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1

Chomarat, M., and P. Mulsant. "Infection Pleurale A Campylobacter Fetus Fetus." Médecine et Maladies Infectieuses 20, no. 11 (November 1990): 584. http://dx.doi.org/10.1016/s0399-077x(05)80163-5.

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2

Eb, F., P. Verharghe, and B. F. K. Odimba. "Cholécystite à Campylobacter fetus ssp fetus." Médecine et Maladies Infectieuses 15, no. 4 (April 1985): 169–72. http://dx.doi.org/10.1016/s0399-077x(85)80273-0.

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3

La Scola, B., S. Chambourlier, and P. Bouillot. "Campylobacter fetus ssp. fetus brain abscess." Journal of Infection 37, no. 3 (November 1998): 309–10. http://dx.doi.org/10.1016/s0163-4453(98)92541-5.

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4

CATES, WILLARD, and E. RUSSELL ALEXANDER. "Sexually Transmitted Diseases and the Fetus." Annals of the New York Academy of Sciences 549, no. 1 Impact on the (December 1988): 1–16. http://dx.doi.org/10.1111/j.1749-6632.1988.tb23952.x.

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5

Cypierre, A., E. Denes, O. Barraud, Y. Jamilloux, J. Jacques, H. Durox, P. Pinet, and P. Weinbreck. "Campylobacter fetus infections." Médecine et Maladies Infectieuses 44, no. 4 (April 2014): 167–73. http://dx.doi.org/10.1016/j.medmal.2014.02.001.

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6

Gal, E., H. Jean-Pierre, and H. Darbas. "Septicémie à Campylobacter fetus ssp. fetus survenue après transfusion sanguine." Médecine et Maladies Infectieuses 15, no. 10 (October 1985): 564–65. http://dx.doi.org/10.1016/s0399-077x(85)80225-0.

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7

Smail, A., J. P. Ducroix, G. Laurens, and J. Baillet. "Spondylodiscite a Campylobacter fetus subspecie (S.S.P.) fetus chez un adulte." Médecine et Maladies Infectieuses 17, no. 5 (May 1987): 264–66. http://dx.doi.org/10.1016/s0399-077x(88)80400-1.

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8

Malani, Anurag N., Preeti N. Malani, and Sandro K. Cinti. "Campylobacter fetus." Infectious Diseases in Clinical Practice 15, no. 2 (March 2007): 119–21. http://dx.doi.org/10.1097/01.idc.0000236974.51334.19.

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9

La Scolea, Leonard J. "Campylobacter fetus subsp. fetus meningitis in a neonate." Clinical Microbiology Newsletter 7, no. 17 (September 1985): 125–26. http://dx.doi.org/10.1016/s0196-4399(85)80024-6.

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10

et al., P. Francioli. "CAMPYLOBACTER FETUS SUBSPECIES FETUS BACTEREMIA." Pediatric Infectious Disease Journal 4, no. 4 (July 1985): 428. http://dx.doi.org/10.1097/00006454-198507000-00042.

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11

Congdon, P. J. "Viral Diseases of the Fetus and Newborn." Archives of Disease in Childhood 60, no. 7 (July 1, 1985): 690. http://dx.doi.org/10.1136/adc.60.7.690.

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12

Mendelson, M. H., P. Nicholas, M. Malowany, and S. Lewin. "Subdural Empyema Caused by Campylobacter fetus ssp. fetus." Journal of Infectious Diseases 153, no. 6 (June 1, 1986): 1183–84. http://dx.doi.org/10.1093/infdis/153.6.1183.

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13

Dronda, Fernando, Isabel García‐Arata, Enrique Navas, and Luis de Rafael. "Meningitis in Adults Due to Campylobacter fetus Subspecies fetus." Clinical Infectious Diseases 27, no. 4 (October 1998): 906–7. http://dx.doi.org/10.1086/517168.

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14

Botelho, Michele Placedino Andrade, Christian Hirsch, Andrey Pereira Lage, Christiane Maria Barcellos Magalhães da Rocha, Elaine Maria Seles Dorneles, Patrícia Gomes Cardoso, and Geraldo Marcio da Costa. "Prevalence of Tritrichomonas foetus and Campylobacter fetus subsp. venerealis among bulls slaughtered in the state of Minas Gerais, Brazil." Semina: Ciências Agrárias 39, no. 5 (September 20, 2018): 2039. http://dx.doi.org/10.5433/1679-0359.2018v39n5p2039.

