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An important area of concern among rural health researchers and policy analysts is the social and ecological correlates of mortality levels. This research is concerned with the empirical relationship between the prevalence of poverty and the mortality experience of different age groups within the population. Poverty is viewed as a characteristic ofthe social organization of local areas and operationalized by employing several indicators, including a measure of rurality. The empirical results indicate that the magnitude of the association between the prevalence of poverty and mortality varies among different age groups. The impact of rurality, while being consistently positive, is shown to be statistically nonsignificant. The research also shows that the availability of primary care is associated with lower mortality.

Division leaders in academic medicine today must have many of the preferred requirements for chief executive officers of large corporations. As academic departments struggle to compete in an increasingly competitive world business climate, many leaders in America are turning to words of wisdom from coaches, some of our most exalted leaders, who truly understand competition.1A stimulating article in theArchives of Internal Medicine, entitled "Triple Threat or Double Fake,"2documents the current difficulty in making individuals or divisions "triple threaters" in efforts to develop excellence in education, teaching, or research, the three missions in academic medicine. Vince Lombardi1offered outstanding advice for our young academic leaders when he stated that "The quality of a person's life is in direct proportion to their commitment to excellence regardless of their chosen field of endeavor." This message has particular merit for academic section leaders. Since medical schools and departments depend

Altered carbohydrate metabolism has been reported during episodes of neo natal infection. To document that there is more rapid glucose disappearance during infection, intravenous glucose tolerance tests (IVGTT) and serial plasma growth hormone and insulin levels were determined in eight full-term neonates during the first three days of an acute episode of infection and during convalescence, 5 to 15 days later. Eight healthy infants were each studied once using the same study protocol. Glucose disappearance rates, measured as Kt of glucose, were increased (p < 0.01) during both the acute septic period (3.7 ± 0.3% disappearance/min; mean ± S.E.M.) and convalescent period (2.5 ± 0.2%/min) when compared with values in control infants (1.3 ± 0.3%/min). Gram-negative, gram-positive, and viral infections were all associated with rapid glucose disposal. The ab normality in carbohydrate homeostasis persisted for at least 5 to 15 days after treatment was begun. Baseline and stimulated (20-minutes post bolus glucose infusion) plasma insulin and growth hormone levels did not differ among the groups. Thus, there is no evidence that hyperinsulinism produced the rapid glucose disappearance rate and enhanced glucose utilization. The reason for the disturbed carbohydrate metabolism in neonatal infections remains un known.

Plasma concentrations of glucose, alanine, and glucagon were measured after 24 hour fasting in newborn and infant sheep and in response to infusion of alanine alone and concurrently with theophylline. The plasma glucagon response to alanine was minimal in newborn sheep; in contrast, alanine produced a brisk response in plasma glucagon concentration in infant sheep. Glucose concentrations were unchanged in both groups. Theophylline enhanced blood glucagon and glucose responses to alanine in newborn animals but had minimal effects on the response of the infant sheep. These data, considered with earlier data in fetal sheep, suggest a progressive maturation of pancreatic islet alpha-cell glucagon secretion in the sheep during the postnatal period and suggest that the blunted glucagon response observed in the neonate is related to immaturity of the glucagon secretion mechanisms rather than deficient synthesis of the hormone. This immaturity may be related to impaired synthesis and/or enhanced degradation of cyclic adenosine monophosphate (cAMP) or to diminished responsiveness to cAMP.

