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Artykuły w czasopismach na temat „Fetus Growth”

Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 25 lipca 2025

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1

Kim, O. H., and K. S. Shinn. "Postnatal growth of fetus-in-fetu." Pediatric Radiology 23, no. 5 (1993): 411–12. http://dx.doi.org/10.1007/bf02011978.

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2

Pilliod, Rachel A., Jessica M. Page, Teresa N. Sparks, and Aaron B. Caughey. "The Growth-Restricted Fetus." Obstetrical & Gynecological Survey 74, no. 7 (2019): 383–85. http://dx.doi.org/10.1097/01.ogx.0000569524.58213.11.

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3

Kamalovna, Sagdullayeva Makhmuda, Ibragimova Shahzoda Abdurahimovna, and Tolmasov Ruzibek. "FETOMETRY OF THE FETUS." American Journal Of Biomedical Science & Pharmaceutical Innovation 03, no. 02 (2023): 24–29. http://dx.doi.org/10.37547/ajbspi/volume03issue01-04.

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The characteristic of the growth rates of various indicators at the stages of screening examination allows us to judge the adaptation processes occurring in the process of fetal growth. And in fetuses of pregnant women in a state of hypothyroidism, the intensity of growth of head parameters was less compared with the parameters of fetuses of healthy pregnant women. In fetuses of pregnant women in a state of hypothyroidism, the biparietal head size is significantly smaller at the stage of the second screening examination than in fetuses of healthy pregnant women.

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4

Denis, Danièle, Maud Righini, Claudie Scheiner, et al. "Ocular Growth in the Fetus." Ophthalmologica 207, no. 3 (1993): 117–24. http://dx.doi.org/10.1159/000310417.

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5

Denis, Danièle, Françoise Faure, Françoise Volot, et al. "Ocular Growth in the Fetus." Ophthalmologica 207, no. 3 (1993): 125–32. http://dx.doi.org/10.1159/000310418.

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6

Shamsuddin, L., and A. K. M. Shamsuddin. "Growth pattern of Bangladeshi fetus." International Journal of Gynecology & Obstetrics 70 (2000): B30. http://dx.doi.org/10.1016/s0020-7292(00)86183-4.

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Harding, JE, and BM Johnston. "Nutrition and fetal growth." Reproduction, Fertility and Development 7, no. 3 (1995): 539. http://dx.doi.org/10.1071/rd9950539.

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Nutrient supply to the fetus is a key factor in the regulation of fetal growth. However, the direct supply of nutrients to provide building blocks for tissue growth is likely to be only a minor component of this regulation. The indirect effects of nutrition on fetal endocrine and metabolic status, and on the interaction between the fetus, placenta and mother all of which must be coordinated to allow fetal growth are also important. Maternal undernutrition may alter the growth of the fetus and its different component tissues in a way which cannot be explained solely on the basis of reduced subs

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8

Firehammer, B. D., and Maryon M. Border. "Bulk growth procedures and a button agglutination test for Campylobacter." American Journal of Veterinary Research 47, no. 7 (1986): 1415–18. https://doi.org/10.2460/ajvr.1986.47.07.1415.

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SUMMARY Bulk-cell yields were obtained from 4 Campylobacter spp incubated aerobically without the use of a special atmosphere. A button agglutination test was developed for quantitation of blood serum antibodies against C fetus subsp venerealis, C fetus subsp fetus, C jejuni, and “C hyointestinalis.” The test was sensitive, and different individuals reading it usually attained the same titers. Cells of C fetus subsp venerealis, C fetus subsp fetus, and “C hyointestinalis” grown aerobically in broth made satisfactory antigens for the button test, but some cell pools of C jejuni had a tendency t

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9

Robinson, J., S. Chidzanja, K. Kind, F. Lok, P. Owens, and J. Owens. "Placental control of fetal growth." Reproduction, Fertility and Development 7, no. 3 (1995): 333. http://dx.doi.org/10.1071/rd9950333.

