This abstract describes both parts of a two part thesis. Part 1 Potential acceptor substrate analogue inhibitors of beta-1,4-galactosyltransferase were proposed and the following compounds were thus synthesised to assist in understanding the mechanism of this enzyme. Octyl 2-acetamido-3,6-di-O- benzoyl-2-deoxy-beta-D-glucopyranoside (13) was synthesised and the 4-hydroxyl group was oxidised to give the corresponding ketone, octyl 2-acetamido-3,6-di-O-benzoyl-2-deoxy-beta-D-xylo-hexopyranosid-4-ulose (15). The ketone (15) was reacted with methoxylamine hydrochloride to give the O-methyloxime, octyl 2-acetamido-3,6-di-O-benzoyl-2,4-dideoxy-4-methoxyimino-beta-D-xylo- hexopyranosid-4-ulose (16), which was reduced to give both the gluco- and galacto-configured O-methylhydroxylamines, octyl 2-acetamido-3,6-di-O- benzoyl-2,4-dideoxy-4-methoxyimino-beta-D-glucopyranoside (17) and octyl 2- acetamido-3,6-di-O-benzoyl-2,4-dideoxy-4-methoxyamino-beta-D- galactopyranoside (18). Both methoxyamino compounds are, however, unstable and hence studies towards the target compounds via an amine at the 4-position were pursued. Octyl 2-acetamido-4-O-acetyl-3,6-di-O-benzyl-2-deoxy-beta-D- galactopyranoside (23) was prepared by displacement of the mesyl group of octyl 2-acetamido-3,6-di-O-benzyl-2-deoxy-4-O-methanesulfonyl-beta-D- glucopyranoside (22) with cesium acetate. Octyl 2-acetamido-3,6-di-O-benzyl-2- deoxy-4-O-methanesulfonyl-beta-D-galactopyranoside (25) was prepared from this and the mesyl group was displaced with sodium azide to give octyl 2-acetamido- 4-azido-3,6-di-O-benzyl-2,4-dideoxy-beta-D-glucopyranoside (26). Octyl 2- acetamido-3,6-di-O-benzoyl-2-deoxy-beta-D-glucopyranoside (13) was reacted with methanesulfonyl chloride to give octyl 2-acetamido-3,6-di-O-benzoyl-2-deoxy-4-O-methanesulfonyl-beta-D-glucopyranoside (28). The mesyl group was displaced with sodium azide to give the galacto-configured azide, octyl 2-acetamido-4- azido-3,6-di-O-benzoyl-2,4-dideoxy-beta-D-galactopyranoside (29). After reduction of the azide functionalities to the corresponding amines access to various amine derivatives will be possible. Part 2 To enable a better understanding of thioglycoside activation by iodine, the following beta-glycosides of 2,3,4,6-tetra-O-benzyl-D-galactopyranoside were synthesised: thiomethyl (39), thiobenzyl (48), thiophenyl (36), p-methoxythiophenyl (44), p-nitrothiophenyl (47) and p-acetamidothiophenyl (51). All of these compounds were treated with iodine in the presence of methanol and rates of reaction were compared. Reactivity was found to depend on the nature of the leaving group. Further studies showed that DDQ in combination with iodine gave rise to substantially enhanced rates of reaction. Similar experiments showed that the nature of the solvent also affected the rate of reaction with reaction in acetonitrile substantially faster than in dichloromethane. Further studies, replacing iodine with either IBr or ICl demonstrated that both of these reagents could activate thioglycosides more rapidly than iodine. All compounds tested can be activated in approximately 1 minute depending on the activator(s) and solvent used. The anomeric ratios of all reactions favoured formation of the methyl a-glycoside. The mechanism of these reactions was studied by analysing the reaction of methyl 2,3,4,6-tetra-O-benzyl-l-thio-beta-D-galactopyranoside (39) with iodine in the absence of methanol. This demonstrated that the thiomethyl glycoside anomerised rapidly; real time N.M.R. studies revealed that the course of the reaction could be followed by N.M.R. An analogous study in the presence of methanol demonstrated that anomerisation also takes place simultaneously with the formation of O-methyl glycosides and can similarly be followed by N.M.R. Activation and glycosylation of thioglycosides with iodine vapour was demonstrated on the surface of silica t.l.c. plates. It may therefore be possible to optimise reaction conditions on t.l.c. plates prior to use of significant quantities of reagents.

