The existence during gestation of an immunological buffer zone at the interface between maternal and foetal tissues

1975 ◽  
Vol 271 (912) ◽  
pp. 343-361 ◽  
Keyword(s):  
Buffer Zone ◽  
Placental Lactogen ◽  
Apical Plasma Membrane ◽  
Hormonal Changes ◽  
Endocrine Activity ◽  
Maternal Tissue ◽  
Local Survival ◽  
Receptor Sites ◽  
Probable Interaction ◽  
Immunological Attack

In mammalian pregnancy the trophoblast normally constitutes an uninterrupted boundary of foetal tissue in immediate contact with maternal tissue, including blood in some species, and is the decisive immunological barrier to rejection of the foetus as an allograft. The ability of the trophoblast to function as a barrier evidently results from its capacity to resist immunological attack by either alloantibody or alloimmune cells and to prevent immunocompetent cells from reaching and damaging the foetus but, as yet, there is no general agreement regarding the means by which it exercises these functions. In view of the dramatic hormonal changes that occur during pregnancy and the undisputed involvement of trophoblast in these endocrine events, the possibility exists of an interaction between the hormones of pregnancy and the immunological phenomena. The present account furnishes evidence that endocrine activity at the maternal surface of the trophoblast, the presumptive site of the immunological frontier between foetus and mother, may be a factor in its local survival at implantation. The placental hormones so far known that are capable of blocking the antigen receptor sites of the mother’s lymphocytes and thus preventing the latter from reacting with the foetal antigens are the glycoprotein, human chorionic gonadotrophin (HCG) and the polypeptide hormone, human chorionic somatomammotrophin (HCS) or human placental lactogen (HPL), both of which are specific to the human placenta. The origin of these hormones, their spatial distribution and their probable interaction with placental steroid hormones are discussed. It is argued that the place of highest concentration of these hormones is on the surface of the syncytial microvilli and the adjacent caviolae of the apical plasma membrane, as well as on the surfaces of the persisting cytotrophoblastic cells of the basal plate (cytotrophoblastic shell), the cell islands and the septa - precisely where the immunological challenge of the foetal allograft to the maternal host occurs. An explanation is offered for the continuing production of the voluminous quantities of these hormones during human pregnancy.

Features hormonal status in pregnant women with benign cervical pathology in anamnesis

2017 ◽  
pp. 71-73
Author(s):  
N.Yu. Bysaha ◽  
Keyword(s):  
Statistical Analysis ◽  
Pregnant Women ◽  
Placental Lactogen ◽  
Control Group ◽  
Hormonal Status ◽  
Hormonal Changes ◽  
Fetoplacental Complex ◽  
History Of ◽  
Objective Study ◽  
Stimulation Of

The objective: study of hormonal status in pregnant women with benign cervical pathology (CP) in anamnesis. Patients and methods. Clinical and statistical analysis of the hormonal status of 100 women with a history of benign CP pathology has been performed. According to the revealed symptoms of CP during colposcopic examination, women were divided into two groups: 100 pregnant women, in whom colposcopic and cytologically signs of CP pathology were not detected, were included in the control group; and 100 women who had a pathology of CP, entered the main group. Results. The study examined hormonal relationships in the system mother–placenta–fetus, namely the level of hormones such as estriol, progesterone, human chorionic gonadotropin, placental lactogen. Hormonal changes in pregnant women and contribute to reducing the immunoreactivity unwanted stimulation of existing benign hyperplastic background processes in the cervix. Conclusion. Determining functional state placenta is an important factor in the timely diagnosis of disorders in the functioning of the system mother–placenta–fetus. Key words: hormonal status, placenta, uterine cervix, fetoplacental complex.

