摘要:

Total serum cholesterol, phospholipids, and triglyceride levels, lipoprotein fractionation, and plasma parathormone levels were measured in a group of 31 nonnephrotic children with various levels of renal function and on hemodialysis. Group A served as controls and consisted of eight healthy children with glomerular filtration rate (GFR) greater than 110 ml/min/1.73 m2. Group B consisted of six children with GFR of 60 to 95 ml/min/1.73 m2. Group C consisted of nine children with GFR of 10 to 40 ml/min/1.73 m2, and group D consisted of eight children on maintenance hemodialysis with GFR of 0 to 5 ml/min/1.73 m2. Among the groups, there were no significant differences in total serum cholesterol and phospholipid levels. A significant (P> 0.05) increase in triglyceride levels was observed in patient groups C and D.Lipoprotein fractionation revealed a significant increase (P> 0.05) in the pre-beta lipoprotein levels (very low density lipoproteins) in patients in group D with 63% of these patients demonstrating a type IV lipoprotein pattern. There were no significant differences observed in the beta lipoproteins (low-density lipoproteins). However, the alpha lipoproteins (high-density lipoproteins) decreased significantly (P> 0.05) in patients whose GFR was below 40 ml/min/1.73 m2(group C) as well as patients in group D.Absolute plasma parathormone levels did not significantly correlate with serum triglyceride levels and remained normal until after the onset of hemodialysis when they increased significantly in all patients.SpeculationEvidence has been accumulating over the past few years that chronic hemodialysis and renal transplant adult patients have shortened survival because of accelerated atherosclerotic cardiovascular disease for which hyperlipidemia could be one of several etiologic factors. Similar epidemiologic studies have not been performed in children. We have demonstrated for the first time in children that alterations in serum triglycerides and alpha lipoproteins (high-density lipoproteins) occur early in chronic renal insufficiency and before the onset of uremia when the glomerular filtration rate falls below 40 ml/min/1.73 m2. These lipid abnormalities become further aggravated with the onset of hemodialysis. If pediatric renal transplant patients show similar lipid abnormalities, then the potential for cardiovascular complications will be of importance in the early medical management of these children.

ISSN:0031-3998    

出版商:OVID    

年代:1981

数据来源: OVID

摘要:

To initiate an investigation into the biochemistry and mechanism of group B β-hemolyticStreptococcusvirulence, bacterial cultures grown in suspension were centrifuged, and the bacteria and media were subjected to extensive fractionation. Each fraction was assayed for physiologic activity by repeated intravenous infusion into adult unanesthetized sheep. Pulmonary artery pressure, arterial Po2, and rectal temperature were monitored. The media fraction, but not the bacteria, contained a component (molecular weight, 2 X 106) composed of 84% carbohydrate and 16% protein with physiological activity. Two mg quantities, when infused, caused the pulmonary artery pressure to increase 100%, Po2to decrease by 20% and chills and fever. The active component could be degraded by hot phenol-water extraction into a pure polysaccharide (molecular weight, 200,000). This lower molecular weight polysaccharide retained the identical physiologic properties when infused in the sheep. The degraded component precipitated with group B-specific antiserum.This study demonstrates that, in the sheep, a pure polysaccharide is the physiologically active part of a high-molecular-weight toxin synthesized by group B β-hemolyticStreptococcustype III and that this component has a different carbohydrate composition from the group B capsular antigen.SpeculationThe clinical syndrome associated with group B β-hemolytic Streptococci in early onset disease is caused by the interactions of an extracellular bacterial component and a specific target tissue in the infected infant.

ISSN:0031-3998    

出版商:OVID    

年代:1981

数据来源: OVID

摘要:

To study the effects of Group B β-hemolyticStreptococcuson the pulmonary circulation and lung fluid balance, live and heat-killed bacteria and their toxin were infused into an awake sheep lung-lymph preparation. In every case, the response was biphasic; there was an initial period of marked pulmonary hypertension and high flow of protein-poor lymph associated with tachypnea, chills, and fever. A second phase followed during which pulmonary vascular pressures returned to near baseline and remained stable, but lymph flow remained high. The changes seen in the initial phase resemble the previously reported response to mechanically increased pulmonary vascular pressure and suggest that the increase in fluid filtration is secondary to increased microvascular pressure. During the second phase after toxin infusion, the increase in lung lymph flow was paralleled by an increase in lymph protein clearance. This cannot be accounted for by the hemodynamic changes alone and suggests that the permeability of lung microvascular walls to protein was increased. It is concluded that group B β-hemolytic streptococcal toxin in the sheep model causes pulmonary hypertension and increased pulmonary vascular permeability.SpeculationThe effects caused by group G β-hemolyticStreptococcustoxin on the pulmonary circulation may be relevant to the pathogenesis of the respiratory distress and shock seen in newborns with this infection. Further understanding of the effects of this toxin could provide means for therapeutic intervention.

