Die histologische Diagnostik stellt in der Hämatologie und Onkologie die Voraussetzung einer differenzierten Therapie dar. Minimal-invasive Eingriffe mittels sonographisch-gesteuerter Punktion zur Gewinnung von zytologischen oder histologischen Material bedeutet sowohl einen zeitlichen Gewinn, als auch eine Herabsetzung des Risikos eines operativen Eingriffs. Mit dem gewonnenen Gewebe werden auch immunhistologische Untersuchungen möglich, die z.B. bei Non-Hodgkin Lymphomen notwendig sind. Zur intensiven Polychemotherapie bei malignen Erkrankungen werden oft zentral-venöse Katheter bzw. Port-Anlagen in große Venen eingeführt. Die Komplikationen und deren Management werden aufgezeigt und diskutiert. Eine sonographisch-gesteuerte Venenpunktionstechnik stellt eine Methode dar, die für die Patienten einen risikoarmen und schnelleren Weg bedeuten und als neu-entwickelte Ein-Personen-Technik auch für den Arzt ein innovatives Vorgehen bei einem potentiell komplikationsträchtigen Eingriff mit größerer Sicherheit durchzuführen. / In hematology and oncology histological diagnosis is an important requirement before differential chemotherapy. Sonographically guided puncture techniques achieving cytological and histological material is a time-saving process with moderate risks for the patients. With this material even immunhistological procedures in malignancies like Non-Hodgkin lymphoma are possible. For intensified chemotherapies in malignant diseases central venous catheter such as port catheters are requiriered. In this thesis complications and their management are shown and discussed. The ultrasounically guided central venous puncture represents a method for fast and low risk procedure for our patients. The one-operator technique represents an innovative and save intervention in a potentially risky procedure for physicians.

Made available in DSpace on 2016-08-10T10:31:04Z (GMT). No. of bitstreams: 1 Alan Soares Machado.pdf: 1017464 bytes, checksum: 18630b283438c7833dbed8bca4d63f3e (MD5) Previous issue date: 2009-02-27 / Fish biomass is one of the success factors during fish transport and pond stocking. This study aimed to evaluate the effect of tilápia stocing density on the time to homeostasis recovery of tilapia after transport. For that, 490 tilapia juvenile around 51,42±8,28g were placed in adapted transport box and transported during five hours. At the end of this period, fish were placed in 500L 18 PVC boxes, filled whit water and maintained whit a volume of 100L, and a mean water flow of 0.05L/s. The tilapia juvenile were randomly distributed in boxes in an entirely random factorial outline of 2 x 3, with two biomasses 10.3 and 15.4 g/L and, three samplings in time, 24, 68 and 168 hours after transport, with three repetitions each. Water physical and chemical parameters were analyzed before and after transport, in the water used from the reservoir, and in the PVC boxes, during the study. Fish blood was collected by puncture from the caudal vasculature, for the determination of the following variables: glucose, hemoglobin, hematocrit, total number of erythrocytes, mean corpuscular volume, cortisol and ions, Na and K. The blood was centrifuged, and the serum stored -20°C until the analyses. The obtained data were submitted to an analysis of variance whit P>0.01 and the averages compared with the Tukey test at 5%. It was concluded that glucose was the best parameter the diagnosis of the occurrence of physiological stress in juvenile tilapia, contrary to expectations. The largest biomass of stand after transport reduced the glycemic content of tilapia, contrary to expectation. There was interaction between biomass and time of storage after transport to the variables blood glucose and hematocrit. This indicates the importance of the period and the condition of proper fish conditioning after transporting on the returning to homeostasis, a procedure that could be used for increased safety in handling subsequent transport in fish farms. You can suggest new research biomass