RÉSUMÉ
Background: Inflammation is a major component of the response to tissue injury caused by myocardial infarction. High-sensitivity C-reactive protein (hs-CRP) levels might be a simple marker of the severity of this inflammatory response, providing prognostic information. Objective: To associate hs-CRP level on admission and other clinical characteristics with in-hospital mortality of patients with acute ST-segment elevation myocardial infarction (STEMI). Methods: A retrospective cohort study of patients admitted with STEMI was carried out. Patients were analyzed regarding clinical characteristics, reperfusion therapy, hs-CRP on admission and outcomes. Continuous variables were analyzed by non-parametric Mann-Whitney U test and categorical variables by chi-square test. A p value of < 0.05 was considered statistically significant. Results: Of the 118 patients analyzed, 20 died during hospitalization. Higher levels of hs-CRP (p = 0.001) and older ages (p = 0.003) were observed among those patients who died. Logistic regression showed that a one unit increase in hs-CRP increased the risk of death by 15% (p = 0.0017), after adjustment for established risk factors. Similarly, each one-year increase in age increases the risk of death by 6.6% (p = 0.003). Conclusion: Our results demonstrate a strong association between hs-CRP obtained on admission and in-hospital mortality after STEMI. It suggests that hs-CRP can be a marker of inflammatory response to myocardial ischemia, providing prognostic information regarding the risk of death
Sujet(s)
Humains , Mâle , Femelle , Adulte d'âge moyen , Protéine C-réactive , Marqueurs biologiques , Infarctus du myocarde/mortalité , Pronostic , Maladies cardiovasculaires/mortalité , Indice de masse corporelle , Études rétrospectives , Facteurs de risque , Mortalité hospitalière , Diabète , Inflammation/physiopathologieRÉSUMÉ
To observe synergistic effects of 999 Ganmaoling (GML) and its Chinese/Western materia medica (CMM and WMM) on pharmacodynamic action and to study underlying mechanisms, their anti-inflammatory, antipyretic effects were compared by assaying the increased capillary permeability induced by glacial acetic acid in mice, ear swelling induced by Xylene in mice, non-specific pleurisy induced by carrageenan in rats, and yeast induced fever in rats. Crystal violet (CV) and microbial activity (XTT) assay were used to evaluate the inhibition of GML and its CMM and WMM on KPN biofilm formation, and scanning electron microscopy (SEM) was applied for observing KPN biofilm morphology changes. The results showed that compared with control group, GML could reduce exudation amount of Evans-Blue and the degree of Ear swelling significantly, and CMM and WMM have no significant effects. The concentration of TNF-α and IL-1β of rat pleural effusion in GML, CMM and WMM group decreased significantly. The concentration of TNF-α, IL-1β and IL-8 in GML group, TNF-α, IL-8 in WMM group and IL-8 in CMM in rats serum decreased significantly. The body temperature in rats decreased significantly in GML and WMM group after 4-8 h of administration. CMM group showed no significant difference in rat body temperature compare with control. Compared with control group, GML (55-13.75 g•L⁻¹) could inhibit KPN biofilm formation and reduce number of viable cells in the KPN biofilm. CMM (45-22.5 g•L⁻¹) and WMM (10 g•L⁻¹) could also inhibit KPN biofilm formation and reduce number of viable cells (P<0.01). Result of SEM also showed that GML (55 g•L⁻¹) and its CMM (45 g•L⁻¹) and WMM (10 g•L⁻¹) could interfere the bacterial arrangement of KPN biofilm and extracellular matrix. GML and its CMM & WMM could inhibit the formation of KPN biofilm, CMM & WMM in GML showed synergism and complementation in inhibit KPN biofilm. Results showed that GML had obvious anti-inflammatory and antipyretic effects and could destruct KPN mature biofilm. WMM and CMM showed obvious synergistic effect against inflammation and inhibition of KPN biofilm formation and reduction of number of viable cells but no same effects against fever.