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Bovine genital campylobacteriosis (BGC) and bovine genital trichomonosis (BGT) are globally widespread, predominantly sexually transmitted diseases that mainly affect herds in which natural mating takes place. Bulls serve as good epidemiological indicators for studying the causative agents of these diseases in cattle herds. The objective of the present work was to determine the prevalence of BGC and BGT among bulls sent to slaughterhouses in southern Minas Gerais, Brazil. Samples of preputial smegma from 200 sexually mature, non-castrated bulls of several ancestries were collected in 2013 from four regional slaughterhouses. The polymerase chain reaction (PCR) was employed to detect Tritrichomonas foetus, Campylobacter fetus subsp. fetus, and C. fetus subsp. venerealis. Isolation also was used aiming to diagnosis of BGT. All smegma samples were negative in culture for T. foetus. Molecular tests revealed 8% (16/200) of animals to be positive for T. foetus, 17.5% (35/200) for Campylobacter. fetus subsp. fetus, and 13.5% (27/200) for C. fetus subsp. venerealis. The results of the present study indicate that T. foetus, C. fetus subsp. venerealis, and C. fetus subsp. fetus are present among bulls slaughtered in southern Minas Gerais, and that BGC and BGT occur in this region. These diseases therefore need to be considered during differential diagnosis of reproductive diseases affecting cattle herds in which natural mating is employed.
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15

de Otero, J., C. Pigrau, M. Buti, and R. Bartolome. "Isolation of Campylobacter fetus Subspecies fetus from a Gluteal Abscess." Clinical Infectious Diseases 19, no. 3 (September 1, 1994): 557–58. http://dx.doi.org/10.1093/clinids/19.3.557.

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16

Lucas, V., M. Derriennic, J. M. Brisseau, J. J. Allioux, and J. H. Barrier. "Spondylodiscite et arachnoïdite a Campylobacter fetus subspecies fetus chez un adulte non immunodeprime." Médecine et Maladies Infectieuses 18, no. 3 (March 1988): 199–200. http://dx.doi.org/10.1016/s0399-077x(88)80129-x.

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17

Scola, Bernard La, Sylvain Chambourlier, Claude Mercier, and Jean-Paul Casalta. "Abdominal aortic aneurysm infected by Campylobacter fetus subsp. Fetus." Clinical Microbiology and Infection 4, no. 9 (September 1998): 527–29. http://dx.doi.org/10.1111/j.1469-0691.1998.tb00409.x.

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18

Shenai, Jayant P. "Infectious Diseases of the Fetus and Newborn Infant." Journal of Perinatology 21, no. 8 (December 2001): 571. http://dx.doi.org/10.1038/sj.jp.7210649.

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19

Wheater, M. "Infectious diseases of the fetus and newborn infant." Archives of Disease in Childhood - Fetal and Neonatal Edition 73, no. 2 (September 1, 1995): F124. http://dx.doi.org/10.1136/fn.73.2.f124.

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20

Johnson, Robert V. "Infectious Diseases of the Fetus and Newborn Infant." Mayo Clinic Proceedings 65, no. 8 (August 1990): 1162–63. http://dx.doi.org/10.1016/s0025-6196(12)62735-9.

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21

Liley, Helen. "INFECTIOUS DISEASES OF THE FETUS AND NEWBORN INFANT." Journal of Paediatrics and Child Health 42, no. 4 (April 2006): 226. http://dx.doi.org/10.1111/j.1440-1754.2006.00842.x.

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22

Isaacs, D. "Infectious Diseases of the Fetus and Newborn Infant." Archives of Disease in Childhood 66, no. 1 Spec No (January 1, 1991): 80. http://dx.doi.org/10.1136/adc.66.1_spec_no.80.

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23

Zajdowicz, Margan. "Infectious Diseases of the Fetus and Newborn Infant." Military Medicine 160, no. 5 (May 1, 1995): 272. http://dx.doi.org/10.1093/milmed/160.5.272b.

