Search

Copyright of Arquivo Brasileiro de Medicina Veterinaria e Zootecnia is the property of Universidade Federal de Minas Gerais, Escola de Veterinaria and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background: Experimental animal research shows that immunologic defenses against tumor cells are disturbed by surgical trauma, resulting in an increased rate of tumor implantation and the growth of subsequent metastases. Minimally invasive surgery is associated with a preservation of postoperative immunologic functions and, in animal models, with decreased tumor growth. The objective was to study the influence of several surgical procedures, approached conventionally and laparoscopically, on interleukin-6 (IL-6) and monocyte-mediated cytotoxicity (MMC).Methods: Five groups of five patients each were included in this prospective study: laparoscopic cholecystectomy (minor trauma) group, Nissen fundoplication (laparoscopic and conventional as moderate trauma) groups, and sigmoid colectomy (laparoscopic and conventional as major trauma) groups. Preoperatively, 1 and 4 days after surgery, IL-6 and MMC against SW948 colon cancer cell line were determined.Results: The IL-6 levels differed significantly between the three laparoscopic procedures (p = 0.004) and increased according to the degree of trauma. There was no significant difference in MMC between the three laparoscopic procedures. However, MMC was suppressed after conventional procedures and preserved after laparoscopic procedures (p = 0.001). There was no correlation between IL-6 levels and changes in MMC.Conclusions: More extensive laparoscopic procedures induce increased levels of IL-6, reflecting higher levels of trauma. Conventional surgical procedures result in depressed MMC in the postoperative period. After laparoscopic procedures, MMC is preserved. These findings may be of importance in preventing implantation and growth of cancer cells spread by surgical manipulation. [ABSTRACT FROM AUTHOR]

Different animal models for peritoneal dialysis (PD) have been used in the past decades to develop PD fluids compatible with patient life and to identify markers of peritoneal fibrosis and inflammation. Only few of those studies have taken into account the importance of uraemia-induced alterations at both systemic and peritoneal levels. Moreover, some animal studies which have reported about PD in a uremic setting did not always entirely succeed in terms of uraemia establishment and animal survival. In the present study we induced uraemia in the recently established mouse PD exposure model in order to obtain a more clinically relevant mouse model for kidney patients. This new designed model reflected both the slight thickening of peritoneal membrane induced by uraemia and the significant extracellular matrix deposition due to daily PD fluid instillation. In addition the model offers the opportunity to perform long-term exposure to PD fluids, as it is observed in the clinical setting, and gives the advantage to knock out candidate markers for driving peritoneal inflammatory mechanisms. [ABSTRACT FROM AUTHOR]

In the present study the migration of human monocytes towards the supernatants of five different human myeloid leukemic cell lines, four different human lymphatic leukemic cell lines and blasts derived from three different patients with acute myeloid leukemia (AML) was studied and the role of monocyte chemoattractant protein (MCP)-1 was established with an ELISA assay. Large differences in migration of monocytes towards the leukemic cell supernatants were shown (variation of approximately 10 to 150% compared to positive control), but high amounts of monocyte migration was always restricted to myeloid leukemic cells (cell lines or patient blasts). MCP-1 turned out to play a major role in the migration, firstly since there was a direct correlation between the amount of migration and the concentration of MCP-1 in the supernatants, and secondly since the addition of anti-hMCP-1 was able to inhibit migration to background level in all cases. Cytotoxicity experiments with a MTT test using MCP-1-stimulated monocytes against two human myeloid leukemic cell lines showed no increase in cell death compared to unstimulated monocytes. It is concluded that monocyte migration towards leukemic cells is restricted to the myeloid lineage and is regulated by MCP-1, which is produced in different amounts by the leukemic cells. Besides, MCP-1 does not increase the direct toxic effects of monocytes on leukemic cells. [ABSTRACT FROM AUTHOR]