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La incidencia de la obesidad, los desórdenes asociados al síndrome metabólico y la diabetes tipo 2 han aumentado en la última década. Estas afecciones pueden estar influenciadas por factores genéticos, ambientales y por vías que conectan el metabolismo con el sistema inmunológico. De esta manera, se observa un metabolismo energético anormal y la inflamación crónica de bajo nivel del tejido adiposo. La incidencia de estos trastornos puede devenir de la susceptibilidad genética y cambios en el estilo de vida de cada individuo. Adicional a esto, se ha sugerido la influencia de la microbiota intestinal en la prevalencia de dichas afecciones. Datos reciente indican que la población de microorganismos residentes en el intestino, puede influir sobre la absorción de nutrientes y el almacenamiento de energía. Todo lo anterior contribuye a un balance energético positivo, consistente en un aumento del aporte energético de la dieta. Se ha relacionado su influencia en los mecanismos de inflamación y respuesta inmune asociados a dicha patología. Se hace necesario conocer con mayor certeza el papel que juega la microbiota intestinal en la aparición de la diabetes en el huésped. En esta revisión se recopilan los resultados recientes obtenidos en estudios recientes que muestran las contribuciones de la microbiota intestinal a la diabetes. Se hace necesario conocer con mayor certeza el papel que juega la microbiota intestinal en la aparición de la diabetes(AU)
The incidence of obesity, disorders associated with metabolic syndrome and type 2 diabetes have increased in the last decade. These conditions can be influenced by genetic, environmental factors and pathways linking metabolism to the immune system. Thus, an abnormal energy metabolism and a low level chronic inflammation of the adipose tissue is observed. The incidence of these disorders can become genetic susceptibility and changes in the lifestyle of each individual. In addition to this, it has been suggested the influence of intestinal microbiota in the prevalence of such conditions. Recent data indicate that the population of microorganisms living in the intestine, can influence nutrient absorption and energy storage. All this contributes to a positive energy balance consisting in increased energy from the diet. It has been implicated in the mechanisms influence of inflammation and immune response associated with such pathology. In-depth knowledge of the role of intestinal microbiota in the onset of diabetes in the host is required. In this review recent results obtained in studies focusing on the contributions of gut microbiota to diabetes are collected(AU)
Sujet(s)
Humains , Mâle , Femelle , Hydrates de carbone alimentaires , Matières grasses alimentaires , Syndrome métabolique X/étiologie , Diabète de type 2/étiologie , Microbiome gastro-intestinal , Obésité , Aliments , Santé publique , Absorption intestinale , Maladies métaboliquesRÉSUMÉ
A periodontite apical é uma doença de origem bacteriana que ativa a liberação local de mediadores pró-inflamatórios capazes de induzir a produção hepática de proteínas de fase aguda, como a proteína C-reativa (CRP). Mesmo pequenos aumentos nos níveis séricos de CRP já estão associados com o aumento do risco cardiovascular. Há na literatura vários estudos avaliando a correlação entre doença periodontal, marcadores inflamatórios (como CRP e IL6) e doenças cardiovasculares, entretanto poucos estudos têm estudado uma possível associação entre a periodontite apical crônica ou história de tratamento endodôntico e doença cardiovascular. O objetivo desta revisão foi investigar as evidências atuais em relação à possível associação entre periodontite apical crônica e o aumento dos níveis séricos de CRP.
Apical periodontitis is a bacteria-induced disease that activates the localized release of pro-inflammatory mediators capable of inducing the production of acute-phase proteins (like C-reactive protein) by the liver. Even mild elevations of serum levels of CRP are associated with higher cardiovascular risk. Literature shows many studies that evaluates the correlation between periodontal disease, inflammatory markers (like CRP and IL6) and cardiovascular diseases. However, few studies have assessed the possible association between chronic apical periodontitis or history of endodontic treatment and cardiovascular diseases. The aim of the present review was to assess the current evidence regarding the possible association between chronic apical periodontitis and elevation of serum CRP.
Sujet(s)
Parodontite périapicale , Maladies parodontales , Protéine C-réactive , Protéine C , Maladies cardiovasculaires , Inflammation , BactériesRÉSUMÉ
Objective To explore the curative effect of ulinastatin against toxic acute kidney injury(AKI) in rats and its mecha-nism .Methods Twenty-four male SD(Sprague Dawley) rats were randomly divided into 3 groups ,control group ,model group and treatment group with 8 rats in each group .Rats were subcutaneously injected gentamicin(300 mg/kg of body weight per day) for 3 days to establish models of toxic AKI .Rats in treatment group were intraperitoneally injected with a 7-day course of ulinastatin(30 000 U/kg of body weight per day) from 4th day .Dectetion of serum level of creatinine and Cystatin-C(Cys C) ,urinary concentra-tion of kidney injury molecule-1 (Kim-1 ) and neutrophil gelatinase-associated lipocalin (NGAL ) ,activity of superoxide dismutase (SOD) and glutathione peroxidase(GSH-Px) ,content of malondialdehyde ,levels of tumour necrosis factor-alpha(TNF-α) and inter-leukin-1β(IL-1β) in homogenate of renal tissues as well as observation of renal pathological changes and semiquantitative score in each group were conducted on 11th day .Results In model group ,degeneration and necrosis of renal tubular epithelial cell ,dilatation of renal tubular cavity and inflammatory cell infiltration in renal interstitial were observed .Renal pathological changes were milder in treatment group ,when compared with the model group .Renal pathological semiquantitative score ,serum level of creatinine and Cys C ,urinary concentration of Kim-1 and NGAL ,content of malondialdehyde ,levels of TNF-α and IL-1β in homogenate of renal tissues were higher in model group than in control group ,while those in treatment group were lower than in model group(P<0 .01 , respectively) .And activity of SOD and GSH-Px in homogenate of renal tissues were lower in model group than in control group ,and those in treatment group were higher than in model group and control group(P<0 .01 ,respectively) .Conclusion Ulinastatin pos-sesses a curative role in toxic AKI in rat via inhibiting oxidative stress and down-regulating levels of proinflammatory factor in renal tissues .
