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Biomedical subjects

R Mitchell

Publications and source records attributed to R Mitchell.

At least 73 records · Page 4Linked to original sources
PubMed1989

The elimination of cross-infection in dental practice--a 5-year follow-up.

A survey in 1983 showed that 16% of general dental practitioners in the Lothian Region wore operating gloves when treating patients; 9% wore them continually and 7% only when performing dento-alveolar surgery. Twelve per cent replied that they would not consider wearing operating gloves and 72% stated that they might consider their use. A similar survey has now been completed 5 years later, involving practitioners in the Lothian and Borders regions. This shows that 163 (97%) of the 168 practitioners who replied now wear operating gloves; 51% restrict their use to the treatment of 'potentially infectious patients' and dento-alveolar surgery; 46% wear them continually. The main objections given to wearing gloves continually were loss of tactile sensation (67%) and cost (13%). The most difficult task to perform wearing gloves was root canal therapy (56%). The majority of practitioners (84%) believed that gloves reduced the dangers of cross-infection. The methods stated to be available for instrument sterilisation in 99.5% of practices were acceptable. This paper proposes that to eliminate cross-infection and protect the dental practitioner, operating gloves should be worn when treating all patients.

Attitude to Health↗
PubMed1989

Novel ligands for the affinity labelling of luteinizing hormone releasing hormone receptors.

A number of novel luteinizing hormone releasing hormone (LHRH) analogues incorporating biotin together with potential covalent attachment sites have been synthesized. Those based on the des-Gly10-[D-Lys6]-LHRH ethylamide peptide backbone resulted in the most useful characteristics of binding to the LHRH receptor in rat anterior pituitary gland membranes. Of these, des-Gly10-[biotinyl-aminoethylglycyl-D-Lys6]-LHRH ethylamide (XBAL) gave the best specific: non-specific binding ratio, with 44 +/- 6% (+/- S.E.M.) of total binding being specific with a Kd of 131 +/- 16 pM (+/- S.E.M., n = 4) as determined by Scatchard analysis. Two methods have been used to covalently crosslink these analogues with the LHRH receptor; photoaffinity labelling and the use of homobifunctional N-hydroxysuccinimide ester crosslinkers. The photoaffinity analogues gave poor specific: non-specific binding ratios. Of the chemical crosslinkers tested, ethylene glycolbis(succinimidylsuccinate) (EGS) was found to be the most efficient at covalently linking the 125I-XBAL bound to the LHRH receptor site. At an EGS concentration of 5 mM, 23 +/- 3% (+/- S.E.M.) of the specific binding of 125I-XBAL was covalently crosslinked.

Affinity Labels↗
PubMed1988

Heterogeneous effects of serotonin in the dorsal horn of rat: the involvement of 5-HT1 receptor subtypes.

The effect of ionophoretically applied serotonin (5-HT) was tested on cutaneous sensory responses of multireceptive dorsal horn neurones in the anaesthetized rat. Three types of 5-HT action were discerned: selective inhibition of nociceptive responses (10/18 cells), non-selective inhibition of responses to both noxious and innocuous stimuli as well as to excitatory amino acids (4/18 cells) and non-selective excitation of evoked responses (1/18 cells). A few cells (3/18) were unaffected by 5-HT. The use of agonists, shown to discriminate between subtypes of 5-HT1 receptor revealed that a 5-HT1A receptor agonist mimicked the non-selective effects of 5-HT, whereas a 5-HT1B receptor agonist mimicked the selective antinociceptive effects of 5-HT. A 5-HT2 receptor agonist, in contrast, was without effect. Both the selective and the non-selective effects were reversed by a 5-HT1 receptor antagonist, but not a 5-HT2 antagonist.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1988

The influence of opioid receptor subtypes on the processing of nociceptive inputs in the spinal dorsal horn of the cat.

Extracellular recordings were made of the cutaneous sensory responses of spinocervical tract (SCT) neurones in the lumbar dorsal horn of anaesthetised and paralysed cats. All of the neurones studied were multireceptive, showing excitatory responses to both innocuous and noxious (thermal and when tested, mechanical) stimuli applied to their cutaneous receptive fields on the ipsilateral hindlimb. The effects of iontophoretically applied opioids were studied on a regular cycle of responses to these cutaneous stimuli and also to D.L-homocysteic acid (DLH). In the first series of experiments, drugs were applied in the vicinity of the SCT neurones. The kappa-receptor agonists dynorphin A(1-13) and U50488H, but not dynorphin A(2-13), the mu-agonist DAGO, or the delta-agonist DADL, caused a selective reduction of the nociceptive responses of the neurones. The corresponding responses to innocuous stimuli or to DLH, and spontaneous activity were unaffected. In the second series of experiments, drugs were applied from a second electrode placed in the region of the substantia gelatinosa directly dorsal to the tip of the recording electrode. Under these conditions, the mu-receptor agonist DAGO, but not the kappa-agonist dynorphin A(1-13) or the delta-agonists DADL, DSLET or DLPEN, showed a selective antinociceptive effect. In both series, the antinociceptive effects of the opioids were readily reversed by iontophoretically applied naloxone. The effect of dynorphin A(1-13) applied close to SCT neurones, but not that of DAGO applied in the region of the substantia gelatinosa, was reversed by the alpha 2-adrenoceptor antagonist, idazoxan. The results indicate that both mu- and kappa-opioid receptors (at anatomically distinct sites) can participate in the selective antinociceptive influence that opioids can exert over somatosensory information ascending to supraspinal levels. The antagonism of kappa-receptor-mediated antinociception by idazoxan is consistent with an interaction of opioid and noradrenaline influences at the level of the dorsal horn.

