RESUMO A ozonioterapia é uma técnica utilizada em diversas especialidades da medicina equina, contudo, são escassos os estudos de sua utilização em cavalos atletas de vaquejada. O presente estudo tem por objetivo avaliar o potencial efeito do gás ozônio administrado por duas diferentes vias sobre os valores hematológicos, bioquímicos e no marcador de estresse oxidativo em cavalos atletas de vaquejada. Para isso, foram utilizados 9 equinos hígidos que seguiram um protocolo de treinamento e foram submetidos a dois tratamentos, com um wash-out de 8 dias entre eles. O grupo de tratamento auto-hemoterapia maior ozonizada (AHTMO) recebeu um volume de 600ml da mistura O2-O3 na concentração de 60 µg/mL e o grupo de tratamento insuflação retal (IR) recebeu 5mL de gás por kg de peso vivo, na concentração de 15µg/ kg, realizado a cada 24h em três dias consecutivos. Os resultados demonstraram-se significativos para hemácias, hematócrito e hemoglobina nas variáveis hematológicas, AST e lactato para as variáveis bioquímicas e para o malondialdeído. Não foram encontradas diferenças estatísticas significativas nas comparações entre grupos de tratamento. Assim, pode-se concluir que não há diferença entre as duas terapias, indicando que as duas técnicas são eficazes para a aplicação da ozonioterapia em cavalos competidores de vaquejada.

ABSTRACT Ozone therapy is a technique used in several specialties of equine medicine; however, there are few studies on its use in vaquejada (cowboy competition) athlete horses. This study aims to evaluate the potential effect of ozone gas administered by two different routes on hematological and biochemical values and the oxidative stress marker in vaquejada athlete horses. For this, nine healthy equines that followed a training protocol and underwent two treatments were used with an 8-day wash-out between them. The major ozonated autohemotherapy (MOA) treatment group received a volume of 600ml of the O2-O3 mixture at a concentration of 60 µg/mL, and the rectal insufflation (RI) treatment group received 5mL of gas per kg of body weight at a concentration of 15µg/kg performed every 24h on three consecutive days. Results were significant for RBC, hematocrit, and hemoglobin in the hematological variables, and AST and lactate for biochemical and malondialdehyde variables. No statistically significant differences were found in comparisons between treatment groups. Thus, we can conclude that there is no difference between the two therapies, indicating that the two techniques are effective for the application of ozone therapy in horses competing for vaquejada.

Adiponectin (APN), an adipose tissue-released adipokine with demonstrated anti-inflammatory and anti-atherogenic properties, is encoded by a gene whose polymorphisms are associated with presence of coronary artery disease (CAD). Serum APN levels are inversely related with presence and complexity of CAD. Within this context, we sought to compare levels of total APN and its high molecular weight form (HMW APN) according to clinical presentation and extent of CAD in patients undergoing elective cardiac catheterization. From March 2008 to June 2010, clinical data and blood samples for APN and HMW APN measurements were collected from 415 subjects undergoing cardiac catheterization at two tertiary centers. CAD extent was estimated by the number of coronary arteries with significant stenosis (≥70% obstruction in a major coronary artery) and by Duke Jeopardy Score (DJS). Serum APN levels were similar between groups with stable or unstable CAD (APN 9.20±5.88 vs 9.47±6.23 μg/mL, P=0.738, and HMW APN 5.31±3.72 vs 5.91±4.16 μg/mL, P=0.255), even after stratification by the number of arteries involved (single-vessel vs multivessel disease: APN 9.39±5.76 vs 9.26±6.27 μg/mL, P=0.871; HMW APN 5.29±3.79 vs 5.83±4.04 μg/mL, P=0.306) and DJS score (APN, P=0.718; HMW APN, P=0.276). We conclude that APN and HMW APN serum levels are similar across clinical presentations and different extents of CAD, despite being significantly lower in the presence of obstructive CAD.

