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Vibrationally and rotationally resolved cross sections and asymmetry parameters for the photoionisation of H2 by 584 and 304 AA radiation are studied for the vibrational states of H2+ from 0 to 12 (14 for the 304 AA line). Vibrationally summed cross sections ( sigma ) and vibrationally averaged asymmetry parameters ( beta ) are evaluated from these results. The calculated ( sigma ) agrees well with the experimental data. The values of ( beta ) are 1.93 and 1.86 for the 584 AA and 304 AA lines, respectively.

The total and differential cross sections for individual rotational and vibrational transitions in the photoionisation of the H2 molecule by 584 AA radiation are calculated in the static-exchange approximation with the addition of the adiabatic dipole polarisation potential. Further, it is demonstrated that the measurement of the relative intensities of the Q and S rotational branches for the transition to the nu 'th vibrational state of H2+ at two angles determine the vibrationally resolved asymmetry parameter beta nu '. The value of beta nu ', obtained from the data of Ruf et al (1983), is 1.87 for nu '=0, and agrees with the calculated value 1.89.

By use of a deconvolution technique to analyse experimental data, it is possible to obtain approximate values of rotationally resolved relative cross sections and asymmetry parameters for the photoionisation of the ground state of N2 to the N2+(X 2 Sigma +g) state with vibrational quantum numbers v'=0 and 1 by He I radiation. The difference of vibrationally resolved asymmetry parameters between the v'=0 and 1 states can be explained by a large variation of rotationally resolved relative cross sections and asymmetry parameters.

We have examined gravida with gestational diabetes mellitus (GDM), as defined by the National Diabetes Data Group (Diabetes 1979; 28:1039), for phenotypic and genotypic heterogeneity. Fasting plasma glucose (FPG) at diagnosis was used for further stratification of GDM according to putative metabolic severity into class A, (FPG < 105 mg/dl [N = 129]), class A2 (FPG 105–129 mg/dl [N = 47]), and class B1 (FPG ≥ 130 mg/dl [N = 23]). All GDM classes tended to be older and heavier than consecutive gravida with documented normal glucose tolerance (controls, N = 148). Subdivision into “lean” and “obese” indicated that plasma immunoreactive insulin (IRI) was greater after overnight fast in the obese of all groups except B1. However, absolute increases in IRI above fasting levels in response to glucose during OGTT were significantly enhanced by obesity only in class A2 gravida. Adjustment for the effects of age and weight by covariate analysis indicated that the IRI response to glycemic stimulation is usually attenuated in all forms of GDM. Mean values for increases in IRI above fasting values during the first 15 min and IRI increments relative to the increases in plasma glucose throughout the 180-min OGTT were below control values in all GDM groups and progressively so, i.e.,A1 < A2 < B1. The absolute insulinopenia was not invariable; a small number of gravida from all GDM groups displayed well-preserved IRI responses to oral glucose. Genotypic evaluation of the GDM population disclosed an increased occurrence of “markers” known to be associated with type I diabetes mellitus. HLA antigens DR3 and DR4 were more frequent in all GDM groups, and the incidence of cytoplasmic islet cell antibodies was enhanced significantly in class A2, and even more so in class B1. Thus, GDM appears to be a heterogeneous entity with substantial phenotypic and genotypic diversity in the mothers. Offspring from some class A1 and diet-treated class A2 gravida were examined to assess whether minimal abnormalities in maternal metabolism suffice to impact on intrauterine development independent of maternal diversity. Amniotic fluid insulin at 36 ± 0.1 wk of gestation and cord plasma C-peptide at birth were increased in offspring of mothers with class A1 GDM, thus indicating that even the mildest forms of GDM can cause accelerated maturation of fetal islet function. Birth weight and symmetry index in the newborn from class A1 arid diet-treated class A2 gravida were significantly increased above control values, even after adjustment for maternal age and weight, thus documenting for the first time that GDM per se can influence the anthropometric characteristics of the neonate. The findings underscore that GDM constitutes an independent risk factor with particular implications for islet and somatic development during fetal life. These unequivocal effects of maternal metabolism on cell development in the fetus may provide the most compelling reason for aggressive approaches to GDM, especially if prospective as well as retrospective studies continue to support their postulated association with increased obesity and diabetes in later life (i.e., “fuel-mediated teratogenesis”; Diabetes 1980; 29:1023).

Altered glucose homeostasis in the neonate often results from antecedent events during fetal life. This article describes the normal and altered development of glucoregulatory capabilities during perinatal life and relates it to problems of hypo- and hyperglycemia in the neonate.

We determined the glycemic response to intravenous lipid infusion alone, lipid with amino acids, or amino acids alone in 15 very small premature infants receiving constant glucose infusion during early life. Infants who received lipid or lipid and amino acids demonstrated significant increases in glucose compared with infants who received amino acids. The combination of lipid and amino acids resulted in an earlier increase than lipid alone. Although plasma insulin did not change in all three groups, infants who received amino acids alone demonstrated an appropriate increase in glucagon. These data suggest that lipid infusion, a commonly used means of providing nutrition to premature infants, may cause significant disturbances in glucoregulation, particularly when administered with amino acids.

