Academic literature on the topic 'Placenta, placental pathology, pathology'
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Journal articles on the topic "Placenta, placental pathology, pathology"
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A., Ashoka, Manjunatha Sarthi, Basavraj A. C., and Mahesh T. K. "Placental pathology and its correlation with immediate feto neonatal outcome." International Journal of Contemporary Pediatrics 6, no. 3 (April 30, 2019): 1108. http://dx.doi.org/10.18203/2349-3291.ijcp20191999.
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Background: Placenta plays a major role in growth and development of the fetus as it helps in both exchange of nutrients and removal of waste. Even though it yields a valuable information of prognostic significance for the newborn, majority of the time it will be discarded after the gross examination. Hence the present study was conducted to determine the placental pathology and its correlation with fetal outcome.Methods: The present study was carried out in Davangere for a period of 2 years. The placenta of 100 parturients, more than 28 weeks of gestation were included for the present study. The data was collected after detailed review of the obstetric case records. Placentas were examined soon after delivery. After the gross examination was complete, the placentas were put in a labelled plastic container. The placentas were re-examined macroscopically again by the pathologist. Cut-section examination was done. Then, at least 4 appropriate blocks were taken for each placenta. They were stained with hematoxylin-eosin stain and examined under the microscope. The histopathological examination was conducted as per proforma.Results: One hundred placentae belonging to one hundred babies were studied among which 80% of the maternal cases had anaemia, 68% were term infant, 37% had IUGR. Eccentric insertion of the cord was observed to be the commonest (51). Marginally inserted membranes were seen most frequently (97).Conclusions: In the present study we conclude that placental reserve is large and small alteration do not affect the pregnancy outcome. The placental changes are not specific to a particular condition affecting the pregnancy.
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Dhawle, Manjusha S., Ashwini R. Tangde, Bhagyashree P. Mundhe, Santosh G. Rathod, and Rajan S. Bindu. "Department of Pathology, Government Medical College and Cancer Hospital, Aurangabad, Maharashtra, India." International Journal of Research in Medical Sciences 5, no. 7 (June 24, 2017): 3214. http://dx.doi.org/10.18203/2320-6012.ijrms20173015.
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Background: The intrauterine existence of fetus is dependent on one vital organ 'the placenta’. The placenta reflects the status of maternal hypertension as it is the mirror of maternal and fetal health. The hypertensive disorders complicate 5-10% of all pregnancies and form a dangerous triad with haemorrhage and infection that contributes greatly to maternal morbidity and mortality. The fetus is dependent on placenta for growth and development. Many disorders of pregnancy like hypertension are accompanied by gross and histological changes in placenta. Aim of the study was to study the various morphological lesions of placenta in pregnancy induced hypertension and compare them with normal pregnanciesMethods: Gross and microscopic examination was conducted on 70 placentas. These included 15 normal placentas and 55 placentas from pregnancy induced hypertension.Results: In PIH, on gross the placenta showed areas of infarction, perivillous fibrin deposition and basal decidual haematoma, while microscopically showed increased syncytial knotting, cytotrophoblasitc proliferation, basement membrane thickening, vasculosyncytial membrane deficiency, infarction and fibrinoid necrosis.Conclusions: Maternal disorders affect the placental histology and can be detected by morphological examination of such placentae. The placenta from hypertensive pregnant women show significant morphological changes as compared to control, which may alter the perinatal outcome.
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Sarode, Ashwini, Anil R. Joshi, and Anjali S. Kulkarni. "The Association of Various Placental Lesions with Perinatal Outcome in Preterm Births." International Journal of Research and Review 8, no. 5 (June 2, 2021): 357–64. http://dx.doi.org/10.52403/ijrr.20210545.
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Objective: Present study was designed to identify various lesions in placenta and investigate their impact on neonatal and perinatal outcome and also to determine the frequency of various inflammatory lesions in placenta. Materials and Methods: Placentae of 60 singleton nonanomalous preterm births were examined at Department of pathology at Tertiary care centre. Complete placental examination including both macroscopic and microscopic examination with the help of Haematoxylin and Eosin staining done. Thereafter placental lesions were classified according to Redline criteria for classification of placental pathology. Thereafter placental lesions were correlated with perinatal mortality and neonatal morbidity in early neonatal period. The relevant clinical details were collected from the obstetric clinical records and neonatal clinical records. Result: We found placental vascular processes as most frequent (73.33%) pathological lesion in our study. Most common inflammatory lesion in our study was chorioamnionitis (15%). Also among placentae of stillbirths, placental vascular lesions were predominant finding present in 85.7% of placentae of stillbirths. Other lesions found in placentae of stillbirths were Immune inflammatory lesions, maternal floor infarction and placenta accreta. Out of total placentae with vasculopathy, 19.2% cases developed neonatal sepsis, in chorioamnionitis group 66.6% live births were having sepsis. In present study we observed higher frequency of resuscitation in babies with placentae having chorioamnionitis. Discussion: This study revealed that the placental pathological findings appear to be correlated with perinatal mortality and early neonatal morbidity. So, examination of the preterm placentae gains importance in early determination of morbidity in infants. Placental findings can help neonatologist in routine diagnosis and management. Keywords: Placenta, Placental pathology, Preterm births, Perinatal outcome.
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Nanda J. Patil, Jyoti S. Tele, Rohit S. Kadam, Pawar S. J, and Sujata M. Kumbar. "Placental pathology in intrauterine fetal death." International Journal of Research in Pharmaceutical Sciences 11, SPL4 (December 21, 2020): 2376–80. http://dx.doi.org/10.26452/ijrps.v11ispl4.4480.
