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Biomedical subjects

K Tyler

Publications and source records attributed to K Tyler.

At least 19 recordsLinked to original sources
PubMed2003

Variability in position of the subthalamic nucleus targeted by magnetic resonance imaging and microelectrode recordings as compared to atlas co-ordinates.

BACKGROUND: Traditional methods for localisation of target nuclei for deep brain stimulation (DBS) have used brain atlas co-ordinates for initial targeting. It is now possible to visualise the subthalamic nucleus (STN) on magnetic resonance imaging (MRI) and determine the individual variability of its position. METHODS: The present study was performed in patients undergoing STN DBS for Parkinson's disease. The STN was directly targeted from axially obtained MRI and verified with microelectrode recordings. Postoperatively, the most effective contact was identified for each patient, and its position was calculated. RESULTS: Fifty electrodes were inserted in 25 patients. The target position varied considerably in relation to the mid-commissural point. The mean effective contact position lies just dorsal to the location of the STN in a standard brain atlas. CONCLUSION: The STN varies in position, and can be accurately targeted from MRI alone.

Adult↗
PubMed2003

Use of the NeuroMate stereotactic robot in a frameless mode for movement disorder surgery.

BACKGROUND/AIMS: To evaluate the use of the NeuroMate stereotactic robot with a novel ultrasound registration system for movement disorder surgery (MDS). METHODS: Using the robot in a frameless mode, 51 patients underwent MDS. Surgical planning was carried out using MRI data obtained more than 24 h before surgery. RESULTS: 37 out of 50 targets in the subthalamic nucleus were satisfactorily identified with a single microelectrode trajectory and the final electrode positions were at a mean distance of 1.7 mm from the calculated target. There was a significant improvement in motor scores of the Unified Parkinson's Disease Rating Scale III (off medication) at 6 (43%) and 18 months (51.7%) compared to pre-operative scores (p < 0.05). CONCLUSIONS: The frameless robot using only MRI data can be used for MDS. The temporal separation of imaging from the surgical procedure provides additional time for detailed image analysis and planning.

Humans↗
PubMed2000

Inhibition of small intestinal secretion by cannabinoids is CB1 receptor-mediated in rats.

We tested the hypothesis that cannabinoids, acting via a neuronal mechanism of action decrease small intestinal secretion. In vitro electrical stimulation induced ileal secretion in rats, that was attenuated by a cannabinoid receptor agonist, WIN 55212-2, (mesylate(R)-(+)-[2, 3-dihydro-5-methyl-3-[4-morpholino)methyl]pyrrolo-[1,2,3-de]-1, 4-benzoxazin-6-yl](1-naphthyl)methanone) but not its optical isomer WIN 55212-3. The inhibition of secretion induced by WIN 55212-2 was reversed by SR141716A (N-(piperidin-1-yl)-5-(4-chlorophenyl)-1(2, 4-dichlorophenyl)-4-methyl-1H-pyrazole-3-carboxamide hydrochloride), a cannabinoid CB1 receptor antagonist. An ileal secretory response stimulated by acetylcholine was unaffected by WIN 55212-2. These findings show that cannabinoids inhibit neurally mediated secretion via cannabinoid CB1 receptors. Thus, cannabinoids may have therapeutic potential for diarrhea unresponsive to available therapies.

Acetylcholine↗
PubMed2000

MEK kinase 1 gene disruption alters cell migration and c-Jun NH2-terminal kinase regulation but does not cause a measurable defect in NF-kappa B activation.

MEK kinase 1 (MEKK1) is a 196-kDa mitogen-activated protein kinase (MAPK) kinase kinase that, in addition to regulating the c-Jun NH(2)-terminal kinase (JNK) pathway, is involved in the control of cell motility. MEKK1(-/-) mice are defective in eyelid closure, a TGFalpha-directed process involving the migration of epithelial cells. MEKK1 expression in epithelial cells stimulates lamellipodia formation, a process required for cell movement. In addition, mouse embryo fibroblasts derived from MEKK1(-/-) mice are inhibited in their migration relative to MEKK1(+/+) fibroblasts. MEKK1 is required for JNK but not NF-kappaB activation in response to virus infection, microtubule disruption, and stimulation of embryonic stem cells with lysophosphatidic acid. MEKK1 is not required for TNFalpha or IL-1 regulation of JNK or NF-kappaB activation in macrophages or fibroblasts. Thus, MEKK1 senses microtubule integrity, contributes to the regulation of fibroblast and epithelial cell migration, and is required for activation of JNK but not NF-kappaB in response to selected stress stimuli.

