Sonochemical assisted synthesis of SrFe12O19 nanoparticles.

We present the synthesis of M-type strontium hexaferrite by sonochemistry and annealing. The effects of the sonication time and thermal energy on the crystal structure and magnetic properties of the obtained powders are presented. Strontium hexagonal ferrite (SrFe12O19) was successfully prepared by the ultrasonic cavitation (sonochemistry) of a complexed polyol solution of metallic acetates and diethylene glycol. The obtained materials were subsequently annealed at temperatures from 300 to 900 °C. X-ray diffraction analysis shows that the sonochemical process yields an amorphous phase containing Fe(3+), Fe(2+) and Sr(2+) ions. This amorphous phase transforms into an intermediate phase of maghemite (γ-Fe2O3) at 300 °C. At 500 °C, the intermediate species is converted to hematite (α-Fe2O3) by a topotactic transition. The final product of strontium hexaferrite (SrFe12O19) is generated at 800 °C. The obtained strontium hexaferrite shows a magnetization of 62.3 emu/g, which is consistent with pure hexaferrite obtained by other methods, and a coercivity of 6.25 kOe, which is higher than expected for this hexaferrite. The powder morphology is composed of aggregates of rounded particles with an average particle size of 60 nm.

Proteomic analysis of MCF-7 breast cancer cell line exposed to leptin.

BACKGROUND: Obesity is a well-known factor risk for breast cancer in postmenopausal women. Circulating leptin levels are increased in obese and it has been suggested to play an important role in mammary tumor formation and progression. To contribute to the understanding of the molecular mechanisms underlying leptin action in breast cancer, our aim was to identify proteins regulated by leptin in MCF-7 human breast cancer cells. METHODS: We used two-dimensional gel electrophoresis (2-DE) and matrix assisted laser desorption/ionization time of flight mass spectrometry (MALDI-TOF MS) to identify proteins affected by leptin. RESULTS: Thirty proteins were found differentially expressed in MCF-7 cells after 48 h leptin exposure. Proteins regulated by leptin included proteins previously implicated in breast cancer such as catechol-o-methyltransferase, cathepsin D, hsp27, serine/threonine-protein phosphatase and regulatory proteins of the Ras signaling pathway. Proteins involved in other cellular functions such as stress response, cytosqueleton remodeling and proteins belonging to ubiquitin-proteasome system, were also identified. Furthermore, leptin-treated cells showed a substantial uptake of the serum carrier proteins albumin and alpha-2-HS-glycoprotein. CONCLUSIONS: This screening reveals that leptin influences the levels of key proteins involved in breast cancer which opens new avenues for the study of the molecular mechanisms linking obesity to breast cancer.

17ß-Estradiol regulates oxidative stress in prostate cancer cell lines according to ERalpha/ERbeta ratio.

Estrogen action is mediated by the two receptor isoforms: estrogen receptor alpha and beta. Both receptors are expressed in human prostate tissue and have different action profiles. ERalpha is positively correlated with the malignancy of prostate cancer, while ERbeta may protect against abnormal prostate cell growth. 17ß-Estradiol (E2), at least in part, induces cancerous transformations by causing deleterious mutations through the formation of reactive oxygen species (ROS). The aim was to study the effect of E2 on oxidative stress and the expression of uncoupling proteins (UCPs) and antioxidant enzymes in several prostate cancer cell lines with different ERalpha/ERbeta ratios. The cell prostate lines with a lower ERalpha/ERbeta ratio had lower oxidative stress, which could be partially explained by the increased expression of antioxidant enzymes and UCPs. Moreover, the action of E2 on the expression of antioxidant enzymes and UCPs was dual and dependent on the ERalpha/ERbeta ratio. Treatments with 0.1 nM E2 in cell lines with high ERalpha/ERbeta ratio produced a decrease in antioxidant enzymes and UCPs levels, with an increase in ROS production. These effects disappeared when the treatment was done in the presence of an ERalpha antagonist (MPP). In the cell lines with greatest levels of ERbeta and the lowest ERalpha/ERbeta ratio, E2 treatment caused the up-regulation of antioxidant enzymes and UCPs with a look-up decrease in ROS production. These effects were reversed when the cells were treated with E2 in the presence of an ERbeta antagonist (R,R-THC). On the whole, our results suggest a dual E2 effect; increasing or decreasing oxidative stress in part by modulation of UCPs and antioxidant enzymes according to the abundance ERbeta and ERalpha/ERbeta ratio in prostate cancer cell lines.