The aim of the research reported in this thesis is to establish the characteristics of paraglacial modification of drift-mantled hillslopes in glaciated upland valleys in Norway and Scotland. Debris flow represents the principal agent of paraglacial sediment reworking, though snow avalanches and slopewash are locally important. Paraglacial hillslope modification is most widespread in areas of thick drift where initial slopes exceed c. 30°, void ratio exceeds c. 0.35, and water input is focused both spatially and temporally. Paraglacially-reworked sediments preserve most of the characteristics of the parent tills, but differ in terms of preferred clast orientation and structural and lithofacies characteristics. Stratigraphic relations between tills and reworked sediments imply cyclic alternation of glacial and paraglacial sediment transport. Paraglacial slope adjustment follows a sequence involving (1) rapid gully incision; (2) widening of gullies, and accumulation of debris cones at the slope foot; (3) reduction and destruction of inter-gully divides, and formation of a slope-foot apron of coalescing cones; (4) extensive exposure of bedrock at the crest of the slope, resulting in sediment exhaustion and progressive stabilisation. Slope profiles tend to converge on a maximum gradient of c. 28° and a concavity index of c. 0.22. At the most active sites, 2-4 m of gully lowering has occurred within decades of deglaciation, implying minimum erosion rates averaging c. 90 mm yr ⁻¹. In Scotland delayed or renewed reworking of drift-mantled slopes has occurred several millennia after deglaciation. Radiocarbon dating of buried palaeosols indicates intermittent drift reworking by debris flows throughout the past 6.5 ka, with some evidence for accelerated activity at c. 2.7-1.7 cal ka BP and after c. 0.7 cal ka BP. Three-dimensional conceptual models are developed to describe the sequence of both immediate and delayed or renewed paraglacial hillslope modification, and the landforms and sediment associations characteristic (and diagnostic) of paraglaciallandsystems in passive continental margins.

The efficiency of a number of experimental techniques for the extraction of total RNA from various cells and tissues (including MDCK strain I cells) was assessed, and the optimal conditions for hybridisation of Na,K-ATPase isoform-specific DNA probes to this RNA were determined. The specificity of hybridisation of DNA probes for the Na,K-ATPase al, a2, a3, and beta1 isoforms was assessed using RNA isolated from rat tissues. The relative abundance of isoform mRNA's in rat kidney, brain, lung, and myocardial tissues was determined by Northern blotting. The abundance of Na,K-ATPase isoforms was also determined in the myocardial tissues of the Milan rat, a hypertensive animal model. Significant differences between the abundance of Na,K-ATPase isoform mRNA's in hypertensive rats and their age and sex matched controls were found. The relative abundance (per ng of total RNA) of al, a3, and beta1 mRNA's in left ventricle and, that of a1, and beta1 mRNA's in right ventricle were significantly decreased in hypertensive rats. The relative abundance (per mug of total RNA) of a2 and beta1 mRNA's in atria was significantly increased in hypertensive rats. These differences found in ventricles and atria were further accentuated by expression of the results per gram wet weight of tissue. The results from ventricular tissues were in contrast to those previously reported by Herrera et al. (1988) who found either increases or no change in the abundance of a1 and beta1 mRNA's in hypertensive rat aorta, skeletal muscle and left ventricle. The differences between these results may be related to the deoxy-corticosterone treatment and high salt diet of the hypertensive rat model used by Herrera et al. (1988). Na,K-ATPase isoform-specific DNA restriction endonuclease fragments were used to investigate the expression of the isoform mRNA's in MDCK strain I cells. Only a1 and beta1 mRNA's was detected on Northern blots, with no detectable a2 or a3 isoform mRNA signals being found in this cell line. [3H]-ouabain binding to cells was used, as an estimate of the cell surface expression of Na,K-ATPase. Possible factors affecting the expression of Na,K-ATPase during the normal cell growth of MDCK strain I cells were investigated. Factors such as cell seeding density, cell growth substrate and the volume of growth medium used, were all found to affect both the level and pattern of expression of Na,K-ATPase during the normal cell growth or culturing cycle. After 2 days of culture the large increases in the expression of Na,K-ATPase assayed in low density compared to high density seeded cells, were not correlated with concomitant changes in the relative abundance of Na,K-ATPase a subunit mRNA. These results indicate that the large changes in cell surface expression of Na,K- ATPase found during cell growth are probably controlled by post transcriptional processes. The effect of certain hormones or their agonists (aldosterone, deoxy-corticosterone, corticosterone, dexamethasone, and tri-iodo thyronine), on the expression of Na,K-ATPase in MDCK strain I cells was also briefly investigated. Under the conditions used, hormone treatment was not found to induce any measurable expression of a2 or a3 mRNA's. The mineralocorticoid aldosterone, and the glucocorticoid corticosterone, both produced small but significant increases in the level of Na,K-ATPase present on the cell membrane, however these increases were not correlated with similar increases in the abundance of both Na,K-ATPase a1 and beta1 mRNA's. The small size of increases in Na,K-ATPase enzyme abundance after hormone treatments and the inability of those treatments to induce consistent increases in Na,K-ATPase mRNA's further suggests that changes in the cell surface expression of Na,K-ATPase in MDCK cells is the result of regulation at a post transcriptional level.

