RESUMO
Emergency obstetric care (EmOC) signal functions are a shortlist of key clinical interventions capable of averting deaths from the five main direct causes of maternal mortality; they have been used since 1997 as a part of an EmOC monitoring framework to track the availability of EmOC services in low- and middle-income settings. Their widespread use and proposed adaptation to include other types of care, such as care for newborns, is testimony to their legacy as part of the measurement architecture within reproductive health. Yet, much has changed in the landscape of maternal and newborn health (MNH) since the initial introduction of EmOC signal functions. As part of a project to revise the EmOC monitoring framework, we carried out a meta-narrative inspired review to reflect on how signal functions have been developed and conceptualised over the past two decades, and how different narratives, which have emerged alongside the evolving MNH landscape, have played a role in the conceptualisation of the signal function measurement. We identified three overarching narrative traditions: 1) clinical 2) health systems and 3) human rights, that dominated the discourse and critique around the use of signal functions. Through an iterative synthesis process including 19 final articles selected for the review, we explored patterns of conciliation and areas of contradiction between the three narrative traditions. We summarised five meta-themes around the use of signal functions: i) framing the boundaries; ii) moving beyond clinical capability; iii) capturing the woods versus the trees; iv) grouping signal functions and v) measurement challenges. We intend for this review to contribute to a better understanding of the discourses around signal functions, and to provide insight for the future roles of this monitoring approach for emergency obstetric and newborn care.
Assuntos
Narração , Feminino , Humanos , Recém-Nascido , Gravidez , Serviços Médicos de Emergência , Serviços de Saúde Materna/tendências , Mortalidade Materna/tendênciasRESUMO
INTRODUCTION: Maternal mortality in Nepal dropped from 553 to 186 per 100 000 live births during 2000-2017 (66% decline). Neonatal mortality dropped from 40 to 21 per 1000 live births during 2000-2018 (48% decline). Stillbirths dropped from 28 to 18 per 1000 births during 2000-2019 (34% decline). Nepal outperformed other countries in these mortality improvements when adjusted for economic growth, making Nepal a 'success'. Our study describes mechanisms which contributed to these achievements. METHODS: A mixed-method case study was used to identify drivers of mortality decline. Methods used included a literature review, key-informant interviews, focus-group discussions, secondary analysis of datasets, and validation workshops. RESULTS: Despite geographical challenges and periods of political instability, Nepal massively increased the percentage of women delivering in health facilities with skilled birth attendance between 2000 and 2019. Although challenges remain, there was also evidence in improved quality and equity-of-access to antenatal care and childbirth services. The study found policymaking and implementation processes were adaptive, evidence-informed, made use of data and research, and involved participants inside and outside government. There was a consistent focus on reducing inequalities. CONCLUSION: Policies and programmes Nepal implemented between 2000 and 2020 to improve maternal and newborn health outcomes were not unique. In this paper, we argue that Nepal was able to move rapidly from stage 2 to stage 3 in the mortality transition framework not because of what they did, but how they did it. Despite its achievements, Nepal still faces many challenges in ensuring equal access to quality-care for all women and newborns.
Assuntos
Mortalidade Infantil , Serviços de Saúde Materna , Mortalidade Materna , Humanos , Nepal , Mortalidade Materna/tendências , Mortalidade Infantil/tendências , Feminino , Recém-Nascido , Gravidez , Lactente , Disparidades em Assistência à Saúde , Qualidade da Assistência à Saúde , Acessibilidade aos Serviços de SaúdeAssuntos
Angiolipoma , Criptorquidismo , Neoplasias Testiculares , Testículo , Humanos , Masculino , Criptorquidismo/diagnóstico , Criptorquidismo/patologia , Criptorquidismo/cirurgia , Neoplasias Testiculares/patologia , Neoplasias Testiculares/diagnóstico , Neoplasias Testiculares/cirurgia , Neoplasias Testiculares/diagnóstico por imagem , Testículo/patologia , Testículo/diagnóstico por imagem , Angiolipoma/patologia , Angiolipoma/diagnóstico , Angiolipoma/cirurgiaRESUMO
RECQL is essential for genomic stability. Here, we evaluated RECQL in 449 pure ductal carcinomas in situ (DCIS), 152 DCIS components of mixed DCIS/invasive breast cancer (IBC) tumors, 157 IBC components of mixed DCIS/IBC and 50 normal epithelial terminal ductal lobular units (TDLUs). In 726 IBCs, CD8+, FOXP3+, IL17+, PDL1+, PD1+ T-cell infiltration (TILs) were investigated in RECQL deficient and proficient cancers. Tumor mutation burden (TMB) was evaluated in five RECQL germ-line mutation carriers with IBC by genome sequencing. Compared with normal epithelial cells, a striking reduction in nuclear RECQL in DCIS was evident with aggressive pathology and poor survival. In RECQL deficient IBCs, CD8+, FOXP3+, IL17+ or PDL1+ TILs were linked with aggressive pathology and shorter survival. In germline RECQL mutation carriers, increased TMB was observed in 4/5 tumors. We conclude that RECQL loss is an early event in breast cancer and promote immune cell infiltration.