Relatively little is known about long term effects of wood smoke on population health. A wood burning marker -- levoglucosan -- was measured using a highly standardized sampling and measurement method in four study areas across Europe (Oslo, the Netherlands, Munich/Augsburg, Catalonia) to assess within and between study area spatial variation. Levoglucosan was analyzed in addition to other components: PM2.5, PM2.5 absorbance, PM10, polycyclic aromatic hydrocarbons (PAH), nitrogen oxides (NOx), elemental and organic carbon (EC/OC), hopanes, steranes and elemental composition. Measurements were conducted at street, urban and regional background sites. Three two-week samples were taken per site and the annual average concentrations of pollutants were calculated using continuous measurements at one background site as a reference. Land use regression (LUR) models were developed to explain the spatial variation of levoglucosan using standardized procedures. Much larger within than between study area contrast in levoglucosan concentration was found. Spatial variation patterns differed substantially from other measured pollutants including PM2.5, NOx and EC. Levoglucosan had the highest spatial correlation with ΣPAH (r = 0.65) and the lowest with traffic markers -- NOx, Σhopanes/steranes (r = -0.22). The correlation of levoglucosan with potassium (K), which is also used as a wood burning marker, was moderate to low (median r = 0.33). Levoglucosan concentrations in the cold (heating) period were between 3 and 20 times higher compared to the warm period. The contribution of wood-smoke calculated based on levoglucosan measurements and previous European emission data to OC and PM2.5 mass were 13 to 28% and 3 to 9% respectively in the full year. Larger contributions were calculated for the cold period. The median model R² of the LUR models was 60 %. In Catalonia the model R² was the highest (71 %). The LUR models included population and natural land related variables but no traffic associated variables. In conclusion, substantial spatial variability was found in levoglucosan concentrations particularly within study areas.Wood smoke contributed substantially to especially wintertime PM2.5 OC and mass. The low to moderate correlation with PM2.5 mass and traffic markers offers the potential to assess health effects of wood smoke separate from traffic-related air pollution. [ABSTRACT FROM AUTHOR]

Long-term exposure to peritoneal dialysis fluid induces morphological alterations, including angiogenesis, leading to a loss of ultrafiltration (UF) capacity. We discuss the effect of different factors in peritoneal dialysis (PD) on angiogenesis. In addition, we describe the process of angiogenesis and the possible role of different cell types in the peritoneum upon PD contributing to new blood vessel formation. Furthermore, we review several interventions used in our rat PD exposure model to decrease angiogenesis in PD. Moreover, we show new data on the use of sunitinib to inhibit angiogenesis in this rat model. Although various interventions seem to be promising, well-randomised clinical trials showing absolute prevention of angiogenesis and UF failure are, yet, still missing. To make real progress in PD treatment, the aim should be to prevent angiogenesis as well as peritoneal fibrosis and PD-induced inflammation. Copyright © 2011 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

BACKGROUND: Several studies have found an effect on mortality of between-city contrasts in long-term exposure to air pollution. The effect of within-city contrasts is still poorly understood. OBJECTIVES: We studied the association between long-term exposure to traffic-related air pollution and mortality in a Dutch cohort. METHODS: We used data from an ongoing cohort study on diet and cancer with 120,852 subjects who were followed from 1987 to 1996. Exposure to black smoke (BS), nitrogen dioxide, sulfur dioxide, and particulate matter < or = 2.5 microm (PM(2.5)), as well as various exposure variables related to traffic, were estimated at the home address. We conducted Cox analyses in the full cohort adjusting for age, sex, smoking, and area-level socioeconomic status. RESULTS: Traffic intensity on the nearest road was independently associated with mortality. Relative risks (95% confidence intervals) for a 10-microg/m(3) increase in BS concentrations (difference between 5th and 95th percentile) were 1.05 (1.00-1.11) for natural cause, 1.04 (0.95-1.13) for cardiovascular, 1.22 (0.99-1.50) for respiratory, 1.03 (0.88-1.20) for lung cancer, and 1.04 (0.97-1.12) for mortality other than cardiovascular, respiratory, or lung cancer. Results were similar for NO(2) and PM(2.5), but no associations were found for SO(2). CONCLUSIONS: Traffic-related air pollution and several traffic exposure variables were associated with mortality in the full cohort. Relative risks were generally small. Associations between natural-cause and respiratory mortality were statistically significant for NO(2) and BS. These results add to the evidence that long-term exposure to ambient air pollution is associated with increased mortality. [ABSTRACT FROM AUTHOR]

