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Purpose: Cognitive impairment is one of the main symptoms of Alzheimer disease and other dementias. Glycyrrhiza uralensis is a natural product that has a protective effect against cognitive impairment. In this study, we investigated whether glycyrrhizic acid, among the main bioactive components of Glycyrrhiza uralensis, has a neuroprotective effect on scopolamine-induced cognitive impairment.Methods: Twenty-week-old male Institute of Cancer Research mice were used in this study. The scopolamine-induced cognitive impairment mice model was used. Glycyrrhizic acid was orally administered to mice once daily for 21 days, while scopolamine (1 mg/kg) treatment was delivered 30 minutes before behavioral tests. Donepezil (2 mg/kg) was used as a positive drug control. To evaluate the effect of glycyrrhizic acid, the following assessments were performed on hippocampal tissue: Y-maze test, acetylcholinesterase activity, antioxidant enzymes’ activity (superoxide dismutase, catalase). Western blotting for phosphor-extracellular signal-regulated kinase, P38, and c-Jun NH2-terminal kinase was conducted.Results: We found that glycyrrhizic acid administration significantly improved scopolamine-induced cognitive impairment in the Y-maze test. The acetylcholinesterase activity, superoxide dismutase, and catalase activity in the glycyrrhizic acid-treated group showed a significant reversal of cognitive impairment compared with the scopolamine-treated group.Conclusions: Our results suggest that glycyrrhizic acid has a neuroprotective effect on cognitive function in scopolamine-induced cognitive impairment.

Purpose: Epidermal growth factor (EGF) has been found to be associated with the development and repair mechanisms of several renal diseases. In this study, we hypothesized that single nucleotide polymorphisms (SNPs) in EGF or its receptor genes might have an association with end-stage renal disease (ESRD) or acute renal allograft rejection (AR) in a Korean population. Methods: Three-hundred and forty seven recipients of the first renal transplants for ESRD, including 63 AR patients along with 289 healthy adults were included in the study. Five EGF gene SNPs (rs11568835, rs11568943, rs2237051, rs11569017, and rs3756261) and four EGFR gene SNPs (rs1140475, rs2293347, rs1050171, and rs6965469) were analyzed. The genotypes of these SNPs were analyzed using the AxiomTM genome-wide human assay. Statistical analysis was performed using SNPStats and Haploview version 4.2 software. Multiple logistic regression models (codominant, dominant, recessive, and Log-additive) were used to estimate the odds ratio (OR), 95% confidence interval (CI), and P value. Results: One SNP (rs11569017) in the EGF gene showed significant association with ESRD but not with AR. Another SNP (rs11568835) in the EGF gene showed significant association with susceptibility to AR but not with ESRD. One SNP (rs1050171) in the EGFR gene showed significant association with susceptibility to AR but not with ESRD. Conclusion: Our findings suggest that SNPs in the EGF and EGFR gene may be associated with the risk of ESRD and AR development in the Korean population.

Objective Renal ischemia/reperfusion (I/R) injury is characterized by the acute deterioration of renal function during ischemia and renal inflammation. Cassia tora has various effects, including antioxidant, antidiabetic, and hypolipidemic properties. In the present study, we investigated whether C tora has a renoprotective effect on I/R-induced acute kidney injury in rats. Methods We fed Sprague-Dawley rats either C tora (100 mg/kg/d) or saline. One week later, ischemia was induced by bilateral renal pedicle occlusion for 30 minutes, followed by reperfusion. Rats were randomized into 3 major groups, which were treated as follows: 1. the sham operation group; 2. the I/R group; and 3. the I/R-C tora group. Results Compared to the sham group, the I/R group had higher levels of blood urea nitrogen and serum creatinine in serum and lower expression of catalase, superoxide dismutase, glutathione peroxidase, antioxidant, and nitric oxide. Compared to the I/R group, the I/R-C tora group had higher expression of catalase, superoxide dismutase, glutathione peroxidase, antioxidant, and nitric oxide, as well as lower levels of blood urea nitrogen and creatinine in serum. Conclusions These results suggest that C tora has significant therapeutic effects in ischemic renal injury.