Assuntos
Neoplasias da Mama , Carcinoma Intraductal não Infiltrante , Humanos , Feminino , Neoplasias da Mama/patologia , Carcinoma Intraductal não Infiltrante/patologia , RecQ Helicases/genética , Predisposição Genética para Doença , Biomarcadores Tumorais/genética , Fatores de Transcrição Forkhead/genéticaRESUMO
Chondroid syringoma is a rare adnexal tumor of skin, with few cases diagnosed on fine needle aspiration cytology (FNAC). Hyaline cell-rich chondroid syringoma (HCRCS) is a very uncommon variant of chondroid syringoma described in histopathologic studies. This variant differs from the usual chondroid syringoma in its site of presentation, cytohistologic features, and morphologically mimics malignant neoplasms. To the best of our knowledge, cytologic features of this entity have never been described. This case report highlights some unusual features of this tumor and discusses the cytologic features of HCRCS along with neoplastic mimics.
Assuntos
Adenoma Pleomorfo , Neoplasias Cutâneas , Neoplasias das Glândulas Sudoríparas , Humanos , Adenoma Pleomorfo/diagnóstico , Adenoma Pleomorfo/patologia , Hialina , Neoplasias das Glândulas Sudoríparas/patologia , Pele/patologia , Neoplasias Cutâneas/patologiaRESUMO
Fine-needle aspiration cytology (FNAC) is often the first-line investigation for detection of any fungal infection. Rhytidhysteron rufulum is an emerging dematiaceous fungus detected as a human pathogen. FNAC combined with molecular techniques helps in the detection of rare fungal species, especially in cases of non-sporulating fungi. We describe the cytomorphologic features of this species in a 62-year immunocompetent male who presented with a localised subcutaneous infection. Molecular studies helped in the final diagnosis.
Assuntos
Ascomicetos , Micoses , Feoifomicose , Humanos , Masculino , Feoifomicose/diagnóstico , Feoifomicose/microbiologia , Micoses/diagnóstico , CitodiagnósticoRESUMO
Myocardial ischemia-reperfusion injury (I/R) causes damage to cardiomyocytes through oxidative stress and apoptosis. We investigated the cardioprotective effects of MnTnBuOE-2-PyP5+ (BMX-001), a superoxide dismutase mimic, in an in vitro model of I/R injury in H9c2 cardiomyocytes. We found that BMX-001 protected against hypoxia/reoxygenation (H/R)-induced oxidative stress, as evident by a significant reduction in intracellular and mitochondrial superoxide levels. BMX-001 pre-treatment also reduced H/R-induced cardiomyocyte apoptosis, as marked by a reduction in TUNEL-positive cells. We further demonstrated that BMX-001 pre-treatment significantly improved mitochondrial function, particularly O2 consumption, in mouse adult cardiomyocytes subjected to H/R. BMX-001 treatment also attenuated cardiolipin peroxidation, 4-hydroxynonenal (4-HNE) level, and 4-HNE adducted proteins following H/R injury. Finally, the pre-treatment with BMX-001 improved cell viability and lactate dehydrogenase (LDH) activity in H9c2 cells following H/R injury. Our findings suggest that BMX-001 has therapeutic potential as a cardioprotective agent against oxidative stress-induced H/R damage in H9c2 cardiomyocytes.
