摘要:

ExtractChanges of incorporation of [3H]thymidine into brain DNA were studied in C57BL/6J mice after perinatal neocerebellar lesion. The destruction of part of the left neocerebellar cortex caused temporary increase of the specific radioactivity of DNA extracted from neocerebellum (15.22 ± 0.57 cpm/mg DNA vs. 4.83 ± 0.40 cpm/mg DNA in controls), from left hemisphere (9.86 ± 0.45 cpm/mg DNA in operated vs. 4.22 ± 0.40 cpm/mg DNA in controls), and from right hemisphere (11.75 ± 0.52 cpm/mg DNA in operated vs. 4.78 ± 0.39 cpm/mg DNA in controls). The labeled DNA was localized both in glia and in neurons in different brain areas. In animals operated upon in adult age, no changes in labeling of brain DNA were observed.SpeculationIt is possible that the described changes of the metabolism of the brain DNA are necessary and precede the “spontaneous nervous reorganization” necessary for the restitution of functions of the damaged brain.

ISSN:0031-3998    

出版商:OVID    

年代:1975

数据来源: OVID

摘要:

ExtractThe nauplii of the brine shrimpArtemia salinaare dependent upon the function of their salt gland to maintain osmotic pressure within narrow limits. A number of drugs interfere with this function and are lethal to the nauplii. Saliva and serum from normal persons, patients with cystic fibrosis, and obligate heterozygotes were tested for lethal effect against brine shrimp nauplii. At salt concentrations between 100 mM and 2.5 M no difference was found among the phenotypes. At lower concentrations a difference was noted occasionally between some normal subjects and some individuals carrying one or two genes for cystic fibrosis. Data from an independent series of experiments indicate that the naupliar deaths result from distorted ratios of Na+/K+and not from a specific gene product. No difference was noted in the O2uptake of nauplii treated with saliva or serum obtained from normal subjects, patients with cystic fibrosis, or obligate heterozygotes.SpeculationThe factor in cystic fibrosis that interferes with resorption of sodium from the parotid gland of the rat does not seem to interfere with the larval salt gland of the brine shrimp. Under the conditions tested, this makes it unlikely that brine shrimp can be used to diagnose cystic fibrosis.

ISSN:0031-3998    

出版商:OVID    

年代:1975

数据来源: OVID

摘要:

ExtractSystemic glucose production rates were evaluated 4 hr after feeding in 14 newborn beagle dogs at ages between 1 and 5 days. After a prime injection of radioisotopic tracers, glucose production was determined during infusion of intermixed tracer [2‐3H]glucose and [1‐14C]glucose at a constant rate. Seven of the newborn dogs served as controls throughout the 3‐hr period of infusion, while seven of their littermates, infused simultaneously, received glucagon at a constant rate of 3.3 &mgr;g/min between 90 and 180 min of study. In control dogs, mean glucose production, determined by dilution of [2‐3H]glucose, was 55 ± 3 &mgr;mol/min · kg body weight. During the control period, their littermates produced glucose at a similar rate; however, glucagon infusion raised glucose production to 81 ± 4 &mgr;mol/min · kg.The average glucose production rate estimated with [1‐14C]glucose was 88% of that with the3H tracer during the initial control period and 77% during the glucagon infusion. In order to confirm that this discrepancy reflected the recycling of14C and the early development of gluconeogenesis, an additional 14 newborn dogs were infused with potential substrates for [14C]glucose. In separate studies, [U‐14C]lactate, [3‐14C]lactate, [U‐14C]alanine, and [6‐14C]‐glucose were incorporated into glucose and [1‐14C]glucose. Quantification of gluconeogenesis by simultaneous infusion of [6‐3H]glucose and [3‐14C]lactate in a 5‐day‐old dog demonstrated that 25% of the glucose produced originated from lactate, whereas 10% was incorporated into carbon 1. Thus, systemic glucose production was established rapidly in newborn dogs and responded to stimulation with glucagon. A significant proportion of the glucose originated from recycling via the gluconeogenic pathway.SpeculationEven in well nourished newborn mammals, recycling of glucose is important in maintaining homeostasis during the postabsorptive period. Based on comparisons between dogs infused with [3‐14C]lactate or [6‐14C]glucose, 25% or more of hepatic glucose production may originate from glucose recycled through lactate and pyruvate. Presumably most of the rest is derived from hepatic glycogen storedin utero..