Objective Hesperidin is a well-known flavanone glycoside copiously found in sweet orange and lemon, which was recently reported to possess significant anti-inflammatory, analgesic, antifungal, antiviral, antioxidant, and anticancer activities. Ischemia-reperfusion (I/R) injury is a major problem after renal transplantation. Furthermore, inflammatory responses to I/R exacerbate the resultant renal injury. In the present study, we investigated whether hesperidin exhibits renoprotective effects against I/R-induced acute kidney injury in a rat model. Methods We fed Sprague-Dawley rats either hesperidin (100 mg/kg/d) or saline. One week later, ischemia was induced by bilateral renal pedicle occlusion for 30 minutes followed by reperfusion. The rats were randomly divided into 3 groups, which were treated as follows: 1. the sham operated group; 2. the I/R group; 3. the I/R-hesperidin group Results Compared to the sham group, the I/R group had higher expression of blood urea nitrogen and serum creatinine and lower expression of catalase, superoxide dismutase, glutathione peroxidase, antioxidants, and nitric oxide. Compared to the I/R group, the I/R-hesperidin group had higher expression of catalase, superoxide dismutase, glutathione peroxidase, antioxidant, and nitric oxide and lower expression of blood urea nitrogen and serum creatinine. Conclusions Hesperidin improved acute renal I/R injury through its antioxidant effects. These findings suggest that hesperidin is a potential therapeutic agent for acute ischemia-induced renal damage.

Background and Aims: The relationship between the promoter polymorphism (−308G/A) of the tumor necrosis factor-alpha (TNF-α) gene and the susceptibility to asthma has been tested in several studies...

Background and objectives: The aim of our study was to evaluate the role of diabetes mellitus (DM) as a significant factor affecting spontaneous stone expulsion, as suggested by previous research. Materials and methods: We investigated the influence of DM on the ureter using a murine model. The mouse-model arm of this study used 20 15 -week-old mice, including 10 normal (control) mice and 10 DM mice. We measured the proximal, middle and distal ureteral smooth muscle thickness in each mouse and the differences among ureteral sections were analyzed. Mouse ureteral specimens were also analyzed via western blotting to detect relative protein expression of phosphor–extracellular signal regulated kinases (P–ERK), phosphor–C–Jun N–terminal kinase (P–JNK), vascular endothelial growth factor (VEGF), and protein kinase C (PKC), which are representative factors involved in cell regulation. Results: We observed significant hyperproliferation of ureteral smooth muscle in DM mice compared to normal mice, which may provoke reduced peristalsis. The ureteral smooth muscle of DM mice was significantly thicker than that of normal mice in all ureteral tissues: proximal (p = 0.040), mid (p = 0.010), and distal (p = 0.028). The relative protein expression of P-ERK (p = 0.005) and P–JNK (p = 0.001) was higher in the diabetic group compared to the normal group. Additionally, protein expression of VEGF (p = 0.002) and PKC (p = 0.001) were remarkably up-regulated in DM mice. Conclusions: Hyperproliferation of ureteral smooth muscle was observed in DM mice, but not in normal mice. The pathways mediated by P–ERK, P–JNK, VEGF, and PKC may play an important role in pathological ureteral conditions.

OBJECTIVE Structural changes of brain areas have been reported in depressive disorder and suicidal behavior (SB), in which TPH1 also has been known as a promising candidate gene. We investigated gray matter volume (GMV) differences, TPH1 rs1800532 and rs1799913 polymorphisms previously found to be associated with depressive disorder and SB, and the relationship between the two markers. METHODS Thirteen depressive disorder patients with suicidal attempts (SA) and twenty healthy controls were included. We examined GMV differences using a voxel-based morphometry and regions of interest analysis. Direct sequencing was used for genotyping. RESULTS The patients showed significant GMV reduction in left cerebral region including middle frontal gyrus, inferior frontal gyrus, and anterior cingulate cortex; in right middle temporal gyrus; in left cerebellar tonsil; and in right cerebral region including precentral gyrus and postcentral gyrus (corrected p