testing at intervals greater than assessed. / A biomassa é um dos fatores para o sucesso no povoamento de viveiros após o transporte de peixes. O presente estudo teve como objetivo avaliar a biomassa de estocagem e seu efeito sobre o tempo de retorno de juvenis de tilápia à homeostase após o transporte. Para tal, 490 juvenis de tilápia de 51,42±8,28g foram colocados em caixa de transporte apropriada e, realizado o transporte por cinco horas. Ao final deste manejo os peixes foram acondicionados em 18 caixas de PVC de 500L, preenchidas com água e mantidas com volume de 100L, e com vazão média de 0,05L/s. Os juvenis de tilápia foram distribuídos aleatoriamente nas caixas compondo delineamento inteiramente casualizado em esquema fatorial 2 x 3, sendo duas biomassas 10,3 e 15,4 g/L e, três amostragens no tempo, 24, 68 e 168 horas após transporte, com três repetições. Os parâmetros físicos e químicos da água foram analisados na caixa de transporte antes e após o transporte, na água do reservatório de abastecimento, e nas caixas de PVC, durante todo o estudo. O sangue foi coletado por punção do vaso caudal, para determinação das seguintes variáveis fisiológicas: glicemia, hemoglobina, hematócrito, número total de eritrócitos, volume corpuscular médio, cortisol e íons, Na e K. O sangue foi centrifugado, e o soro armazenado a -20º C até a realização das análises. Os dados obtidos foram submetidos à análise de variância com 0,01 < P &#8804; 0,05, e as médias comparadas pelo teste de Tukey a 5%. Concluiu-se que a glicemia foi o parâmetro de melhor diagnóstico da ocorrência de estresse fisiológico em juvenis de tilápia. A maior biomassa de povoamento após o transporte reduziu o teor glicêmico da tilápia, contrariando a expectativa. Houve interação entre biomassas e tempo de estocagem após transporte para as variáveis glicemia e hematócrito. Isto indica a importância do período e da condição de condicionamento adequado dos peixes após transporte para o retorno a homeostase, procedimento que poderia ser adotado para maior segurança em manejo subsequente ao transporte nas pisciculturas. Pode-se sugerir ainda novas pesquisas testando biomassas em intervalos superiores aos avaliados.

O pacu, Piaractus mesopotamicus Holmberg, 1887 (Characiformes, Characidae), é uma das principais espécies da fauna aquática brasileira, com grande potencial para aqüicultura interior. Estudos sobre nutrição e determinação de exigências nutricionais são ferramentas para embasar a formulação de dietas completas e consolidar a piscicultura intensiva e viável da espécie. A suplementação dietética com vitamina C tem importância na eficiência alimentar, sanidade dos estoques e na economicidade das dietas e da criação. O objetivo deste projeto foi determinar as exigências nutricionais em vitamina C de alevinos de pacu. Os peixes (9,06 ± 1,40 g) foram alimentados com dietas contendo diferentes teores de vitamina C, ad libitum, duas vezes ao dia, durante 63 dias, e avaliados quanto ao desempenho, medido pelo ganho de peso (GDP), consumo de ração, conversão alimentar (CA), taxa de crescimento específico (TCE) e sanidade, considerando-se a incidência de sinais de deficiência em vitamina C e alterações hematológicas - contagem de eritrócitos (GV), hematócrito (HCT), hemoglobina (Hb), volume corpuscular médio (VCM) e leucócitos totais (GB). As rações semipurificadas foram suplementadas com dez níveis de inclusão: 0 (controle), 50, 100, 150, 200, 250, 300, 500, 700 e 900 mg de vitamina C (monofosfato de ácido ascórbico) kg -1 , em delineamento inteiramente ao acaso, com quatro repetições por tratamento. O efeito dos níveis de vitamina C sobre as variáveis foi analisado por regressão polinomial linear e regressão não-linear segmentada, para a determinação de valores ótimos de suplementação. A análise das variáveis de desempenho não detectou diferença entre os tratamentos (P>0,05). As regressões para peso final (PF) e GDP indicaram tendência linear positiva com maiores doses de vitamina C e o nível ótimo estimado para