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Los mecanismos fisiopatológicos de la malaria placentaria son hasta el momento poco comprendidos, y el daño placentario derivado de la infección por Plasmodium spp se ha relacionado con eventos adversos del embarazo que afectan directamente el desarrollo del feto. Las concentraciones placentarias de algunas citocinas como la IL-10, TNF-alfa y TGF-beta y glicosaminoglicanos como el CSA, HA y HS podrían estar participando de forma reguladora en los eventos inflamatorios placentarios durante la infección por Plasmodium spp.
The pathophysiological mechanisms of placental malaria are until now poorly understood and the placental damage resulting from infection by Plasmodium spp has been linked to adverse pregnancy events that directly affect fetal development. Placental concentrations of some cytokines such as IL-10, TNF-alpha and TGF-beta and glycosaminoglycans such as CSA, HA and HS could be involved in a regulatory role in placental inflammation during infection by Plasmodium spp.
Sujet(s)
Humains , Femelle , Grossesse , Glycosaminoglycanes , Paludisme/immunologie , Paludisme/parasitologie , Placenta/immunologie , Placenta/parasitologie , Plasmodium , Complications parasitaires de la grossesseRÉSUMÉ
O avanço tecnológico trouxe aumento na quantidade e na variedade de agentes eliminados na atmosfera, tendo relação direta com o aumento de partículas de poluição do ar e com a ocorrência de mortes por falência cardíaca, infarto agudo do miocárdio e arritmias. Muitos estudos já relataram que o aumento de material particulado (MP <10 nM) induz ao estresse oxidativo que, por sua vez, pode causar inflamação, aumentando a expressão de citocinas inflamatórias. Especificamente no miocárdio, quando agredido, ocorre necrose dos cardiomiócitos, apoptose, ativação do sistema complemento, acúmulo de células inflamatórias na área infartada e na área remota, tendo como mediadores dessa perda celular a inflamação e o estresse oxidativo. Essa cadeia complexa de eventos promove intenso remodelamento molecular e celular na região infartada e em regiões distantes a ela. Visto a poluição atuar tanto na inflamação quanto no estresse oxidativo, e esses serem mecanismos de lesão miocárdica, nossa hipótese é que a poluição poderia ser um amplificador dessa lesão. O objetivo deste trabalho foi avaliar o papel da poluição no remodelamento estrutural, geométrico e funcional do coração em modelo experimental de infarto do miocárdio. Para tal, foram analisados o acúmulo de colágeno intersticial no miocárdio, a inflamação, o estresse oxidativo e a apoptose. Foram estudados 75 ratos wistar divididos em 5 grupos: controle (CT), grupo controle exposto à poluição (CTP), grupo infartado (IAM), infartado exposto à poluição (IAM G1) e grupo exposto à poluição antes e após o infarto (IAM G2). Os métodos utilizados foram: histologia para análise morfométrica, RT-PCR real time para citocinas inflamatórias e apoptose, ecocardiograma para anatomia e função cardíaca e ELISA para avaliação do estresse oxidativo. Os resultados mostraram maior deposição de colágeno intersticial no ventrículo esquerdo nos grupos CTP, IAM, IAM G1 e IAM G2, quando comparados ao grupo controle (p <= 0,001). No VD, houve...