Heparan sulfate proteoglycans (HSPGs) are well known for their proposed role in glomerular filtration. In addition, HSPGs can bind the leukocyte adhesion molecule L-selectin and chemokines, suggesting a role in inflammation. We examined a panel of biopsies representing different human primary kidney diseases for L-selectin and monocyte chemoattractant protein-1 (MCP-1) binding. In various renal diseases, L-selectin and MCP-1 binding to interstitial perivascular matrix HSPGs is increased, which is significantly associated with leukocyte influx. In proteinuric diseases, including membranous glomerulopathy, minimal change disease, but also IgA nephropathy and lupus nephritis, increased binding of L-selectin and MCP-1 to tubular epithelial cell (TEC) HSPGs is observed, which colocalizes with increased basolateral syndecan-1 and anti-heparan sulfate 10E4 staining. Short-hairpin RNA-mediated silencing demonstrates that syndecan-1 on TECs indeed mediates L-Selectin binding. Increased TEC expression of IL-8 in biopsies of proteinuric patients suggests that the increase in luminal protein may activate TECs to increase expression of L-selectin and MCP-1 binding syndecan-1. Strikingly, urinary syndecan-1 from proteinuric patients is less capable of binding L-selectin compared with urinary syndecan-1 from healthy controls, although syndecan-1 concentrations are similar in both groups. Together, our data show pronounced tubulo-interstitial HSPG alterations in primary kidney disease, which may affect the inflammatory response. [ABSTRACT FROM AUTHOR]

Background: The greater omentum is frequently involved in the course of gastrointestinal and ovarian tumors. Therefore, common practice in surgical treatment for especially gastric and ovarian cancer includes removal of the greater omentum. Paradoxically, many immune cells, such as macrophages that accumulate in so-called milky spots, reside within the omentum and are cytotoxic against tumor cells ex vivo. Consequently, omental macrophages might play an important role in killing tumor cells, and may hereby prevent development into local peritoneal recurrences. In the present study, we therefore evaluated the role of the omentum and the clinical relevance of omentectomy in minimal residual disease (MRD). Methods: Tumor cell dissemination patterns on the omentum in a rat model were examined using DiI-labelled CC531s tumor cells. Additionally, intra peritoneal (i.p.) tumor load was investigated in rats that underwent omentectomy or sham laparotomy followed by i.p. injection of CC531s cells on day 21, which represented MRD. Results: At 4 h post injection, tumor cells predominantly adhered on milky spots. Number of cells thereafter declined rapidly suggesting initial tumor killing functions in these specific immune aggregates. Despite initial reduction observed in milky spots, numbers of tumor cells however increased at fatty tissue stripes that border the omentum. This indicated proliferation at these locations, which corresponded to macroscopic observations of the omenta on day 21 after tumor cell injection. Omentectomy resulted in reduced intra-abdominal tumor load, which was completely attributable to the absence of the omentum, as tumor development did not differ on other sites. Even in the MRD group microscopic clusters of tumor cells located in the omentum eventually developed into macroscopic nodules. Conclusion: Since the ability of omental milky spots is, even in MRD, insufficient to prevent intra abdominal tumor outgrowth, omentectomy, which reduces tumor load, is recommended in surgical treatment of intra abdominal tumors that are prone to disseminate intraperitoneally. [ABSTRACT FROM AUTHOR]

Macrophages play a role in the host defence against cancer. Little is known about changes in macrophage populations during early metastatic growth. To evaluate the distribution, number and phenotype of macrophages in the development of hepatic metastases in a rat model (Wag/Rij rats and syngeneic CC531 colon carcinoma cell line), an immunohistochemical study was performed with the monoclonal antibodies EDI (monocytes, and all macrophages), ED2 (resident tissue macrophages, like Kupffer cells) and ED3 (a subpopulation of macrophages which may play a role in the recruitment of lymphocytes). OX19 and Hisl4 were used to identify lymphocytes. In this study a new monoclonal antibody CC52 is described, which recognizes the CC531 tumour cell line. Liver metastases were induced by injection of CC531 colon carcinoma cells into a mesenteric vein. Rats were killed at various intervals. Results show three major macrophage populations during hepatic tumour growth: (1) on day 3, infiltrates are observed around the micrometastases, which contain mainly newly recruited macrophages (EDI + and ED2- ); (2) after 7 days, ED3-positive (ED3 +) macrophages together with T lymphocytes are found in the infiltrates; (3) an increase in the number of ED2-positive (ED2+) Kupffer cells is observed in the liver parenchyma after 14 days. In conclusion, the present results suggest that various populations of macrophages, newly recruited (EDI +) as well as resident Kupffer cells (ED2+), are involved in the immune response against tumour cell deposits in the liver. [ABSTRACT FROM AUTHOR]

