Shape-changing shell-like structures.

Plants such as Dionaea muscipula (Venus Flytrap) can change the shape of their shell-like leaves by actively altering the cell pressures. These leaves are hydraulic actuators that do not require any complex controls and that possess an energy efficiency that is unmatched by natural or artificial muscles (Huber et al 1997 Proc. R. Soc. A 453 2185-205). We extend our previous work (Pagitz et al 2012 Bioinspir. Biomim. 7 016007) on pressure-actuated cellular structures by introducing a concept for shape-changing shell-like structures that can significantly alter their Gaussian curvature. The potential of this concept is demonstrated by a hemispherical shell that can reversibly change the sign of its Gaussian curvature. Furthermore, it is shown that a snap-through behaviour, similar to the one known from Dionaea muscipula, can be achieved by lowering the pressure in a single layer of cells.

Unconventional therapy use among children with cancer in Saskatchewan.

The study aimed to estimate the prevalence of unconventional therapy use among children with cancer in Saskatchewan, including identification of the most commonly used therapies, and to describe families' expectations and experiences in doing so. Researchers used a cross-sectional survey design with semi-structured telephone interviews to suit the descriptive and exploratory inquiry and the population focus. The personal telephone interviews occurred during the fall and winter of 1996 to 1997, with the parents coming from a wide range of geographic areas in the province of Saskatchewan. Parents of all children who were aged 14 years or younger when diagnosed with cancer during 1994 and 1995 in Saskatchewan and still living at the time of the study were identified through the provincial cancer registry with the assistance of the Saskatchewan Cancer Agency. Of the 44 families participating (92% of those eligible), 36% reported using unconventional therapy for their child's cancer; another 21% considered it. Reasons included complementing medical treatment, coping with side effects; making the child stronger; and stopping the cancer. Experiences were generally positive. Reasons for not using unconventional therapies included the child doing well and parents placing confidence in the medical system. Parents identified a need for better quality information about unconventional therapies. Unconventional therapies play a substantial complementary role in cancer care for children. Families need support to identify safe and potentially helpful therapies when they choose that route. This requires: more research about therapies' effectiveness; more accessible, quality information; and more training for health professionals in understanding and discussing unconventional therapies. There is considerable research showing that use of unconventional therapies, also known as complementary or alternative therapies, is high among adult cancer patients. Although it is likely reasonable to assume this may also be true for children, there is almost no research on children's use of unconventional therapies for cancer. Knowing the extent of children's use of unconventional therapies and whether those experiences have been beneficial or harmful is essential for parents and health professionals making quality care decisions for children.

Quantifying aggregation of IgE-FcepsilonRI by multivalent antigen.

Aggregation of cell surface receptors by multivalent ligand can trigger a variety of cellular responses. A well-studied receptor that responds to aggregation is the high affinity receptor for IgE (FcepsilonRI), which is responsible for initiating allergic reactions. To quantify antigen-induced aggregation of IgE-FcepsilonRI complexes, we have developed a method based on multiparameter flow cytometry to monitor both occupancy of surface IgE combining sites and association of antigen with the cell surface. The number of bound IgE combining sites in excess of the number of bound antigens, the number of bridges between receptors, provides a quantitative measure of IgE-FcepsilonRI aggregation. We demonstrate our method by using it to study the equilibrium binding of a haptenated fluorescent protein, 2,4-dinitrophenol-coupled B-phycoerythrin (DNP25-PE), to fluorescein isothiocyanate-labeled anti-DNP IgE on the surface of rat basophilic leukemia cells. The results, which we analyze with the aid of a mathematical model, indicate how IgE-FcepsilonRI aggregation depends on the total concentrations of DNP25-PE and surface IgE. As expected, we find that maximal aggregation occurs at an optimal antigen concentration. We also find that aggregation varies qualitatively with the total concentration of surface IgE as predicted by an earlier theoretical analysis.

A comparison of low-dose maintenance treatment with enprostil against ranitidine in the prevention of duodenal ulcer recurrence.

Enprostil, a prostaglandin E2 analogue, is effective in healing acute duodenal ulcer but its value in preventing recurrence, when given daily for maintenance therapy, is uncertain. In this three-centre study we compared enprostil and ranitidine maintenance therapy; the latter is known to reduce duodenal ulcer relapse rates. Patients whose duodenal ulcers had been healed by treatment with an H2-receptor antagonist were randomized to receive single-blind treatment with either 35 micrograms enprostil (n = 64) or 150 mg ranitidine (n = 64) at bedtime for periods of up to 1 year. Endoscopy was routinely performed at 3 months at one centre, and at 6 and 12 months at all three centres, or whenever ulcer symptoms recurred. Clinical assessment and laboratory investigations were performed every 3 months. Relapse, defined as recurrent ulcer with or without pain, or erosions with pain, was significantly greater in patients on enprostil, the comparative rates at 3, 6 and 12 months were: enprostil 23, 31 and 36% ranitidine 6, 12 and 17% (P = 0.013; P = 0.03 and P = 0.03, respectively). Thirty-one patients reported adverse events, the most common being headache (enprostil = 6, ranitidine = 2) and mild diarrhoea (enprostil = 6, ranitidine = 0). Four patients on enprostil were withdrawn for adverse events, although none terminated because of diarrhoea. There were no clinically significant changes in haematology or biochemistry. Enprostil may reduce duodenal ulcer relapse but at a dose of 35 micrograms nightly, it is less effective than 150 mg ranitidine nightly.