Using ESR dimer-radical equilibrium techniques the heat of formation, △Hf0, of the pentamethylcyclopentadienyl radical was determined as 7.4 kcal mol−1, and hence SEMeH was calculated to be 37.9 kcal mol−1. It was attempted to determine △Hf0 for the pentaethyl- and pentamethoxycarbonylcyclopentadienyl radicals, but this proved unsuccessful. From appearance energy measurements, △Hf0 (Pentadienyl) was determined to be 49.6 kcal mol−1 Using photoacoustic calorimetry, the C3-H bond dissociation energy of penta−1,4-diene and several 3-substituted pentadienes were determined; i.e. for penta−1,4-diene (DH° (C3-H) = 76.6±0.6 kcal mol−1), 3-methyl- penta−1,4-diene (DH°(C3-H) = 76.6±0.6 kcal mol−1) and 3-hydroxypenta−1,4-diene (DH°(C3-H) = 69.0±0.6 kcal mol−1). ESR exchange broadening methods were used to show that SEESR (3-methylpentadienyl) is virtually the same as that of the parent pentadienyl radical, (i.e. 25 kcal mol−1). The 3-hydroxypentadienyl, l-hydroxy-3-methylpentadienyl and l-trimethylsilyloxy-3-methylpentadienyl radicals were generated, but exchange broadening was not observed in the accessible temperature range. Sulphonate esters were examined as a potential source of free radicals. The reaction of simple alkyl alkanesulphonates with photochemically generated trimethyltin radicals in the cavity of an ESR spectrometer gave the corresponding alkanesulphonyl radicals. Good ESR spectra were obtained when sulphonyl radicals, generated from sulphonate esters, were used to form adduct radicals with alkenes of the type CH2=CHR where R is an electron releasing substituent, (R = OMe, OBun, SPh, SiME3). Delocalised radicals were generated from sulphonate esters which contained a terminal alkenyl or alkynyl substituent. For example, the reaction of allyl methanesulphonate with photochemically generated trimethyltin radicals in the cavity of an ESR spectrometer gave good spectra of the allyl radical. The pent-4-ene-1-sulphonyl radical was generated from the corresponding sulphonyl chloride using several different radical initiator systems (tri-n-butyltin hydride, triphenylsilane, hexa-n-butylditin, 9-trimethylstannyl-9,10-dihydroanthracene, copper (II) chloride and tris (triphenylphosphine) ruthenium (II) chloride). The radical was found to cyclise in a predominantly endo-fashion to give 3-chlorotetrahydrothiopyran-1,1-dioxide, the exact proportion of endo- and exo-products depending on the temperature. The hex-5-ene-1-sulphonyl radical was found to give thiepane-1,1- dioxide, also the product of endo-cyclisation. The inclusion of a bulky ring substituent forced the cyclohexenylethanesulphonyl radical to cyclise in the exo-mode to give 2-chloro-9-thiabicyclo[4.3.0]nonane-9,9-dioxide. Dialkyltellurides and dialkylditellurides gave the corresponding alkyl radical on photolysis in the cavity of an ESR spectrometer. For example, diallyltelluride gave good spectra of the allyl radical. Under thermolysis conditions, a nitrosodurene spin trap was employed to observe the trapped alkyl radicals. It is believed that certain of the trapped radicals were tellurium-centred species.