We measured several growth stimulating variables in growth retarded (small-for-gestational-age [SGA]) rat fetuses on days 18, 19, 20, and 21 of their 21.5-day gestation. Bilateral maternal uterine artery ligation on day 18 was used to retard fetal growth, and fetuses of sham and nonoperated (normal) mothers served as controls. SGA fetuses had the lowest body and placental weights, while sham fetuses had intermediate weights from days 19 to 21. Similarly, SGA fetuses had the most profound alterations in arteriovenous PO 2 , PCO 2 , and pH, while sham fetuses had significant but less severe alterations. Fetal plasma concentrations and fetal/maternal ratios of glucose were significantly diminished in SGA fetuses on days 18 and 19; sham fetuses had intermediate values on day 19. Plasma concentrations and fetal/maternal ratios of leucine, isoleucine, and valine, but not the other amino acids, were significantly diminished in SGA fetuses on days 18, 19, and 20. Plasma insulin concentrations were significantly diminished in SGA fetuses on days 19 and 20, and hepatic concentrations of glycogen were significantly diminished on all days. Despite significantly elevated plasma glucagon concentrations in SGA fetuses, hepatic cytosolic phosphoenolpyruvate carboxykinase (PEPCK) activity was not elevated. These data indicate that bilateral uterine artery ligation retards fetal growth in the rat by altering gas exchange and limiting fuel availability. The limited insulin in SGA fetuses might further have retarded growth. Despite the acknowledged role of glucagon as a potent stimulator of gluconeogenic enzyme induction during the perinatal period, significantly elevated glucagon concentrations in the SGA fetus failed to stimulate PEPCK.

To determine whether administration of human placental lactogen (hPL) to pregnant rats during late gestation might enhance fetal growth, we implanted osmotically driven minipumps to provide 75 micrograms h PL/24 h on day 14 of the rat's 21.5-day gestation. This substantially increased maternal and fetal plasma hPL concentrations. By day 18, hPL fetuses were significantly heavier and had larger placentas than controls. From this point until term, their rate of growth (1.20 g/24 h) significantly exceeded that of controls (0.95 g/24 h). Birth weights differed significantly (hPL 5.86 +/- 0.08 g; controls 5.20 +/- 0.08 g, p less than 0.001). This increase was due primarily to significant increases in the growth of the liver and carcass. Enhanced glucose availability was in part responsible for this phenomenon inasmuch as plasma glucose concentrations were significantly increased in hPL maternal rats from days 15 to 19. This resulted on days 18 and 19 in significantly increased plasma glucose and insulin concentrations in hPL fetuses. Fetal/maternal glucose ratios did not differ between hPL and control fetuses. Fetal heptic glycogen concentrations were significantly increased on day 18 and 19 but were similar to controls from day 20 until birth. These observations suggest that increased maternal glucose availability with consequent stimulation of fetal insulin secretion accelerated the growth of hPL fetuses. However, maternal and fetal plasma glucose concentrations and fetal plasma insulin and hepatic glycogen concentrations on days 20 and 21 were normal, suggesting that other factors also were responsible for sustaining the accelerated fetal growth on these days.(ABSTRACT TRUNCATED AT 250 WORDS)

We determined the incidence of pneumothorax in 295 infants (mean birthweight, 1,917 gm) with the respiratory distress syndrome (RDS) treated according to the same protocol. Fifty-five infants (mean birthweight, 1,594 gm) developed pneumothorax (incidence, 19%); incidence varied with severity of RDS and intensity of respiratory assistance. Pneumothorax occurred in 3.5% (2 of 58) of infants who received no assisted ventilation and in 11% (14 of 124) of infants who received continuous positive airway pressure (CPAP) as the only form of assisted ventilation; the difference between these two groups is not significant. Forty-nine infants initially treated with CPAP later required mechanical ventilation with positive end-expiratory pressure (PEEP). Pneumothorax occurred in 12 of the 49 (24%) and in 21 of 64 (33%) of those infants initially treated with PEEP; the incidence of pneumothorax for both these groups was significantly higher than for those treated with no assisted ventilation or CPAP only. To assess the value of frequent measurement of vital signs, blood gas tensions, and pH in the recognition of pneumothorax, we analyzed these variables by the cumulative sum statistical technique. We noted the following significant changes associated with pneumothorax: arterial blood pressure, heart rate, and respiratory rate decreased in 77% of cases; pulse pressure narrowed in 51% of cases; Po2 decreased in 17 of 20 cases in which ventilatory settings were constant for at least three hours prior to pneumothorax. However, pH and PCO2 showed no consistent changes. Frequent measurements of vital signs and Po2 aid in the early diagnosis of pneumothorax.

