Resin modified glass ionomer cements. In vitro microleakage in direct class V and class II sandwich restorations

Microleakage of conventional chemically cured and resin modified glass ionomer cements (GIC), a compomer and a composite resin was studied in vitro in direct class V and class II GIC/composite sandwich fillings. None of the restorative techniques investigated completely resisted microleakage at both the occlusal and gingival margins. The dentinal gingival margins exhibited the highest leakage pattern. The compomer and the resin modified GIC showed a better seal than the chemically cured GIC's. The use of a liner as separating agent between composite resin and GIC in the class II sandwich fillings did not improve the seal. The results suggest that the initial bond obtained immediately after light curing of the resin modified GIC's is stronger than that for chemically cured GIC's. The contradictory results of dye leakage studies reported in the literature are discussed and in vivo evaluations are suggested necessary to predict clinical performance.     

Regulation of insulinoma cell proliferation and insulin accumulation by peptides and second messengers

The regulation of clonal rat insulinoma (RINm5F) cell proliferation and hormone accumulation was investigated with the aim of identifying putative compounds capable of inducing differentiation, i.e. decreased growth and increased insulin accumulation, by the tumor cells. In particular, interest was focused on the role of a number of peptides as well as pharmacological probes modulating various signal transduction systems and which have been shown to regulate normal beta-cell proliferation and insulin accumulation. Growth hormone stimulated insulin accumulation and inhibited DNA synthesis, whereas galanin and insulin-like growth factor I caused a moderate suppression of insulin accumulation but did not affect proliferation, while epidermal growth factor, transforming growth factor beta, platelet-derived growth factor, acidic and basic fibroblast growth factor, bradykinin and somatostatin were virtually inactive on all parameters tested. Exogenous prostaglandins E2 and F1 alpha were inactive, while the cycloxygenase inhibitor indomethacin slightly suppressed insulin accumulation. The cytokine IL-1 beta caused a significant decrease in both beta-cell mitogenesis and insulin accumulation, effects that were mediated through nitric oxide generation. The vitamin A derivative retinyl acetate slightly inhibited serum-stimulated DNA synthesis, but did not affect insulin accumulation. The vitamin E alpha-tocopherol significantly enhanced insulin release but did not affect mitogenesis. By contrast, gamma-tocopherol was inactive on both these parameters. The alpha-adrenergic agonist clonidine evoked a slight inhibition of serum-stimulated DNA synthesis, without influencing insulin accumulation, whereas phenylephrine did not affect any of these parameters. Carbamylcholine increased insulin accumulation, but not cell proliferation, whereas the adenylyl cyclase activator forskolin suppressed mitogenesis but did not affect insulin accumulation. Inhibition of protein kinase C with staurosporine or prolonged treatment with phorbol ester suppressed DNA synthesis, as did the tyrosine kinase inhibitor genistein. Stimulating Ca2+ influx by closing ATP-dependent K+ channels with glibenclamide enhanced DNA synthesis, while opening of these channels with diazoxide suppressed cell growth. Conversely, preventing Ca2+ influx by the Ca2+ channel antagonist D-600, chelating intracellular Ca2+ by fura-2 AM or inhibiting the Ca2+/calmodulin-dependent protein kinase by calmidazol resulted in a decreased DNA synthesis. On the other hand, uncontrolled influx or mobilization of Ca2+ by ionomycin or thapsigargin resulted in an arrested DNA synthesis. The present paper shows that RINm5F insulinoma cell proliferation and insulin accumulation can be modulated by various peptidergic and pharmacological agents regulating certain signal transduction pathways. However, mitogenesis in the insulinoma cells seemingly is controlled in a vastly different manner in comparison to that in normal beta-cells. The most spectacular finding in this screening study, i.e. that growth hormone, contrarily to its effect on normal beta-cells, suppresses insulinoma cell growth, merits further elucidation of the underlying mechanisms. Possibly the hormone might become of utility in a clinical setting in the treatment of patients with insulin-producing tumors.     

Cryo-ultramicrotomy and myofibrillar fine structure: a review.