ISSN:0031-3998    

出版商:OVID    

年代:1981

数据来源: OVID

摘要:

The present study was designed to evaluate the red blood cell (RBC) radiolabeling technique utilizing the short half-lived radio-nuclide technetium-99m and to compare the results with the well-recognized standard chromium-51 method. The procedure was evaluated in a canine and a newborn lamb model utilizing dual radionuclide labeling and counting techniques. With the express purpose of providing a significant radiation dose reduction, the procedure presented was adapted for utilization in a neonatal patient population. Statistical analysis of the data revealed that there was no significant difference in the radiolabeling efficiency for the two methods (Cr-51, 86.6%; Tc-99m, 92.4%). Assessment of thein vivostability for technetium-99m RBCs showed that less than a 4% loss of radiolabel from the RBC was seen in a 4-hr time span in the canine model (15 min, 90.5%; 2 hr, 88.9%; 4 hr, 86.6%) when compared to the 15 min equilibrium sample.Evaluation of newborn lamb RBC volumes showed that the technetium-99m RBC volume did not significantly differ from the chromium-51 labeling technique (Cr-51, 24.0 ml/kg; Tc-99m, 23.2 ml/kg). Summarization of the whole-body radiation dose showed that greater than a 30-fold reduction in absorbed dose was achieved in the newborn (Cr-51,30.0 mrad; Tc-99m, 0.9 mrad). The modified procedure presented for the radiolabeling of the RBC with the short half-lived radionuclide technetium-99m provides a technique comparable to the utilized standard chromium-51 RBC method, yet with a large reduction in absorbed radiation dose. This procedure is presented as a superior technique for the determination of pediatric RBC volumes.SpeculationDemonstration of the efficacy of radionuclide dilution techniques in two species (animal models) predicates for the application of this procedure in neonates. The accurate assessment of circulating red blood cell volume affords the neonatologist a unique management tool while accruing significant radiation dose reduction using the short half-lived technetium-99m rather than the standard chromium-51 technique.

ISSN:0031-3998    

出版商:OVID    

年代:1981

数据来源: OVID

摘要:

In a review of 13 documented cases of fetal alcohol syndrome (FAS), an increased incidence of life-threatening bacterial infections as well as a propensity to minor infections was observed. Five of 13 patients had had at least one episode of pneumonia, two had meningitis, and one had sepsis. A comprehensive immunologic evaluation of FAS was completed, and results were compared to an age-matched control group of children with intrauterine growth retardation without FAS.Children with FAS were shown to have decreased E rosette-forming lymphocytes (35 ± 5%versus55 ± 5% or 1328 ± 274versus2333 ± 112 per mm3), low EAC rosette-forming lymphocytes (15 ± 2%versus18 ± 1% or 524 ± 109versus740 ± 75 per mm3), and diminished mitogen-induced stimulation responses to mitogens: 31616 ± 5337versus58076 ± 4455 cpm for phytohemagglutinin, 17582 ± 5436versus35018 ± 5346 for pokeweed mitogen, and 32460 ± 7044versus54996 ± 5531 for concanavalin A,P< 0.05. Nine patients had dysgammaglobulinemia. FAS subjects also had a marked eosinophilia (624 ± 154versus72 ± 27 mm3). Other parameters of immune function including absolute lymphocyte and neutrophil counts, total hemolytic complement, delayed cutaneous hypersensitivity, and nitroblue tetrazolium dye reduction assays, were not different from control children. Impairment of immunity may explain an increased susceptibility to infection in FAS.SpeculationDefects in host defense and propensity to infection are attributable to intrauterine exposure to high levels of alcohol. Such abnormalities are not related to the degree of postnatal growth retardation nor to degree of malnutrition and do not correct with increasing age. Subsequent disease processes associated with defects in immunity such as malignancy or autoimmunity could result from this exposure to alcohol during fetal development.