O paciente, um menino brasileiro de família japonesa e pais consagüíneos, é portador de deficiência concomitante de C9 (C9D) e Fator (F) H. Detectamos níveis reduzidos de FH (16,8µg/mL), C3 e FB no seu soro. O Western Blot confirmou a ausência da proteína de 150 kDa (FH). Sua mãe também apresentou níveis reduzidos de FH (140,5µg/mL), C3 e FB, enquanto o pai e a irmã apresentaram níveis reduzidos de FH. C9 também estava reduzido no soro do paciente (5,6µg/mL). O seqüenciamento do cDNA de FH do paciente revelou a presença de uma substituição homozigota G453A, codificando uma His127Arg. Esta substituição é também homozigota na mãe e provavelmente altera a estrutura terciária do FH e/ou seu perfil de secreção, uma vez que o FH é produzido pelos fibroblastos do paciente. O seqüenciamento de fragmentos do DNA genômico de C9 do paciente revelou a ausência da mutação Arg95, principal causa de C9D entre japoneses. O paciente é portador de uma mutação missense que possivelmente impede a secreção de FH, contudo, não pudemos identificar mutações envolvidas na C9D do paciente. / Our proband, Brazilian from a family of Japanese descent and history of consanguinity, carries C9 (C9D) and FH deficiencies. He was referred with severe recurrent pneumonia. FH (16,8 µg/mL), C3 and FB were present in the patient at low levels. Western blot assays confirmed the complete absence of 150 kDa (FH). His mother also had FH (140,5 µg/mL), C3 and FB low levels, while his father and sister presented only FH low levels. C9 was present in low levels (5,6 µg/mL) and only a very faint ~70 kDa band (expected size) was detected. Sequencing of proband?s FH cDNA revealed a homozygous G453A substitution, encoding a His127Arg. This substitution is also homozygous in the mother and may alter FH protein tertiary structure and/or its secretion profile, as we detected FH production in patient?s fibroblast. Sequencing of proband?s C9 genomic DNA fragments revealed the absence of Arg95 mutation, main cause of C9D in other C9D Japanese patients. The proband carries a missense mutation that may impair the FH secretion, but we couldn?t identify mutations explaining its C9D.

O paciente, um menino brasileiro de família japonesa e pais consagüíneos, é portador de deficiência concomitante de C9 (C9D) e Fator (F) H. Detectamos níveis reduzidos de FH (16,8µg/mL), C3 e FB no seu soro. O Western Blot confirmou a ausência da proteína de 150 kDa (FH). Sua mãe também apresentou níveis reduzidos de FH (140,5µg/mL), C3 e FB, enquanto o pai e a irmã apresentaram níveis reduzidos de FH. C9 também estava reduzido no soro do paciente (5,6µg/mL). O seqüenciamento do cDNA de FH do paciente revelou a presença de uma substituição homozigota G453A, codificando uma His127Arg. Esta substituição é também homozigota na mãe e provavelmente altera a estrutura terciária do FH e/ou seu perfil de secreção, uma vez que o FH é produzido pelos fibroblastos do paciente. O seqüenciamento de fragmentos do DNA genômico de C9 do paciente revelou a ausência da mutação Arg95, principal causa de C9D entre japoneses. O paciente é portador de uma mutação missense que possivelmente impede a secreção de FH, contudo, não pudemos identificar mutações envolvidas na C9D do paciente. / Our proband, Brazilian from a family of Japanese descent and history of consanguinity, carries C9 (C9D) and FH deficiencies. He was referred with severe recurrent pneumonia. FH (16,8 µg/mL), C3 and FB were present in the patient at low levels. Western blot assays confirmed the complete absence of 150 kDa (FH). His mother also had FH (140,5 µg/mL), C3 and FB low levels, while his father and sister presented only FH low levels. C9 was present in low levels (5,6 µg/mL) and only a very faint ~70 kDa band (expected size) was detected. Sequencing of proband?s FH cDNA revealed a homozygous G453A substitution, encoding a His127Arg. This substitution is also homozygous in the mother and may alter FH protein tertiary structure and/or its secretion profile, as we detected FH production in patient?s fibroblast. Sequencing of proband?s C9 genomic DNA fragments revealed the absence of Arg95 mutation, main cause of C9D in other C9D Japanese patients. The proband carries a missense mutation that may impair the FH secretion, but we couldn?t identify mutations explaining its C9D.