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Placenta is the most accessible and readily evaluable specimen which is mirror image of pregnancy. The objective here is to study the histomorphological changes in placenta in cases of intrauterine fetal deaths and to study correlation of placental findings with causes of fetal death which is significant to understand. The present cross sectional study was carried out in Department of Pathology of a tertiary care hospital from June 2015 to May 2017. Study of Placental Pathology in Intrauterine Fetal Death cases comprised of 99 placentas. The present study was undertaken to study the placental pathology in cases of intrauterine fetal death. IUFD was found to be more common in primigravida 50/99 (50.50%) mothers. Placental study gives useful morphological information regarding the abnormality of pregnancy. Gross and microscopic examination of the placenta plays an important role in identifying the underlying causes of fetal death and helps prevent further recurrence by making appropriate interventions during the next pregnancy. Study of placental pathology gives clues to events occurring throughout gestation and can potentially help to answer, questions concerning pregnancy management and risk assessment of future pregnancies. It will help the researchers who are doing the research in the field of placental pathology in the days to come.
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Shanes, Elisheva D., Leena B. Mithal, Sebastian Otero, Hooman A. Azad, Emily S. Miller, and Jeffery A. Goldstein. "Placental Pathology in COVID-19." American Journal of Clinical Pathology 154, no. 1 (May 22, 2020): 23–32. http://dx.doi.org/10.1093/ajcp/aqaa089.
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Abstract Objectives To describe histopathologic findings in the placentas of women with coronavirus disease 2019 (COVID-19) during pregnancy. Methods Pregnant women with COVID-19 delivering between March 18, 2020, and May 5, 2020, were identified. Placentas were examined and compared to historical controls and women with placental evaluation for a history of melanoma. Results Sixteen placentas from patients with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) were examined (15 with live birth in the third trimester, 1 delivered in the second trimester after intrauterine fetal demise). Compared to controls, third trimester placentas were significantly more likely to show at least one feature of maternal vascular malperfusion (MVM), particularly abnormal or injured maternal vessels, and intervillous thrombi. Rates of acute and chronic inflammation were not increased. The placenta from the patient with intrauterine fetal demise showed villous edema and a retroplacental hematoma. Conclusions Relative to controls, COVID-19 placentas show increased prevalence of decidual arteriopathy and other features of MVM, a pattern of placental injury reflecting abnormalities in oxygenation within the intervillous space associated with adverse perinatal outcomes. Only 1 COVID-19 patient was hypertensive despite the association of MVM with hypertensive disorders and preeclampsia. These changes may reflect a systemic inflammatory or hypercoagulable state influencing placental physiology.
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Ojha, Kamala, Suniti Rawal, and Abhimanyu Jha. "Placental Pathology in Severe Pre-eclampsia and Eclampsia." Nepalese Medical Journal 1, no. 1 (June 22, 2018): 32–35. http://dx.doi.org/10.3126/nmj.v1i1.20397.
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Introduction: Hypertensive disorders complicating pregnancy contribute significantly to maternal and perinatal morbidity and mortality. Since placenta is the functional unit between the mother and fetus examination of placenta can give an idea about prenatal experience of fetus. The aim is to observe the morphology and histopathology of placenta in pregnancy with severe preeclampsia / eclampsia between 20-42 weeks of gestation.Materials and Methods: This was a prospective, descriptive study carried out in the Department of Obstetrics and Gynaecology and Department of Pathology at Institute of Medicine, Tribhuwan University Teaching Hospital, TUTH for one year, starting from 15th May 2015 - 14th May 2016. A total 55 placentas, 48 of severe preeclampsia and 7 of eclampsia were collected and placental morphometric parameters, gross and histopathological features were examined.Results: It was found that placental morphometric parameters were significantly reduced. Histopathological study showed significant number of syncytial knots, areas of fibrinoid necrosis, hyalinization and calcification. These placental findings were associated with significantly decreased weight of fetus at birth.Conclusions: Preeclampsia and eclampsia cause significant placental morphometric and histological changes which in turn adversely affects neonatal birth weight.Nepalese Medical Journal, vol.1, No. 1, 2018, page: 32-35
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Ernst, Linda M., and Vinita Parkash. "Placental Pathology in Fetal Bartter Syndrome." Pediatric and Developmental Pathology 5, no. 1 (January 2002): 76–79. http://dx.doi.org/10.1007/s10024-001-0092-4.
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Bartter syndrome, which presents clinically with polyuria, urinary potassium loss, hypokalemia, hypercalciuria, and alkalosis, is an autosomal recessive disorder with mutations in genes encoding the Na-K-2Cl cotransporter, the chloride channel CLC-NKB, and the potassium channel ROMK. Prenatal diagnosis of Bartter syndrome is now possible; however, there are no reports of the placental pathology associated with fetal Bartter syndrome. We present the placental pathologic findings in two siblings with fetal Bartter syndrome. Both pregnancies were complicated by polyhydramnios and preterm delivery. The first pregnancy delivered at 30 weeks, and Bartter syndrome was diagnosed in the perinatal period. The subsequent pregnancy required periodic therapeutic amniocentesis secondary to massive polyhydramnios and delivered at 32 weeks gestation. The suspicion of fetal Bartter syndrome was very high in this second pregnancy, and the infant was confirmed to have Bartter syndrome subsequently. Both placentas were large for gestational age, weighing greater than the 95th percentile. Microscopic examination showed extensive subtrophoblastic basement membrane mineralization (special stains positive for iron and calcium) in the chorionic villi. This striking finding was present in both placentas. Subtrophoblastic mineralization has been described in the literature in placentas of fetuses with abnormalities including anencephaly, trisomy 21, and other congenital abnormalities; however, it has also been described in normal pregnancies. Mechanisms of calcification in the placenta are not well understood, but these striking cases suggest that defects in fetal renal excretion of ions can lead to dystrophic calcification within the placenta, particularly in a subtrophoblastic pattern.
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Bockoven, Crystal, Roland D. Gastfield, Thomas Victor, Palamadai N. Venkatasubramanian, Alice M. Wyrwicz, and Linda M. Ernst. "Correlation of Placental Magnetic Resonance Imaging With Histopathologic Diagnosis: Detection of Aberrations in Structure and Water Diffusivity." Pediatric and Developmental Pathology 23, no. 4 (December 23, 2019): 260–66. http://dx.doi.org/10.1177/1093526619895438.
