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The synthesis of a bis(arylphosphinito)amide pincer ligand P2ONO− designed to form two six-membered rings upon metallation is reported. Phosphination of a known bis(phenolato)amide ONO3− scaffold led to isolation of two isomers: the intended H(P2ONO) preligand with an amine moiety is formed as a kinetic product, which isomerizes via net oxidative addition of the amine N−H to phosphorous to yield a benzoxazaphosphole-containing thermodynamic product. Both isomers undergo productive metallation with NiBr2(dimethoxyethane) to produce the same complex, (P2ONO)NiBr. Treatment with triethylborohydride furnished the terminal hydride complex (P2ONO)NiH. The bromide and hydride complexes enabled comparisons of the steric and electronic properties of the P2ONO− ligand with other amide-based pincers.

Recent approaches to the homogeneous conversion of synthesis gas to organic chemicals and fuels are reviewed. Progress in this field is placed in the context of important industrially practiced transformations, such as the Fischer–Tropsch process for conversion of synthesis gas to higher alkanes, as well as previous attempts to produce a viable homogeneous alternative. Approaches to homogeneous syngas conversion discussed in some detail include the reduction of transition metal carbonyl complexes by main group hydrides or transition metal hydrides; unusual routes to formyls including radical-based late transition metal chemistry; early metal and lanthanide reductive couplings; cluster chemistry; and Lewis acid-assisted transformations. Our current research combines a number of these concepts in an attempt to convert syngas selectively to multicarbon organic fragments.

The mechanism by which low affinity adhesion molecules function to produce stable cell-cell adhesion is unknown. In solution, the interaction of human CD2 with its ligand CD58 is of low affinity (500 mM-1) and the interaction of rat CD2 with its ligand CD48 is of still lower affinity (40 mM-1). At the molecular level, however, the two systems are likely to be topologically identical. Fluorescently labeled glycosylphosphatidylinositol-anchored CD48 and CD58 were prepared and incorporated into supported phospholipid bilayers, in which the ligands were capable of free lateral diffusion. Quantitative fluorescence imaging was used to study the binding of cell surface human and rat CD2 molecules to the fluorescent ligands in contact areas between Jurkat cells and the bilayers. These studies provide two major conclusions. First, CD2/ligand interactions cooperate to align membranes with nanometer precision leading to a physiologically effective two-dimensional affinity. This process does not require the intact cytoplasmic tail of CD2. Second, the degree of membrane alignment that can be achieved by topologically similar receptors deteriorates with decreasing affinity. This suggests an affinity limit for the ability of this mode of cooperativity to achieve stable cell-cell adhesion at approximately 10 mM-1.

The effects of different cations on the hydrodynamic radius (RH) of a 48-bp synthetic DNA are measured by time-resolved fluorescence polarization anisotropy of intercalated ethidium. Relative statistical errors in RH are only approximately 1%. With increasing cation concentration, Na+ causes a small decrease in RH, Cs+ causes a somewhat larger decrease by up to 0.5 A at 100 mM, and (CH3CH2)4N+ causes an increase in RH by approximately 0.5 A at 100 mM. The qualitatively different effects of these monovalent cations indicates that the changes in RH with cation concentration do not arise primarily from electrolyte friction. Divalent cations cause much larger increases in RH with increasing cation concentration. Mg2+ causes an increase in RH by up to 1.0 A at 24.4 mM, and Mn2+ causes an increase in RH by up to 1.6 A at 24.4 mM. These effects are independent of DNA concentration. There is some positive correlation between the order of effects of the different cations on RH and the order of their effects on interhelical hydration forces. It is suggested that these different ions affect RH either by altering the hydration layer or possibly by some effect on DNA structure, such as stabilizing bends.

The seasonal course of carbon dioxide assimilation, leaf conductance, transpiration, leaf temperature, xylem pressure potentials, growth, foliage macro- and micronutrient element concentrations, and water- and nitrogen-use efficiencies were measured in juvenile, small-adult, and large-adult western juniper ( Juniperus occidentalis ) growing under ambient field conditions in eastern Oregon to explore the timing of, and seasonal limitations on, those processes. Highest daily total assimilation occurred during July and August; over the 15 month period juveniles had significantly higher daily total assimilation and transpiration per gram foliage than small adults or large adults. As soil water became limiting, total daily assimilation of juveniles and small adults declined to levels similar to those of large adults. Juveniles had the highest leaf conductance flux densities in all except three measurement periods, when leaf conductances in all three morphotypes were equally low. Juveniles also had the tightest stomatal control over water loss; however, during periods of low soil water, juveniles had the most negative xylem pressure potentials. Soil drought affected leaf conductance independent of plant water potentials or vapor pressure deficits. Juveniles had the capacity for higher carbon dioxide assimilation over a broader range of stomatal resistances and xylem pressure potentials than did small or large adults. Foliage nitrogen concentrations were usually highest in small adults and large adults. High rates of transpiration may be required to acquire an adequate supply of nitrogen, but nitrogen did not appear to be allocated preferentially to photosynthetic compounds. Potential photosynthetic nitrogen-use efficiences of J. occidentalis were very low compared with other growth forms. Branchlet elongation was greatest in June and July. Juveniles were more responsive to the changing environment than were small adults; large adults had the least seasonal variation in measured proceses.