Asthma is a serious disease around the world. It is caused by genetic and environmental factors. Epigenetics is the study of heritable changes in gene expression without changes of deoxyribonucleic acid (DNA) sequences. The gene expression change is due to methylation on DNA. Traditional Korean Medicine (TKM) uniquely classifies patients with asthma according to their symptoms. The present study is investigated to find a novel epigenetic marker of diagnosis for Korean asthma patients using Korean differentiation syndrome category in TKM. We recruited 62 patients with asthma from departments of respiratory medicine in hospitals. They are classified by symptom diagnosis and questionnaire to the deficiency syndrome (DS) group and excess syndrome (ES) group. And their DNA was extracted from peripheral blood. To investigate novel epigenetic markers on classification by Korean differentiation syndrome category, methylation analysis was performed using next generation sequencing (NGS), Agilent SureSelect Human Methyl-Seq which is a tool from Agilent Technologies company. In analysis of differential methylated epigenetic markers between the DS group and the ES group, total of 8 sites in exon region in [meprin (a cell surface glycoprotein), A5 antigen (a developmentally-regulated cell surface protein), and receptor protein-tyrosine phosphatase mu (MAM) domain containing glycosylphosphatidylinositol anchor 1] (MDGA1) gene were considered to be closely associated with differentiation syndrome category in Korean asthma patients. The methylation within MDGA1 gene could be regarded as an epigenetic candidate marker for Korean differentiation syndrome category in Korean asthma patients.

The prostatic hyperplasia in benign prostatic hyperplasia (BPH) leads to obstructive micturition symptoms. Previous studies showed that pontine micturition center (PMC), ventrolateral periaqueductal gray (vlPAG), and medial preopticnucleus (MPA) regions in the brain have been known to regulate the urinary bladder function. The present study shows the influences of Panax ginseng on nerve growth factor (NGF) expressions in PMC, vlPAG, and MPA regions in the brain. Wistar rats were used for the present study. The rats split into four groups; 4 groups (n=6) in control group, BPH-induced group, BPH-induced and P. ginseng-treated group, and BPH-induced and finasteride-treated group. BPH in rats was induced by testosterone and the animals were evaluated for NGF expression in PMC, vlPAG, and MPA regions in the brain. The NGF expression was identified using immunohistochemistry (IHC). The NGF expression by IHC showed spots with dark brown color. In our results, NGF expressions in PMC, vlPAG, and MPA regions in the brainstem of the BPH-induced group showed increase than the control animal. These increased NGF expressions in three regions were decreased using treatment with P. ginseng (200mg/kg). These results suggest that P. ginseng has therapeutic effects on the symptoms of BPH and is associated with the regulation of NGF expression in the brain. In conclusion, the administration of P. ginseng helps nerve growth factor activation.

A recent study reported that Panax ginseng (P. ginseng) has a protective effect on the development of benign prostatic hyperplasia (BPH). KH053 is used as a new herbal prescription consisting of P. ginseng and bee-pollen. The present study aimed to investigate whether the KH053 has inhibition effects on the development of benign prostatic hyperplasia (BPH) using an animal model with testosterone induced BPH. The experiment was carried out in forty male Wistar 7week old rats that were divided into four groups (control group, BPH group, positive group, and KH053 group). One group was used as the control and the three groups received subcutaneous injections of testosterone 20mg/kg for 4weeks to induce BPH. One of them received KH053 by oral gavage daily at doses of 200mg/kg concurrently with the testosterone. The positive group received finasteride at a dose of 1mg/kg with testosterone. After 4weeks, all rats were sacrificed and analyzed for prostate weight, and growth factors. Results revealed that, compared to rats in the BPH group, KH053 showed that the prostate weight and dihydrotestosterone (DHT) levels in serum were significantly decreased and the decreases in hyperplasia in prostate were also observed. In addition, immunohistochemistry (IHC) also revealed that the protein expressions of growth factors [transforming growth factor β1 (TGF-β1) and vascular endothelial growth factor (VEGF)] in prostate tissue were decreased in the KH053 group. In conclusion, these results suggest that KH053, comprising P. ginseng and bee-pollen, inhibits the development of BPH in Wistar rat model and might be used as functional food for BPH.

BACKGROUND Secretoglobin family 3A member 2 (SCGB3A2) plays an important role in secreting lung surfactant protein, which is a downstream target of thyroid transcription factor. MATERIAL AND METHODS We investigated whether single-nucleotide polymorphisms (SNPs) of SCGB3A2 gene contribute to susceptibility to asthma. To explore this possible association, 2 promoter SNPs (rs6882292, 659 G/A and rs1368408, -112 G/A) and missense SNP (rs151333009, stop codon) were tested in SCGB3A2 gene in 101 asthma patients and 377 healthy control subjects. SNPStats was used to obtain odds ratio (OR), 95% confidence intervals (CI), and P value adjusted for age and sex as covariables. Logistic regression method in each model (dominant, recessive, and log-additive) was applied to analyze genetic data. RESULTS rs151333009 SNP showed a monomorphic genotype. Two promoter SNPs (rs6882292, -659 G/A and rs1368408, -112 G/A) showed significant association with asthma (rs6882292, OR=2.66, 95% CI=1.42-5.01, p=0.0033 in dominant model, OR=2.45, 95% CI=1.33-4.54, p=0.0055 in log-additive model; rs1368408, OR=1.59, 95% CI=1.02-2.49, p=0.041 in dominant model, OR=3.02, 95% CI=1.15-7.90, p=0.03 in recessive model, OR=1.63, 95% CI=1.63, 95% CI=1.12-2.37, p=0.012 in log-additive model). CONCLUSIONS These results suggest that the promoter SNPs (rs6882292 and rs1368408) of SCGB3A2 gene may contribute to susceptibility to asthma in a Korean population.