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The placenta exerts its effects on the growth of the fetus from the beginning of pregnancy via metabolic and endocrine mechanisms. To achieve this, the placenta exchanges a wide array of nutrients, endocrine signals, cytokines and growth factors with the mother and the fetus. These exchanges modulate or programme fetal growth and development. This review concentrates on the function and structure of the placenta in humans and in animals, and the effects of experimental perturbation of placental size and function on fetal growth. The consequences for fetal growth of varying the abundance of pep

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10

Hart-Elcock, Laura, R. D. Baker, and H. W. Leipold. "Growth of the Early Bovine Fetus." Journal of Veterinary Medicine Series A 37, no. 1-10 (1990): 294–99. http://dx.doi.org/10.1111/j.1439-0442.1990.tb00908.x.

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11

Mathai, M., S. Thomas, A. Peedicayil, A. Regi, P. Jasper, and R. Joseph. "Growth pattern of the Indian fetus." International Journal of Gynecology & Obstetrics 48, no. 1 (1995): 21–24. http://dx.doi.org/10.1016/0020-7292(94)02237-2.

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12

Hema, Karumpuzha R., and Richard Johanson. "Management of the growth-restricted fetus." Obstetrician & Gynaecologist 2, no. 2 (2000): 13–20. http://dx.doi.org/10.1576/toag.2000.2.2.13.

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13

Ziyadinov, A. A., and V. A. Novikovа. "Pregestational risks of insufficient fetus growth." Obstetrics and gynecology: News, Opinions, Training 11, no. 3 (2023): 44–51. http://dx.doi.org/10.33029/2303-9698-2023-11-3-44-51.

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14

Ганчар, Е. П. "Molecular Predictors of Fetus Growth Delay." Репродуктивное здоровье. Восточная Европа 13, no. 4 (2023): 346–57. http://dx.doi.org/10.34883/pi.2023.13.4.004.

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Цель. На основании изучения метаболического профиля свободных аминокислот у женщин в 1-м триместре беременности создать метод прогнозирования задержки роста плода. Материалы и методы. На 1-м этапе произведен забор плазмы крови у 518 женщин в сроке беременности 11–13 недель. Плазма криоконсервирована в условиях умеренно низкой температуры (–80 °С). Произведен анализ исходов беременности и родов. На 2-м этапе в исследование включено 50 пациенток: 1-я группа (основная) – 29 пациенток с подтвержденным диагнозом задержки роста плода; 2-я группа (контрольная) – 21 женщина с беременностью без осложне

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15

Cosmi, Erich, Tiziana Fanelli, Silvia Visentin, Daniele Trevisanuto, and Vincenzo Zanardo. "Consequences in Infants That Were Intrauterine Growth Restricted." Journal of Pregnancy 2011 (2011): 1–6. http://dx.doi.org/10.1155/2011/364381.

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Intrauterine growth restriction is a condition fetus does not reach its growth potential and associated with perinatal mobility and mortality. Intrauterine growth restriction is caused by placental insufficiency, which determines cardiovascular abnormalities in the fetus. This condition, moreover, should prompt intensive antenatal surveillance of the fetus as well as follow-up of infants that had intrauterine growth restriction as short and long-term sequele should be considered.

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16

Owens, JA. "Endocrine and substrate control of fetal growth: placental and maternal influences and insulin-like growth factors." Reproduction, Fertility and Development 3, no. 5 (1991): 501. http://dx.doi.org/10.1071/rd9910501.

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Fetal growth is largely controlled by the interaction of the genome with the availability of oxygen and glucose and by endocrine responses to variations in their supply. Insulin-like growth factor II (IGF-II), and probably IGF-I, modulate fetal growth. Insulin and thyroid hormones are controlled by the supply of glucose and oxygen, respectively, and they influence fetal growth, partly via IGF-I. Circulating IGF-I and -II are controlled acutely and chronically by glucose availability to the fetus. The transfer of substrates from the mother to the fetus is determined by placental transfer capaci

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17

Tudehope, David I. "Neonatal aspects of intrauterine growth retardation." Fetal and Maternal Medicine Review 3, no. 1 (1991): 73–85. http://dx.doi.org/10.1017/s0965539500000450.