Abstract Antimicrobial resistance in Escherichia coli isolated from pet dogs can be considered a potential threat of infection for the human population. Our objective was to characterize the resistance pattern, extended spectrum beta-lactamase production and genetic relatedness of multiresistant E. coli strains isolated from dogs (n = 134), their owners (n = 134), and humans who claim to have no contact with dogs (n = 44, control), searching for sharing of strains. The strains were assessed for their genetic relatedness by phylogenetic grouping and pulsed-field gel electrophoresis. Multiresistant E. coli strains were isolated from 42 (31.3%) fecal samples from pairs of dogs and owners, totaling 84 isolates, and from 19 (43.1%) control group subjects. The strains showed high levels of resistance to ampicillin, streptomycin, tetracycline, trimethoprim and sulfamethoxazole regardless of host species or group of origin. The blaTEM, blaCTX-M, and blaSHV genes were detected in similar proportions in all groups. All isolates positive for bla genes were ESBL producers. The phylogenetic group A was the most prevalent, irrespective of the host species. None of the strains belonging to the B2 group contained bla genes. Similar resistance patterns were found for strains from dogs, owners and controls; furthermore, identical PFGE profiles were detected in four (9.5%) isolate pairs from dogs and owners, denoting the sharing of strains. Pet dogs were shown to be a potential household source of multiresistant E. coli strains.

Dilated cardiomyopathy can be the end-stage form and common denominator of several cardiac disorders of known cause, such as hypertensive, ischemic, diabetic and Chagasic diseases. However, some individuals have clinical findings, such as an increase in ventricular chamber size and impaired contractility (classical manifestations of dilated cardiomyopathy) even in the absence of a diagnosed primary disease. In these patients, dilated cardiomyopathy is classified as idiopathic since its etiology is obscure. Nevertheless, regardless of all of the advances in medical, pharmacological and surgical procedures, the fate of patients with dilated cardiomyopathy (of idiopathic or of any other known cause) is linked to arrhythmic episodes, severe congestive heart failure and an increased risk of sudden cardiac death. In this review, we will summarize present data on the use of cell therapies in animal models of dilated cardiomyopathies and will discuss the few clinical trials that have been published so far involving patients affected by this disease. The animal models discussed here include those in which the cardiomyopathy is produced by genetic manipulation and those in which disease is induced by chemical or infectious agents. The specific model used clearly creates restrictions to translation of the proposed cell therapy to clinical practice, insofar as most of the clinical trials performed to date with cell therapy have used autologous cells. Thus, translation of genetic models of dilated cardiomyopathy may have to wait until the use of allogeneic cells becomes more widespread in clinical trials of cell therapies for cardiac diseases.

The aim of this study was to determine if bone marrow mononuclear cell (BMMC) transplantation is safe for moderate to severe idiopathic dilated cardiomyopathy (IDC). Clinical trials have shown that this procedure is safe and effective for ischemic patients, but little information is available regarding non-ischemic patients. Twenty-four patients with IDC, optimized therapy, age 46 ± 11.6 years, 17 males, NYHA classes II-IV, and left ventricular ejection fraction <35% were enrolled in the study. Clinical evaluation at baseline and 6 months after stem cell therapy to assess heart function included echocardiogram, magnetic resonance imaging, cardiopulmonary test, Minnesota Quality of Life Questionnaire, and NYHA classification. After cell transplantation 1 patient showed a transient increase in enzyme levels and 2 patients presented arrhythmias that were reversed within 72 h. Four patients died during follow-up, between 6 and 12 weeks after therapy. Clinical evaluation showed improvement in most patients as reflected by statistically significant decreases in Minnesota Quality of Life Questionnaire (63 ± 17.9 baseline vs 28.8 ± 16.75 at 6 months) and in class III-IV NYHA patients (18/24 baseline vs 2/20 at 6 months). Cardiopulmonary exercise tests demonstrated increased peak oxygen consumption (12.2 ± 2.4 at baseline vs 15.8 ± 7.1 mL·kg-1·min-1 at 6 months) and walked distance (377.2 ± 85.4 vs 444.1 ± 77.9 m at 6 months) in the 6-min walk test, which was not accompanied by increased left ventricular ejection fraction. Our findings indicate that BMMC therapy in IDC patients with severe ventricular dysfunction is feasible and that larger, randomized and placebo-controlled trials are warranted.

