Experimental study of an asymmetric valveless pump to elucidate insights into strategies for pediatric extravascular flow augmentation.

Asymmetric pumping is a sub-category of valveless pumping in which a flexible tube is rhythmically compressed in the transverse symmetry plane. Due to the resulting asymmetry between the suction and discharge pipes, a net pumping head is achieved. Asymmetric pumping is regarded as one of the main mechanisms responsible for the Liebau effect in addition to impedance pumping. However, there remains a paucity of research surrounding the governing parameters of asymmetric pumping. Here, we conducted an experimental study of the performance of an asymmetric pump, with an aim to assess its potential for extravascular flow augmentation. A custom flexible latex tube and experimental platform were developed for this purpose. We tested various tube thicknesses and pinching frequencies. Our results demonstrate that the performance is within the range of physiological requirements for pediatric circulatory devices (~ 1 L/min and < 30 mmHg). We conclude that due to the absence of reverse flow and its mechanical simplicity, pure asymmetric pumping is promising for selected cardiovascular applications with less complexity than other valveless techniques.

Cytokines - their pathogenic and therapeutic role in chronic viral hepatitis.

Cytokines make up a network of molecules involved in the regulation of immune response and organ functional homeostasis. Cytokines coordinate both physiological and pathological processes occurring in the liver during viral infection, including infection control, inflammation, regeneration, and fibrosis. Hepatitis B and hepatitis C viruses interfere with the complex cytokine network brought about by the immune system and liver cells in order to prevent an effective immune response, capable of viral control. This situation leads to intrahepatic sequestration of nonspecific inflammatory infiltrates that release proinflammatory cytokines, which in turn favor chronic inflammation and fibrosis. The therapeutical administration of cytokines such as interferon alpha may result in viral clearance during persistent infection, and revert this process.

[Cyclosporin A causes oxidative stress and mitochondrial dysfunction in renal tubular cells]. / La ciclosporina A origina estrés oxidativo y disfunción mitocondrial en células tubulares renales.

Reactive oxygen species (ROS) have been implicated in cyclosporin A (CsA) nephrotoxicity. As mitochondria are one of the main sources of ROS in cells, we evaluated the role of CsA in mitochondrial structure and function in LLC-PK1 cells. We incubated cells with CsA 1 microM for 24 hours and studies were performed with flow citometry and confocal microscopy. We studied mitochondrial NAD(P)H content, superoxide anion (O2.-) production (MitoSOX Red), oxidation of cardiolipin of inner mitochondrial membrane (NAO) and mitochondrial membrane potential (DIOC2(3)). Also we analyzed the intracellular ROS synthesis (H2DCF-DA) and reduced glutation (GSH) of cells. Our results showed that CsA decreased NAD(P)H and membrane potential, and increased O2.- in mitochondria. CsA also provoked oxidation of cardiolipin. Furthermore, CsA increased intracellular ROS production and decreased GSH content. These results suggest that CsA has crucial effects in mitochondria. CsA modified mitochondrial physiology through the decrease of antioxidant mitochondrial compounds as NAD(P)H and the dissipation of mitochondrial membrane potential and increase of oxidants as O2.-. Also, CsA alters lipidic structure of inner mitochondrial membrane through the oxidation of cardiolipin. These effects trigger a chain of events that favour intracellular synthesis of ROS and depletion of GSH that can compromise cellular viability. Nephrotoxic cellular effects of CsA can be explained, at least in part, through its influence on mitochondrial functionalism.

[All-trans retinoic acid induces apoptosis in human mesangial cells: involvement of stress activated p38 kinase]. / El ácido retinoico todo-trans induce apoptosis en células mesangiales humanas: implicación de la quinasa activada por estrés p38.

All-trans retinoic acid (AR-t) is used for treating acute promyelocytic leukemia and renal cell carcinoma and it also has therapeutic value in several animal models of renal disease. Among its renal targets, mesangial cells have been widely studied: they have both retinoic acid receptors (RAR) and retinoid X receptors (RXR) and the cell growth is inhibited when human mesangial cells are incubated with 1-10 microM AR-t. Although his effect has been related with the antiproliferative action of AR-t, there are no studies on the involvement of apoptosis in AR-t induced cell growth when higher concentrations of retinoid are used. Our studies show that 25 microM AR-t triggers mesangial cell apoptosis assessed by light and fluorescence microscopy (Giemsa stain and acridine orange stain, respectively), DNA electrophoresis, flow cytometry (annexin-V) and immunocytochemistry (TUNEL). AR-t induced apoptosis was not inhibited by preincubation with the RXR pan-antagonist HX531 nor with the RAR pan-antagonist AGN 193109, this suggesting RAR and RXIR are not involved in AR-t induced cell death. Previous results of our group showed that ERK (extracellular regulated kinase) and INK (c-Jun kinase), two members of the MAP (mitogen activated protein) kinase family, are involved in non apoptotic effects of AR-t on mesangial cells. Therefore we focussed on the stress activated p38 kinase, the third member of the MAPK family, to investigate its involvement in AR-t induced apoptosis. The results confirmed a role of p38 since: 1) preincubation with B5203589, a p38 inhibitor, inhibited ARA induced apoptosis; 2) incubation with AR-t induced p38 phosphorilation after few minutes and p38 remained phosphorilated for at least 8 hours and 3) AR-t induced p38 phosphorilation was inhibited by SB203589. These data suggest that AR-t might have toxic side effects on the kidney but also suggest that AR-t could be an useful inhibitor of pathological mesangial cell expansion.