Rheumatoid arthritis (RA) is a chronic disease. It causes chronic inflammation of the joint. Recent studies suggested that interleukin 4 (IL4) contributes to susceptibility and severity of rheumatoid arthritis (RA). Especially, it was reported that promoter polymorphism (−590, T/C) of IL4 gene has been associated with susceptibility of RA. The aim of present study was to investigate whether the promoter polymorphism (−590, T/C) of IL4 gene is associated with the susceptibility of RA using meta-analysis. And in order to perform meta-analysis, comprehensive meta analysis program was used. Genetic models (co-dominant, dominant, recessive, and allele) were used to determine odds ratios (ORs), 95% confidence intervals (CIs), and P values. Nine case-control studies with case and control design were included in this meta-analysis. Overall, meta-analysis revealed a strong association with susceptibility of RA [OR = 1.303, 95% CI = 1.093–1.554, P = 0.003 in allele model (C vs. T); OR = 1.247, 95% CI = 1.054–1.474, P = 0.010 in dominant model (CC vs. CT + TT); OR = 2.148, 95% CI = 1.263–3.651, P = 0.005 in recessive model (CC + CT vs. TT)]. Our data demonstrated that promoter polymorphism (−590, T/C) of IL4 gene may be contributed to susceptibility of RA. However, more studies with a larger sample size are needed to provide more precise evidence.

To investigate the contribution of the interleukin-6 receptor (IL-6R) gene single nucleotide polymorphisms (SNPs) to the neurological status of Korean patients with ischemic stroke (IS), two SNPs of the IL-6R gene (rs4845617, 5 UTR; rs2228144, Ala31Ala) were selected. IS patients were classified into clinical phenotypes according to two well-defined scores: the National Institutes of Health Stroke Survey (NIHSS) and the Modified Barthel Index scores. There were 121 IS patients and 291 control subjects. The SNP rs4845617 significantly contributed to the neurological status of patients with IS (P = 0.011 in codominant model 2, P = 0.006 in recessive model, and P = 0.008 in log-additive model). Allele frequencies of rs4845617 and rs2228144 demonstrated no significant difference in IS patients and controls. The AG and GG haplotypes differed between the NIHSS 1 (NIHSS scores < 6) group and the NIHSS 2 (NIHSS scores ≥ 6) group in patients with IS (P = 0.014, P = 0.0024). These results suggest that rs4845617 of the IL-6R gene is associated with the neurologic status of Korean patients with IS.

Objective To investigate whether four single nucleotide polymorphisms (SNPs) rs2293054 [Ile734Ile], rs1047735 [His902His], rs2293044 [Val1353Val], rs2682826 (3'UTR) of nitric oxide synthase 1 (NOS1) are associated with the development and clinical phenotypes of ischemic stroke. Methods We enrolled 120 ischemic stroke patients and 314 control subjects. Ischemic stroke patients were divided into subgroups according to the scores of the National Institutes of Health Stroke Survey (NIHSS

Chronic prostatitis typically occurs in aging men, and its symptoms include frequent and painful urination. In recent study, several studies have shown that Korean red ginseng (KRG) can be used in the prevention and treatment of various diseases. The objective of this study is to investigate whether KRG can play a role in repressing the development of chronic nonbacterial prostatitis (CNP) in male Wistar rats. To induce CNP, rats were castrated and beta-estradiol (0.25 mg/kg) was subcutaneously (s.c.) injected daily. 7-week-old male Wistar rats were divided into 5 groups (the normal group, CNP group, positive group, and KRG group (0.25g/kg) and another KRG (0.50g/kg) group. After 4 weeks, all rats were sacrificed and their prostate and serum were analyzed. Compared to the positive group, the KRG groups (0.25g/kg and 0.50g/kg) showed similar protective properties on CNP based on the histopathologic morphology of the prostate and the inflammation cytokines in the prostate tissue. Also, results of the immunohistochemistry staining showed that expression levels of vascular endothelial growth factor A (VEGFA), interleukin 6 (IL6), interleukin 1 beta (IL-1ß), tumor necrosis factor (TNF-alpha), and cytochrome c oxidase subunit II (COX2) were also decreased in KRG group (0.25g/kg) and KRG group (0.50g/kg). These results suggested that KRG inhibited the development of CNP and might a useful herbal treatment or functional food for CNP.