Animals↗
PubMed1988

Antibody that blocks stimulation of cortisol secretion by adrenocorticotrophic hormone in Addison's disease.

To investigate whether Addison's disease may in some cases be due to the blocking of adrenocorticotrophic hormone's action at the adrenal cortex by antibodies IgG isolated from a woman with Addison's disease associated with the autoimmune polyglandular syndrome type I was studied. Its effects on guinea pig adrenal cells in vitro were investigated and compared with those of IgG from three normal subjects and IgG obtained commercially. IgG from the patient inhibited the stimulation of cortisol secretion by adrenocorticotrophic hormone by 77 (SD 2)% and 57 (12)% at concentrations of 0.5 and 0.05 g/l, respectively; IgG prepared five months after she had started treatment with replacement steroids inhibited cortisol secretion by 74 (1)% (0.5 g/l) and 51 (15)% (0.05 g/l). The other IgGs had no inhibitory effects. The IgG from the patient and that obtained commercially did not inhibit the stimulation of cortisol secretion by dibutyryl cyclic adenosine monophosphate or precursors of cortisol. None of the IgGs bound to adrenocorticotrophic hormone. These results suggest that the IgG from the patient acted against the receptor for adrenocorticotrophic hormone, and its presence may explain the patient's raised concentrations of adrenocorticotrophic hormone, failure to respond to exogenous adrenocorticotrophic hormone, and normal basal cortisol concentrations. Addison's disease may thus in some instances be a receptor antibody disease.

Addison Disease↗
PubMed1988

Expression of human basic fibroblast growth factor cDNA in baby hamster kidney-derived cells results in autonomous cell growth.

Growth factor over-production by responsive cells might contribute to their autonomous proliferation as well as their acquisition of a transformed phenotype in culture. Basic fibroblast growth factor (bFGF) has been shown to induce transient changes in cell behavior that resemble those encountered in transformed cells. In addition, several types of human tumor cells have been shown to produce bFGF. To determine directly the role that bFGF might play in the induction of the transformed phenotype, we have introduced a human bFGF cDNA expression vector into baby hamster kidney-derived (BHK-21) fibroblasts. One of the BHK transfectants, termed clone 19, expresses the bFGF mRNA and produces biologically active bFGF that accumulates to a high concentration inside the cells. These properties correlate with the ability of the cells to grow in serum-free medium without the addition of exogenous bFGF. Clone 19 cells also proliferated in soft agar, indicating that constitutive expression of the bFGF gene results in a loss of anchorage-dependent growth.

Animals↗
PubMed1988

LKE red cell antigen and its relationship to P1 and Pk: serological study of a large family.

The fourth example of human anti-LKE was identified in the serum of an antenatal patient. Study of the red cells of the proband and her family confirmed the recessive inheritance of the LKE- phenotype. The blood groups of the family confirmed that Pk expression is greater on cells from LKE- members than on those from LKE+ members. In this family, the expression of LKE varied with the P1 phenotype. LKE- individuals occurred with an incidence of 0.0017 in the donor population of the Glasgow and West of Scotland Region.

Blood Group Antigens↗
PubMed1988

Antinociceptive actions of descending dopaminergic tracts on cat and rat dorsal horn somatosensory neurones.