PF foi de 423,1 mg de vitamina C kg -1 . O ganho de peso relativo médio dos tratamentos foi de 460,8%. Houve efeito linear negativo das doses de vitamina C sobre as médias de CA (P=0,038) e foi determinado o valor de 635,7 mg kg -1 de dieta no ponto de quebra (P=0,068). O valor médio de CA para os tratamentos foi de 0,95. As médias de TCE não diferiram (P>0,05) e o valor médio encontrado foi de 2,72% dia -1 . As médias das variáveis hematológicas não diferiram (P>0,05). A GV teve efeito linear negativo na regressão com o aumento da vitamina C na dieta (P<0,05). Foi encontrado efeito quadrático (P=0,024) para o HCT na regressão linear e o valor ótimo determinado pela regressão não-linear segmentada foi de 254,0 mg kg -1 . Existiu fraca evidência linear positiva para os dados de VCM na análise de regressão não-linear segmentada (P=0,090), com valor estimado de 109,7 mg de vitamina C kg -1 de dieta no ponto de quebra. Houve fraca evidência linear negativa na regressão para as médias de Hb (P=0,103) e as médias de contagem de leucócitos totais (GB) não diferiram (P>0,05). Os exames radiológicos não detectaram deformidades estruturais nos peixes analisados. O nível de 254,0 mg de vitamina C kg -1 de dieta foi suficiente para garantir a sanidade e desempenho adequados para o pacu. / The pacu Piaractus mesopotamicus Holmberg, 1887 (Characiformes, Characidae), is one of the main species of the Brazilian aquatic fauna with great potential for inland aquaculture. Studies on nutritional requirements of the species are important tools to establish the basis for the formulation of complete diets and consolidate the intensive and viable farming of the species. Dietary vitamin C supplementation plays an important role in feed efficiency, sanity of the stocks and economical viability of fish diets. The objective of this study was to determine nutritional requirements of vitamin C of fingerling pacu (9.06 ± 1.40 g), fed diets containing different levels of vitamin C, ad libitum, twice a day for 63 days, through the performance indexes weight gain (WG), feed consumption, feed conversion rate (FCR), specific growth rate (SGR); sanity through incidence of vitamin C deficiency signals, and hematological analyses - red blood cells counting (RBC), hematocrit (HCT), hemoglobin (Hb), mean corpuscular volume (MCV), and total white blood cells counting (WBC). Semi-purified diets were supplemented with 0 (control), 50, 100, 150, 200, 250, 300, 500, 700, and 900 mg of vitamin C (ascorbic acid monophosphate) kg -1 , and fed to fish in a totally randomized design with four replicates. Effects of dietary levels of vitamin C on performance parameters were analyzed by linear polynomial regression and non-linear segmented regression. No differences were detected among treatments (P>0.05). Regression analysis for final weight (FW) and WG indicated positive, linear tendency with larger vitamin C doses, the best level for FW being 423.1 mg of vitamin C kg -1 diet. The average relative weight gain of fish was 460.8%. There was linear, negative effect of vitamin C doses on the averages FCR (P=0.038), reaching the break point at 635.7 mg vitamin C kg -1 diet (P=0.068), and average FCR=0.95 for all treatments. The average SGR (2.72% day -1 ) did not differ among treatments (P>0.05). Averages of hematological variables did not differ (P>0.05). RBC had negative linear effect with increasing dietary vitamin C (P <0.05). A quadratic effect was determined for HCT (P=0.024); the break point of the non-linear segmented regression was 254.0 mg vitamin C kg -1 diet. There was a low, positive linear evidence for MCV (P=0.090), the break point standing at 109.7 mg of vitamin C kg -1 of diet. There was low, negative linear evidence for average Hb (P=0.103), and the averages for WBC did not differ (P>0.05) among treatments. Radiological exams did not detect structural deformities in the analyzed fish. The level of 254.0 mg vitamin C kg -1 diet was enough to allow sanity and appropriate performance of fingerling pacu.

