Biomedical subjects

Eun A Choi

Publications and source records attributed to Eun A Choi.

6 recordsLinked to original sources

PubMed2006

Id-1 gene downregulation by sulindac sulfide and its upregulation during tumor development in gastric cancer.

The molecular mechanisms underlying the chemopreventive effects of NSAIDs are not well understood and remain the subject of debate. One of the mechanistic possibilities involves alterations in gene expression. We examined gene expression profiles in SNU601 gastric cancer cells treated with sulindac sulfide (50 microM) for 24 hr. Microarray analysis showed that 1.3% (105/8170) of genes were induced or repressed more than 3-fold in cells treated with sulindac sulfide. Seven genes were selected and confirmed by reverse transcription-polymerase chain reaction. Inhibitor of differentiation/DNA binding-1 (Id-1) was downregulated in SNU601 cells treated with sulindac sulfide. Id-1 expression level was decreased dose-dependently by sulindac sulfide. In addition, the expression pattern of Id-1 was inversely related to that of nm23. We also examined Id-1 expression in human gastric cancer tissues and compared it with clinicopathologic parameters to study its biologic role in the cancers. Id-1 was frequently and strongly expressed in gastric cancer tissues compared with that in adjacent nonmetaplastic mucosa. Its immunoreactivity scores were positively correlated to Ki67 labeling indices and tumor progression, and is higher in intestinal type than in diffuse type. In summary, a number of genes, both induced and repressed, could be important in mediating sulindac sulfide-induced cell death in gastric cancer cells. Id-1, one of the repressed genes, is upregulated in gastric cancers and has positive role in tumor progression and histogenesis of intestinal-type cancers.

Adult↗

PubMed2006

Altered responsivity to central administrations of corticotropin-releasing factor in rats with a history of opiate exposures.

The authors studied the effects of a history of opiate exposures on behavioral responses to intracerebroventricular (ICV) microinjections of the stress-related peptide corticotropin-releasing factor (CRF). Rats were injected for 10 days with morphine (10 mg/kg) or saline, and 1 or 7 days later they received an ICV microinjection of CRF (0.5 microg or 2.5 microg) or artificial cerebrospinal fluid. Microinjections of CRF produced anxiety-like behavior, locomotor activity, and self-grooming. The anxiogenic response was altered so that morphine-treated rats showed reduced responses to 0.5-microg CRF but showed exaggerated responses to 2.5-microg CRF 1 or 7 days after last opiate exposure. These findings suggest that alterations in central CRF circuits may underpin the increased vulnerability to anxiety observed following opiate exposures.

Animals↗

PubMed2005

Expression of cardiovascular and behavioural components of conditioned fear to context in T4 spinally transected rats.

A spinal cord transection at the fourth thoracic level (T4) results in paraplegia. It also removes supraspinal control of sympathetic outflow to most viscera and their blood vessels but spares the heart. We studied the effects of such a transection on the expression of the conditioned fear response to context, which includes freezing, 22 kHz ultrasonic vocalisations, a marked pressor response and a slowly rising tachycardia. Rats implanted with radiotelemetric probes were fear conditioned, tested, then transected at T4 and finally re-tested 4 weeks after transection. Baseline blood pressure in transected animals was the same as in intact animals but baseline heart rate was 127 bpm higher. There were clear signs of fear in the transected animals: although freezing occurred in the upper part of the body only, there was a 3 fold increase in the number of ultrasonic vocalisations, most probably due to paralysis of abdominal muscles that made expirations shorter and therefore more frequent. The pressor response of fear was initially the same as in intact animals but controls revealed that this was due to handling during transfer to the aversive context. The rest of the pressor response was markedly reduced (70%) confirming that it depends in large part on a sympathetically mediated increase in vascular resistance in the lower part of the body. The cardiac response was characterized by an initial bradycardia followed by a marked tachycardia, which is consistent with a baroreceptor-mediated reflex response to the altered pressor changes. Finally, none of these changes was observed when the same experiment was repeated in sham transected animals. Thus, the pressor response of fear is in large part mediated by the thoracic cord below T4 and the baroreflex is not inhibited but maintained during conditioned fear.

