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C McIntosh

Publications and source records attributed to C McIntosh.

At least 37 records · Page 2Linked to original sources
PubMed1992

Isolation of a neuropeptide from locust corpus cardiacum which influences ileal transport.

1. Schistocerca gregaria ion-transport peptide (Scg-ITP) was isolated from aqueous extracts of the corpus cardiacum by a four-step procedure, utilizing reverse-phase high-performance liquid chromatography for separation and stimulation of a Cl(-)-dependent short-circuit current (Isc) across locust ilea as the bioassay. 2. Scg-ITP has an unblocked N terminus and an apparent relative molecular mass of 7700. Thirty-one residues (of an estimated 65) were identified by sequence analysis. 3. Scg-ITP is structurally related to a crustacean family of neuropeptides which includes the crustacean hyperglycaemic hormones from the shore crab Carcinus maenas and the crayfish Orconectes limosus and moult-inhibiting hormone and vitellogenesis-inhibiting hormone from the lobster Homarus americanus. 4. Scg-ITP has no sequence homology with neuroparsins (Nps). Nps are the only other neuropeptides isolated to date that might regulate reabsorption in an insect hindgut (rectum).

Amino Acid Sequence↗
PubMed1991

Variations in the carcinogenicity of tremolite dust samples of differing morphology.

Six samples of tremolite of different morphological type were prepared as dusts of respirable size and used in intraperitoneal injection studies in rats. Three "asbestiform" tremolites produced mesotheliomas in almost all animals, although with significantly different tumor-induction periods. A brittle type of fibrous tremolite which, when manipulated to prepare "respirable dust," produced a sample with relatively few asbestiform fibers remaining nonetheless produced tumors in 70% of rats. Two samples of nonfibrous tremolite produced respirable dust samples containing numerous elongated fragments with aspect ratios greater than 3:1, which therefore fitted the definition of respirable fibers. Both these samples produced relatively few tumors, although one had more long "fibers" than did the brittle tremolite that produced 70% of tumors. This study has therefore demonstrated that different morphologic forms of tremolite produce dusts with very different carcinogenic potential. Carcinogenicity does not depend simply on the number of elongated particles injected, and we need to develop methods of distinguishing carcinogenic tremolite fibers from relatively innocuous tremolite dusts, with similar numbers of elongated particles of similar aspect ratios.

Animals↗
PubMed1991

Ultrasonic detection of parathyroid adenomas.

High-resolution real time sonography was used to evaluate patients with suspected primary hyperparathyroidism. A total of 12 consecutive patients was scanned pre-operatively. The sensitivity of the procedure was 92% and the specificity 97%. In our hospital sonography is the procedure of choice for localizing enlarged parathyroid glands prior to surgical exploration.

Adenoma↗
PubMed1990

Augmentation of release of gastric somatostatin-like immunoreactivity by adenosine, adenosine triphosphate and their analogs.

The effect of adenosine, adenosine 5'-triphosphate (ATP) and ATP analogs on basal gastric somatostatin-like immunoreactivity (SLI) release was studied using the vascularly perfused rat stomach. The release of gastric SLI was stimulated by adenosine (0.6-60 microM) concentration dependently, while the release of immunoreactive gastrin was inhibited by 1 and 10 microM adenosine. The stimulatory action of adenosine was probably mediated by adenosine receptors because the receptor antagonist, 8-phenyltheophylline, abolished the action of adenosine. In addition, the adenosine-induced release of SLI was not mediated by a cholinergic or beta-adrenergic mechanism, since atropine, hexamethonium or propranolol did not block the action of adenosine. Dipyridamole enhanced the adenosine-stimulated, but not 2-chloroadenosine-induced SLI release. Since the adenosine analog, 2-chloroadenosine, is resistant to the adenosine uptake mechanism, it is likely that adenosine-stimulated release of gastric SLI is due to the activation of extracellular receptors. ATP also stimulated gastric SLI release. The analogs alpha,beta-methyleneadenosine triphosphate and diphosphate, which are resistant to metabolic breakdown, did not stimulate basal SLI release, while gamma,beta-methyleneadenosine triphosphate, which can be metabolized, increased the release of SLI. In addition, the ATP-induced release of SLI was abolished by 8-phenyltheophylline. Therefore, the action of ATP is likely to be a result of its metabolism to adenosine.

2-Chloroadenosine↗
PubMed1989

Calcium-antagonist receptors in the atrial tissue of patients with hypertrophic cardiomyopathy.

