Scanning magnetoresistance microscopy of atom chips.

Surface based geometries of microfabricated wires or patterned magnetic films can be used to magnetically trap and manipulate ultracold neutral atoms or Bose-Einstein condensates. We investigate the magnetic properties of such atom chips using a scanning magnetoresistive (MR) microscope with high spatial resolution and high field sensitivity. By comparing MR scans of a permanent magnetic atom chip to field profiles obtained using ultracold atoms, we show that MR sensors are ideally suited to observe small variations of the magnetic field caused by imperfections in the wires or magnetic materials which ultimately lead to fragmentation of ultracold atom clouds. Measurements are also provided for the magnetic field produced by a thin current-carrying wire with small geometric modulations along the edge. Comparisons of our measurements with a full numeric calculation of the current flow in the wire and the subsequent magnetic field show excellent agreement. Our results highlight the use of scanning MR microscopy as a convenient and powerful technique for precisely characterizing the magnetic fields produced near the surface of atom chips.

Nasal polyposis: clinical course during 20 years.

BACKGROUND: The etiology of nasal polyposis is mainly unknown although it has been connected with many clinical conditions. The long-term clinical course of nasal polyposis is largely unknown, because long-term followup studies on the recurrence of nasal polyposis have rarely been reported. OBJECTIVE: The aim of the study was to find out the clinical course of nasal polyposis over a long period of time. PATIENTS AND METHODS: Our report describes a 20-year follow-up study of 41 patients with nasal polyps. These patients had surgery for nasal polyp disease 20 years previously and they were initially grouped according to occurrence of (1) acetylsalicylic acid (ASA) intolerance, (2) atopic allergy (AT), and (3) intrinsic allergy-like disease (INTR). Patients were now re-examined, sinus computed tomography (CT) scanning was made, and a biopsy from polyp or from mucosa of the middle turbinate was taken. RESULTS: Anterior rhinoscopy revealed polyps in 35 of 41 patients. Thus nasal polyposis was still active in 85% of patients after 20 years. Mucosal changes in paranasal sinuses were found in every patient. Anosmia or hyposmia was found in 61% (25/41) of the patients. Eight patients had had 11 or more surgical operations during the 20-year period. Of these, 88% (7/8) belonged to the ASA group. Bronchial asthma was found in all ASA intolerance patients (11/11), and in 36% (4/11) of AT and in 16% (3/19) of INTR patients, respectively. CONCLUSION: Because of the high recurrence tendency and insidious symptoms of nasal polyposis, patients will require followup for the rest of their lives.

Vascular permeability factor/vascular endothelial growth factor in nasal polyps.

Although the aetiology of polyps is still, for the most part, unknown, the disease is known to involve tissue oedema. Vascular permeability/vascular endothelial growth factor (VPF/VEGF) is a major inducer of angiogenesis and capillary permeability. This study investigated VPF/VEGF expression in biopsies of nasal polyps from 39 patients and in healthy nasal mucosa from 10 patients by immunohistochemical staining. Staining for VPF/VEGF in the mucosal surface and in the glandular epithelium of nasal polyps was weaker than in normal controls. In two patients, strong staining for VPF/VEGF was found in a granular pattern in mast cells, while the mast cells in other polyposis patients appeared to be largely degranulated. VPF/VEGF was not seen in the mast cells of control patients. Although expression of VPF/VEGF was not increased in the epithelium of the nasal polyps, VPF/VEGF secreted from mast cells may take part in nasal polyp formation.

TCR-CD4 and TCR-TCR interactions as distinctive mechanisms for the induction of increased intracellular calcium in T-cell signalling.

Specific activation of CD4 T cells involves recognition of a peptide: MHC class II complex by the heterodimeric alpha beta TCR and its CD4 co-receptor. The activation of T cells initiates a signal transduction cascade that includes a substantial and rapid increase in cytosolic calcium. In this work we study the role of the interactions between the TCR and the CD4 molecule in inducing this [Ca2+]i increase in the cloned CD4 T-cell line D10. Ligating CD3 or the TCR with mAb leads to proliferation of this cloned line and an increase in intracellular free calcium. An exceptional antibody, 16A, was able to stimulate proliferation but did not induce an increase in intracellular free calcium, even when extensively cross-linked with anti-Ig. However, when 16A was cross-linked to CD4 a rise in [Ca2+]i was observed. This demonstrated the ability of TCR-CD4 interactions to trigger a [Ca2+]i response in a situation where no signal was obtained from TCR-TCR interactions. Because CD4 molecules can associate with the TCR, we also studied whether CD4 is involved in the observed increases in intracellular free calcium obtained with other anti-TCR antibodies. This was examined in CD4-negative T cells transfected with cDNA encoding the D10 TCR. These cells could be induced to flux calcium by the same anti-TCR antibodies that gave this response in D10 cells, and again 16A failed to induce such a response. In the transfectants, anti-CD3 antibodies, in contrast to TCR antibodies, could induce a calcium signal in the absence of cross-linking by anti-Ig indicating that CD3 antibodies may signal distinctly from alpha beta TCR ligation. These studies document that antibodies binding different TCR/CD3 epitopes signal distinctively, and that CD4 can participate in, but is not absolutely required for, the induction of increased intracellular calcium.

