Is floral diversification associated with pollinator divergence? Flower shape, flower colour and pollinator preference in Chilean Mimulus.

BACKGROUND AND AIMS: Adaptation to different pollinators is thought to drive divergence in flower colour and morphology, and may lead to interspecific reproductive isolation. Floral diversity was tested for association with divergent pollinator preferences in a group of four closely related wildflower species: the yellow-flowered Mimulus luteus var. luteus and the red-pigmented M. l. variegatus, M. naiandinus and M. cupreus. METHODS: Patterns of pollinator visitation were evaluated in natural plant populations in central Chile, including both single-species and mixed-species sites. Floral anthocyanin pigments were identified, and floral morphology and nectar variation were quantified in a common garden experiment using seeds collected from the study sites. KEY RESULTS: Mimulus l. luteus, M. l. variegatus and M. naiandinus are morphologically similar and share a single generalist bumblebee pollinator, Bombus dahlbomii. Mimulus cupreus differs significantly from the first three taxa in corolla shape as well as nectar characteristics, and had far fewer pollinator visits. CONCLUSIONS: This system shows limited potential for pollinator-mediated restriction of gene flow as a function of flower colour, and no evidence of transition to a novel pollinator. Mimulus cupreus may experience reduced interspecific gene flow due to a lack of bumblebee visitation, but not because of its red pigmentation: rare yellow morphs are equally undervisited by pollinators. Overall, the results suggest that factors other than pollinator shifts may contribute to the maintenance of floral diversity in these Chilean Mimulus species.

Intrinsic hyperreactivity of mucosal T cells to interleukin-2 in pediatric Crohn's disease.

OBJECTIVES: To cells play a crucial role in many chronic inflammatory diseases. Mucosal T cells are particularly important in the pathogenesis of Crohn's disease (CD). We investigated the response of T cells in CD and other intestinal inflammatory conditions to interleukin-2 (IL-2), a cytokine essential for T-cell activation, growth, and function. STUDY DESIGN: T-cell reactivity was assessed by measuring growth induced by IL-2 in mucosal endoscopic biopsy specimens obtained from children with CD, ulcerative colitis, indeterminate colitis, and chronic nonspecific colitis and from children without gastrointestinal inflammation. RESULTS: CD mucosal T cells grew remarkably and significantly more than T cells from normal, ulcerative colitis, and chronic nonspecific colitis mucosa. T cells from indeterminate colitis mucosa grew similarly to those of CD mucosa. The enhanced growth response in CD was independent of disease location, presence or absence of intestinal inflammation, treatment, disease duration, or clinical activity. CONCLUSION: Mucosal T cells from children with CD exhibit an intrinsic hyperreactivity to IL-2. This may represent a primary pathogenic abnormality in this condition.

Presymptomatic late-infantile metachromatic leukodystrophy treated with bone marrow transplantation.

At 8 months of age, before clinical neurologic deterioration, the younger of two sisters with metachromatic leukodystrophy received a transplant of bone marrow from her haploidentical, heterozygote mother. Compared with the course in the older, affected, untreated sibling, the onset of neurologic regression was delayed 1 year and progressed at a slower rate.

Active and passive transport of sodium and potassium ions in erythrocytes of severely malnourished Jamaican children.

Erythrocytes of normal and malnourished children, both marasmic and oedematous (kwashiorkor), were equilibrated in standard incubation medium and their ion transport via the Na/K pump and the pathways of passive permeation were measured as unidirectional fluxes of 86Rb (as a congener of K) and 22Na. Cells of children with kwashiorkor exhibited a 65 per cent higher ouabain-sensitive K(Rb) influx ('pump rate') than those of normal or marasmic children. When allowance was made for cytoplasmic Na concentration, the pump rate was slower in younger (12 months and under) normal children than in older children. Judged by the same criterion, cells of older marasmic children also had slower steady-state pump activity. The passive permeation of K through the residual 'leak' pathway (ie, ouabain-and-bumetanide-insensitive influx) and Na permeation (ouabain-and-bumetanide-insensitive Na efflux) were greater in malnourished children than in normal children by a factor of two or more. During treatment for malnutrition, both Na-pump activity and ouabain binding increased rapidly in marasmic children. Passive permeation did not return to normal levels in malnourished children during the period of hospitalization.

Differential requirements for platelet aggregation and inhibition of adenylate cyclase by epinephrine. Studies of a familial platelet alpha 2-adrenergic receptor defect.

We describe a family whose members have impaired platelet aggregation and secretion responses to epinephrine with normal responses to adenosine diphosphate and collagen. Platelet alpha 2-adrenergic receptors (measured using 3H methyl-yohimbine) were diminished in the propositus (78 sites per platelet), his two sisters (70 and 27 sites per platelet), and parents (37 and 63 sites per platelet), but not in two maternal aunts (12 normal subjects, 214 +/- 18 sites per platelet; mean +/- SE). However, the inhibition of cyclic adenosine monophosphate (cAMP) levels by epinephrine in platelets exposed to 400 nmol/L PGI2 was similar in the patients and five normal subjects (epinephrine concentration for 50% inhibition, 0.04 +/- 0.01 mumol/L v 0.03 +/- 0.01 mumol/L; P greater than .05). In normal platelets, the concentration of yohimbine (0.18 mumol/L) required for half maximal inhibition of aggregation induced by 2 mumol/L epinephrine was lower than that for inhibition of its effect on adenylate cyclase (1.6 mumol/L). In quin2 loaded platelets, thrombin (0.1 U/mL) stimulated rise in cytoplasmic Ca2+ concentration, [Ca2+]i, was normal in the two patients studied. The PGI2 analog ZK 36,374 completely inhibited thrombin-induced rise in [Ca2+]i; the reversal of this inhibition by epinephrine was normal in the two patients. Thus, despite the impaired aggregation response to epinephrine, platelets from these patients have normal ability to inhibit PGI2-stimulated cAMP levels. These patients with an inherited receptor defect provide evidence that fewer platelet alpha 2-adrenergic receptors are required for epinephrine-induced inhibition of adenylate cyclase than for aggregation.

The hemostatic system in children undergoing intensive plasma exchange.

We report the effects on the hemostatic system of intensive plasma exchange therapy using replacement fluids devoid of plasma coagulation proteins. Five children were studied during ten exchanges. There were no hemorrhagic episodes clearly attributable to the plasma exchange, but one patient developed recurrent thrombosis of the vascular access used for the procedure. Plasma values of the various coagulation factors (II to XII) were decreased by 35 to 67% immediately following the plasmapheresis. The mean decrease in levels of antithrombin III antigen and activity and of plasminogen were 58, 60, and 66%, respectively. The recurrent thrombosis of the vascular access in one of the patients, and the decrease in antithrombin III and plasminogen values in plasma following plasmapheresis in all patients, suggest that there is increased potential for thrombosis in patients undergoing intensive plasmapheresis, despite the depletion of coagulation factors. At 24 hours following plasmapheresis the values for all factors were within normal limits, attesting to the ability of the synthetic mechanisms in children to replenish hemostatic factors rapidly.

The Aicardi syndrome versus congenital infection: diagnostic considerations.

The Aicardi syndrome consists of agenesis of the corpus callosum, infantile spasms, a characteristic lacunar chorioretinopathy, mental subnormality, and costovertebral anomalies. All patients have been female. Its clinical similarity to several congenital intrauterine infections, particularly toxoplasmosis, is reinforced by the erroneous diagnosis of congenital infection initially made in the two patients reported here. Reasons for this confusion are outlined, and methods for a clinical differentiation between the Aicardi syndrome and the congenital infections are discussed.