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PubMed2001

Middle cerebral artery Doppler in severe intrauterine growth restriction.

OBJECTIVE: To examine longitudinal changes in middle cerebral artery blood flow assessed by Doppler in severely growth restricted fetuses. METHODS: Eighteen structurally normal singleton pregnancies complicated by suspected intrauterine growth restriction were monitored by serial measurement of the pulsatility index of the middle cerebral artery over 7 to 72 days. Outcome measures included indication for delivery, umbilical venous pH and admission to and length of stay in neonatal intensive care. RESULTS: Thirteen fetuses demonstrated severe intrauterine growth restriction based on subsequent birth weights being below the 2.5th centile, two had intrauterine growth restriction (birth weights between the 2.5th and 5th centiles), and three had birth weights between the 5th and 50th centiles. The middle cerebral artery pulsatility index showed rapid and sharp changes between examinations in those severely growth restricted fetuses which required delivery before 34 weeks. This pattern was not obvious in severely growth restricted fetuses delivered after 34 weeks, or in those less severely growth restricted, regardless of the gestation at delivery. Changes in middle cerebral artery pulsatility index contributed to the decision to deliver in three cases. The middle cerebral artery pulsatility index demonstrated greater variation in those fetuses with cord pHs of less than 7.25. The length of stay in neonatal intensive care decreased with increasing gestational age and birth weight. CONCLUSIONS: The difference in the pattern of change in middle cerebral artery pulsatility index in intrauterine growth restricted fetuses may be a reflection of maturity in addition to the degree of fetal compromise. The decision to deliver was multifactorial. The middle cerebral artery pulsatility index only influenced the decision to deliver when changes in other parameters were evident.

Amniotic Fluid↗

PubMed2001

Ventriculovascular physiology of the growth-restricted fetus.

OBJECTIVES: To examine the mechanisms by which intrauterine growth restriction may influence later cardiovascular risk by comparing the ventriculovascular physiology of gestational age- and weight-matched growth-restricted and normal fetuses. DESIGN: A prospective longitudinal observational study of 20 normal fetuses studied from 20 weeks to term at monthly intervals was compared with a growth-restricted cohort examined in the interval between diagnosis and delivery. The last values before delivery of the growth-restricted cohort were compared with the normal cohort in two analyses matched for weight and for gestation. Arterial and venous vessel wall physiology and aortic pulse wave velocity were examined longitudinally in the thoracic descending aorta and inferior vena cava using an ultrasonic phase-locked echo-tracking system. Serial echocardiographic examinations were performed assessing structure, ventricular dimensions, function and Doppler flows. RESULTS: There was a linear increase in cardiac preload and relative pulse amplitude in the inferior vena cava with gestation. In normal fetuses, the aortic pulse wave velocity, maximum incremental and late decremental velocities increased with gestation whilst the relative pulse amplitude decreased reflecting falling distal impedance. In both age- and weight-matched analyses, the growth-restricted fetuses showed significantly reduced values reflecting the chronic fetal ventriculovascular responses to increased placental impedance. Pulse wave velocity increased with gestation and was significantly less in the growth-restricted cohort. CONCLUSIONS: Growth restriction is associated with abnormal ventriculovascular physiology that represents a successful adaptive response to raised placental impedance and reduction in wall stress as evidenced by the lower fetal pulse wave velocity in growth-restricted fetuses. However, whilst fetal adaptive mechanisms may aid survival they may result in cerebral and vascular abnormalities that prejudice later cardiovascular health.

Aorta, Thoracic↗

PubMed2003

Vision and driving self-restriction in older adults.

OBJECTIVES: To assess driving self-restriction (vision related and nonvision related) in relation to vision test performance of older adults. DESIGN: Cross-sectional study. SETTING: Population-based cohort of community-dwelling older adults. PARTICIPANTS: Six hundred twenty-nine current drivers aged 55 and older had driving behavior, health, and physical function assessed and vision function tested in 1993-95. MEASUREMENTS: Self-report of driving restriction as vision or non-vision related and performance on a comprehensive battery of vision tests (visual acuity; contrast sensitivity; effects of illumination level, contrast, and glare on acuity; visual fields with and without attentional load; color vision; temporal sensitivity; and the effect of dim light on walking ability). RESULTS: Demographic, health, and functional characteristics differed significantly between restrictors and nonrestrictors but not between vision- and nonvision-related restrictors. Controlling for potential confounding, only vision-related driving self-restriction was significantly associated with reduced performance on nonstandard measures of acuity. Poor depth perception was significantly associated with restriction for both vision- and nonvision-related reasons. Poor performance on attentional visual field tests, analyzed individually and in combination with standard field tests, was not associated with driving self-restriction. CONCLUSION: Older adults with early changes in spatial vision function and depth perception appear to recognize their limitations and restrict their driving even if they do not acknowledge the visual impairment as the cause for restriction. Poor visual attention, a risk factor for crashes, may not be recognized. Additional studies of driving self-restriction in relation to risk factors for crashes in older adults may help refine this strategy of reducing driving-related injury and death.