The stimulation of sodium transport by aldosterone

1971 ◽  
Vol 262 (842) ◽  
pp. 323-332 ◽  
Keyword(s):  
Protein Synthesis ◽  
Active Transport ◽  
Sodium Transport ◽  
Apical Plasma Membrane ◽  
Transport Pathway ◽  
Receptor Sites ◽  
Rna And Protein Synthesis ◽  
Inhibitor Of Protein Synthesis ◽  
Stimulation Of

Aldosterone, the major sodium retaining hormone in man, will stimulate active transport of sodium across the urinary bladder of the toad, Bufo marinus in vitro , at physiological concentrations of the hormone.The in vitro action of aldosterone is mimicked by steroid hormones with known mineralocorticoid properties and it is competitively inhibited by other analogues, e.g. spironolactone and cortisone. Aldosterone is bound to physiological receptor sites within the transporting epithelial cells, chiefly within the nuclei, and is displaced from these binding sites specifically by structural analogues including other mineralocorticoids. Effects of aldosterone are dependent upon availability of metabolizable substrates to support the active transport of sodium. Although the stimulation of sodium transport by aldosterone can be specifically inhibited by actinomycin D, an inhibitor of RNA synthesis, and by puromycin, an inhibitor of protein synthesis, direct evidence of stimulation of new RNA and protein synthesis during the latent period with physiological concentrations of aldosterone is still lacking. It is possible, however, that the amounts of RNA and protein that are involved are too small to be detected by available techniques. Evidence is summarized which leads us to conclude that the increased sodium transport induced by aldosterone is the consequence of a reduced resistance of the apical plasma membrane of the transporting epithelia to the entry of sodium into the transport pathway.

scholarly journals A Case of Improvement of Insulinoma Symptoms in Pregnancy

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A985-A986
Author(s):  
Shumail Syed ◽  
Andrea George
Keyword(s):  
Insulin Resistance ◽  
Spiral Ct ◽  
Placental Lactogen ◽  
Focal Lesion ◽  
Protective Mechanism ◽  
Surgical Removal ◽  
Hormonal Changes ◽  
Placental Growth Hormone ◽  
Pancreatic Neck ◽  
In Pregnancy

Abstract Background: Insulinomas are rare tumors with an incidence of approximately 4 cases per million person per year. Only 39 cases of pancreatic neuroendocrine tumors have been reported in pregnancy. We report a case of pregnancy protecting the mother from manifesting the symptoms of insulinoma. Clinical Case: This case describes a 25-year old female who initially noticed symptoms of generalized weakness and oral tingling sensation in Fall 2018. She became pregnant in March 2019. She noticed an immediate reduction of the intensity of her symptoms during pregnancy. Her pregnancy was uneventful, and she delivered a healthy newborn in November 2019. Two months postpartum, she had worsening symptoms including syncopal episodes, confusion, difficulty ambulating and visual changes that improved with PO intake specifically carbohydrate intake. She was evaluated in March 2020 and labs showed the following: venous glucose 32 mg/dL, C-peptide 1.7 nmol/L, BOHB 0.4 mmol/L, Insulin 6.1 microU/ml, Proinsulin 25.8 pmol/L, IGF-2 354 ng/mL, negative insulin antibodies and negative oral hypoglycemic agent screen. TSH was unremarkable and AM cortisol was 16.1 mcg/dL. She was started on diazoxide twice a day. She underwent MRI of abdomen, which was negative followed by an EUS which was also negative. She had run out of her diazoxide and became severely symptomatic resulting in an ER visit where she was found to be hypoglycemic. Further evaluation was done with a Triple Phase spiral CT which showed a 1 cm arterial enhancing focal lesion within the pancreatic neck compatible with insulinoma. This was further evaluated with EUS FNA which confirmed the diagnosis of insulinoma on pathology. Her chromogranin A was 46.5 ng/mL. She is scheduled for surgical removal of the lesion. Conclusion: Pregnancy leads to an increased insulin resistance through hormonal changes with increased expression of placental growth hormone, human placental lactogen and the placental variant of corticotrophin-releasing hormone (via ACTH and cortisol production), TNF-alpha and leptin. These changes that increase the insulin resistance act as a protective mechanism against the detrimental effects of an insulinoma. Pregnancy most likely also delayed the diagnosis of the insulinoma in this patient. Further research is warranted to evaluate the effects of an insulinoma on the mother and fetus. References: 1) Lowy AJ, Chisholm DJ. Insulinoma masked by pregnancy. Intern Med J. 2001 Mar;31(2):128-9. doi: 10.1046/j.1445-5994.2001.00017.x. PMID: 11480477.

