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Biomedical subjects

S Meghji

Publications and source records attributed to S Meghji.

71 records · Page 4Linked to original sources
PubMed1989

Enhanced presynaptic facilitation of vascular adrenergic neurotransmission in spontaneously hypertensive rats.

1. The interaction between the vascular renin-angiotensin system and presynaptic beta-adrenoreceptors was examined in male and female normotensive and spontaneously hypertensive rats, using the in vitro perfused mesentery preparation. 2. Enhancement of the pressor response to periarterial nerve stimulation by isoprenaline was shown to be significantly greater in preparations from male and female spontaneously hypertensive rats compared to corresponding preparations from normotensive Wistar rats. 3. In preparations from normotensive and hypertensive animals, the potentiating effect of isoprenaline was prevented by pretreatment with propranolol or ICI 118 551, but not atenolol, implicating a beta 2-adrenoreceptor. 4. Angiotensin II enhanced the responses to peripheral nerve stimulation in preparation from normotensive and hypertensive animals. Enhancement was significantly greater in preparations from hypertensive animals. 5. The potentiation caused by isoprenaline was blocked by the angiotensin II receptor antagonist [Sar1-Ile8] angiotensin II, and by captopril. The potentiation following angiotensin II was unaffected by ICI 118 551. 6. These results suggest that stimulation of presynaptic beta 2-adrenoreceptors activates a localized angiotensin II system. No significant differences in this facilitatory system were observed between male and female animals, but the potentiation caused by activation of this system was considerably greater in the spontaneously hypertensive rats.

Adrenergic beta-Antagonists↗
PubMed1989

Magnets and orthodontics.

The first part of this paper is a literature review of magnets and their uses in orthodontics. The biological safety of magnets is considered and a report is given of experiments carried out on rat osteosarcoma cell line UMR-106. The second part of the paper describes a case where neodynium-iron-boron magnets were used to assist eruption of an unerupted, vertically impacted upper right canine. Previously, space was available for this tooth, but it failed to show signs of eruption. Following surgical attachment of a magnet, and the use of a second magnet attached to an upper removable appliance, rapid eruption occurred producing a favourable position for bonding.

Animals↗
PubMed1988

Parathyroid hormone and prostaglandin E2 stimulate both inositol phosphates and cyclic AMP accumulation in mouse osteoblast cultures.

Parathyroid hormone (PTH) and prostaglandin E2 (PGE2) are physiological agonists which stimulate bone cells to resorb bone, a process by which the mineralized extracellular bone matrix is dissolved. Bone resorption has a key role in the maintenance of plasma calcium levels. It has been established that both PTH and PGE2 activate adenylate cyclase in osteoblasts, but it is apparent that (1) the two agents have qualitatively different effects on osteoblasts, and (2) the generation of cyclic AMP cannot account for all the effects of PTH on bone cell metabolism. Others have demonstrated that PTH and PGE2 may also elevate intracellular calcium levels, but the mechanism by which this is achieved has not been fully defined. Here we have investigated the effects of PTH on neonatal mouse osteoblasts in culture and shown that physiological concentrations of the hormone (50 nM) caused a small increase (22%) in total inositol phosphates accumulation, with a larger increase (40%) in inositol trisphosphate. We found that this activation occurred at lower concentration than was necessary to activate adenylate cyclase. PGE2 was a more effective activator of inositol phosphates accumulation than PTH, causing up to 300% increase in the total inositol phosphates after 30 min. Both PTH and PGE2 stimulated cyclic AMP accumulation, but the activation of adenylate cyclase by forskolin did not enhance inositol phosphates production. We conclude that both PTH and PGE2 stimulate phosphoinositide turnover in mouse osteoblasts and suggest that this mechanism may contribute to their elevation of intracellular calcium in bone cells.

Animals↗
PubMed1988

Heterogeneity of bone resorbing factors produced by unstimulated murine osteoblasts in vitro and in response to stimulation by parathyroid hormone and mononuclear cell factors.

The bone resorbing activity of factors released from monolayer cultures of osteoblasts (OB) was examined by measurement of calcium released by neonatal mouse calvaria in vitro. Unstimulated conditioned media (CM) were found to contain significant bone resorbing activity, which was partially inhibited by indomethacin, dexamethasone and nordihydroguaiaretic acid. Ultrafiltration of CM (molecular weight cut-off of 5000) revealed bone resorbing activity in the filtrate and retentate. Fractionation of the CM by high-performance liquid chromatography revealed four major peaks of bone resorbing activity. Stimulation of the OB by mononuclear cell factor and parathyroid hormone significantly increased the synthesis and/or release of these factors with a relatively greater increase of lipid-soluble, low molecular-weight activity. These results suggested an important role for relatively small non-popular mediators in hormonally stimulated bone resorption.