Technological improvement has brought an increased amount and range of agents disposed in the atmosphere. Moreover, there is a direct relationship with increased air pollution with the occurrence of deaths because heart failure, acute myocardial infarction and arrhythmias. Many studies have reported that the increase of particulate matter (<10 nM) induces oxidative stress which can cause inflammation increasing the expression of inflammatory cytokines. Specifically, in the myocardium affected by an ischemic process, cardiomyocytes necrosis, apoptosis, activation of the complement system, inflammatory cell accumulation in the infarcted area and in remote area occurs. The pathways for this cell loss also include inflammation and oxidative stress. This complex chain of events promotes intense molecular and cellular remodeling in the infarcted region and in regions distant to it. However, the available literature does not correlate the influence of exposure to pollution with remodeling, inflammation and oxidative stress specifically in the myocardium. The aim of this study was to evaluate the role of pollution in structural, geometric and functional remodeling in the heart using an experimental model of myocardial infarction. This study, analyzed the accumulation of interstitial collagen in the myocardium, as well as inflammation, oxidative stress and apoptosis 75 rats were divided into five groups: control group (CT), control group exposed to pollution (CTP), myocardial infarcted group (MI), infarcted group immediately exposed to pollution (MI G1) and infarcted previously exposed to pollution and kept on that after infarction (MI G2). The methods that was used: histology for morphometric analysis, real time RT-PCR for inflammatory cytokines and apoptosis, echocardiography for cardiac anatomy and function and ELISA to assess oxidative stress. The results showed greater deposition of interstitial collagen in the left ventricle in groups CTP, MI, MI G1 and MI G2...
Sujet(s)
Animaux , Mâle , Rats , Pollution de l'air , Inflammation , Infarctus du myocarde , Stress oxydatif , Rat Wistar , Dysfonction ventriculaire , Remodelage ventriculaireRÉSUMÉ
A anemia é uma comorbidade prevalente e marcadora de pior prognóstico em pacientes com insuficiência cardíaca (IC). Sua relevância clínica, bem como a fisiopatologia e abordagem terapêutica nesses pacientes são temas de destaque na literatura especializada. Nessa revisão são descritos os conceitos atuais sobre a fisiopatologia da anemia na IC, os critérios diagnósticos e as indicações da suplementação de ferro, ao mesmo tempo em que são analisados criticamente os principais estudos que ofereceram evidências sobre os benefícios dessa suplementação. São abordados os quatro componentes principais da anemia: doença crônica, dilucional, "renal" e disabsortiva. Nos pacientes com IC, os critérios para o diagnóstico são os mesmos utilizados na população geral: níveis de ferritina sérica inferiores a 30 mcg/L em pacientes não nefropatas e menores que 100 mcg/L ou ferritina sérica entre 100-299 mcg/L com saturação de transferrina menor que 20% em pacientes com doença renal crônica. Finalmente, são discutidas as possibilidades terapêuticas da anemia nessa população específica de pacientes.
Anemia is a prevalent comorbidity and marker of a poorer prognosis in patients with heart failure (HF). Its clinical relevance, as well as its pathophysiology and the clinical management of these patients are important subjects in the specialized literature. In the present review, we describe the current concepts on the pathophysiology of anemia in HF, its diagnostic criteria, and the recommendations for iron supplementation. Also, we make a critical analysis of the major studies showing evidences on the benefits of this supplementation. The four main components of anemia are addressed: chronic disease, dilutional, "renal" and malabsorption. In patients with HF, the diagnostic criteria are the same as those used in the general population: serum ferritin levels lower than 30 mcg/L in patients without kidney diseases and lower than 100 mcg/L or serum ferritin levels between 100-299 mcg/L with transferring saturation lower than 20% in patients with chronic kidney diseases. Finally, the therapeutic possibilities for anemia in this specific patient population are discussed.
Sujet(s)
Humains , Anémie par carence en fer , Défaillance cardiaque , Anémie par carence en fer/complications , Anémie par carence en fer/diagnostic , Anémie par carence en fer/traitement médicamenteux , Anémie par carence en fer/physiopathologie , Compléments alimentaires , Médecine factuelle , Ferritines/sang , Défaillance cardiaque/complications , Défaillance cardiaque/physiopathologie , Antianémiques/usage thérapeutique , Composés du fer/usage thérapeutique , Fer/sang , Facteurs de risqueRÉSUMÉ
A proteína PGC1α é um co-ativador de transcrição gênica que desempenha papel importante na regulação de uma série de fenômenos metabólicos que compreendem desde o controle da termogênese e mitocondriogênese até a regulação da secreção de insulina e a produção hepática de glicose. Como vários dos fenômenos biológicos controlados direta ou indiretamente pela PGC1α tem importância vital, a regulação dos níveis de PGC1α nos tecidos deve ser finamente ajustada. Nos últimos anos, inúmeros estudos exploraram os mecanismos envolvidos com o controle da expressão gênica e tradução da PGC1α. Entretanto, apenas alguns poucos estudos avaliaram a degradação da mesma. Um dos mais importantes mecanismos envolvidos com a regulação funcional e da meia-vida de proteínas é a ubiquitinação, que pode direcionar proteínas alvo ao proteassoma para degradação ou a outras modificações pós-traducionais. O objetivo do presente estudo foi avaliar a participação de uma proteína com atividade deubiquitinase e ubiquitina ligase, a A20, na manutenção da homeostase do tecido adiposo de animais submetidos à dieta rica em gordura e voluntários humanos magros e obesos antes e após cirurgia de redução de peso. Foram utilizados o tecido adiposo branco visceral e subcutâneo e o tecido adiposo marrom de camundongos Swiss machos submetidos a 16 semanas de dieta hiperlipídica e o tecido adiposo subcutâneo de voluntários magros e obesos antes e após a cirurgia bariátrica. Esses tecidos foram avaliados quanto ao conteúdo protéico e expressão gênica da proteína A20, e sua associação com a PGC1α por imunoprecipitação e imunofluorescência, bem como a ubiquitinação desta última. Os resultados obtidos a partir do tecido adiposo de humanos mostram uma diminuição na expressão da proteína A20 nos pacientes antes e após a cirurgia bariátrica com relação aos voluntários magros.