Background Immunoglobulin A nephropathy (IgAN) is the most common primary glomerulonephritis worldwide. Recent evidence suggests that genetic factors are related to the pathogenesis of IgAN. We conducted a genome-wide association study (GWAS) to identify novel genetic susceptibility loci for IgAN in a Korean population. Methods We enrolled 188 biopsy-confirmed IgAN cases and 455 healthy controls for the discovery stage and explored associations between IgAN and single nucleotide polymorphisms (SNPs) using a customized DNA chip. The significant SNPs from the discovery samples were then selected for replication in an independent cohort with 310 biopsy-confirmed IgAN cases and 438 healthy controls. Results In the first stage, two SNPs (rs10172700 in LOC105373592 and rs2296136 in ANKRD16) were selected for further association analysis in the next stage. In the replication cohort, rs2296136 in ANKRD16 was significantly associated with IgAN (odds ratio [OR] = 1.40, 95% confidence interval [CI] 0.99–1.98, p = 0.05 in log-additive model, OR = 1.55, 95% CI = 1.06–−2.27, p = 0.02 in dominant model, and OR = 0.70, 95% CI = 0.17–−2.84, p = 0.62 in recessive model). rs2296136 in ANKRD16 also showed a significant association with IgAN in the entire study population combining GWAS and replication study (p = 0.0045 in log-additive model, p = 0.0027 in dominant model, and p = 0.76 in recessive model). Conclusions The SNPs identified in the present study could be good candidate markers for predicting IgAN in Koreans, although further experimental validation is needed.

BACKGROUND Ischemic stroke and myocardial infarction are fatal diseases and are among the top 10 causes of death in Korea, including arterial thromboembolic events. Many previous studies have described the function of interleukin-6 (IL-6) in arterial thromboembolic events and the association between promoter single-nucleotide polymorphism (SNP) (rs1800795; -174, G/C) of the IL-6 gene. However, these results were controversial. Therefore, we performed a meta-analysis to more precisely assess the association between the SNP of the IL-6 gene and susceptibility to arterial thromboembolic events. MATERIAL AND METHODS We used PubMed, Embase, Google Scholar, and Korean Studies Information Service System (KISS) electronic databases. Comprehensive Meta-analysis software (Corporation, NJ) was used to evaluate the relationship between rs1800795 SNP of IL-6 gene and risk of arterial thromboembolic events. Odds ratio (OR), 95% confidence interval (CI), and P value were also calculated. The 13 eligible studies were analyzed in the meta-analysis. RESULTS The present meta-analysis found that rs1800795 SNP of IL-6 gene is not significantly associated with susceptibility to arterial thromboembolic events (C allele vs. G allele, OR=1.04, 95% CI=0.91-1.19, P=0.619; CC vs. CG+GG, OR=1.09, 95% CI=0.91-1.31, P=0.364; CC+CG vs. GG, OR=0.97, 95% CI=0.78-1.21, P=0.763, respectively), and the SNP of IL-6 gene also did not show any significant association with ischemic stroke or myocardial infarction (P>0.05 in each model). CONCLUSIONS We found that rs1800795 SNP of IL-6 gene was not related to arterial thromboembolic events. However, further study will be needed to confirm these results.