As células sangüíneas originam-se da medula óssea através da célula tronco que sofre processo de proliferação, diferenciação e maturação no microambiente hematopoiético. O microambiente hematopoiético é uma estrutura altamente organizada composta de células estromais, moléculas da matriz extracelular (MEC) e citocinas. A desnutrição protéico-energética diminui a produção de células sangüíneas e interfere na defesa do organismo. Neste trabalho estudamos os efeitos da desnutrição protéica (dieta contendo 4% de caseína) sobre a MEC da medula óssea em camundongos. Avaliamos a composição da MEC através de SDS-PAGE 7,5% e Western blot para Fibronectina (FN), laminina (LN) e trombospondina (TSP). Verificamos a capacidade da MEC aderir e sustentar proliferação da célula mielóide FDC-P1, na ausência e na presença de citocinas (GM-CSF e IL3). Avaliamos também a capacidade de ligação destas citocinas na MEC. O perfil eletroforético mostrou diferenças nas proteínas da MEC do animal desnutrido em relação ao controle. Através da densitometria dos géis observamos nas amostras obtidas do animal desnutrido, maior intensidade nas bandas de peso molecular 220, 182, 108 e 56 KDa em relação ao controle. Em 72 KDa a banda foi mais intensa nas amostras dos animais controles. A banda de 60 KDa foi evidenciada apenas nas amostras obtidas dos animais desnutridos. As bandas de 123 e 49 KDa foram evidenciadas apenas nas amostras dos animais controles. A expressão de FN, LN e TSP foi maior nas amostras obtidas dos animais desnutridos. Os ensaios de adesão e proliferação na presença e ausência de citocinas não apresentaram diferenças significativas entre as amostras. Quando avaliamos a capacidade da MEC ligar-se ao GM-CSF, houve maior interação com a MEC proveniente do animal desnutrido do que a MEC do animal controle. O teste de ligação para o IL3 não mostrou diferenças entre as amostras. Esses achados sugerem que a desnutrição protéica induz modificações na MEC, alterando o microambiente hematopoiético. / Blood cells have their origin at the bone marrow through the stem cell which undergoes a proliferation, differentiation and maturation process in the hematopoietic microenvironment. The hematopoietic environment is a highly organized structure formed by stromal cells, extracellular matrix (ECM) molecules, and cytokines. Protein-energy malnutrition reduces the production of blood cells, interfering with the defense of the organism. In the present work we have studied the effects protein malnutrition has on the ECM of bone marrow in mice. We have evaluated ECM composition by means of SDS PAGE 7,5% and Western blot for fibronectin (FN), laminin (LN) and thrombospondin (TSP). We assessed the capacity ECM has in adhesion and support of proliferation of the FDC-P1 myeloid cell both in the absence and in the presence of GM-CSF and IL3 cytokines. We have also measured the binding capacity of these cytokines in the ECM. The electrophoresis profile showed the existence of differences between the ECM proteins in the undernourished animal and the control. Using gel densitometry, we observed in samples from the undernourished animal a greater intensity of bands of 220, 182, 108, 60 and 56 KDa molecular weight as compared to control. At 72 KDa the band was more intense on samples from control animals. The 60 KDa band was evident only on samples taken from undernourished animals. The 123 and 49 KDa bands were evident on control animals only. Expression of FN, LN, and TSP was greater on samples from undernourished animals. Adhesion and proliferation assays, both in the presence and in the absence of cytokines, did not show significant differences among samples. When we evaluated the capacity ECM has to bind to GM-CSF, a greater interaction was seen with the ECM from the undernourished animal than the ECM from the control. Binding test for IL3 showed no differences existed among samples. Such findings suggest protein malnutrition causes alterations of the ECM, modifying the hematopoietic microenvironment.

