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Stable isotopes of calcium are used safely as tracers for calcium in human populations ranging in age from infants to postmenopausal women. Thermal ionization mass spectrometry is used to measure calcium isotope ratios with relative accuracies of about 1% for natural abundance ratios at precisions of about 1% relative to the mean. Perturbations of natural abundance ratios are determined for the calcium in blood, urine, and feces with a limit of detection of about 2 delta % excess. The mathematical rationale for clinical studies of fractional absorption of dietary calcium and the kinetics of calcium's internal distribution are presented.

The occurrence and properties of PTH-related peptide (PTH-RP) in milk was investigated. PTH-RP was purified to homogeneity from human and bovine milk using heat and acid to precipitate milk proteins followed by ion exchange chromatography and reverse-phase HPLC. The peak of PTH-RP from HPLC was detected using a sensitive bone cell bioassay. A single band of peptide was detected on silver-stained polyacrylamide gels, which migrated as a 20-21-kDa macromolecule. PTH-RP isolated from either human or bovine milk had similar electrophoretic mobilities on sodium dodecyl sulfate-polyacrylamide gel electrophoresis. The partially purified bovine PTH-RP stimulated cAMP production in UMR106-01 and OK cell lines and elicited a concentration-dependent inhibition of sodium-dependent phosphate transport in OK cells. Incubation of milk extracts with an anti-PTH antiserum did not affect their bioactivity, whereas an antihuman PTH-RP 1-34 antiserum markedly reduced the cAMP response of UMR106-01 cells to the immunoabsorbed milk extracts. A PTH antagonist, norleu PTH 3-34, blocked the stimulation of cAMP production in UMR106-01 cells treated with milk extracts. PTH-RP immunoreactivity and bioactivity occurred in milk extracts of diverse animals from both eutherian and metatherian (marsupial) species. Porcine colostrum also had immunoreactive PTH-RP, although the levels were lower than the immunoreactive PTH-RP concentrations observed in milk samples collected at 7 and 14 days of lactation. Thus, a 20-21-KDa PTH-RP is secreted into milk where it could play a role in the development of suckling, newborn animals.

Twenty-seven sick premature infants with serum calcium concentrations less than 6.0 mg/dl during the first day of age were enrolled in a prospective controlled study involving two treatment regimens--calcium given as a bolus or a drip--or no treatment. Mean total calcium concentration was 5.5 +/- 0.8 mg/dl, and ionized calcium was 3.1 +/- .3 mg/dl, with no significant difference between treatment groups. By 24 hours, in all groups total calcium had increased to greater than 6.0 mg/dl (bolus 6.5 +/- 1.1, drip 7.0 +/- 0.4, control 6.6 +/- 0.4) and ionized calcium to greater than 3.5 mg/dl (bolus 3.9 +/- 0.3, drip 3.6 +/- 0.6, control 3.6 +/- 0.3). Ionized and total calcium concentrations were significantly correlated (r = 0.562; P less than 0.001), but total calcium did not predict ionized calcium in any group. These data support the concept that, even in sick infants, early neonatal hypocalcemia is a physiologic phenomenon that may not require treatment.

Lung, liver, kidney, and rib specimens were obtained at autopsy from 66 sudden infant death syndrome (SIDS) infants and 23 infants who died suddenly from other causes between the ages of 4-26 wk. Tissue levels of lead and cadmium were measured by atomic absorption spectroscopy and are expressed as microgram/g dry weight. Because these metals are cumulative with age in storage tissues, the levels were corrected for age (adjusted to age 13 wk). The SIDS liver and rib specimens contained significantly more lead than non-SIDS tissues (liver, 1.095 microgram/g versus 0.761 microgram/g, P less than 0.05; rib, 1.754 microgram/g versus 1.041 microgram/g, P less than 0.01, respectively). There were no significant differences in cadmium concentration between the SIDS and non-SIDS tissues. All four tissues showed significant increases with age in both lead and cadmium concentrations in SIDS. The increase in lung lead concentration with age was significantly greater in SIDS than in non-SIDS cases, P less than 0.05. In non-SIDS only kidney cadmium showed an increase with age (P less than 0.0001). These data collectively suggest an increased exposure of the SIDS infant to lead either prenatally and/or postnatally. Any physiologic effects of the increased tissue lead levels are unknown. They may be only a marker of the known epidemiology of SIDS.