Animals↗

PubMed2005

The midbrain periaqueductal gray and fear extinction: opioid receptor subtype and roles of cyclic AMP, protein kinase A, and mitogen-activated protein kinase.

Four experiments studied the opioid receptor subtype and signal transduction mechanisms mediating fear extinction in the ventrolateral quadrant of the midbrain periaqueductal gray (vlPAG). Microinjection of a mu- but not a delta- or kappa-opioid receptor antagonist into the vlPAG retarded extinction. Extinction was also dose-dependently retarded by vlPAG infusions of a cyclic AMP (cAMP) analog but was unaffected by infusions of a protein kinase A activator or a mitogen-activated protein kinase inhibitor across wide dose ranges. The results show that fear extinction occurs via activation of vlPAG mu-opioid receptors and involves reductions in cAMP. These mechanisms are different from the cellular mechanisms for extinction in the amygdala and from the known cellular mechanisms for opioid analgesia in the vlPAG.

Analysis of Variance↗

PubMed2004

Sentinel lymph node biopsy after neoadjuvant chemotherapy.

BACKGROUND: We surveyed single-center and multi-center studies pertaining to sentinel lymph node biopsy (SLNB) after neoadjuvant chemotherapy to compare the results with those of our current study to evaluate the feasibility and accuracy of SLNB after neoadjuvant chemotherapy. METHODS: From October 2001 to July 2003, 80 patients who had neoadjuvant chemotherapy underwent curative surgery and axillary lymph node dissection (ALND) after SLNB at the Center for Breast Cancer, National Cancer Center. A MEDLINE search was performed using the keywords breast cancer, sentinel lymph node biopsy, and neoadjuvant chemotherapy. RESULTS: Our results showed that 42 (52.6%) of 80 patients had downstaging of the primary tumor; 9 patients (11.3%) had pathologic complete response (pCR) and 33 (41.3%) had pathologic partial response (pPR). 26 patients (32.5%) showed complete axillary clearance after neoadjuvant chemotherapy. Among them, 5 patients (6.3%) revealed pCR of both the primary tumor and axillary metastasis. SLNB was successful in 61 of 80 patients (76.3%) and there were 3 false negatives, yielding a false negative rate (FNR) of 7.3% (3/41), a negation prediction value (NPV) of 87.0%(20/23), and an accuracy of 95.1% (58/61). Thirteen out of 16 studies retrieved by to MEDLINE pertaining SLNB after neoadjuvant chemotherapy concluded its feasibility and accuracy with a identification rate of 82%-100% and a FNR of 17-100%. CONCLUSION: Most studies, including ours, concluded that SLNB after neoadjuvant chemotherapy is accurate and could be an alternative to ALND.

Adult↗

PubMed2002

Pleiotrophin (PTN) and midkine (MK) mRNA expression in eutopic and ectopic endometrium in advanced stage endometriosis.

Endometriosis is characterized by the ectopic implantation of endometrium on peritoneal surfaces. Angiogenic and growth factors may play a significant role in the pathogenesis of endometriosis. Midkine (MK) and pleiotrophin (PTN) are two related peptides associated with carcinogenesis and angiogenesis. To test the hypothesis that a higher expression of MK and PTN in ectopic and eutopic endometrium from women with endometriosis might favour increased angiogenesis and growth with subsequent ectopic implantation, we investigated PTN and MK expression by quantitative competitive PCR (QC-PCR) in endometrium from 30 women with severe, stages III and IV endometriosis and from 30 women without endometriosis. Total RNA was extracted and reverse transcribed into cDNA, and QC-PCR was performed to evaluate PTN and MK mRNA expression. Results were analysed by analysis of variance. Eutopic endometrium from endometriosis patients showed increased expression of MK and PTN mRNA compared with endometrium from normal women in the luteal phase (P < 0.05). MK and PTN mRNA expression in ectopic endometrium was significantly lower than that in eutopic endometrium from women with and without endometriosis (P < 0.05). Our results suggest increased MK and PTN expression may be related to the initiation of ectopic endometrial implants and peritoneal invasion.

Adult↗