Les plaquettes sanguines sont des cellules qui ont un rôle majeur au cours des processus de l'hémostase primaire et jouent un rôle primordial dans l'immunité innée mais aussi adaptative. Ces cellules anucléées ont une capacité sécrétoire très importante de facteurs solubles notamment de cytokines, de chimiokines (CK/CH) et de facteurs immunomodulateurs. L'émergence du rôle inflammatoire des plaquettes sanguines dans la communauté scientifique a soulevé de nombreuses questions auxquelles nous essayons de répondre dans ce manuscrit. La majorité de ces questions repose sur la capacité de ces cellules anucléées à répondre de manière régulée à des stimuli complexes. Nos investigations pour répondre à ces questions ont été réalisées dans un contexte transfusion sanguine. Au cours de nos travaux, nous avons mis en évidence la corrélation des profils de sécrétion plaquettaire avec les récepteurs membranaires et les voies de signalisations intraplaquettaires engagées. Les plaquettes expriment plusieurs récepteurs immunitaires sur leur surface notamment les " Pattern recognition receptors " (PRR) et des récepteurs aux CK/CH. Nous avons démontré et caractérisé la fonction d'un nouveau récepteur plaquettaire, le Siglec-7. Ce récepteur est localisé dans les granules a ; son expression sur la membrane est corrélée avec l'état d'activation plaquettaire. Le Siglec-7 a une avidité élevée avec les molécules composées d'α2,8-disialyl (NeuAcα2,8NeuAcα2,3Gal) et de α2,6-sialyl (Gal-b1,3[NeuAcα2,6]HexNAc) (comme les gangliosides GD2, GD3 et GT1b). L'engagement de ce récepteur peut induire l'apoptose plaquettaire par la voie intrinsèque et extramitochondriale. Ce processus nécessite l'engagement du récepteur GPIIbIIIa et P2Y1 et la signalisation de la voie de PI3k. Nous avons également étudié et mis en évidence une composante inflammatoire multifactorielle dans les effets indésirables des receveurs (EIR) et trouvé dans les concentrés plaquettaires (CP), plusieurs facteurs solubles ayant une valeur prédictive élevée pour la survenue des EIR, notamment le sCD40L et l'IL-13. Nous avons confirmé que la concentration de ces facteurs augmente au cours de temps de stockage des CP, étant, en partie, responsable du taux élevé de l'EIR des CP âgés. Enfin, en plus de la conservation, les processus de préparation des CP peuvent aussi avoir des impacts sur les propriétés inflammatoires des plaquettes. Ces travaux montrent que la réponse inflammatoire plaquettaire est régulée en fonction du stimulus, permettant d'argumenter sur le rôle présumé de sentinelle des plaquettes sanguines humaines. Ainsi, mes travaux s'inscrivent dans la ré-exploration de la fonction inflammatoire des plaquettes sanguines et l'étude du rôle des plaquettes comme cellules de l'immunité à composante inflammatoire

The Chronic Myeloid Leukemia (CML) is a clonal hematopoietic stem cell disorder characterized by the t(9:22) genetic translocation and expression of the oncogenic tyrosine kinase BCR-ABL . A first BCR-ABL Tyrosine Kinase Inhibitor (TKI), Imatinib (IM), was identified that inhibits proliferation of BCR-ABL expressing hematopoietic cells and leads to disease remission. However, BCR-ABL mRNA remains detectable in the most immature HSCs and discontinuation of IM results in clinical relapse. STAT5 factors play a crucial role in the CML pathogenesis of human primary CML cells. However, the contribution of the two related STAT5 genes, STAT5A and STAT5B, was unknown. We used an RNAinterference based strategy to analyze STAT5A or STAT5B roles in normal and CML cells. We showed that STAT5A/5B double knock-down (KD) triggers normal and CML cell apoptosis and suppressed long-term clonogenic potential of immature hematopoietic stem and progenitor cells known to be resistant to TKI treatment and responsible for residual disease. STAT5A loss alone was ineffective at impairing growth of both normal and CML cells under standard conditions. In contrast, STAT5A loss was sufficient to enhance Reactive Oxygen Species (ROS) which correlated with enhanced DNA damages in both normal and leukemic cells. We reported that STAT5A regulates oxidative stress through unconventional mechanisms, in a non-transcriptional-dependent