyst inboth Schiff base formation and in subsequent abstraction ofthe C4-hydroxyl proton.     

Effect of vanadium and chromium on the microstructural features of V–Cr–Mn–Ni spheroidal carbide cast irons

The objective of this investigation is to study the influence of vanadium（5.0wt%–10.0wt%） and chromium（0–9.0wt%） on the microstructure and hardness of Cr-V-Mn-Ni white cast irons with spheroidal vanadium carbides. The alloys＇ microstructural features are presented and discussed with regard to the distribution of phase elements. The structural constituents of the alloys are spheroidal VC, proeutectoid cementite, ledeburite eutectic, rosette-shaped carbide eutectic（based on M7C3）, pearlite, martensite, and austenite. Their combinations and area fraction（AF） ratios are reported to be influenced by the alloys＇ chemical composition. Spheroidized VC particles are found to be sites for the nucleation of carbide eutectics. Cr and V are shown to substitute each other in the VC and M7C3 carbides, respectively. Chromium alloying leads to the formation of a eutectic（γ-Fe ＋ М7С3）, preventing the appearance of proeutectoid cementite in the structure. Vanadium and chromium are revealed to increase the total carbide fraction and the amount of austenite in the matrix. Cr is observed to play a key role in controlling the metallic matrix microstructure.     

Yield stress distribution in injection‐moulded glassy polymers

A methodology for structural analysis simulations is presented that incorporates the distribution of mechanical properties along the geometrical dimensions of injection‐moulded amorphous polymer products. It is based on a previously developed modelling approach, where the thermomechanical history experienced during processing was used to determine the yield stress at the end of an injection‐moulding cycle. Comparison between experimental data and simulation results showed an excellent quantitative agreement, both for short‐term tensile tests as well as long‐term creep experiments over a range of strain rates, applied stresses, and testing temperatures. Changes in mould temperature and component wall thickness, which directly affect the cooling profiles and, hence, the mechanical properties, were well captured by the methodology presented. Furthermore, it turns out that the distribution of the yield stress along a tensile bar is one of the triggers for the onset of the (strong) localization generally observed in experiments. © 2015 Society of Chemical Industry     

Cardiovascular effects of platelet-activating factor

Sudden release of platelet-activating factor (PAF) into the circulation can cause hypotension, tachycardia, and circulatory collapse. To further examine this response, we performed detailed studies of cardiovascular function after PAF administration to young domestic pigs and newborn piglets. Our results indicate that circulatory dysfunction after PAF reflects severe constriction of pulmonary resistance vessels and consequent acute right ventricular failure. Although PAF-induced coronary artery constriction and contractile depression may be complicating problems, left ventricular underperfusion and dysfunction after PAF are mainly the result of systemic arterial hypotension and diminished left ventricular filling. The adverse hemodynamic effects of PAF are accompanied by substantial release of thromboxane A₂ (TxA₂). These effects are mimicked by the TxA₂ agonist U-46619 and partially blocked by specific and nonspecific inhibitors of TxA₂ synthesis (OKY-046 and indomethacin). Even more potent blockade of PAF action is exerted by the TxA₂ receptor blocker, SQ 29,548. Taken together, these findings indicate that severe pulmonary vascular constriction and hemodynamic collapse soon after intravenous PAF are at least partially mediated by PAF-induced TxA₂ release. Tachyphylaxis to PAF influence has been observed in studies of leukocyte and platelet function. We hypothesized that tachyphylaxis to PAF might also occur in our studies of constrictor responses in pulmonary vessels. Recently, we have examined the capacity of PAF to produce sustained pulmonary vasoconstriction in openchested, anesthetized newborn piglets. Infusions sufficient to produce 100% increase in mean pulmonary artery pressure after 3 min showed no loss of efficacy when sustained for 30 min. The same was true for infusions of U-46619. Thus, the pulmonary vasoconstrictor influence of PAF or U-46619 is not readily diminished by tachyphylaxis. These findings favor the viewpoint that PAF or TxA₂ release during inflammatory processes could have prolonged adverse actions on pulmonary and systemic circulations. Based on a paper presented at the Third International Conference on Platelet-Activating Factor and Structurally Related Alkyl Ether Lipids, Tokyo, Japan, May 1989. The opinions or assertions contained here are those of the authors. They do not reflect the views of the Department of Defense or the Uniformed Services University of the Health Sciences. The experiments reported here were conducted according to the principles set forth in the “Guide for the Care and Use of Laboratory Animals,” Institute of Laboratory Animal Resources, U.S. Department of Health and Human Services (NIH Publ. 85-23, 1985).     

A new serum alpha-amylase assay of high sensitivity

This four-week study included 336 patients aged eleven to 80 years with complaints suggestive of stress-related emotional lability, and was intened to discover a possible relationship between the effects of pimozide and the initial psychic defence phenomena in this condition: the discouragement type of reaction was registered in 243 cases, overcompensation in 80, and a mixture of the two in the remaining 13. In most cases, the daily dose of pimozide remained close to the initial 2 mg, and treatment could be entirely discontinued after three-four weeks in five patients. Control evaluation after two and four weeks revealed a significant improvement of all pathological scores of a 17-item questionnaire, but failed to show any susbstantial difference between the three subgroups. No side-effects were reported.     

Natural history and evaluation of ST segment changes and MB CK release in acute myocardial infarction

The experimental evidence relating ST segment elevation in the electrocardiogram to the progress and extent of ischaemic myocardial damage is discussed. There are difficulties in applying this to patients: the reproducibility of praecordial mapping was tested using a multiple analysis of variance. This showed that factors such as time after the onset of myocardial infarction and posture can affect measurements of sigmaST elevation significantly. There was a pattern of changes in segmaST elevation and of changes in plasma MB CK activity in a group of patients with uncomplicated anterior infarction. A significant byt weak correlation was found between sigmaST elevation in the first hour and the total MB CK activity released into the plasma, but not at any other time. The use of sigmaST elevation as a measure of the extent of ischaemic damage is unreliable. In 5 patients with a variety of complications of acute anterior infarction, changes in sigmaST elevation werr significantly different from the uncomplicated group, and MB CK release profiles suggested further necrosis. The pattern and time course of ST segment changes may be of use in assessing the progress of ischaemic myocardial damage.