Aged↗

PubMed1987

Effects of food restriction on cortisol, TSH and iodothyronine concentrations in the plasma of the newborn lamb.

The influence of food restriction, applied from birth to 36 h post partum, on neonatal thyroid function was studied in newborn Limousin x Romanov lambs. The control animals (n = 18) had free access to the mother and suckled ad libitum. Restricted lambs (n = 16) were removed from the mother and received limited amounts of colostrum in proportion to birth weight; 8 lambs were supplemented with lactose (30 g/l of colostrum). Plasma glucose and free fatty acid levels were significantly lower in restricted lambs, whereas urea levels were elevated. Plasma cortisol concentrations in control animals decreased during the period studied, but rose during the first 8 h of life in restricted lambs. Lactose supplementation only partially restored glucose and urea levels. Food restriction induced considerable modifications in neonatal thyroid function. The postpartum rise in plasma thyroid-stimulating hormone (TSH), thyroxine (T4) and free T4 levels occurring in control lambs was inhibited in restricted animals. However, the surge in plasma triiodothyronine (T3) levels was not affected, suggesting that this change was not related to physiological neonatal TSH hypersecretion. Thereafter, thyroid hormone concentrations decreased sharply during food restriction, whereas reverse T3 levels remained higher than in the controls. In response to these T4 and T3 deficiencies, plasma TSH levels rose only in lactose-supplemented animals. In agreement with the significant modifications in the values of the T3/free T4 and reverse T3/free T4 ratios, the abrupt changes in T3 and reverse T3 levels suggest that food restriction affected the peripheral conversion of T4 into T3 and reverse T3.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1998

On the mechanism of the effects of potassium restriction on blood pressure and renal sodium retention.

Dietary potassium restriction increases sodium and chloride retention, whereas potassium administration promotes both diuresis and natriuresis. In epidemiologic and clinical studies, potassium intake is inversely related to blood pressure and is lower in blacks than in whites. The present studies examined the mechanism by which potassium restriction fosters sodium conservation and the impact of race on this response. Twenty-one healthy black and white men and women ingested an isocaloric, potassium-restricted diet (20 mmol/d) containing 180 mmol/d of sodium with and without a potassium supplement (80 mmol/d) for 9 days on two occasions. Additionally, eight of these subjects ingested the same diets for 3 days followed by a water load to determine free water clearance before and during the early phase of dietary potassium restriction. During potassium restriction, mean arterial pressure (MAP) derived from 24-hour blood pressure measurements was higher (85.7 +/- 1.6 mm Hg v 82.0 +/- 1.3 mm Hg; P < 0.001), cumulative sodium excretion lower (984 +/- 59 mmol/d v 1,256 +/- 58 mmol/d; P < 0.001), and weight greater (71.1 +/- 2.1 kg v 69.3 +/- 2.2 kg; P < 0.001). Blacks displayed no greater increase in MAP, although they excreted less sodium overall and less potassium on the potassium-supplemented diet. After a water load, minimum urine osmolality (Uosm) was lower (53.0 +/- 3.0 mOsm/L v 65.6 +/- 3.5 mOsm/L; P = 0.01) and free water clearance greater (4.44 +/- 0.59 mL/min v3.72 +/- 0.58 mL/min; P = 0.009) during potassium restriction. In conclusion, in healthy, normotensive subjects, potassium restriction was associated with an increase in blood pressure and volume expansion effected by increased renal sodium and chloride retention. Potassium restriction was also associated with increased free water clearance and enhanced diluting capacity consistent with augmentation of Na+, K+:2Cl- cotransporter activity in the thick ascending limb of Henle. This mechanism may play an important role in the renal adaptation required for potassium conservation, but at the expense of sodium chloride retention and an elevation in blood pressure.