Peroxisome proliferator-activated receptor γ coactivator 1 alpha (PGC-1α) plays an important role in whole body metabolism and, particularly in glucose homeostasis. Its expression is tightly regulated and, small variations in tissue levels can have a major impact in a number of physiological and pathological conditions. Recent studies have shown that the ubiquitin/proteasome system plays a role in the control of PGC-1α degradation. Here we evaluated the interaction of PGC-1α with the protein A20, which plays a dual-role in the control of the ubiquitin/proteasome system acting as a deubiquitinase and as an E3 ligase. We employed immunoprecipitation, quantitative real-time PCR and immunofluorescence staining to evaluate PGC-1α, A20, PPARγ and ubiquitin in the adipose tissue of humans and mice. Our results show that, in distinct sites of the adipose tissue A20 binds to PGC-1α. At least in the subcutaneous fat of humans and mice the levels of PGC-1α decrease during obesity, while its physical association with A20 increases. The inhibition of A20 leads to a reduction of PGC-1α and PPARγ expression, suggesting that A20 acts as a protective factor against PGC-1α disposal. Thus, we provide evidence that mechanisms regulating PGC-1α ubiquitination are potentially involved in the control of the function of this transcriptional co-activator.
Sujet(s)
Humains , Animaux , Mâle , Femelle , Souris , Graisse abdominale , Obésité , Tissu adipeux , Inflammation , UbiquitinesRÉSUMÉ
Se presentan los mecanismos patogénicos más conocidos en la infección por Plasmodium falciparum durante la fase eritrocitaria y extraeritrocitaria. La obstrucción vascular, explicada por los fenómenos de secuestro de glóbulos rojos parasitados y la formación de rosetas, mediados por diversos ligandos y receptores endoteliales, además de los procesos inflamatorios instaurados ante la presencia del parásito, son aspectos centrales en la patogenia de la malaria que permiten explicar. A partir de eventos como la lesión y la destrucción de eritrocitos, hepatocitos y células endoteliales, la pérdida de integridad del endotelio y la activación de promotores de daño celular y de apoptosis, se explican alteraciones como el aumento de la permeabilidad vascular, la hipoxia y el metabolismo anaerobio, que conducen tanto a lesiones localizadas en órganos como cerebro y pulmón, como a un estado de acidosis generalizada y falla multisistémica.
The most recognized pathogenic mechanisms of the infection with Plasmodium falciparum, during both the erythrocytic and exo-erithrocytic stages are presented. Vascular obstruction explained by the sequestration of parasitized red blood cells and erythrocyte rosetting, mediated by different endothelial ligands and receptors, in addition to the inflammatory processes induced by the presence of the parasite, are central aspects in the pathogenesis of malaria that explain the processes of damage, dysfunction and cell death in various organs. Alterations such as increased vascular permeability, hypoxia and anaerobic metabolism leading to localized lesions in organs such as brain and lung, as well as to a generalized acidotic state with multisystem failure can be explained by events such as the injury and destruction of erythrocytes, hepatocytes and endothelial cells, the loss of endothelial integrity, and the activation of cell damage and apoptosis promoters.
