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Provides insights on how visiting professors might affectively contribute as members of faculty and questions the emphasis to methodology at the expense of the commitment to the ideological and moral base of social work. (Editor/PG)

A 5'-nucleotidase with unique specificity has been identified in the soluble fraction of normal human erythrocytes. It mediates the hydrolytic dephosphorylation of pyrimidine 5'-ribosemonophosphates but is catalytically ineffective with purine nucleotides or with the 2'-, 3'-, or cyclic isomers of pyrimidine nucleotides. Activities at 37 degrees in dialyzed hemolysates of nromal human erythrocytes averaged 7.3 and 6.2 mumol of Pi liberated per hour per g of hemoglobin for the substrates UMP and CMP, respectively. Activity with TMP as substrate was approximately one-half as much as with UMP or CMP. Apparent Michaelis constants were 0.33 mM UMP, 0.15 mM CMP, and 1.0 mM TMP. Magnesium was required for optimal activity, and this cation could not be replaced by Mn2+. Maximum activity was obtained between pH 7.0 and 7.5 with rapid decreases in more alkaline media and moderate decreases with acidification. The enzyme was quite sensitive to heat and was strongly inhibited by AMP, by some purine bases, and by both purine and pyrimidine nucleosides. Divalent cations of heavy metals were also strongly inhibitory, as were agents active against sulfhydryl groups. The presence of substrates and/or 2-mercaptoethanol provided considerable protection against some of these deleterious agents and conditions. Pyrimidine 5'-nucleotidase activity in hemolysates was clearly distinguishable from erythrocyte acid phosphatase and from leukocyte and serum alkaline phosphatases and nucleotidases.

Solutions of tetraheptylammonium bromide, iodide, nitrate, or perchlorate in ethyl bromide behave as anionic liquid membranes with ideality degrees close to 100%. In the cases of tetra­ heptylammonium fluoride, or chloride, the ideality degrees are about 80%. A picture of the charac­teristics and structures of this class of membranes is given

Two brothers with congenital nonspherocytic hemolytic anemia and neurologic disease were found to have erythrocyte and leukocyte phosphoglycerate kinase deficiency. Elevated levels of red cell dihydroxyacetone phosphate and 2,3-diphosphoglycerate were documented as well. Erythrocyte phosphoglycerate kinase deficiency is X-chromosome linked, and the present report brings the number of male hemizygous individuals to five. All are mentally retarded and some have additional neurologic defects

The electronic absorption spectrum of NF3 was investigated for the first time. At the lowest pressures, the long wavelength limit of absorption is at about 960 A in agreement with the lowest ionization potential of the molecule (939 A). Quantitative intensity measurements showed a smooth decrease of the absorption coefficients to effectively zero at about 1800 A, with no indication of even partly resolved electronic transitions. Comparisons with the electronic spectrum of ammonia are discussed. The molecular dipole moment is used to obtain an equivalent orbital representation of the NF3 wave function.

Dipole strengths of various heteronuclear diatomic molecules are calculated for high and low energy transitions of one spectral type, 1Σ-1Σ, σ-σ. Through the use of increasingly accurate ground state wavefunctions it is possible to display the sensitivity of the transition probabilities to known approximations in the wavefunction. Selfconsistent field and configuration interaction effects are compared and contrasted.

IT is now clear that hereditary hemolytic anemias not associated with hemoglobinopathy or with the thalassemia syndromes are frequently due to inherited deficiencies in one or another of the enzymes upon which the erythrocyte is dependent to meet its energy needs. The non-nucleated, relatively metabolically impoverished adult human red cell has limited resources and places major dependence upon energy derived from the conversion of glucose to lactate – chiefly via the anaerobic Embden–Meyerhof pathway, but to a lesser but still important extent by way of the oxidative hexose monophosphate shunt. In the former diphosphopyridine nucleotide (NAD) is cycled to its . . .

Data on the singlet-triplet absorption spectra and phosphorescent lifetimes of the group IV tetraphenyls are presented. The singlet-triplet transition probability is found to increase with increasing atomic number of the central metallic atom. This leads to phosphorescent lifetimes (~10 −4 sec) and singlet-triplet extinction coefficients (of order unity) for the heavier tetraphenyls, which are quite unusual for transitions of aromatic pi electrons. This represents a further example of the “atomic number effect”.