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Objective Noninvasive methods to identify placental pathologic conditions are being sought in order to recognize these conditions at an earlier stage leading to improved clinical interventions and perinatal outcomes. The objective of this study was to examine fixed tissue slices of placenta by T2- and diffusion-weighted magnetic resonance imaging (MRI) and correlate the images with placental pathologic findings defined by routine gross and histologic examination. Methods Four formalin-fixed placentas with significant placental pathology (maternal vascular malperfusion, chronic villitis of unknown etiology, and massive perivillous fibrin deposition) and 2 histologically normal placentas were evaluated by high-resolution MRI. Representative placental slices were selected (2 cm long and 10 mm wide) and rehydrated. Imaging was performed on a Bruker Avance 14.1 T microimager. Diffusion-weighted images were acquired from 16 slices using slice thickness 0.5 mm and in-plane resolution approximately 100 µm × 100 µm. T2 maps were obtained from the same slices. T2 relaxation time and apparent diffusion coefficient (ADC) were acquired from representative regions of interest and compared between normal and diseased placentas. Results In T2- and diffusion-weighted images, the placental microstructure differed subjectively between diseased and normal placentas. Furthermore, diseased placentas showed statistically significantly longer mean T2 relaxation times and generally higher mean ADC. Conclusion Diffusion- and T2-weighted MRI can potentially be used to detect significant placental pathology by using T2 relaxation time and ADC as markers of altered placental microstructure.
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Ramachandran, Amrutha. "Analysis of placental pathology and fetal outcome." International Journal of Reproduction, Contraception, Obstetrics and Gynecology 7, no. 4 (March 27, 2018): 1322. http://dx.doi.org/10.18203/2320-1770.ijrcog20180996.
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Background: A careful examination of placenta along with microscopic study may frequently point to the cause of perinatal death. The American College of Pathologists has provided guidelines for the examination of placenta. Aim of this study was to illustrate the gross and histopathological changes in placenta in certain normal and abnormal pregnancies and to analyse the relationship of placental pathology with fetal outcome.Methods: A prospective study of 120 deliveries at a tertiary teaching centre in India. Each placenta was studied macroscopically and sent to the pathology department for histological examination. The study included placentas of normal pregnancies and those with maternal high-risk features. The placenta was fixed in formalin and 6 sections were taken. The paraffin sections were studied for vessel wall thickening, infarction, villitis, chorioangiosis, calcification and intervillous hemorrhage. The primary outcome variables were fetal and neonatal morbidity. Abnormal fetal /neonatal events in each histological group were compared with the normal group using Ψ2 test for homogeneity. For cell frequencies less than 5, Fischer exact test was used.Results: Vessel wall thickening was demonstrated in 54/120 patients (45%). 7 out of 54 (12.96%) fetuses were still born in this group compared to 2/30 (6.67%) with normal histology (p value <0.05). Infarcts were demonstrated in 15/120 (12.5%). The occurrence of abnormal neonatal events in this group was significant p <0.01.Conclusions: Placental histological features of vessel wall thickening, and infarction is associated with abnormal fetal and neonatal outcome. Larger studies are required to establish the inference.
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Levy, RA, E. Avvad, J. Oliveira, and LC Porto. "Placental pathology in antiphospholipid syndrome." Lupus 7, no. 2_suppl (February 1998): 81–85. http://dx.doi.org/10.1177/096120339800700218.
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One of the major targets of antiphospholipid antibodies (aPL) is the placenta, the evolution of which during pregnancy has been well documented. Histopathological findings are related to gestational age, and several physiologic and pathologic alterations that occur during its development. The major findings in placentae from aPL positive patients are thrombosis, acute atherosis, a decreased number of syncytio-vascular membranes, increased number of syncytial knots and obliterative arteriopathy. These findings are not specific to the antiphospholipid syndrome (APS) and sometimes do not correlate with the fetal outcome. Histopathological study of placentae may elucidate mechanisms of action of aPL in fetal loss and other obstetric complications. In addition, it may assist in the investigation of the differential diagnosis between APS and pregnancy-induced hypertension. Immunohistochemical studies of local placental proteins contribute to this differential diagnosis.
Dissertations / Theses on the topic "Placenta, placental pathology, pathology"
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Mukherjee, Anika. "Pattern Recognition and Machine Learning as a Morphology Characterization Tool for Assessment of Placental Health." Thesis, Université d'Ottawa / University of Ottawa, 2021. http://hdl.handle.net/10393/42731.
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Introduction: The placenta is a complex, disk-shaped organ vital to a successful pregnancy and responsible for materno-fetal exchange of vital gases and biochemicals. Instances of compromised placental development or function – collectively termed placenta dysfunction - underlies the most common and devastating pregnancy complications observed in North America, including preeclampsia (PE) and fetal growth restriction (FGR). A comprehensive histopathology examination of the placenta following delivery can help clarify obstetrical disease etiology and progression and offers tremendous potential in the identification of patients at risk of recurrence in subsequent pregnancies, as well as patients at high risk of chronic diseases in later life. However, these types of examinations require a high degree of specialized training and are resource intensive, limiting their availability to tertiary care centers in large city centres. The development of machine learning algorithms tailored to placenta histopathology applications may allow for automation and/or standardization of this important clinical exam – expanding its appropriate usage and impact on the health of mothers and infants. The primary objective of the current project is to develop and pilot the use of machine learning models capable of placental disease classification using digital histopathology images of the placenta.