ISSN:0031-3998    

出版商:OVID    

年代:1975

数据来源: OVID

摘要:

ExtractThe effects of birth and norepinephrine on hepatic glucose production, glycogenolysis, and gluconeogenesis were examined in livers isolated from fetal dogs at term, littermates 3 hr after delivery, and newborn dogs 1‐5 days old. Livers were perfused in pairs with medium containing [6‐3H]glucose (6 mM) and [3‐14C]lactate (10 mM) ± a pharmacologic amount of norepinephrine (10‐6M). Changes in glucose production rates were correlated with changes in the enzymatic activities controling gluconeogenesis.Net glucose production was <0.48 &mgr;mol/min · g liver in both fetal and 3 hr liver but stabilized above 1 &mgr;mol/min · g later during the first day. Initially, mobilization of the fetal hepatic glycogen accounted for glucose output. Subsequently, incorporation of lactate into glucose rose from negligible fetal rates to 0.19 &mgr;mol/min · g and accounted for 21% of net glucose production onday 3.Maximal pyruvate carboxylase activity and mitochondrial CO2fixation increased postnatally and correlated directly with net glucose production, glucose production from glycogen, and glucose production from lactate.Fetal liver did not respond to norepinephrine. Therafter, norepinephrine increased hepatic glucose production by stimulating glycogen breakdown. Postnatal acceleration of glucose production and the response to norepinephrine occurred only after induction of mitochondrial CO2fixation. Duringday 1the decline of hepatic glycogen in response to norepinephrine correlated with both CO2fixation and lactate incorporation into glucose. Thus, initiation of gluconeogenesis after birth may have been required for the postnatal acceration of hepatic glucose production and for the regulation of glycogenolysis by norepinephrine.SpeculationA multiple system for hormonal plus neural initiation of hepatic glucose production after birth may protect the newborn mammal from cessation of the maternal supply of glucose and other substrates. Events such as relative hypoglycemia postnatally or intermittent hypoxia prenatally initiate pancreatic glucagon or sympathetic neural norepinephrine release, both of which stimulate hepatic glucose release. Shortly after birth, the target organ, liver, responds appropriately to both the pancreatic and neural hormones.

ISSN:0031-3998    

出版商:OVID    

年代:1975

数据来源: OVID

摘要:

ExtractUrea cycle function was evaluated in liver obtained from six patients with Reye's syndrome and from five control subjects. Reye's syndrome patients demonstrated normal activities for the extramitochondrial portion of the urea cycle, but showed marked abnormalities of the mitochondrial enzymes,i.e.,carbamyl phosphate synthetase (CPS) and ornithine transcarbamylase (OTC) (Tables 2, 3). CPS activity was reduced to less than 15% of control values in all four patients from whom tissues was obtained during the first 72 hr after the onset of encephalopathy. Two patients from whom tissue was not obtained until after 9 days of symptoms showed no reduction in CPS activity. The OTC activity was also reduced (3‐67% of control values) in the four patients from whom tissue was obtained early in the illness. In addition, greater than 60% reduction in Vmaxand Kmfor carbamyl phosphate was noted in all four patients in whom sample size permitted kinetic analysis, including both patients in whom CPS and OTC activity were not markedly reduced. The same kinetic abnormality as well as decreased CPS activity were experimentally produced in normal rat liver incubated in the presence of 1.0 mM 4‐pentenoic acid, a short chain fatty acid and known hepatic mitochondrial toxin (Table 4).SpeculationAbnormalities of the mitochondrial portion of the urea cycle are a frequent occurrence in Reye's syndrome. This appears to be an acquired and reversible process that can probably be produced by a number of etiologic agents, of which endogenous or exogenous short chain fatty acids may be included.

ISSN:0031-3998    

出版商:OVID    

年代:1975

数据来源: OVID

摘要:

ExtractMost investigators studying changes in body composition during growth agree to the desirability of having longitudinal data. A group of 110 boys and 126 girls, studied annually for 4‐5 years with 880 measurements of total body K in a 2&pgr; liquid scintillation whole body counter, had total body K vs. height and total body K vs. weight data that fit previously described regression lines.SpeculationGiven an adequate diet and environment, children increase their total body K in a predictable amount in reference to skeletal growth.

ISSN:0031-3998    

出版商:OVID    

年代:1975

数据来源: OVID

摘要:

