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Role of Cerebrospinal Fluid Biomarkers in Clinical Trials for Alzheimer’s Disease Modifying Therapies
Ju-HeeKang, Na-YoungRyoo, DongWunShin, JohnQTrojanowski, LeslieM.Shaw 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 10 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2014, Vol.18 No.6 1 447-456 (10 pages)
aspects of analysis of these biomarkers is an essential prerequisite to the clinical uses. To accomplish this, global efforts are underway to standardize CSF biomarker measurements and a quality control program supported by the Alzheimer’s Association. The current review summarizes therapeutic targets of developing drugs in AD pathophysiology, and provides the most recent advances in the clinical utility of CSF biomarkers and the integration of CSF biomarkers in current clinical trials. -
Exendin-4 Improves Nonalcoholic Fatty Liver Disease by Regulating Glucose Transporter 4 Expression in ob/ob Mice
SeokKim, JaehoonJung, HwajinKim, RokWonHeo, Chin-okYi, JungEunLee, ByeongTakJeon, Won-HoKim, JongRyealHahm, GuSeobRoh 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 7 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2014, Vol.18 No.4 8 333-339 (7 pages)
Exendin-4 (Ex-4), a glucagon-like peptide-1 receptor (GLP-1R) agonist, has been known to reverse hepatic steatosis in ob/ob mice. Although many studies have evaluated molecular targets of Ex-4, its mechanism of action on hepatic steatosis and fibrosis has not fully been determined. In the liver, glucose transporter 4 (GLUT4) is mainly expressed in hepatocytes, endothelial cells and hepatic stellate cells (HSCs). In the present study, the effects of Ex-4 on GLUT4 expression were determined in the... -
Cyclophilin A as a New Therapeutic Target for Hepatitis C Virus- induced Hepatocellular Carcinoma
JinhwaLee 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 9 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2013, Vol.17 No.5 1 375-383 (9 pages)
Hepatocellular carcinoma (HCC) related to hepatitis B virus (HBV) and hepatitis C virus (HCV) infections is thought to account for more than 80% of primary liver cancers. Both HBV and HCV can establish chronic liver inflammatory infections, altering hepatocyte and liver physiology with potential liver disease progression and HCC development. Cyclophilin A (CypA) has been identified as an essential host factor for the HCV replication by physically interacting with the HCV non structural protein... -
Prolyl 4 Hydroxylase: A Critical Target in the Pathophysiology of Diseases
RaviKant, AnjanaBali, NirmalSingh, AmteshwarSinghJaggi 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 10 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2013, Vol.17 No.2 1 111-120 (10 pages)
Prolyl 4 hydroxylases (P4H) are iron- and 2-oxoglutamate-dependent dioxygenase enzymes and hypoxia-inducible transcription factor (HIF)-P4Hs play a critical role in the regulating oxygen homeostasis in the local tissues as well in the systemic circulation. Over a period of time, a number of prolyl hydroxylase inhibitors and activators have been developed. By employing the pharmacological tools and transgenic knock out animals, the critical role of these enzymes has been established in the... -
CTLA-4-Tg/CD-28-KO Mice Exhibit Reduced T Cell Proliferation in vivo Compared to CD-28-KO Mice in a Graft-versus-host Disease Model
Jong-SunYoo, Yun-JungLee, JooWonYoon, KyeongEunHyung, KwangWooHwang 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 5 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2012, Vol.16 No.5 10 349-353 (5 pages)
Activated T cells express inhibitory receptors such as CTLA-4 that can downregulate immune responses. Blockade of or genetic deficiency in CTLA-4 can result in autoimmunity. Therefore, strategies to increase the inhibitory function of CTLA-4 may be attractive in settings of undesirable T cell responses such as autoimmunity or transplant rejection. We have tested the hypothesis that transgenic constitutive expression of CTLA-4 can further attenuate immune responses when compared with normal... -