Methods: 1) A systematic review was conducted to identify the current methods being applied to automate histopathology screening to inform experimental design for later components of the project. Of 230 peer-reviewed articles retrieved in the search, 18 articles met all inclusion criteria and were used to develop guidelines for best practices. 2) To facilitate machine learning model development on placenta histopathology samples, a villi segmentation algorithm was developed to aid with feature extraction by providing objective metrics to automatically quantify microscopic placenta images. The segmentation algorithm applied colour clustering and a tophat transform to delineate the boundaries between neighbouring villi. 3) As a proof-of-concept, 2 machine learning algorithms were tested to evaluated their ability to predict the clinical outcome of preeclampsia (PE) using placental histopathology specimens collected through the Research Centre for Women’s and Infant’s Health (RCWIH) BioBank. The sample set included digital images from 50 cases of early onset PE, 29 cases of late onset PE and 69 controls with matching gestational ages. All images were pre-processed using patch extraction, colour normalization, and image transformations. Features of interest were extracted using: a) villi segmentation algorithm; b) SIFT keypoint descriptors (textural features); c) integrated feature extraction (in the context of deep learning model development). Using the different methods of feature extraction, two different machine learning approaches were compared - Support Vector Machine (SVM) and Convolutional Neural Network (CNN, deep learning). To track model improvement during training, cross validation on 20% of the total dataset was used (deep learning algorithm only) and the trained algorithms were evaluated on a test dataset (20% of the original dataset previously unseen by the model).
Results: From the systematic review, 5 key steps were found to be essential for machine learning model development on histopathology images (image acquisition and preparation, image preprocessing, feature extraction, pattern recognition and classification model training, and model testing) and recommendations were provided for the optimal methods for each of the 5 steps. The segmentation algorithm was able to correctly identify individual villi with an F1 score of 80.76% - a significantly better performance than recently published methods. A maximum accuracy of 73% for the machine learning experiments was obtained when using textural features (SIFT keypoint descriptors) in an SVM model, using onset of PE disease (early vs. late) as the output classification of interest.
Conclusion: Three major outcomes came of this project: 1) the range of methods available to develop automated screening tools for histopathology images with machine learning were consolidated and a set of best practices were proposed to guide future projects, 2) a villi segmentation tool was developed that can automatically segment all individual villi from an image and extract biologically relevant features that can be used in machine learning model development, and 3) a prototype machine learning classification tool for placenta histopathology was developed that was able to achieve moderate classification accuracy when distinguishing cases of early onset PE and late onset PE cases from controls. The collective body of work has made significant contributions to the fields of placenta pathology and computer vision, laying the foundation for significant progress aimed at integrating machine learning tools into the clinical setting of perinatal pathology.
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Donohoe, Siobhan. "An investigation of antiphospholipid antibody associated obstetric complications." Thesis, University College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.312964.
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DeFranco, Emily A. "Placental pathologic aberrations in cases of familial idiopathic spontaneous preterm birth." University of Cincinnati / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1282578435.
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Widdows, Kate Louise. "Gestational related morphological abnormalities in placental villous trophoblast turnover in compromised pregnancies." Thesis, Brunel University, 2009. http://bura.brunel.ac.uk/handle/2438/4444.
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Human placental villi are covered by a layer of trophoblast epithelia in direct contact with maternal blood, which exist in a constant steady-state of turnover and renewal ensuring both maternal and fetal health. The process of trophoblast turnover involves proliferation, differentiation and fusion of cytotrophoblast cells to form a terminally differentiated outer syncytiotrophoblast layer which functions as the active transport compartment between mother and fetus. Alterations in the balance between these three processes are thought to diminish both the structural and functional integrity of the syncytiotrophoblast, potentially leading to placental insufficiency associated with severe complications of pregnancy such as pre-eclampsia (PET), intrauterine growth restriction (IUGR) and sudden infant death syndrome (SIDS). Placentas from early (<32 weeks) and late-onset (>33 weeks) pregnancies complicated by PET, IUGR, SIDS and gestational age-matched controls were systematically uniform randomly sampled to assess the morphological basis of placental villous structure and trophoblast turnover (villi, cytotrophoblast, syncytiotrophoblast, apoptotic syncytial knots) using unbiased stereological techniques (volumes and numbers). Villous cytotrophoblast proliferation was assessed using double immunohistochemistry for Ki67 and cytokeratin 7 (CK-7). Severe early-onset IUGR placentas (n=5) were smaller displaying significant reductions in the total number of CT cells, within which the density of proliferating CT was further reduced by 50%. Syncytiotrophoblast volume and number was significantly reduced with an increase in apoptotic syncytial knots. Late-onset IUGR placentas (n=4) also displayed significant reductions in the total number of CT and proliferating CT, but were not associated with changes in the density of proliferating CT. SCT numbers were significantly reduced with an increase in apoptotic knots. Placentas from severe early-onset PET (n=11) were similar to preterm controls, except for a significant increase in apoptotic syncytial knots. However, late-onset PET (n=6) displayed a significant decrease in total CT number, the percentage of which undergoing proliferation was significantly increased for structural villi. There were increased numbers of apoptotic syncytial knots in peripheral villi.
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Rabie, Ursula. "The contribution of the placenta to the diagnosis of congenital tuberculosis." Thesis, Stellenbosch : Stellenbosch University, 2014. http://hdl.handle.net/10019.1/86623.
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Thesis (MMed)--Stellenbosch University, 2014.ENGLISH ABSTRACT: The aim of this pilot project was to determine whether mothers with laboratory confirmed or clinically suspected tuberculosis (TB) had evidence of TB in the placenta. A secondary objective was to correlate evidence of placental TB with neonatal outcome. A total of 56 placentas were examined to determine if there were any specific histopathological features predictive of tuberculosis together with Ziehl-Neelsen (ZN) staining. A total of 30 cases were positive for maternal TB and one case was a false positive maternal diagnosis of TB, whilst 25 cases were negative for maternal TB. Biopsies from these 56 placentas were collected for conventional PCR from the paraffin embedded tissue blocks. The performance of these two diagnostic modalities (histopathology and PCR) was assessed coll ectively and individually, and compared to the neonatal outcome (presence or absence of active clinical mycobacterial tuberculosis infection) and evidence of maternal pulmonary and extra pulmonary tuberculosis. The recognition of specific sites of lesions in the placenta (e.g. membranes vs. intervillous space) may lead to an understanding of the pathogenic mechanisms involved in matern alfetal transmission of tuberculosis, and thereby pave the way for further studies in understanding the pathogenesis of congenital TB. Invaluable knowledge was obtained in the diagnoses of M.tuberculosis in the placenta as it was found that micro abscesses and intervillositis were strong indicators of TB infection in the placenta, however, ZN staining still remains the gold standard for diagnosing M.tuberculosis infection in the placenta. PCR is found to have limitations, because only M.tuberculosis DNA is amplified and does not distinguish live from dead bacteria. The conclusion reached is that PCR is of limited value in the diagnosis of active M.tuberculosis infection in the placenta using FFPE tissue, while certain histological changes may be indicative of such infection; however confirmation of the organism by ZN staining is still essential.