After myocardial infarction (MI), activation of the immune system and inflammatory mechanisms, among others, can lead to ventricular remodeling and heart failure (HF). The interaction between these systemic alterations and corresponding changes in the heart has not been extensively examined in the setting of chronic ischemia. The main purpose of this study was to investigate alterations in cardiac gene and systemic cytokine profile in mice with post-ischemic HF. Plasma was tested for IgM and IgG anti-heart reactive repertoire and inflammatory cytokines. Heart samples were assayed for gene expression by analyzing hybridization to AECOM 32k mouse microarrays. Ischemic HF significantly increased the levels of total serum IgM (by 5.2-fold) and total IgG (by 3.6-fold) associated with a relatively high content of anti-heart specificity. A comparable increase was observed in the levels of circulating pro-inflammatory cytokines such as IL-1β (3.8X) and TNF-α (6.0X). IFN-γ was also increased by 3.1-fold in the MI group. However, IL-4 and IL-10 were not significantly different between the MI and sham-operated groups. Chemokines such as MCP-1 and IL-8 were 1.4- and 13-fold increased, respectively, in the plasma of infarcted mice. We identified 2079 well annotated unigenes that were significantly regulated by post-ischemic HF. Complement activation and immune response were among the most up-regulated processes. Interestingly, 21 of the 101 quantified unigenes involved in the inflammatory response were significantly up-regulated and none were down-regulated. These data indicate that post-ischemic heart remodeling is accompanied by immune-mediated mechanisms that act both systemically and locally.

Patients with metabolic syndrome are at high-risk for development of atherosclerosis and cardiovascular events. The objective of this study was to examine the major determinants of coronary disease severity, including those coronary risk factors associated with metabolic syndrome, during the early period after an acute coronary episode. We tested the hypothesis that inflammatory markers, especially highly sensitive C-reactive protein (hsCRP), are related to coronary atherosclerosis, in addition to traditional coronary risk factors. Subjects of both genders aged 30 to 75 years (N = 116) were prospectively included if they had suffered a recent acute coronary syndrome (acute myocardial infarction or unstable angina pectoris requiring hospitalization) and if they had metabolic syndrome diagnosed according to the National Cholesterol Education Program/Adult Treatment Panel III. Patients were submitted to a coronary angiography and the burden of atherosclerosis was estimated by the Gensini score. The severity of coronary disease was correlated (Spearman’s or Pearson’s coefficient) with gender (r = 0.291, P = 0.008), age (r = 0.218, P = 0.048), hsCRP (r = 0.256, P = 0.020), ApoB/ApoA ratio (r = 0.233, P = 0.041), and carotid intima-media thickness (r = 0.236, P = 0.041). After multiple linear regression, only male gender (P = 0.046) and hsCRP (P = 0.012) remained independently associated with the Gensini score. In this high-risk population, male gender and high levels of hsCRP, two variables that can be easily obtained, were associated with more extensive coronary disease, identifying patients with the highest potential of developing new coronary events.

Therapy with bone marrow-derived cells has been used in ischemic patients with reported success. The aim of this study was to determine the therapeutic efficacy of fresh and frozen human umbilical cord blood cells (hUCB) in Wistar rats submitted to permanent occlusion of the left coronary artery. Three hours after myocardial infarction, 2 x 10(7) hUCB cells or vehicle were administered by intramyocardial injection. The animals were divided into five groups: control (N = 10), sham operated (N = 10), infarcted that received vehicle (N = 9), infarcted treated with cryopreserved hUCB (N = 7), and infarcted treated with fresh hUCB (N = 5). Cardiac function was evaluated by electrocardiogram (ECG) and echocardiogram (ECHO) before cell therapy, and by ECG, ECHO, cardiopulmonary test, and left ventricular pressure measurements 3 weeks later. After 3 weeks, both groups treated with hUCB still had Q wave present in L1, âQRS >90° and reduced shortening fraction (less than 50%). In addition, cardiac indexes of left ventricular contractility and relaxation were 5484 ± 875 and -4032 ± 643 mmHg (cryopreserved hUCB) and 4585 ± 955 and -2862 ± 590 mmHg (fresh hUCB), respectively. These values were not statistically different from those of saline-treated animals. Cardiopulmonary exercise test profile was typical of infarcted hearts; exercise time was about 14 min and maximal VO2 was 24.77 ± 5.00 mL·kg-1·min-1. These data show that hUCB therapy did not improve the cardiac function of infarcted animals or prevent cardiac remodeling.