Ackmann, Charlotte Osmotische Induktion des Komplementfaktors C9 in retinalen Pigmentepithelzellen Universität Leipzig, Dissertation 98 Seiten, 208 Literaturangaben, 28 Abbildungen, 8 Tabellen Die altersbedingte Makuladegeneration (AMD) ist die häufigste Ursache für Erblindung bei Erwachsenen in den industrialisierten Ländern. Die AMD ist unter anderem eine chronisch entzündliche Erkrankung, bei der die Aktivierung der alternativen Komplementkaskade eine Rolle spielt. Daneben erhöht Bluthochdruck, der auch durch eine salzreiche Ernährung getriggert wird, das Risiko an einer AMD zu erkranken. Untersucht wurde die Genexpression des Komplementfaktors C9 unter verschiedenen pathologischen Bedingungen in humanen retinalen Pigmentepithel (RPE)-Zellen sowie deren Wirkung auf die physiologischen Eigenschaften der Zellen. Gezeigt wird, dass die Expression des C9 Gens in humanen RPE-Zellen spezifisch durch Hyperosmolarität, Hypoxie und oxidativen Stress induziert wird. Die Menge an C9 Protein wurde durch Hyperosmolarität leicht aber signifikant erhöht. Die hyperosmotische Induktion der C9 mRNA ist abhängig von der Aktivierung der Signalproteine p38 MAPK, ERK1/2, JNK, PI3K, sowie der Transkriptionsfaktoren STAT3 und NFAT5 während für die Hypoxie-induzierte C9 mRNA Expression nur eine Beteiligung des Transkriptionsfaktors STAT3 nachgewiesen wurde. Die Aktivierung verschiedener Signalwege durch Hyper-osmolarität und Hypoxie lässt vermuten, dass eine hohe Kochsalzaufnahme auch unter normoxischen Verhältnissen die Eigenschaften RPE-Zellen verändert. Hyperosmolarität hemmt die Proliferation und Migration der RPE-Zellen, während chemische Hypoxie nur die Proliferationsrate verringert. Die Wirkung einer erhöhten extrazellulären NaCl-Konzentration auf die C9 mRNA Expression wird über zwei Mechanismen vermittelt: über die Erhöhung der extrazellulären Osmolarität und über die Veränderung des NaCl-Gradienten über der Plasmamembran. Die NaCl Wirkung über den veränderten NaCl-Gradienten lässt vermuten, dass eine übermäßige Aufnahme von Kochsalz nicht nur über die Erhöhung des Blutdruckes die Pathogenese der AMD stimuliert, sondern dass Kochsalz auch eine direkte stimulierende Wirkung auf RPE-Zellen besitzt. Diese Vermutung könnte erklären, weshalb hoher Blutdruck ein Risikofaktor der AMD ist, aber Medikamente zur Behandlung des Bluthochdruckes das Risiko der AMD nicht verändert.

An advisory program to determine the timing of fungicide application for control of early leafspot of peanut, caused by Cercospora arachidicola, was developed based on growth responses of the pathogen to specific environmental conditions. The advisory program (89-ADV) assigned time-duration values to conditions conducive for infection (TDVi). Cumulative TDVi levels were used to determine when fungicide applications were needed. Various spray thresholds (TDVi=48, 72, 96, 120) of the 89-ADV program were compared to a 14-day spray schedule and an advisory program that was released to growers in 1981 (81-ADV). Leafspot incidence, area under the disease progress curve (AUDPC), spray number, yield and value were used to evaluate the performance of spray programs. Preliminary trials used Florigiant peanut and the fungicide chlorothalonil (1.26 kg/ha). The 89-ADV program with TDVi=48 performed exceptionally well for three consecutive years in field tests and in simulated disease environments reconstructed from historical weather data. Benefits of this program compared to the 81-ADV program included significant improvement of leafspot control, and improved crop yield and value. Based on performance, the 89-ADV program was delivered to growers as the on-line peanut leafspot advisory in 1989. Subsequent evaluations of the 89-ADV program included cultivars and fungicides in large multi-factorial experiments. Three classes of cultivars were identified: class I or highly susceptible, Florigiant and NC 9; class II or moderately susceptible, NC 7 and NC-V11; and class III or moderately resistant, NC 6. The efficiency of fungicide sprays was improved through effective leafspot control with about three fewer sprays per season than the 14-day spray schedule when chlorothalonil at 1.26 kg/ha, diniconazole at 140 g/ha or terbutrazole at 126 g/ha was applied on class I cultivars according to the TDVi=48 threshold of the 89-ADV program. The same efficiency was achieved when chlorothalonil or terbutrazole was applied on class II cultivars according to the TDVi=96. Cupric hydroxide at 1.79 kg/ha plus sulfur at 1.04 kg/ha or terbutrazole at 126 kg/ha with TDVi=96 as well as chlorothalonil at 1.26 kg/ha with TDVi=120 resulted in efficient control of disease on the class III cultivar. The spray adjuvant SoyOil 937® at 0.5% of spray volume consistently improved the performance of chlorothalonil, and allowed a reduction of application rate from 1.26 to 0.95 kg/ha without sacrificing disease control. The integrated use of cultivar resistance, fungicide, spray adjuvant, and TDVi thresholds of the 89-ADV program contributed to a reduction of fungicide input and improved disease control. / Ph. D.

