Anther and pollen development in some species of Poaceae (Poales).

Anther and pollen development were studied in Olyra humilis Nees, Sucrea monophylla Soderstr, (Bambusoideae), Axonopus aureus P. Beauv., Paspalum polyphyllum Nees ex Trin. (Panicoideae), Eragrostis solida Nees, and Chloris elata Desv. (Chloridoideae). The objective of this study was to characterise, embryologically, these species of subfamilies which are considered basal, intermediate and derivate, respectively. The species are similar to each other and to other Poaceae. They present the following characters: tetrasporangiate anthers; monocotyledonous-type anther wall development, endothecium showing annular thickenings, secretory tapetum; successive microsporogenesis; isobilateral tetrads; spheroidal, tricellular, monoporate pollen grains with annulus and operculum. Nevertheless, the exine patterns of the species studied are distinct. Olyra humilis and Sucrea monophylla (Bambusoideae) show a granulose pattern, whereas in the other species, it is insular. In addition, Axonopus aureus and Paspalum polyphyllum (Panicoideae) have a compactly insular spinule pattern, while Chloris elata and Eragrostis solida (Chloridoideae) show a sparsely insular spinule pattern. The exine ornamentation may be considered an important feature at the infrafamiliar level.

The serologic response of horses to equine arteritis virus as determined by competitive enzyme-linked immunosorbent assays (c-ELISAs) to structural and non-structural viral proteins.

In an effort to further characterize the humoral immune response of horses to equine arteritis virus (EAV), direct and competitive enzyme-linked immunosorbent assays (c-ELISAs) were developed using monoclonal and polyclonal anti-sera to structural (G(L), N and M) and non-structural (nsp1) viral proteins. A nsp1-specific monoclonal antibody was produced to facilitate development of a c-ELISA to this protein. Data obtained using the various c-ELISAs confirm that the M protein is a major target of the antibody response of horses to EAV. However, none of the c-ELISAs that were developed were as sensitive in detecting EAV-specific antibodies in horse sera as the existing serum neutralization test.

[Space occupying lesion in the anterior mediastinum in a patient with Basedow disease and previously diagnosed osteosarcoma]. / Raumforderung im vorderen Mediastinum bei einer Patientin mit Morbus Basedow und einem Osteosarkom in der Vorgeschichte.

HISTORY AND CLINICAL FINDINGS: A 24-year-old woman with osteosarcoma of the right thigh, diagnosed 12 years ago, complained at a follow-up examination of decreased exercise tolerance, increased nervous tension, heat intolerance, weight loss, hair loss and irregular stools. Examination revealed tachycardia (100/min), mild exophthalmus and a small goitre. INVESTIGATIONS: A decreased basal TSH level (0.002 mU/ml), raised peripheral thyroid hormone (fT4 6.7 ng/dl, total T3 7.8 micrograms/l) and a TSH receptor antibody titre of 33.4 U/l) were compatible with immune type Graves' disease. Radiology revealed an upper mediastinal space-occupying lesion which scintigraphically was separate from thyroid tissue. A metastasis of the osteosarcoma or thymus hyperplasia were considered the most likely cause. TREATMENT AND COURSE: The mediastinal lesion regressed under thyrostatic treatment with carbimazole (20 mg daily by mouth). But the clinical picture, localization and negative scintigraphy provided the diagnosis of transitory thymus hyperplasia in the course of Graves' disease. CONCLUSION: In immune type Graves' disease with a mediastinal space-occupying lesion, not only intrathoracic goitre but also thymus hyperplasia should be considered in the differential diagnosis.

Analysis of the coding sequence for the GM-CSF receptor alpha and beta chains in patients with juvenile chronic myeloid leukemia (JCML).

Peripheral blood granulocyte-macrophage progenitors (CFU-GMs) from patients with juvenile chronic myeloid leukemia (JCML) are able to proliferate spontaneously in the absence of exogenous growth factors and studies have shown that these progenitors display a hypersensitive growth response to GM-colony-stimulating factors (CSFs) in culture. We screened RNA from six patients with JCML for mutations in the GM-CSF receptor (GM-CSFR) coding sequence using RT-PCR-SSCP. Altered patterns were found in five patients for the GM-CSFR alpha chain, and in five patients for the beta chain. Two nucleotide substitutions accounted for all alpha chain abnormalities; one was conservative for Val333 and the other caused an Ala17-->Gly substitution. Both had previously been detected in normal controls. Sequencing of beta chain abnormalities revealed four base substitutions. Three were previously described polymorphisms, one causing a Pro603-->Thr substitution and two conservative point mutations involving Ser426 and Pro648. A further nucleotide mutation, which resulted in a Glu249-->Gln substitution, was also found but is not thought to be of pathological significance. Polymorphisms of the GM-CSFR alpha and beta chains are common, but pathogenic point mutations of the GM-CSFR are infrequent in patients with JCML and are unlikely to be involved in the hypersensitivity to GM-CSF demonstrated by progenitor cells.