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24

Saiman, Lisa. "Infectious Diseases of the Fetus and Newborn Infant." JAMA 307, no. 17 (May 2, 2012): 1865. http://dx.doi.org/10.1001/jama.307.17.1865.

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25

Barton, Leslie L. "Infectious Diseases of the Fetus and Newborn Infant." JAMA: The Journal of the American Medical Association 274, no. 15 (October 18, 1995): 1248. http://dx.doi.org/10.1001/jama.1995.03530150072042.

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26

Rupar, David G. "Infectious Diseases of the Fetus and Newborn Infant." JAMA: The Journal of the American Medical Association 264, no. 22 (December 12, 1990): 2940. http://dx.doi.org/10.1001/jama.1990.03450220108037.

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27

Barton, L. L. "Infectious Diseases of the Fetus and Newborn Infant." JAMA: The Journal of the American Medical Association 285, no. 21 (June 6, 2001): 2788–89. http://dx.doi.org/10.1001/jama.285.21.2788.

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28

Akli, J., J. Penot, D. Levallois, P. Rodon, J. P. Ramain, M. Germain, M. D. Coulee, and P. Choutet. "Septicemie a Campylobacter fetus ssp fetus: Une observation traitee en monotherapie par la ciprofloxacine." Médecine et Maladies Infectieuses 19, no. 10 (October 1989): 474–75. http://dx.doi.org/10.1016/s0399-077x(89)80140-4.

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29

May, Th, J. M. Rousselot, F. Mory, and Ph Canton. "Infection neonatale a Campylobacter fetus subsp fetus. A propos d'une observation traitee par imipenem." Médecine et Maladies Infectieuses 20, no. 5 (May 1990): 255–56. http://dx.doi.org/10.1016/s0399-077x(05)81138-2.

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30

Nishikubo, Masashi, Seiko Nasu, Hayato Maruoka, Tomoya Kawabata, Mika Ikeda, and Hiroaki Nishioka. "Sequential breast implant infections due to Campylobacter fetus subsp. fetus." Journal of Infection and Chemotherapy 27, no. 7 (July 2021): 1080–83. http://dx.doi.org/10.1016/j.jiac.2021.01.012.

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31

Howe, R. A., T. Clarke, M. H. Wilcox, P. Vandamme, and R. C. Spencer. "Campylobacter fetus subspecies fetus septicaemia: SDS-PAGE as an aid to speciation." Journal of Infection 31, no. 3 (November 1995): 229–32. http://dx.doi.org/10.1016/s0163-4453(95)80032-8.

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32

Levy, C., E. M. Mamizuka, C. Zapata, and H. Fernandez. "Bactériémie avec péricardite à Campylobacter fetus subsp. fetus chez une femme avec bêta-thalassémie majeure." Médecine et Maladies Infectieuses 28, no. 2 (February 1998): 216–17. http://dx.doi.org/10.1016/s0399-077x(98)80012-7.

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33

Texier, J., P. Couzigou, M. Mormede, J. Fourche, and C. Beraud. "Isolement d'un Campylobacter fetus ssp fetus d'un liquide d'ascite lors d'une septicémie chez un cirrhotique." Médecine et Maladies Infectieuses 15, no. 4 (April 1985): 173–74. http://dx.doi.org/10.1016/s0399-077x(85)80275-4.

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34

Wallace, Madison L., and Ken S. Rosenthal. "Vaccine protection of the mother, the fetus, neonates and infants." AIMS Allergy and Immunology 8, no. 2 (2024): 124–45. http://dx.doi.org/10.3934/allergy.2024007.

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Pregnant women, the fetus, neonates, and young infants are at an increased risk for serious diseases from many infections due to their immunocompromised or immunonäive statuses. Vaccines are available for many diseases, but not all of the serious infectious diseases for which these individuals are at risk. Some of these vaccines can be administered to the mother either prior to or during pregnancy. The antibodies that are generated can benefit the mother, the fetus, and the neonate. Other vaccines can be administered to the neonate soon after birth to elicit important protections. This review outlines the available vaccines and the need and potential for new vaccines for pathogens that challenge pregnant women, the fetus, neonates, and the infant.
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35

Goldfarb, Johanna. ":Infectious Diseases of the Fetus and Newborn, 5th Edition." Clinical Infectious Diseases 33, no. 3 (August 2001): 417–18. http://dx.doi.org/10.1086/321865.