We rendered pregnant rats chronically hyperinsulinemic to determine the effect of reduced maternal metabolic fuel availability on fetal growth and development. We implanted osmotically driven insulin loaded minipumps on day 14 (term 21.5 days) in pregnant rats. This significantly increased maternal plasma concentrations of insulin and reduced glucose from day 15 until term. From day 17 until birth, fetal growth was significantly less for hyperinsulinemic mothers (term birth weight 4.53 +/- 0.07 versus 5.64 +/- 0.06 g, p less than 0.001). In fetuses of hyperinsulinemic mothers plasma glucose and insulin concentrations were significantly reduced while glucagon concentrations were increased. Total plasma amino acids were significantly reduced in maternal rats and their fetuses from days 17 to 19 while arteriovenous blood gas tensions and pH did not differ between fetuses of hyperinsulinemic and control mothers. Small for gestational age newborn pups of hyperinsulinemic mothers were hypoglycemic for the first 240 min of life as a result of limited hepatic glycogen stores and a delay in the normally expected induction of hepatic cytosolic phosphoenolpyruvate carboxykinase. This occurred despite significant increases in neonatal plasma glucagon concentrations. These data indicate that limitation of maternal glucose and amino acids with normal placental gaseous exchange retards fetal growth, limits hepatic glycogen deposition, and delays neonatal phosphoenolpyruvate carboxykinase induction. Limited fetal insulin secretion resulting from diminished maternal fuel availability may have also been a factor in retarding growth. The delay in phosphoenolpyruvate carboxykinase induction despite enhanced glucagon secretion during fetal and neonatal life suggests a specific "resistance" to this hormone in the rat growth retarded by limited metabolic fuel availability.

The velocities of electrostatically sprayed droplets were measured by means of a new holographic technique employing two pulsed dye lasers of different wavelength, by which a pair of holograms at desired time interval were recorded in two different films. The motion of one droplet particle was analyzed in a one-dimensional situation. The theoretical results indicate that the particles are accelerated in the strong-field region up to about 8 m s −1 and then decelerated towards an equilibrium velocity due to the drag of the air on the particles. The velocity profiles derived theoretically are of the same order of magnitude. It should be noticed, however, that the air flow entrained by the spray possibly influences the motion of the particles.

Summary A new instrument has been developed and is now in use on shop floor for inspecting chatter marks sometimes generated by the grinding and the ultra-precision machining process. The instrument is able to measure both geometrical waviness and fluctuation of glossiness of the finished surface. The instrument principally consists of an optical lever and phototransistor and detects two analogue signals separately, corresponding to local deviations of the surface inclination and the glossiness. The detected surface inclination signal that contains influence of the glossiness deviation is then processed by a computer for delineating the true height variation, namely waviness, of the measured surface. Analyses are demonstrated on test samples finished by the grinding and the ultra-precision machining process. The instrument is capable of analysing surfaces finished to 0.1 μm waviness or even less.

We characterized some of the consequences of intrauterine growth retardation in rat pups growth retarded [small for gestational age (SGA)] due to bilateral maternal uterine artery ligation. Pups of sham and nonoperated (normal) mothers served as controls. SGA pups had significantly reduced body and carcass mass throughout the study while body mass did not differ between sham and normal pups after 4 days. Brain mass was similar in the three groups at any age, while at 21 days and later, SGA liver weight as % body mass exceeded that of sham or normals. At 21 days, a 48-h fast reduced plasma glucose significantly in SGA compared to sham and normal pups; SGA plasma insulin was decreased and glucagon increased. Hepatic phosphoenolpyruvate carboxykinase activity and glycogen content were similar among groups. SGA pups did have significantly reduced plasma alanine and elevated betahydroxybutyrate levels. No differences in the responses to fasting occurred at 28 or 35 days. These data indicate that intrauterine growth retardation has profound effects on postnatal growth and metabolism.

For use in practical equipment, GaAs MESFET's need Schottky gates with high energy tolerance against electrostatic discharge. This paper describes the design and fabrication technology related to the monolithic integration of protective diodes into low-noise GaAs MESFET's. A new diode structure, the grooved sidewall junction diode (GSJD), is proposed which is well suited for suppressing deterioration of the FET's RF performance. The GSJD was successfully integrated into the dual-gate low-noise GaAs FET for use in a UHF TV tuner. High energy tolerance of 50 erg was obtained in the device with a noise figure of 1.2 dB at 1 GHz.

The author explained N. M. Bronze and compared it to ordinary manganese bronze with high and moderate manganese content in regard to the main qualities required for marine propellers, namely, 1. Resistance to corrosion and erosion by sea water, 2. Tensile strength etc., and homogeneity of material, 3. Casting and machining properties, 4. Cost, 5. Suitability for repair by welding, fairing, etc., all based on the results of tests actually carried out on propeller castings and gave a conclusion as to the general superiority of N. M. Bronze over the others.