scholarly journals Therapeutic plasma exchange for the management of severe gestational hypertriglyceridaemic pancreatitis due to lipoprotein lipase mutation

2020 ◽  
Vol 2020 ◽  
Author(s):  
Albert S Kim ◽  
Rashida Hakeem ◽  
Azaliya Abdullah ◽  
Amanda J Hooper ◽  
Michel C Tchan ◽  
...  
Keyword(s):  
Plasma Exchange ◽  
Lipoprotein Lipase ◽  
Therapeutic Plasma Exchange ◽  
Placental Lactogen ◽  
Pharmacological Intervention ◽  
List Type ◽  
Hormonal Changes ◽  
Changes In Pregnancy ◽  
Preconception Counselling ◽  
In Pregnancy

Summary A 19-year-old female presented at 25-weeks gestation with pancreatitis. She was found to have significant hypertriglyceridaemia in context of an unconfirmed history of familial hypertriglyceridaemia. This was initially managed with fasting and insulin infusion and she was commenced on conventional interventions to lower triglycerides, including a fat-restricted diet, heparin, marine oil and gemfibrozil. Despite these measures, the triglyceride levels continued to increase as she progressed through the pregnancy, and it was postulated that she had an underlying lipoprotein lipase defect. Therefore, a multidisciplinary decision was made to commence therapeutic plasma exchange to prevent further episodes of pancreatitis. She underwent a total of 13 sessions of plasma exchange, and labour was induced at 37-weeks gestation in which a healthy female infant was delivered. There was a rapid and significant reduction in triglycerides in the 48 h post-delivery. Subsequent genetic testing of hypertriglyceridaemia genes revealed a missense mutation of the LPL gene. Fenofibrate and rosuvastatin was commenced to manage her hypertriglyceridaemia postpartum and the importance of preconception counselling for future pregnancies was discussed. Hormonal changes in pregnancy lead to an overall increase in plasma lipids to ensure adequate nutrient delivery to the fetus. These physiological changes become problematic, where a genetic abnormality in lipid metabolism exists and severe complications such as pancreatitis can arise. Available therapies for gestational hypertriglyceridaemia rely on augmentation of LPL activity. Where there is an underlying LPL defect, these therapies are ineffective and removal of triglyceride-rich lipoproteins via plasma exchange should be considered. Learning points: Hormonal changes in pregnancy, mediated by progesterone,oestrogen and human placental lactogen, lead to a two- to three-fold increase in serum triglyceride levels. Pharmacological intervention for management of gestational hypertriglyceridaemia rely on the augmentation of lipoprotein lipase (LPL) activity to enhance catabolism of triglyceride-rich lipoproteins. Genetic mutations affecting the LPL gene can lead to severe hypertriglyceridaemia. Therapeutic plasma exchange (TPE) is an effective intervention for the management of severe gestational hypertriglyceridaemia and should be considered in cases where there is an underlying LPL defect. Preconception counselling and discussion regarding contraception is of paramount importance in women with familial hypertriglyceridaemia.

scholarly journals Hormonal regulation of tight junction closure in the mouse mammary epithelium during the transition from pregnancy to lactation

2001 ◽  
Vol 170 (2) ◽  
pp. 347-356 ◽  
Author(s):  
DA Nguyen ◽  
AF Parlow ◽  
MC Neville
Keyword(s):  
Tight Junction ◽  
Hormonal Regulation ◽  
Mammary Epithelium ◽  
Fluorescein Isothiocyanate ◽  
Pregnant Mouse ◽  
Placental Lactogen ◽  
Hormonal Changes ◽  
Ru 486 ◽  
Pregnant Mice ◽  
Delayed Closure