cAMP inhibits the OKT3-induced increase in cytoplasmic free calcium in the Jurkat T cell line: the degree of inhibition correlates inversely with the amount of CD3 binding ligand used.

We have investigated the effect of cAMP concentration on the CD3-mediated rise in intracellular Ca2+ induced by anti-CD3 monoclonal antibody in the human T cell leukemia line Jurkat. Forskolin, prostaglandin E2 (PGE2) and dibutyryl cAMP (db-cAMP) were used to increase intracellular cAMP concentrations. Treatment of Jurkat cells with forskolin or db-cAMP for 3 h inhibited the subsequent rise in intracellular Ca2+ concentration induced by an optimally mitogenic dose of 100 ng/ml of the anti-CD3 OKT3, whereas PGE2 counteracted the Ca2+ rise only marginally. The inhibitory effect of forskolin and PGE2 on the Ca2+ signal correlated with their abilities to induce increased cAMP levels in Jurkat cells. The suppression of the Ca2+ response was dependent on the concentration of the cAMP-elevating agent and the time of pre-incubation with the drug. The cAMP-mediated inhibition of the Ca2+ response diminished or disappeared when increasing concentrations of OKT3 were used to stimulate the rise in intracellular Ca2+ concentration. The results indicate that cAMP participates in the regulation of T lymphocyte activation at the level of signal transduction. Our findings, which stress the crucial role of the concentration of the ligand used to trigger Ca2+ responses, provide an explanation to previous contradictory reports on the impact of cAMP on the signal transduction in T cells.

A morphologic and fluorophotometric analysis of the corneal endothelium in long-term extended wear soft contact lens wearers.

Eleven extended wear soft contact lens wearers with an average of 4 years of wear underwent corneal fluorophotometry and quantitative specular microscopy. Compared to age-matched controls, a significant increase in mean endothelial permeability was found in the contact lens group, indicating a defect in their endothelial barrier function. A significant increase in the mean endothelial pump rate was also noted in the contact lens group. In addition, mean corneal thickness was significantly greater in the contact lens group. No significant difference was noted between the two groups in mean cell area and figure coefficient; however, the coefficient of variation was significantly higher in the contact lens group. Duration of contact lens wear correlated positively with coefficient of variation. An inverse correlation was noted between contact lens oxygen transmissibility and cell area, as well as corneal thickness. These data suggest both a morphologic and functional defect in the corneal endothelium of long-term extended wear soft contact lens wearers.

Kinetics of Ca2+ uptake into lectin-induced secondary lymphocytes during reactivation with concanavalin A or interleukin 2.

The kinetics of Ca2+ uptake into lectin-induced secondary lymphocytes was studied during reactivation to DNA synthesis with concanavalin A (Con A) or interleukin 2 (IL-2). IL-2 did not cause any significant uptake of Ca2+ into the lymphocytes, while Con A induced an accumulation of Ca2+ into the lymphocytes which reached a maximum 1 to 2 h after the addition of the lectin. The time during which Ca2+ uptake occurred corresponded to the time of dependence on extracellular Ca2+ for lectin-induced DNA synthesis. The increased rate of Ca2+ accumulation and the shortened Ca2+ dependence period of secondary lymphocytes as compared with primary lymphocytes could explain the ability of secondary lymphocytes to display an accelerated response, in terms of DNA synthesis, to re-stimulus.

Effects of calmodulin antagonists Cd2+ and trifluoperazine on mixed lymphocyte culture cell-mediated lysis and antibody-dependent cell cytolysis.

The effects of two substances with calmodulin-antagonistic properties, cadmium and trifluoperazine, were studied on mixed lymphocyte culture-cell mediated lysis (MLC-CML) and antibody-dependent cell cytolysis (ADCC). Both cadmium and trifluoperazine readily inhibited MLC-CMC, while ADCC was inhibited only to a small extent or not at all. Trifluoperazine almost completely inhibited phagocytosis in cells whose ability to lyse antibody-coated red blood cells was unimpaired. The results suggests a striking difference in the extent in which calmodulin mediated processes take part in MLC-CML on the one hand and ADCC on the other. This indicates a profound dissimilarity in the mechanisms of these two types of cell-mediated lysis.