Background: Posttransplantation diabetes mellitus (PTDM) is an important metabolic complication after renal transplantation. Activation of the innate immune system via toll-like receptors (TLRs) is implicated in the pathogenesis of insulin resistance and deficiency. Although links between diabetes, dysregulated innate immune responses, and the TLR signaling pathway have been reported, no study so far has investigated their associations with PTDM. In this study, we ascertained whether single nucleotide polymorphisms (SNPs) in TLRs are associated with PTDM in the Korea population. Methods: A total of 305 patients who received renal transplants without previously diagnosed diabetes were included. We analyzed the association between PTDM development and 6 SNPs within 2 genes of TLR2, 1 gene of TLR4, and 3 genes of TRL6. Results: Of 305 patients, PTDM developed in 51 patients (16.6%). Patients in the PTDM group were older than those in the non-PTDM group (45.56 ± 1.28 vs. 38.28 ± 0.71 years). Patients with PTDM had significantly higher allele frequency compared to those without PTDM for the TLR4 rs1927914*T, TLR6 rs3775073*A, TLR6 rs3821985*C, and TLR6 rs1039559*C alleles. Of the 6 SNPs, rs1927914 in the TLR4 gene and rs1039559 in the TLR6 gene were significantly associated with the development of PTDM after adjustment for age, gender, and tacrolimus usage. Conclusions: Our study demonstrates a significant association between SNPs rs1927914 in TLR4 and rs1039559 in TLR6 and PTDM in the renal transplantation recipient group. These data suggest that the activation of the innate immune system and inflammation via TLR activation might have an essential role in the pathogenesis of PTDM in renal transplantation.

Benign prostatic hyperplasia (BPH) is considered the most common prostate disease in elderly men. Recent studies have suggested that specific polymorphisms might be contributed to risk factors for development of BPH. The aim of present study is to investigate whether promoter single nucleotide polymorphisms (SNPs) of the NDUFA4, mitochondrial complex associated (NDUFA4) gene are risk factors for BPH in Korean men. To evaluate the associations between promoter SNPs (rs17163801, rs17163803, rs1681288, and rs3761817) of NDUFA4 gene and clinical progress of BPH, one hundred eighty one BPH patients were recruited from Department of Urology at Kyung Hee Hospital. Prostate volume, international prostate symptom score (IPSS), and prostate specific antigen (PSA) were measured. For genetic analysis, SNPStats and SPSS 22.0 were performed. Genetic models (codominant, dominant, recessive, and log-additive models) were applied to calculate the odds ratio (OR), 95% confidence interval (CI), and P value. Among tested four SNPs, three promoter SNPs (rs17163803, rs1681288, and rs3761817) showed significant associations with prostate volume after Bonferroni’s correction (rs17163803, OR=3.00, 95% CI=1.31-6.84, Pc=0.036 in codominant 1 model; rs1681288, OR=3.53, 95% CI=1.65- 7.56, Pc=0.004 in codominant 1 model; OR=2.98, 95% CI=1.47-6.05, Pc=0.0072 in dominant model; rs3761817, OR=3.86, 95% CI=1.79-8.31, Pc=0.004 in codominant 1 model; OR=3.25, 95% CI=1.59- 6.62, Pc=0.0032 in dominant model; OR=2.19, 95% CI=1.21-3.99, Pc=0.0296). The results of present study demonstrate that specific promoter polymorphisms (rs17163803, rs1681288, and rs3761817) of the NDUFA4 gene might be associated with prostate enlargement in Korean men.

Estrogens and estrogen receptors (ESRs) have been implicated in the stimulation of aberrant prostate growth and the development of prostate diseases. The aim of the present study was to investigate four single nucleotide polymorphisms (SNPs) of the ESR2 gene in order to examine whether ESR2 is a susceptibility gene for benign prostatic hyperplasia (BPH). In order to evaluate whether an association exists between ESR2 and BPH risk, four polymorphisms [rs4986938 (intron), rs17766755 (intron), rs12435857 (intron) and rs1256049 (Val328Val)] of the ESR2 gene were genotyped by direct sequencing. A total of 94 patients with BPH and 79 control subjects were examined. SNPStats and Haploview version 4.2 we used for the genetic analysis. Multiple logistic regression models (codominant1, codominant2, dominant, recessive and log-additive) were produced in order to obtain the odds ratio, 95% confidence interval and P-value. Three SNPs (rs4986938, rs17766755 and rs12435857) showed significant associations with BPH (rs4986938, P=0.015 in log-additive model; rs17766755, P=0.033 in codominant1 model, P=0.019 in dominant model and P=0.020 in log-additive model; rs12435857, P=0.023 in dominant model and P=0.011 in log-additive model). The minor alleles of these SNPs increased the risk of BPH, and the AAC haplotype showed significant association with BPH (χ2=6.34, P=0.0118). These data suggest that the ESR2 gene may be associated with susceptibility to BPH.