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The growth-retarded fetus is susceptible to intrauterine death, perinatal asphyxia and subsequently neonatal morbidity. Recent technical advances have only moderately increased the obstetrician's ability to recognize the fetus with intrauterine growth retardation (IUGR) prior to delivery, compared with two decades ago when less than one-third of such infants were identified before labour and delivery.

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18

Syusyuka, V. G., N. G. Kolokot, and I. F. Belenichev. "Oxidative stress markers in pregnant women with fetus growth inhibition and their influence on results of labour process." HEALTH OF WOMAN, no. 8(144) (October 31, 2019): 48–52. http://dx.doi.org/10.15574/hw.2019.144.48.

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The objective: estimate the oxidative stress markers and their influence on result of labour process of pregnant women with fetus growth inhibition. Materials and methods. The complex examination of 63 pregnant women was made in term of 28–34 weeks of gestation and in dynamics (examination in 3–4 weeks). І group includes 33 pregnant women with fetus growth inhibition. Group ІІ was presented by 30 pregnant women without fetus growth inhibition. Markers of oxidative modification of proteins were analyzed in blood serum by means of spectrophotometric method and glutathione level was analyzed by f

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19

Kaku, Shoji, Fuminori Kimura, and Takashi Murakami. "Management of Fetal Growth Arrest in One of Dichorionic Twins: Three Cases and a Literature Review." Obstetrics and Gynecology International 2015 (2015): 1–4. http://dx.doi.org/10.1155/2015/289875.

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Progressive fetal growth restriction (FGR) is often an indication for delivery. In dichorionic diamniotic (DD) twin pregnancy with growth restriction only affecting one fetus (selective fetal growth restriction: sFGR), the normal twin is also delivered prematurely. There is still not enough evidence about the optimal timing of delivery for DD twins with sFGR in relation to discordance and gestational age. We report three sets of DD twins with sFGR (almost complete growth arrest affecting one fetus for ≥2 weeks) before 30 weeks of gestation. The interval from growth arrest to delivery was 21–24

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20

Maria, Tzitiridou-Chatzopoulou, and F. Zymperdikas Vasileios. "Preterm birth and its effects on craniofacial and dentoalveolar growth." World Journal of Advanced Research and Reviews 22, no. 1 (2024): 563–65. https://doi.org/10.5281/zenodo.14206359.

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Premature or preterm birth is a condition that takes place either before the 37<sup>th</sup> week of gestation or when the weight of the neonate is lower than 2500 grams (Paulsson et al., 2004; Cortines and Costa, 2016). Several factors that are related to the mother or the fetus have been considered as potential causes for this condition, whereas there is a consensus that there are potential parameters that could lead to premature birth which still remain to be identified (Hohoff et al., 2005; Seow, 1997). Despite the fact that the incidence of neonatal mortality owing to premature birth has

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21

Morrison, Janna L., and Kimberley J. Botting. "Does a growth-restricted fetus have fewer cardiomyocytes than a normally grown fetus?" Expert Review of Obstetrics & Gynecology 7, no. 4 (2012): 301–3. http://dx.doi.org/10.1586/eog.12.30.

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22

R., Vijaya Kumar Reddy* Dr. Uppu Ravi Babu &. K.Prudvi Raju. "AN APPROACH TO MONITOR FETUS GROWTH AND ITS WEIGHT ESTIMATION USING ULTRASOUND." INTERNATIONAL JOURNAL OF ENGINEERING SCIENCES & RESEARCH TECHNOLOGY 6, no. 8 (2017): 263–66. https://doi.org/10.5281/zenodo.843930.