1. The actions of dopamine (DA) and DA receptor specific agonists and antagonist ionophoretically applied in the spinal dorsal horn, and of focal electrical stimulation in the region of the supraspinal DA cell groups (A9 and A11) were assessed on the somatosensory responses of dorsal horn neurones, in both the rat and cat. The neurones tested were multireceptive, giving reproducible responses to both noxious (using a mechanical pinch or radiant heat) and innocuous (using a motorized brush) cutaneous stimuli, as well as to ionophoretically applied DL-homocysteic acid (DLH, a direct excitant). In the cat, all neurones tested were identified as belonging to the spinocervical tract (SCT) and were located in the dorsal horn laminae III-V, whilst in the rat, spinothalamic tract (STT) and spinomesencephalic (SMT) neurones located in the region of lamina I and laminae III-V were tested. 2. Ionophoretically applied DA and RU24213, a D2 DA receptor agonist, caused a selective inhibition of the responses to noxious stimuli of SCT, STT and SMT neurones, whilst the responses to non-nociceptive stimuli, spontaneous activity and DLH-evoked activity were unaffected. This action was reversed in the presence of sulpiride, the highly selective D2 DA receptor antagonist. Neither sulpiride alone nor SKF38393, a D1 DA receptor agonist, altered evoked or spontaneous activity when ionophoretically applied. 3. Focal electrical stimulation in the region of the A11, but not the A9, DA cell group selectively suppressed nociceptive responses of spinal, multireceptive neurones in the rat. This stimulus-evoked effect was consistently and rapidly reversed by ionophoresis of sulpiride, in the vicinity of the dorsal horn neurone being tested. In contrast, naloxone and idazoxan (RX781094), an alpha 2-antagonist, were not effective. 4. This study presents data supporting a selective antinociceptive role for DA at the spinal level, where it has a widespread antinociceptive influence, on cells in both the superficial and deeper dorsal horn. The A11 DA cell group was shown to be a supraspinal site from which a selective antinociceptive action could be electrically evoked and which was mediated by DA at the level of the dorsal horn.

Action Potentials↗
PubMed1988

The role of protein kinase C in LHRH-induced LH and FSH release and LHRH self-priming in rat anterior pituitary glands in vitro.

We have investigated the role of protein kinase C (PKC) in LHRH-induced LH and FSH secretion and LHRH priming. Hemipituitary glands from prooestrous rats were incubated with agents known to affect PKC and with or without LHRH, during which time the secretion of gonadotrophins was measured. Phorbol esters and phospholipase C, activators of PKC, released LH and FSH in a concentration-dependent manner and potentiated the LHRH-induced secretion of gonadotrophins in parallel with their ability to release these hormones alone. Inhibitors of PKC had either no effect on LH release (1-(5-isoquinolinesulphonyl)-2-methylpiperazine hydrochloride) or they augmented LHRH-induced gonadotrophin release (polymyxin B and 8-(N,N-diethylamino) octyl-3,4,5-trimethoxybenzoate). Neither the activators nor the inhibitors of PKC, when present with LHRH, caused any change in LHRH priming, even though the activators alone produced a release of gonadotrophins that showed a temporal pattern similar to that produced by LHRH priming. The profiles of effects on LH and FSH secretion were always qualitatively similar. These results show that PKC may be involved in general regulation of gonadotrophin release but that it is not important in acute responses to LHRH nor in LHRH self-priming.

Animals↗
PubMed1988

Facilitated calcium mobilization and inositol phosphate production in the priming effect of LH-releasing hormone in the rat.

The ability of LHRH to induce Ca2+ mobilization and production of inositol phosphates in rat anterior pituitary tissue in vitro was investigated in relation to the self-priming effect of LHRH. Prior exposure to LHRH (which caused a characteristic potentiation of subsequent secretory responses) specifically enhanced LHRH-induced inositol phosphate production and mobilization of intracellular Ca2+ stores. LHRH-induced influx of Ca2+ through dihydropyridine-sensitive Ca2+ channels was unaltered, as was ligand binding to LHRH receptors. These data suggest that a novel facilitation of signalling may occur in the phospho-inositide-Ca2+ mobilization response mechanism during LHRH priming, and that this may represent an important means of regulating cellular responsiveness in gonadotrophs.

Animals↗
PubMed1988

Addition of growth hormone secretion signal to basic fibroblast growth factor results in cell transformation and secretion of aberrant forms of the protein.

Basic fibroblast growth factor (bFGF) is a potent mitogen for a wide variety of cell types. Unlike most growth factors, the primary translation product for bFGF appears to lack a secretory signal peptide. To explore the normal mode of bFGF release, as well as to investigate the growth factor's oncogenic potential, expression vectors were created for a bFGF cDNA and for a chimeric molecule in which the bFGF coding sequence was linked to the human growth hormone signal peptide sequence. Transfection of NIH3T3 cells with the bFGF cDNA vectors caused the synthesis of high levels of biologically active, cell-associated bFGF, but no evidence of transformation was detected. In contrast, the chimeric bFGF-signal peptide expression vector induced foci of transformation at a very high frequency. The transformed cells grew in soft agar and were tumorigenic in nude mice. The majority of the immunoreactive bFGF species made by the transformed cells was found in the conditioned medium and appeared to be posttranslationally modified, indicating that the chimeric bFGF-signal peptide molecule was processed through the secretory pathway. The secreted bFGF exhibited little mitogenic activity, suggesting that interaction of bFGF with its receptor likely occurs while the fusion protein is being processed along the secretory pathway.

Animals↗