Animals↗
PubMed1988

Stimulation of bone resorption by lipoxygenase metabolites of arachidonic acid.

We have studied the effect of leukotrienes, (LT): B4, C4, D4 and E4 and the hydroxyeicosatetraenoic acids (HETEs) 5-HETE and 12-HETE on bone resorption in vitro. Resorption was measured by colorimetric assay of calcium released from neonatal mouse calvaria maintained in organ culture for 72h. All the LTs and HETEs stimulated bone resorption, with optimum responses at picomolar or nanomolar concentrations. The responses were biphasic, with a decreasing effect at higher concentrations. In contrast, prostaglandin E2 (PGE2) stimulated resorption only at 10nM and above. Indomethacin partially inhibited resorption by LTB4, LTC4 and LTD4, but did not affect resorption stimulated by LTE4, 5-HETE and 12-HETE. These results indicate that lipoxygenase products of arachidonic acid are highly potent bone resorbing factors and may play an important role in the localised bone loss associated with inflammatory lesions.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1988

Macromolecular osteolytic factor synthesised by squamous carcinoma cell lines from the head and neck in vitro is interleukin 1.

Three human cell lines derived from oro-pharyngeal squamous cell carcinomas of the head were investigated for bone-resorbing activity in vitro. Culture media from all three spontaneously produced a non-dialysable osteolytic factor with activity in three in vitro assays for interleukin 1 (IL1), viz. the lymphocyte activating factor (LAF) assay, stimulation of collagenase synthesis by articular chondrocytes, and stimulation of prostaglandin E2 synthesis by fibroblasts. Addition of anti-human IL1 antibody to the culture media abolished all the bone-resorbing activity. Fractionation of the cell culture media by high performance liquid chromatography (HPLC) showed a single peak of activity in the chondrocyte assay with an apparent mol.wt of 15-17,000. This co-eluted with activity in a preparation of IL1 from rat peritoneal macrophage cultures. These results indicate that IL1 is responsible for the prostaglandin-independent bone resorbing activity synthesised by these cells in vitro, and may contribute to the bone destruction associated with the tumour.

Bone Resorption↗
PubMed1988

Effect of capsular material from Haemophilus actinomycetemcomitans on bone collagen synthesis in vitro.

Capsular material was extracted from Haemophilus actinomycetemcomitans, an organism associated with localised juvenile periodontitis, and examined for its effect on the in vitro synthesis of collagen and DNA in mouse calvaria. The material was found to cause a significant inhibition of both collagen and DNA synthesis at concentrations as low as 10 ng ml-1. The ability of capsular material to inhibit bone formation, together with its previously described bone resorbing activity, suggests that it may contribute to the rapid alveolar bone loss which is characteristic of localised juvenile periodontitis.

Animals↗
PubMed1987

Stabilisation of collagen by betel nut polyphenols as a mechanism in oral submucous fibrosis.

Treatment of reconstituted collagen fibrils and pieces of rat dermis with the crude extract, purified tannins or (+)-catechin from betel nut (Areca catechu) increases their resistance to both human and bacterial collagenases in a concentration-dependent manner. These tanning agents may stabilise collagen in vivo following damage to the oral epithelium, and promote the sub-epithelial fibrosis which occurs in betel nut chewers.

Animals↗
PubMed1987

Stimulation of human fibroblast collagen synthesis in vitro by gamma-aminobutyric acid.

Human buccal mucosa fibroblasts were exposed in culture to gamma-aminobutyric acid (GABA) and the areca alkaloid arecaidine. Both GABA and arecaidine stimulated collagen synthesis and proliferation in a concentration-dependent manner, with arecaidine consistently producing the greater stimulation. Prior exposure to GABA or arecaidine for 5 days caused the cells to become insensitive when challenged with either drug.

Arecoline↗
PubMed1987

An in-vitro comparison of human fibroblasts from normal and oral submucous fibrosis tissue.

Fibroblasts cultured in vitro from normal buccal tissue and from tissue from oral submucous fibrosis (OSF) associated with betel-nut chewing showed no significant difference in their rates of proliferation in culture, nor in the rate at which they hydrolysed the betel nut alkaloid arecoline to arecaidine. Basal rates of collagen synthesis were slightly higher in the OSF cells but, on addition of arecoline, the rate of collagen synthesis in normal and OSF cells was stimulated to the same level.

Arecoline↗
PubMed1987

Interleukin-1-like activity in capsular material from Haemophilus actinomycetemcomitans.

