Cessation of migraine with aura following removal of left atrial myxoma.
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Female↗
Biomedical subjects
L Caputi
Publications and source records attributed to L Caputi.
Neuroprotective actions in vivo and electrophysiological actions in vitro of 202W92.
202W92 (R-(-)-2,4-diamino-6-(fluromethyl)-5-(2,3,5-trichlorophenyl)pyrimidine) is a novel compound in the same chemical series as the antiepileptic drug lamotrigine and the neuroprotective sipatrigine. Here 202W92 was quantitatively assessed as a neuroprotective agent in focal cerebral ischaemia, and as an inhibitor of sodium and calcium channels and of synaptic transmission. In the rat permanent middle cerebral artery occlusion (MCAO) model of acute focal ischaemia, 202W92 reduced infarct volume by 75% in cortex and by 80% in basal ganglia, with ED(50) approximately 2 mg/kg (single i.v. dose, 10 min post-occlusion). In whole-cell current recordings from single cells, 202W92 completely and reversibly inhibited voltage gated sodium channels (IC(50) 3 x 10(-6) M) in rat freshly-isolated cortical neurons and in the GH(3) pituitary cell line. 202W92 also inhibited a nifedipine-sensitive fraction (approximately 35%) of native high-voltage-activated (HVA) calcium current in rat cortical neurons (IC(50) 15 x 10(-6) M) and weakly inhibited low-voltage-activated (LVA) calcium currents of the recombinant alpha1I-mediated T-type (IC(50)>100 x 10(-6) M). The drug inhibited the amplitude and frequency of 4-aminopyridine-evoked glutamatergic excitatory post-synaptic currents (EPSCs). In conclusion, 202W92 is an effective neuroprotective agent when administered post-ischaemia and a potent sodium channel inhibitor in vitro.
Animals↗
Group I mGluRs coupled to G proteins are regulated by tyrosine kinase in dopamine neurons of the rat midbrain.
Metabotropic glutamate receptors (mGluRs) modulate neuronal function via different transduction mechanisms that are either dependent or independent on G-protein function. Here we investigated, using whole cell patch-clamp recordings in combination with fluorimetric measurements of intracellular calcium concentration ([Ca(2+)](i)), the metabolic pathways involved in the responses induced by group I mGluRs in dopamine neurons of the rat midbrain. The inward current and the [Ca(2+)](i) increase caused by the group I mGluR agonist (S)-3,5-dihydroxyphenylglycine (DHPG, 100 microM) were permanently activated and subsequently abolished in cells loaded with the nonhydrolizable GTP-analogue GTP-gamma-S (600 microM). In addition, when GDP-beta-S (600 microM) was dialyzed into the cells to produce the blockade of the G proteins, the DHPG-dependent responses were reduced. When the tissue was bathed with the phospholipase C inhibitor 1-[6[[(17 beta)-3-methoxyestra-1,3,5(10)-trien-17-yl]amino]exyl]-1H-pyrrole-2,5-dione (10 microM), the DHPG-induced calcium transients slightly diminished but the associated inward currents were not affected. Interestingly, a substantial depression of the DHPG-induced inward current and transient increase of [Ca(2+)](i) was caused by the protein tyrosine kinase inhibitors tyrphostin B52 (40 microM) and 4',5,7-trihydroxyisoflavone (genistein; 40 microM), whereas genistein's inactive analogue 4',5,7-trihydroxyisoflavone-7-glucoside (40 microM) was ineffective. The blockade of the Src family of tyrosine kinase by 4-amino-5-(4-methylphenyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimidine (20 microM), mitogen-activated protein kinase by 2'-amino-3' methoxyflavone (50 microM), and protein kinase C by staurosporine (1 microM) had no effect on the cellular responses caused by DHPG. The mGluR5-selective antagonist 2-methyl-6-(phenylethynyl)-pyridine (10--100 microM) did not affect the actions of DHPG. Thus our results indicate that the responses, mainly mediated by mGluRs1 in dopamine neurons, are activated by intracellular mechanisms coupled to G proteins and regulated by tyrosine kinases.
Animals↗
Is pyloric function preserved in pylorus-preserving pancreaticoduodenectomy?
OBJECTIVE: To assess the function of the pylorus after pylorus-preserving pancreaticoduodenectomy (PPPD) done for periampullary or pancreatic cancer. DESIGN: Prospective, observational controlled clinical study. SETTING: Teaching hospital, Italy. SUBJECTS: 17 patients who had undergone PPPD, and 15 healthy control subjects. INVESTIGATIONS: Endoscopy to check for gastritis and marginal ulcers and 24 h-pH monitoring and 99mTc HIDA scintigraphy to detect jejunogastric reflux. Scintigraphy was also used to evaluate gastric and jejunal transit after a solid meal labelled with 99mTc colloid sulphur. MAIN OUTCOME MEASURES: Signs of delayed gastric emptying, jejunogastric reflux and gastric outlet obstruction in the short and long term. RESULTS: In the early postoperative period only 1 patient had delayed gastric emptying. In the long term, two patients had symptoms of dyspepsia and 8/11 showed alkaline reflux with persistent gastric pH more than 4 for more than 12 hours; 3 had histological signs of gastritis. There was no difference in gastric emptying compared with controls, but three patients had prolonged emptying time (T1/2 more than 85 minutes). Endoscopy findings correlated with pH monitoring results. CONCLUSIONS: After PPPD, most patients have abnormal pyloric function, but it is clinically evident in only a small proportion.
Adult↗
The integration of theoretical constructs into the design of computer assisted instruction.
The authors believe that for computer assisted instruction to be an effective instructional tool, it must incorporate the most current theoretical principles related to learning and instruction. To assist future developers of computer assisted instruction, the authors review some of the major constructs from the theoretical foundations of various disciplines and then illustrate the integration of these constructs in the design of a software program entitled SOS--Strategies for Problem Solving.
Computer-Assisted Instruction↗
A cognitive approach to classifying instructional software.
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Computer-Assisted Instruction↗
TLC at college of DuPage.
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Computer-Assisted Instruction↗
Welcome to TLC General Hospital.
This article discusses the development of the computer program titled TLC General Hospital, then offers hints and ideas for nurses contemplating the development of their own instructional packages.
Computer Simulation↗