The pancreatic alpha and beta cell responses to glucose and deoxyglucose infusion were studied in nine healthy newborn lambs at 24 to 36 hours of age. Steady-state glucose infusion resulted in a significant, though obtunded, increase in plasma insulin concentrations within 45 minutes; glucose/insulin ratios were higher than fetal values observed in similar studies (5.6 vs. 0.88, p

The extent and significance of spontaneous glucagon secretion in the immediate postnatal period were investigated in groups of normal infants studied cross-sectionally and longitudinally. Arginine-and alanine-stimulated glucagon secretion was also studied. Plasma glucagon concentrations were correlated with prevailing glucose and insulin concentrations. The characteristic fall in blood glucose, reaching a nadir within hours of birth, was associated with a significant increase in glucagon concentration. Despite persistence of relative glucopenia, glucagon did not change appreciably between 2 and 24 h of life. A further significant elevation in glucagon concentration occurred from day 1 to day 3 of life associated with a return of glucose to euglycemic levels. In contrast to the sluggishness of pancreatic glucagon release, glucagon-like immunoreactivity rose markedly to mean levels of approximately 2,000 pg/ml after introduction of formula feeding. No significant changes in insulin levels were observed in these studies. Arginine infusion via an umbilical vein catheter into six infants within 6 h of birth elicited a brisk, almost threefold increment in glucagon concentration (from 339±85 to 940±254 pg/ml) in blood obtained from, or close to, the portal circulation. Bolus injection of alanine (1 mmol/kg) into a peripheral vein to six infants resulted in significant increments in glucagon (mean maximal, 128 pg/ml) as well as glucose and insulin. The observations suggest that spontaneous glucagon secretion may be an important factor in neonatal glucose homeostasis. Secretion seems more brisk in response to amino acid stimulation than to a falling glucose concentration.

The growth hormone responses to arginine infusion and to insulin-induced hypoglycemia were studied in 13 patients with neoplastic disease after treatment with radiation and chemotherapy. Patients who received intensive cranial radiation (greater than 2,400 rads) had no response to either arginine or insulin; those who received moderate cranial radiation (greater than or equal to 2,400 rads) had GH response to arginine but not to insulin; patients receiving no cranial radiation responded to both arginine and insulin. These data support the hypothesis that GH secretion in response to arginine infusion has a different mechanism in contrast to the response to insulin-induced hypoglycemia and that the latter is more vulnerable to cranial radiation.

The ketogenic diet is a well-established, but relatively infrequently used, therapy for intractable seizures in children. Currently, the standard ketogenic diet is formulated using medium chain triglyceride (MCT) oil as its major caloric source. Cost, availability, and gastrointestinal side effects limit its use in some cases. We report the successful substitution of corn oil for MCT oil in six children treated with the ketogenic diet for intractable seizures. In each case, the corn oil ketogenic diet was effective, well-tolerated by the patient and parents, and free of clinical toxicity. Corn oil also has the major advantages of being much less expensive and more available than MCT oil. Its use in the ketogenic diet appears to be effective, safe, and practical.( J Child Neurol 1988;3:21-24)...

Summary: Hyperviscosity was produced in one member of each of 7 sets of twin newborn lambs by an exchange transfusion with 500 ml maternal packed red blood cells. The remaining seven control twin lambs underwent an identical exchange with maternal whole blood. Postexchange hematocrits were 63 ± 6 and 29.0 ± 3% (mean ± S.E.), respectively (P ≤0.01). Whole blood viscosity measured at 3 rpm increased from 3.2 ± 0.4 centipoise (cps) to 14.4 ±6.1 cps in the lambs made hyperviscous (P ≤0.01) and remained unchanged in the control lambs (2.2 ± 0.2 versus 2.8 ± 0.3 cps). A 2-hr steady state glucose infusion was performed on each lamb before and after the packed cell or whole blood exchange transfusion. Mean steady state plasma glucose concentrations were significantly decreased from pre-exchange steady state glucose infusion levels in the same lambs made hyperviscous (P ≤0.05), whereas steady state glucose levels increased from pre-exchange levels in the twin lambs exchanged with maternal whole blood. Mean plasma insulin and glucagon values for the hyperviscous and control lambs remained unchanged during the glucose infusion. Speculation: The fmding of an abnormality in glucose homeostasis in the absence of a hormonal or substrate disturbance in hyperviscous lambs suggests that there may be rapid glucose utilization from increased cerebral extraction of glucose and/or a reduction in endogenous glucose production caused by sluggish hepatic circulation.