AFRIKAANSE OPSOMMING: Die hoofdoelwit van hierdie projek was om vas te stel of moeders met bevestigde of vermoedelike TB enige indikasie van TB in die plasenta toon. ‘n Tweede doelwit was om die neonatale uitkoms teenoor die plasentale TB te korreleer. ‘n Totale getal van 56 plasentas is ondersoek om vas te stel of daar enige spesifieke histopatologiese indikasies is van tuberkulose met die hulp van die ZN spesiale kleuring. Die totale getal positiewe vir TB was 30 asook ‘n vals positiewe geval vir TB en daar was 25 TB negatiewe gevalle. Ses en vyftig biopsies is versamel van paraffien in gebedteerde weefsel vir die gebruik in PKR. Die uitvoering van hierdie twee diagnostiese modaliteite is elk individueel ondersoek asook gesamentlik om dit te vergelyk met die neonatale uitkoms (m.a.w die teenwoordigheid of aanwesigheid van mikobakteriale tuberkulose infeksie) asook die teenwoordigheid van moederlike pulmunere en ekstra-pulmunere tuberkulose. Die spesifieke ligging van die letsels in die plasenta (bv. membrane vs. intervillus spasie) kan lei tot verbeterde begrip van die patogeniese meganismes betrokke in die moeder fetale oordrag van tuberkulose en dit kan lei tot toekomstige navorsing. Waardevolle kennis is opgedoen in die diagnose van M.tuberkulose in die plasenta, want die letsels van mikro abbesses en intervillisitus gee ‘n goeie aanduiding van TB infeksie in die plasenta. Die ZN kleuring bly nog steeds die standaard metode om M.tuberculose in die plasenta te diagnoseer. PKR het baie limiete want dit kan slegs die M.tuberkulose DNA vermeningvuldig, maar dit kan nie onderskeid tref tussen lewendige en dooie bakterie nie. The slotsom in hierdie projek is dat PKR ‘n be pperkte waarde het in die diagnose van aktiewe M .tuberkulose in die plasenta, deur die gebruik van formalien gefikseerde paraffien ingebedteerde weefsel nie terwyl sekere histologiese veranderinge ‘n aa nduiding van sodanige infeksie kan wees maar dat dit deur die spesiale kleruring (ZN) bevestig moet word.
National Health Laboratory Service (NHLS)
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Лазоренко, В. В. "Роль плацентарних макрофагів в розвитку патоморфологічних змін плаценти в умовах плацентарної недостатності та інфекційної патології посліду." Thesis, Видавництво СумДУ, 2012. http://essuir.sumdu.edu.ua/handle/123456789/26913.
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Cantón, Germán José. "Immunopathogenesis of bovine neosporosis throughout gestation." Thesis, University of Edinburgh, 2013. http://hdl.handle.net/1842/8798.
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Despite Neospora caninum being recognised as a major cause of bovine abortion, its pathogenesis is only partially understood. Evidence of immune mediated placental pathology has been reported as being responsible for compromising pregnancy probably due to an exacerbated Th1 immune response at the maternal-foetal interface. Different clinical outcomes are known to follow experimental infections at different stages of gestation, with foetal death being the most common finding during early gestation infections, and the birth of live congenitally infected calves following infection in mid or late gestation. The aim of the current study was to characterise the placental cellular immune responses and cytokine expression following experimental Neospora infection during pregnancy. Placentomes were collected from cattle experimentally inoculated with the tachyzoites of the Nc-1 strain during early, mid and late gestation. Inflammation in early gestation was generally moderate to severe. Differently in mid gestation, inflammation was mild to moderate and minimal to mild in late gestation. Generally cellular infiltrates were mainly characterised by the presence of CD3+, CD4+ and γδ T-cells; whereas CD8+ and NK cells were less numerous. Macrophages were detected in larger numbers during later time-points after infection. A moderate to severe infiltration of IL-12, IFN-γ and TNF-α expressing cells was observed in the placentas collected in early gestation. This infiltration was more pronounced in the samples of placentome collected from dams carrying a dead foetus or in those that had aborted, compared with mothers carrying live foetuses at the time of sampling. The distribution of the cellular subsets observed in the three studies was similar. However, cellular infiltrates were more severe following infection during the first trimester in comparison to the second and third trimester. Similarly, the infiltration of Th1 cytokine expressing-cells was more severe in early gestation compared with the milder and more minimal infiltrations observed following N. caninum infection in mid and late gestation, respectively. These results may explain the milder clinical outcome observed when animals are infected in later stages of pregnancy.
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Cisse, Ouma. "Conséquences transgénérationnelles d'une programmation fœtale par dénutrition maternelle et d'un régime hyperlipidique chez le rat : focus sur le placenta." Phd thesis, Université du Droit et de la Santé - Lille II, 2013. http://tel.archives-ouvertes.fr/tel-01064268.