Assuntos
Metaloporfirinas , Mimetismo Molecular , Traumatismo por Reperfusão Miocárdica , Miócitos Cardíacos , Estresse Oxidativo , Superóxido Dismutase , Superóxido Dismutase/metabolismo , Miócitos Cardíacos/efeitos dos fármacos , Miócitos Cardíacos/metabolismo , Estresse Oxidativo/efeitos dos fármacos , Traumatismo por Reperfusão Miocárdica/prevenção & controle , Metaloporfirinas/metabolismo , Metaloporfirinas/farmacologia , Sobrevivência Celular/efeitos dos fármacos , Lactato Desidrogenases/metabolismo , Linhagem Celular , Animais , Ratos , Cardiolipinas/metabolismo , Mitocôndrias/efeitos dos fármacos , Mitocôndrias/metabolismo , Metabolismo Energético/efeitos dos fármacos , Apoptose/efeitos dos fármacosRESUMO
Neointimal hyperplasia is characterized by a loss of the contractile phenotype of vascular smooth muscle cells (VSMCs). Our group has recently shown that VSMC proliferation and migration are mediated by lysophosphatidic acid (LPA) during restenosis, but the role of autotaxin (ATX; lysophospholipase D), which produces LPA, remains unclear. Endothelial denudation of the mouse carotid artery was performed to induce neointimal hyperplasia, and the extent of damage caused by the ATX-LPA axis was assessed in VSMCs. We observed the upregulation of ATX activity (p < 0.0002) in the injured carotid artery using an AR2 probe fluorescence assay. Further, the tissue carotid LPA levels were elevated 2.7-fold in carotid vessels, augmenting neointimal hyperplasia. We used an electrical cell-substrate impedance sensor (ECIS) to measure VSMC proliferation and migration. Treatment with an ATX inhibitor (PF8380) or LPA receptor inhibitor (Ki16425) attenuated VSMC proliferation (extracellular signal-regulated kinases) activity and migration in response to recombinant ATX. Indeed, PF8380 treatment rescued the aggravated post-wire injury neointima formation of carotid arteries. The upregulation of ATX following vessel injury leads to LPA production in VSMCs, favoring restenosis. Our observations suggest that inhibition of the ATX-LPA axis could be therapeutically targeted in restenosis to minimize VSMC phenotypic modulation and inflammation after vascular injury.
Assuntos
Miócitos de Músculo Liso , Neointima , Camundongos , Animais , Hiperplasia/patologia , Neointima/patologia , Fenótipo , Miócitos de Músculo Liso/patologia , Proliferação de Células , Movimento Celular , Células Cultivadas , Modelos Animais de DoençasRESUMO
Autotaxin (ATX) is an extracellular secretory enzyme (lysophospholipase D) that catalyzes the hydrolysis of lysophosphatidyl choline to lysophosphatidic acid (LPA). The ATX-LPA axis is a well-known pathological mediator of liver fibrosis, metastasis in cancer, pulmonary fibrosis, atherosclerosis, and neurodegenerative diseases. Additionally, it is believed that LPA may cause vascular permeability. In ischemic stroke, vascular permeability leading to hemorrhagic transformation is a major limitation for therapies and an obstacle to stroke management. Therefore, in this study, we generated an endothelial-specific ATX deletion in mice (ERT2 ATX-/-) to observe stroke outcomes in a mouse stroke model to analyze the role of endothelial ATX. The AR2 probe and Evans Blue staining were used to perform the ATX activity and vascular permeability assays, respectively. Laser speckle imaging was used to observe the cerebral blood flow following stroke. In this study, we observed that stroke outcomes were alleviated with the endothelial deletion of ATX. Permeability and infarct volume were reduced in ERT2 ATX-/- mice compared to ischemia-reperfusion (I/R)-only mice. In addition, the cerebral blood flow was retained in ERT2 ATX-/- compared to I/R mice. The outcomes in the stroke model are alleviated due to the limited LPA concentration, reduced ATX concentration, and ATX activity in ERT2 ATX-/- mice. This study suggests that endothelial-specific ATX leads to increased LPA in the brain vasculature following ischemic-reperfusion and ultimately disrupts vascular permeability, resulting in adverse stroke outcomes.