The contribution to the intensity of atomic and molecular electronic transitions beyond the Hartree—Fock, or independent‐particle model, is examined by means of ``many‐electron theory'' (MET). The contribution is of first order in the wavefunctions of the combining states.MET analysis of the off‐diagonal matrix element for the transition probability in the frozen‐core approximation yields physically interesting expressions which are applied to atomic and molecular examples. Considerable improvement in calculated atomic (e.g., Be resonance transition) and molecular (e.g., π—π* transitions) intensities are obtained when analysis shows that ground‐state ``hole pairs'' are strongly scattered into the orbital sea of the excited state.The uses of energies and operators in the calculation of electronic intensities is also examined. The relation between the expectation values of operators ∇ and r which replaces the widely used off‐diagonal hypervirial theorem in the absence of exact wavefunctions is given.

Hereditary hydroxyacl-glutathione hydrolase (Glyoxalase II) deficiency was demonstrated in both homozygous and heterozygous form in kindred in which hereditary elliptocytosis was inherited independently. Homozygotes and heterozygotes for the enzyme deficiency were clearly differentiated by direct enzyme assay and a variety of indirect methods. Four homozygotes exhibited 10 per cent or less of normal activity. Leukocytes do not share the deficiency. Lactoyl-glutathione lyase (Glyoxalase I) activity was entirely normal in both leukocytes and erythrocytes, and was three times more active than Glyoxalase II. Glyoxalase II deficiency was traceable through three generations, was transmitted as an autosomal recessive trait and was not associated with discernible clinical or hematological abnormalities. It did not appear to worsen clinical manifestations of hereditary elliptocytosis where the two abnormalities coexisted.

The semi-empirical free electron theory with inclusion of interelectronic and electron-nuclear molecular integrals is used to examine the spectroscopic properties of the trans-polyenes. The molecular integrals were calculated at many values ofQ, the free electron theory length parameter. Comparisons are made to equivalent LCAO-MO methods, especially in regard to molecular coulomb and exchange integrals, singlet-triplet separations and parametric dependence. The FET viriel theorem is examined.

The LCAO–MO–CI method is applied to the study of the electronic transition moment of the Lyman bands of H2 (B 1Σu+–X 1Σg+) over the range of internuclear separations 1 ≤ R ≤ 6 a.u. It is found that configuration interaction is responsible for a strong nonlinear variation of the transition moment with internuclear distance (maximum transition moment at 3.0 a.u.). Comparison with other calculations indicates that the method is applicable to more complicated molecules and permits the examination of how individual electron correlation effects contribute to the transition moment.

The absorption and emission spectra of carbon, silicon, germanium, tin, and lead tetraphenyl are reported in their entirety. The two electronic transitions observed in absorption are shown to be analogous to those of benzene and benzene derivatives. Vibrational structure is analyzed and correlated for all five tetraphenyls. Two electronic transitions are observed in emission. The emitting levels are the lowest members of the singlet and triplet systems. The effect of atomic number of the central atom on the rate of intersystem crossing is a corollary of the usual atomic number effect on the radiative lifetime of the triplet state.

The characteristic features of the Rydberg transitions in a polyatomic molecule are examined with emphasis on their extravalence‐shell nature. It is made plausible that in molecular orbital perturbation theory the corresponding Hartree—Fock atomic orbital of principal quantum number n is a zero‐order approx‐imation to the Rydberg orbital. Calculations without integral approximations are carried out for the low‐lying states of H2O. The ASP—SCF—LCAO—MO treatment of the H2O ground state provides the core. The mean singlet—triplet absorption spectrum of H2O is fairly well reproduced by the calculation. The calculated oscillator strength of B1(3s)←A1, 1×10—2, and the calculated symmetry‐induced splitting of the 3p Hartree—Fock atomic orbital in C2v symmetry into B1 and A1 components, 2200 cm—1, are also in satisfactory agreement with experiment, 3×10—2 and 1500 cm—1, respectively.

