CLINICAL POTASSIUM PROBLEMS

Alterations in serum potassium are common in many diseases. In a series of 390 determinations of serum potassium, the levels found were low in 24 per cent and high in 2.6 per cent.The major causes of low serum potassium are (1) decreased potassium intake due to intravenous feedings which do not contain potassium; (2) increased loss of potassium in the urine due to accelerated tissue breakdown, or renal lesions; (3) loss from the gastrointestinal tract due to diarrhea, or fistulae, and (4) shift between serum and cells, due to metabolic causes, drugs or changes in pH.The major cause of high serum potassium is uremia with renal retention.Clinical symptoms and signs of low body potassium include muscle weakness and paralysis, which may lead to death in respiratory failure if not corrected, tachycardia, gallop rhythm, dilatation of the heart. The electrocardiogram shows inverted, low amplitude, or isoelectric T waves and a prolonged QT interval.Potassium chloride orally, subcutaneously or intravenously is recommended for use in the treatment of potassium deficits. It should not be used in the presence of oliguria or anuria or dehydration. The amounts of potassium necessary to correct deficits vary widely and cannot be predicted from the serum level. Special reference is made to the prevention and therapy of potassium deficits in diabetic acidosis.High serum potassium levels are difficult to correct. Suggested measures are administration of glucose, insulin or calcium, gastric or peritoneal lavage or use of the artificial kidney.     

Theoretical prediction of devitrification tendency: determination of critical warming rates without using finite expansions

Previously, critical warming rates vcr above which ice did not have enough time to crystallize had been roughly evaluated for many wholly amorphous aqueous solutions. These evaluations were obtained by extrapolation of the linear variation of the devitrification temperature Td with log v, where v is the warming rate, observed experimentally between 2.5 and 80 degrees C/min. Theory also gives such a linear variation, but only using the first term of a finite expansion. The other terms can be neglected only for small variations of Td. These evaluations were sufficient for classification of the solutions, but large errors were made in vcr. A new and more accurate method of determination of the variation of Td with v is presented here. The general equation giving in our models the derivative of the quantity of ice formed versus temperature T is differentiated, instead of integrated using a finite expansion. This gives an explicit expression of v versus Td assuming that the ratio xd of the quantity of ice formed at Td to the total quantity of ice formed on warming is constant. Experimentally, xd is constant within a good approximation. Theoretical curves representing the variation of Td with v have been drawn for solutions of 35 or 45% (w/w) 1,2-propanediol in water. Td never reaches the temperature of the end of melting Tm, but as v tends toward infinity, Td tends toward an asymptotic value of 0.96Tm for 35% solute. For that solution, above about 10(3) degrees C/min, Td deviates appreciably from linearity with log v, but 1/Td remains almost linear with log v up to Td congruent to 0.95Tm. Therefore, systematic comparison of the theoretical variation of Td with v with a linear variation of 1/Td with log v has been done, varying the parameters of the equations within the entire experimental range. Similar conclusions can be given for all the solutions. Experimentally for Td = 0.95Tm, the quantity of ice crystallized is generally less than 0.1% of the solution, reaching 1% only once. Therefore, a new definition of the critical warming rate vcr has been used, corresponding to extrapolation of the linear variation of 1/T with log v up to Td = 0.95Tm. New values of vcr have been calculated for all the binary systems previously studied. The order of the solutions is almost the same, but the new values of vcr are significantly smaller than the former.     

Experimental dissection of devitrification in aqueous solutions of 1,3-butanediol

Devitrification is a major problem which must be overcome for successful organ cryopreservation. Devitrification can be initiated on fracture planes and on bubbles, but the focus of attention here is on devitrification by ordinary heterogeneous and homogeneous mechanisms, which are the most relevant for organ preservation by vitrification. The purpose of the present studies was to define the devitrification process: to determine nucleation rates, ice-crystal growth rates, and the distribution of ice-crystal size and to evaluate the applicability of existing quantitative models of these processes which have successfully approximated the behavior of other aqueous systems. The present work was done using differential scanning calorimetry and cryomicroscopy. The amount of ice formed has been estimated for highly concentrated solutions. Kinetic parameters are presented here for isothermal conditions and continuous heating rate experiments. The classical theory based on the Johnson-Avrami equation has been evaluated and the results are compared with the theory of Boutron. The agreement is good for the continuous heating rate conditions, but results differ for the isothermal conditions.     

Four new species of Cerambycidae (Coleoptera) from Paraguay

Four new species of Cerambycidae are described from Paraguay: Eranina tomentilla (Hemilophini); Mimasyngenes concolor (Desmiphorini); Recchia drechseli (Aerenicini); and Microibidion bimaculatum (Neoibidionini). The new species are included in known keys.     