Assuntos
Fibrose Pulmonar , Acidente Vascular Cerebral , Animais , Camundongos , Modelos Animais de Doenças , Diester Fosfórico Hidrolases/genética , Acidente Vascular Cerebral/genéticaRESUMO
Lysophosphatidic acid (LPA), a multifunctional endogenous phospholipid, plays a vital role in cellular homeostasis and the malignant behavior of cancer cells through G-protein-coupled receptors. However, the role of LPA in ß-catenin-mediated gastric cancer is unknown. Here, we have noted the high expression of LPAR2 in human gastric cancer tissues, and that LPA treatment significantly increased the proliferation, migration, and invasion of human gastric cancer cells. Results from our biochemical experiments showed that an LPA exposure increased the expression of ß-catenin and its nuclear localization, increased the phosphorylation of glycogen synthase kinase 3ß (GSK-3ß), decreased the expression of Axin2, and increased the expression of the target genes of the ß-catenin signaling pathway. The LPA2 receptor (LPAR2) antagonist significantly reduced the LPA-induced nuclear localization of ß-catenin, the primary signaling event. The knockdown of LPAR2 in the gastric cancer cell lines robustly reduced the LPA-induced ß-catenin activity. An LPA exposure increased the ATP production by both oxidative phosphorylation and glycolysis, and this effect was abrogated with the addition of an LPAR2 antagonist and XAV393, which stabilizes the Axin and inhibits the ß-catenin signaling pathway. Based on our findings, the possibility that LPA contributes to gastric cancer initiation and progression through the ß-catenin signaling pathway as well as by the dysregulation of the energy metabolism via the LPAR2 receptor and Axin2, respectively, provides a novel insight into the mechanism of and possible therapeutic targets of gastric cancer.
Assuntos
Proteína Axina , Metabolismo Energético , Receptores de Ácidos Lisofosfatídicos , Neoplasias Gástricas , beta Catenina , Humanos , Proteína Axina/genética , Proteína Axina/metabolismo , beta Catenina/metabolismo , Linhagem Celular Tumoral , Glicogênio Sintase Quinase 3 beta/metabolismo , Receptores de Ácidos Lisofosfatídicos/genética , Receptores de Ácidos Lisofosfatídicos/metabolismo , Neoplasias Gástricas/metabolismo , Neoplasias Gástricas/patologiaRESUMO
Reactive oxygen species (ROS), a by-product of aerobic life, are highly reactive molecules with unpaired electrons. The excess of ROS leads to oxidative stress, instigating the peroxidation of polyunsaturated fatty acids (PUFA) in the lipid membrane through a free radical chain reaction and the formation of the most bioactive aldehyde, known as 4-hydroxynonenal (4-HNE). 4-HNE functions as a signaling molecule and toxic product and acts mainly by forming covalent adducts with nucleophilic functional groups in proteins, nucleic acids, and lipids. The mitochondria have been implicated as a site for 4-HNE generation and adduction. Several studies clarified how 4-HNE affects the mitochondria's functions, including bioenergetics, calcium homeostasis, and mitochondrial dynamics. Our research group has shown that 4-HNE activates mitochondria apoptosis-inducing factor (AIFM2) translocation and facilitates apoptosis in mice and human heart tissue during anti-cancer treatment. Recently, we demonstrated that a deficiency of SOD2 in the conditional-specific cardiac knockout mouse increases ROS, and subsequent production of 4-HNE inside mitochondria leads to the adduction of several mitochondrial respiratory chain complex proteins. Moreover, we highlighted the physiological functions of HNE and discussed their relevance in human pathophysiology and current discoveries concerning 4-HNE effects on mitochondria.
Assuntos
Aldeídos , Estresse Oxidativo , Camundongos , Humanos , Animais , Espécies Reativas de Oxigênio/metabolismo , Peroxidação de Lipídeos/fisiologia , Aldeídos/metabolismo , Mitocôndrias/metabolismoRESUMO
RecQ helicases participate in a variety of DNA metabolic processes through their multiple biochemical activities. In vitro characterization and cellular studies have suggested that RECQ1 (also known as RECQL or RECQL1) performs its diverse functions through specific interactions with DNA and protein partners. We have taken an unbiased approach to determine the contribution of RECQ1 in genome maintenance and as a putative susceptibility factor in breast cancer. Here, we provide methodology to map the genome-wide binding sites of RECQ1 together with the profiling of RECQ1-dependent transcriptome to investigate its role in gene regulation. The described approach will be helpful to develop a mechanistic framework for elucidating critical functions of RECQ1 and other RecQ homologs in distinct chromatin and biological contexts.