Animals↗
PubMed2000

Recombinant human interleukin-11 modulates ion transport and mucosal inflammation in the small intestine and colon.

Human recombinant interleukin 11 (rhIL-11) is a cytokine that suppresses the clinical signs of colitis in animal models of inflammatory bowel disease (IBD) and may be an effective therapeutic agent in the treatment of IBD. The objective of the current study was to investigate whether rhIL-11 was capable of reversing abnormalities in secretomotor function associated with gut inflammation. We investigated the effects of rhIL-11 on epithelial electrogenic ion transport in the jejunum and colon. Application of rhIL-11 (10 to 10,000 ng/ml) at either the luminal or serosal side of mucosal sheets isolated from control rats induced a concentration-dependent reduction of transmural potential difference (PD) in the jejunum and decreased the short-circuit current (Isc), representative of active electrogenic transport, in the colon. To investigate the effect of rhIL-11 on an inflamed gut, we isolated jejunal and colonic tissue from HLA-B27 transgenic rats with active inflammation of the bowel that represents an animal model of IBD. In jejunum and colon isolated from HLA-B27 transgenic rats, basal electrogenic ion transport was significantly attenuated and, under these conditions, rhIL-11 caused no changes in either transmural PD or Isc. However, in HLA-B27 rats, pretreatment with subcutaneous doses of rhIL-11 suppressed the symptoms of diarrhea, normalized myeloperoxidase activity in the jejunum and colon and healed mucosal injury. In the jejunum from HLA-B27 rats, healing of the intestinal inflammatory response enhanced basal transmural PD and the rhIL-11-duced changes in mucosal ion transport resembled those seen in uninflamed controls. Conversely, in the colon, healing of the mucosa did not normalize basal active ion transport nor did it reverse the inhibition of rhIL-11-induced changes in colonic Isc. Our results suggest that endogenous IL-11 may act as a modulator of epithelial transport under physiologic conditions and may act as a potent anti-inflammatory cytokine during active intestinal inflammation.

Animals↗
PubMed1999

Five familial cases of opsismodysplasia substantiate the hypothesis of autosomal recessive inheritance.

We describe a family with two marriages of first cousins and a total of five children with opsismodysplasia. The diagnosis was based on clinical, radiological, and immunhistochemical findings. Helpful to the diagnosis was the testing with type I collagen antibodies, showing abnormally high levels in the hypertrophic area of growth cartilage. This observation supports the hypothesis of autosomal recessive transmission of opsismodysplasia.

Bone and Bones↗
PubMed1999

Anti-diarrhoeal effects of seirogan in the rat small intestine and colon examined in vitro.

BACKGROUND: Seirogan is a beechwood extract composed of guaiacol, creosol and other related phenolic compounds which is widely used as an anti-diarrhoeal agent in Asia. Abnormalities in water and electrolyte transport are often the cause of diarrhoea, but the mechanism of action of seirogan on small intestinal and colonic mucosal ion transport is unknown. AIM: To examine the effect of seirogan on electrogenic ion transport in vitro. METHODS: Sheets of rat jejunum and colon were mounted in Ussing chambers, and transmural potential difference (PD) was used as an electrical marker of changes in mucosal ion transport. Hypersecretory conditions were induced by acetylcholine (ACh). RESULTS: Serosal or mucosal application of seirogan (0.1-100 microg/mL) decreased basal jejunal transmural PD. Pre-treatment of the tissue with the neurotoxin, tetrodotoxin, did not inhibit the seirogan-induced changes in basal electrical activity. Seirogan had no effect on basal transmural PD in the ileum and colon. Under ACh-induced hypersecretory conditions in the small intestine and colon, addition of serosal or mucosal seirogan produced antisecretory effects determined indirectly by measurement of transmural PD. CONCLUSION: The ability of seirogan to decrease basal transmural PD in the jejunum, and inhibit the ACh-induced electrical responses, may contribute to its anti-diarrhoeal action.