Adult↗

PubMed2001

Protein restriction and dexamethasone as a model of protein hypercatabolism in dogs: effect of glutamine on leucine turnover.

To determine (1) whether protein restriction, combined with glucocorticosteroid treatment, can be used as a hypercatabolic model and (2) if so, whether glutamine attenuates protein wasting in this model, the effects of protein restriction, dexamethasone, and glutamine on leucine metabolism were assessed in dogs. A control group (n = 8) received a maintenance diet; another group (n = 8) received a protein-restricted diet either (1) alone; (2) along with a 7-day corticoid treatment; or (3) along with a 7-day corticoid treatment and a 7-hour intravenous (IV) glutamine infusion. The last day of each regimen, dogs underwent an IV isotope infusion in the fasting state, with a 3-hour NaH(13)CO3 infusion to assess CO2 production, and immediately thereafter, a 3-hour (13)C-leucine infusion to assess leucine appearance rate (Ra), oxidation (Ox), and nonoxidative leucine disposal (NOLD), expressed as micromol x kg(-1) x h(-1). Protein restriction was associated with a 24% decline in leucine Ra (223 +/- 16 v 298 +/- 17; P <.01), an index of whole body proteolysis, and a 29% decline in NOLD (180 +/- 15 v 223 +/- 13; P <.01), an index of whole body protein synthesis. In the protein-restricted group, dexamethasone treatment was associated with a 32% increase in Ra, (295 +/- 28 v 223 +/- 16; P <.05), a 186% increase in Ox (120 +/- 14 v 43 +/- 4; P <.001), with no change in NOLD, when compared with the protein-restricted alone. After protein restriction + dexamethasone, glutamine infusion induced a 40% increase in plasma glutamine (1,090 +/- 70 v 780 +/- 29 micromol x L(-1); P <.01), but failed to alter Ra, Ox, or NOLD. These results suggest that (1) in dogs, protein restriction combined with a 7-day course of dexamethasone results in alterations in leucine kinetics similar to those observed in stress-induced protein wasting in humans, and (2) in that model, a 7-hour IV glutamine infusion in the fasting state does not significantly attenuate protein wasting.

Animals↗

PubMed2001

Effects of maternal iron restriction on placental vascularization in the rat.

To investigate the effects of maternal iron deficiency and anaemia on the placenta the composition and vascularization of the placental labyrinth was investigated in iron-restricted rats. Rats in the experimental groups were placed on iron-restricted diets either 1 or 2 weeks before mating and continued on these diets throughout gestation. Placentae were studied at day 21 of gestation. Tissue sections were stained with lectin to allow identification of fetal capillaries and analyzed using stereological techniques. Capillary surface area density and total capillary surface area were decreased in both iron-restricted groups compared with the control group. Capillary length density was decreased in both iron-restricted groups compared with the control group. Total capillary length was significantly reduced in the 1-week, but not in the 2-week, iron-restricted group compared with the control group. Endothelial cell volume was increased in both iron-restricted groups compared to the controls. There were no significant differences in the volume of fetal capillaries, the volume of the maternal blood spaces or the surface area of the maternal-fetal interface between the control and iron-restricted groups. Labyrinthine volume, labyrinthine tissue volume and the surface area of the maternal fetal interface were increased in the 2-week group when compared with the 1-week group. These changes in placental vascularization may contribute to the fetal growth retardation observed in iron-restricted litters.

Anemia, Iron-Deficiency↗

PubMed1997

Increased incidence of fetal growth restriction in association with breech presentation in preterm deliveries < 32 weeks.