We report sensitive radioimmunoassay procedures for glucagon-like immunoreactivity and for pancreatic glucagon, with use of antisera generated in rabbits by the injection of glucagon covalently coupled to thyroglobulin. Optimum assay conditions were determined. These assays have absolute limits of sensitivity of 10 to 20 pg, an intra-assay coefficient of variation of 8%, and an inter-assay coefficient of variation of up to 22%. In human infants 30 minutes after birth, glucagon concentration was 227 ± 27 pg/ml (SEM), and glucagon-like immunoreactivity increased sharply with oral feeding. In children and adolescents, plasma glucagon concentrations during fasting, the increase in response to arginine stimulation, and the suppression after oral glucose loading were similar to values previously reported in adults. Problems inherent in the methodology for measuring plasma glucagon are discussed.

SummaryThe presence of chronic, experimentally induced hypercholesterolemia in rhesus monkeys led to atypical patterns of lipid response during acute pneumococcal infection. When compared to infection in previously normal monkeys, hypercholesterolemic monkeys showed an impaired synthesis of cholesterol with accumulation of squalene in the plasma, an increased conversion of newly formed cholesterol to an esterified form, and an impaired utilization of triglycerides.

Extract: Experimentally induced endotoxemia in the rhesus monkey produced a two- to fourfold increase in plasma triglyceride concentration; glucose administration partially prevented this rise. Plasma free fatty acid and phospholipid values were depressed 40–50% of control values whereas cholesterol values were unchanged. Endotoxin-treated monkeys displayed slowed glucose disappearance (K values, 2.2 versus 1.1) and higher levels of sugar in blood when given glucose (72 ± 8 mg/100 ml versus 151 ± 11 mg/100 ml). These studies indicate that endotoxin has a marked effect on the pattern of substrate utilization by the host. Speculation: Alterations in lipid and carbohydrate metabolism affecting substrate utilization of the host may account for many of the clinicopathologic events associated with endotoxemia. Therapeutic measures designed to increase the availability of metabolic fuels for efficient cellular fuel utilization might be of value to patients during endotoxemia.

Constant glucose infusions to the sheep fetus in utero with the use of the chronic catheterized preparation produced a significant improvement in fetal blood gases and pH (pH, 7.37 ± 0.02 vs. 7.42 ± 0.01; Po 2 , 14 ± 1.4 vs. 19 ± 1.5 mm. Hg; and Pco 2 , 58 ± 1.5 vs. 44 ± 1.7 mm. Hg; mean ± S.E.M. of pre- and postinfusion values.) Similar changes were not observed after an acute intravenous-bolus injection of glucose. These results may be explained on the basis of improved circulatory and perfusion status of the fetal-placental unit when a sustained increase in fetal blood glucose level was achieved by constant glucose infusion.

The bidirectional transfer of radioiodine-labeled glucagon was investigated in the pregnant ewe late in gestation. Specific immunoprecipitation was used to identify 125I or 131I-glucagon in maternal and fetal plasma following direct injection into the fetus or simultaneous injections into the mother and fetus (dual label experiments). No placental transfer of labeled glucagon was detected, either in the fetal to maternal direction (5 studies), or in the maternal to fetal direction (2 studies). (Endocrinology 93: 1435, 1973)

Endotoxin in the neonatal rat produced marked elevations of plasma triglycerides, free fatty acids, and phospholipids. Incorporation of 3H-acetate into total lipids and cholesterol fraction of the brain was increased in rats given endotoxin, while incorporation into the phospholipid fraction in both brain and liver was decreased. These studies suggest that changes in plasma lipids provide not only a sensitive index of endotoxemia in the neonatal rat, but also reflect marked alterations in substrate utilization of the host during stress.