Animals↗
PubMed1998

Cardiac tamponade in a postpartum woman with Lemierre's syndrome.

A 23-year-old primigravida with Lemierre's syndrome developed pericardial tamponade secondary to mediastinal infection and anticoagulant therapy. Intrathoracic echocardiographic diagnosis during a period of cardiac arrest led to urgent pericardiocentesis and successful resuscitation.

Adult↗
PubMed1995

Magnetic resonance imaging in phenylketonuria: reversal of cerebral white matter change.

OBJECTIVES: To investigate the extent to which the abnormalities in cerebral white matter in adolescents and adults with phenylketonuria (PKU) are reversible. METHOD: Magnetic resonance imaging (MRI) of the brain was repeated in 41 patients with PKU (age range, 14 to 49 years) after an interval (median, 9 months; range, 3 to 12 months) of dietary intervention. Scans were scored according to the extent of the white matter involvement. After an initial MRI, five patients returned to a strict low-phenylalanine diet with amino acid supplement; 21 patients started a low-protein diet (1 gm/kg) with amino acids supplement; and 15 patients made no dietary alteration. RESULTS: Scans improved in all five patients who returned to a strict low-phenylalanine diet, in 5 of the 21 patients on the low-protein diet plus amino acid supplement, and in 4 of the 15 patients who made no dietary change. There was a significant association between change in the MRI findings and in the blood phenylalanine concentration (Pearson correlation: r = 0.55; p < 0.0002) and between change in the MRI and in the phenylalanine level at the time of the second scan (r = 0.58; p < 0.0001). Improvement was seen primarily in those in whom phenylalanine levels were reduced to less than 900 mumol/L. There was no obvious change in MRI score after 3 weeks of strict phenylalanine restriction for the two adults who underwent serial scanning. CONCLUSION: The MRI changes in PKU are at least partially reversible by lowering the blood phenylalanine concentration.

Adolescent↗
PubMed1994

Magnetic resonance imaging of the brain in phenylketonuria.

Abnormalities of magnetic resonance imaging (MRI) of the brain occur in some patients with phenylketonuria but the clinical importance of this finding is not clear. In order to determine the frequency and functional significance of changes on MRI we investigated 77 adolescent and adult patients with phenylketonuria. Patients aged 14-49 years and taking a restricted diet of 1 g/kg protein underwent clinical examination, IQ testing, neurophysiological investigation, and MRI of the brain. Patients aged between 10-14 years taking a low phenylalanine diet with amino acid supplements had MRI of the brain only. Biochemical control was assessed from: the lifetime blood phenylalanine determined from the mean blood concentration throughout life; the accumulated time for each patient that phenylalanine was < 120 mumol/L; the accumulated time for each patient that phenylalanine was > 1200 mumol/L); mean blood concentration in the first 4 years of life; and the mean blood phe concentration in the 5 years prior to imaging. MRI changes, compatible with a disturbance in the water content of white matter, were present in all but 1 patient. The severity of abnormality was most strongly associated with the blood phenylalanine concentration at the time of imaging. Clinical and neurophysiological abnormalities were less common and usually mild. 3 patients had prolonged central motor conduction time, 7 had prolonged visual evoked potentials, and 5 had impaired peripheral sensory nerve conduction. There was no significant association between the extent of MRI abnormalities and IQ, and the presence of neurophysiological, or clinical abnormalities. An abnormal brain scan in PKU may reflect present biochemical control rather than indicate significant neurological damage. As yet there is little evidence that in most patients with PKU these MRI changes are of clinical importance.

Adolescent↗
PubMed1994

Comparison of a PCR-based diagnostic assay for Mycoplasma pulmonis with traditional detection techniques.

Current diagnosis of infection by Mycoplasma pulmonis, an important pathogen of laboratory rodent colonies worldwide, is based on serological, histopathological and culture techniques which can be slow and unreliable. A polymerase chain reaction (PCR) assay for M. pulmonis diagnosis was compared to current diagnostic methods. This PCR based technique allows a more specific, sensitive and rapid diagnosis of M. pulmonis from various tissues by comparison with culture and histopathology.