Sujet(s)
Humains , Paludisme à Plasmodium falciparum/parasitologie , Plasmodium falciparum/pathogénicité , Érythrocytes/parasitologie , Hémolyse , Inflammation/parasitologie , Paludisme à Plasmodium falciparum/immunologieRÉSUMÉ
<p><b>OBJECTIVE</b>To evaluate the anti-inflammatory property of the leaf exacts of Gendarussa vulgaris (G. vulgaris) Nees.</p><p><b>METHODS</b>G. vulgaris Nees of the family Apocynaceae is a medium sized tree grown in semishade or no shade and is common in the Ernad and Nilambur taluks of Kerala.Various parts of this plant have been used in the treatment of ulcers, sores, inflammation, dyspepsia, healing of wounds, etc. The present study aimed at the evaluation of anti-inflammatory property of the aqueous and alcoholic extracts of the leaves by both in vitro and in vivo methods. In vitro method was estimated by human red blood cell membrane stabilisation (HRBC) method and in vivo method was estimated on the carrageenan induced paw oedima.</p><p><b>RESULTS</b>Both the methods showed significant anti-inflammatory property of the different extracts tested.</p><p><b>CONCLUSIONS</b>The alcoholic extract at a concentration of 300 mg/mL showed potent activity on comparing with the standard drug diclofenac sodium.</p>
Sujet(s)
Animaux , Femelle , Humains , Mâle , Rats , Anti-inflammatoires , Apocynaceae , Chimie , Oedème , Traitement médicamenteux , Allergie et immunologie , Phytothérapie , Extraits de plantes , Feuilles de plante , Chimie , Rat Wistar , Arbres , ChimieRÉSUMÉ
ObjectiveTo investigate the effects of rosiglitazone, the agent of highly selective peroxisome proliferator-activated receptor-γ agonist, on the renal injury of rats with severe acute pancreatitis. MethodsFifty-four male Wistar rats were randomly (random number) divided into three groups : sham operation group ( SO group), severe acute pancreatitis group ( SAP group ) and rosiglitazone pretreatment group (ROSI group) . Severe acute pancreatitis model was induced by retrograde infusion of 5% sodium taurocholate into the biliopancreatic duct. Rosiglitazone (6 mg/kg) dissolved in 10% DMSO were injected into the femoral vein 30 minutes prior to the modeling. The solution of 10% DMSO was given to rats of SO group and SAP group. Rats were sacrificed 3, 12 and 24 h after modeling. The levels of serum amylase, serum creatinine, urea nitrogen, urinary albumin, urinary lgG and αl-microglobulin were measured and analyzed statistically. Kidney tissue samples were stained respectively with hematoxylin and eosin for histopathological evaluation.Results The levels of serum amylase, serum creatinine, urea nitrogen, urinary albumin, urinary IgG and αl-microglobulin were significantly increased (P < 0. 05 )after modeling, while lesser increases were found in ROSI group 12 h and 24 h after modeling (P <0. 05)compared with those in SAP group. ConclusionsRenal injury can be induced by severe acute pancreatitis,while Rosiglitazone protects rats from renal injury in the setting of severe acute panereatitis.
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El ojo, además de entregarnos el sentido de la visión, también nos permite conocer la salud general del organismo. Muchas enfermedades sistémicas se manifiestan en el órgano visual antes, durante o después del debut de ellas a nivel sistémico. Este compromiso visual es variado y depende de la enfermedad en cuestión, destacando la escleritis, uveítis y vasculitis retinales. Conocer el estado ocular permitirá al clínico realizar diagnósticos más asertivos y oportunos, realizar el tratamiento más adecuado y definir pronóstico en varias enfermedades, que tienen al globo ocular como un órgano blanco. El objetivo de esta revisión es atraer la atención del lector sobre el compromiso oftalmológico en varias enfermedades
The eye besides giving us sight, it let us know the general health of the whole body as well. Many systemic diseases become evident in the visual organ before, during or after its systemic onset. The visual involvement in these diseases is wide and depends on the underlying disease. It is worth to stand out the escleritis, uveitis and retinal vasculitis. The knowledge of the ocular health will let the physician to diagnose more accurately and in time, to start the most appropriate treatment and to define the prognosis of several diseases that have the eye as a target organ. The aim of this review is to draw the reader's attention to the ophthalmic involvement in several systemic diseases
Sujet(s)