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Analysis the growth of a fetus is essential and most important at pregnancy time. For this, we have to consider the fetal biometric measurements. Normally to check the growth of a fetus we used to measure weight of the fetal. The weight estimation is done by using ultrasound image where gynaecologist proper observation required and image quality. And the accuracy of the weight estimation of the fetal during scanning process depends upon fetal biometric parameters like Biparietal diameter (BPD), Head circumference (HC) Crown Rump Length (CRL), Femur length (FL), Humerus Length (HL) and abdomina

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23

Hiraoka, Takanori, Takafumi Kudo, and Yasuo Kishimoto. "Catecholamines in Experimentally Growth-Retarded Rat Fetus." Asia-Oceania Journal of Obstetrics and Gynaecology 17, no. 4 (2010): 341–48. http://dx.doi.org/10.1111/j.1447-0756.1991.tb00284.x.

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24

Baschat, Ahmet A., and Chris R. Harman. "Antenatal assessment of the growth restricted fetus." Current Opinion in Obstetrics and Gynecology 13, no. 2 (2001): 161–68. http://dx.doi.org/10.1097/00001703-200104000-00011.

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25

Galan, Henry L. "Timing Delivery of the Growth-Restricted Fetus." Seminars in Perinatology 35, no. 5 (2011): 262–69. http://dx.doi.org/10.1053/j.semperi.2011.05.009.

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26

Gardiner, H., J. Brodszki, and K. Maršál. "Ventriculovascular physiology of the growth-restricted fetus." Ultrasound in Obstetrics and Gynecology 18, no. 1 (2001): 47–53. http://dx.doi.org/10.1046/j.1469-0705.2001.00436.x.

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27

Sims, D. G. "Doppler studies in the growth retarded fetus." BMJ 294, no. 6571 (1987): 577. http://dx.doi.org/10.1136/bmj.294.6571.577-a.

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Whittle, M. J., and K. P. Hanretty. "Doppler studies in the growth retarded fetus." BMJ 294, no. 6572 (1987): 644. http://dx.doi.org/10.1136/bmj.294.6572.644-a.

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29

Takeda, Y., M. Nakabayashi, and M. Iwashita. "Intrauterine Treatment of the Growth Retarded Fetus." Journal of Perinatal Medicine 18, s1 (1990): 108. http://dx.doi.org/10.1515/jpme.1990.18.s1.108.

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30

Vora, Neeta L., and Nancy Chescheir. "Delivery of the growth restricted preterm fetus." Lancet 385, no. 9983 (2015): 2126–28. http://dx.doi.org/10.1016/s0140-6736(14)62455-7.

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Mol, Ben. "Delivery of the growth-restricted preterm fetus." Lancet 386, no. 10001 (2015): 1336. http://dx.doi.org/10.1016/s0140-6736(15)00327-x.

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Bekedam, D. J., G. H. A. Visser, J. J. de Vries, and H. F. R. Prechtl. "Motor behaviour in the growth retarded fetus." Early Human Development 12, no. 2 (1985): 155–65. http://dx.doi.org/10.1016/0378-3782(85)90178-1.

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Maršál, Karel. "Physiological adaptation of the growth-restricted fetus." Best Practice & Research Clinical Obstetrics & Gynaecology 49 (May 2018): 37–52. http://dx.doi.org/10.1016/j.bpobgyn.2018.02.006.

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Clifton, V., A. Osei-Kumah, N. Hodyl, N. Scott, and M. Stark. "036. SEX SPECIFIC FUNCTION OF THE HUMAN PLACENTA: IMPLICATIONS FOR FETAL GROWTH AND SURVIVAL." Reproduction, Fertility and Development 21, no. 9 (2009): 9. http://dx.doi.org/10.1071/srb09abs036.

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The placenta plays a central role in the development of the fetus by modulating the supply of nutrients and oxygen throughout pregnancy. We have identified that the placenta adapts to the presence of a maternal pathophysiology in a sexually dimorphic manner which results in differences in fetal growth. We have reported that the female fetus reduces her growth in response to chronic maternal asthma which ensures her survival in the presence of an acute asthma exacerbation. Conversely the male fetus continues to grow normally in the presence of maternal asthma but this is associated with a poor

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35

Ross,, J. C., P. V. Fennessey, R. B. Wilkening, F. C. Battaglia, and G. Meschia. "Placental transport and fetal utilization of leucine in a model of fetal growth retardation." American Journal of Physiology-Endocrinology and Metabolism 270, no. 3 (1996): E491—E503. http://dx.doi.org/10.1152/ajpendo.1996.270.3.e491.