ISSN:0031-3998    

出版商:OVID    

年代:1981

数据来源: OVID

摘要:

The activity of phenyl-N-methyl transferase (PNMT), the adrenomedullary enzyme which catalyzes theN-methylation of norepinephrine (NE) to epinephrine (E) is induced by endogenous glucocorticoid hormones secreted by the adrenal cortex. We quantitated the urinary output of NE and E before, during, and after insulin-induced hypoglycemia in patients with pituitary dysfunction. Plasma concentrations of cortisol, growth hormone, and glucagon were measured simultaneously. The study population was comprised of nine healthy controls (group 1), eight children with growth hormone deficiency (group 2), and eight children with combined growth hormone and cortisol deficiencies (group 3). Recovery from acute hypoglycemia was similar in all groups. Mean plasma glucagon values reached a maximum at 30 min after insulin injection, and no significant differences were observed among the groups. Plasma cortisol levels were similar in groups 1 and 2, maximum values ocurring at 45 min after insulin. Patients in group 3 did not increase their cortisol concentrations above 5.5 μg/d despite a greater than 50% drop in blood glucose. Mean urinary E output of all groups increased significantly above pretest values (groups 1 and 2,P< 0.001; and group 3,P< 0.01), whereas NE levels were unchanged. After hypoglycemia, the mean E increments in the control and cortisol-deficient groups were not significantly different.The data can be interpreted in two ways. Endogenous cortisol production in ACTH-deficient bypopituitary children is sufficient to maintain PNMT activity at a level needed for synthesis of E from NE. Alternatively, cortisol may not be essential for E release during acute hypoglycemia because hypothalamic regulatory mechanisms supervene, and direct neural stimulation promotes PNMT activity and synthesis of E.We conclude that patients with cortisol and growth hormone deficiencies are able to recover from acute hypoglycemia when hepatic glycogen stores are adequate because there is sufficient release of E or because other adrenergic mechanisms stimulate glucagon release and hepatic glycogenolysis.SpeculationAlthough children with cortisol and growth hormone deficiencies are able to recover from acute hypoglycemia, many do not tolerate a prolonged fast because of diminished gluconeogenesis and depletion of hepatic glycogen.

ISSN:0031-3998    

出版商:OVID    

年代:1981

数据来源: OVID

摘要:

Because the rabbit kidney is being used as an experimental model with increasing frequency, this study was designed to measure the relationships between cell number, size, and contents in the developing rabbit. Kidney slice extracellular and intracellular fluid spaces, high in the fetus and neonate, declined as the rabbits matured, being paralleled by changes in body fluid spaces. Although the cellular contents of both sodium and potassium were increased in the young kidney, intracellular sodium concentration was slightly lower in the fetal (43.6 mEq/liter) and 2-wk kidneys (44.5 mEq/liter) than in the mature kidney (51.7 mEq/liter). Intracellular potassium concentrations were similar in all age groups (163 to 167 mEq/liter). Tissue protein content was similar during development. In contrast, DNA content and the number of nuclei in kidney tissue were high in the fetus (DNA, 59.9 mg/g solids; nuclei, 3.9 x 109/g solids), decreasing in postnatal life (DNA in adult, 18.2 mg/g solids; nuclei in adult, 1.0 x 109/g solids). In association with this, the diameter of proximal tubular cells increased with maturation. These data should be valuable to those interested in kidney development.

ISSN:0031-3998    

出版商:OVID    

年代:1981

数据来源: OVID

摘要:

The pH of gastric fluid was measured in rat fetuses during the last 3 days of gestation. On day 19, the gastric pH was close to neutral. During the night of day 20, the pH was clearly lowered (6.11 ± 0.15 units), this decrease becoming more marked on the following day. At birth (day 22), just before the first feeding, the pH of gastric fluid reached the mean value of 2.98 ± 0.14 units. This drop in gastric pH was concomitant with an increase in chloride concentration whereas the gastric Pco2remained constant. These results imply that in term rat fetuses, the gastric mucosa secretes fixed acid, very likely hydrochloride acid.The administration of acetazolamide (inhibitor of carbonic anhydrase) to 20-day-old fetuses did not suppress the spontaneous acidification of gastric fluid, although the enzyme activity was reduced by approximately 80%. Moreover, the gastric pH in acetazolamide-injected fetuses was markedly lower than in the noninjected littermates. The administration of NaCl solution (acetazolamide vehicle) had no effect on the carbonic anhydrase activity but clearly decreased the pH of gastric fluid. Thus, the drop of gastric pH produced by injection of acetazolamide or saline solution alone probably results from a stress effect of puncture.In fetuses from adrenalectomized, metopirone-treated mothers, the injection of NaCl solution no longer had effect on the pH of gastric fluid whereas triamcinolone injection produced a clear decrease in the gastric pH 3 hr later.SpeculationCorticosteroids could play an important role in the development of H+generation processes in parietal cells during the fetal period of life.