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36

Agarwal, Krishna, and Ramesh Agarwal. "Effects of Maternal Autoimmune Diseases on Fetus and Neonates." Journal of Neonatology 20, no. 2 (June 2006): 172–75. http://dx.doi.org/10.1177/0973217920060210.

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37

Taylor, Paul M. "Neonatal-Perinatal Medicine: Diseases of the Fetus and Infant." JAMA: The Journal of the American Medical Association 260, no. 17 (November 4, 1988): 2580. http://dx.doi.org/10.1001/jama.1988.03410170128059.

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38

Elcuaz, Rosa, Ana Ma Cañas, Bernardo Lafarga, Ma Eugenia Arkuch, Jerónima Artiles, and Saturnino Suarez. "Spontaneous Peritonitis due to Campylobacter fetus ssp. fetus in a patient with cirrhosis." Clinical Microbiology Newsletter 20, no. 8 (April 1998): 72–73. http://dx.doi.org/10.1016/s0196-4399(00)80023-9.

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39

Grogono-Thomas, R., J. Dworkin, M. J. Blaser, and D. G. Newell. "Roles of the Surface Layer Proteins ofCampylobacter fetus subsp. fetus in Ovine Abortion." Infection and Immunity 68, no. 3 (March 1, 2000): 1687–91. http://dx.doi.org/10.1128/iai.68.3.1687-1691.2000.

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ABSTRACT The role of the surface (S)-layer proteins of Campylobacter fetus subsp. fetus has been investigated using an ovine model of abortion. Wild-type strain 23D induced abortion in up to 90% of pregnant ewes challenged subcutaneously. Isolates recovered from both dams and fetuses expressed S-layer proteins with variable molecular masses. The spontaneous S-layer-negative variant, strain 23B, neither colonized nor caused abortions in pregnant ewes. A series of isogenic sapA and recA mutants, derived from 23D, also were investigated in this model. A mutant (501 [sapA recA +]) caused abortion in one of five challenged animals and was recovered from the placenta of a second animal. Another mutant (502 [sapA recA]) with no S-layer protein expression caused no colonization or abortions in challenged animals but caused abortion when administered intraplacentally. Mutants 600(2) and 600(4), both recA, had fixed expression of 97- and 127-kDa S-layer proteins, respectively. Two of the six animals challenged with mutant 600(4) were colonized, but there were no abortions. As expected, all five strains recovered expressed a 127-kDa S-layer protein. In contrast, mutant 600(2) was recovered from the placentas of all five challenged animals and caused abortion in two. Unexpectedly, one of the 16 isolates expressed a 127-kDa rather than a 97-kDa S-layer protein. Thus, these studies indicate that S-layer proteins appear essential for colonization and/or translocation to the placenta but are not required to mediate fetal injury and that S-layer variation may occur in a recA strain.
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40

Park, Che Yon, and Hyunjin Cho. "Prevention and Management of Perinatal Major Infectious Diseases." Journal of The Korean Society of Maternal and Child Health 24, no. 3 (July 31, 2020): 133–43. http://dx.doi.org/10.21896/jksmch.2020.24.3.133.

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Perinatal infection is the leading cause of fetal and neonatal mortality and is directly related to childhood morbidity. Perinatal infections cause abnormal growth, delayed development, and many other clinical problems in newborns. In particular, TORCH syndrome can cause serious fetal and neonatal health problems through vertical infection, and timely diagnosis and treatment through regular antenatal examinations are important. There are no therapeutic options or vaccines for parvovirus or cytomegalovirus. Therefore, prevention is the most important method. In the case of toxoplasmosis, prenatal education is important because it can be prevented through hygiene management, although there are therapeutic drugs. Syphilis has a high prevalence, so early diagnosis is important. Rubella and varicella zoster infections can lead to fatal results in vertical transmission to the fetus. Therefore, preconception vaccination should be performed. Women with herpes simplex, which has a high prevalence in the community, need to be mindful when choosing a childbirth method by evaluating the infection through regular prenatal care to prevent vertical infection. Seasonal flu is rarely transmitted vertically to the fetus, but the morbidity and mortality risk to the mother is higher than that of the general population. Thus, prevention through vaccination is important. Lastly, coronavirus disease 2019 (COVID-19) infection has yet to be well studied, although the mother's morbidity and mortality are similar to those of the general population and there is no evidence of vertical infection. Since the findings of the effects on the mother and fetus are limited, transmission should be prevented through social distancing and personal hygiene practices.
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41