This paper describes the activity of a bacterial surface component (capsular material, CM) in biological assays for interleukin-1 (IL-1). CM from the periodontal pathogen Haemophilus actinomycetemcomitans was tested in the following in vitro assays: mouse thymocyte proliferation (LAF assay), stimulation of collagenase and prostaglandin (PG) E2 synthesis by articular chondrocytes, and stimulation of PGE2 synthesis by fibroblasts. In all these assays, CM gave a response similar to an IL-1 preparation. This ability to mimic IL-1 suggests an important role for CM in both cell-mediated immunity and connective tissue destruction in localized juvenile periodontitis (LJP).

Animals↗
PubMed1986

Stimulation of human buccal mucosa fibroblasts in vitro by betel-nut alkaloids.

Oral submucous fibrosis (OSF) is characterized by excessive collagen production by mucosal fibroblasts and is associated with the habitual chewing of betel-nuts (Areca catechu); nut extracts stimulate fibroblast activity in vitro. The metabolism of arecoline, the major alkaloid in the nut, by human buccal mucosa fibroblasts in vitro was investigated; alkaloid metabolites extracted from culture media were analysed by gas chromatography and thin-layer chromatography. [3H]-arecoline was metabolized predominantly to [3H]-arecaidine and this was accompanied by a concentration-dependent stimulation of collagen synthesis and cell proliferation. Arecaidine was a more potent stimulator than arecoline. The rate of hydrolysis of a series of synthetic arecaidine esters (methyl, ethyl, butyl, propyl and pentyl) by fibroblasts was closely correlated with the extent of stimulation of collagen synthesis. Thus fibroblasts are responsive to the major metabolite of arecoline and hydrolysis of the ester group may be necessary for this action. Exposure of buccal mucosa fibroblasts to these alkaloids in vivo may contribute to the accumulation of collagen in OSF.

Alkaloids↗
PubMed1986

In vitro inhibition of lipopolysaccharide-induced bone resorption by polymyxin B.

Lipopolysaccharide (LPS) purified from Haemophilus actinomycetemcomitans stimulates resorption and inhibits collagen synthesis in mouse calvaria bones in vitro. Addition of polymyxin B caused a dose-related inhibition of LPS-stimulated bone resorption and reversal of the inhibition of collagen synthesis. A polymyxin B to LPS ratio of 2:1 prevented bone resorption and restored collagen synthesis to control levels. The activity of polymyxin B was specific for LPS as bone resorption induced by prostaglandin E2 or parathyroid hormone was unaffected at similar concentrations. These results indicate that polymyxin B and its analogues may have potential in the treatment of periodontal disease by reducing bone loss induced by lipopolysaccharides.

Animals↗
PubMed1984

Evidence for fibroblasts as the major source of prostacyclin and prostaglandin synthesis in dental cyst in man.

Periodontal cysts synthesize large amounts of prostaglandins and collagenase which probably cause the localized bone destruction essential for intraosseous cyst growth. Fragments of cyst wall, and fibroblasts cultured from them, synthesized prostacyclin (PGI2) in addition to prostaglandin E2 (PGE2), PGF2 alpha and collagenase in vitro. Soluble products from cultures of unstimulated and phytohaemagglutinin-stimulated blood mononuclear cells enhanced the synthesis of these prostaglandins in monolayer cultures of cyst-wall fibroblasts. It is therefore proposed that cyst capsule fibroblasts are the major source of these bone-resorbing factors, acting under the stimulus of lymphocytes and monocytes in chronically inflamed cysts. Cysts which were not infiltrated by chronic inflammatory cells (follicular cysts, a keratocyst, an ameloblastoma, and an aneurysmal bone cyst) also produced prostaglandins and collagenase, indicating that the stimulatory mechanism for the production of bone-resorbing factors in these cysts may differ from that in periodontal cysts.

6-Ketoprostaglandin F1 alpha↗
PubMedDate not supplied

Prostaglandin synthesis in the pathogenesis of fronto-ethmoidal mucoceles.

The fronto-ethmoidal mucocele is a rare condition capable of expansion and erosion of bone. Its etiology is attributed to obstruction of the fronto-nasal duct and inflammation. To elucidate the role of inflammation, mucocele fragments and fibroblasts cultured from them were examined in vitro to assess prostaglandin E2 synthesis. The cultured fibroblasts when stimulated with mononuclear cell culture supernatant produced significant levels of prostaglandin E2 and collagenase, compared with normal frontal sinus mucosa fibroblasts removed at craniotomy. These significantly elevated mucocele levels of prostaglandin E2 (p = less than 0.001) suggest that lining fibroblasts are a major source of bone-resorbing factors, acting under the stimulus of lymphocytes and monocytes and which operate at the mucocele-bone interface, facilitating expansion. This situation closely parallels that already established in odontogenic cysts.

Dinoprostone↗