Nella presente ricerca sono stati esaminati gli spettri d'assorbimento nell'ultravioletto vicino, di una serie di complessi di cobalto bivalente e cobalto trivalente, con l'α-α′ dipiridile e l'o-o′ fenatrolina. I risultati ottenuti confermano che i composti del Co bivalente non portano sensibili alterazioni allo spettro d'assorbimento delle basi chelanti, in relazione alla asuscettivia magnetica che corrisponde a quella di Co2+. Per contro i complessi del Co trivalente presentano uno spostamento batocromico della prima banda a 2800 A° del dipiridile e a 2650 A° della fenantrolina e la scomparsa della seconda banda rispettivamente a 2350 A° per il dipiridile e a 2275 A° per la fenantrolina, in accordo con l'intervento nei complessi cobaltici degli orbitali 3d del metallo, come risulta anche dal loro diamagnetismo.

Atypical cases of heritable hemolytic anemia have been noted that conform clinically and biochemically to anemias of the pyruvatekinase (PK)-deficient type, except for the presence of apparently adequate quantities of erythrocyte-PK activity by the usual assay procedure. Investigations of four such anomalous cases, occurring in two unrelated families, are presented. Erythrocytes contained a kinetically aberrant isozyme of pyruvate kinase (PK2). Michaelis constants for the pathologic isozyme relative to phosphoenolpyruvate were over 10-fold greater than control values, but no kinetic abnormality was evident for the second substrate, adenosine diphosphate. PK2 exhibited a pH optimum almost 1 U lower than the wild enzyme form (PK1). Significant differences were also evident in the functional stabilities of the isozymes. Leukocytes were unaffected. Family studies revealed paternal heterozygosity for quantitative PK deficiency of the usual type. Clinically normal maternal relatives and some siblings demonstrated intermediate deviations in erythrocyte-PK kinetics and reaction characteristics compatible with coexistence of normal PK1 and kinetically abnormal PK2. Hemolytic anemia in the propositi appeared to require simultaneous inheritance of the gene governing PK2 production and its presumed allele resulting in quantitative PK deficiency. Both genetic defects were traced through three generations, the defective gene in both instances apparently resident on autosomes. A revision of the PK assay technique is suggested, since catalytic inefficiency of PK2 was manifested only at low substrate concentrations and was therefore undetectable at the relatively high phosphoenolpyruvate levels employed in the conventional assay.

SUMMARY. A unique mutant form of erythrocyte pyruvate kinase has been found associated with chronic haemolytic anaemia in a child who is apparently doubly heterozygous for the mutant isoenzyme and for pyruvate kinase deficiency of the classical quantitative type. Clinical and laboratory findings conformed closely to those typically observed in homozygous pyruvate kinase deficiency anaemia. Assayed in fresh haemolysates, the isoenzyme exlubited reduced optimal activity (c 45% of normal) and an increased Michaelis constant for phosphoenolpyruvate (four to five times greater than normal). The kinetic anomaly was only partially corrected by activation with fructose-I,&&sphosphate. Despite some common characteristics, this isoenzyme appears distinct from others reported in the literature and lends support to the polymorphous nature of heritable haemolytic anaemias secondary to defective pyruvate kinase. Pyruvate kinase (PK) (ATP :pyruvate phosphotransferase, EC 2.7.1.40) catalyses the conversion of phosphoenolpyruvate (PEP) and adenosine &phosphate (ADP) to pyruvate and adenosine triphosphate (ATP). This constitutes a critical ATP regenerating reaction in mature human erythrocytes which must rely almost exclusively upon glycolysis to fulfil energy requirements. Homozygously inherited deficiency of the enzyme is often the only definable biochemical lesion in cases of congenital nonspherocytic haemolytic anaemia. No longer entirely tenable, it was the initial presumption that haemolysis occurred in such cases when the quantity of functional enzyme had been degraded to levels incompatible with effective glycolysis. More recent evidence indicates that abnormal isoenzymes of PK also exist which may be associated with haemolytic anaemia despite being highly active in vitro under optimal assay conditions. One such isoenzyme demonstrated markedly impaired kinetics with an elevated Michaelis-Menten constant (K,,,) for one of its substrates, PEP (Paglia et al, 1968). It was postulated that this mutant enzyme might be as rate limiting in glycolysis as normal PK which was quantitatively deficient, since in both instances intracellular PEP concentrations would have to rise appreciably before effective catalysis could occur.

