Biomedical subjects

Kisok Kim

Publications and source records attributed to Kisok Kim.

6 recordsLinked to original sources

PubMed2005

Effect of subchronic acrylamide exposure on the expression of neuronal and inducible nitric oxide synthase in rat brain.

Acrylamide (ACR) is a known industrial neurotoxic chemical. Evidence suggests that ACR neurotoxic effect is related to brain neurotransmission disturbances. Since nitric oxide (NO) acts as a neurotransmission modulator and is produced by nitric oxide synthase (NOS), the neuronal NOS (nNOS) and inducible NOS (iNOS) expression pattern were determined in rat cerebral cortex and striatum after subchronic exposure to ACR. Using immunocytochemistry, the neuronal count of nNOS or optical density of iNOS from sections at three coronal levels, bregma 1.0, -0.4, and -2.3 mm, were compared between ACR-treated and control rats. At all three levels, nNOS expressions were uniformly decreased in most of the neocortical subregions following the treatment of ACR. At bregma level 1.0 mm, total numbers of nNOS expressing neurons were significantly decreased to 58.7% and 64.7% of the control in the cortex and striatum of ACR-treated rats, respectively. However, at the bregma level -2.3 mm, ACR treatment did not produce a significant difference in the numbers of nNOS expressing neurons both in the cortex and striatum. Contrary to nNOS, iNOS expressions were consistently increased to approximately 32% in the neocortex and 25% in the striatum, following the subchronic ACR treatment. These data suggest that subchronic ACR exposure involves compensatory mechanism on nNOS and iNOS expression to maintain the homeostasis of NO at the rostral part of the neocortex and the striatum. However, in the caudal brain, increased iNOS expression did not suppress nNOS expression. Therefore, the present study is consistent with the hypothesis that ACR toxicity is mediated through the disturbance to the NO signaling pathway and exhibits a rostrocaudal difference through the differential expressions of nNOS and iNOS in the neocortex and the striatum.

Acrylamide↗

PubMed2004

3-monochloropropane-1,2-diol does not cause neurotoxicity in vitro or neurobehavioral deficits in rats.

3-monochloro-1,2-propanediol (3-MCPD) is a contaminant of acid-hydrolyzed vegetable protein. Several reports have suggested that chronic exposure to 3-MCPD could produce neurotoxicity in vitro or neurobehavioral effects in experimental animals. The present study further explored the in vitro neurotoxic effects of 0.1-100 microM 3-MCPD on PC12 and N18D3 cell lines. In addition, to investigate the effects of repeated ingestion of 3-MCPD on neurobehavioral impairments parameters in rats, motor activity, landing foot splay, and grip strength tests were performed, following treatment with 3-MCPD at dose levels of 10, 20, and 30 mg/kg per day for 11 weeks. We demonstrated that no significant neurotoxic effects were present in 3-MCPD-treated rats compared to saline-treated control rats, whereas, acrylamide, used as a positive control, induced significant deficits in all neurobehavioral parameters in both male and female rats. On the other hand, body weight gain was significantly decreased in high dose 3-MCPD-treated male rats as well as in acrylamide-treated rats. Taken together, these results suggest that 3-MCPD, at the dose levels used for this study, does not produce in vitro neurotoxicity or neuromotor deficits in vivo.

Animals↗

PubMed2004

Six regularities of source recognition.

In recent work, researchers have shown that source-recognition memory can be incorporated in an extended signal detection model that covers both it and item-recognition memory (A. Hilford, M. Glanzer, K. Kim, & L. T. DeCarlo, 2002). In 5 experiments, using learning variables that have an established effect on item recognition, the authors tested further implications of that extended model. The results establish 6 source-recognition regularities that support the model. An important regularity in that set is the linkage of source and item recognition: Any learning variable that increases item recognition increases source recognition.

Humans↗

PubMed2004

The effect of PARP inhibitor on ischaemic cell death, its related inflammation and survival signals.

Poly(ADP-ribose) polymerase (PARP) plays an important role in ischaemic cell death, and 3-aminobenzamide (3-AB), one of the PARP inhibitors, has a protective effect on ischaemic stroke. We investigated the neuroprotective mechanisms of 3-AB in ischaemic stroke. The occlusion of middle cerebral artery (MCA) was made in 170 Sprague-Dawley rats, and reperfusion was performed 2 h after the occlusion. Another 10 Sprague-Dawley rats were used for sham operation. 3-AB was administered to 85 rats 10 min before the occlusion [3-AB group (n = 85) vs. control group without 3-AB (n = 85)]. Infarct volume and water content were measured, brain magnetic resonance imaging, terminal deoxynucleotidyltransferase (TdT)-mediated dUTP-biotin nick end-labelling (TUNEL) and Cresyl violet staining were performed, and immunoreactivities (IRs) of poly(ADP-ribose) polymer (PAR), cleaved caspase-3, CD11b, intercellular adhesion molecule-1 (ICAM-1), cyclooxygenase-2 (COX-2), phospho-Akt (pAkt) and phospho-glycogen synthase kinase-3 (pGSK-3) were compared in the peri-infarcted region of the 3-AB group and its corresponding ischaemic region of the control group at 2, 8, 24 and 72 h after the occlusion. In the 3-AB group, the infarct volume and the water content were decreased (about 45% and 3.6%, respectively, at 24 h), the number of TUNEL-positive cells was decreased (about 36% at 24 h), and the IRs of PAR, cleaved caspase-3, CD11b, ICAM-1 and COX-2 were significantly reduced, while the IRs of pAkt and pGSK-3 were increased. These results suggest that 3-AB treatment could reduce the infarct volume by reducing ischaemic cell death, its related inflammation and increasing survival signals. The inhibition of PARP could be another potential neuroprotective strategy in ischaemic stroke.

Animals↗

PubMed2003

Perinatal exposure to aluminum alters neuronal nitric oxide synthase expression in the frontal cortex of rat offspring.

Disturbance of the neuronal nitric oxide signaling pathway by chronic exposure to aluminum (Al) in drinking water may be a causal factor of neurological disorders in offspring. In order to investigate the relationship between Al administration and expression of neuronal nitric oxide synthase (nNOS), the numbers and distribution patterns of nNOS-immunoreactive neurons were examined in the frontal cortex of offspring after exposure to 0, 5, and 10 mM of Al in drinking water during prenatal and neonatal periods. At the bregma 0.20 level, the number of nNOS-positive neurons was significantly increased (10%) and decreased (17%) following exposure to 5 and 10 mM of Al in drinking water, respectively. The change was more severe in the upper layer than in deep layer of the cortex. In contrast, at the bregma -2.80 level, the number and distribution pattern was not significantly changed following exposure to Al. These data suggest that Al toxicity may be mediated through disturbances to the nitric oxide signaling pathway and exhibits a biphasic effect, especially in the frontal area of the cortex. In addition, the results suggest that impaired expression of nNOS plays an important role in the development of neurological syndrome caused by an exposure to Al during the early developmental stage.

Aluminum↗

PubMed2002

Regularities of source recognition: ROC analysis.

Source memory has become the focus of a growing number of investigations in a variety of fields. An appropriate model for source memory is, therefore, of increasing importance. A simple 2-dimensional signal-detection model of source recognition is presented. The receiver operating characteristics (ROCs) obtained from 3 experiments are then used to test the model. The data demonstrate 3 regularities: convex ROCs, z-ROCs with linear slopes of 1.00, and slightly concave z-ROCs. Two of these regularities support the model. The 3rd requires a revision of the model. This revised model is fitted to the data. The implications of these regularities for other theories are also discussed.

Adolescent↗