Mesothelial cells that line the peritoneal cavity are capable of producing several proinfiammatory cytokines such as interleukin-6 and interleukin-8. Since they are the most numerous cell in the peritoneal cavity when the lining mesothelial cells are included, they may play a major role in the local antibacterial defence mechanism. Cancer antigen (CA)125 is expressed by mesothelial cells (as by other coelomic epithelium-derived cells) and might therefore be considered a marker of the mesothelium. The aim of this study was to determine whether CA125 is a bulk or an activation stage mesothelial cell marker. A positive correlation was found between the mesothelial cell number and the CA125 concentration in dialysate of stable PD patients ( = 0.03). CA125 release by mesothelial cell cultures during confluence showed that the release per cell was constant in time. Stimulation of mesothelial cells in a confiuential phase with IL1β, TNFα, IFNγ and TGFβ did not result in an increase in CA125 release. Cell lysis showed that CA125 is also present intracellularly. This implies that release of intracellular CA125 can be a disturbing factor in interpreting the CA125 concentration of dialysate in situations where mesothelial cell death may occur, such as in peritonitis. It can be concluded, that our data show that dialysate CA125 is a bulk marker for the mesothelial cell mass in stable PD patients and can thus provide data on the state of the peritoneal membrane in the follow-up of the individual patient. [ABSTRACT FROM PUBLISHER]

We analysed the peritoneal cellular immune system 24-48 h before the onset of a clinical peritonitis. Peritoneal cells were obtained from the overnight dialysis effluents 1 or 2 days (day-1 and day-2) preceding the day of peritonitis, the last overnight effluent before the peritonitis effluent (day P), and the first peritonitis effluent. Nine peritonitis episodes of six patients were studied. The number of Fc receptor positive cells, the chemotactic activity, and immunophenotype of the peritoneal cell population at day-2 and day-1 were similar to the postperitonitis control effluent. However, immunophagocytosis and phagocytosis capacity of the peritoneal macrophages was decreased in five of six episodes at day-2 and -1 compared to control peritoneal macrophages. The overnight effluents of day P revealed a moderate influx of neutrophilic granulocytes and an increase of bacterial killing capacity and chemotactic activity. Activation of the peritoneal T cells at day P was shown by the increase in MHC class II positive T cells and an increase in the CD4/CD8 ratio. Bacterial cell cultures of the effluents were positive in three episodes 24-48 h before peritonitis, and of all overnight effluents at day P. These results indicate that malfunctioning of phagocytosis by peritoneal macrophages may contribute to the development of a CAPD peritonitis. [ABSTRACT FROM PUBLISHER]

In the present study about 03% to F6% of human bronchoalveolar lavage (BAL) cells were identified as typical dendritic cells (DC), having an irregular outline, lobulated nucleus, and clear distinguishable acid phosphatase activity or EBM11 (anti-CD68) reactivity in a spot near the nucleus. After DC enrichment, using transient adherence to plastic, FcR-panning, and a density metrizamide gradient, a population containing 7-8% typical DC was obtained. This DC-enriched low density fraction, containing the highest percentages of DC, very strongly induced T cell proliferation in an allogeneic mixed leucocyte reaction (MLR), which was significantly higher than that induced by other partly (un)fractionated BAL cells. These data indicate that DC seem to be the major accessory cells in the BAL fluid, and therefore may be important in the regulation of T cell immune responses in the lung. [ABSTRACT FROM AUTHOR]

In this study the antigen-presenting capacity of human peritoneal cells and the influence of continuous ambulant peritoneal dialysis (CAPD) were studied. On average 6% of the peritoneal cells were dendritic cells (DC), with no difference between CAPD and control peritoneal cells, DC were enriched by selecting for non-adherent, Fc receptor-negative, low density cells. A typical spot-like CD68 positivity was seen in DC, in contrast to the pancytoplasmic staining pattern in macrophages. Peritoneal DC morphologically and functionally showed features of cells belonging to the DC lineage. Peritoneal DC were superior antigen-presenting cells for both allo-antigen, and Candida albicans antigen or purified protein derivative. CAPD peritoncal macrophages were two- to threefold better stimulator cells for allogeneic T cells compared with control macrophages. The level of integrins/adhesins or MHC class I or II, as measured semi-quantitatively on the FACS, could not account for this phenomenon. In addition, a double chamber system showed that dialysate-activated macrophages produced soluble factors that could enhance DC-induced allogeneic T cell proliferation, in conclusion, human peritoneal cells contain a relatively high percentage of classical DC. CAPD treatment does not impair the antigen-presenting capacity of peritoneal cells, but instead upregulates the allo-antigen-presenting capacity of peritoneal macrophages. [ABSTRACT FROM AUTHOR]