Begum, Shamsun Nahar, Nazneen Kabir, and Fahima Akhter. "Prenatal Management of Compromised Fetus." Bangladesh Journal of Obstetrics & Gynaecology 28, no. 2 (October 23, 2016): 92–99. http://dx.doi.org/10.3329/bjog.v28i2.30097.

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Compromised fetuses are those who are at increased risk in intrauterine life due to various factor resulting in increased mortality & morbidity. Fetal compromise in pregnancy is difficult to assess. Diagnostic skills for fetal diseases have improved enormously, but therapeutic approaches remains limited. “The Fetus should be considered as a separate individual and fetal medicine now needs to move into phase of evidence based management. Due to relative rarity of fetal disorder, a multicentre study is needed and this is the challenge for the next decade of fetal medicine.Bangladesh J Obstet Gynaecol, 2013; Vol. 28(2) : 92-99
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42

Forster, Dominik, Jan Hendrik Schwarz, Katrin Brosinski, Ulrich Kalinke, Gerd Sutter, and Asisa Volz. "Obstetric Ultrasonography to Detect Fetal Abnormalities in a Mouse Model for Zika Virus Infection." Viruses 12, no. 1 (January 7, 2020): 72. http://dx.doi.org/10.3390/v12010072.

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In 2015 Zika virus (ZIKV) emerged for the first time in South America. The following ZIKV epidemic resulted in the appearance of a clinical phenotype with microcephaly and other severe malformations in newborns. So far, mechanisms of ZIKV induced damage to the fetus are not completely understood. Previous data suggest that ZIKV may bypass the placenta to reach the fetus. Thus, animal models for ZIKV infection are important to facilitate studies about ZIKV infection during pregnancy. Here, we used ultrasound based imaging (USI) to characterize ZIKV induced pathogenesis in the pregnant Type I interferon receptor-deficient (IFNAR-/-) mouse model. Based on USI we suggest the placenta to be a primary target organ of ZIKV infection enabling ZIKV spreading to the fetus. Moreover, in addition to direct infection of the fetus, the placental ZIKV infection may cause an indirect damage to the fetus through reduced uteroplacental perfusion leading to intrauterine growth retardation (IUGR) and fetal complications as early as embryonic day (ED) 12.5. Our data confirmed the capability of USI to characterize ZIKV induced modifications in mouse fetuses. Data from further studies using USI to monitor ZIKV infections will contribute to a better understanding of ZIKV infection in pregnant IFNAR-/- mice.
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43

Yadav, Mukesh Kumar, Zeeshan Ahmed Khan, Jing-Hua Wang, and AbuZar Ansari. "Impact of Gut–Brain Axis on Hepatobiliary Diseases in Fetal Programming." Journal of Molecular Pathology 5, no. 2 (May 16, 2024): 215–27. http://dx.doi.org/10.3390/jmp5020014.

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The hepatobiliary system is vital for the biotransformation and disposition of endogenous molecules. Any impairment in the normal functioning of the hepatobiliary system leads to a spectrum of hepatobiliary diseases (HBDs), such as liver cirrhosis, fatty liver, biliary dyskinesia, gallbladder cancer, etc. Especially in pregnancy, HBD may result in increased maternal and fetal morbidity and mortality. Maternal HBD is a burden to the fetus’s growth, complicates fetal development, and risks the mother’s life. In fetal programming, the maternal mechanism is significantly disturbed by multiple factors (especially diet) that influence the development of the fetus and increase the frequency of metabolic diseases later in life. Additionally, maternal under-nutrition or over-nutrition (especially in high-fat, high-carbohydrate, or protein-rich diets) lead to dysregulation in gut hormones (CCK, GLP-1, etc.), microbiota metabolite production (SCFA, LPS, TMA, etc.), neurotransmitters (POMC, NPY, etc.), and hepatobiliary signaling (insulin resistance, TNF-a, SREBPs, etc.), which significantly impact fetal programming. Recently, biotherapeutics have provided a new horizon for treating HBD during fetal programming to save the lives of the mother and fetus. This review focuses on how maternal impaired hepatobiliary metabolic signaling leads to disease transmission to the fetus mediated through the gut–brain axis.
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44