Breech presentation and fetal growth restriction (FGR) are each related independently with preterm delivery. This study was designed to assess the possible relationship between breech presentation and FGR in deliveries at < 32 weeks' gestation. From an established database of 465 consecutive deliveries at < 32 weeks of nonhypertensive, nondiabetic patients with singleton nonanomalous fetuses, those in whom birth weight, body length, fetal presentation (vertex or breech), and amniotic fluid volume (AFV) had been assessed were studied. Fetal growth restriction (defined as symmetric if both birth weight and body length were < 10th percentile and asymmetric if only the birth weight was < 10th percentile) was studied in relation to maternal age, parity, tobacco use, fetal presentation, AFV, membrane status, and gestational age at delivery. Statistical analyses included contingency tables and analysis of variance, with p < 0.05 considered significant. Two hundred ninety-eight patients met the inclusion criteria. In these patients 85 (28.5%) fetuses were breech and 213 (71.5%) cephalic. A total of 56 (19%) fetuses were growth restricted. Of these, 31 (10.4%) were symmetrically and 25 (8.3%) asymmetrically growth restricted. The incidence of symmetric growth restriction in the breech-presenting fetuses was 16% (n = 14) versus 8% (n = 17) in the cephalic-presenting fetuses, and of asymmetric growth restriction 12% (n = 10) versus 7% (n = 15), (overall p = 0.03). Fetal growth restriction was not associated with significant differences in maternal age, parity, smoking, AFV, membrane status, or gestational age at delivery (each p > 0.10). In preterm deliveries at < 32 weeks' gestation, breech presentation is associated with an increased incidence of intrauterine growth restriction, independent of clinical confounders.

Amniotic Fluid↗

PubMed2000

Preterm fetal growth restriction is associated with increased parathyroid hormone-related protein expression in the fetal membranes.

OBJECTIVE: Parathyroid hormone-related protein has roles in normal fetal growth, placental calcium transport, and vascular tone regulation; these factors are compromised in growth-restricted fetuses. Our objective was to determine whether intrauterine parathyroid hormone-related protein expression was increased in association with fetal growth restriction. STUDY DESIGN: The expression of parathyroid hormone-related protein was examined in intrauterine tissues from women with idiopathic fetal growth restriction with preterm (n = 8-10) and term (n = 8-10) gestations and from gestation-matched control subjects. The abundance and immunoreactive content of parathyroid hormone-related protein messenger ribonucleic acid were determined by Northern blot and radioimmunoassay, respectively, in the placenta, amnion, and chorion-decidua. RESULTS: The expression of parathyroid hormone-related protein messenger ribonucleic acid was increased in the amnion (placental and reflected) in association with preterm fetal growth restriction (P <.05). Both parathyroid hormone-related protein messenger ribonucleic acid and protein expression were increased in chorion-decidua in association with preterm fetal growth restriction (P <.05). In term gestations both parathyroid hormone-related protein messenger ribonucleic acid and protein expression were greater in amnion over placenta than in reflected amnion (P <.05); these in turn were greater than those in chorion-decidua (P <.05). No significant changes were detected in parathyroid hormone-related protein messenger ribonucleic acid or in protein expression in association with term fetal growth restriction. CONCLUSION: Either parathyroid hormone-related protein messenger ribonucleic acid or protein expression, or both, was increased in the fetal membranes in association with fetal growth restriction in preterm but not term gestations, suggesting that parathyroid hormone-related protein may be involved in the pathogenesis of preterm fetal growth restriction.

Amnion↗

PubMed2000

Neutrophil activation in preeclampsia and isolated intrauterine growth restriction.

OBJECTIVE: Neutrophils have been implicated in the pathogenesis of preeclampsia. Because preeclampsia and intrauterine growth restriction result from similar placental lesions, the aim of this study was to investigate neutrophil activation in isolated intrauterine growth restriction relative to preeclampsia and uncomplicated pregnancy. Polymorphonuclear neutrophil activation was analyzed by measuring cell surface and soluble cell adhesion molecule expressions. STUDY DESIGN: L -Selectin (CD62L ) and CD11b surface expressions on polymorphonuclear neutrophils were analyzed in 13 women with preeclampsia, 11 women with isolated intrauterine growth restriction, and 17 age- and gestation-matched control women by means of a standardized quantitative flow cytometry assay. Serum levels of soluble L -selectin were measured by enzyme-linked immunosorbent assay. RESULTS: Neutrophils from women with isolated intrauterine growth restriction and women with preeclampsia displayed higher levels of CD11b and lower levels of CD62L than did neutrophils from healthy pregnant women. Soluble L -selectin serum levels were significantly increased in the preeclampsia and intrauterine growth restriction groups relative to normal values. No significant difference in the levels of CD11b, CD62L, and soluble L -selectin were observed between women with isolated intrauterine growth restriction and those with preeclampsia. Leukocyte activation was not correlated with disease severity. CONCLUSION: The observed alteration in polymorphonuclear neutrophil adhesion molecule expressions and increased serum soluble L -selectin levels are consistent with activation of peripheral blood neutrophils occurring in isolated intrauterine growth restriction in a manner similar to that seen in preeclampsia. This evidence of neutrophil activation may help to advance our understanding of the disease process in isolated intrauterine growth restriction.