manner. We further showed that, in contrast to primary cells at diagnosis, IM-resistant cells exhibited enhanced STAT5A dependence, by being sensitive to STAT5A single KD. To investigate the molecular basis of STAT5A activity in TKI-resistance and oxidative stress, we performed a transcriptomic analysis of STAT5 regulated genes. We identified Axl, which encodes a receptor tyrosine kinase, recently shown to be crucial in TKI-resistant CML cells. Specifically, Axl expression is enhanced by STAT5A. We investigated the role of Axl and we found that Axl KD did not affect survival of IM-sensitive CML cells. However, Axl KD decreased survival of IM-resistant cells, miming the activity of STAT5A. Moreover, Axl loss increased ROS levels in CML cells, promoting STAT5A anti-oxidant activity. We further sought to determine the expression of the Axl ligand, Gas6. Gas6 expression is dramatically reduced in CML primary cells at diagnosis compared to healthy cells. The strong and consistent down-regulation of Gas6 in CML cells suggested a possible role in the pathophysiology. Collectively, our findings highlight the pro-survival, stress protection and drug resistance roles of STAT5 factors, providing new understanding for medical treatment of CML patients. We suggest that STAT5A acts in synergy with Axl to face exogenous insults and propose a new mechanism by which CML cells increase their proliferation and reduce their motility by down-regulating Gas6 expression.

Les réactions de type hypersensibilité parfois observées au début de séances d'hémodialyse ont été corrélées à la présence, dans les bains de dialyse, d'endotoxines ou lipopolysacharides (LPS) provenant de bactéries de type gram négatif. Nous nous sommes tout d'abord attachés au développement d'un système de production de bains de dialyse stériles et apyrogènes qui soit intégrable au matériel existant. Notre étude nous a permis de rejeter les dispositifs d'ultrafiltration utilisant des membranes organiques planes ou des membranes minérales tubulaires. Nous avons proposé l'emploi d'un hémofiltre à fibres creuses en polyamide qui s'avère un bon compromis puisque, dans des conditions de contamination normales, le bain produit est stérile et apyrogène et la faible perte de charge générée par le filtre permet son intégration aux générateurs de bains existants. Nous avons également déterminé plus précisément la masse moléculaire des LPS par électrophorèse et par filtrations successives sur des membranes de seuils de coupure décroissants. Nous avons ainsi pu mettre en évidence les LPS après filtration sur des membranes de 5 kDa pour les LPS de type R. Dans une dernière étape, nous avons cherché à modifier la membrane de dialyse pour augmenter sa rejection des LPS. Un revêtement de la face dialysat de la membrane par un polymère organique polycationique nous a permis d'obtenir des absorptions notables de LPS. La conjonction des deux méthodes que nous avons proposées, ultrafiltration des bains de transfert des LPS vers le compartiment sanguin. Des essais cliniques nous permettront de valider ce procédé.

Uncovering the chromosomal abnormalities associated with human malignancy can provide significant insights into the molecular basis of tumorigenesis, as well as identifying potential targets for therapy. The present study set out to examine the genetic characteristics of t(2;7)(p11-12;q21-22) translocations arising in conjunction with chronic B-cell neoplasia. Using long-range PCR, a t(2;7) was initially mapped in an individual presenting with the preclinical entity CD5- monoclonal B-cell lymphocytosis. This revealed a breakpoint at 2p11.2 localized to the recombination signal of the immunoglobulin kappa (IGK) variable gene IGKV3-15, and a breakpoint at 7q21.2 located 520 bp upstream of cyclin dependent kinase 6 (CDK6). The same approach was subsequently employed to elucidate near-identical t(2;7) breakpoints in 4 additional cases presenting with chronic lymphocytic leukemia or indolent non-Hodgkin lymphomas. The remarkable consistency of these translocations implicates the dysregulation of CDK6 via translocation to IGK as a recurrent pathomechanism during the emergence of B-cell lymphoproliferative disorders.