Central effects of nicotinamide and inosine which are not mediated through benzodiazepine receptors.

The actions of nicotinamide and inosine were investigated on rat cerebellar Purkinje cells using ionophoretic and extracellular recording techniques. Ionophoretic application of nicotinamide or inosine showed that they were potent inhibitors of Purkinje cell firing. This inhibition differed from that induced by benzodiazepines in that it was not reversed by the GABA antagonists bicuculline methiodide and picrotoxin. RO 15-1788, the specific benzodiazepine antagonist, did not reverse the effects of nicotinamide. Chlordiazepoxide has been shown to increase significantly social interaction between pairs of male rats and this increase can be reversed by RO 15-1788, 20 mg kg-1 i.p. Nicotinamide also caused a small increase in social interaction but this effect was not reversed by the benzodiazepine antagonist. Inosine did not increase social interaction. [3H]-flunitrazepam binding studies showed that nicotinamide and inosine have only low affinities for the benzodiazepine binding site. These results suggest that while nicotinamide may exert some neuronal depressant and anxiolytic activity, its site of action appears not to be associated with the benzodiazepine receptor site. Similarly, inosine exerts a neuronal depressant effect dissimilar from that of benzodiazepines.

The action of gamma-aminobutyric acid (GABA) and ethylenediamine (EDA) on Limulus and Helix central neurones and rat cerebellar and sympathetic ganglion neurones.

Intracellular recordings were made from central Limulus and Helix neurones and extracellular recordings from rat cerebellar Purkinje cells and sympathetic ganglia. The actions of gamma-aminobutyric acid (GABA) and ethylenediamine (EDA) and related analogues on these preparations were investigated. On Limulus neurones inhibited by GABA, EDA and piperazine were 81 and 186 times respectively less potent than GABA. Both the GABA and EDA events were chloride mediated, having similar reversal potentials and were reversibly antagonised by picrotoxinin. The EDA response persisted in high magnesium Ringer. On Helix neurones inhibited by GABA, EDA was 92 times less potent while on neurones excited by GABA, EDA was 9.25 times less potent. The other analogues tested had little or no GABA-like effect on either preparation. On rat cerebellar Purkinje cells, EDA was equipotent with GABA and both compounds were antagonised by bicuculline. Flurazepam only potentiated the action of EDA on 3 out of 23 cells tested while the GABA response of all 23 cells was potentiated by the benzodiazepine. Diaminopropionic acid was a weak inhibitor of cerebellar Purkinje cell firing but flurazepam potentiated this response in 6 out of 10 cells tested. On rat cervical ganglion neurones, EDA was half the potency of GABA and likewise the other analogues were less potent than GABA as depolarising agents. Incubation with glutamic acid decarboxylase inhibitors had no effect on the EDA response. Cross desensitisation between GABA and EDA was demonstrated using the ganglion preparation.(ABSTRACT TRUNCATED AT 250 WORDS)

Inhibition of estrogen-induced sexual receptivity of female hamsters: comparative effects of progesterone, dihydrotestosterone and an estrogen antagonist.

In the first experiment ovariectomized female hamsters were administered varying dosages of progesterone (P), dihydrotestosterone (DHT) or CI-628 at the same time (concurrently) as estrogen (EB) or 48 hr after EB (sequentially). All groups also received 500 microgram P 4 hr before being tested for sexual receptivity. P was more effective in reducing receptivity when given sequentially with estrogen than when given concurrently. Thus, the inhibitory effect of P increased with an increased interval between EB and P treatment. More CI-628 than P was required to inhibit lordosis and unlike P, CI-628 was equally effective when given concurrently with EB as when given sequentially. DHT did not inhibit receptivity when given in either paradigm. In the second experiment ovariectomized hamsters were treated with varying dosages of DHT 12 hr before EB. An amount of DHT which had no effect in Experiment 1 significantly inhibited receptivity when given 12 hr before EB. The relative inhibitory effects of these three compounds were discussed in terms of the possible similarities and differences in their mechanisms of action for inhibiting lordosis.

The excitation and inhibition of sexual receptivity in female hamsters by progesterone: time and dose relationships, neural localization and mechanisms of action.

Ovariectomized hamsters were administered estradiol benzoate (EB) and 44 h later, progesterone (P.) Lordosis behavior was induced. When an additional dose of P was given up to 24 h prior to or 24 h after the EB, EB-P facilitation of lordosis was inhibited. Additional hamsters were given varying doses of P (25-200 mu) following EB using both excitatory and inhibitory paradigms. Inhibition of EB-induced lordosis was effected with a lower dose of P than was the facilitation of EB induced lordosis by P. Hamsters were also given intracerebral implants of P using excitatory and inhibitory paradigms. No excitatory loci were found. Inhibition of EB-induced lordosis was effected by implants in the posterior hypothalamus and anterior mesencephalon, but not by diencephalic implants. Other hamsters were administered tritiated estradiol (E2) plus P prior to, concurrent with, or shortly after the E2. P had no effect upon the accumulation of E2 by any brain sites, although E2 was found to concentrate to a greater degree in the diencephalon than in the mesencephalon or cortex. The estrogen-induced depletion and replenishment of hypothalamic cytosol estrogen receptors was also studied. Concurrent P treatment had no effect upon the receptor depletion-replenishment process. It was concluded that P can both facilitate and inhibit estrogen-induced lordosis and that the inhibitory effects of P are not upon estrogen-sensitive cells in the brain.