以上ノ所見ニヨリテ余等ハ次ノ如ク結論セント欲ス.1). 膜樣迷路ノ壁ハ結締織性ノ固有膜及ビ上皮細胞ヨリ形成サル.2). 固有膜ハ場所ニヨリテ厚サヲ異ニスルモ一般ニ透明ナ可成リ強ク光線ヲ屈折スル同質性ノ外觀ヲ呈ス.3). 上皮細胞ハ稍々扁平多角形ノ細胞ニシラ原形質内ニハ核ニ近ク微細ナル顆粒ヲ僅カニ有シ, 核ハ卵圓形ニシテ核染色質ハ著名ナリ.4). 磚状上皮細胞ハ場所ニヨリテ其ノ高サ, 大サヲ異ニス.5). 色素細胞ハ比較的大ナル高キ細胞ニシテ原形質ニハ chondriokonten ノ密ニ排列スルヲ認メ, 核ハ表面ニ近ク圓形, 卵圓形時トシテハ不正ナル形ヲ呈シ核染質ハ多シ.6). 有毛細胞ハ長樽状ヲ呈シ其ノ長サハ常ニ一定セズ. 原形質ハ一般ニ顆粒ニトミ下方ニ楕圓又ハ圓形ノ核ヲ有ス.7). 絲状細胞ハ細長キ原形質ト比較的大ナル核ヲ有シ核ノ存在スル部分ハ膨大ス.8). 色素細胞ハ Foramen utriculo-sacculare ノ周圍ニモ認メラル.9). Perimaculare Zelleu ハ多列體ニ配列シ原形質ニ密ニ存在スル大量ノKornchen ヲ有シ, 核ハ一般ニ太ク且ツ卵圓形ナリ.10). Proto-Plasmatische Zellen ハー或ハ多列的ニ散在シ原形質ハ比較的狹クシテ少量ノ Plastosomen ヲ含ム.

Streptomyces azureus carried one copy or less of plasmid pSA1, which elicited pocks at 0.1 to 1.0%. Strain PK100 was isolated from the wild-type strain after UV irradiation. PK100 carried approximately 20 to 30 copies of pSA1.1, a derivative of pSA1. Plasmid pSA1.1 elicited pocks at 100% and inhibited spore and thiostrepton production.

A guided-wave acousto-optic device will certainly serve important functions such as deflection, modulation and switching of laser light beams in future optical communication and processing systems. We had experimentally demonstrated, for the first time, a high-performance guided-wave acousto-optic light beam deflector by employing blazed grating couplers as shown in Fig.11. In order to realize their high coupling efficiency, the blazed grating couplers had been developed by the reactive ion-beam etching(RIBE) technique using holographically produced photoresist gratings as masks2.

We determined if reducing litter number by selective fetal ablation (A) might enhance the growth of the surviving fetuses. On day 14 of the rat's 21.5-day gestation, we ligated branches of the uterine artery at their secondary division. Each of these branches supplies a placenta and its fetus, and ligation kills them. Every other fetus in litters of eight to 14 fetuses was ablated. Each A maternal rat was matched to a control with an equal number of fetuses. Ablation reduced fetal number (from 8–14 to 4–7) and increased fetal growth (birth weight 5.84 ± 0.05 versus 5.20 ± 0.05 g, p < 0.001). In the A but not control litters, newborn body mass was negatively related to litter number. Fetuses of A litters had increased carcass, liver, and brain mass. On days 18 and 19, fetal plasma glucose concentrations, fetal/maternal glucose ratios, insulin concentrations, and hepatic glycogen concentrations were increased suggesting that A increases glucose provision to the surviving fetuses. Although these observations imply that A enhances glucose provision resulting in stimulated growth of insulin-sensitive tissues, the growth of the brain, purportedly a tissue not sensitive to insulin, was also increased. In addition, the growth rate of A fetuses continued to be increased on days 20 and 21 despite normal fetal plasma glucose and insulin. These observations indicate that with A, factors other than insulin also stimulated growth. Of note, newborn A pups developed hypoglycemia at 20 and 60 min as a result of increased insulin secretion. Newborn A pups also failed to increase hepatic cytosolic phosphoenolpyruvate carboxykinase. Selective uterine artery ligation is reproducible, relatively easy to implement, and may prove to be useful for studying the phenomenon of accelerated fetal growth.

We studied the effects of glucose, alanine, and saline infusion in newborn guinea pigs. After acute (24–30 h after delivery) or prolonged (96–100 h after delivery) starvation, alanine or glucose infusion significantly increased liver glycogen concentration. Alanine infusion increased plasma glucose concentration and urea production rate (UrP). After acute starvation, a continuous 12-hour glucose infusion did not affect either plasma alanine concentration or UrP; however, after prolonged starvation, glucose infusion significantly reduced both variables. After prolonged starvation, the newborn guinea pig mobilizes alanine for gluconeogenesis. Increased protein catabolism is a consequence of this process. Glucose infusion negates the need for gluconeogenesis and spares body protein.