The effects of oral alanine feeding on glucose homeostasis were evaluated in 21 infants who were small for gestational age and 26 who were appropriate for gestational age. In the first 24 hours, basal plasma alanine concentrations were higher in the former. Oral alanine feedings produced a significant rise over baseline levels of plasma alanine and glucagon concentrations in both groups. The blood glucose and plasma insulin concentrations also increased significantly in infants who were appropriate but not in those who were small for gestational age. At 25 to 96 hours of age, plasma glucagon, insulin and blood glucose concentrations did not change after the alanine feeding in either group. These data indicate that in the normally nourished infant (appropriate forgestational age), gluconeogenic amino acid (alanine) enhances hepatic glucose output. This phenomenon is not observed in the mainourished infants (small for gestational age), a point that may reflect decreased glycogen stores and ineffective gluconeogenic enzyme system in such infants.

The effectiveness of orally administered activated charcoal in simulated acute barbiturate and glutethimide poisoning was assessed in fasting dogs. Twenty grams of activated charcoal was administered 30 minutes after a hypnotic dose of secobarbital, phenobarbital, or glutethimide. Differences greater than 50 per cent between control and experimental serum drug concentrations indicated significant inhibition of systemic absorption; this effect persisted over a 24 hour period. These studies show that activated charcoal is extremely effective in reducing barbiturate and glutethimide absorption in vivo and that the activated charcoal-drug complexes formed are essentially stable throughout the gastrointestinal tract.

An attempt was made to determine if correlations exist among plasma concentrations of alanine, the major amino acid substrate for gluconeogenesis, and plasma concentrations of glucose, glucagon, and insulin in normal newborn infants. The effects of an intravenous infusion of cl -alanine (1 mMl/kg) to six neonates was also determined. Although a peak in alanine concentration coincided with a nadir in glucose concentration at 12 hours of life, no correlation existed between the observed changes in alanine and glucose, or alanine and glucagon. Infused alanine caused increases in both plasma glucose and glucagon concentrations, as in the adult; the responses, however, were of small magnitude. Our data indicate that reduced blood glucose concentrations in the normal newborn infant are not due to a deficiency of alanine substrate for gluconeogenesis. And, although alanine stimulates secretion of glucagon, there is no consistent correlation between plasma alanine and glucose, or plasma alanine and glucagon concentrations during the early neonatal period. thus the key factors in control of glucose concentrations in the newborn period cannot be deduced from simple relationships of these plasma constituents.

A propos de l'observation d'une fille de 8 ans atteinte du syndrome de Donohue, nombre des expressions phenotypiques de ce syndrome sont compatibles avec des taux supraphysiologiques du facteur de croissance epidermique. Cependant, etant donnee la diversite des manifestations phenotypiques, elles peuvent ou non avoir une meme cause et il apparait important de confirmer les presentes donnees sur d'autres cas du syndrome

3. Lewis R, and Gorbach S: Actinomyces viscosus in man, Lancet 1:641, 1972. 4. Adeniyi-Jones C, Menielly JA, and Matthews WR: Actinomyces viscosus in a branchial cyst, J Clin Pathol 60:711, 1973. 5. Gutschik E: Endocarditis caused by Actinomyces viscosus, Scand J Infect Dis 8:271, 1976. 6. Leers WD, Dussault J, Mullens JE, and Volpe R: Suppurative thyroiditis: An unusual case caused by Actinomyces naeslundi, Can Med Assoc J 101:56, 1969. 7. Georg LK, Pine L, and Gerencser MA: Actinomyces viscosus, comb. nov., a catalase positive, facultative member of the genus Actinomyces, Int J Syst Bacteriol 19:291, 1969. 8. Gerencser MA, and Slacik JM: Identification Of human strains of Actinomyces viscosus, Appl Microbiol 18:80, 1969. 9. Turner OW, Robertson BS, and Langton RW: Cellmediated immune response to products of Actinomyces viscosus cultures, Infect Immun 14:372, 1976. 10. Engel D, VanEpps D, and Clagett J: In vivo and in vitro studies on possible pathogenic mechanism of Actinomyces viscosus , Infect Immun 14:548, 1976.