Incorporation of eel electroplax acetylcholinesterase into black lipid membranes. A possible model for the cholinergic receptor

Addition of low concentrations of acetylcholine or carbamylcholine to solutions bathing a black lipid membrane into which electroplax acetylcholinesterase has been incorporated elicits a dramatic increase in the membrane conductance. This change is prevented or reversed by addition of neostigmine or atropine to the system. The magnitude of the conductance increase of the acetylcholinesterase-treated membrane is proportional to the fourth power of the carbamylcholine concentration and, at constant carbamylcholine concentration, to the fourth power of the enzyme concentration in the medium.     

Stoichiometric relation of protein components in cerebral myelin from different species

Abstract— In cerebral myelin from man, ox, rabbit, guinea pig and chicken, the amounts of proteolipid protein, basic protein and the fraction of further protein components were found to be present in a fixed ratio of 5·0: 3·5: 2·0 by weight. The molecular weights of 25,000 and 35,000 as obtained for the basic protein and proteolipid protein might indicate that cerebral myelin contains one molecule of basic protein per molecule of proteolipid protein. This fixed ratio of protein components was found to be changed in myelin from the PNS and in cerebral myelin from rat and carp, with their exceptional basic proteins. Using the polyacrylamide-gel electrophoresis it was possible to demonstrate that a homogeneous structural protein (the Folch-Lees proteolipid protein) constitutes about 50 percent of the total amount of myelin proteins in all species studied. An attempt was made to correlate myelin protein and lipid patterns from various species.     

Modification of the aggregation state of the multifunctional enzyme complex catalyzing the first steps in pyrimidine biosynthesis in the course of development of Drosophila melanogaster

Mutations at the bithoraxoid (bxd) and postbithorax (pbx) loci cause a transformation of posterior haltere to posterior wing. It has previously been shown that pbx and $\text{pbx}\text{Ubx}{}^{101}$ cause this transformation by affecting the maintenance (or cell heredity function) of determination so that the transformed cells are indistinguishable from normal wing cells, and have no “memory” of having been part of a haltere disk (Adler, 1978a). I report here that Tp(3) $\text{bxd}{}^{100}\text{Ubx}{}^{101}$ and bxd¹, pbx, e^w both cause the transformation of posterior haltere to posterior wing in the same way as pbx. On the other hand, bxd¹, $\text{bxd}{}^1\text{Ubx}{}^{101}$, bxd^51j, $\text{bxd}{}^{\mathrm{<mtext>51</mtext><mtext>j</mtext>}}\text{Ubx}{}^{101}$, and $\text{bxd}{}^{\mathrm{<mtext>51</mtext><mtext>j</mtext>}}\text{red pbx}$ cause this same transformation of posterior haltere to posterior wing by interfering with the expression of the determined state so that the developmental information of posterior haltere is “misread” as posterior wing. The transformed cells in these disks retain the memory of having been part of a haltere disk; that is, these posterior cells that would secrete wing cuticle during metamorphosis regenerate anterior haltere structures. Thus it appears clear that it is possible to uncouple the expression and cell heredity functions of determination in the haltere disk of Drosophila.     

Insights into dimerization and four-helix bundle formation found by dissection of the dimer interface of the GrpE protein from Escherichia coli

The GrpE heat shock protein from Escherichia coli has a homodimeric structure. The dimer interface encompasses two long alpha-helices at the NH(2)-terminal end from each monomer (forming a "tail"), which lead into a small four-helix bundle from which each monomer contributes two short sequential alpha-helices in an antiparallel topological arrangement. We have created a number of different deletion mutants of GrpE that have portions of the dimer interface to investigate requirements for dimerization and to study four-helix bundle formation. Using chemical crosslinking and analytical ultracentrifugation techniques to probe for multimeric states, we find that a mutant containing only the long alpha-helical tail portion (GrpE1-88) is unable to form a dimer, most likely due to a decrease in alpha-helical content as determined by circular dichroism spectroscopy, thus one reason for a dimeric structure for the GrpE protein is to support the tail region. Mutants containing both of the short alpha-helices (GrpE1-138 and GrpE88-197) are able to form a dimer and presumably the four-helix bundle at the dimer interface. These two mutants have equilibrium constants for the monomer-dimer equilibrium that are very similar to the full-length protein suggesting that the tail region does not contribute significantly to the stability of the dimer. Interestingly, one mutant that contains just one of the short alpha-helices (GrpE1-112) exists as a tetrameric species, which presumably is forming a four-helix bundle structure. A proposed model is discussed for this mutant and its relevance for factors influencing four-helix bundle formation.