Electronically soft phases in manganites.

The phenomenon of colossal magnetoresistance in manganites is generally agreed to be a result of competition between crystal phases with different electronic, magnetic and structural order; a competition which can be strong enough to cause phase separation between metallic ferromagnetic and insulating charge-modulated states. Nevertheless, closer inspection of phase diagrams in many manganites reveals complex phases where the two order parameters of magnetism and charge modulation unexpectedly coexist. Here we show that such experiments can be naturally explained within a phenomenological Ginzburg-Landau theory. In contrast to models where phase separation originates from disorder or as a strain-induced kinetic phenomenon, we argue that magnetic and charge modulation coexist in new thermodynamic phases. This leads to a rich diagram of equilibrium phases, qualitatively similar to those seen experimentally. The success of this model argues for a fundamental reinterpretation of the nature of charge modulation in these materials, from a localized to a more extended 'charge-density wave' picture. The same symmetry considerations that favour textured coexistence of charge and magnetic order may apply to many electronic systems with competing phases. The resulting 'electronically soft' phases of matter with incommensurate, inhomogeneous and mixed order may be general phenomena in correlated systems.

Ultrastructural localization of anionic sites and lectin-binding sites in sarcoid human alveolar macrophages during interaction with T-lymphocytes.

Sarcoidosis alveolitis is caused by an unknown stimulus activating alveolar macrophages (AM) and T-lymphocytes. During antigen presentation, the complex HLA class II molecule/processed peptide, on the surface of sarcoid AM, induces the T-lymphocyte to proliferate. Altered glycosylation patterns of cell surface glycoproteins such as class II molecules in inflammatory states, may enhance the antigen-presenting capability of AM. In order to know if anionic sites and lectin-binding sites take part in the process of antigen presentation by alveolar macrophages, cells obtained from bronchoalveolar lavage of patients with pulmonary sarcoidosis were incubated with cationized ferritin (CF) and colloidal gold complexed lectins (BSL-I-A4; RCA-I; RCA-II; WGA) for 30 min at 4 degrees C. After incubation, the cells were fixed with 4% paraformaldehyde, 2% glutaraldehyde, postfixed, and Epon embedded. The CF particles were uniformly distributed over the entire cell surface of the lymphocyte, and formed clusters on the surface of the macrophage mainly at the adhesion region between the AM and the lymphocytes. We found enhanced binding of BSL-I-A4 by AM, while WGA and RCA were poorly taken up by these cells. Gold-BSL-I-A4 was distributed randomly on the plasma membrane of the AM, and clustered in the adhesion region with lymphocytes. These results suggest that anionic sites and alpha-D-N-acetyl-galactosamine residues labeled with gold-BSL-I-A4 may be involved in the process of antigen presentation by sarcoid alveolar macrophages.

Ultrastructural study of expression of adhesion molecules between blood monocytes and alveolar macrophages from patients with pulmonary sarcoidosis.

Pulmonary sarcoidosis is a chronic inflammatory disorder characterized by the presence of activated T cells and alveolar macrophages at sites of inflammation. These cells are recovered from bronchoalveolar lavage (BAL) from sarcoid patients in order to evaluate the expression of various markers on cell surfaces that should determine the diagnosis in sarcoidosis. In this work we compared the expression of VLA-4, VLA-5, Mac-1, ICAM-1 and VCAM- 1 adhesion molecules, at ultrastructural level, between blood monocytes and alveolar macrophages obtained from BAL, from patients with pulmonary sarcoidosis. Cells obtained from blood and BAL were fixed, embedded in LRWhite and then ultrathin sections were incubated with monoclonal antibodies against VLA-4, VLA-5, Mac-1, ICAM-1 and VCAM-1. The results showed a more evident labelling of all adhesion molecules on alveolar macrophages when compared to blood monocytes. The labelling was seen at cell surface, at cytoplasm and small vacuoles. The differences on adhesion molecule distributions from blood monocytes to alveolar macrophages suggest that changes in the expression of these molecules occur during pulmonary inflammatory response. Lymphocytes from BAL or blood had a weak label for these molecules.

Cardiopulmonary disease in Manson's schistosomiasis.

Five patients with cardiopulmonary manifestations of Manson's schistosomiasis are described. Two patients had pulmonary hypertension, two had cyanosis and one had the very rare combination of both. The results of routine pulmonary function tests--not sufficiently studied in this form of schistosomiasis--are discussed in detail. Aside from a tendency to hyperventilate, found in all cases, the only significant abnormality encountered was hypoxemia due to increased right-to-left shunt in the cyanotic patients. Although more studies are needed, the results suggest that the pulmonary lesions are mainly vascular in nature. The pathogenesis of cyanosis in this disease is briefly discussed.

Calcaneal "L" osteotomy: a retrospective study.

In this retrospective study of 36 patients and 58 feet, the "L" shaped osteotomy of the calcaneus body was investigated. The procedure, designed to add intrinsic stability to the shape of the osteotomy, was performed to correct triplane deformities of the heel in a variety of pathologic foot types. A retrospective analysis of clinical and radiographic data suggests that this procedure is a valuable alternative for surgical treatment of deformities of the calcaneus. Advantages appear to be predictability, stability, and versatility with respect to triplane reduction of deformities. A reliable method of evaluating calcaneal position both perioperatively and intraoperatively is also presented.