Detailed dietary records were obtained from 30 women with the irritable bowel syndrome and 25 healthy, asymptomatic women. Stool transit times and wet stool weights were measured. Analysis of the dietary data revealed no significant difference between energy, protein, fat, carbohydrate, or total fiber intakes. Total dietary fiber intake was 17 g/day in the irritable bowel group and 18 g/day in the control group, but vegetable fiber intake was significantly lower in the patients (6.6 g/day) than the controls (8.2 g/day). Cereal and fruit fiber were comparable for both groups as were the stool transit times and wet stool weights. These results do not support the hypothesis that symptoms of the irritable bowel syndrome are directly related to total or cereal fiber depletion.

Twenty-eight premature infants of mean gestation 30.9 +/- 2.5 weeks and mean birth weight 1175 +/- 206 g had repeated serum calcitonin concentrations determined over the first 12 weeks of life. Serum calcitonin concentrations slowly fell but remained elevated even at 12 weeks of age [normal adult = 71 +/- 48, 1 week (N = 15) = 327 +/- 167, 3 week (N = 23) = 270 +/- 129, 6 week (N = 16) = 249 +/- 154, 9 week (N = 13) = 214 +/- 108, 12 week (N = 12) = 174 +/- 11]. Throughout this period, serum total calcium was normal or low (8.4 +/- .8-9.3 +/- 1.0). Serum phosphorus was normal or low (6.0 +/- 1.4-6.5 +/- 1.0), and serum magnesium was normal (1.7 +/- 0.24-1.8 +/- 0.34). The reason for the sustained elevation of serum calcitonin in these very small, sick, premature infants in unclear.

Because of concern about tissue uptake of pasticizers used in medical equipment, di-(2-ethylhexyl) phthalate was measured by gas chromatography-mass spectrometry in neonatal heart and gastro-intestinal tissue. Seventeen infants who had umbilical catheterization alone or with administration of blood products, and 13 stillborn or older controls were studied. The mean levels of the plasticizer for heart residue and pressed extract in the study group --1.27 plus or minus 0.42 and 0.66 plus or minus 0.22 mug per gram respectively--were significantly (pgreater than 0.005) higher than the corresponding control levels (less than 0.07 plus or minus 0.03 and less than 0.07 plus or minus 0.04 mug per gram). Higher levels were associated with larger amounts of blood products, more extensive use of catheters, and early death. Levels in gastrointestinal tissue from three infants who had died of necrotizing enterocolitis were significantly (less than 0.05) higher than those in gastrointestinal tissue from infants without this disease. Thus, plasticizer from medical use of plastics does accumlate in tissues of critically ill infants.

25-Hydroxyvitamin D-binding capacity and affinity were studied in human cord, adult, and maternal sera, and in sera from women receiving oral contraceptives, by in vitro satuaration analyses employing dextran-coated charcoal to adsorb unbound sterol. 25-Hydroxyergocalciferol and 25-hydroxycholecalciferol were equipotent in their ability to displace 3H 25-hydroxycholecalciferol from human serum binding sites. At 0C, the apparent dissociation constant for the serum binding of 25-hydroxycholecalciferol was low (Kd=8x 10-10M). Cord and adult sera had a similar 25-hydroxycholecalciferol binding capacity (1.8 x 10-6M), but the binding capacity of maternal sera and the sera from women receiving oral contraceptives was significantly higher. At physiological serum concentrations of 25-hydroxyvitamin D (5 x 10-8M), only 2-3% of human serum 25-hydroxyvitamin D-bindig sites are occupied.

Six cases of endoscopically documented acute oesophagitis during therapy with emepronium bromide (Cetiprin) for urinary symptoms are described. The oesophagitis was associated with acute severe retrosternal pain and dysphagia which resolved spontaneously on stopping medication. The potential of this drug to induce severe oesophageal inflammation and ulceration should be emphasised.

Craniofacial pain can be one of the more intractable problems that presents to the GDP. One management route can be referral to a specialist pain relief unit, where the facilities and expertise will be available for diagnosis, counselling, drug management and invasive therapy. In this article the authors describe the results achieved at one such unit, over a one-year period, for a group of 34 craniofacial pain sufferers. At the end of the year 30 patients reported total or partial relief from their pain.