Extract: Twenty-four studies were conducted in 14 sheep fetuses to investigate the pancreatic islet α and β cell responses to substrate infusions. The studies were conducted between 100 days gestation and near term, using indwelling vascular catheters for infusions and blood sampling. Constant glucose infusions (6 mg/kg/min) produced a significant rise in the mean concentration of insulin in plasma by 105 min, but no change in glucagon in plasma was observed. Near term (>135 days) the mean plasma insulin increment with constant glucose infusion was significantly greater and occurred sooner than in fetuses early in gestation (

The effects of Triton WR 1339 on plasma lipids were studied in fasted and glucose-loaded rhesus monkeys. This compound produced a marked linear increase in plasma triglycerides (TG) during the first 4 hours of a 5-hour study period. Triglyceride secretion rates were determined in fasted and in glucose-loaded monkeys. Free fatty acid values (FFA) were depressed, while cholesterol and phospholipid values were unchanged. No evidence of hepatocellular or other tissue damage was noted at necropsy. These studies suggest that Triton administration is valuable in assessing rates of basal hepatic TG secretion in the rhesus monkey. (Modified author abstract)

Sandfly fever was found to stimulate a series of changes in the plasma concentration of lipids and their transport lipoproteins when the disease was induced experimentally in healthy young adult men, who had been equilibrated for 17 days on a constant liquid diet containing 40 per cent of calories as fat. Plasma values for total and esterified cholesterol, phospholipids, free fatty acids, and free glycerol declined in conjunction with, or prior to, the onset of fever, as did both the cholesterol and protein components of the low density lipoproteins. Concentrations of these moieties remained depressed for varying periods thereafter. Plasma triglyceride values also fell initially but then rose above base line in early convalescence. These lipid changes seemed compatible with a concept, (1) that the use of triglycerides and other lipids as metabolic fuel was increased prior to and during the early febrile period, and (2) that mechanisms that mediated metabolic responses to even a mild self-limited virus infection took precedence over some of the ordinary demands of energy balance.

Humoral and cellular immune responses to several antigens were compared in control and hypercholesterolemic groups of monkeys. Chronic hypercholesterolemia, with concomitant hyperphospholipidemia and hypotriglyceridemia, was produced experimentally by feeding monkeys a high-fat, high-cholesterol diet. When studied prior to infection, hypercholesterolemic monkeys exhibited impaired development of precipitating antibodies against ovalbumin, enhanced sensitivity to tuberculin antigen (stimulated apparently by mycobacterial components in complete Freund adjuvant), and an increased rate of clearance of colloidal carbon from blood. During pneumococcal infection the ability of neutrophiles from hypercholesterolemic monkeys to reduce nitroblue tetrazolium dye showed an increase greater than that of control monkeys; both groups exhibited increased but comparable final clearance rates of colloidal carbon, although the increment of increase was smaller in hypercholesterolemic monkeys.

A 9-month Mexican-American female has been followed for episodic hypoglycemia first documented in the immediate postnatal period. Three convulsions occurred with glucose levels (BS) 20 mg%. Physical exam has been normal to date. A 4 hr. fast resulted in hypoglycemia (30 mg%) and mild lacticacidemia. Basal and stimulated plasma growth hormone, glucagon and cortisol were normal. IV GTT normal; (K =1.6). Glucagon increased BS two-fold. Plasma insulin was < 5 μU/ml during hypoglycemia. IV substrate infusion results were: Fasting alanine levels also were increased. A liver biopsy, at 5 1/2 months, showed reduced levels of pyruvate carboxylase and markedly low or undetectable levels of PEPCK. All other gluconeogenic and glycogenolytic enzymes were normal. The data are compatible with an inborn error in gluconeogenesis at the level of PEPCK. The pyruvate carboxylase reduction is likely a secondary effect. This child represents the first documented case of PEPCK deficiency.