Mechanical alloying of biocompatible Co-28Cr-6Mo alloy.

We report on an alternative route for the synthesis of crystalline Co-28Cr-6Mo alloy, which could be used for surgical implants. Co, Cr and Mo elemental powders, mixed in an adequate weight relation according to ISO Standard 58342-4 (ISO, 1996), were used for the mechanical alloying (MA) of nano-structured Co-alloy. The process was carried out at room temperature in a shaker mixer mill using hardened steel balls and vials as milling media, with a 1:8 ball:powder weight ratio. Crystalline structure characterization of milled powders was carried out by X-ray diffraction in order to analyze the phase transformations as a function of milling time. The aim of this work was to evaluate the alloying mechanism involved in the mechanical alloying of Co-28Cr-6Mo alloy. The evolution of the phase transformations with milling time is reported for each mixture. Results showed that the resultant alloy is a Co-alpha solid solution, successfully obtained by mechanical alloying after a total of 10 h of milling time: first Cr and Mo are mechanically prealloyed for 7 h, and then Co is mixed in for 3 h. In addition, different methods of premixing were studied. The particle size of the powders is reduced with increasing milling time, reaching about 5 mum at 10 h; a longer time promotes the formation of aggregates. The morphology and crystal structure of milled powders as a function of milling time were analyzed by scanning electron microscopy and XR diffraction.

Auto-positive end-expiratory pressure during tracheal gas insufflation: testing a hypothetical model.

OBJECTIVE: The major benefit of tracheal gas insufflation (TGI) is an increase in CO2 elimination efficiency by removal of CO2 from the anatomical deadspace. In conjunction with mechanical ventilation, TGI may also alter variables that affect CO2 elimination, such as minute ventilation and peak airway pressure (peak Paw) and cause the development of auto-positive end-expiratory pressure (auto-PEEP). We tested the hypothesis that TGI-induced auto-PEEP alters ventilatory variables. We predicted that TGI-induced auto-PEEP offsets the beneficial effects of TGI on CO2 elimination and that keeping total PEEP (ventilator PEEP + auto-PEEP) constant enhances the CO2 elimination efficiency afforded by TGI. DESIGN: Prospective study of two series of patients with acute respiratory distress syndrome receiving mechanical ventilation. SETTING: Intensive care units at a university medical center. PATIENTS: Each series consisted of eight sequential hypercapnic patients. INTERVENTIONS: In series 1, we examined the effect of continuous TGI at 0 and 10 L/min on PaCO2, without compensating for the development of auto-PEEP. In series 2, we examined this same effect of continuous TGI while reducing ventilator PEEP to keep total PEEP constant. TGI-induced auto-PEEP was calculated based on dynamic compliance measurements during zero TGI flow conditions (deltaV/deltaP) after averaging the two baseline values for peak Paw and tidal volume and assuming compliance did not change between the zero TGI and TGI flow conditions (deltaVTGI/deltaPTGI). MEASUREMENTS AND MAIN RESULTS: In series 1, total PEEP increased from 13.2 +/- 3.2 cm H2O to 17.8 +/- 3.5 cm H2O without compensation for auto-PEEP (p = .01). PaCO2 decreased (p = .03) from 56.2 +/- 10.6 mm Hg (zero TGI) to 52.9 +/- 9.3 mm Hg (TGI at 10 L/min), a 6% decrement. In series 2, total PEEP was unchanged (p = NS). PaCO2 decreased (p = .03) from 59.5 +/- 10.4 mm Hg (zero TGI) to 52.2 +/- 8.3 mm Hg (TGI at 10 L/min), a 12% decrement. There was no significant change in PaO2; there were no untoward hemodynamic effects in either series. CONCLUSIONS: These data are consistent with the hypothesis that mechanical ventilation + TGI causes an increase in auto-PEEP that can blunt CO2 elimination. In addition to the ventilator modifications necessary to keep ventilatory variables constant when TGI is used, it is also necessary to reduce ventilator PEEP to keep total PEEP constant and further enhance CO2 elimination efficiency.

Tracheal gas insufflation. Limits of efficacy in adults with acute respiratory distress syndrome.