Hypertrophic cardiomyopathy is characterized by a nondilated, hypertrophied left ventricle in the absence of any overt cause. A possible role of adrenergic innervation or of cellular calcium regulation is suggested by the presence of hyperdynamic left ventricular function and by the clinical and symptomatic improvement seen in patients treated with beta-receptor antagonists or calcium antagonists. Therefore, we measured the density of calcium-antagonist receptors and beta-adrenoceptors in the atrial myocardium of 16 patients with hypertrophic cardiomyopathy and 19 patients with various other cardiac disorders. For comparison, we also measured the number of voltage-sensitive sodium channels. Calcium-antagonist binding sites, measured as the amount of dihydropyridine bound to atrial tissue, were increased by 33 percent in patients with hypertrophic cardiomyopathy (mean [+/- SD], 397 +/- 104 fmol per milligram of protein in patients with hypertrophic cardiomyopathy, as compared with 299 +/- 108 in patients with other cardiac disorders; P less than 0.01). The densities of saxitoxin-binding sites on voltage-sensitive sodium channels and beta-adrenoceptors were the same in the two groups, although the density of beta-adrenoceptors was higher in atrial samples from patients receiving beta-receptor antagonists (165 +/- 86 fmol per milligram of protein [patients receiving beta-blockers] vs. 85 +/- 60 [patients not receiving beta-blockers]; P less than 0.04). The increase in the number of calcium-antagonist receptors in hypertrophic cardiomyopathy suggests that abnormal calcium fluxes through voltage-sensitive calcium channels may play a pathophysiologic part in the disease.

Adolescent↗
PubMed1989

CF and emphysema.

Explore the source record for details and available documents.

Cystic Fibrosis↗
PubMed1988

Pulmonary clearance of UICC amosite fibres inhaled by rats during chronic exposure at low concentration.

Clearance of UICC amosite asbestos from the lungs during chronic--that is, repeated--exposure was investigated by using the scanning electron microscope to measure lung burdens from rats which had inhaled amosite asbestos at an approximately constant concentration of 0.1 mg/m3 or, equivalently, 20 fibres/ml for seven hours a day, five days a week for up to 18 months. The lung burdens were compared with previous results for higher exposure concentrations of 1 and 10 mg/m3. Those previous lung burdens had been measured using other analytical methods (infrared spectrophotometry) that were not suitable for the new lower lung burdens. Taken together, these results showed lung burdens rising pro rata with exposure concentration and exposure time. This accumulation of lung burden has been described by a kinetic model that takes account of the sequestration of material at locations in the lung from where it cannot be cleared. Unlike some earlier models in which lung burdens eventually reach a plateau with equilibrium between deposition and clearance during chronic exposure, this sequestration model shows lung burdens continuing to rise with exposure time. The latest results reported here support the application of such a model to lower exposure concentrations closer to those of asbestos in workplaces.

Animals↗
PubMed1985

Anti-MAG antibody and antibody complexes: detection by radioimmunoassay.

A radioimmunoassay (RIA) for measuring isotype-specific antibodies to the myelin-associated glycoprotein (MAG) was developed using radiolabeled CNS MAG in a double-antibody precipitation system. Anti-MAG activity was detected by RIA only in patients with neuropathy and anti-MAG M proteins. Anti-MAG IgM or IgG antibodies were not detected in serum of patients with Guillain-Barré syndrome, chronic relapsing polyneuritis, or multiple sclerosis (MS). Some patients with anti-MAG IgM M proteins also had complexes of IgG or IgA bound to the M protein. In one patient, anti-CNS MAG activity was detected by RIA, but not by ELISA or immunoblot. Anti-MAG antibody activity in patients with neuropathy seems to be isotypically restricted, and there is no evidence for antibody reactivity to MAG in other demyelinating diseases.

Antibodies, Anti-Idiotypic↗
PubMed1985

Unmasking of the cardiovascular effects of carbohydrate in subjects with sympathetic denervation.

The cardiovascular, biochemical and hormonal effects of a standard meal and two differing carbohydrates have been studied in normal subjects and in patients with autonomic failure (AF) and impaired cardiovascular reflexes. In the normal subjects blood pressure (BP) was unchanged after a meal and oral glucose. In AF patients, however, there was a marked and prolonged fall in BP after the meal. A similar fall occurred after oral glucose with only a small fall after oral xylose. In normal subjects, the meal and glucose raised plasma noradrenaline levels, unlike in AF patients, in whom noradrenaline and adrenaline levels were unchanged. In normal subjects with intact autonomic reflexes there are minimal cardiovascular effects induced by a meal or glucose. In AF subjects neural mechanisms are impaired, which probably unmasks the primary effects of food ingestion. The ability of glucose, but not xylose, to induce a similar degree of hypotension suggests that insulin may play an important role in postcibal hypotension.

Aged↗
PubMed1984

Contractile effects of cysteamine on the guinea-pig ileum.