Adult↗

PubMed2000

Expectant management of severe preterm preeclampsia: is intrauterine growth restriction an indication for immediate delivery?

OBJECTIVE: Expectant management of severe preterm preeclampsia is gaining widespread acceptance in clinical practice. The objective of our study was 2-fold-to determine the frequency of fetal deterioration with expectant management of severe preterm preeclampsia and to evaluate whether the presence of intrauterine growth restriction on admission is associated with a shorter admission-to-delivery interval or more deliveries resulting from nonreassuring fetal status in comparison with pregnancies with preeclampsia but without intrauterine growth restriction. STUDY DESIGN: This was an observational study of women with singleton pregnancies at <34 completed weeks' gestation who were admitted to the hospital with the diagnosis of severe preeclampsia and managed expectantly. Fetal status on admission, admission-to-delivery interval, indication for delivery, and neonatal outcome were examined. RESULTS: Forty-seven women were studied during a 3-year period (1996-1999). Gestational age at admission was 29.8 +/- 2.6 weeks. The mean admission-to-delivery interval for the entire group was 6.0 +/- 5.1 days; in 42.5% delivery was for fetal indications. In comparison with the absence of intrauterine growth restriction, the presence of intrauterine growth restriction at admission resulted in a significantly shorter admission-to-delivery interval (3.1 +/- 2.1 vs 6.6 +/- 6.1 days; P <.05). Most fetuses with intrauterine growth restriction (85.7%) were delivered before 1 week. Although 57% of fetuses with intrauterine growth restriction were delivered for fetal indications, versus 39% of fetuses without intrauterine growth restriction, these rates were not found to be significantly different. Neonatal outcomes, as reflected by Apgar scores, number of admissions to and duration of stay in the neonatal intensive care unit, and neonatal mortality rates, were similar. CONCLUSION: Pregnancies complicated by severe preterm preeclampsia and the presence of intrauterine growth restriction at admission may not benefit from expectant management beyond the 48 hours needed for betamethasone to act. Furthermore, all patients may benefit from close fetal monitoring before delivery because of the high rate of intervention for deteriorating fetal status.

Adolescent↗

PubMed2001

Effects of intrauterine growth restriction on lung liquid dynamics and lung development in fetal sheep.

OBJECTIVE: The aim of this study was to determine the effects of intrauterine growth restriction on fetal lung liquid and lung development. STUDY DESIGN: Intrauterine growth restriction was induced in 7 fetal sheep from 120 to 140 days' gestation (term, approximately 147 days' gestation) by umbilicoplacental embolization. We used 6 control fetuses. Volumes and production rates of fetal lung liquid were measured, and lungs were removed post mortem (140 days' gestation) for analysis of concentrations of deoxyribonucleic acid, protein, and messenger ribonucleic acid for surfactant proteins A, B, and C. RESULTS: Umbilicoplacental embolization induced fetal hypoxemia, hypoglycemia, and intrauterine growth restriction. At 140 days' gestation lung weight was reduced by 34%, and the fetal lung liquid production rate (15.9 +/- 1.8 mL/h for intrauterine growth restriction vs 24.8 +/- 3.9 mL/h for control) and volume (110.9 +/- 16.3 mL for intrauterine growth restriction vs 178.1 +/- 11.9 mL for control) were reduced in the intrauterine growth restriction group. After adjustment for body weight, however, values were not different from those in the control group. Pulmonary deoxyribonucleic acid and plasma cortisol concentrations were elevated by intrauterine growth restriction, but levels of messenger ribonucleic acid for surfactant proteins were unchanged. CONCLUSION: In intrauterine growth restriction, lung liquid and lung growth were proportionate to body weight, and surfactant protein expression was unaffected. Alterations in lung deoxyribonucleic acid concentrations suggest that the lungs may be structurally immature.

Animals↗

PubMed2001

Early and persistent reduction in umbilical vein blood flow in the growth-restricted fetus: a longitudinal study.