In mechanically ventilated adults with acute respiratory distress syndrome (ARDS), peak airway pressures (Paw(peak)) above 35 cm H(2)O may increase the risk of barotrauma or volutrauma. Tracheal gas insufflation (TGI), an adjunctive ventilatory technique, may facilitate a reduction in set inspiratory pressure in these patients, and thereby in the tidal volume (VT) and Paw(peak) used in their ventilation, without a consequent increase in arterial carbon dioxide tension (PaCO(2)). The purpose of this study was to: (1) assess the limits of efficacy of continuous TGI at two levels of decreased mechanical ventilatory support; and (2) determine an appropriate time interval after initiation of TGI at which to evaluate response. We prospectively studied eight adults with ARDS and increased airway pressures (40.2 +/- 2.7 cm H(2)O) who were managed with pressure-control ventilation (PCV). After obtaining baseline ventilatory and hemodynamic measures, we initiated TGI at 10 L/min, adjusting ventilator positive-end expiratory pressure (PEEP) to maintain baseline VT, and decreased the set inspiratory pressure by 5 cm H(2)O. Data were obtained after 30 and 60 min. Set inspiratory pressure was then decreased by an additional 5 cm H(2)O (total: 10 cm H(2)O), and data were again obtained after 30 min. Baseline (zero TGI) measures were then again recorded. Thirty minutes after decreasing the set inspiratory pressure by 5 cm H(2)O with TGI at 10 L/min, there was a 15% decrease in Paw(peak) and a 16% decrease in VT as compared with their baseline values. However, Pa(CO(2)) remained constant (59 +/- 10 mm Hg versus 57 +/- 6 mm Hg) (p = NS). There was no change in Pa(O(2)) or in hemodynamic variables, and no differences between variables, at 30 min versus 60 min in seven subjects. The remaining subject did not tolerate the reduction in set inspiratory pressure for 60 min. Thirty minutes after the set inspiratory pressure was decreased by 10 cm H(2)O with TGI at 10 L/min, there was a 26% decrease in Paw(peak) and a 26% decrease in VT. However, Pa(CO(2)) increased by 19% and Pa(O(2)) decreased by 13%. Six subjects completed this phase of the protocol for 30 min, and one subject completed it for 60 min. TGI can be used to rapidly facilitate a 5 cm H(2)O reduction in set inspiratory pressure without an increase in Pa(CO(2)). The ability to achieve a 5 cm H(2)O reduction in set inspiratory pressure without adverse physiologic effects was evident within 30 min. Attempts to further reduce set inspiratory pressure were not successful.

Tracheal gas insufflation improves ventilatory efficiency during metacholine-induced bronchospasm.

INTRODUCTION: Barotrauma and cardiovascular insufficiency are frequently encountered problems in patients with acute bronchospastic disease who require mechanical ventilation. Permissive hypercapnia is a recognized strategy for minimizing these adverse effects; however, it has potential risks. Tracheal gas insufflation (TGI) has been shown to increase carbon dioxide elimination efficiency and thus could permit mechanical ventilation at lower peak airway pressures without inducing hypercapnia. However, caution exists as to the impact of TGI on lung volumes, given that expiratory flow limitation is a hallmark of bronchospastic disease. PURPOSE: To examine these issues, we studied ventilatory and hemodynamic effects of continuous TGI as an adjunct to mechanical ventilation before and after methacholine-induced bronchospasm. MATERIALS AND METHODS: Ten anesthetized, paralyzed dogs were ventilated on volume-controlled mechanical ventilation during administration of continuous TGI (0, 2, 6, and 10 L/min) while total inspired minute ventilation (ventilator-derived minute ventilation plus TGI) was kept constant. In an additional step, with TGI flow of 10 L/min, total inspired minute ventilation was decreased by 30%. RESULTS: PaCO2 decreased (44 +/- 7 mm Hg at zero flow to 34 +/- 7 mm Hg at 6 L/min and 31 +/- 6 mm Hg at 10 L/min, respectively, P < .05), as did the dead space to tidal volume ratio at TGI of 6 and 10 L/min compared with zero flow. There were no significant changes in end-expiratory transpulmonary pressure, mean arterial pressure, or cardiac output. During the highest TGI flow (10 L/min), with a 30% reduction of total inspired minute ventilation, both PaCO2 and peak airway pressure remained less than during zero flow conditions. CONCLUSION: We conclude that TGI increases carbon dioxide elimination efficiency during constant and decreased minute ventilation conditions without any evidence of hyperinflation or hemodynamic instability during methacholine-induced bronchospasm.