Cysteamine (beta-mercaptoethylamine HCl) (1.0-40.0 mM) induced a concentration-dependent increase in tonic and phasic contractions of segments of guinea-pig ileum in vitro. Myenteric plexus-longitudinal muscle (MPLM) preparations also responded with an increase in tonic contractions but phasic contractions were either greatly reduced or absent, indicating that these were a response of the circular muscle. Atropine (5 microM) inhibited the cysteamine-induced contractions, whereas hexamethonium and guanethidine had no effect, suggesting that cysteamine was acting at least partly via a cholinergic mechanism involving muscarinic receptors. Tetrodotoxin increased the phasic contractions of ileal segments, but had no effect on the tonic component. Treatment of MPLM preparations with morphine (1 microM) resulted in a small reduction in responsiveness to cysteamine, and blocked electrically-induced contractions by at least 90%. Since morphine acts by inhibiting acetylcholine release via hyperpolarization of intrinsic neurones, a small but significant part of the cysteamine-induced contractions probably resulted from stimulation of acetylcholine release from intrinsic neurones. Following a response to high cysteamine concentrations (greater than 15 mM) tissues were refractory to subsequent cysteamine administration. Cross-desensitization between cysteamine and acetylcholine also occurred, as short-term (1-3 min) incubation of MPLM preparations with high concentrations of either compound (1-10 microM acetylcholine or 20 mM cysteamine) resulted in a reduced responsiveness to both. A reduced sensitivity to acetylcholine or cysteamine was obtained following long-term (45 min) incubation with acetylcholine (1 microM). Removal of Na+ from the incubation medium negated this effect. In contrast, the refractoriness to acetylcholine or cysteamine following long-term (45 min) incubation with cysteamine (20 mM) was accentuated in low Na+ medium. It is suggested that cysteamine induces a contraction of both the circular and longitudinal muscle of the guinea-pig ileum by stimulating the release of acetylcholine from intrinsic neurones, by an action at the level of the smooth muscle muscarinic receptor, and possibly by a non-cholinergic mechanism. However, the mechanisms by which acetylcholine and cysteamine induce tissue refractoriness probably differ.

Animals↗
PubMed1984

Effect of cysteamine on secretion of gastrin and somatostatin from the rat stomach.

Cysteamine (beta-mercaptoethylamine HCl) administration to rats induces a hypergastrinemia and a reduction in gastric tissue somatostatin content. The possibility that this reduction may contribute to the elevated gastrin levels has been investigated in the isolated perfused rat stomach. Cysteamine (1 mM) rapidly increased immunoreactive gastrin release to levels ranging between 41% and 125% above basal. Increasing the dose to 10 mM caused a 1148% increase in immunoreactive gastrin. Secretion of somatostatinlike immunoreactivity did not change. Perfusion of gastric inhibitory polypeptide (1 nM) induced a sustained increase in somatostatinlike immunoreactivity secretion and a transient rise in gastrin. Addition of 10 mM cysteamine during gastric inhibitory polypeptide perfusion caused a 300% increase in immunoreactive gastrin. These levels were lower than in response to cysteamine alone. The results demonstrate that cysteamine can stimulate immunoreactive gastrin secretion without any change in somatostatinlike immunoreactivity release. When somatostatinlike immunoreactivity secretion is stimulated by an agent such as gastric inhibitory polypeptide, the cysteamine-induced release of immunoreactive gastrin is attenuated, suggesting the presence of a functional linkage between somatostatin and gastrin under these conditions.

Animals↗
PubMed1981

Vagal release of IR-VIP and IR-gastrin from the isolated perfused rat stomach.

The effects of electrical stimulation of the vagus at varying pulse widths on the release of immunoreactive VIP (IR-VIP) and IR-gastrin have been investigated, using the isolated perfused rat stomach preparation. Electrical stimulation of vagal trunks at a pulse width of 0.1 msec duration yielded no change in basal IR-VIP levels whereas a pulse width of 5.0 msec produced a prompt sustained increase. Stimulation at either pulse width evoked gastrin release. Atropine blocked the vagal release of IR-gastrin but not IR-VIP whereas hexamethonium blocked both responses. Exogenously administered porcine VIP, at concentrations mimicking endogenously released levels, was used in an attempt to reproduce the effects observed by vagal stimulation. Exogenous VIP had no effect on gastrin or somatostatin-like immunoreactivity (SLI) release. These in vitro studies support a role for VIP as a neurotransmitter released from the stomach by low-threshold non-cholinergic vagal fibres, but involving autonomic ganglia.

Animals↗
PubMed1981

Somatostatin and gastrin release into the gastric lumen in rats.

Somatostatin and gastrin release into the gastric lumen was investigated in anaesthetized, vagally intact rats. The stomach was perfused at a flow rate of 0.5 mL.min-1. During perfusion with 0.1 M HCl or buffers of varying pH the somatostatin ans gastrin concentrations in the perfusate were less than 10 pg.mL -1 and approximately 30 pg.mL-1, respectively. Peptone caused a gastrin concentrations in the perfusate were less than 10 pg.mL-1 and approximately 30 pg.mL-1, respectively. Peptone caused a slight pH-independent increase in somatostatin release; gastrin release was unchanged despite an increase in serum gastrin from a basal of 15 +/- 4 to 155 +/- 34 pg.mL-1 during peptone stimulation. intravenous infusion of carbachol (1 microgram.kg-1.min-1) strongly stimulated luminal somatostatin and gastrin release (from 5 +/- 1 to 192 +/- 52 pg.mL-1 and from 27 +/- 5 to 198 +/- 41 pg.mL-1, respectively) during perfusion with 0.1 M HCl. Phosphate buffer perfusion at pH 7.5 abolished the cholinergic-mediated somatostatin release but the gastrin response was unaffected. It is suggested that changes of luminal hormone concentrations in the rat stomach do not reflect the secretory activity of the endocrine cells in the gastric mucosa.

Animals↗