Fetal and maternal compartments differ in factors shown to regulate 24.25 dihydroxyvitamin D [24,25(OH)2D] metabolism [calcium, phosphorus, and parathyroid hormone (PTH)] such that one might predict that maternal serum 24,25(OH)2D levels are decreased and fetal 24,25(OH)2D concentrations are increased. To evaluate this, 25-hydroxyvitamin D (25OHD), 24,25(OH)2D, calcium, magnesium, calcitonin, and PTH were measured in 24 paired maternal and cord sera. The mean maternal serum 24,25(OH)2D concentration (2.9 +/- 0.26 ng/ml) was significantly lower than that of nonpregnant females (3.9 +/- 0.37 ng/ml). Mean serum PTH and calcitonin levels were, however, normal in maternal sera. The normal elevations of PRL, estrogen, and placental lactogen in serum of pregnant women could possibly decrease 24,25(OH)2D production, as seen in animal experimental systems. There was no correlation (R = -0.25) between 24,25(OH)2D levels in maternal and cord sera, as predicted; however, mean (+/-SE) fetal 24,25(OH)2D (2.5 +/- 0.26 ng/ml) was similar to the mean maternal concentration and significantly below the mean level in normal adults. The low fetal 24,25(OH)2D concentration may be due to 1) decreased 24-hydroxylase capacity of the fetus; 2) regulation by fetal factors other than calcium, phosphorus, and PTH; or 3) increased utilization of 24,25(OH)2D possibly for fetal bone mineralization.

Deficiencies of various vitamin and minerals per se have been suggested as possible causes of sudden infant death syndrome (SIDS). Further, a deficiency of essential minerals may lead to enhanced toxicity of toxic elements, in particular, lead and cadmium to explore the possibility of mineral deficiencies or interactions with the toxic metals, lead and cadmium, lung, liver, kidney, and rib specimens were obtained at autopsy from 66 SIDS infants and 23 infants who died suddenly from other cases. Tissue copper, zinc, calcium, and magnesium were measured by atomic absorption spectroscopy. No differences were found between SIDS and non-SIDS for any element in any tissue except for more magnesium in the liver (P less than 0.0001) and less copper in the lungs (P less than 0.02) in the SIDS group. Only sporadic interactions between toxic and essential elements could be found. We found no evidence of any essential mineral deficiencies per se or significant interactions of essential and toxic minerals that might potentiate the effects of toxic metals. The physiologic significance, if any, of the higher liver magnesium and lower lung copper found in SIDS is unclear.

A patient who developed signs of acute bowel obstruction following upper intestinal endoscopy is described. Relations of endoscopy to the symptoms and therapeutic measures are discussed.

To further define control of mineral homeostasis during lactation, 28 lactating (L) and 20 nonlactating (NL) women were studied at 6 weeks post partum. Serum and urine calcium, magnesium, and phosphorus were normal and the same in both groups. 25-Hydroxyvitamin D (25-OHD) was the same (L, 18.6 +/- 4.8; NL, 17.0 +/- 5 ng/ml) in spite of a twofold higher intake of vitamin D in the lactating group. The serum fractions containing 24,25-dihydroxyvitamin D (24,25(OH)2D) were lower than in nonpregnant adults in both groups but significantly lower (P less than 0.05) in lactating than in nonlactating women (L, 1.67 +/- 1.7; NL, 2.46 +/- 1.3 ng/ml). 1,25-Hydroxyvitamin D (1,25-(OH)2D) was normal in both groups (L, 25.8 +/- 8.6, NL, 31.8 +/- 8.1 pg/ml). Parathyroid hormone (PTH) was normal in both groups (L, 5.6 +/- 2.0; NL, 7.2 +/- 1.9 microliters Eq/ml), and calcitonin (HCT) was equally detectable. As expected, prolactin was higher in the lactating group (L, 46 +/- 36; NL, 14.3 +/- 14.9 ng/ml). Serum prolactin levels had no correlation with serum 1,25(OH)2D. Estradiol was significantly (P less than 0.02) lower in lactating women (L, 78 +/- 23; NL, 105 +/- 28 pg/ml). One could speculate that the lower levels of estradiol in the presence of low 24,25(OH)2D and normal HCT allow bone resorption to occur at a rate adequate to supply the mineral needs of lactation without elevations of either PTH or 1,25(OH)2D.