Closure of the tight junctions of the mammary epithelium has been shown to accompany the onset of copious milk secretion or lactogenesis, stage 2, in both goats and humans. Here we use injection of [(14)C]sucrose and FITC-albumin (fluorescein isothiocyanate-albumin) into the mammary duct to follow the course of tight junction closure during lactogenesis in mice. To examine the hormonal changes responsible, we ovariectomized day 16 or 17 pregnant mice and found that closure followed ovariectomy with a mean delay of 13.6+/-1.5 (s.e.m. ) h. That progesterone withdrawal is the trigger for closure was shown by the finding that injection of progesterone within 4 h of ovariectomy delayed closure and that closure occurred after injection of the progesterone antagonist RU 486 in intact late pregnant mice. Endocrine ablation studies showed that low to moderate concentrations of corticosterone and either placental lactogen or prolactin are necessary for tight junction closure triggered by progesterone withdrawal. Thus the hormonal requirements for tight junction closure are similar to those shown by other investigators to promote lactogenesis, stage 2. Further, the tight temporal control of tight junction permeability suggests that ovariectomy of the late pregnant mouse may be a good model for molecular studies of the lactogenic switch.

Bovine Placental Lactogen Is a Potent Stimulator of Growth and Displays Strong Binding to Hepatic Receptor Sites of Coho Salmon

1994 ◽  
Vol 95 (1) ◽  
pp. 31-41 ◽  
Author(s):  
Robert H. Devlin ◽  
John C. Byatt ◽  
Ewen McLean ◽  
Timothy Y. Yesaki ◽  
Gwen G. Krivi ◽  
...  
Keyword(s):  
Coho Salmon ◽  
Placental Lactogen ◽  
Strong Binding ◽  
Potent Stimulator ◽  
Receptor Sites

scholarly journals The Prolactin Family of Hormones as Regulators of Maternal Mood and Behavior

2021 ◽  
Vol 2 ◽  
Author(s):  
Teodora Georgescu ◽  
Judith M. Swart ◽  
David R. Grattan ◽  
Rosemary S. E. Brown
Keyword(s):  
Mental Health Problems ◽  
Maternal Mental Health ◽  
Brain Regions ◽  
Placental Lactogen ◽  
Hormonal Changes ◽  
Aberrant Expression ◽  
Major Barrier ◽  
Pregnancy And Lactation ◽  
Lactogenic Hormones ◽  
And Behavior

Transition into motherhood involves profound physiological and behavioral adaptations that ensure the healthy development of offspring while maintaining maternal health. Dynamic fluctuations in key hormones during pregnancy and lactation induce these maternal adaptations by acting on neural circuits in the brain. Amongst these hormonal changes, lactogenic hormones (e.g., prolactin and its pregnancy-specific homolog, placental lactogen) are important regulators of these processes, and their receptors are located in key brain regions controlling emotional behaviors and maternal responses. With pregnancy and lactation also being associated with a marked elevation in the risk of developing mood disorders, it is important to understand how hormones are normally regulating mood and behavior during this time. It seems likely that pathological changes in mood could result from aberrant expression of these hormone-induced behavioral responses. Maternal mental health problems during pregnancy and the postpartum period represent a major barrier in developing healthy mother-infant interactions which are crucial for the child's development. In this review, we will examine the role lactogenic hormones play in driving a range of specific maternal behaviors, including motivation, protectiveness, and mother-pup interactions. Understanding how these hormones collectively act in a mother's brain to promote nurturing behaviors toward offspring will ultimately assist in treatment development and contribute to safeguarding a successful pregnancy.

scholarly journals Neuroendocrinology of Pregnancy: Participation of Sex Hormones

2021 ◽  
Author(s):  
Luz Irene Pascual Mathey
Keyword(s):  
Immune System ◽  
Thyroid Hormones ◽  
Sex Hormones ◽  
Chorionic Gonadotropin ◽  
Human Chorionic Gonadotropin ◽  
Fetal Development ◽  
Placental Lactogen ◽  
Physiological Adaptation ◽  
Hormonal Changes ◽  
Human Placental Lactogen