We present two techniques of facial injectable resorbable filling, using hyaluronic acid (HA), and the different results obtained with both methods, based on physical principles of sustentation, intending to demonstrate how theese techniques can optimize and rationalize the use of the filling substance, contributing to enhance the results and cost-benefit relation. We also make a general presentation of the basic principles that remodel the cutaneous tissue using facial filling methods, as well as the importance of the clinical evaluation to achieve a fine diagnostic, emphasizing the limits when selecting the patient, listing the important and ethical points related to the use of facial filling procedures.

Presentamos dos técnicas de relleno facial utilizando ácido hialurónico y los resultados obtenidos con este método desarrollado por nosotros en base a los principios físicos de sustentación, para optimizar y racionalizar el material de relleno y mejorar los resultados, especialmente la relación costo-beneficio. Hacemos también una presentación general de los principios básicos para conseguir remodelar el tejido cutáneo empleando técnicas de relleno facial. Señalamos la importancia de la evaluación clínica para llegar a un buen diagnóstico, haciendo hincapié en los límites de selección del paciente y enumeramos los puntos importantes y éticos en el uso de materiales de relleno.

We investigated whether liver injury by dual exposure to ethanol and carbon tetrachloride (EtOH + CCl4) for 15 weeks would persist after hepatotoxic agents were removed (EtOH + CCl4/8wR). After 15 weeks of hepatic injury with ethanol (5.5%, m/v) and carbon tetrachloride (0.05, mL/kg, ip), 5 of 11 female Wistar rats were sacrificed. The other 6 rats were maintained for an additional 8 weeks without hepatotoxic agents. Ultrasonography showed increased liver echogenicity and dilation of portal vein caliber in both groups (EtOH + CCl4: 0.22 ± 0.01 cm, P < 0.001; EtOH + CCl4/8wR: 0.21 ± 0.02 cm, P < 0.01) vs control (0.16 ± 0.02 cm). Histopathology showed regenerative nodules in both experimental groups. Histomorphometry revealed increased fibrosis content in both groups (EtOH + CCl4: 12.6 ± 2.64%, P < 0.001; EtOH + CCl4/8wR: 10.4 ± 1.36%, P < 0.05) vs control (2.2 ± 1.21%). Collagen types I and III were increased in groups EtOH + CCl4 (collagen I: 2.5 ± 1.3%, P < 0.01; collagen III: 1.3 ± 0.2%, P < 0.05) and EtOH + CCl4/8wR (collagen I: 1.8 ± 0.06%, P < 0.05; collagen III: 1.5 ± 0.8%, P < 0.01) vs control (collagen I: 0.38 ± 0.11%; collagen III: 0.25 ± 0.06%). Tissue transglutaminase increased in both groups (EtOH + CCl4: 66.4 ± 8%, P < 0.01; EtOH + CCl4/8wR: 58.8 ± 21%, P < 0.01) vs control (7.9 ± 0.8%). Cirrhosis caused by the association of CCl4-EtOH remained for at least 8 weeks after removal of these hepatotoxic agents. Ultrasound images can be a useful tool to evaluate advanced hepatic alterations.

RESUMO O objetivo do trabalho foi avaliar a resistência antimicrobiana de cepas de Salmonella isoladas de águas de escaldamento, evisceração e resfriamento; de carcaças não evisceradas, evisceradas e resfriadas; penas e fezes frente à ação de antimicrobianos de uso comum. Foram coletadas 288 amostras e isoladas 29 cepas de Salmonella spp., dentre elas S. Kentucky (34,5%); S. Enteritidis (20,8%); S. Anatum e S. Enterica subsp. Enterica 8,20:-:z6 (13,8%); S. Typhimurium (6,9%);S. Enterica subsp. Enterica 4,5, 12:i:-, S. Saintpaul e S. Tennessee 3,4%. O teste de sensibilidade frente a 12 agentes antimicrobianos foi realizado com as amostras de Salmonella spp. isoladas e seguiu a metodologia de Kirby-Bauer, 25 (86,2%) amostras foram resistentes ao aztreonam e à ampicilina, 21 (72,4%) à tetraciclina e 16 (55,2%) à amoxicilina/ácido clavulânico e sulfazotrim. Os isolados apresentaram menor resistência à gentamicina , com uma amostra (3,45%) resistente, duas (6,9%) amostras foram resistentes à amicacina. Nenhuma das amostras testadas apresentou 100% de resistência ou sensibilidade aos antimicrobianos utilizados. As amostras de Salmonella spp. foram em grande proporção resistentes aos princípios antimicrobianos normalmente utilizados em avicultura, estes dados servem como alerta contra o uso indiscriminado de antibióticos, que pode contribuir para a seleção de cepas resistentes, agentes de doenças transmissíveis por alimentos em seres humanos.