Serial concentration values of 25-hydroxyvitamin D (25-OHD) were determined in the sera of term, premature, and twin infants. In infants born at term with normal concentrations of 25-OHD in cord blood, serial concentrations of 25-OHD remained normal; in infants born at term with low concentrations of 25-OHD in cord blood, serial concentrations of 25-OHD increased. In premature infants with normal concentrations of 25-OHD in cord blood, serial concentrations of 25-OHD decreased; in premature infants with low values of 25-OHD in cord blood, serial concentrations of 25-OHD did not increase until a postconceptual age of 36 to 38 weeks. The concentrations of 25-OHD in the sera of twin infant pairs followed parallel courses. Oral and intravenous supplementation of vitamin D did not significantly increase the concentrations of 25-OHD in serum of premature infants. These findings suggest that a decreased rate of 25-hydroxylation of vitamin D may be a factor impairing homeostasis of 25-OHD in premature infants.

Bathing with soap containing hexachlorophene was instituted during two major staphylococcal epidemics in a Neonatal Intensive Care Unit. Infants who weighed less than 1,200 gm, those with a postconceptional age of less than 35 weeks, and those with large areas of abraded skin were at highest risk to achieve elevated blood HCP concentrations. T 1/2 of HCP ranged from 6.1 to 44.2 hours and appeared to follow first order kinetics. Time of peak blood concentrations of HCP following a bath ranged from 6 to 10 hours. One infant with liver disease achieved a concentration of HCP of 4,350 ng/ml after seven baths and developed clinical symptoms consistent with HCP toxicity.

A self-consistent description is given for the propagation of a weak optical probe beam through a homogeneously broadened two-level medium in the presence of a strong, collinear, near-resonant pump beam. The propagation of the probe beam is given in terms of bichromatic natural modes, which contain frequency components symmetrically displaced from that of the pump beam. The two frequency components have a definite relative amplitude and phase, which are determined solely by the frequency detunings of the optical fields from the atomic resonance and by the intensity of the pump field. A simple method for calculating these natural modes is derived, and their importance in describing nearly degenerate four-wave mixing, optical bistability, and the stability of homogeneously broadened ring lasers is discussed.

Mortality from neonatal meningitis due to gram-negative microorganisms remains 50% despite use of aminoglycoside antibiotics. Blood was obtained on 238 occasions from 77 neonates with putative or documented sepsis; paired blood and cerebrospinal fluid (CSF) samples were obtained on 14 occasions from ten neonates with meningitis. Kanamycin and gentamicin were measured by a radioisotopic assay procedure. Kanamycin was administered at 15 mg/kg/day in three divided doses intravenously; serum concentrations peaked at one hour (mean, 7.77mug/ml). Gentamicin was administered at 7.5 mg/kg/day in three divided doses intravenously; serum concentrations peaked at two hours (mean, 5.34mug/ml). Both aminoglycosides generally were nondetectable within the CSF; survival of neonates with gram-negative meningitis correlated specifically with the sensitivity of their isolates to ampicillin which was administered concurrently. This study suggests that alternative approaches to the treatment of neonatal sepsis should be explored; administration of an antibiotic which crosses the blood-cerebrospinal fluid barrier more readily should be considered.

A study was undertaken to determine the practicality of replacing rigid sigmoidoscopy with flexible fibresigmoidoscopy. A total of 388 examinations were performed and complete examination was possible in 79% of patients in less than 10 minutes. Abnormalities were found in 18% of patients; colorectal polyps and tumours were identified in 11% of patients. No complications occurred and the investigation was well tolerated. Fibresigmoidoscopy is a practical, safe procedure for routine use in the outpatient setting and has several advantages over rigid sigmoidoscopy.

We have developed a method for measuring true fractional calcium absorption (alpha) in premature infants using two stable isotopes of calcium and tested it in seven studies in seven infants (birth weight 1543 +/- 65 g, gestation 32.8 +/- 7 wk). A total of 7.5 micrograms/kg 46Ca was given as a single intravenous bolus. Immediately thereafter 1.25 mg/kg of 44Ca was given in a single gavage feeding of standard infant formula (Enfamil). A metabolic isolette was used to obtain 4-h collections of urine for 24 h total. 46Ca and 44Ca were measured in urine by thermal ionization mass spectroscopy and expressed as the ratio to naturally occurring 48Ca. The differences in the 46Ca/48Ca and 44Ca/48Ca ratios from natural levels (delta % excess 46Ca and delta % excess 44Ca) were calculated. Percent absorption (alpha) equals a constant times cumulative delta % excess 44Ca/delta % excess 46Ca. The calculation of alpha is independent of urine volume or concentration. The delta % excess 46Ca, showed the expected multiexponential decline as a function of time, and delta % excess 44Ca usually peaked during a 4- to 8-h urine collection. Calculations of alpha using increasingly long sampling times showed that a plateau had been reached by 12 h. alpha values calculated after 16-24 h in the seven infants at 2 wk of age were 41, 48, 45, 46, 25, 55, and 51%. Repeat studies at 3 wk of age were 46, 60, and 54%. These values are somewhat higher than net percent calcium absorption values reported for standard formula and thus appear very appropriate.(ABSTRACT TRUNCATED AT 250 WORDS)