OBJECTIVE: We have previously shown, in a cross-sectional study, that the reduction in umbilical vein blood flow in intrauterine growth-restricted fetuses is due to reduced umbilical vein velocity. The purpose of this longitudinal study in intrauterine growth-restricted fetuses was to determine whether the umbilical vein velocity reduction, which, in turn, reduces blood flow, persists throughout gestation or represents a late event that precedes indicated delivery. STUDY DESIGN: Twenty-one intrauterine growth-restricted fetuses with an abnormal umbilical artery velocimetry underwent serial sonographic and Doppler examinations from 23 to 36 weeks of gestation. Umbilical vein diameter and velocity were measured, and umbilical vein absolute (milliliters per minute) and weight-specific blood flow (milliliters per minute per kilogram) were calculated. Umbilical vein diameter, velocity, and blood flow were expressed per abdominal circumference. Intrauterine growth-restricted findings were compared to local reference data. RESULTS: Intrauterine growth-restricted fetuses showed persistent reductions in umbilical vein blood flow per abdominal circumference and weight-specific blood flow (milliliters per minute per kilogram) from the time of diagnosis of intrauterine growth-restriction. Umbilical vein velocity was reduced in the intrauterine growth-restricted fetuses, although umbilical vein diameter did not change. CONCLUSION: Reduction of umbilical vein blood flow is an early finding in intrauterine growth-restricted fetuses, and it can persist for several weeks until delivery. This reduction in blood flow is due to reduced umbilical vein velocity.

Adult↗

PubMed2003

Intrauterine growth restriction is accompanied by decreased renal volume in the human fetus.

OBJECTIVE: Intrauterine growth-restricted fetuses are at risk for the development of adult hypertension and related cardiovascular diseases. Congenital oligonephropathy has been postulated as the primary mechanism. The objective of our study was to determine whether ultrasonically obtained in utero measurements of renal volume or renal artery Doppler blood flow differ between fetuses that are intrauterine growth restricted and fetuses that are not. STUDY DESIGN: The study population consisted of women who were referred for a prenatal ultrasound evaluation at a large community medical center. The women were divided into two groups: women with fetal biometry that was consistent with intrauterine growth restriction and women with biometry within normal range. Information was collected on maternal demographics and other factors known to affect fetal growth. We performed detailed fetal renal anthropomorphic and Doppler blood flow measurements in addition to standard fetal biometric measurements on all patients, specifically comparing renal volume and renal artery flow data between the two groups. RESULTS: No differences were observed in maternal age, race, parity, or fetal gestational age. Renal volume in the intrauterine growth-restricted fetuses was 31% (95% CI, 20%-40%), which was less than that in the group of fetuses that were not intrauterine growth restricted after an adjustment was made for gestational age. The ratio of renal volume to estimated fetal weight was 15% (95% CI, 1%-26%), which was less than the same ratio in the fetuses that were not intrauterine growth restricted. There were no differences seen in the renal artery Doppler measurements. CONCLUSION: Intrauterine growth restriction appears to be associated with a decrease in fetal renal volume. Because renal volume is a likely proxy for nephron number, this study supports the hypothesis that intrauterine growth restriction may be linked to congenital oligonephropathy and potentially to hypertension in later life.

Adult↗

PubMed1980

Akvr-1, a dominant murine leukemia virus restriction gene, is polymorphic in leukemia-prone wild mice.

We describe a restriction gene (Akvr-1, for AKR virus restriction) that is polymorphic for two alleles, Akvr-1R (restrictive) and Akvr-1r (susceptible), in a feral population of mice (Mus) musculus domesticus) at a squab farm near Lake Casitas (LC) in southern California. Akvr-1k is a dominant allele that exhibits 100% penetrance in prevention of viremia of AKR endogenous retrovirus and of virus-mediated lymphoma in LC (Akvr-1RR) X AKR F1 hybrids. The restriction phenotype segregates as a single Mendelian locus in backcrosses to AKR mice. Akvr-1R likewise is effective in restriction of NB-tropic Moloney murine leukemia virus-induced viremia and NB-tropic Friend virus-induced splenomegaly but fails to restrict expression or pathogenesis of LC-derived amphotropic retrovirus. Pleiotropic restriction of AKR, Friend, and Moloney ecotropic viruses, but not of amphotropic virus, suggests that the viral targets of Akvr-1 in the three ecotropic viruses are similar to each other and distinct from the target in the LC-amphotropic virus. The relationship of Akvr-1 to previously reported murine restriction loci Fv-1, Fv-2, and Fv-4 is discussed.

AKR murine leukemia virus↗

PubMed1984

Effects of food restriction on aging: separation of food intake and adiposity.