On a note une incidence elevee de meningite chez les prematures traites pour hydrocephalie post-hemorragique. Il se peut que cette hydrocephalie altere l'integrite de la barriere hematoencephalique, augmentant de ce fait le risque de meningite lorsqu'une bacteriemie survient. Le role des ponctions lombaires est mal elucide. On recommande de limiter le traitement par ponction lombaire a certains cas

To determine the mechanism of alteration in glucose homeostasis associated with maternal isoxsuprine administration, isoxsuprine or 0.04 M saline was administered intravenously for 3 hours to term pregnant and age-matched virgin rats. Isoxsuprine infusion significantly increased plasma glucose and insulin concentrations and decreased hepatic glycogen stores in both. Compared to rat pups of saline infused mothers, pups of isoxsuprine infused mothers had significantly elevated plasma glucose concentrations for the first 4 hours of life and plasma insulin concentrations for the first two. Plasma glucose concentrations for the offspring of isoxsuprine treated mothers then decreased significantly and remained so until 16 hours of age. Hepatic glycogen concentrations were significantly less in rat pups of isoxsuprine treated mothers at birth and for the first 4 hours of life. In a limited number of studies, isoxsuprine was present at birth in substantial quantities (80-85% of maternal levels) in the plasma of rat pups of isoxsuprine infused mothers. These data suggest that maternal isoxsuprine therapy mobilizes hepatic glycogen and results in maternal hyperlgycemia. Maternal isoxsuprine infusion may directly deplete fetal hepatic glycogen and result in transient fetal and neonatal hyperglycemia. the in utero depletion of glycogen and possibly, the early stimulation of insulin production may be responsible for the later significant decreases in plasma glucose in the offspring of isoxsuprine treated mothers.

We provided parenteral nutrition to 40 very low birth-weight premature infants (birth weight 815 +/- 17 grams, gestational age 27 +/- 2 weeks) with a superior vena cava catheter. To avoid the risk of transport, catheterization was performed under sterile conditions in the intensive care nursery. The central venous catheter facilitated administration of calories to sustain growth, especially in infants whose catheters remained in place for 3 weeks or longer. The overall incidence of catheter related sepsis was high (30%) but the majority of cases were due to Staphylococcus epidermidis and resolved without incident. Other complications of parenteral nutrition were minimal. This approach is a safe and effective means of providing nutrition to the very low birth-weight infant.

We determined the effects of feeding, starvation, and glucose infusion after starvation in newborn guinea pigs. We determined the rate of 14 C-leucine incorporation into skeletal muscle (Ks) as a measure of muscle protein synthesis and the rate of excretion of 3-methylhistidine as a measure of muscle myofibrillar protein catabolism (Kc). Fed newborns, who were in positive nitrogen balance, had the highest Ks and lowest Kc, while starved newborns had the lowest Ks and highest Kc. Infusing glucose after starvation decreased net protein catabolism and Kc, but did not increase Ks. The magnitude of change of Kc in response to starvation and glucose infusion was much greater than Ks. Changes in catabolic rate may influence net muscle protein balance ro a greater degree than changes in synthetic rate.

We determined the incidence of pneumothorax in 295 infants (mean birthweight, 1,917 gm) with the respiratory distress syndrome (RDS) treated according to the same protocol. Fifty-five infants (mean birthweight, 1,594 gm) developed pneumothorax (incidence, 19%); incidence varied with severity of RDS and intensity of respiratory assistance. Pneumothorax occurred in 3.5% (2 of 58) of infants who received no assisted ventilation and in 11% (14 of 124) of infants who received continuous positive airway pressure (CPAP) as the only form of assisted ventilation; the difference between these two groups is not significant. Forty-nine infants initially treated with CPAP later required mechanical ventilation with positive end-expiratory pressure (PEEP). Pneumothorax occurred in 12 of the 49 (24%) and in 21 of 64 (33%) of those infants initially treated with PEEP; the incidence of pneumothorax for both these groups was significantly higher than for those treated with no assisted ventilation or CPAP only. To assess the value of frequent measurement of vital signs, blood gas tensions, and pH in the recognition of pneumothorax, we analyzed these variables by the cumulative sum statistical technique. We noted the following significant changes associated with pneumothorax: arterial blood pressure, heart rate, and respiratory rate decreased in 77% of cases; pulse pressure narrowed in 51% of cases; Po2 decreased in 17 of 20 cases in which ventilatory settings were constant for at least three hours prior to pneumothorax. However, pH and Pco2 showed consistent changes. Frequent measurements of vital signs and Po2 aid in the early diagnosis of pneumothorax.

The mechanism of the neurologic complications associated with primary atypical pneumonia is unknown. To examine the ability of Mycoplasma pneumoniae to enter the brain of experimental animals, the organism was inoculated into adult and suckling mice by various routes. After intranasal infection, M. pneumoniae was isolated from brains and lungs of both groups of mice. After intracerebral inoculation, the high levels of the mycoplasma persisted for two months or more in the brains of suckling mice. In addition, after intravenous infection, the systemic spread of infection occurred in the mice treated with high doses of cyclophosphamide. Our results suggest that M. pneumoniae may be able to reach the brain via blood and it may occur with relative ease in compromised hosts.