Assuntos
Neoplasias da Mama , RecQ Helicases , DNA/química , Feminino , Regulação da Expressão Gênica , Predisposição Genética para Doença , Humanos , RecQ Helicases/genética , RecQ Helicases/metabolismoRESUMO
Background: RECQL (also known as RECQ1 and RECQL1) is a gene of recent interest in breast cancer and an association between high levels of RECQL protein in breast cancer tumour cells and good survival of patients has been reported. Methods: To validate this association, we measured the RECQL protein levels in tumours of 933 breast cancer patients using immunohistochemistry analysis and followed the patients for death from breast cancer. Results: Women with a level of RECQL protein above the 75th percentile had better 15-year disease-specific survival among ER-positive patients (62.5% vs. 48.7%, HR= 0.72, 95%CI= 0.52-0.98, p-value = 0.04), but not among ER- patients (48.9% vs. 48.0%, HR= 1.07, 95%CI= 0.67-1.69, p-value= 0.79). Among the ER-negative patients, high RECQL protein levels were associated with better survival among women who received tamoxifen treatment (67.0% vs. 51.5%, HR= 0.64, 95%CI= 0.41-0.99, p-value= 0.04). Conclusion: RECQL might be a new predictive marker for tamoxifen treatment among ER-positive patients.
RESUMO
Reactive oxygen species (ROS) cause oxidative stress by generating reactive aldehydes known as 4-hydroxynonenal (4-HNE). 4-HNE modifies protein via covalent adduction; however, little is known about the degradation mechanism of 4-HNE-adducted proteins. Autophagy is a dynamic process that maintains cellular homeostasis by removing damaged organelles and proteins. In this study, we determined the role of a superoxide dismutase (SOD) mimetic MnTnBuOE-2-PyP5+ (MnP, BMX-001) on rotenone-induced 4-HNE aggresome degradation in HL-1 cardiomyocytes. A rotenone treatment (500 nM) given for 24 h demonstrated both increased ROS and 4-HNE aggresome accumulation in HL-1 cardiomyocytes. In addition, cardiomyocytes treated with rotenone displayed an increase in the autophagy marker LC3-II, as shown by immunoblotting and immunofluorescence. A pre-treatment with MnP (20 µM) for 24 h attenuated rotenone-induced ROS formation. An MnP pre-treatment showed decreased 4-HNE aggresomes and LC3-II formation. A rotenone-induced increase in autophagosomes was attenuated by a pre-treatment with MnP, as shown by fluorescent-tagged LC3 (tfLC3). Rotenone increased tubulin hyperacetylation through the ROS-mediated pathway, which was attenuated by MnP. The disruption of autophagy caused HL-1 cell death because a 3-methyladenine inhibitor of autophagosomes caused reduced cell death. Yet, rapamycin, an inducer of autophagy, increased cell death. These results indicated that a pre-treatment with MnP decreased rotenone-induced 4-HNE aggresomes by enhancing the degradation process.
Assuntos
Miócitos Cardíacos , Rotenona , Autofagossomos/metabolismo , Autofagia , Miócitos Cardíacos/metabolismo , Espécies Reativas de Oxigênio/metabolismo , Rotenona/metabolismo , Rotenona/toxicidadeRESUMO
Endothelial permeability is a major complication that must be addressed during stroke treatment. Study of the mechanisms underlying blood−brain barrier (BBB) disruption and management of the hypoxic stress-induced permeability of the endothelium following reperfusion are both urgently needed for stroke management. Lysophosphatidic acid (LPA), a bioactive lipid essential for basic cellular functions, causes unfavorable outcomes during stroke progression. LPA-producing enzyme autotaxin (ATX) is regulated in ischemic stroke. We used an electrical cell-substrate impedance sensor (ECIS) to measure endothelial permeability. Mitochondrial bioenergetics were obtained using a Seahorse analyzer. AR-2 probe fluorescence assay was used to measure ATX activity. LPA increased endothelial permeability and reduced junctional protein expression in mouse brain microvascular endothelial cells (MBMEC). LPA receptor inhibitors Ki16425 and AM095 attenuated the LPA-induced changes in the endothelial permeability and junctional proteins. LPA significantly diminished mitochondrial function in MBMEC. ATX was upregulated (p < 0.05) in brain microvascular endothelial cells under hypoxic reperfusion. ATX activity and permeability were attenuated with the use of an ATX inhibitor in a mouse stroke model. The upregulation of ATX with hypoxic reperfusion leads to LPA production in brain endothelial cells favoring permeability. Inhibition of the ATX−LPA−LPAR axis could be therapeutically targeted in stroke to achieve better outcomes.