Animals↗
PubMed1991

Evidence that calcium channel blockade prevents cyclosporine-induced exacerbation of renal ischemic injury.

The following study was performed to determine whether calcium channel blockers, delivered before or after an ischemic insult, were effective at reducing cyclosporine-induced exacerbation of renal ischemic injury. When cyclosporine (5 mg/kg) was administered intravenously to rats after 30 min of renal ischemia, GFR fell by 60% compared with values observed in rats subjected to ischemia alone (190 +/- 30 vs. 330 +/- 40 microliters/min/100 g; P less than 0.05). Pretreatment with verapamil (10 micrograms/kg/min delivered intravenously) prevented the fall in GFR (320 +/- 70 microliters/min 100 g), as did pretreatment with nitrendipine, 1 micrograms/kg/min (460 +/- 90 microliters/min/100 g). Verapamil was less effective if given after the ischemia-cyclosporine insult (GFR 260 +/- 90 microliters/min/100 g), and nitrendipine given at this time had no beneficial effect at all (GFR 180 +/- 10 microliters/min/100 g). The doses of calcium channel blockers used had no protective effect on renal ischemic injury alone. Blood pressure during study ranged between 105 and 119 mm Hg with minor differences between groups. Sodium and potassium excretion and urinary flow rates were similar in all groups, except for a slight increase in sodium excretion in verapamil-treated rats. These values demonstrate that calcium channel blockers ameliorate the exacerbation or renal ischemic injury induced by cyclosporine if given before but not after the ischemia-cyclosporine insult. The protective effect of these agents, used preischemia in cyclosporine-treated rats, is observed with intravenous use of the drugs at doses that have no protective effect on renal ischemic injury alone.

Animals↗
PubMed1986

In vitro antimicrobial activity of six pulp-capping agents.

The antimicrobial activity of six commonly used pulp-capping agents was compared to reagent Ca(OH)2 by means of an in vitro microbiologic assay. Microbial samples were collected from deep carious lesions in each of twelve teeth and plated onto T-soy blood agar. Uniform disks of each pulp-capping agent were pressed slightly below the surface of each agar dish, and zones of bacterial inhibition were measured at 24 hours to the nearest 0.1 mm. All agents, including IRM, demonstrated significantly more antimicrobial activity than reagent Ca(OH)2 with the exception of Pulpdent. This tends to indicate that the antibacterial properties associated with these capping compounds are not entirely due to the high pH associated with Ca(OH)2.

Bacteria↗
PubMed1986

Beta adrenergic control of extrarenal potassium disposal. A beta-2 mediated phenomenon.

Beta adrenergic control of extrarenal potassium disposal was evaluated by examining the effects of physiologic doses of beta adrenergic agonists and antagonists on potassium tolerance in acutely nephrectomized rats. Following an acute intravenous potassium load (0.17 mEq/100 g over 60 min), the plasma potassium concentration rose significantly less in animals concomitantly treated with epinephrine at a dose that raises plasma epinephrine concentration to levels found during surgical stress (maximum plasma K 2.2 vs. 2.9 mEq/1 in controls receiving KCl alone; p less than 0.005). Similar results were observed with the selective beta-2 agonists salbutamol and terbutaline. Conversely, the rise in plasma potassium concentration was significantly greater in rats treated with low-dose propranolol (beta-1 + beta-2 blockade) and with butoxamine (beta-2 blockade) compared to control animals. In contrast, the selective beta-1 blocking agent metoprolol had no effect on potassium tolerance. Alterations in potassium tolerance following the administration of various beta adrenergic agonists and antagonists could not be explained by changes in plasma insulin, renin, or glucose concentration or by differences in the acid-base or hemodynamic status of the animals. The data suggest that beta adrenergic control of extrarenal potassium disposal occurs with physiologic stimulation or blockade of the beta-2 receptor site.

Acid-Base Equilibrium↗
PubMed1983

The effect of dexamethasone on renal potassium excretion and acute potassium tolerance.