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Placental transport and fetal utilization of leucine were studied at 130 days of gestation in six control ewes and in seven ewes in which intrauterine growth retardation (IUGR) had been induced by exposure to heat stress. Leucine fluxes were measured during simultaneous intravenous infusion of L-[1-13C]leucine into the mother and L-[1-14C] leucine into the fetus. In the IUGR group, the following leucine fluxes, expressed as micromol/min/kg fetus, were reduced compared with control: net uterine uptake (3.44 vs. 8.56, P<0.01), uteroplacental utilization (0.0 vs. 4.7, P<0.01), fetal disposa

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36

V.A., Puchkov, G. Siusiuka V., Deinichenko O.V., Sergienko M.Yu., Boguslavska N.Yu., and Babinchuk O.V. "The current state of the problem, clinical-pathogenetic approaches to the diagnosis and management tactics of fetal growth restriction." Reproductive Health of Woman, no. 5 (July 31, 2024): 74–83. https://doi.org/10.30841/2708-8731.5.2024.310397.

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Fetal growth restriction is a common complication of pregnancy with a complex etiology and limited possibilities of diagnosis and treatment. The relevance of this difficult obstetric problem is determined by various published diagnostic criteria, relatively low detection rates, and limited options for prevention and treatment.Fetal growth restriction is defined as the inability of the fetus to reach its genetically determined growth potential, most often due to abnormal placentation. Forms of fetal growth restriction with early or late onset are distinguished based on the gestational age deter

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37

Hyatt, Melanie A., Helen Budge, David Walker, Terence Stephenson, and Michael E. Symonds. "Ontogeny and Nutritional Programming of the Hepatic Growth Hormone-Insulin-Like Growth Factor-Prolactin Axis in the Sheep." Endocrinology 148, no. 10 (2007): 4754–60. http://dx.doi.org/10.1210/en.2007-0303.

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The liver is an important metabolic and endocrine organ in the fetus, but the extent to which its hormone receptor sensitivity is developmentally regulated in early life is not fully established. Therefore, we examined developmental changes in mRNA abundance for the GH receptor (GHR) and prolactin receptor (PRLR) plus IGF-I and -II and their receptors. Fetal and postnatal sheep were sampled at either 80 or 140 d gestation, 1 or 30 d, or 6 months of age. The effect of maternal nutrient restriction between early gestation to midgestation (i.e. 28–80 d gestation, the time of early liver growth) o

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38

Shenai, Ashwini. "Hormones Influencing Growth of the Fetus: A Review." Research Journal of Pharmacy and Technology 8, no. 6 (2015): 749. http://dx.doi.org/10.5958/0974-360x.2015.00119.5.

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Murtazina, Nuriya I., Elena D. Lutsai, and Sofya V. Ershova. "Growth rate of thyroid gland in human fetus." Science and Innovations in Medicine 6, no. 2 (2021): 4–7. http://dx.doi.org/10.35693/2500-1388-2021-6-2-4-7.

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Objectives to determine the thyroid gland growth rate in the intermediate fetal period of human ontogenesis. Material and methods. The thyroid glands of 60 male and female fetuses aged from 14 to 27 weeks were the subject of this research. The material was divided according to fetus age in three groups: Group I from 14 to 18 weeks, Group II from 19 to 22 weeks and Group III from 23 to 27 weeks. Results. The study revealed the increase in all dimensions of thyroid gland related to the increase of fetus age. During the intermediate fetal period of ontogenesis, the growth varied from

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40

Chard, T. "Hormonal control of growth in the human fetus." Journal of Endocrinology 123, no. 1 (1989): 3–9. http://dx.doi.org/10.1677/joe.0.1230003.

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Tyson, R. Weslie, and Barton C. Staat. "The Intrauterine Growth-Restricted Fetus and Placenta Evaluation." Seminars in Perinatology 32, no. 3 (2008): 166–71. http://dx.doi.org/10.1053/j.semperi.2008.02.005.