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Le concept de DOHaD (Developmental Origins of Health and Disease) qui découle de la théorie de Barker, replace l'origine des maladies métaboliques de l'adulte au moment du développement fœtal et/ou périnatal. De nombreuses données épidémiologiques indiquent qu'une dysnutrition maternelle (dénutrition, surnutrition) a des répercussions sur la croissance fœtale qui se traduisent par une anomalie du poids à la naissance (retard de croissance intra utérin : RCIU / gros poids de naissance : Macrosomie) et prédisposent l'individu au développement des maladies métaboliques. Afin de mieux comprendre les mécanismes susceptibles de transmettre de génération en génération cette vulnérabilité métabolique, nous avons développé un modèle transgénérationnel chez le rat associant la programmation fœtale chez la F0 par dénutrition maternelle (modèle FR30) et une dysnutrition chez la F1 avec un régime alimentaire hyperlipidique.Nos résultats montrent qu'une restriction alimentaire de 70% durant toute la grossesse (modèle FR30) contribue à une sensibilité accrue chez la descendance F1 femelle au développement de traits de syndrome métabolique. Les femelles F1 issues de mères dénutries présentent à l'âge adulte une intolérance au glucose et une hyperleptinémie. Les femelles de la F1 soumises à un régime hyperlipidique " high fat " (HF) ne présentent pas d'obésité que ce soit celles issues de mères contrôle que de mères dénutries. La faible appétence du régime, et la carence en hydrates de carbone qui l'accompagnent ne permettent pas le développement de l'obésité. En revanche, ce régime accentue les perturbations métaboliques chez des animaux sensibilisés par la programmation.Lorsque les femelles F1 sont mises en reproduction, on observe qu'en réponse à la programmation fœtale (FR) et/ou au régime alimentaire (Standard ou HF) la trajectoire de croissance dans la descendance F2 conduit à des phénotypes différents à la naissance. Les nouveau-nés de mères F1 issues de mères C ou FR et ayant suivi un régime HF en prégestation et en gestation (C HF-HF et FR HF-HF) ont un RCIU. A l'inverse, les nouveau-nés issus de mères F1 issues de mères dénutries et ayant eu un régime HF en prégestation puis un régime standard durant la gestation (FR HF-S) ont une macrosomie. Les perturbations métaboliques et hormonales des mères F1 ne pouvant expliquer à elles seules la survenue de ces phénotypes, nous nous sommes intéressés à l'organe situé à l'interface entre les compartiments maternels et fœtaux permettant le dialogue entre la mère et le fœtus : le placenta.L'analyse morphologique et moléculaire du placenta nous indique que cet organe est non seulement sensible aux modifications métaboliques de la mère, mais s'adapte à la demande du fœtus. On observe de fortes variations géniques qui se traduisent par une surexpression ou sous expressions géniques selon le phénotype observé RCIU ou macrosomie. Il est important de noter que les variations présentent un dimorphisme sexuel. Nos travaux suggèrent donc que les phénotypes de RCIU ou macrosomie sont le résultat d'anomalies métaboliques et hormonales maternelles mais également de l'adaptation génique placentaire sexe-spécifique.
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Anto, Enoch Odame. "Evaluation of suboptimal health status and prospective levels of oxidative stress biomarkers and angiogenic growth mediators with placental anatomy and pathology in normotensive and preeclamptic births." Thesis, Edith Cowan University, Research Online, Perth, Western Australia, 2020. https://ro.ecu.edu.au/theses/2317.
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Preeclampsia (PE) is the leading cause of poor maternal and perinatal outcomes in both developed and developing countries. Even though the condition is treatable in the developed world, mothers from developing countries still suffer dramatic events due to limited resources. There is the need to identify readily available measures in addition to existing biomarkers that can predict PE. Thus, this thesis evaluated suboptimal health status (SHS) and prospective levels of oxidative stress (OS) biomarkers and angiogenic growth mediators (AGMs) with placental anatomy and pathology in normotensive and preeclamptic births in a Ghanaian Population.
This longitudinal nested case-control study was based on the Ghanaian Suboptimal Health Status Cohort Study (GHOACS) that recruited 593 normotensive pregnant women (NTN-PW) at baseline (10-20 weeks gestation) from the Komfo Anokye Teaching Hospital between June 2017 and May 2019. Suboptimal health status, a subjective health measure was evaluated using the Suboptimal Health Status Questionnaire-25 (SHSQ-25) at baseline, and participants were subsequently classified into suboptimal health status (SHS) and optimal health status (OHS). Baseline participants were followed at 21-31 weeks, 32-42 weeks of pregnancy and 48 hours-2 weeks postpartum. Of the 593, 488 pregnant mothers aged 18-45 years completed the study and 105 were lost to follow-up. Data on sociodemographic, clinical, obstetric and anthropometric characteristics were collected from participants in addition to urine and venous blood samples. The panel of objective biomarkers of AGMs (placental growth factor [PIGF], vascular endothelial growth factor-A [VEGF-A], soluble endoglin [sEng] and soluble VEGF receptor-1 also known as soluble fms-like tyrosine kinase [sFlt-1]) in addition to OS biomarkers (8-epiprostaglandinF2 alpha [8-epi-PGF2α], 8-hydroxy-2-deoxyguanosine [8-OHdG] and total antioxidant capacity [TAC]) were evaluated across the 4-time sampling periods (10-20, 21-31, 32-42 weeks, and 48 hours-2 weeks postpartum) using ELISA. Placenta tissues were collected after delivery and examined for macroscopical, histopathological and immunohistochemical analyses. Data were analysed using SPSS, GraphPad Prism, XLSTAT and R Core.