The role of hydrogen peroxide in the contractile response to angiotensin II.

In the last years, reactive oxygen species (ROS) have been proposed as mediators of proliferative/hypertrophic responses to angiotensin II (Ang II), both in vivo and in vitro. However, the hypothesis that the Ang II-dependent cell contraction could be mediated by ROS, particularly H2O2, has not been tested. Present experiments were devoted to test this hypothesis and to analyze the possible mechanisms involved. Catalase (CAT) prevented the increased myosin light chain phosphorylation and the decreased planar cell surface area (PCSA) induced by 1 microM Ang II in cultured rat vascular smooth muscle cells (VSMC). This preventive effect of CAT was also detected when 1 microM platelet-activating factor (PAF) was used as a contractile agonist instead of Ang II. Similar results were found when using horseradish peroxidase as an H2O2 scavenger or cultured rat mesangial cells. In vascular smooth muscle cells, CAT modified neither the binding of labeled Ang II nor the Ang II-induced inositol 1,4,5-trisphosphate (IP3) synthesis. However, it completely abolished the Ang II-dependent calcium peak, in a dose-dependent fashion. CAT-loaded cells (increased intracellular CAT concentration over 3-fold) did not show either a decreased PCSA or an increased intracellular calcium concentration after Ang II treatment. Ang II stimulated the H2O2 synthesis by cultured cells, and the presence of CAT in the extracellular compartment significantly diminished the Ang II-dependent increased intracellular H2O2 concentration. The physiological importance of these findings was tested in rat thoracic aortic rings: CAT prevented the contraction elicited by Ang II. In summary, present experiments point to H2O2 as a critical intracellular metabolite in the regulation of cell contraction.

[Pott's puffy tumor]. / Tumor blando de Pott.

Between the complications of frontal sinusitis orbital or intracranial are the most frequent encountered (meningitis, abscesses and empyemas). All are secondary to thrombophlebitis of veins communicating the intracranial cavity with the frontal sinus. Frontal osteomyelitis secondary to sinusitis, the so-called Pott's puffy tumor, is a much more rare aftermath in the antibiotic epoch. Pott's puffy tumor must be suspected in patients with frontal headache followed by frontal oedema. Concerning the diagnosis clinical suspicion is essential and must be settled throughout computerized tomography and/or magnetic resonance or even bone scintiscan. The paper report 2 cases, one an orbital periostitis, at the beginning of the disease, which was recovered with medical antibiotic treatment and another one, an osteomyelitis somewhat evolved requiring surgery through frontal osteoplasty. Perusal of etiology, pathogenesis, diagnosis and treatment of this complication.

Nefrectomia en donante vivo: Abordaje subcostal anterior extraperitoneal / Nephrectomy in living-donor

Se presentan siete pacientes a quienes se les ha practicado nefrectomía por ser donantes vivos intrafamiliares, mediante abordaje anterior extraperitoneal; se informan las ventajas de esta cirugía comparadas con el abordaje clásico de la lumbotomia ampliada

Cyclosporine increases local glomerular synthesis of reactive oxygen species in rats: effect of vitamin E on cyclosporine nephrotoxicity.

BACKGROUND: We report an investigation of the effects of cyclosporine (CsA) on kidney function, the glomerular synthesis of reactive oxygen species, the peroxidation of lipids, and the levels of thromboxane B2 (TXB2). The effect of the simultaneous administration of the antioxidant vitamin E (Vit E) and CsA in rats was also evaluated. METHODS: Adult male Wistar rats were treated for 30 days with CsA (30 mg/kg/day), with Vit E (0.05 mg/ml), with CsA plus Vit E, or with the vehicle used for administration of CsA, namely 12.6% ethanol. RESULTS: CsA induced kidney failure and increased the glomerular synthesis of superoxide anion, H2O2, malonyldialdehyde, and TXB2. Vit E minimized the adverse effects of CsA on kidney function and the glomerular synthesis of these compounds. CONCLUSIONS: Our results suggest that the acute decrease in glomerular filtration rate induced by CsA might be mediated by the synthesis of reactive oxygen species and subsequent peroxidation of lipids, which increases the levels of TXB2. Treatment with Vit E prevented these effects, suggesting a possible role for antioxidants in the prevention of CsA nephrotoxicity.