Unexpected, sustained ventricular tachyarrhythmia after cardiac operations is differentiated from sustained ventricular tachycardia and ventricular fibrillation from known antecedent causes, such as recent or perioperative myocardial infarction, low cardiac output, preoperative ventricular arrhythmia, sympathomimetic drugs, drug toxicity, and metabolic abnormalities. Sixteen of 2364 patients (0.68%) who underwent heart operations met strict exclusion criteria for unexpected sustained ventricular tachyarrhythmia that occurred 1 hour to 12 days after operation. Recurrent ventricular tachyarrhythmias occurred in 12 patients; three died (21%), despite resuscitation from the initial episode. All patients had significant preoperative left ventricular dysfunction and 14 had ejection fractions below 30%. Fifteen of the 16 patients had monomorphic ventricular tachycardia at the initial episode. Empirically prescribed therapy was not effective in suppressing ventricular tachyarrhythmias inducible by programmed stimulation during postevent electrophysiologic studies in 10 of the 13 survivors. Inducibility was eventually prevented by drugs in nine patients, three patients received automatic implantable cardiac defibrillators, and one patient underwent successful catheter ablation of ventricular tachycardia. No patient died of recurrent ventricular tachyarrhythmias during the follow-up of 8 to 55 (mean 29) months after hospital discharge.

5-Hydroxytryptophan (5-HTP) elevated serum corticosterone concentrations when administered either intraperitoneally (i.p.) or intraventricularly. Inhibition of aromatic L-amino acid decarboxylase outside of the blood-brain barrier antagonized the corticosterone response, but only when the 5-HTP was given i.p. Stimulation of the pituitary-adrenocortical system by fenfluramine was not affected by 5,7-dihydroxytryptamine pretreatment, whereas the stimulation produced by quipazine administration was blocked by lesions of the basomedial hypothalamus. These results suggest that serotonergic drugs can act at multiple sites (i.e., both central and peripheral) to evoke a pituitary-adrenocortical response.

Pyknocytosis is a rare cause of haemolytic anaemia in utero and in the neonatal period. Two unusually severe cases of infantile pyknocytosis in 2 siblings are described. The first sibling, a male infant, was delivered prematurely at 37 wk. At birth the child had moderately severe jaundice and hepatosplenomegaly. The cord blood film showed marked pyknocytosis with numerous nucleated red cells. During the first 6 h of life the child developed clinical and laboratory evidence of disseminated intravascular coagulation. An attempt was made to do exchange transfusion but the child died 6 h after birth. The autopsy showed evidence of marked extramedullar erythropoiesis consistent with intrauterine haemolytic anaemia. The second infant of the parents was closely monitored during pregnancy as the history in the first infant had suggested severe intrauterine haemolysis. Amniocentesis was performed at 33 wk and 35 wk of gestation and showed an increase in bilirubin suggestive of a moderately severely affected infant. The baby was delivered by caesarean section at 35 wk and at birth showed evidence of haemolytic anaemia. Cord blood:haemoglobin 11.2 g/dl; PCV 36%; MCV 104 μ m 3 ; MCHC 32.7%; MCH 34 pg; reticulocyte count 21.3%; 126 nucleated red cells per 100 white cells; WCC 12,900 × 10 3 and platelet count 273 × 10 3 . Peripheral blood showed marked pyknocytosis very similar to the blood film of the first infant. The investigations to exclude enzyme deficiencies such as G6-PD, P-K. and glutathione reductase were normal. β -lipoproteins were also normal. No Heinz bodies were detected. To control hyperbilirubinaemia, the baby required 3 exchange transfusions. Despite exchange transfusions pyknocytosis persisted with evidence of recurrence of anaemia. The pyknocytosis and haemolytic anaemia persisted until 4 mth of age. A previous report suggested that the erythrocyte abnormality may have resulted from a plasma factor present in the affected infants. However, in our patient red cell morphology was not corrected by incubating the red cells with fresh plasma, nor were normal erythrocytes affected when incubated with the infant’s plasma. It would appear therefore that the erythrocyte abnormality is a transient but intrinsic abnormality of red cell membrane.