Tris caused the distention of the Golgi cisternae in primary cultured rat hepatocytes and perturbed the functions occurring there. Proteolytic cleavage of precursors of both albumin and complement C3 was inhibited, whereas that of prohaptoglobin was not affected by Tris. These effects on the proteolytic cleavages resemble those of acidotropic amines (Oda, K., and Ikehara, Y. (1985) Eur. J. Biochem. 152, 605-609; Oda, K., Koriyama, Y., Yamada, E., and Ikehara, Y. (1986) Biochem. J. 240, 739-745). However, the effects of Tris significantly differed from acidotropic amines on the basis of its effects on the processing of N-linked oligosaccharides of glycoproteins. Both alpha 1-protease inhibitor and haptoglobin secreted from the Tris-treated cells were found to contain almost equal amounts of endo-beta-N-acetylglucosaminidase H-sensitive and -resistant oligosaccharides, whereas the glycoproteins from both the control and methylamine-treated cells were resistant to the enzyme. The endo-beta-N-acetylglucosaminidase-sensitive oligosaccharides were analyzed to be Man8-5GlcNAc by high resolution gel permeation chromatography, suggesting that trimming of alpha-mannose residues from the precursor Man9GlcNAc2 is incomplete in the Tris-treated cells. On the other hand, Tris did not significantly inhibit incorporation of radioactive monosaccharides (N-acetylglucosamine, galactose, and fucose) into the glycoproteins. However, two-dimensional gel electrophoresis in combination with neuraminidase digestion demonstrated that sialylation was markedly inhibited by Tris. Taken together, our results reveal that Tris inhibits not only the sialic acid addition which takes place in the trans Golgi region, but also the trimming step of high mannose-type oligosaccharides, which is thought to occur before glycoproteins reach the trans Golgi region.

We measured the residual placental blood volume (RPBV) of 20 infants delivered at term by cesarean section of women not in labor. In all cases, the umbilical cord was clamped within 40 seconds of birth. RPBV decreased significantly with increasing age at cord clamping. In addition, RPBV for infants with cords clamped within 20 seconds of birth correlated inversely with maternal systolic blood pressure (mean RPBV = 54.8 ml. per kilogram at 105 torr and 28.4 ml. per kilogram at 148 torr). However, RPBV did not correlate with maternal blood pressure for the whole group of 20 infants or for those with cords clamped later than 20 seconds after birth. These data indicated that in infants delivered by cesarean section placental transfusion is time related during the first 40 seconds of life and that maternal blood pressure also influences the magnitude of placental transfusion during the first 20 seconds after birth. Analysis of data from this study combined with data from a previous study shows that after 40 seconds the net flow between placenta and infant reverses and that cord clamping delayed beyond this point is accompanied by a rise in RPBV back to the level found when the cord was clamped before 20 seconds.

The class II HLA antigens, Ia antigens, are essential for cellular recognition and cooperation in immune response [1, 2]. A cluster of genes encoding these class II antigens has been mapped in the HLA-D region of human chromosome 6. Serological as well as cellular reagents allowed the identification of two sets of molecular entities that display a similar function and tissue distribution to HLA-D products. These antigens, named DR and DQ, are composed of two noncovalently associated glycosylated 33 000 dalton α (heavy) and 28 000 dalton β (light) chains. The latter carries the main polymorphic determinants. Recently, another human class II antigen, named DP, has been defined by cellular assay which is encoded in subregions distinct from DR and DQ [3, 4]. DP antigens control a secondary lymphocyte reaction and are encoded in a region centromic to the DR loci. Further, biochemical data and genetic approach with cloned DNA probes provide evidence for several other distinct α and β chains of human Ia molecules [5–9].

Infant mice (2 to 4 days old) were exposed to living Mycoplasma pneumoniae. The organisms were isolated in the order of 10(3) to 10(4) colony-forming units from the lungs of mice for 2 weeks after infection. Mononuclear cell infiltration was present in the lungs of infected mice. The specific IgG antibodies to membrane proteins of M. pneumoniae in the sera of infected mice were detected by enzyme-linked immunosorbent assay for about 800 days. In immunoblotting analysis, a 160-kilodalton (kDa) protein strongly reacted with the infected mouse sera. The dams immunized with membrane proteins conferred passive immunity on their offspring via colostrum. Specific IgG antibody appeared in the serum of infant mice that were given mouse anti-M. pneumoniae serum or convalescent human patient serum orally. These mice were also protected from challenge with M. pneumoniae. The immunoblotting patterns of patient sera were similar to those of infected mouse sera. The infant mouse model may be useful to investigate the host immune responses to M. pneumoniae.