ExtractAmniotic and allantoic fluid samples were obtained at the time of uterotomy from healthy pregnant ewes at various times during gestation. In most instances maternal and fetal blood was collected simultaneously. Serum thyroxine (T4) and triiodithyronine (T3) and free T4were measured in most samples. To determine whether conjugates of T4were present in amniotic and allantoic fluids, T4was measured before and after 24‐hr acid hydrolysis. T4and T3turnover from amniotic fluid were measured using kinetic methods after intravenous or intraamniotic fluid injection of radiolabeled hormones.T3was unmeasurable (< 15 ng/100 ml) in amniotic and allantoic fluids as well as in most fetal serum samples. T4levels in amniotic fluid were low before 120 days of gestation (0.17 ± 0.03 &mgr;g/100 ml; mean and SEM) and increased progressively thereafter to term. The mean (and SEM) concentration between 124 and 152 days was 0.33 ± 0.03 &mgr;g/100 ml. T4concentrations in allantoic fluid were relatively high before 120 days (0.57 ± 0.01 &mgr;g/100 ml) and did not increase with progression of the pregnancy. There were no correlations between amniotic and allantoic fluid T4concentrations, between amniotic fluid T4, and either maternal or fetal serum T4levels, or between allantoic fluid T4and maternal or fetal serum T4at any time during gestation. Mean free T4concentrations were similar in fetal serum and amniotic fluid and higher than values in maternal serum or allantoic fluid.Mean amniotic and allantoic fluid T4concentrations by radioimmunoassay (RIA) increased significantly after acid hydrolysis, suggesting that one‐third to one‐half the T4in these fluids is present as T4conjugate.Radiolabeled T4or T3was injected into amniotic fluid and recovery of hormone label was measured in serum and tissues at 24 hr for comparison with recoveries after intravenous injection. Mean T4radioactivity in several organs or tissues was nearly identical whether the hormone was injected intravenously or into amniotic fluid. In addition, the total residual labeled T4or T3in the fetal sheep (percentage dose per fetus) at the time of killing was similar after intravenous and intra‐amniotic fluid injection. Chromatograms of butanol‐ammonia extracts of fetal sera after intraamniotic or intravenous injection of labeled T4were similar and showed predominantly T4; a significant iodide peak was observed as well as a small peak of radioactivity with an RFcorresponding to that of T4conjugate.The results indicate that there are low but measurable concentrations of T4in amniotic and allantoic fluids of pregnant sheep. There appears to be minimal exchange of hormone between allantoic and amniotic fluid. Amniotic fluid T4levels, in contrast to allantoic fluid concentrations, increase progressively during the last half of gestation. Although free T4concentrations are similar in amniotic fluid and in fetal serum, and are higher than in allantoic fluid or maternal serum, the lack of correlation between T4levels in either fluid and T4levels in fetal or maternal serum suggests that amniotic or allantoic fluid T4levels do not reliably reflect thyroid status of the fetus or the mother. Rather, both must be represented in some way. Finally, T4and T3appear to be rapidly and quantitatively absorbed from amniotic fluid by the sheep fetus.SpeculationThe present results suggest that amniotic fluid T4is derived both from the mother and the fetus so that measurement of amniotic fluid T4would not seem to be a reliable approach to intrauterine diagnosis of fetal thyroid status. Amniotic fluid T4is turned over rapidly by the fetus, presumably via swallowing and absorption from the fetal gut so that the fetus might acquire maternal thyroid hormones via amniotic fluid even though placental transfer of thyroid hormones is minimal. This route of maternal T4entry to the fetus must be of minimal quantitative significance, however, since the serum T4concentration in the athyroid sheep fetus is very low. It should be possible, however, to provide thyroid hormone therapy to the fetus via amniotic fluid injection; this approach allows direct intrauterine therapy of fetuses in whom there is a high index of suspicion of hypothyroidism.

ISSN:0031-3998    

出版商:OVID    

年代:1975

数据来源: OVID

摘要:

ExtractThere were little or no indications of differences in sleep outcomes between the sexes. Results indicate a disturbance of sleep on initial laboratory nights relative to later nights. The results reported here clearly document the persistence of these effects from year to year. For the most part, sleep characteristics during the 4 years immediately after onset of puberty appear to represent a typical phase in the gradual patterns of changes across all ages. Total sleep time decreased markedly from 560 min in age range 10‐12 to 424 min in age range 20‐29, with our puberty subjects at intermediate levels. Puberty subjects had an average of 2.5 awakenings/night in the first 2 years as compared with 1.2/night in the last 2 years. The number of sleep stage shifts during the night varied around a constant mean value of approximately 37/night throughout all ages. The number of rapid eye movement (REM) periods during the night decreased sharply for individuals from childhood (6.9/night) through adolescence (4.0/night), remaining constant thereafter. Percentages of the various sleep stages were fairly constant for individuals from age range 10‐12 through age 30‐39. Our puberty subjects had percentage profiles in near perfect agreement with the normal ontogenetic process. Normative data suggest that slow wave sleep reaches a peak at some point during the teen years.SpeculationStability of sleep rather than its disruption may prove to be the rule rather the exception. Sleep may be refractory to developmental change. This may have survival value.

ISSN:0031-3998    

出版商:OVID    

年代:1975

数据来源: OVID

摘要:

ExtractSulfadimethoxine significantly reduced plasma bilirubin levels and altered the tissue bilirubin distribution in both the newborn and the adult Gunn rat. The majority of the unbound bilirubin appeared to distribute preferentially to the intestine and liver in the newborn, whereas in the adult the unbound bilirubin was taken up primarily by the liver. The bilirubin content of brain tissue from both age groups was significantly higher after sulfadimethoxine treatment.SpeculationA decrease in the available extravascular bilirubin binding sites, indicated by an increased concentration of bilirubin in the carcass and an apparent decreased capacity of the liver of the newborn Gunn rat to bind bilirubin, would suggest that kernicterus in the Gunn rat neonate is associated with increased bilirubin concentrations in the brain. However, the similar uptake of bilirubin by the brain tissue of both the newborn and the adult Gun rat raises the question of increased sensitivity of the newborn brain to bilirubin toxicity.

ISSN:0031-3998    

出版商:OVID    

年代:1975

数据来源: OVID

ISSN:0031-3998    

出版商:OVID    

年代:1975

数据来源: OVID