There were significant associations between SHS and imbalances in AGMs and OS (Study I: cross-sectional). The incidence of PE was high among SHS pregnant women (30.7%) compared to OHS pregnant women (8.8%), and SHS was an independent risk indicator for PE (Study II: longitudinal nested case-control). Compared to using the biomarkers alone, combining biomarkers of AGMs and OS, particularly 8- OHdG/PlGF ratio measured at 21-31 weeks (mid-pregnancy) yielded the best area under the curve, sensitivity, specificity, positive and negative predicted values for predicting the likelihood of SHS and OHS pregnant women developing PE (Study III: longitudinal nested case-control). Placental abnormalities and imbalance in the expression of AGMs and OS were associated more with SHS pregnant mothers who developed PE, particularly early-onset PE than late-onset PE (Study IV: case-control). In contrast to normotensive pregnancy, longitudinal profiling of AGMs and OS showed different patterns across the 4-time sampling periods with significant imbalance among SHS more than OHS mothers who later developed PE. Unlike, the single biomarkers, combined AGMs and OS ratios measured at mid-pregnancy yielded more significant hazard ratios in association with PE development (Study V: longitudinal cohort).
Thus, combined evaluation of SHS, biomarkers of AGMs and OS together with placental examination increased the understanding of the aetiology, diagnosis and prognosis of PE, and created a window of opportunity for developing potentially predictive, preventive and personalised medicine in both high-and low-resource maternal and child health settings.
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Gouny-Doridot, Ludivine. "Rôle du facteur de transcription STOX1 dans la physiopathologie de la prééclampsie : apport d'un modèle cellulaire et d'un modèle murin de transgénèse additive." Phd thesis, Université René Descartes - Paris V, 2013. http://tel.archives-ouvertes.fr/tel-01015874.
Full textAbstract:
La prééclampsie est une maladie fréquente de la grossesse, caractérisée par l'apparition de novo d'une hypertension et d'une protéinurie à partir de la 20ème semaine d'aménorrhée. Ces symptômes s'aggravent au long de la grossesse, conduisant éventuellement à la mort maternelle en l'absence de prise en charge médicalisée. La thérapeutique définitive l'extraction du placenta, et donc du fœtus, ce qui induit une importante prématurité iatrogène. Les causes restent mal définies, mais il est bien admis que des anomalies au niveau de la mise en place du placenta sont au cœur de sa physiopathologie. Un défaut d'invasion trophoblastique des artères spiralées utérines semble être une constante de la maladie. Des données épidémiologiques démontrent qu'il existe une forte composante génétique dans la prééclampsie, et en 2005, un clonage positionnel dans des familles hollandaises, aboutit à l'identification de STOX1 comme le premier gène lié à cette maladie. STOX1 code un facteur de transcription intervenant dans le contrôle de la prolifération et de l'invasion des trophoblastes. Dans notre laboratoire, l'étude de STOX1 a été initiée par surexpression dans des cellules de choriocarcinome humain (modèle de trophoblastes) suivie d'une analyse transcriptomique. Celle-ci a révélé que les altérations d'expression génique observées suite à la surexpression de STOX1 étaient significativement corrélées à celles trouvées dans des placentas prééclamptiques. La création de souris transgéniques exprimant la version humaine de STOX1 sous le contrôle d'un promoteur ubiquitaire a alors été entreprise. Mes travaux de thèse ont principalement consisté à caractériser le phénotype de ces souris. Nous avons décidé de croiser des mâles transgéniques avec des souris sauvages afin de limiter l'expression du transgène à l'unité fœto-placentaire. Ces souris sauvages développent au cours de leur gestation une hypertension sévère, et une protéinurie. Elles constituent donc un nouveau modèle de prééclampsie. De plus, nous avons observé des anomalies que l'on trouve également chez les patientes : une fibrose rénale, une élévation des taux sériques de facteurs pro-angiogéniques (le récepteur soluble du VEGF et l'endogline soluble). Ces souris ont également des marqueurs d'hypertrophie cardiaque, attestant de l'impact sévère de l'hypertension. Pour mieux comprendre comment STOX1 peut induire ce syndrome, nous avons étudié son impact dans le modèle cellulaire surexprimant STOX1 et nous avons pu montré une altération de la gestion du stress oxydatif et de la fonction mitochondriale. En conclusion, nous avons obtenu et caractérisé un modèle de prééclampsie sévère, le seul existant montrant un phénotype hypertensif très marqué et très précoce. Ce modèle est un outil puissant pour découvrir de nouvelles voies impliquées dans la physiopathologie de la prééclampsie, pour rechercher de potentiels marqueurs diagnostiques précoces, tester des approches thérapeutiques innovantes et explorer les mécanismes responsables des conséquences à long terme de la prééclampsie.
Books on the topic "Placenta, placental pathology, pathology"
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S, Heller Debra, and Joshi Vijay V. 1936-, eds. Handbook of placental pathology. 2nd ed. London: Taylor & Francis, 2006.
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1942-, Kaufmann Peter, ed. Pathology of the human placenta. 2nd ed. New York: Springer-Verlag, 1990.
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1942-, Kaufmann Peter, and Baergen Rebecca N, eds. Pathology of the human placenta. 5th ed. New York: Springer, 2005.
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1942-, Kaufmann Peter, ed. Pathology of the human placenta. 4th ed. New York: Springer, 2000.
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1942-, Kaufmann Peter, ed. Pathology of the human placenta. 3rd ed. New York: Springer-Verlag, 1995.
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Khong, T. Yee, Eoghan E. Mooney, Peter G. J. Nikkels, Terry K. Morgan, and Sanne J. Gordijn, eds. Pathology of the Placenta. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-97214-5.
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Benirschke, Kurt, Graham J. Burton, and Rebecca N. Baergen. Pathology of the Human Placenta. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-23941-0.
Full textBook chapters on the topic "Placenta, placental pathology, pathology"
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Sato, Yuichiro. "Placental Pathology." In Preterm Labor and Delivery, 225–43. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-9875-9_23.
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Fox, Harold. "Placental Pathology." In Intrauterine Growth Restriction, 187–201. London: Springer London, 2000. http://dx.doi.org/10.1007/978-1-4471-0735-4_10.
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Turowski, Gitta, Susan Arbuckle, and W. Tony Parks. "The Placental Pathology Report." In Pathology of the Placenta, 371–77. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-97214-5_57.
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Morgan, Terry K. "Frontiers in Placental Pathology." In Pathology of the Placenta, 379–82. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-97214-5_58.