We previously reported an obtunded plasma glucagon response to stimuli in fetal sheep and suggested that relative hypoglucagonemia in the neonatal period might explain the tendency to hypoglycemia. The present studies were conducted to further test this hypothesis. Glucagon responses to alanine were measured after 4 or 24 hr. fast in 10 newborn and 5 infant lambs (3 months). With 24 hr. fasting glucose and alanine decreased 32 and 35% respectively (p < 0.05) in the newborns but glucagon levels did not increase (121 ± 31 vs. 101 ± 15 pg/ml). In response to alanine infusions glucagon increased 32% (p < .01) in the 4 hr. and 38% (p < .01) in the 24 hr. fasted newborns. Infant lambs fasted 24 hr. displayed similar glucose and glucagon levels to the newborn animals, but alanine levels were lower (p < .001). In response to alanine, glucagon increased 214% above base line (p < .001), a response significantly greater than that in the newborn animals. Theophylline pretreatment of newborn lambs augmented the glucagon response to alanine to levels observed in infant sheep (Δ = 245%, p < .01). These data show 1) residual immaturity of pancreatic glucagon secretion in neonatal sheep 2) maturation of this response with age and 3) that the diminished responsiveness in the newborn period may be related to a functional immaturity of the cyclic AMP generating system.

Glucose (G) disposal rate, plasma insulin (I) and plasma alanine (A) levels were studied in 8 full term infants (mean age=25 days) during acute infection and convalescence, 2 days and 8 days following antibiotic therapy for septicemia in 6 infants and/or meningitis in 5. Five infants had gram positive; 2, gram negative; and I, viral infection. Following a 1-2 hour constant G infusion (6 mg/kg/min), baseline G, I, and A samples were obtained. An intravenous glucose tolerance test (GTT) was performed giving 1 gm/kg G (in 50% solution). Peripheral blood G was obtained for calculation of G disposal rate (Kt) and at 30 to 45 min. for plasma 1 levels. Four non-septic infants underwent similar studies. The results show that (1) glucose utilization is enhanced during the acute phase of infection, and although decreased, remains high during convalescence (Kt acute=3.7 ± 0.3 vs. control = 1.8 ± 0.1, p

The decline in blood glucose (G) level during the immediate neonatal period has been attributed partly to sluggish glucagon (GN) release and relative deficiency in gluconeogenesis. This hypothesis was tested by measuring plasma G, GN, and insulin (I) response to oral feeding of 0.5 gm/kg of L-alanine in 40 AGA term, 10 AGA preterm and 16 SGA infants, age 1-4 days. Universally noted was an increase in G levels when baseline G levels were 60 mgjC. This was not related to gestational age, postnatal age, AGA or SGA. AGA term infants had a significant increase in I (6.4 ± 0.7 to 10.9 ± 1.7 μU/ml, M ± SEM, p < .05), at 1 hr. and GN at 1/2, 1, and 4 hrs. (300%, 228%, and 28% above baseline respectively, p

The etiology of the Prader-Willi Syndrome is obscure. Although the clinical characteristics (obesity, mental retardation, hypotonia and hypogonadism) suggest hypothalamic dysfunction, this has not been documented. We have studied two patients (15 and 22 yr.) with this disorder in whom clinico-pathologic correlation was possible. Both were severely obese (150 and 190 kg) with glucose intolerance. Cold exposure (4° C for 1 hr.) produced an abnormal decrease in body temperature in one child. Plasma growth hormone (GH) did not increase with arginine-insulin, or L-dopa stimulation. Plasma cortisol showed a diurnal variation but blunted response to hypoglycemia. Basal T4 and TSH were normal and the TSH, T4 and T3 responses to TRH were normal in both patients. Basal testosterone was low in both individuals and LH and FSH responses to LRH were blunted. Clomiphene stimulation failed to augment plasma gonadotropin levels. The pituitary glands were of decreased weight but neither the pituitary nor hypothalamus was abnormal on light microscopy. These studies indicate abnormal hypothalamic-pituitary function in both patients. Involvement of the temperature control center, absent clomiphene response, abnormal GH responsiveness and normal anatomical findings support the formulation of a functional hypothalamic abnormality.