Tracheal gas insufflation during pressure-control ventilation: effect of using a pressure relief valve.

OBJECTIVES: Pressure-control ventilation minimizes alveolar overdistention by limiting peak airway pressure, but a consequence of this pressure limitation may be a reduction in tidal volume with subsequent hypercarbia. Tracheal gas insufflation (TGI) can be used in combination with pressure-control ventilation to augment CO2 elimination. During pressure-control ventilation with continuous TGI, we observed that peak airway pressure increased above the set inspiratory pressure. Based on this observation, we investigated the ability of the pressure-control ventilator circuit to compensate for continuous TGI and the effect of insertion of a pressure relief valve to eliminate over-pressurization. SETTING: University research laboratory. DESIGN: Using an artificial lung model, we studied the effects of continuous TGI with varying catheter flows (0, 2, 6, and 10 L/ min); ventilator frequencies (10 and 20 breaths/min); inspiratory duty cycles (0.33, 0.50, and 0.67); lung compliance (0.01, 0.02, and 0.04 L/cm H2O); and airway resistance (5, 20, and 50 cm H2O/L/sec) on: a) peak airway pressure; b) total inspiratory tidal volume; c) ventilator-derived tidal volume; and d) intrapulmonary pressure at end-exhalation (auto-PEEP). Tests were performed with and without a pressure relief valve whose threshold "pop-off" pressure was adjusted to match the set inspiratory pressure (35 cm H2O) for a total of 432 experimental conditions. MEASUREMENTS AND MAIN RESULTS: Our data demonstrate that pressure-control ventilation augmented with continuous TGI can increase peak airway pressure above set inspiratory pressure due to delivery of a higher than intended tidal volume. Predisposing conditions include catheter flow rates of 6 and 10 L/min, long inspiratory time, low compliance, and low resistance. With the pressure relief valve, peak airway pressure was maintained at the set inspiratory pressure and total inspiratory tidal volume remained constant. CONCLUSION: A pressure relief valve is a necessary adjunct to maintain peak airway pressure at set inspiratory pressure and keep total inspiratory tidal volume constant when continuous TGI is administered in conjunction with pressure-control ventilation.

New ventilatory strategies in acute respiratory failure.

New management options for acute respiratory failure aim at avoiding ventilator-induced lung injury while maintaining adequate gas exchange. Selected approaches examined in this article include methods to augment carbon dioxide elimination with tracheal gas insufflation, venovenous extracorporeal carbon dioxide removal, and intravascular oxygenation. Improving oxygenation can be accomplished by judicious use of positive end-expiratory pressure, venoarterial extracorporeal membrane oxygenation, and pharmacologic intervention with inhaled nitric oxide.

Quantification of thrombelastographic changes after blood component transfusion in patients with liver disease in the intensive care unit.

Thrombelastography (TEG) can be used to monitor hemostasis and guide transfusion therapy during orthotopic liver transplantation. However, data are limited regarding the type and quantity of blood components necessary for TEG-guided blood component transfusion in coagulopathic critically ill patients with liver disease. We evaluated changes in four thrombelastogram variables (reaction time, thrombin constant time, alpha angle, and maximum amplitude) in whole blood samples after 74 separate blood component transfusions in 60 critically ill patients with a coagulopathy and liver disease. Only platelets significantly improved TEG variables in patients who received a single type of blood component. Each unit of platelets decreased the reaction and thrombin constant time by 0.43 (P < 0.05) and 0.82 (P < 0.005) min, respectively, increased the alpha angle by 1.5 degrees (P < 0.005), and the maximum amplitude by 1.4 mm (P < 0.005). In patients who received multiple blood components, cryoprecipitate decreased the thrombin constant time by 0.56 min/U (P < 0.05), and each unit of platelets decreased the thrombin constant time by 0.39 min (P < 0.005), and increased the alpha angle and maximum amplitude by 0.63 degrees (P < 0.05) and 0.99 mm (P < 0.005), respectively. We conclude that platelet transfusions, alone or in combination with other blood components, are most effective for improving abnormal TEG variables in coagulopathic critically ill patients with liver disease.

Cardiopulmonary responses to continuous positive airway pressure in acute asthma.