The beta subunit common to the GM-CSF, IL-3 and IL-5 receptors is highly polymorphic but pathogenic point mutations in patients with acute myeloid leukaemia (AML) are rare.

The intracytoplasmic tail of the granulocyte-macrophage colony-stimulating factor receptor (GM-CSFR) beta c chain is essential for the activation of ligand-mediated signal transduction pathways in myeloid cells. Alterations in this region could deregulate normal signalling processes. We have therefore used RT-PCR-SSCP analysis of the receptor tail to look for point mutations in RNA from 35 patients with acute myeloid leukaemia (AML) and 10 haematologically normal controls. Patterns differing from those of the haemopoietic cell line TF-1 were detected in 25/35 (71%) AML patients and 8/10 (80%) normal controls. A total of six base substitutions were identified by sequencing. Three were conservative for the amino acid involved, three led to amino acid differences, valine652-->methionine, glycine647-->valine and proline603-->threonine. One alteration was found only in a normal control, the other five were all found in both AML patients and normal controls suggesting that they were DNA polymorphisms. Two substitutions were particularly common with allele frequencies of 0.23 (G1972-->A, unchanged proline648) and 0.13 (C1306-->T, unchanged serine426). These results indicate that the GM-CSFR beta c chain is highly polymorphic but point mutations of the intracytoplasmic tail do not appear to contribute frequently to the pathogenesis of AML.

Analysis of mutations in the GM-CSF receptor alpha coding sequence in patients with acute myeloid leukaemia and haematologically normal individuals by RT-PCR-SSCP.

Mutations of signal transducing molecules such as Ras have been shown to confer a growth advantage in leukaemic blasts and contribute to the pathogenesis of the disease. Alterations of signal transducing molecules other than Ras may play a role in leukaemogenesis. Knowledge of such mutations could also further our understanding of the normal signalling processes. We have therefore studied the coding sequence of the GM-CSF receptor alpha chain (GM-CSFR alpha) in patients with acute myeloid leukaemia (AML) and non-AML controls using single strand conformation polymorphism (SSCP) analysis. Abnormalities were detected in 4/32 AML patients (13%) and 2/15 non-AML controls (13%). Direct sequencing of PCR products revealed five different base substitutions. Three were conservative, two caused amino acid changes. The base substitution leading to amino acid change alanine to glycine at position 17 was found in both an AML patient and a control. It lies in the signal sequence and does not affect the mature protein. The other base change altering arginine to glutamine at position 164 is unlikely to influence the receptor structure as this structural position in the chain is not well conserved in members of the cytokine receptor family. Both amino acid changes were constitutive alterations as they could be demonstrated in the patients' children. The base changes described in the AML patients thus represent polymorphisms and do not contribute to the pathogenesis of AML.

Interferon-gamma inhibits the efficacy of interleukin 1 to generate a Th2-cell biased immune response induced by Leishmania major.

Splenic adherent cells from L. major-infected resistant and susceptible mice were restimulated in vitro and analyzed for the expression of IL-1 activity. Three weeks or later after infection, cells from parasite infected susceptible BALB/c mice produced substantially more IL-1 activity than those from non-infected controls or from L. major-infected resistant C57BL/6 animals. More than 95% of the IL-1 bioactivity was mediated by IL-1 alpha, as determined by blocking experiments with an anti-IL-1 alpha antiserum. The strain-specific differences in IL-1 production correlated with different accumulation of IL-1 producing adherent cells in the spleens of infected animals, but also with different IL-1 producing capacity on a per cell basis. When adherent cells were mixed with syngeneic IFN-gamma producing CD4+ T lymphocytes from L. major-infected C57BL mice or from animals that had been pretreated with anti-CD4 monoclonal antibody prior to infection, the level of detectable IL-1 decreased depending on the number of T cells added. This inhibition could be blocked completely with an anti-IFN-gamma antibody. No such effect was seen, when CD4+ cells were used that were derived from parasite-infected BALB/c mice and did not produce IFN-gamma. In contrast to L. major, L. donovani antigen not only failed to induce IL-1 production, but also dose-dependently suppressed the IL-1 activity elaborated by L. major antigen. We conclude from these data that IFN-gamma effectively inhibits the efficacy to IL-1 to generate to Th2-cell biased immune response induced by L. major. A T cell independent and as yet unknown mechanism to inhibit the IL-1 response is used by L. donovani.