Uncovering the chromosomal abnormalities associated with human malignancy can provide significant insights into the molecular basis of tumorigenesis, as well as identifying potential targets for therapy. The present study set out to examine the genetic characteristics of t(2;7)(p11-12;q21-22) translocations arising in conjunction with chronic B-cell neoplasia. Using long-range PCR, a t(2;7) was initially mapped in an individual presenting with the preclinical entity CD5- monoclonal B-cell lymphocytosis. This revealed a breakpoint at 2p11.2 localized to the recombination signal of the immunoglobulin kappa (IGK) variable gene IGKV3-15, and a breakpoint at 7q21.2 located 520 bp upstream of cyclin dependent kinase 6 (CDK6). The same approach was subsequently employed to elucidate near-identical t(2;7) breakpoints in 4 additional cases presenting with chronic lymphocytic leukemia or indolent non-Hodgkin lymphomas. The remarkable consistency of these translocations implicates the dysregulation of CDK6 via translocation to IGK as a recurrent pathomechanism during the emergence of B-cell lymphoproliferative disorders.

[Truncated abstract] Fetal inflammatory response syndrome (FIRS) has only recently been recognised as an important cause of spontaneous preterm delivery (PTD). In addition, it has been associated with a number of other short-term and long-term adverse neonatal outcomes, including early onset neonatal sepsis, necrotising enterocolitis, periventricular leucomalacia, cerebral palsy, and bronchopulmonary dysplasia, although the causal mechanisms are unclear. The hallmark of FIRS is histologic chorioamnionitis (HCA). Mothers with HCA are often asymptomatic and it remains unclear whether elevated maternal inflammatory markers, such as C-reactive protein (CRP) and procalcitonin (PCT), are predictive of preterm birth. Furthermore neonatal inflammatory markers such as CRP, PCT, white cell count (WCC) and absolute neutrophil count (ANC), are commonly used in clinical practice to diagnose infection in the neonatal period. Although both intrauterine inflammation and FIRS may have effects on inflammatory markers for up to 10 days following delivery, the extent to which intrauterine infection and FIRS confound these diagnostic surrogates of neonatal infection is unknown. This work addressed the hypothesis that HCA is associated with inflammatory changes that may be detected in the: (a) maternal circulation at the time of delivery, (b) umbilical cord blood at delivery and (c) post-natal circulation within the first 48 hours of life. The primary aim of this study was to investigate the relationship between the presence of HCA and maternal inflammatory markers (serum CRP and PCT on the day of delivery) as well as neonatal inflammatory markers (haematological parameters, CRP and PCT up to 48 hours following delivery). ... Cord platelet counts were likely affected by platelet activation. For both intra-rater and inter-rater reproducibility, the corrected WCC, ANC and NRBC were shown to be reliable with an ICC of >0.90 for all comparisons. However, I:T ratio was poorly reproducible. HCA appears to be a minor inflammatory insult for the mother. In the majority of cases it is asymptomatic and results in minor increases in PCT and CRP levels on the day of delivery. Conversely HCA results in significant inflammatory changes in the newborn that can be seen in the cord blood. Sensitive markers of inflammation in the cord blood are significantly higher in affected infants (CRP and PCT), while less sensitive markers, such as WCC and ANC are not significantly different. This study has shown that fetal inflammation has sustained effects on CRP and haematological parameters in early neonatal life; CRP, WCC and ANC are significantly higher in newborns exposed to HCA, peaking 24 hours following delivery. These effects may confound the interpretation of common diagnostic tests for early onset neonatal sepsis. Conclusion: HCA results in mild elevations in CRP and PCT in the cord blood. Over the subsequent 24 hours CRP, WCC and ANC increase significantly in these neonates. Intrauterine exposure to HCA may influence surrogate diagnostic markers for early onset sepsis in newborn infants. Future research to investigate novel diagnostic markers, such as CD64 and soluble triggering receptor expressed on myeloid cells (TREM-1), or enhanced microbiological molecular diagnosis, will help distinguish true invasive infection from HCA-driven inflammation in the newborn infant.