Assuntos
Permeabilidade Capilar , AVC Isquêmico , Animais , Modelos Animais de Doenças , Células Endoteliais/metabolismo , Lisofosfolipídeos/metabolismo , Camundongos , Diester Fosfórico Hidrolases/metabolismo , ReperfusãoRESUMO
DNA helicase RECQ1 (also known as RECQL or RECQL1) is a candidate breast cancer susceptibility gene significantly correlated with clinical outcomes of sporadic breast cancer patients. Prior studies have suggested that RECQ1 maintains genomic stability by regulating a wide variety of core cellular functions including DNA replication, DNA damage response, and transcription. However, it is unclear which, if any, of these are the primary functions of RECQ1 as related to its role in suppressing breast cancer. We describe here an unbiased integrative genomics approach that enabled us to discover a previously unknown regulatory role of RECQ1 in promoting Estrogen Receptor alpha (ERα) expression and the expression of specific ERα target genes in ER positive breast cancer cells. We discuss potential future applications of similar experimental strategies in advancing the mechanistic understanding and elucidating specific new details of genome-wide functions of RECQ1 and other RecQ helicases in maintaining genomic stability and preventing cancer.
Assuntos
Neoplasias da Mama , RecQ Helicases , Neoplasias da Mama/genética , Receptor alfa de Estrogênio/genética , Feminino , Predisposição Genética para Doença , Instabilidade Genômica , Humanos , RecQ Helicases/genéticaRESUMO
Research is needed to understand why some countries succeed in greater improvements in maternal, late foetal and newborn health (MNH) and reducing mortality than others. Pathways towards these health outcomes operate at many levels, making it difficult to understand which factors contribute most to these health improvements. Conceptual frameworks provide a cognitive means of rendering order to these factors and how they interrelate to positively influence MNH. We developed a conceptual framework by integrating theories and frameworks from different disciplines to encapsulate the range of factors that explain reductions in maternal, late foetal and neonatal mortality and improvements in health. We developed our framework iteratively, combining our interdisciplinary research team's knowledge, experience and review of the literature. We present a framework that includes health policy and system levers (or intentional actions that policy-makers can implement) to improve MNH; service delivery and coverage of interventions across the continuum of care; and epidemiological and behavioural risk factors. The framework also considers the role of context in influencing for whom and where health and non-health efforts have the most impact, to recognize 'the causes of the causes' at play at the individual/household, community, national and transnational levels. Our framework holistically reflects the range of interrelated factors influencing improved MNH and survival. The framework lends itself to studying how different factors work together to influence these outcomes using an array of methods. Such research should inform future efforts to improve MNH and survival in different contexts. By re-orienting research in this way, we hope to equip policy-makers and practitioners alike with the insight necessary to make the world a safer and fairer place for mothers and their babies.
Assuntos
Saúde do Lactente , Mortalidade Infantil , Feminino , Humanos , Recém-Nascido , Saúde MaternaRESUMO
OBJECTIVES: Peritoneal fluid cytology is done routinely in cases with serous carcinoma of ovary. However, morphologic features of borderline serous tumors (BSTs) of ovary in ascitic fluid have been rarely described. The aim of our study was to evaluate the morphologic features of BST with and without ascitic fluid involvement (BST+ and BST-, respectively) and compare with those of serous carcinomas, both in conventional and liquid-based cytology (LBC) smears. MATERIAL AND METHODS: Out of 30 BST cases reported in 3 years, seven cases had BST+. We compared the cytomorphology of seven cases of BST+, seven cases of BST-, and seven cases of serous adenocarcinoma with positive ascitic fluid cytology. Both conventional and LBC smears were studied in all cases and compared. Histopathology of omentum in these cases was also studied. RESULTS: Most cases with BST+ had regular papillary fragment borders with nuclei showing mild-to-moderate pleomorphism, fine nuclear chromatin with small nucleoli as compared with serous carcinomas all of which had irregular borders with moderate-to-severe nuclear pleomorphism, coarse chromatin, and macronucleoli. CONCLUSION: A combination of cytoarchitectural and nuclear features can help in suspecting BST in ascitic fluid. Ascitic fluid cytology together with tissue histology can increase the rate of the detection of peritoneal implants.