Effects of lipoic acid in hexacarbon-induced neuropathy.

The effects of lipoic acid on hexacarbon neurotoxicity in rats were investigated. Rats were exposed by inhalation to n-hexane for 24 hours/day, 7 days/week, up to a total period of 9 weeks. Eight animals were exposed to 700 ppm n-hexane only, and eight animals were exposed to 700 ppm n-hexane and additionally received 100 mumol/kg lipoic acid PO daily. Clinical status of the animals was evaluated by examination of general condition, motor performance tests and neurophysiological measurements of caudal nerve motor conduction velocity. Results showed that animals exposed to 700 ppm n-hexane developed severe motor neuropathy leading to paralysis by the 6th week. Motor distal latencies of these animals were severely prolonged. In contrast, in animals treated with lipoic acid the onset of motor neuropathy was delayed for approximately 3 weeks as could be demonstrated by motor performance tests and measurements of motor distal latencies.

Relationship between the airway response to inhaled sulfur dioxide, isocapnic hyperventilation, and histamine in asthmatic subjects.

To determine whether bronchoconstriction induced by sulfur dioxide can be predicted by the airway response to inhaled histamine, we exposed on two days 46 patients with asthma to air or 0.5 ppm SO2. The exposure protocol consisted of 10 min of tidal breathing followed by 10 min of isocapnic hyperventilation at a rate of 30 l/min. Airway response was measured before (baseline) and after hyperventilation in terms of specific airway resistance, SRaw. Exposure to air increased baseline mean (SD) SRaw from 6.27 (2.12) to mean (SD) maximum post-hyperventilation SRaw of 9.10 (4.38) cmH2O*s (P less than 0.0001). Exposure to SO2 increased mean (SD) baseline SRaw from 6.93 (3.29) to mean (SD) maximum post-hyperventilation SRaw of 18.21 (18.69) cmH2O*s (P less than 0.0001). Mean (SD) effect of SO2 defined as difference between maximum post-hyperventilation SRaw after SO2 versus air was 9.11 (16.14) cm H2O*s. When evaluated individually, 26 and 34 of the 46 patients showed an airway response to hyperventilation of air and SO2, respectively. Airway response to histamine was determined as the histamine concentration necessary to increase specific airway resistance by 100%, PC100SRaw. The airway response after SO2 and PC100SRaw showed a weak but significant correlation (R = -0.48), whereas the responses to hyperventilation and SO2 did not correlate. We suggest that the mechanisms by which histamine and SO2 exert their bronchomotor effects are different and that in asthmatic patients the risk of pollutant-induced asthmatic symptoms can be poorly predicted by histamine responsiveness.

Comparing the effects of perinatal and later childhood lead exposure on neuropsychological outcome.

Blood lead values (PbB) from cord blood and maternal samples as well as present PbB from venous blood samples were available for 114 six- to seven-year-old children living in or near the city of Nordenham (FRG). These children represented 30% of all children born between July 1975 and August 1976 in the district hospital (N = 383). The range of cord blood PbB was 4-31 micrograms/100 ml (mean = 8.2 micrograms/100 ml) and of maternal PbB was 4-30 micrograms/100 ml (mean = 9.3 micrograms/100 ml), whereas the range for present PbB was 3.9-22.8 micrograms/100 ml (mean = 8.2 micrograms/100 ml). The degree of correlation between maternal and cord blood PbB was 0.79, despite the poor technical quality of many cord blood samples as compared to maternal blood samples (less coagulation). These children were given a battery of neurophysiological and neuropsychological tests. The present report is restricted to psychological performance measures. The test battery covered intelligence (reduced Wechsler Intelligence Scale for Children), visual-motor performance (Bender Test, GFT), serial reaction performance (Wiener Reaction Device), and cued as well as choice reaction times. After correction for confounding by means of stepwise multiple-regression analysis, few significant associations between blood lead levels and performance deficit occurred. In general the degree of association was somewhat stronger for present PbB than for perinatal PbB: With increasing present PbB there was a borderline drop of performance IQ (P less than 0.1), as well as a significant disruption of serial reactions, which was more pronounced for the difficult (P less than 0.01) than for the easier version of the Wiener Device (P less than 0.05). A similar but less pronounced pattern of associations was observed for maternal PbB but not for cord blood PbB. Some influence of perinatal lead exposure on later performance can, thus, still be detected if, in addition to cord blood PbB, maternal PbB is taken into account as well.