A combination of predispositions and exposures as responsible for acute eosinophilic pneumonia.

BACKGROUND: Acute eosinophilic pneumonia (AEP) is a rare febrile illness which is characterized by respiratory failure and often requires mechanical ventilation. The causes and sequence of events of this disease at a biochemical and histological level remain largely unknown. In this article we report the exceptional case, possibly unique, of a patient who developed AEP and three pneumothoraces within less than one month during her hospitalization. CASE PRESENTATION: A 39-year-old German woman was admitted to our hospital for a laparoscopy-assisted vaginal hysterectomy under general anaesthesia. The surgical intervention was followed by peritonitis in the early postoperative course. Following anaesthesia induction with propofol/midazolam and during the prolonged therapy with several broad-spectrum antibiotics, she developed AEP and three spontaneous (one left-sided and two right-sided) pneumothoraces, the latter ones observed in quick succession. Symptoms, laboratory markers, and chest radiology significantly improved after a one-day treatment with methylprednisolone. CONCLUSIONS: On the whole, these pathological occurrences, together with similar cases reported in literature, can support the conclusion of possible predisposing genetic factors at the lung tissue level of AEP patients, a view that might shed new light on the pathogenesis of this disease. To provide a coherent pattern that explains the reported evidence for AEP and pneumothoraces, independently from the causative stimulus, the supposed molecular mutations could be localized in the connective tissue rather than in the epithelial cells. In order to interpret clinical and laboratory evidence, as well as to support the main conclusions, the important part of scientific research here presented can also assist physicians in making more informed decisions for the treatment of patients with pulmonary infiltrates.

The how, when, and why of the aging signals appearing on the human erythrocyte membrane: an atomic force microscopy study of surface roughness.

We recently developed an atomic force microscopy-based protocol to use the roughness of the plasma membrane of erythrocytes (red blood cells, RBCs) as a morphological parameter, independently from the cell shape, to investigate the membrane-skeleton integrity in healthy and pathological cells. Here we apply the method to investigate a complex physiological phenomenon, the RBCs aging, that plays a major role in the regulation of the RBCs' turnover. The aging, monitored morphologically and biochemically, has been accelerated and modulated by preventing oxidative stresses as well as the effects of proteases and divalent cations, and by artificially consuming the intracellular adenosine triphosphate. The collected data evidence that the progression of aging causes a drastic decrease of the measured roughness that is diagnostic of a progressive, adenosine triphosphate-dependent alteration of the membrane-skeleton properties. Finally, the degree of reversibility of such effects has been investigated as a function of aging time, enabling the detection of irreversible transformation in the RBCs' structure and metabolism.

Erythrocyte death in vitro induced by starvation in the absence of Ca(2+).

Human erythrocytes (RBCs), stored at 4 degrees C under nominal absence of external energy sources and calcium ions, show a gradual decrease in membrane roughness (R(rms)) at the end of which the appearance of morphological phenomena (spicules, vesicles and spherocytes) is observed on the cell membrane, phenomena that can mainly be ascribed to the ATP-dependent disconnection of the cortical cytoskeleton from the lipid bilayer. After depletion of the intracellular energy sources obtained under the extreme conditions chosen, treatment with a minimal rejuvenation solution makes the following remarks possible: (i) RBCs are able to regenerate adenosine triphosphate (ATP) and 2,3-bisphosphoglycerate only up to 4 days of storage at 4 degrees C, whereas from the eighth day energy stocks cannot be replenished because of a disorder in the transmembrane mechanisms of transport; (ii) the RBCs' roughness may be restored to the initial value (i.e. that observed in fresh RBCs) only in samples stored up to 4-5 days, whereas after the eighth day of storage the rejuvenation procedure appears to be inefficient; (iii) membrane physical properties - as measured by R(rms) - are actually controlled by the metabolic production of ATP, necessary to perform the RBCs' basic functions; (iv) once energy stores cannot be replenished, a regulated sequence of the morphological events (represented by local buckles that lead to formation of spicules and vesicles of the lipid bilayer with generation of spherocytes) is reminiscent of the RBCs' apoptotic final stages; (v) the morphological phenomenology of the final apoptotic stages is passive (i.e. determined by simple mechanical forces) and encoded in the mechanical properties of the membrane-skeleton; and (vi) necrotic aspects (e.g. disruption of cell membrane integrity, so that intracellular protein content is easily released) ensue when RBCs are almost totally (> or =90%) depleted in an irreversible way of the energetic stores.