Cilostazol Decreases Ethanol-Mediated TNFalpha Expression in RAW264.7 Murine Macrophage and in Liver from Binge Drinking Mice
YounJuLee, JongRyeolEun 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 8 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2012, Vol.16 No.2 8 131-138 (8 pages)
Alcoholic hepatitis is a leading cause of liver failure in which the increased production of tumor necrosis factor Ձ (TNFՁ) plays a critical role in progression of alcoholic liver disease. In the present study, we investigated the effects of cilostazol, a selective inhibitor of type III phosphodiesterase on ethanol-mediated TNFՁ production in vitro and in vivo, and the effect of cilostazol was compared with that of pentoxifylline, which is currently used in clinical trial.... -
CD40 Co-stimulation Inhibits Sustained BCR-induced Ca2＋ Signaling in Response to Long-term Antigenic Stimulation of Immature B Cells
YenHoangNguyen, Ki-YoungLee, TaeJinKim, SungJoonKim, TongMookKang 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 9 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2011, Vol.15 No.3 9 179-187 (9 pages)
Regulation of B cell receptor (BCR)-induced Ca2＋ signaling by CD40 co-stimulation was compared in long-term BCR-stimulated immature (WEHI-231) and mature (Bal-17) B cells. In response to long-term pre-stimulation of immature WEHI-231 cells to Ձ-IgM antibody (0.5∼48 hr), the initial transient decrease in BCR-induced [Ca2＋]i was followed by spontaneous recovery to control level within 24 hr. The recovery of Ca2＋ signaling in WEHI-231 cells was not due to restoration of internalized... -
Matrix Metalloproteinase Inhibitors Attenuate Neuroinflammation Following Focal Cerebral Ischemia in Mice
CheolHongPark, TaeKyeongShin, HoYounLee, SoJungKim, WonSukLee 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 7 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2011, Vol.15 No.2 7 115-121 (7 pages)
The aim of this study was to investigate whether matrix metalloproteinase (MMP) inhibitors attenuate neuroinflammation in an ischemic brain following photothrombotic cortical ischemia in mice. Male C57BL/6 mice were anesthetized, and Rose Bengal was systemically administered. Permanent focal ischemia was induced in the medial frontal and somatosensory cortices by irradiating the skull with cold white light. MMP inhibitors, such as doxycycline, minocycline, and batimastat, significantly reduced... -
Loss of hsp70.1 Decreases Functional Motor Recovery after Spinal Cord Injury in Mice
HyunJeongKim, Ji-InJung, YoungkyungKim, Jae-SeonLee, YoungWookYoon, JunesunKim 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 5 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2010, Vol.14 No.3 7 157-161 (5 pages)
Heat shock proteins (HSPs) are specifically induced by various forms of stress. Hsp70.1, a member of the hsp70 family is known to play an important role in cytoprotection from stressful insults. However, the functional role of Hsp70 in motor function after spinal cord injury (SCI) is still unclear. To study the role of hsp70.1 in motor recovery following SCI, we assessed locomotor function in hsp70.1 knockout (KO) mice and their wild-type (WT) mice via the Basso, Beattie and Bresnahan (BBB)... -
Inhibition of eNOS/sGC/PKG Pathway Decreases Akt Phosphorylation Induced by Kainic Acid in Mouse Hippocampus
SangHyunLee, JongSeonByun, PilJaeKong, HeeJaeLee, DukKyungKim, HaeSungKim, Jong-HeeSohn, JaeJunLee, , SoYoungLim, WanjooChun, SungSooKim 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 7 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2010, Vol.14 No.1 6 37-43 (7 pages)
production of NO and that NO stimulates soluble guanylate cyclase (sGC), which results in accumulation of cGMP and subsequent activation of the protein kinase G (PKG). It has been also reported that PKG activates PI3K/Akt signaling. Therefore, it is possible that PI3K, Akt, eNOS, sGC, and PKG form a loop to exert enhanced and sustained activation of Akt. However, the existence of this loop in eNOS-expressing cells, such as endothelial cells or astrocytes, has not been reported. Thus, we examined...