We have shown that childhood obesity is associated with hyperinsulinemia involving the acute and chronic pools of insulin similarly. To define the mechanism(s) responsible for this, we have measured the response of plasma insulin, glucagon, growth hormone (GH) and free fatty acids (FFA) to various stimuli in 10 obese children and matched lean controls. To allow direct assessment of the uptake of glucose by peripheral tissue (impedance) we have utilized the technique of Shen (continuous infusions of glucose, insulin, epinephrine and propranolol) to suppress endogenous insulin secretion and hepatic glucose output. All patients had normal glucose tolerance. Basal insulin levels (94 vs. 10 μU/ml) and tissue impedance (247 vs. 86) were increased (p < 0.01) in obese patients. Younger obese children (3-6 yr.) had intermediate plasma insulin and tissue impedance values (30 and 168). The plasma glucagon and GH responses to arginine were blunted in obese patients. Fasting FFA and triglyceride (TG) levels and the FFA and TG responses to oral lipomul and heparin were similar in both groups. These studies demonstrate progressive impairment of glucose uptake by peripheral tissues in childhood obesity and suggest a basic tissue defect in carbohydrate metabolism.

The ICU Syndrome, manifested by anxiety, depression, hallucinations, and delirium, has been reported to occur in children but has not been well documented. The purpose of this study was to determine factors associated with the development of ICU Syndrome in children. Forty-three children between the ages of 6 and 17 years were studied, 18 in ICU and 25 on general wards. The Hospital Observed Behavior Scale (HOBS) was developed to describe acute adverse psychological reactions in four areas: anxiety, depression, delirium, and withdrawal. The Diagnostic Interview for Children and Adolescents (DICA) was administered to each subject and the DICA-P to each subject's parent to elicit any pre-existing psychopathology. Additional data collected included demographics, diagnosis, prognosis, previous admissions, duration of parental visitation (PV), amount of sleep, and medications. Good interrater reliability was found for the HOBS (r=0,63, p< 0.000001). Sixteen subjects demonstrated behavior clinically consistent with the ICU Syndrome, 11 ICU and 5 ward subjects. The mean HOBS scores were statistically different for those with and without the ICU Syndrome (9.3 ± 4.1 vs. 3.9 ± 3.6; p< 0.0005). Factors positively correlated with the mean HOBS were pre-existing anxiety disorder and race (black); negatively correlated was PV (p < 0.10). We conclude that the ICU Syndrome may be reliably diagnosed using HOBS and that it may occur in patients in both ICU and ward settings.

The significance of key substrate-hormone interrelations in neonatal glucose (G) homeostasis, was ascertained by measurements of plasma G, alanine (A), glucagon (GLU) and insulin (I) In the immediate hrs and days after birth. The effect of an A infusion was also studied. In cross-sectional studies over the initial 12 hrs of life, G fell (77 ± 6 mg% @ 1/2 hr to 57 ± 5 mg% @ 1-1/2 hrs) while GLU increased (224 ± 27 pg/ml to 420 ± 81 pg/ml) significantly, but A and I remained unchanged. When infants were sampled sequentially the fall in G (cord 133 ± 21 to 49 ± 14 mg%) and rise in GLU (83 ± 27 to 139 ± 41 pg/ml) during the first 2 hrs post birth was confirmed. G and GLU remained stable during the next 10 hrs but rose after 24 hrs; highest values were observed on day 3 (61 ± 6 mg% and 243 ± 30 pg/ml). Plasma A rose progressively; the peak at 12 hrs coinciding with the nadir of G. An increase in A also occurred from days 1 to 3. I remained unchanged throughout the period of observation. An I.V. infusion of 1mM/Kg A into 6 fasting infants at 12 hrs produced an elevation of plasma GLU at 15 min (208 ± 27 to 293 ± 62 pg/ml)and an increase in G at 30 min (47.8 ± 3.1 to 54.7 ± 1 rag%). Thus, in the neonate GLU secretion occurs in response to the stimulus of G need or gluconeogenic amino acid infusion. No consistent relation of endogenous A to G or GLU levels was observed but the response to A infusion suggests a potential role for this substrate in neonatal G homeostasis.