In the past, the techniques of electron microscopy and X-ray diffraction have both been very informative about the ultrastructure of the muscle myofibril But X-ray diffraction patterns are difficult to interpret unambiguously and until now specimen preservation in plastic embedded muscle has been sufficiently poor to make it difficult to use electron micrographs of muscle as a means of interpreting the available X-ray diffraction evidence. The possibility of using ultrathin sections of frozen muscle, in which the disruptive steps of chemical dehydration and plastic embedding can be avoided, promises to help to bridge the information gap between present X-ray and electron microscope results. For this reason we here review the application of the cryosectioning technique to muscle, we assess the technique in terms of the improvements in preservation which have so far been obtained and which might be expected and we discuss some of the many potential advantages and uses of this technique for studies of muscle ultrastructure and function. It is concluded that this technique should be developed vigorously since it promises to play a very important role in muscle research in the future.     

The detailed structure of delamination fracture surfaces in graphite/epoxy laminates

Delamination fracture surfaces of angle-ply graphite/epoxy specimens failed in tension were studied in the SEM. The fracture surfaces contain resin-rich and resin-poor areas, with the former showing imprints from fibres while the latter show debonded fibres. A delamination crack propagates in the outer parts of the plies adjacent to the resin-rich interlaminar region and alternates from one ply to the adjacent ply and back as it propagates. The serrations formed in between fibres in the outermost parts of plies are tilted. The sense of the tilt is in agreement with the direction of the major tensile principal stress. The delamination is suggested to proceed in steps including debonding of fibres, crack opening by the major principal tensile stress and linking together of these fractures.     

Contribution of prostaglandins to the adenosine triphosphate-induced contraction of rabbit urinary bladder

1 Adenosine 5'-triphosphate (ATP) produced an initial rapid, phasic contraction and a later, slowly developing tonic contraction in the isolated detrusor of the rabbit but mainly a rapid, phasic response in the guinea-pig bladder. 2 Electrical field stimulation elicited only a rapid, phasic contraction in both rabbit and guinea-pig bladders. 3 Prostaglandin synthesis inhibition by means of indomethacin and suprofen abolished the tonic response to ATP in the rabbit detrusor, leaving the phasic part of the contraction almost unaffected. The ATP-induced contraction in guinea-pig bladder was not influenced by indomethacin. 4 The contractile response of rabbit urinary bladder to prostaglandins F2 alpha and E2 and to carbachol were not significantly influenced by indomethacin. The contractions induced by the prostaglandins were similar to the tonic response to ATP. 5 Tetrodotoxin, atropine, phentolamine, and theophylline did not alter the ATP-induced contraction. However, the calcium antagonists, nifedipine and nimodipine, abolished the phasic ATP response and greatly reduced the tonic part of the contraction. 6 Tachyphylaxis occurred on repeated addition of ATP; the response to field stimulation was progressively reduced only after indomethacin pretreatment. 7 ATP and prostaglandins may contribute to the non-adrenergic, non-cholinergic component of the excitation of rabbit and guinea-pig bladder.     

Stillbirth is no longer managed as a nonevent: a nationwide study in Sweden

BACKGROUND: Giving birth to a stillborn child is a tragedy. The aim of this study is to investigate the meeting of mothers with their stillborn children and the women's experiences of support during and after the delivery. METHODS: In a nationwide study in Sweden, data from 636 women who gave birth to a stillborn or live baby were collected by means of an anonymous postal questionnaire in 1994. RESULTS: Among the 314 women who gave birth to a stillborn child, nearly every mother had seen her child, and 80 percent had carressed her baby. More than 90 percent of the mothers stated that the medical staff showed respect, and about 80 percent of the mothers stated that staff exhibited tenderness toward their dead children. The mother's assessment of respect and tenderness to her child by medical staff was almost identical between stillbirths and live births. Nearly 70 percent of the women reported that the hospital had good routines to support mothers of stillborn children. Feelings of sadness and having been deeply hurt or angered by the medical staff's behavior were reported by 37 percent of the women. A difficult balance is still to be achieved between women being forced to encounter the baby when not yet ready versus others who wish the staff had given more encouragement. The value of properly taken photographs is described. CONCLUSIONS: Treating stillbirth as a nonevent has been largely, if not entirely, abandoned in Sweden. Most mothers of a stillborn child experience that the medical staff treat their dead children appropriately.