SAXS studies of the thermally-induced fusion of diblock copolymer spheres: formation of hybrid nanoparticles of intermediate size and shape.

Dilute dispersions of poly(lauryl methacrylate)-poly(benzyl methacrylate) (PLMA-PBzMA) diblock copolymer spheres (a.k.a. micelles) of differing mean particle diameter were mixed and thermally annealed at 150 °C to produce spherical nanoparticles of intermediate size. The two initial dispersions were prepared via reversible addition-fragmentation chain transfer (RAFT) dispersion polymerization of benzyl methacrylate in n-dodecane at 90 °C. Systematic variation of the mean degree of polymerization of the core-forming PBzMA block enabled control over the mean particle diameter: small-angle X-ray scattering (SAXS) analysis indicated that PLMA39-PBzMA97 and PLMA39-PBzMA294 formed well-defined, non-interacting spheres at 25 °C with core diameters of 21 ± 2 nm and 48 ± 5 nm, respectively. When heated separately, both types of nanoparticles regained their original dimensions during a 25-150-25 °C thermal cycle. However, the cores of the smaller nanoparticles became appreciably solvated when annealed at 150 °C, whereas the larger nanoparticles remained virtually non-solvated at this temperature. Moreover, heating caused a significant reduction in mean aggregation number for the PLMA39-PBzMA97 nanoparticles, suggesting their partial dissociation at 150 °C. Binary mixtures of PLMA39-PBzMA97 and PLMA39-PBzMA294 nanoparticles were then studied over a wide range of compositions. For example, annealing a 1.0% w/w equivolume binary mixture led to the formation of a single population of spheres of intermediate mean diameter (36 ± 4 nm). Thus we hypothesize that the individual PLMA39-PBzMA97 chains interact with the larger PLMA39-PBzMA294 nanoparticles to form the hybrid nanoparticles. Time-resolved SAXS studies confirm that the evolution in copolymer morphology occurs on relatively short time scales (within 20 min at 150 °C) and involves weakly anisotropic intermediate species. Moreover, weakly anisotropic nanoparticles can be obtained as a final copolymer morphology over a restricted range of compositions (e.g. for PLMA39-PBzMA97 volume fractions of 0.20-0.35) when heating dilute dispersions of such binary nanoparticle mixtures up to 150 °C. A mechanism involving both chain expulsion/insertion and micelle fusion/fission is proposed to account for these unexpected observations.

Impact of enteral feeding on gastric tonometry in healthy volunteers and critically ill patients.

BACKGROUND: Enteral feeding may interfere with gastric tonometry measurement. The effect of enteral nutrition on gastric tonometry has not been fully documented. METHODS: Seven healthy volunteers and nine stable intensive care unit (ICU) patients with poor tolerance of gastric feeding were investigated. Consecutive continuous postpyloric and gastric feeding, both at two different rates (40 and 100 ml. h-1, respectively), and an intragastric 200 ml nutrition bolus were studied. Gastric intramucosal PCO2 (PiCO2) was measured by air tonometry and in patients a gastric intramucosal-arterial PCO2 difference (PCO2 gap) was calculated. Hemodynamics and blood gases were also measured. RESULTS: In volunteers, PiCO2 remained stable during the postpyloric phase. During continuous gastric feeding PiCO2 did not change significantly, although in 4 volunteers PiCO2 increased >0.5 kPa. PiCO2 decreased significantly after gastric bolus from 6.9+/-0.4 to 6.1+/-0.5 kPa (P<0.05). Eight patients had an increased PCO2 gap (>1 kPa) at baseline (1.8+/-0.6 kPa). PCO2 gap changes during the whole study were not statistically significant. However, during the postpyloric phase (or immediately afterwards), the PCO2 gap increased by more than 0.5 kPa in 5 patients. After gastric bolus, a decrease in PCO2 gap >0.5 kPa was seen in 5 patients. CONCLUSION: In volunteers, postpyloric feeding does not interfere with gastric tonometry measurement and gastric bolus leads to a PiCO2 decrease. The impact of postpyloric and gastric feeding on gastric tonometry in ICU patients with compromised gut is variable.

[Acute respiratory distress syndrome]. / Akutní respiracní distress syndrom.

Acute respiratory distress syndrome (ARDS) is the general term used for severe acute respiratory failure of diverse aetiology. It is associated with a high morbidity, mortality (50-70%), and financial costs. Regardless of aetiology, the basic pathogenesis of ARDS is a systemic inflammatory response leading to a diffuse inflammatory process that involves both lungs, thus causing diffuse alveolar and endothelial damage with increased pulmonary capillary permeability and excessive extravascular lung water accumulation. ARDS is commonly associated with sepsis and multiple organ failure. The clinical picture involves progressive hypoxaemia, radiographic evidence of pulmonary oedema, decreased lung compliance and pulmonary hypertension. Despite the scientific and technological progress in critical care medicine, there is no specific ARDS therapy available at the moment and its management remains supportive. Therapeutic goals include resolution of underlying conditions, maintenance of acceptable gas exchange and tissue oxygenation and prevention of iatrogenic lung injury. Many new specific therapeutic strategies have been developed, however, most of them require further scientific evaluation. The paper reviews definition, basic pathogenesis and pathophysiology of ARDS and discusses current concepts of therapeutic possibilities of ARDS.

Continuous venovenous hemodiafiltration (CVVHDF) with citrate anticoagulation in the treatment of a patient with acute renal failure, hypercalcemia, and thrombocytopenia.

A 72-year-old patient with multiple myeloma was admitted to the intensive care unit because of hypercalcemic crisis and acute renal failure. After 7 days of comprehensive therapy including diuretics steroids, calcitonin, and intermittent hemodialysis (IHD) with low-calcium dialysate, calcium still reached high levels between IHD treatments and thrombocytopenia developed after chemotherapy. CVVHDF with calcium-free bicarbonate dialysate was started. Anticoagulation with 2.2% citrate was performed in order to chelate calcium, and thus treat the hypercalcemia, and to provide regional anticoagulation, and thus reduce the risk of bleeding due to thrombocytopenia. CVVHDF with citrate anticoagulation was continued for 6 days, and standard heparin anticoagulation was started when the hypercalcemia and thrombocytopenia abated.