Kinetics of long-term (72 hr) calcium content during mitogen activation of cultured human T lymphocytes.

In vitro stimulation of human blood lymphocytes with mitogen resulted in an increased intracellular content of Ca2+ per unit cell volume. This increase in Ca2+ content of lectin-activated cells reached a maximum after 24 hr of culture and thereafter slowly declined. Brief treatment of cells at 24 hr of culture with the Ca2+ ionophore A23187 in combination with EGTA resulted in a larger release of Ca2+ from cells in mitogen-stimulated cultures than from cells in control cultures. This indicates that the Ca2+ is accumulated intracellularly but is readily exchangeable. At 24 hr of culture the increase in cellular Ca2+ correlated well with the proliferative response as measured by 3H-thymidine incorporation. Ca2+ influx at 24 and 48 hr of culture was markedly enhanced in the mitogenically stimulated cells as compared either to cells cultured for 1 and 72 hr or cells cultured without mitogen.

Effects of Cd2+ upon Ca2+ fluxes and proliferation in concanavalin A-stimulated lymphocytes.

The mitogenic response of human peripheral blood lymphocytes to the lectin concanavalin A (conA) is inhibited by micromolar concentrations of CdCl2. This inhibition is partially relieved by an increase in the external Ca2+ concentration (from 0.6 to 2.2 mM). The initial rate of conA-induced 45Ca2+ influx is unaltered by CdCl2, although the level of 45Ca2+ accumulation increases. The basal rate of 45Ca2+ entry is not measurably disturbed by CdCl2 (100 microM). The steady-state efflux of 45Ca2+ and the calmodulin-activated (Ca2+ + Mg2+)-ATPase activity of erythrocyte ghosts are inhibited by CdCl2 (10 microM). Thus, the mechanism behind the Cd2+-induced suppression of the mitogenic response to conA is not due to alteration of mitogen-stimulated Ca2+ influx. We suggest that Cd2+ competes with Ca2+ for intracellular Ca2+-binding molecules, such as calmodulin, essential for the induction of cell proliferation.

Colecistite aguda em compartimento distal de vesicula bilobada com septacao transversal. / Acute cholecystitis in distal compartment of bilobate gallbladder with transversal septation

Trata-se de um caso raro, num menino de 10 anos que apresentava crises de dor no hipocondrio direito e epigastrico, em consequencia de colecistite aguda. No entanto os exames habitualmente realizados nesta situacao, revelaram-se normais. A suspeita diagnostica de anomalia de forma de vesicula so foi possivel na ocasiao pelo estudo laparoscopico, com o diagnostico definitivo atraves de cirurgia e estudo radiologico transoperatorio. Estes confirmaram a presenca de vesicula com septacao transoperatorio. Estes confirmaram a presenca de vesicula com septacao transversal, com formacao consequente de dois compartimentos isolados e com colecistite aguda no distal. Este tipo de anomalia de forma e extremamente raro. Mais raro ainda e a instalacao concomitante de colecistite aguda. Na literatura existe um caso descrito de colecistite aguda, mas em vesicula dupla

Concanavalin A binding and Ca2+ fluxes in rat spleen cells.

Addition of the mitogenic lectin concanavalin A to rat spleen cells results in a small increase in the steady-state Ca2+ content of the cells. 45Ca2+ fluxes were measured under conditions where artifacts due to Ca2+ binding to concanavalin A could be excluded. Both 45Ca2+ influx into and efflux from these cells are significantly activated by the lectin. If 45Ca2+ is added 30 min after concanavalin A the rate of influx is further enhanced. The increase in 45Ca2+ influx correlates well with binding of concanavalin A to the cells. At low concentrations (optimal mitogenic) of the lectin (1 and 3 micrograms/ml) no significant increase in 45Ca2+ influx occurs but an increase in 45Ca2+ efflux is still observed. The results suggest that concanavalin A binding to the cell surface causes an increase in Ca2+ influx into the cells and that activation of Ca2+ efflux occurs as a response to an increase in the cytosolic Ca2+ activity. Thus, Ca2+ may well play a role in triggering lymphocyte activation.

Cistos solitarios, nao parasitados de figado. / Solitary non-parasitic hepatic cysts

Os autores apresentam sua experiencia com tres casos de cistos isolados de figado, nao parasitado. Abordam o quadro clinico, os meios de diagnostico e a conduta cirurgica. Chamam a atencao para o diagnostico diferencial como o cisto hidatico, especialmente, quando o doente provem de zona endemica