Background: We report the outcome of 67 patients after endovascular treatment of chronic cerebro-spinal venous insufficiency in patients with multiple sclerosis. Material and methods: For evaluating outcome, patients were divided into three groups with respective outcome after three, six and twelvemonths. Assessment of outcome was done by a disease-specific quality-of-life score that reflects the physical health (physical health composite, PHC) and mental health (mental health composite, MHC) by a score. Results: Improvement in PHC was significant (P < 0.05) in the three- and six-month groups. Improvement in MHC was only significant (P < 0.05) in the three-month group. Conclusion: In conclusion, we can state that the result of endovascular treatment seems to decay although the baseline is still higher than preoperative. To confirm this finding, this study needs to be reproduced in a larger patient population. [ABSTRACT FROM AUTHOR]

Abdominal surgery induces an inflammatory reaction that activates a cascade of immunological events leading to increased postoperative intra-abdominal tumor recurrence. Subject for discussion is the mechanism by which postoperative intraabdominal tumor development is stimulated. Laparotomized groups enabled people to evaluate local and systemic effects of surgery on tumor development, whereas in thoracotomized groups only systemic effects were measured. The surgical intraperitoneal microenvironment enhances adhesion of free tumor cells rather than it affects growth of micrometastases. Additionally, local factors as well as systemic immune suppression as a result of surgery play an important role in facilitation of intra-abdominal tumor development.

The application of animal models to study the biocompatibility of bicarbonate-buffered peritoneal dialysis solutions. Patients treated with peritoneal dialysis (PD) are at risk for development of ultrafiltration failure and peritonitis. These two significant complications can result in the termination of PD treatment. The relative unphysiologic composition of the currently used standard peritoneal dialysis fluids (PDF) is considered to be a major cause for the development of morphologic changes of the peritoneal membrane, ultimately resulting in ultrafiltration failure and probably contributing to changes in local defense mechanisms with the associated increased risk of peritonitis. In recent years, a major research focus has become the development of new and improved PD solutions. This has resulted in the development of an amino-acid–based PDF, a glucose polymer–based PDF, and several bicarbonate-buffered PDF. Typically, the first phase of biocompatibility testing of new PD solutions involves in vitro testing, employing isolated cells such as peritoneal macrophages or cell culture systems using human peritoneal mesothelial cells. The results of such evaluations are useful in providing insights into the biocompatibility performance of any given formulation, but suffer from several disadvantages, which can be better addressed using animal models. In vivo studies using animals permit the analysis of biocompatibility under conditions that allow for cell-to-cell interactions and dynamic changes in solution composition that more closely mimic the clinical situation. In this paper, we will review the use of animal models for the study of PDF biocompatibility and their application to the assessment of bicarbonate-buffered PDF. [ABSTRACT FROM AUTHOR]

Abstract: Land-use regression models have increasingly been applied for air pollution mapping at typically the city level. Though models generally predict spatial variability well, the structure of models differs widely between studies. The observed differences in the models may be due to artefacts of data and methodology or underlying differences in source or dispersion characteristics. If the former, more standardised methods using common data sets could be beneficial. We compared land-use regression models for NO2 and PM10, developed with a consistent protocol in Great Britain (GB) and the Netherlands (NL). Models were constructed on the basis of 2001 annual mean concentrations from the national air quality networks. Predictor variables used for modelling related to traffic, population, land use and topography. Four sets of models were developed for each country. First, predictor variables derived from data sets common to both countries were used in a pooled analysis, including an indicator for country and interaction terms between country and the identified predictor variables. Second, the common data sets were used to develop individual baseline models for each country. Third, the country-specific baseline models were applied after calibration in the other country to explore transferability. The fourth model was developed using the best possible predictor variables for each country. A common model for GB and NL explained NO2 concentrations well (adjusted R 2 0.64), with no significant differences in intercept and slopes between the two countries. The country-specific model developed on common variables for NL but not GB improved the prediction. The performance of models based upon common data was only slightly worse than models optimised with local data. Models transferred to the other country performed substantially worse than the country-specific models. In conclusion, care is needed both in transferring models across different study areas, and in developing large inter-regional LUR models. [Copyright &y& Elsevier]