Restricted feeding of rodents increases longevity, but its mechanism of action is not understood. We studied the effects of life-long food restriction in genetically obese and normal mice of the same inbred strain in order to distinguish whether the reduction in food intake or the reduction in adiposity (percentage of fatty tissue) was the critical component in retarding the aging process. This was possible because food-restricted obese (ob/ob) mice maintained a high degree of adiposity. In addition to determining longevities, changes with age were measured in collagen, immune responses, and renal function. Genetically obese female mice highly congenic with the C57BL/6J inbred strain had substantially reduced longevities and increased rates of aging in tail tendon collagen and thymus-dependent immune responses, but not in urine-concentrating abilities. When their weight was held in a normal range by feeding restricted amounts, longevities were extended almost 50%, although these food-restricted ob/ob mice still had high levels of adiposity, with fat composing about half of their body weights. Their maximum longevities exceeded those of normal C57BL/6J mice and were similar to longevities of equally food-restricted normal mice that were much leaner. Food restricted ob/ob mice had greatly retarded rates of collagen aging, but the rapid losses with age in splenic immune responses were not mitigated. Thus, the extension of life-span by food restriction was inversely related to food consumption and corresponded to the aging rate of collagen. These results suggest that aging is a combination of independent processes; they show that reduced food consumption, not reduced adiposity, is the important component in extending longevity of genetically obese mice.

Adipose Tissue↗

PubMed1986

Rapid degradation restricts measles virus matrix protein expression in a subacute sclerosing panencephalitis cell line.

Measles virus matrix protein expression is restricted in the persistently infected brain cells of patients with the chronic neurological disease subacute sclerosing panencephalitis (SSPE). Prior studies of the nature of this restriction have identified polyadenylylated matrix gene-encoded RNA transcripts unable to direct effective translation. The defective nature of these mRNAs readily accounted for the inability to detect matrix protein in these persistently infected cells and suggested that in SSPE the restriction of matrix protein expression is achieved by preventing its synthesis. Recently, however, we reported evidence that matrix protein is synthesized in at least one example of this persistent infection, the SSPE cell line IP-3-Ca. In this case, failure of matrix protein to accumulate normally accounted for its restricted expression [Sheppard, R. D., Raine, C. S., Bornstein, M. B. & Udem, S. A. (1985) Science 228, 1219-1221]. To clarify the nature of the restriction displayed by IP-3-Ca cells, the synthesis and fate of the matrix protein of this SSPE cell line were examined in detail. No evidence of constraints on the efficiency of matrix protein mRNA transcription or translation was found. Instead, the restricted expression proved to be the result of rapid posttranslational degradation of matrix protein. We suggest that matrix protein gene mutations incurred in the course of genome replication are likely to be responsible for the diversity of observed mechanisms restricting matrix protein expression. In that event, the nature and position of the nucleotide substitution(s) would be the determinants of the level at which restricted expression is achieved.

Cell Line↗

PubMed1980

The response of liver enzymes to feed restriction and subsequent ad lib. feeding in the laying hen.

1. The effects of restricted feeding, and ad lib. feeding following food restriction, on hepatic carbohydrate and lipid metabolism in the laying hen were studied. 2. The birds were allocated to four groups and given either 92, 84 or 75 g/d or allowed ad lib. access to food. 3. Food restriction significantly reduced liver total lipid content compared with ad lib.-fed control birds and this was reflected in reduced hepatic lipogenic enzyme activities. 4. When birds from the restricted regimens were allowed free access to food they initially consumed more food than the control group but after 2 weeks of ad lib. feeding the food consumptions of the birds in all the groups were similar. 5. Concomitant with the increase in food intake there were also increases in liver lipid content and hepatic lipogenic enzyme activities. After 18 d of ad lib. feeding these measurements were similar in the previously restricted birds and the ad lib.-fed control group. 6. Despite these effects on lipid metabolism, food restrictio, and the subsequent release from food restriction, had no significant effects on the specific activities of the glycolytic enzymes examined. 7. Although there were large increases in liver lipid content following release from feed restriction no birds died from, or showed any of the symptoms of, fatty liver-haemorrhagic syndrome. This suggests that, in the absence of any other factor which may be involved in the syndrome, these high liver lipid contents were not, alone, sufficient to cause FLHS. The results also indicate that free access to food following food restriction is unlikely to be a major factor in initiating the syndrome.

Animals↗