In order to further characterize the kaliuretic action of dexamethasone, the effect of the hormone on renal electrolyte excretion and potassium tolerance was evaluated. In the first set of experiments, dexamethasone was administered acutely to unreplaced adrenalectomized rats, to adrenalectomized rats replaced with a single daily injection of dexamethasone (10 micrograms/100 g X day), and to intact control rats. After dexamethasone injection (10 micrograms/100 g), urinary potassium excretion increased by 105% in unreplaced adrenalectomized rats (0.99 +/- 0.13 to 2.02 +/- 0.26 mueq/min, P less than 0.005) and by 59% in rats maintained on glucocorticoid (0.87 +/- 0.10 to 1.38 +/- 0.18 mueq/min, P less than 0.05). The kaliuresis in adrenalectomized rats was associated with a significant increase in phosphate excretion and by a tendency for urinary chloride excretion to rise. In contrast, potassium excretion was unchanged by dexamethasone in control rats. These results indicate that the kaliuretic effect of dexamethasone is influenced by the degree of glucocorticoid deficiency before hormone administration. An additional study with K loading was performed in these same three groups of rats to evaluate the effect of dexamethasone replacement on potassium tolerance. Adrenalectomized rats maintained in daily dexamethasone replacement received an additional dose of hormone (50 micrograms/100 g) before study. After KCl, plasma potassium concentration rose significantly higher in unreplaced adrenalectomized rats vs. control (2.2 +/- 0.2 vs. 1.3 +/- 0.4 meq/liter, P less than 0.05) and peak renal potassium clearance was significantly blunted (577 +/- 90 vs. 1104 +/- 120 microliter/min. P less than 0.001). This impairment in potassium tolerance could not be attributed to hypotension, acidemia, diminished urinary flow, or sodium delivery in the distal nephron in unreplaced adrenalectomized rats but may be explained by decreased renal perfusion since glomerular filtration rate at the end of study was lower than in controls. Dexamethasone replacement improved potassium tolerance (peak delta Pk = 1.7 +/- 0.1 meq/liter) and renal potassium clearance (942 +/- 60 microliter/min). These data demonstrate that dexamethasone, at the high dose employed during KCl loading, improves renal potassium tolerance by enhancing renal K clearance in adrenalectomized rats. These results explain our previous report of near normal potassium excretion in glucocorticoid replaced adrenalectomized rats.

Adrenalectomy↗
PubMed1982

The effect of dexamethasone on renal electrolyte excretion in the adrenalectomized rat.

The acute effect of low and high doses of dexamethasone on renal electrolyte excretion was examined in chronically (2--3 weeks) adrenalectomized rats and was compared with that of aldosterone. At the lowest effective dose (2 micrograms/100 g BW) dexamethasone injection produced a 70% increase in urinary potassium (K) excretion (0.99 +/- 0.06 to 1.70 +/- 0.20 mueq/min; P less than 0.005) but had no effect on sodium excretion. In contrast, low doses of aldosterone (2.5 micrograms/100 g BW) caused a significant decrease in urinary sodium excretion (6.23 +/- 1.2 to 2.75 +/- 0.7 mueq/min; P less than 0.01) but had no influence on renal potassium excretion (UKV). Higher doses of dexamethasone (10, 20 and 50 micrograms/100 g BW) produced a greater kaliuresis, increasing UKV by more than 100% over baseline and higher (P less than 0.05) than values after a low dose of dexamethasone, but again failed to lower sodium excretion. The increase in UKV after all doses of dexamethasone occurred in association with a significant increase in urinary K concentration; at higher doses of dexamethasone there was a variable increase in urine flow. The increase in UKV was not secondary to an increase in plasma K concentration nor was it associated with a rise in blood pressure or glomerular filtration rate after dexamethasone administration. These findings demonstrate that, in the adrenalectomized rat, acute administration of low and high doses of dexamethasone increases urinary K excretion without affecting sodium excretion. In contrast, aldosterone has little effect on K excretion but significantly decreases sodium excretion. These results indicate that the kaliuresis observed after dexamethasone cannot be attributed to a mineralocorticoid property of the hormone.

Adrenalectomy↗