The effects of nasal continuous positive airway pressure (CPAP) on expiratory flow, arterial blood gas tensions, cardiovascular status, and dyspnea were studied in 21 patients with acute asthma. Therapy consisted of the following CPAP sequence: 30 minutes at 5 cm H2O, 20 minutes at 0 cm H2O, 30 minutes at 7.5 cm H2O, and 20 minutes at 0 cm H2O. Six control patients were fitted with a CPAP mask but given no positive-pressure therapy. Significant reductions in respiratory rate occurred from a baseline of 22.0 +/- 1.0 to 19.8 +/- 3.8 breaths/min at CPAP 5 cm H2O and to 19.4 +/- 4.3 breaths/min at CPAP 7.5 cm H2O (P < .05). No significant change occurred in forced expiratory volume in 1 second (FEV1), heart rate, mean arterial blood pressure, or arterial blood gas tension with either level of CPAP. Dyspnea, as assessed by a breathlessness score, improved during CPAP therapy (P < .05). These levels of CPAP were tolerated without deleterious side effects. In comparison, the control group showed no change in heart rate, respiratory rate, or breathlessness score during the study period. These data show that application of CPAP in acute asthma reduces respiratory rate and dyspnea with no untoward effects on gas exchange, expiratory airflow, or hemodynamics.

Continuous positive airway pressure in COPD patients in acute hypercapnic respiratory failure.

We used mask continuous positive airway pressure (CPAP) in seven patients with acute hypercapnic respiratory failure in an attempt to avoid endotracheal intubation and mechanical ventilation. Mask CPAP was started at 5 cm H2O and then increased to a maximum of 10 cm H2O depending on the clinical response. In five patients, CPAP significantly improved gas exchange; four of these patients were weaned to oxygen by face mask without needing intubation. In two patients, gas exchange deteriorated even with CPAP of 10 cm H2O. No barotrauma or adverse hemodynamic effects were associated with CPAP. We conclude that a trial of mask CPAP may be warranted before intubation of an alert, acutely hypercapnic patient with COPD.

The role of fiberoptic bronchoscopy for diagnosis of pulmonary tuberculosis in patients at risk for AIDS.

In patients with acquired immunodeficiency syndrome (AIDS)-associated pulmonary Mycobacterium tuberculosis (MTB) (group 1), we analyzed whether the addition of transbronchial biopsy (TBB) and bronchial brushings augmented the diagnostic MTB yield over nonbiopsy sampling. Positive acid-fast bacilli (AFB) smears from combined sputum, bronchoalveolar lavage (BAL), and washings were 30 percent compared with 37 percent when brushings and TBB were added (p = NS). The addition of TBB increased culture yield from 96 percent to 100 percent (p = NS). Similar results were seen in patients with pulmonary MTB without human immunodeficiency virus (HIV) risk factors (group 2). Group 1 patients most commonly had a nonspecific inflammation on TBB histopathology and had a lower incidence of granuloma formation than group 2 (p less than 0.05). Our results suggest that more invasive sampling with bronchial brushings and TBB does not contribute to the microscopic, bacteriologic, or histopathologic diagnosis of pulmonary MTB, independent of AIDS risk factors.

Ciliary motility in two patients with yellow nail syndrome and recurrent sinopulmonary infections.

The yellow nail syndrome (YNS) is described as a combination of yellow nails, chronic lymphedema, pleural effusions, and recurrent sinopulmonary infections, but all these features need not be present for the diagnosis. The mechanism that renders patients with this syndrome susceptible to respiratory infections is not known. To determine whether abnormal ciliary motility is a predisposing factor, in vitro ciliary beat frequency (CBF) was measured in two patients with YNS and recurrent respiratory infections. In each case, the CBF was within normal limits (12 Hz). These data suggest that abnormal ciliary motility is not a pathophysiologic mechanism of recurrent sinopulmonary infections in YNS.

Noncardiogenic pulmonary edema following laser therapy of a tracheal neoplasm.

Nd-YAG laser phototherapy has been demonstrated to be effective for the treatment of airways obstruction caused by tracheal tumors. Pulmonary edema has been reported as a complication following acute relief of an upper airway obstruction. We describe a case where laser photoresection of an endotracheal malignancy resulted in acute pulmonary edema. It is important to recognize this potential cause of respiratory deterioration following successful phototherapy to obstructing lesions of the upper airways.