ABSTRACT The aim of this study was to evaluate the level of antibiotic resistance of Salmonella strains isolated from scald, evisceration, and chiller water; non-eviscerated, eviscerated, and chilled carcasses; feathers; and feces collected in six chicken abattoirs. The 29 Salmonella strains belonged to S. Kentucky (34.5%); S. Enteritidis (20.8%); S. Anatum e S. Enterica subsp. Enterica 8,20:-:z6 (13.8%); S. Typhimurium (6.9%); S. Enterica subsp. Enterica 4,5, 12:i:-, S. Saintpaul and S. Tennessee (3.4%). All strains were submitted to antibiotic resistance test following Kirby-Bauer methodology, 25 (86.2%) strains were resistant to aztreonam and to ampicilin, 21 (72.4%) to tetracycline and 16 (55.2%) to amoxicilin/clavulanic acid and to sulfazotrim. Only one strain (3.45%) was gentamicin resistant. Two strains (6.9%) were resistant to amicacin. Resistance and susceptibility to all antibiotics tested was not detected.Salmonella strains were total or partially resistant to the antibiotics frequently used in aviculture. These note-worthy data draw attention to a danger of indiscriminate use of antibiotics in aviculture that may contribute for selection of resistant strains and this can cause foodborne infections in humans.

Gap junctions are intercellular channels which connect adjacent cells and allow direct exchange of molecules of low molecular weight between them. Such a communication has been described as fundamental in many systems due to its importance in coordination, proliferation and differentiation. Recently, it has been shown that gap junctional intercellular communication (GJIC) can be modulated by several extracellular soluble factors such as classical hormones, neurotransmitters, interleukins, growth factors and some paracrine substances. Herein, we discuss some aspects of the general modulation of GJIC by extracellular messenger molecules and more particularly the regulation of such communication in the thymus gland. Additionally, we discuss recent data concerning the study of different neuropeptides and hormones in the modulation of GJIC in thymic epithelial cells. We also suggest that the thymus may be viewed as a model to study the modulation of gap junction communication by different extracellular messengers involved in non-classical circuits, since this organ is under bidirectional neuroimmunoendocrine control.

Gap junctions are clusters of intercellular channels directly connecting the cytoplasm of adjacent cells. These channels are formed by proteins named connexins and are present in all metazoan organisms where they serve diverse functions ranging from control of cell growth and differentiation to electric conduction in excitable tissues. In this overview we describe the presence of connexins in the cardiovascular and lympho-hematopoietic systems giving the reader a summary of the topics to be covered throughout this edition and a historical perspective of the discovery of gap junctions in the immune system.

We report results obtained with sera from 58 chronic chagasic patients that were evaluated for effects on heart rate and atrioventricular (AV) conduction in isolated rabbit hearts and screened for the presence of muscarinic and beta-adrenergic activity. We show that sera from 26 patients decreased heart rate, while 10 increased it and 22 had no effect. Additionally, sera from 20 of the 58 patients blocked AV conduction. Muscarinic activation seems to be involved in both effects, but is not the only mechanism, since atropine did not antagonize the decrease in heart rate in 23% of sera or AV block in 40%. Sera from patients with complex arrhythmias were significantly more effective in depressing both heart rate and AV conduction. Sera that induce increases in heart rate seem to operate exclusively through beta-adrenergic activation. Two of these sera, evaluated with respect to intercellular communication in primary cultures of embryonic cardiomyocytes were able to block gap junction conductance evaluated by a dye injection technique after 24-h exposure. The mechanisms underlying this uncoupling effect are currently being investigated.