Cyclosporin A-induced hydrogen peroxide synthesis by cultured human mesangial cells is blocked by exogenous antioxidants.

Cyclosporin A (CsA) is the immunosupressor most widely used in transplanted patients for preventing organ rejection, but it has some toxic side effects in vascular beds and kidney. The purpose of this work was to study if H2O2, a reactive oxygen species, is involved in the CsA-induced toxic effects on kidney in vitro. Human mesangial cells (HMC) in culture were incubated in presence of CsA (10[-5]-10[-8]M) and H2O2 was measured by flow cytometry. The specificity of the probe used in this method was demonstrated as fluorescence was not detected when superoxide anion generated through a Xanthine-Xanthine oxidase system was present, but fluorescence was noted when H2O2 was present in the incubation medium, both directly and after addition of superoxide dismutase to the medium thus promoting H2O2 synthesis. CsA induced a significant dose and time-response increased H2O2 synthesis by cultured HMC. This increase appeared 5 min after CsA addition, being maximal between 15-45 min at CsA concentration of 10(-7)M. When HMC were preincubated with antioxidants as vitamin E or selenium, the CsA-induced H2O2 production was partially blocked. In addition, selenium also induced an increased activity of glutathion peroxidase in HMC after 24 hours of incubation, suggesting that it exerted its H2O2 scavenging action through the modulation of the activity of this enzyme.

[Lateral cervical branchial cysts: a retrospective study]. / Quistes branquiales cervicales laterales: un estudio retrospectivo.

The cause of lateral cervical branchial cysts is debated. Some authors claim that they are congenital, whereas others believe that they are acquired, being their likely origin cystic degeneration of the cervical lymph nodes. Their protocol of study and differential diagnosis with respect to malignant neck masses are of special interest. A retrospective clinical study was made of 13 cervical branchial cysts seen by one of the authors over a decade-long period. Based on the results, their probable origin is discussed and a study protocol is proposed. Although it has been discussed by some authors, we conclude that the origin of branchial cysts cannot be determined through this type of clinical study. Computed tomography and fine-needle aspiration currently are essential diagnostic methods in the study protocol of these lesions.

Cyclosporine A nephrotoxicity: role of thromboxane and reactive oxygen species.

The main adverse effect of cyclosporine A (CyA) is nephrotoxicity. CyA increases urinary concentrations of thromboxane A2 (TXA2), a potent vasoconstrictor that can be involved in kidney failure induced by CyA. Furthermore, it has been postulated that a relationship exists between oxygen free radicals and the synthesis of arachidonate metabolites in experimental models of CyA nephrotoxicity. We studied the effect of vitamin E (VitE), an oxygen free radical scavenger, on renal function, on glomerular synthesis of thromboxane B2 (TXB2), and on free radicals in rats treated with CyA. Four groups of male Wistar rats were studied: (1) a control group; (2) a group given VitE at 0.05 mg/dl in drinking water for 25 days; (3) a group given CyA at 50 mg/kg body weight/day orally for 10 days; and (3) a group given Vit E + CyA, in which rats were provided with drinking water containing VitE for 15 days and afterwards were treated with VitE and CyA for 10 days. Renal function parameters and glomerular synthesis of TXB2, superoxide anion (02.-), malondialdehyde (MDA), and hydrogen peroxide (H202) were evaluated. CyA decreased body weight, caused deterioration of kidney function and increased glomerular synthesis of TXB2, O2.-, MDA, and H202. Pretreatment with VitE prevented the effects of CyA on kidney function and decreased glomerular synthesis of these mediators. In conclusion, CyA induced glomerular synthesis of reactive oxygen species (ROS) and TxB2. Pretreatment with VitE inhibited acute renal failure induced by CyA, probably by scavenging free radicals and by inhibiting the synthesis of TXB2.

Helicobacter pylori infection in the Colombian Andes: a population-based study of transmission pathways.

In 1992, the authors studied Helicobacter pylori infection and exposures relevant to person-to-person, waterborne, foodborne, and zoonotic transmission in a census sample of 684 2-9-year-old children in Aldana, Nariño, a rural community in the Colombian Andes. H. pylori prevalence, as determined by the 13C-urea breath test, was 69%, and prevalence increased from 53% in 2 year-olds to 87% in 9 year-olds. Beginning at 3 years of age, a higher percentage of males compared with females were infected. Odds ratios were estimated by multivariate logistic regression to control for mutual confounding by transmission-pathway proxy variables and socioeconomic indicators. Among transmission-pathway proxies, the strongest predictor of H. pylori status was the number of persons who lived in the home, with the number of children apparently being of greater importance than the number of adults. Swimming in rivers, streams, or pools increased the odds of infection, as did using streams as a drinking water source. Children who frequently consumed raw vegetables were more likely to have the infection, and children who had contact with sheep also had increased prevalence odds. Because the results did not implicate a single mode of transmission, the possibility of multiple pathways is indicated.