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1.
Journal of the Korean Society of Emergency Medicine ; : 19-26, 2021.
Article in Korean | WPRIM | ID: wpr-875100

ABSTRACT

Objective@#This study is to measure the high sensitivity C-reactive protein (hs-CRP) value in acute myocardial infarction (AMI) patients who arrive within 6 hours of the symptom manifestation and see how the resulting value affects the short term prognosis in AMI patients. @*Methods@#This study was conducted on 118 patients who had less than 6 hours of onset-to-door time among 149 patients who were diagnosed with myocardial infarction in emergency room and undergo percutaneous coronary intervention (PCI) for 2 years from September 2017. The group including main adverse cardiovascular outcomes were compared in the patients according to the blood test figures (hs-CRP on admission [CRP1], CRP velocity [CRPv], post-PCI hs-CRP [CRP2], and CRP difference values [CRP2-1]). @*Results@#In this study, the average of the hs-CRP values of AMI patients arriving within 6 hours of the symptom manifestation was 2.2±2.3 mg/L. CRP velocity that corrected the CRP value to the elapsed time after the onset of symptoms and N-terminal probrain natriuretic peptide (NT-proBNP) appeared to be significantly correlated with the occurrence of main adverse cardiovascular outcomes (P=0.03). @*Conclusion@#The hs-CRP values of AMI patients arrived within 6 hours of the symptom manifestation showed the mean risk group. CRPv and NT-proBNP showed a significant casual relationship with main adverse cardiovascular outcomes.

2.
International Neurourology Journal ; : 137-149, 2021.
Article in English | WPRIM | ID: wpr-898769

ABSTRACT

Purpose@#Adenosine monophosphate-activated protein kinase (AMPK) is thought to inhibit cell proliferation or promote cell death, but the details remain unclear. In this study, we propose that AMPK inhibits the expression of anti-apoptotic B-cell lymphoma 2 (Bcl-2) by relying on the hypoxia-inducible factor 1 alpha (HIF-1α)-induced caveolin-1 (Cav-1) expression pathway in noninvasive human bladder tumor (RT4) cells. @*Methods@#In cells exposed to a hypoxic environment (0.5% oxygen), the levels of expression and phospho-activity of the relevant signaling enzymes were examined via Western blots and reverse transcription-polymerase chain reaction. Cell proliferation was assessed using a Cell Counting Kit-8 assay. @*Results@#The level of expression of Cav-1 was very low or undetectable in RT4 cells. Hypoxia was associated with significantly decreased cell growth, along with marked induction of HIF-1α and Cav-1 expression; additionally, it suppressed the expression of the antiapoptotic marker Bcl-2 while leaving AMPK activity unchanged. Under hypoxic conditions, HIF-1α acts as a transcription factor for Cav-1 mRNA gene expression. The cell growth and Bcl-2 expression suppressed under hypoxia were reversed along with decreases in the induced HIF-1α and Cav-1 levels by AMPK activation with metformin (1mM) or phenformin (0.1mM). In addition, pretreatment with AMPK small interfering RNA not only increased the hypoxia-induced expression of HIF-1α and Cav-1, but also reversed the suppression of Bcl-2 expression. These results suggest that HIF-1α and Cav-1 expression in hypoxic environments is regulated by basal AMPK activity; therefore, the inhibition of Bcl-2 expression cannot be expected when AMPK activity is suppressed, even if Cav-1 expression is elevated. @*Conclusions@#For the first time, we find that AMPK activation can regulate HIF-1α induction as well as HIF-1α-induced Cav1 expression, and the hypoxia-induced inhibitory effect on the antiapoptotic pathway in RT4 cells is due to Cav-1-dependent AMPK activity.

3.
International Neurourology Journal ; : 137-149, 2021.
Article in English | WPRIM | ID: wpr-891065

ABSTRACT

Purpose@#Adenosine monophosphate-activated protein kinase (AMPK) is thought to inhibit cell proliferation or promote cell death, but the details remain unclear. In this study, we propose that AMPK inhibits the expression of anti-apoptotic B-cell lymphoma 2 (Bcl-2) by relying on the hypoxia-inducible factor 1 alpha (HIF-1α)-induced caveolin-1 (Cav-1) expression pathway in noninvasive human bladder tumor (RT4) cells. @*Methods@#In cells exposed to a hypoxic environment (0.5% oxygen), the levels of expression and phospho-activity of the relevant signaling enzymes were examined via Western blots and reverse transcription-polymerase chain reaction. Cell proliferation was assessed using a Cell Counting Kit-8 assay. @*Results@#The level of expression of Cav-1 was very low or undetectable in RT4 cells. Hypoxia was associated with significantly decreased cell growth, along with marked induction of HIF-1α and Cav-1 expression; additionally, it suppressed the expression of the antiapoptotic marker Bcl-2 while leaving AMPK activity unchanged. Under hypoxic conditions, HIF-1α acts as a transcription factor for Cav-1 mRNA gene expression. The cell growth and Bcl-2 expression suppressed under hypoxia were reversed along with decreases in the induced HIF-1α and Cav-1 levels by AMPK activation with metformin (1mM) or phenformin (0.1mM). In addition, pretreatment with AMPK small interfering RNA not only increased the hypoxia-induced expression of HIF-1α and Cav-1, but also reversed the suppression of Bcl-2 expression. These results suggest that HIF-1α and Cav-1 expression in hypoxic environments is regulated by basal AMPK activity; therefore, the inhibition of Bcl-2 expression cannot be expected when AMPK activity is suppressed, even if Cav-1 expression is elevated. @*Conclusions@#For the first time, we find that AMPK activation can regulate HIF-1α induction as well as HIF-1α-induced Cav1 expression, and the hypoxia-induced inhibitory effect on the antiapoptotic pathway in RT4 cells is due to Cav-1-dependent AMPK activity.

4.
Journal of the Korean Society of Emergency Medicine ; : 463-472, 2009.
Article in Korean | WPRIM | ID: wpr-207286

ABSTRACT

PURPOSE: Early goal-directed therapy (EGDT) has been known to reduce the mortality of patients with severe sepsis and septic shock. We wanted to determine the clinical effectiveness of implementing EGDT as a protocol in the emergency department (ED). METHODS: A prospective, non-blinded, interventional study was conducted for 14 months at a university hospital ED (EGDT group). And a medical records of patients who were treated with the same diagnosis were reviewed retrospectively during same durations 4 years ago (non-EGDT group). Data were collected for age, sex, simplified acute physiology score (SAPS) III, sources of infection, length of stay (LOS) in the intensive care unit (ICU) and in the hospital, and 1- and 28-day mortality. RESULTS: 59 patients were enrolled in the non-EGDT group and 41 in the EGDT group. Age, sex, SAPS III, ICU LOS, hospital LOS, and 1- and 28-day mortality were not significantly different between the groups. CONCLUSION: In our study, implementation of an EGDT protocol in ED couldn't improve the prognosis of patients with severe sepsis and septic shock.


Subject(s)
Humans , Emergencies , Hospitals , Intensive Care Units , Length of Stay , Medical Records , Prognosis , Prospective Studies , Retrospective Studies , Sepsis , Shock, Septic
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