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S Y Lok

Publications and source records attributed to S Y Lok.

6 recordsLinked to original sources
PubMed2000

Prostate cancer: MR imaging and thermometry during microwave thermal ablation-initial experience.

Percutaneous interstitial microwave thermoablation of locally recurrent prostate carcinoma was continually guided with magnetic resonance (MR) imaging. Phase images and data were obtained with a rapid gradient-echo technique and were used to derive tissue temperature change on the basis of proton-resonance shift. Thermally devitalized regions correlated well with the phase image findings. MR imaging-derived temperatures were linearly related to the fluoroptic tissue temperatures. MR imaging can be used to guide thermoablation.

Aged↗
PubMed1995

Primary renal artery dissection.

A typical case of primary renal artery dissection, an unusual entity causing renal infarction, is described. This abnormality, masquerading as renal colic, affects otherwise-healthy middle-aged men. Angiography, which will confirm the diagnosis, should precede nephrectomy, because vascular repair may be feasible.

Adult↗
PubMed1992

Efflux of glutamate produced by short ischemia of varied severity in rat striatum.

BACKGROUND AND PURPOSE: Evidence has accumulated suggesting that ischemia-induced neuronal damage may be linked to an extracellular overflow of glutamate. The purpose of this study was to provide new information about the time course of the increase in extracellular glutamate concentration associated with moderate and severe ischemia, and its relationship with electrical changes including anoxic depolarization. METHODS: Changes in the extracellular concentration of glutamate were continuously monitored in the rat striatum by microdialysis. Ischemia was induced by four-vessel occlusion for 3 or 5 minutes, and in some cases its severity was increased with a neck tourniquet. The severity of ischemia was assessed by electroencephalogram and direct current potential recording to detect anoxic depolarization. RESULTS: In all experiments, the extracellular glutamate concentration began to increase shortly after the onset of ischemia and steadily rose throughout the ischemic period. Increases up to 35.0 mumol/l (2-3 mumol/l baseline; p less than 0.005) were observed when ischemia provoked the rapid occurrence of a large and sustained anoxic depolarization. Relatively smaller but still significant increases (6.9 mumol/l; p less than 0.005) were observed in penumbral conditions (electroencephalogram loss without anoxic depolarization). Glutamate began to be cleared immediately after reperfusion and 90% of released glutamate was cleared within 5 minutes, even when the preceding ischemia had been severe. CONCLUSIONS: We propose that the extracellular glutamate concentration may not reach critical levels during short episodes of penumbral ischemia, but this might happen with a longer ischemic period.

Animals↗
PubMed1992

Changes in extracellular glutamate concentration produced in the rat striatum by repeated ischemia.

BACKGROUND AND PURPOSE: Evidence suggesting that ischemia-induced neuronal damage may be linked to an extracellular overflow of glutamate has accumulated, and previous studies have shown that repetitive ischemic insults may have a cumulative effect. The purpose of this study was to investigate changes in the extracellular glutamate concentration produced by repeated brief ischemic episodes of varied severity. METHODS: Four consecutive 3- or 5-minute periods of bilateral hemispheric ischemia were produced in rats, each ischemic period followed by 27 minutes of reperfusion. Extracellular glutamate in the striatum was monitored using microdialysis, and the electroencephalogram and extracellular direct current potential were recorded in the same tissue site to assess the severity of ischemia. RESULTS: The results suggest that the kinetics of the increase in the extracellular glutamate concentration produced by a brief ischemic episode are similar, irrespective of whether it is a single insult or part of a repeated sequence. In all cases, the extracellular glutamate concentration increased throughout ischemia and returned to its preischemic level early during reperfusion. The pattern of changes in the ischemia-induced glutamate overflow during repetitive insults varied with the severity of ischemia, in common with the pattern of changes in the direct current potential, supporting the concept that ionic changes associated with anoxic depolarization are a major determinant of ischemia-induced glutamate overflow. CONCLUSIONS: There may be no cumulative effect of brief repeated episodes of ischemia on the extracellular glutamate concentration, even though repeated 5-minute ischemic episodes apparently caused progressive deterioration of ionic homeostasis in some cases.

Animals↗
PubMed1991

Changes in rat brain extracellular glutamate concentration during seizures induced by systemic picrotoxin or focal bicuculline injection: an in vivo dialysis study with on-line enzymatic detection.

An on-line enzymatic assay of dialysis fluid has been used to monitor the extracellular glutamate concentration in the rat hippocampus. Perfusion with artificial cerebrospinal fluid containing a glutamate uptake inhibitor (either dihydrokainate or 4,4'-diisothiocyanatostilbene-2,2' disulfonic acid) produced a marked stable increase in glutamate concentration; 10 min perfusion with 100 mM K+ produced a transient increase. Sustained epileptiform EEG discharges were induced in the hippocampus by focal injection of bicuculline into the piriform cortex or by systemic injection of picrotoxin. Extracellular glutamate did not change significantly during seizure activity, either in the absence or in the presence of glutamate uptake inhibitors. It is concluded that seizure activity is not necessarily accompanied by an overall increase in extracellular glutamate concentration.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