Pregnancy is characterized by hormonal changes, critical for the mother’s physiological adaptation, exercising a role in the fetus’s development, maintenance, protection, and nutrition. Since born, the neuroendocrine system’s involvement is necessary to prevent the embryo from being rejected by the mother’s immune system. These changes are regulated by fluctuations in hormones such as Progesterone, Testosterone, Androstenedione, Dehydroepiandrosterone, Estradiol, Prolactin, human Placental Lactogen, human Chorionic Gonadotropin, and Thyroid hormones, which promote the mother’s development and the fetus (maternal-fetal development). Therefore, given the great importance of these hormones during pregnancy, this chapter will explain the preclinical and clinical participation of sex hormones in maternal-fetal development.

Sites of Adsorption of the Bacteriophages T3 and T5 on the Wall of Escherichia Coli B.

1967 ◽  
Vol 25 ◽  
pp. 96-97
Author(s):  
Manfred E. Bayer
Keyword(s):  
Escherichia Coli ◽  
Cell Wall ◽  
Electron Microscope ◽  
Uranyl Acetate ◽  
E Coli ◽  
Receptor Sites ◽  
Rigid Cell Wall ◽  
Host Cell Surface ◽  
Bacterial Viruses ◽  
Escherichia Coli B

Bacterial viruses adsorb specifically to receptors on the host cell surface. Although the chemical composition of some of the cell wall receptors for bacteriophages of the T-series has been described and the number of receptor sites has been estimated to be 150 to 300 per E. coli cell, the localization of the sites on the bacterial wall has been unknown.When logarithmically growing cells of E. coli are transferred into a medium containing 20% sucrose, the cells plasmolize: the protoplast shrinks and becomes separated from the somewhat rigid cell wall. When these cells are fixed in 8% Formaldehyde, post-fixed in OsO4/uranyl acetate, embedded in Vestopal W, then cut in an ultramicrotome and observed with the electron microscope, the separation of protoplast and wall becomes clearly visible, (Fig. 1, 2). At a number of locations however, the protoplasmic membrane adheres to the wall even under the considerable pull of the shrinking protoplast. Thus numerous connecting bridges are maintained between protoplast and cell wall. Estimations of the total number of such wall/membrane associations yield a number of about 300 per cell.

Ultrastructural morphology of nontumorous lactotrophs in human pituitaries exposed to high prolactin levels

1987 ◽  
Vol 45 ◽  
pp. 896-897
Author(s):  
S. Jalalah ◽  
K. Kovacs ◽  
E. Horvath
Keyword(s):  
Anterior Pituitary ◽  
Secretory Activity ◽  
Pituitary Hormones ◽  
Feedback Mechanism ◽  
Endocrine Activity ◽  
Hormone Synthesis ◽  
Anterior Pituitary Hormones ◽  
Negative Feedback Mechanism ◽  
Ultrastructural Morphology ◽  
Transmission Electron

Lactotrophs, as many other endocrine cells, change their morphology in response to factors influencing their secretory activity. Secretion of prolactin (PRL) from lactotrophs, like that of other anterior pituitary hormones, is under the control of the hypothalamus. Unlike most anterior pituitary hormones, PRL has no apparent target gland which could modulate the endocrine activity of lactotrophs. It is generally agreed that PRL regulates its own release from lactotrophs via the short loop negative feedback mechanism exerted at the level of the hypothalamus or the pituitary. Accordingly, ultrastructural morphology of lactotrophs is not constant; it is changing in response to high PRL levels showing signs of suppressed hormone synthesis and secretion.By transmission electron microscopy and morphometry, we have studied the morphology of lactotrophs in nontumorous (NT) portions of 7 human pituitaries containing PRL-secreting adenoma; these lactotrophs were exposed to abnormally high PRL levels.

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