Interesting similarities in the vacuum ultraviolet spectra of oxygen-containing molecules have been noted previously (1, 2). In the present work the basis of this classification is discussed from the viewpoint of the Rydberg states of these molecules. Sections I and II describe some of the characteristics of Rydberg spectra, especially with regard to the expected differences between lower and higher members of the same series. The splitting of np type orbitals in C2v symmetry is calculated as a function of principal quantum number n. In Section III the spectra of the simple oxygen-containing polyatomic molecules are correlated on the basis of their term values relative to the ionization potential of the nonbonding oxygen electrons.

Twenty-one enzymatic activities and red cell glutathione content are compared in cord blood, dyserythropoietic disorders, normal subjects, and subjects with hemolytic syndromes and reticulocytosis approximating that of the newborn. The dyserythropoietic states are heterogeneous and include several hereditary disorders, "preleukemia" and overt leukemia, refractory anemia with and without marrow ringed sideroblasts, and folate deficiency. Many activities exceeded those of cord erythrocytes and "high reticulocyte" controls by one or even several standard deviations. The low phosphoglycerate kinase and glutathione peroxidase and relatively low ribosophosphate pyrophosphokinase and adenine-phosphoribosyl transferase of cord erythrocytes were mimicked uncommonly. Pyruvate kinase was often relatively or absolutely low and sometimes dramatically so. Enzyme ratios were grossly aberrant. Capricious very high individual activities occurred in some instances. The heterogeneous nature of case material, including both hereditary and acquired syndromes, renders it difficult to interpret similarities often seen from case to case and sometimes to cord blood patterns on the basis of the reversion to fetal erythropoiesis as a common denominator. Rather, the cyto- and karyokinetic abnormalities characterizing dyserythropoiesis of diverse etiologies may result in exaggerations and distortions of a normal asynchronism in loss of functional genetic material governing enzyme synthesis as the nucleus degenerates and cytoplasmic organelles are lost.

Summary. In one type of hereditary dyserythropoietic anaemia, HEMPAS (hereditary erythroblastic multinuclearity with a positive acidified-serum test) striking increases in the activity of some, but not all, erythrocyte enzymes have been detected in three cases. Since there was only minimal reticulocytosis, these enzyme changes cannot be accounted for by the presence of a young erythrocyte population. It is suggested that the enzymatic abnormalities of HEMPAS result from abnormal karyo- and cyto-kinesis of the erythroid precursors.

HE human mature erythrocyte is metabolically underprivileged. It lacks a nucleus, deoxyribonucleic acid (DNA), ribonucleic acid (RNA), an intact Krebs’ cycle or cytochrome system and the capacity to perform oxidative phosphorylation. Its metabolic requirements, small but definite, are largely satisfied by the conversion of glucose to lactate via the EmbdenMeyerhof and hexose monophosphate oxidative shunt pathways. Reduced triphosphopyridine nucleotide (NADPH) generated in the latter is recycled to triphosphyridine nucleotide (NADP) chiefly in the process of conversion of oxidized glutathione to the reduced form by the enzyme glutathione reductase. Maintenance of glutathione in the reduced state appears important in protection against certain drug challenges and oxidative stresses. Net synthesis of high energy phosphate bonds in the form of adenosine triphosphate (ATP) is derived from glycolysis, and the Embden-Meyerhof pathway of metabolism of glucose also provides a mechanism whereby NAD is converted to NADH and cycled back

Schools of social work in the United States and in Canada have for many years, supported and encouraged their faculty to accept visiting professorships or research appointments in foreign schools of social work. This program has benefited both faculty and students through enriched course content. However, only in recent years have more than a few faculty from foreign schools of social work joined the faculties of schools of social work in the United States and Canada as visiting professors. There is no question that these faculty members have made a contribution to social work education in the schools where they were resident. This author provides insights on how visiting professors might affectively contribute as members of faculty and questions the emphasis we are presently giving to methodology at the expense of our commitment to the ideological and moral base of social work.