Fetal hyperinsulinemia is a well-known correlate of accelerated fetal growth; the consequences of fetal hyperinsulinemia upon fetal and neonatal glucoregulation are less well understood. We injected rat fetuses of a litter on day 18 of gestation with either 5 units of long acting insulin (I) or 154 mmol/L NaCl. Twelve hours after injection, the wet and dry mass of total body and liver of I fetuses significantly exceeded that of controls. At birth (day 21.5), newborn I pups weighed 5.86 ± .08 g, and controls, 5.48 ± .05 g, (P < .001). On day 18, within one hour of injection, fetal plasma insulin concentrations were significantly elevated and remained so for 24 hours. Mothers of I fetuses had significant elevations of plasma insulin at 1, 3, and 6 hours, and they developed transient hypoglycemia. Plasma glucose concentrations in I fetuses were significantly diminished at 1, 3, and 6 hours and then achieved control levels by 12 hours. Fetal hypoglycemia resulted from an apparent direct effect of insulin upon fetal tissue and from the maternal hypoglycemia. Hypoglycemic I fetuses demonstrated a sluggish α-cell response; they failed to increase plasma glucagon one hour after insulin injection. Values were significantly increased three hours after injection. At birth, I pups became hypoglycemic relative to controls. This was, in part, due to their significantly elevated plasma insulin concentrations at 120 and 240 minutes (120 minutes, 43.8 ± 8 v 17.5 ± 6 μU/mL, P < .001). Plasma glucagon was significantly increased in I pups at 240 minutes. During the neonatal period, pups who had undergone intrauterine insulin injection did not mobilize glycogen or induce hepatic cytosolic phosphoenolpyruvate carboxykinase to the same extent as controls. Insulin injection to the fetus accelerates growth and causes fetal hypoglycemia by decreasing maternal glucose and increasing fetal tissue uptake of glucose. The intriguing observation of sustained neonatal hyperinsulinemia remains unexplained.

We have attempted to use perinatal islet performance as an index of the impact of maternal fuels during fetal development. Accordingly, we analyzed cord plasma for C-peptide and amniotic fluid (secured several weeks before delivery) for immunoreactive insulin in infants of mothers with normal metabolism (NM), gestational diabetes (GDM), and tightly regulated White Class B or Class C insulin-dependent diabetes mellitus (IDDM). We tried to subdivide mothers with GDM on the basis of severity by distinguishing between those with fasting plasma glucose within the normal range for pregnancy (i.e., less than 105 mg/dl and those with fasting plasma glucose of 105 mg/dl or greater). Most of the latter were treated with insulin whereas the former received diet alone. We found that cord plasma levels of C-peptide in infants of mothers with GDM < 105, GDM ≥ 105, and IDDM did not differ significantly from one another; all were approximately twofold greater than in infants from mothers with NM. Values for insulin and ratios of insulin/glucose in amniotic fluid were also increased and to a similar degree in all three diabetic groups; all exceeded the findings in the NM group. Our results indicate that islet function is enhanced at birth in the offspring of mothers with even the mildest forms of untreated gestational diabetes (i.e., GDM < 105) to a degree that is not appreciably different than in more severe forms of diabetes receiving tightly regulated insulin therapy. The augmented B-cell secretion cannot be ascribed to intrapartum events, since similar changes were also found in amniotic fluid secured several weeks before delivery. We conclude that neonatal insulin secretion may constitute an exquisitely sensitive index of the effects of ambient fuels during intrauterine life. Neonatal B-cell function thereby may provide a useful yardstick for the retrospective evaluation of maternal glucoregulation during late gestation.

The proposition that Borderline Personality Disorders (BPDs) are atypical forms of affective disorder is reviewed in the light of pharmacological, outcome and clinical studies. The case can be summarized briefly as follows: that the basic underlying cause of borderline symptomatology is an effective disorder; that mood disturbance, which is viewed as primarily biological, is more important than developmental experience and life events in maintaining borderline personality features; that therapies aimed at treating the mood disorder should therefore be expected to relieve the personality disorder. However, the pharmacological studies suggest that antidepressant medications have been largely ineffective in treating well defined BPD, except in the presence of coexisting depressive disorder. Indeed low dose antipsychotics have a demonstrated efficacy in the treatment of BPD, which does not strengthen the case for an affective etiology. Follow-up studies of BPDs suggest that dramatic characterological features seen at the time of index hospitalization tend to recede by the time patients are in their 30s, that major affective disorders fail to emerge over time, and that long-term marginal functioning derives from long-term maladaptive patterns across a variety of areas. Clinical studies suggest that 20-60 per cent of patients with BPD have a concomitant depressive disorder. Conversely the prevalence of personality disorders in depressions varies with depressive category, with considerably higher incidence of personality disturbance found in non-endogenous depression. The high rate of coexistence of these two disorders does not imply causality or primacy, in the sense that it is the affective disorder which brings out and causes the personality disorder. The review concludes that the assertion that BPD represents atypical affective disorder begs the possibility that it is precisely in having borderline features that they are atypical, and hence distinct.