Humains , Uvéite/thérapie , Vascularite rétinienne/étiologie , Sarcoïdose/complications , Uvéite/immunologie , Uvéite/thérapie , Maladies inflammatoires intestinales/complications , Antigène HLA-B27 , Syndrome uvéo-méningo-encéphalique/complications , Maladie de Behçet/complications , Vascularite systémique/complications , Maladies articulaires/complications , Lupus érythémateux disséminé/complicationsRÉSUMÉ
A presença de desnutrição tem sido associada a inflamação e estresse oxidativo (EO) em pacientes em hemodiálise (HD) crônica. Objetivo: Verificar a associação entre marcadores do estado nutricional, incluindo a gordura corporal (GC), marcadores inflamatórios e de EO em pacientes HD. Métodos: Estudo transversal, realizado em 40 pacientes em HD. O estado nutricional foi avaliado por avaliação subjetiva global modificada (SGAm), equivalente protéico do aparecimento de nitrogênio total normalizado (PNAn), albumina sérica (Alb-s), índice de massa corporal (IMC), GC e massa corporal magra (MCM), inflamação e EO foram avaliadas através da proteína C- reativa de (IL-6), produtos protéicos de oxidação avançada (PPOA), 8-hidroxideoxiguanosina (8OHdG) e pentosidina, respectivamente. Resultados: Trinta e sete por cento dos pacientes apresentavam algum grau de desnutrição avaliada pela SGAm. A mediana e variação da GC (Kg) foram de 16,2 (5,3 - 36,7). Com relação aos marcadores inflamatóriose de EO, houve uma correlação positiva e significativa entre IMC e PCRas (R= 0,37; p= 0,02), GC e PCRas (R= 0,32; p= 0,04) e entre PCRas e IL-6 (R= 0,51; p= 0,0007). Correlação negativa foi encontrada entre Alb-s e PCRas (R= -0,31; p= 0,05). Apenas no sexo masculino, a PCRas apresentou relação com IMC (R=0,54; p=0,01) e com a GC (R=0,52; p=0,01). Nenhuma associação foi encontrada entre marcadores inflamatórios e de EO. Conclusão: Marcadores de desnutrição e de excesso de peso não foram correlacionados com EO. A associação da PCRas com IMC e GC somente no sexo masculino pode sugerir diferenças na resposta inflamatória entre os sexos.
The presence of malnutrition has been associated with inflammation and oxidative stress (OS) in patients on hemodialysis (HD) disease. Objective: To investigate the association between markers of nutritional status, including body fat (BF), inflammatory markers and EO in HD patients. Methods: Cross-sectional study in 40 HD patients. Nutritional status was assessed by subjective global assessment modified (SGAM), protein equivalent of total nitrogen appearance normalized (PNAN), albumin (Alb-s), body mass index (BMI), GC and lean body mass (LBM) , inflammation and EO were evaluated by C-reactive protein (IL-6), advanced oxidation protein products (PPOA), 8-hidroxideoxiguanosina (8OHdG) and pentosidine, respectively. Results: Thirty-seven percent of patients had some degree of malnutrition assessed by SGAM. The median and range of the GC (kg) were 16.2 (5.3 to 36.7). Regarding markers inflamatóriose EO, there was a significant positive correlation between BMI and hsCRP level (R = 0.37, p = 0.02), GC and hsCRP level (R = 0.32, p = 0.04) and between hsCRP level and IL-6 (R = 0.51, p = 0.0007). Negative correlation was found between s-Alb and hsCRP level (R = -0.31, p = 0.05). Only in males, the hsCRP level was correlated with BMI (R = 0.54, p = 0.01) and BA (R = 0.52, p = 0.01). No association was found between inflammatory markers and EO. Conclusion: Markers of malnutrition and overweight were not associated with EO. The association of hsCRP level with BMI and BF only in males may suggest differences in inflammatory response between the sexes.
Sujet(s)
Humains , Mâle , Femelle , Adulte d'âge moyen , Indice de masse corporelle , Dialyse rénale/statistiques et données numériques , Stress oxydatif/physiologie , Évaluation de l'état nutritionnelRÉSUMÉ
Este estudo faz uma revisão atualizada da prevalência do Trichomonas vaginalis na população geral, bem como sua complexa interação com o hospedeiro e as consequências da infecção não diagnosticada. O Trichomonas vaginalis é um parasita extracelular das mucosas, especialmente a vaginal, que causam descarga vaginal, irritação e inflamação, podendo ser assintomático em quase 1/3 dos casos. Atualmente tem sido pouco encontrado em alguns centros, mas continua como causa importante de vulvovaginites no mundo, mantendo-se com taxas de 10% dos corrimentos vaginais em vários estudos epidemiológicos. É abordada a complexa relação parasita-hospedeiro, em que a resposta imunológica predispõe vaginose bacteriana e infecção pelo HIV, por mobilização das células de defesa (leucócitos, linfócitos T CD4 e macrófagos). As formas de diagnóstico são apontadas para facilitar a compreensão do diagnóstico. Foram apontadas ainda as formas de tratamento e em especial as dificuldades com casos de resistência medicamentosa.