Durante o ciclo menstrual, o endométrio se torna receptivo à chegada do \"futuro embrião\". Estes eventos são regulados pela liberação de progesterona durante a fase secretória do ciclo, que aumenta a secreção do componente C3 do Sistema Complemento (SC). Neste período, também foi observado o aumento fisiológico da expressão de algumas proteínas reguladoras do SC (CRPs) como: C1Inh, C4bp, DAF, CD59 e clusterina, oque sugere uma forte regulação da atividade deste sistema, favorável à implantação e ao desenvolvimento embrionário. Modificações na expressão destas proteínas poderiam resultar em aborto espontâneo recorrente (AER).Neste trabalho estudou-se a expressão endometrial de DAF e CD59 noendométrio de pacientes com AER, durante a fase secretória do ciclo. Adicionalmente, verificou-se a ativação do SC através da presença do neoantígeno de C9 neste mesmo material. A casuística foi composta de nove mulheres férteis normais (Grupo Controle) e doze mulheres com AER (Grupo Aborto), todas analisadas durante a fase secretória do ciclo. A técnica utilizada para detecção destas proteínas foi a imunohistoquímica. O neoantígeno deC9 não foi detectado em nenhum dos grupos, tanto nas glândulas quanto no estroma endometrial. DAF e CD59 foram detectados tanto no Grupo Controle quanto no Grupo Aborto.Houve expressão nitidamente mais acentuada de ambas as CRPs, DAF e CD59, durante a fase secretória intermediária do Grupo Aborto, embora sem diferença estatística. Houve expressão para DAF e CD59 no estroma endometrial de ambos os grupos. Assim, os resultados deste trabalho apontam para a ausência do neoantígeno de C9 no endométrio humano normal e no endométrio humano de patologias como o AER. As CRPs, DAF e CD59, se mostraram presentes tanto no endométrio humano normal quanto no endométrio humano patológico por AER, com destaque para o aumento da expressão de DAF e CD59 na sub-fase intermediária secretória do ciclo menstrual, período crítico para a implantação, sugerindo que alguma alteração neste período possa resultar na posterior perda gestacional. / In the cycle menstrual, the endometrium becomes ready to the arrived of embryo future. These events are controlled by mechanisms like, liberation of progesterone during the secretory phase of cycle, that increases the secretion of C3 component of Complement System (CS). In this period, it was also observed the physiologic increase of the expressionof some CS regulatory proteins (CRPs) like: C1Inh, C4bp, DAF, CD59 and clusterin, a fact suggesting strong regulation of the activity this system. Changes in this regulation can be harmful to implantation and to embryonary development, causing recurrent spontaneous abortion (RSA). To goal of the present study is to evaluate the endometrial expression of the Membrane Complex Atack (MAC) of CS, representing by neoantígen C9, in the normal and patologic human endometrium with RSA during the secretory phase of the menstrual cycle and of the CRPs, DAF e CD59, in the patologic human endometrium with RSA during the secretory phase, contributing to better understanding of the CS regulation in the endometrium in no physiologic conditions. The study group consisted of twelve endometrial biopsy, during the secretory phase of the menstrual cycle, of women with RSA of no apparent cause, compared to a control group of nine endometrial biopsy, in the same phase, of normal fertile women evaluated to endometrial expression of the neoantígen C9, DAF e CD59 by the immunochemistry technique. Neoantigen C9 was not detected in any group, in the secretory phase of the menstrual cycle in the endometrial glandular epithelium and stromal cells. DAF e CD59 were expressed in both groups during the secretory phase. DAF e CD59 were detected more intensely during the intermediate secretory phase of the Abortion Group when compared to the Control Group. Meanwhile, it not detected any significance difference. There was expression of DAF e CD59 in the stromal cells to the both groups. In summary, we data show that neoantígeno de C9 isn\'t expressed in the normal and patologic human endometrium, and the CRPs, DAF e CD59, are expressed in the normal and patologic human endometrium, predominating in the intermediary secretory phase of the cycle compared to the controls suggesting that some changes in the implantation period can result in the future gestational loss.