Tu, Zheng-Chao, Floyd E. Dewhirst, and Martin J. Blaser. "Evidence that the Campylobacter fetus sap Locus Is an Ancient Genomic Constituent with Origins before Mammals and Reptiles Diverged." Infection and Immunity 69, no. 4 (April 1, 2001): 2237–44. http://dx.doi.org/10.1128/iai.69.4.2237-2244.2001.

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ABSTRACT Campylobacter fetus bacteria, isolated from both mammals and reptiles, may be either subsp. fetus or subsp.venerealis and either serotype A or serotype B. Surface layer proteins, expressed and secreted by genes in the saplocus, play an important role in C. fetus virulence. To assess whether the sap locus represents a pathogenicity island and to gain further insights into C. fetusevolution, we examined several C. fetus genes in 18 isolates. All of the isolates had 5 to 9 sapA orsapB homologs. One strain (85-387) possessed bothsapA and sapB homologs, suggesting a recombinational event in the sap locus betweensapA and sapB strains. When we amplified and analyzed nucleotide sequences from portions of housekeeping generecA (501 bp) and sapD (450 bp), a part of the 6-kb sap invertible element, the phylogenies of the genes were highly parallel. Among the 15 isolates from mammals, serotype A and serotype B strains generally had consistent positions. The fact that the serotype A C. fetus subsp. fetus and subsp. venerealis strains were on the same branch suggests that their differentiation occurred after the type A-type B split. Isolates from mammals and reptiles formed two distinct tight phylogenetic clusters that were well separated. Sequence analysis of 16S rRNA showed that the reptile strains form a distinct phylotype between mammalian C. fetus and Campylobacter hyointestinalis. The phylogenies and sequence results showing that sapD and recA have similar G + C contents and substitution rates suggest that the sap locus is not a pathogenicity island but rather is an ancient constituent of the C. fetus genome, integral to its biology.
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45

Das, Bibhuti, Shashi Raj, and Robert Solinger. "Natriuretic Peptides in Cardiovascular Diseases of Fetus, Infants and Children." Cardiovascular & Hematological Agents in Medicinal Chemistry 7, no. 1 (January 1, 2009): 43–51. http://dx.doi.org/10.2174/187152509787047667.

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46

Halliday, H. L. "Diseases of the Fetus and Newborn: Pathology, Radiology and Genetics." Archives of Disease in Childhood 64, no. 10 (October 1, 1989): 1519. http://dx.doi.org/10.1136/adc.64.10.1519-a.

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47

Goldsmith, Jay P. "INFECTIOUS DISEASES OF THE FETUS AND NEWBORN INFANT, 6TH EDITION." Shock 25, no. 4 (April 2006): 427. http://dx.doi.org/10.1097/01.shk.0000223840.63640.62.

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48

Carapetis, Jonathan R. "Infectious diseases of the fetus and newborn infant (5th edn)." International Journal of Infectious Diseases 6, no. 2 (June 2002): 152. http://dx.doi.org/10.1016/s1201-9712(02)90081-0.

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49

Rutledge, Joe. "Diseases of the fetus and newborn: Pathology, radiology, and genetics." Human Pathology 21, no. 4 (April 1990): 461–62. http://dx.doi.org/10.1016/0046-8177(90)90218-t.

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50

Breeze, A. C. "Infectious diseases of the fetus and newborn infant, 6th edn." Archives of Disease in Childhood - Fetal and Neonatal Edition 92, no. 2 (February 6, 2007): F156. http://dx.doi.org/10.1136/adc.2006.102566.

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