Apolipoproteins are important in the structure and metabolism of lipoproteins, and alterations in levels of apoproteins or in their interrelations occur in some forms of hyperlipemia. Pregnancy is regularly accompanied by hyperlipoproteinemia, but while data on lipoprotein lipids is available, the apopipoproteins have not been studied. To characterize the lipemia of pregnancy more completely, we studied some of the apolipoproteins in plasmas of pregnancy women. Thirty-eight normal fasting women were studied between the 18th and 39th weeks of gestation and again 23 plus or minus 17 weeks after delivery. Eight additional women were sampled every 4-6 wk during the second and third trimesters of gestation. Plasma and lipoprotein lipids were assayed by standard procedures and Apolipoprotein B (ApoB) was measured by radioimmunoassay. The interrelations of Apolipoprotein A (ApoA) in high-density lipoprotein (HDL) and of Apolipoprotein C (ApoC) in very-low-density lipoprotein (VLDL) were assessed by disc gel electrophoresis in four women during the last trimester of gestation and again 6-8 mo post partum and in four nongravid controls. Gestational triglycerides (TG) and cholesterol (Chol) were elevated in 95% of the pregnant women. TG in lipoproteins rose progressively during gestation, with VLDL-TG rising the most. Low-density lipoprotein (LDL) and HDL became enriched by TG relative to other components. Total-and VLDL-ApoB increased, while LDL-ApoB remained unchanged, resulting in a change in the density distribution of ApoB. (VLDL-ApoB X 100/total ApoB rose from 3.6% to 6.7%, P less than 0.02.) The accumulation of TG-rich LDL and the increases of VLDL-ApoB may be the result of changes in the rates of secretion or intravascular catabolism of VLDL. Which process is altered remains to be determined. The relative amounts of ApoC-II and ApoC-III in VLDL and the ApoA-I/ApoA-II ratios in HDL were unchanged in pregnancy. These results differ from those seen following high-carbohydrate diets.

Among the many theories put forth to explain sudden infant death syndrome (SIDS) is a theory of vitamin D deficiency. 25-Hydroxyvitamin D (25-OHD) serum concentrations were measured in 31 SIDS and 24 postmortem control infants. 25-OHD was 19.0 +/- 7.9 mg/ml in SIDS, 16.9 +/- 5.2 ng/ml in acute death control infants, and 11.9 +/- 4.4 ng/ml in in-hospital deaths. For four "near miss" infants the mean serum 25-OHD concentration was 21.1 +/- 4.1 ng/ml. The mean serum 25-OHD concentration of 39 living premature or small-for-gestational-age infants at 3 months of age was 26 +/- 9.9. Serum calcium and serum copper concentrations were also the same in SIDS and control infants. Parathyroid hormone was measured in ten and was detectable in five SIDS infants. These data eliminate a simple vitamin D deficiency or a 25-OHD deficiency as a significant contribution to the pathophysiology of SIDS.

Clinical details of 30 Caucasian women suffering from the irritable bowel syndrome were analyzed. Dietary fiber intakes, stool transit time, and stool weights were compared between groups of differing bowel habit and no statistically significant differences were found. A significant correlation between the clinical severity and the anxiety score on the Middlesex Hospital Questionnaire was present, but there was no correlation with other psychoneurotic traits or self-rating depression scores. Two to 3-year follow-up after management with a high fiber diet in 14 patients, showed that symptoms had improved greatly in seven, were unchanged in five, and were worse in two. Although dietary fiber had increased by a mean of 6.7 g/day, the clinical course could not be correlated with the amount of fiber consumed nor was it possible to predict the course of the individual patient from any clinical or psychological score. Despite persistence of symptoms at follow-up these were generally less severe and associated with significant decreases in anxiety, somatic and self-rating depression scores with the somatic score correlating with a decrease in clinical severity.