Acid alpha-glucosidase [EC 3.2.1.3] was purified from pig liver by a procedure including Sephadex G-100 affinity chromatography. Electrophoresis on SDS-polyacrylamide gel of the purified enzyme indicated the presence of two components with molecular weights of 73K and 64K. The two components of the enzyme were completely separated, in reasonable yield, by chromatography on a DEAE-5PW column. Both components catalyzed the hydrolysis of the alpha-1,4 and alpha-1,6 linkages of glycogen, maltose, isomaltose, dextrin, and a synthetic glucoside at acid pH. The pH optima of both components were 4.3 for maltase and glucoamylase, and 4.8 for isomaltase and dextrinase. But as to the activity on 4MU-alpha-Glc, the pH optimum of the larger component was 4.8 and that of the smaller component 5.3. The Km values of both components for 4MU-alpha-Glc, maltose, glycogen, isomaltose, and dextrin were 1.0 X 10(-4) M, 9.1 X 10(-3) M, 16.7 mg/ml, 6.7 X 10(-2) M, and 12.5 mg/ml, respectively. Erythritol, Tris, and turanose inhibited the two components competitively. The Ki values of the larger component were 5.0 X 10(-2) M, 13.3 X 10(-3) M, and 3.2 X 10(-3) M, and those of the smaller component were 2.5 X 10(-2) M, 6.1 X 10(-3) M, and 4.7 X 10(-3) M, for erythritol, Tris, and turanose, respectively.

Membranous and soluble forms of rat liver alkaline phosphatase were selectively prepared by extracting microsomes with n-butanol at pH 8.5 and 5.5, respectively, and purified in homogeneous forms by the method previously established (Miki et al. (1986) Eur. J. Biochem. 160, 41-48). When subjected to polyacrylamide gel electrophoresis, the two forms migrated to the same position in the presence of sodium dodecyl sulfate, while the membranous form remained at the top of gels in the absence of the detergent. Treatment of the membranous form with phosphatidylinositol-specific phospholipase C resulted in its conversion to a soluble form with the same electrophoretic mobility even in the absence of the detergent as that of the soluble form extracted at pH 5.5. Automated Edman degradation analysis showed that the two forms have the same N-terminal amino acid sequence up to the 30th residue determined. Chemical analyses of hydrolysates of the two forms by gas-liquid chromatography demonstrated that the membranous form contains palmitic acid, stearic acid, and inositol, while the soluble form contains inositol but is devoid of the fatty acids. Taken together, these results suggest that rat liver alkaline phosphatase is covalently attached to phosphatidylinositol acylated with palmitic acid and stearic acid, which functions as the membrane-anchoring domain of the enzyme molecule.

We studied the effects of acute starvation and refeeding on muscle protein synthesis and degradation in young rats. As measures of synthesis, we determined muscle RNA concentration and the rate of incorporation of [14C]leucine into skeletal muscle protein (Sm). As an estimate of nitrogen retention we measured urea production (UrP). Starvation reduced these variables significantly. One refeeding period returned Sm to control values, only partially restored RNA concentration, and increased UrP. We determined the urinary excretion rate of 3-methylhistidine (3-MH) as a measure of the rate of myofibrillar protein degradation. Excretion of 3-MH was lowest in control and highest in starved rats. Refeeding decreased 3-MH excretion to a level midway between control and starved animals. Growth was attended by high rates of synthesis and low rates of degradation. Starvation depressed synthesis and increased degradation. With refeeding, synthesis increased and degradation decreased, compared with the starved state.

Human malignant melanoma cell lines have been divided into three broad groups on the basis of morphology, pigmentation, tyrosinase levels, the 2-dimensional electrophoretic patterns of their [3H]glucosamine-labeled glycoproteins and the presence or absence of an extracellular matrix of fibronectin. The most pigmented cell lines were characterized by the synthesis of a novel glycoprotein with a molecular weight of 75,000 and the absence of a fibronectin matrix. As cultured skin melanocytes also had these characteristics, this group of melanomas appears to be the most differentiated. Melanoma cell lines in the amelanotic group were characterized by the synthesis of high levels of HLA-DR antigen and by the production of an extracellular fibronectin matrix.

We measured blood glucose concentrations and glucose turnover rates in 24 hr fasted, conscious, unrestrained pregnant rats and nongravid controls on days 18, 19, and 20 of gestation. Turnover measurements were secured with simultaneous equilibrium infusions of D-(6-3H) and D-(6-14C) glucose so that gluconeogenic recycling could also be determined. “Steady state” values for blood glucose in the mother after 24 hr of fasting did not significantly differ on each of the days, and these concentrations were significantly lower than the values in 24 hr fasted nongravid rats. At 18 days gestation, glucose turnover did not differ from nongravid values. By contrast, values for glucose turnover after 24 hr fasting increased significantly and progressively in the 19 and 20 day pregnant rats. The increase in turnover correlated with the increasing growth of the conceptus. The ratio between D-(6-14C) glucose and D-(6-3H) turnover remained constant (and the same as in the nongravid rats) during all 3 days of gestation suggesting that rates of glucose recycling remained unaltered. These longitudinal studies indicate that the factors contributing to the pattern of “accelerated starvation” during dietary deprivation in pregnancy may vary as pregnancy progresses. The exaggerated lowering of blood glucose which accompanies fasting occurs before total glucose turnover increases. This could provide a potential mechanism for conserving maternal glucose. Since transplacental transfer of glucose is concentration-dependent, the early establishment of a lower “steady state” for circulating glucose could diminish the magnitude of loss of this key nutrient to the fetus.