Durante o ciclo menstrual, o endométrio se torna receptivo à chegada do \"futuro embrião\". Estes eventos são regulados pela liberação de progesterona durante a fase secretória do ciclo, que aumenta a secreção do componente C3 do Sistema Complemento (SC). Neste período, também foi observado o aumento fisiológico da expressão de algumas proteínas reguladoras do SC (CRPs) como: C1Inh, C4bp, DAF, CD59 e clusterina, oque sugere uma forte regulação da atividade deste sistema, favorável à implantação e ao desenvolvimento embrionário. Modificações na expressão destas proteínas poderiam resultar em aborto espontâneo recorrente (AER).Neste trabalho estudou-se a expressão endometrial de DAF e CD59 noendométrio de pacientes com AER, durante a fase secretória do ciclo. Adicionalmente, verificou-se a ativação do SC através da presença do neoantígeno de C9 neste mesmo material. A casuística foi composta de nove mulheres férteis normais (Grupo Controle) e doze mulheres com AER (Grupo Aborto), todas analisadas durante a fase secretória do ciclo. A técnica utilizada para detecção destas proteínas foi a imunohistoquímica. O neoantígeno deC9 não foi detectado em nenhum dos grupos, tanto nas glândulas quanto no estroma endometrial. DAF e CD59 foram detectados tanto no Grupo Controle quanto no Grupo Aborto.Houve expressão nitidamente mais acentuada de ambas as CRPs, DAF e CD59, durante a fase secretória intermediária do Grupo Aborto, embora sem diferença estatística. Houve expressão para DAF e CD59 no estroma endometrial de ambos os grupos. Assim, os resultados deste trabalho apontam para a ausência do neoantígeno de C9 no endométrio humano normal e no endométrio humano de patologias como o AER. As CRPs, DAF e CD59, se mostraram presentes tanto no endométrio humano normal quanto no endométrio humano patológico por AER, com destaque para o aumento da expressão de DAF e CD59 na sub-fase intermediária secretória do ciclo menstrual, período crítico para a implantação, sugerindo que alguma alteração neste período possa resultar na posterior perda gestacional. / In the cycle menstrual, the endometrium becomes ready to the arrived of embryo future. These events are controlled by mechanisms like, liberation of progesterone during the secretory phase of cycle, that increases the secretion of C3 component of Complement System (CS). In this period, it was also observed the physiologic increase of the expressionof some CS regulatory proteins (CRPs) like: C1Inh, C4bp, DAF, CD59 and clusterin, a fact suggesting strong regulation of the activity this system. Changes in this regulation can be harmful to implantation and to embryonary development, causing recurrent spontaneous abortion (RSA). To goal of the present study is to evaluate the endometrial expression of the Membrane Complex Atack (MAC) of CS, representing by neoantígen C9, in the normal and patologic human endometrium with RSA during the secretory phase of the menstrual cycle and of the CRPs, DAF e CD59, in the patologic human endometrium with RSA during the secretory phase, contributing to better understanding of the CS regulation in the endometrium in no physiologic conditions. The study group consisted of twelve endometrial biopsy, during the secretory phase of the menstrual cycle, of women with RSA of no apparent cause, compared to a control group of nine endometrial biopsy, in the same phase, of normal fertile women evaluated to endometrial expression of the neoantígen C9, DAF e CD59 by the immunochemistry technique. Neoantigen C9 was not detected in any group, in the secretory phase of the menstrual cycle in the endometrial glandular epithelium and stromal cells. DAF e CD59 were expressed in both groups during the secretory phase. DAF e CD59 were detected more intensely during the intermediate secretory phase of the Abortion Group when compared to the Control Group. Meanwhile, it not detected any significance difference. There was expression of DAF e CD59 in the stromal cells to the both groups. In summary, we data show that neoantígeno de C9 isn\'t expressed in the normal and patologic human endometrium, and the CRPs, DAF e CD59, are expressed in the normal and patologic human endometrium, predominating in the intermediary secretory phase of the cycle compared to the controls suggesting that some changes in the implantation period can result in the future gestational loss.