Nine premature infants developed radiographic and biochemical rickets at a mean +/- SD of 12.6 +/- 2.8 weeks of age. Serum 25-hydroxyvitamin D concentrations were all low, with a mean of less than 3.6 +/- 2.1 ng/ml. The mean average daily intake of vitamin D since birth had been 300 +/- 181 IU, and the mean average daily intake during the week of diagnosis was 587 +/- 313 IU. All of the infants were extremely premature (mean weight 948 +/- 153 gm, mean gestation 27.7 +/- 1.1 weeks), and were being fed either a low-calcium "human milk-like" formula or a soy formula. It is postulated that low-calcium intake may have increased 25-OHD utilization in the face of a decreased ability of the extremely premature infant to produce 25-OHD. Because of multiple factors leading to both decreased production and possible increased utilization of 25-OHD, such infants have an increased requirement for vitamin D to maintain normal serum 25-OHD concentrations, and daily intakes of at least 400 IU vitamin D orally must be assured. Serum 25-OHD measurements and radiographs may be important in following infants at risk.

A fatal case of mepivacaine poisoning in a newborn infant is reported. Regional brain tissue concentrations of mepivacaine were determined by a sensitive and specific gas chromatographic-mass spectrometric method. The brain tissue levels in this patient were higher than those previously reported, possibly due to alkalosis occurring several hours prior to the infant's death.

The mean +/- SEM of the cord, 48-hr, and 7-day values for serum calcium, magnesium, human calcitonin (HCT), parathyroid hormone (PTH), and 25-hydroxy-vitamin D (25-OHD) for premature and term infants can be seen in Table 1. Mean cord calcium concentrations were similar for term and premature infants. Serum calcium concentrations fell in both term and premature infants at 48 hr, but decreased more in the premature infants (from 10.23 +/- 0.30 to 8.74 +/- 0.19 mg/dl) than in the term infants (from 10.5 +/- 0.26 to 9.6 +/- 0.23 mg/dl). Serum calcium values increased from 48 hr to 7 days in both groups, and there was no significant difference between term and premature infants' serum calcium concentrations (10.6 +/- 0.28 and 10.12 +/- 0.3 mg/dl, respectively) at that time. There was no significant difference between term and premature cord serum magnesium concentrations. Serum magnesium concentrations increased similarly by 48 hr in both groups and remained at these concentrations at 7 days of life. Serum HCT concentrations were elevated above normal adult levels (71.9 +/- 6.6 pg/ml, 81% less than 100 pg/ml, n = 63) in both premature and term cord sera, but premature cord concentrations (146 +/- 24 pg/ml) were significantly higher than term cord concentration (91 +/- 21 pg/ml). Both term and premature infants displayed a 2-3-fold increase in serum HCT by 48 hr and a partial fall by 7 days to concentrations still above those seen in cord sera (Fig. 1). Nine of 10 premature and 9 of 10 term infants had undetectable PTH concentrations in cord sera. In two premature infants, PTH serum concenttration remained undetectable at 48 hr. However, the majority of both premature and term infants had elevated levels of PTH at 48 hr. The mean PTH concentrations were lower but still elevated at 7 days with the suggestion of higher concentrations in premature infants (Fig 2). There were no significant differences in serum 25-OHD concentrations between term and premature sera at birth or at 7 days. There was a weakly positive correlation between 25-OHD and cord calcium (r = 0.45, P less than 0.05), and a negative correlation between cord calcium and 48-hr PTH (r = -0.53, P less than 0.01). Calcium and magnesium were significantly positively correlated in 48-hr (r = 0.83) and 7-day (r = 0.84) sera in premature infants but not in term infants. Cord 25-OHD and cord HCT levels were significantly positively correlated (r = 0.80, P less than 0.01) in the term infants but not the premature infants.

Eight-week randomized cross-over studies in three separate groups of 10 healthy volunteers were undertaken to determine the effects of daily dietary supplementation with pectin (12 g/day), cellulose (15 g/day) and lignin (12 g/day) on serum lipid levels. Detailed dietary records were kept throughout the study and there was no significant change in dietary intakes except for the fiber supplement. Neither pectin, cellulose, nor lignin significantly altered serum total cholesterol, triglycerides, high-density lipoprotein cholesterol, or the ratio of high-density lipoprotein to total cholesterol in healthy normolipidemic subjects over four weeks.