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Bahtiyar, Mert Ozan, and Joshua A. Copel. "Cardiac Changes in the Intrauterine Growth-Restricted Fetus." Seminars in Perinatology 32, no. 3 (2008): 190–93. http://dx.doi.org/10.1053/j.semperi.2008.02.010.

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BOTSIS, D., N. VRACHNIS, and G. CHRISTODOULAKOS. "Doppler Assessment of the Intrauterine Growth-Restricted Fetus." Annals of the New York Academy of Sciences 1092, no. 1 (2006): 297–303. http://dx.doi.org/10.1196/annals.1365.027.

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Abitbol, M. Maurice. "Growth of the fetus in the abdominal cavity." American Journal of Physical Anthropology 91, no. 3 (1993): 367–78. http://dx.doi.org/10.1002/ajpa.1330910309.

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Chareonsirisuthigul, Takol, Suchin Worawichawong, Rachanee Parinayok, Patama Promsonthi, and Budsaba Rerkamnuaychoke. "Intrauterine Growth Retardation Fetus with Trisomy 16 Mosaicism." Case Reports in Genetics 2014 (2014): 1–3. http://dx.doi.org/10.1155/2014/739513.

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Fetal trisomy 16 is considered uniformly lethal early in gestation. It has been reported to be associated with the variability of clinical features and outcomes. Mosaic trisomy 16 leads to a high risk of abnormality in prenatal cases. Intrauterine growth retardation (IUGR) is a common outcome of mosaic trisomy 16. Herein, we report on the case of Thai male IUGR fetus with trisomy 16 mosaicism. The fetal body was too small. Postmortem investigation of placenta revealed the abnormality including small placenta with furcated cord insertion and single umbilical cord artery. Cytogenetic study demon

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46

Fry, Gordon, Deborah Pittinaro, and Shirley Eberly. "Pulsatile versus continuous growth in the human fetus." American Journal of Obstetrics and Gynecology 191, no. 6 (2004): S167. http://dx.doi.org/10.1016/j.ajog.2004.10.492.

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Baschat, Ahmet Alexander. "Venous Doppler Evaluation of the Growth-Restricted Fetus." Clinics in Perinatology 38, no. 1 (2011): 103–12. http://dx.doi.org/10.1016/j.clp.2010.12.001.

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Denis, D., O. Burguiere, F. Oudahi, and C. Schemer. "Measurement of facial growth in the human fetus." Graefe's Archive for Clinical and Experimental Ophthalmology 233, no. 12 (1995): 756–65. http://dx.doi.org/10.1007/bf00184086.

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Khajuria, Ruchi, and Megha Sharma. "Histopathology of placenta in intrauterine growth restriction (IUGR)." International Journal of Research in Medical Sciences 7, no. 3 (2019): 889. http://dx.doi.org/10.18203/2320-6012.ijrms20190943.

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Background: Birth of healthy term baby depends on normal placenta. IUGR is a condition associated with placental insufficiency. There is a close relationship between IUGR and placental qualitative changes. The aim of the present study was to evaluate the morphological and histological changes in placentas of IUGR fetuses and in placentas of normal uncomplicated pregnancies and to determine the relationship that exists between morphological change and frequency of IUGR.Methods: In a cross sectional study conducted in the department of Pathology, GMC Jammu, a total of 60 placenta were received,

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WARSHAW, JOSEPH B. "Intrauterine Growth Retardation: Adaptation or Pathology?" Pediatrics 76, no. 6 (1985): 998–99. http://dx.doi.org/10.1542/peds.76.6.998.

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Intrauterine growth retardation can result from a variety of environmental or genetic influences on fetal growth.1 The sequelae of intrauterine growth retardation resulting from impairment of nutrient flow from mother to fetus are well known and include low birth weight with sparing of brain growth, polycythemia, and hypoglycemia resulting from decreased storage fuels and defective gluconeogenesis. Despite the generally held assumption that nutritionally related intrauterine growth retardation (either maternal malnutrition or impaired uteroplacental blood flow) represents a serious pathologic

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