ISSN:0031-3998    

出版商:OVID    

年代:1981

数据来源: OVID

摘要:

The basic pathogenetic defect in patients with Bartter's syndrome remains unknown, although the possibility that a defect in membrane ion transport underlies the syndrome has been explored by several investigators. The purpose of the present study was to investigate abnormalities in erythrocyte sodium transport in five patients with Bartter's syndrome and to examine the effect of treatment with prostaglandin synthetase inhibitors on these abnormalities.In five patients with Bartter's syndrome, the rate of passive sodium leak from the erythrocyte was 1.04 ± 0.21 mmoles of sodium per liter of erythrocytes per hr, compared to 0.39 ± 0.06 mmoles of sodium per liter of erythrocytes per hr in controls (P< 0.025). Treatment with prostaglandin synthetase inhibitors had little effect on this erythrocyte sodium transport abnormality. After treatment with either acetylsalicylic acid at a dosage of 50 mg/kg/day or indomethacin at a dosage of 100 mg/day, the rate of passive sodium leak averaged 0.96 ± 0.10 mmoles of sodium per liter of erythrocytes per hr in the patients with Bartter's syndrome.In vitrothere was no significant effect of prostaglandin E2on erythrocyte sodium transport, nor did a lowered potassium concentrationin vitroreproduce the changes in sodium transport which we had noted in patients with Bartter's syndrome.We would conclude that one of the basic abnormalities in patients with Bartter's syndrome is a disorder in electrolyte transport at the level of the cell membrane. Prostaglandin synthetase inhibitors have been demonstrated to reverse many of the secondary manifestations of Bartter's syndrome, but they did not seem to affect the membrane transport defect.SpeculationThe most basic defect described to date in patients with Bartter's syndrome may be an abnormality in electrolyte transport at the level of the cell membrane. The abnormality does not appear to be altered by treatment with prostaglandin synthetase inhibitors; perhaps this explains the failure of these agents to totally correct the clinical syndrome.

ISSN:0031-3998    

出版商:OVID    

年代:1981

数据来源: OVID

摘要:

To evaluate the impact of malnutrition on the developing gut, we studied small bowel structure, epithelial renewal, and enzymes in suckling rats deprived of adequate nutrient from birth. Rat pups were suckled by foster dams fedad libitumone of three isocaloric, semipurified diets containing 6,9, or 25% (control) protein throughout gestation and lactation. An additional control group consisted of pups raised with their natural, chow-fed mothers. Although survival of the pups, 98% in the chow-fed and 25% protein groups, decreased to 83% in the 9% groups and 53% in the 6% protein groups, body and gut weights were remarkably uniform within each study group. Mean body weight, gut weight, villus height, and crypt depth were markedly and significantly less in the 6 and 9% pups when compared with those in the chow and 25% control groups, the 6% group being significantly more affected was than the 9% group (P< 0.001). Pups raised by chow-fed mothers also weighed significantly less (P< 0.001) than did those raised by dams fed the 25% protein diet. Total small intestinal protein and DNA content of mucosal scrapings were less in 6 than 9% rat pups (P< 0.001), which in turn were less than those in the 25% group (P< 0.05). The protein/DNA ratio in the small intestine of the 6% animals only was reduced when compared with the 25% group (P< 0.05). Epithelial cell migration assessed by autoradiography with [3H]thymidine was significantly slower in both proximal and distal intestinal segments of the 6% animals when compared with those from the 25% group (P< 0.001). Incorporation of the3H, seen by autoradiography after 1 hr, was also signficantly decreased in the 6% group (P< 0.001). Calculated for the total small intestine, lactase, sucrase, alkaline phosphatase, and thymidine kinase activities were significantly diminished (P≤ 0.001) in the 6% animals compared with 25% controls. Calculated in relation to mucosal protein content and compared with 25% controls, sucrase and alkaline phosphatase activities were significantly decreased (P< 0.001) in both proximal and distal small intestinal segments of the 6% animals, but thymidine kinase activity was decreased only in the distal segment (P< 0.001). However, lactase specific activity was increased in both proximal and distal segments from the 6% group (P< 0.001). Further studies of this phenomenon demonstrated a significant increase in intracellular acid β-galac-tosidase (P< 0.001), particularly in the distal intestinal segment, but also a marked increase in brush border β-galactosidase.Our data demonstrate that in the small intestinal mucosa of the suckling rat, chronic malnutrition causes a decreased number of cells and impaired epithelial proliferation. These abnormalities reflect a profound direct impact of malnutrition on the gut of the young animal and demonstrate a delay in the normal pattern of postnatal maturation of the small intestinal epithelium.

ISSN:0031-3998    

出版商:OVID    

年代:1981

数据来源: OVID