Serial measurements of vitamin D-binding protein (DBP) were made in 28 infants of 29.7 +/- 2 weeks gestation and 1162 +/- 344 g birthweight. Mean (+/- SD) values (micrograms per ml) were: cord, 375 +/- 97; 1 week, 396 +/- 82; 3 weeks, 382 +/- 67; 6 weeks, 393 +/- 78; 9 weeks, 372 +/- 120; and 12 weeks, 490 +/- 130. At 12 weeks of age (40-42 weeks postconceptual age), DBP, 25-hydroxyvitamin D (25OHD), calcium, phosphorus, copper, and albumin were all significantly increased (by paired t test). At this point, but not earlier, DBP was correlated with 25OHD (r = 0.69; P less than 0.01) and phosphorus (r = 0.49; P less than 0.05), and 25OHD was correlated with phosphorus (r = 0.48; P less than 0.05) and calcium (r = 0.44; P less than 0.05). This may represent a concomitant maturation of the liver's protein synthetic abilities and the absorption and/or 25-hydroxylation in the liver of the parent vitamin D.

We measured serum concentrations of thyroxine (T4), triiodothyronine (T3), reverse T3, free T4, thyroid-stimulating hormone, and cortisol in 62 victims of sudden infant death syndrome (SIDS) in 30 infants who died of known causes and in 15 living controls. The mean T3 value was elevated in 69% of those with SIDS. 37% of the others who died, and in no control infants. After excluding those who died of known cause who had abnormal thyroid function (abnormal postmortem concentrations of T4, free T4, or reverse T3), the T3 values were elevated in 63% of those remaining. When the data were analyzed on the basis of case histories and autopsy findings, those infants who were in good health and died suddenly of accidental causes had an elevation in mean T3 similar to that seen in SIDS victims; those who died under conditions known to alter thyroid metabolism did not. The T4, free T4, reverse T3, thyroid-stimulating hormone, and cortisol values were not useful in differentiating those with SIDS from the living controls, or those who were healthy at the time of death. We were unable to find any difference in T3 serum concentrations between the total group who had SIDS and those who had SIDS with minor infections, with petechiae on intrathoracic organs, with premature birth, or those who were resuscitated. Our data point out the importance of using appropriate controls when evaluating SIDS. The normal reverse T3 values in SIDS, as well as confirmation of the normal T4 and free T4 values, constitute evidence against chronic persistent alveolar hypoventilation or prolonged episodes of hypoxia immediately preceding death from SIDS.

Sera were obtained during the last trimester from both black and white women receiving prenatal care for determinations of calcium, magnesium, and 25-hydroxyvitamin D (25-OHD). The mean serum 25-OHD concentrations were 15.4 +/- 5.9 ng, per milliliter (S.D.) in February (n = 56) and 42.1 +/- 13.9 ng.per milliliter in August (n = 61). There was no significant racial difference in serum 25-OHD in February or August. No seasonal difference in calcium was noted but magnesium concentrations were lower in August. No correlation existed between serum 25-OHD and serum calcium or magnesium, parity, time from last pregnancy, maternal age, or social class. Concentrations of 25-OHD showed weak correlations with vitamin D intake (r = 0.32) and duration of gestation (r = 0.26) in the winter only. These data suggest that, regardless of race, ultraviolet exposure is the major determinant of maternal serum 25-OHD concentration in St. Louis. Dietary intake and and other factors may be important during periods of decreased ultraviolet exposure.

Randomized cross-over studies were undertaken to determine the effects of daily dietary supplements of pectin (12 g/d), cellulose (15 g/d) and lignin (12 g/d) on stool characteristics of healthy volunteers. Detailed dietary records were kept throughout the study. Stool collections over 48 h were used to determine mean stool pH and weight. The single stool transit time was measured using radio-opaque markers. Pectin did not significantly alter the mean stool pH, transit time or 24 h wet weight. Cellulose lowered the mean stool pH from 6.38 to 6.12, decreased mean stool transit time by 27% and increased mean wet stool weight by 57%. Lignin lowered the mean pH from 6.34 to 6.25, decreased the stool transit time by 20% and increased stool weight by 27% but these changes were not statistically significant. These findings have shown that individual fibre components have different colonic metabolic effects and support the view that associations between dietary fibre intakes and diseases such as colorectal cancer should be evaluated with regard to the type of fibre components consumed.