This study is an updated review of Trichomonas vaginalis prevalence in the general population as well as its complex interaction with the host and the consequences of undiagnosed infection. The Trichomonas vaginalis is an extracellular parasite of the mucous membranes, especially the vagina, causing vaginal discharge, irritation and inflammation and may be asymptomatic in nearly one third of cases. Currently, little has been found in some centers, but remains a important cause of vulvovaginitis in the world keeping up with rates of 10% of vaginal discharge in several epidemiological studies. This involves complex host parasite relationship where the immune response predisposes to bacterial vaginosis and HIV infection by mobilizing defense cells (leukocytes, CD4 T lymphocytes and macrophages). The forms of diagnosis are pointed to facilitate understanding of the diagnosis. We also pointed the way to treatment and in particular the difficulties with cases of drug resistance.
Sujet(s)
Humains , Femelle , Trichomonas vaginalis , Maladies du vagin , Maladies sexuellement transmissiblesRÉSUMÉ
In recent years, a new alternative for the treatment of human inflammatory diseases, such as Crohn's disease, by oral administration of eggs from the swine parasitic nematode Trichuris suis has attracted attention, based on the capacity of helminths to polarize T helper cells (Th) to Th2 type which inhibits inflammation. In the present review the mechanisms used by parasitic helminths to modify the host immune response are analyzed and their potential use for the treatment of a variety of inflammatory diseases is discussed.
En años recientes ha llamado la atención una nueva alternativa para el tratamiento de enfermedades inflamatorias de humanos, como la enfermedad de Crohn, por medio de la administración oral de huevos del nematodo parásito de cerdos Trichuris suis, con base en la capacidad que tienen los helmintos de polarizar la respuesta de las células T cooperadoras (Th) a una de tipo Th2 que inhibe la inflamación. En la presente revisión se analizan los mecanismos que utilizan los helmintos parásitos para modificar la respuesta inmunitaria del portador y se discute su uso potencial para el tratamiento de una variedad de enfermedades inflamatorias.
RÉSUMÉ
La infección por Helicobacter pylori produce, en algunos pacientes, inflamación crónica en el estómago, gastritis atrófica y cáncer gástrico. Los mecanismos moleculares que conducen de la infección a la inflamación crónica y al cáncer son desconocidos. La magnitud y el proceso de la inflamación dependen del tipo de cepa de H. pylori y de la respuesta del hospedero ante la infección. Esta respuesta inflamatoria está regulada por citoquinas, algunas de las cuales han sido asociadas con cambios en la secreción de ácido en el estómago y con el riesgo de desarrollar cáncer gástrico y varias lesiones gástricas precancerosas. Sin embargo, la relación entre citoquinas y cáncer gástrico no es del todo clara. Esta revisión se enfoca en los procesos inflamatorios asociados con el desarrollo del cáncer gástrico.
Helicobacter pylori infection results, in some patients, in chronic inflammation of the stomach, atrophic gastritis and gastric cancer. The molecular mechanisms that lead from infection to chronic inflammation and gastric cancer are not understood. The degree of inflammation varies and depends on the H. pylori strain and the host response against the infection. The inflammatory response is regulated by cytokines, some of which have been associated with acid gastric secretion changes and with increased risk of stomach cancer and some precancerous lesions. Nevertheless, the relationship between cytokines and gastric cancer is not clear yet. This review focuses on the inflammatory processes associated with the development of gastric malignancies.
Sujet(s)
Humains , Helicobacter pylori , Inflammation , Tumeurs de l'estomacRÉSUMÉ
From May to November 2001, among 32 241 patients met 3 772 who had allergic dematology inflamation of many causes, 35 of them contacted cosmetics. In general, 91.43% of the patients are women and 8.57% are men, 51.4% range from 20-29 years old of age. 62.86% are state servants and students. 68.6% of the patients were affected after contacting cosmetic for one year. 65.71% are affected on the face and 37.14% had an antecedent of allergy.
Sujet(s)
Épidémiologie , CosmétiquesRÉSUMÉ
At Hospital No175 from 1998 to 2001, the study was conducted on 152 subjects (78 female, 74 male), no statistically significant difference of age, divided into various groups: group of due to stone (40 subjects), group of AIGB combining with stenosis of MBD (42 subjects). Two control group comprise of IGB due to stone (36 subjects), group of stenosis of MBD due to stone (34 subjects). In AIGB the dimention of gall bladder (+B) was not enlarged. The variation of this dimention relates to the severity of stenosis of MBD or the shrinkage of the GB. Murphy sign varies according to the severity of stenosis. The signs in internal wall of GB is the main symptoms reflecting the variation of the wall and the condition in GB. Acute damage of the wall of GB does not change sigificantly the ultrasonic sign of chronic inflammation in the wall of GB. For strenthening the accurary of the diagnosis it must not any sign note solitarily but it has to combine 2-3 signs