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Pantham, Priyadarshini, Francesca Soncin, Kathy Zhang-Rutledge, Srimeenakshi Srinivasan, Leah M. Lamale-Smith, Louise C. Laurent, and Mana M. Parast. "Innovations in Placental Pathology." In Benirschke's Pathology of the Human Placenta, 837–67. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-84725-8_31.
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Prins, Jelmer Riemer, Neil Sebire, Asma Khalil, and Sanne Jehanne Gordijn. "Imaging of Placental Pathology." In Benirschke's Pathology of the Human Placenta, 869–86. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-84725-8_32.
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Heller, Debra S. "Placental Mesenchymal Dysplasia." In Pathology of the Placenta, 127–30. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-97214-5_16.
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Benirschke, Kurt, Graham J. Burton, and Rebecca N. Baergen. "Placental Types." In Pathology of the Human Placenta, 27–39. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-23941-0_4.
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Benirschke, Kurt, and Peter Kaufmann. "Placental Types." In Pathology of the Human Placenta, 1–12. New York, NY: Springer New York, 1990. http://dx.doi.org/10.1007/978-1-4757-4193-3_1.
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Benirschke, Kurt, and Peter Kaufmann. "Placental Membranes." In Pathology of the Human Placenta, 130–79. New York, NY: Springer New York, 1990. http://dx.doi.org/10.1007/978-1-4757-4193-3_7.
Full textConference papers on the topic "Placenta, placental pathology, pathology"
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Weed, Benjamin, Ali Borazjani, Sourav Patnaik, Rajkumar Prabhu, Thomas Franz, M. F. Horstemeyer, Lakiesha Williams, and Jun Liao. "Stress State Dependence of Human Placenta Mechanical Behavior." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53775.
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Maternal trauma affects 5–8% of all pregnancies and is the leading nonobstetric cause of maternal death in the United States [1]. The most common cause of trauma is motor vehicle accident (MVA) and the most common pathology is abruptio placentae, detachment of the placenta from uterus, which leads to serious maternal and fetal consequences [2].
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Gordon, Laurel A., Kaavya Adam, Kristen Kelly, Amanda T. Harrington, and Sachin Amin. "Comparison Of Placental Pathology And Placental Culture As Predictors Of Clinical Sepsis In Neonates." In AAP National Conference & Exhibition Meeting Abstracts. American Academy of Pediatrics, 2021. http://dx.doi.org/10.1542/peds.147.3_meetingabstract.687-a.
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Lukovnikova, L. V., L. A. Lelbiks, and E. E. Lesiovskaya. "EFFECT OF NICKEL AND ITS INSOLUBLE INORGANIC COMPOUNDS ON REPRODUCTIVE FUNCTION OF WHITE RATS." In The 16th «OCCUPATION and HEALTH» Russian National Congress with International Participation (OHRNC-2021). FSBSI “IRIOH”, 2021. http://dx.doi.org/10.31089/978-5-6042929-2-1-2021-1-326-329.
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Abstract. Introduction. The problem of women's health protection in enterprises producing and using nickel and its compounds is particularly relevant, since women make up a significant contingent of workers at some stages of production. Nickel and its compounds are used in the production of high-alloy steels, alloys with copper, chromium, aluminum, as a catalyst in the processes of hydrogenation of fats, in the production of batteries, nickel-plating of metal products. In case of violations of the technological process, labor protection conditions, workers may be exposed to nickel aerosol and its oxides. Purpose. To study the effect of nickel and its insoluble compounds on the reproductive function of white rats. Method of research. The studies were carried out on sexually mature female white rats weighing 180-200 g with a stable estrous cycle lasting 4-6 days. Experimental studies were conducted in accordance with national and international regulatory requirements ensuring humane treatment of animals used in experiments: Directive 2010/63/EU of the European Parliament and of the Council of the European Union of September 22, 2010 on the protection of animals used in scientific purposes, Order of the Ministry of Health of the Russian Federation of 01.04.2016 No. 199n «On approval of the Rules of good laboratory Practice». The industrial conditions for the action of aerosol of insoluble nickel compounds were simulated in a special chamber with an individual intake of aerosol into the breathing zone at a concentration of 0.2 mg / m3 daily for 4 hours during the entire gestation period. The animals were assessed for the dynamics of body weight on the 1st, 8th, 14th and 20th days of pregnancy. On the 20th day of pregnancy, the number of yellow bodies of pregnancy, placentas and fetuses was determined, pre-, post-implantation and total intrauterine death, average length and weight of fetuses, and average placenta weight were calculated. The total number of pregnant females and fetuses was recorded with the subsequent calculation of the number of fetuses per female. Results. The action of an aerosol of insoluble nickel compounds at a concentration of 0.2 mg / m3 in this mode did not lead to a violation of the reproductive function of white rats in all the studied parameters. Conclusion. The experimental data obtained indicate that insoluble nickel compounds at the level of the maximum permissible concentrations for the air of the working area will not pose a risk of developing reproductive health pathology in working women.
Reports on the topic "Placenta, placental pathology, pathology"
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Feng, Zhichao, Zhimin Yan, and Qianyun Liu. MRI Signs for Prenatal Prediction of Placenta Accreta Spectrum Disorders and Invasiveness in High-risk Pregnant Women: A Systematic Review and Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, November 2022. http://dx.doi.org/10.37766/inplasy2022.11.0003.
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Review question / Objective: This meta-analysis aimed to identify the significant MRI signs for placenta accreta spectrum in high-risk pregnant women and to determine their diagnostic value. Condition being studied: Placenta accreta spectrum (PAS) is a dangerous complication in pregnancies with increasing incidence worldwide, in which the villous tissue adheres or invades the uterine wall. Eligibility criteria: Articles assessing the diagnostic performance of MRI signs for PAS and/or placenta percreta in high-risk pregnant women underwent full-text review. Included studies required confirmation of diagnosis based on intraoperative and/or pathologic findings.