Objectives Fas is the prototypic representative of the death receptor subgroup of the tumor necrosis factor (TNF) receptor family. Recently, single nucleotide polymorphisms (SNPs) of the Fas or Fas ligand (FasL) genes have been shown to be associated with an increased risk of several cancers and with the prognosis of several cancers. The objective of this study was to evaluate the association between the SNPs of the Fas and FasL genes and papillary thyroid cancer (PTC) and to assess the relationship between these SNPs and the clinicopathological characteristics of PTC. Methods Five SNPs located within the two genes of Fas and FasL were genotyped using direct sequencing in 94 patients with PTC and 364 healthy controls. Genetic data were analyzed using commercially available software. And, the statistical analyses were performed according to clinicopathologic characteristics of PTC. Results Genotyping analysis demonstrated that the intron SNP (rs1571013), promoter SNP (rs1800682) and 3′-UTR SNP (rs1468063) of Fas were significantly associated with the development of PTC. We also detected a significant difference between patients with PTC and healthy controls with respect to Fas gene allele frequencies. Furthermore, we found that the 3′-UTR SNP (rs1468063) of Fas was associated with the multifocality of cancer [dominant model, OR 0.28, p = 0.028; log-additive model, OR 0.43, p = 0.033]. Conclusion We observed a significant association between SNPs of the Fas gene and the development of PTC. In addition, there was a significant association between a Fas SNP and the multifocality of PTC.

Background. Interleukin-1β(IL-1β) plays an important role as a mediator of various inflammatory responses in chronic periodontitis. Several studies have investigated the potential relationship between IL-1βpolymorphism (rs16944) and susceptibility to chronic periodontitis; inflammatory process is involved, but conclusions is still controversial.Objective. The aim of this study was to determine whether the IL-1βpolymorphism (rs16944) is associated with susceptibility to chronic periodontitis.Material and Methods. For the case-control study, 51 patients with chronic periodontitis and 33 healthy control patients were recruited in the study. Genotyping was conducted by direct sequencing. SNPStats and SPSS 18.0 were used for the analysis of genetic data and to evaluate odds ratios, 95% confidence intervals, andPvalues; logistic regression models were used. And to perform meta-analysis, studies about IL-1βpolymorphism (rs16944) and chronic periodontitis were searched in PubMed, Embase, Google Scholar, and Korean Studies Information Service System (KISS) electronic databases until July 2017.Results. In our case-control study, no significant relationship was revealed between IL-1βpolymorphism (rs16944) and chronic periodontitis (P>0.05in each model). When combined with the previous studies in the meta-analysis, the result was not associated with chronic periodontitis in any of the models (CC vs. CT + TT: OR = 0.97, 95% CI = 0.762–1.246; CC + CT vs. TT: OR = 0.90, 95% CI = 0.658–1.232; and C vs. T: OR = 0.93, 95% CI = 0.774–1.128). The subgroup analysis stratified by ethnicity showed a weak association between the IL-1βpolymorphism (rs16944) and chronic periodontitis in the Caucasian population (recessive model, OR = 1.34, 95% CI = 1.017–1.758,P=0.037).Conclusion. Evidences from a case-control study and the meta-analysis suggest that IL-1βpolymorphism (rs16944) is not associated with susceptibility to chronic periodontitis.

This study was carried out to investigate the effects of the Achyrantes japonica (A. japonica) extract on serum level of hormones from osteoporosis induced ovariectomized rats. Two month-old rats were ovariectomized (OVX), remained untreated for 8 weeks, and were subsequently administered A. japonica (300 mg/kg) every day for 8 weeks. We examined the effects of treated A. japonica every 10 days on ovariectomy-related changes in Insulin-like Growth Factors (IGF), Insulin-like Growth Factor binding protein-3 (IGBF-3), Estrogen, Calcium, and Phosporus. After 8 weeks, the serum levels of IGF-I, -II, and IGFBP-3 were higher presented as compared to the other two groups (P< 0.05), in the A. japonica extract treatment on OVX rats. Bone alkaline phosphatase levels were increased through A. japonica extract treatment in OVX rats compared to the other two groups. There were no differences between OVX and A. japonica extract treated OVX rats in serum levels of estrogen, but estrogen levels for the sham group were higher than for the other two groups. A. japonica extract is increased to serum levels of IGFs and IGFBP-3 of osteoporosis induced by ovariectomized rats. Thus, the results reveal that the A. japonica extract is a possible role for improvement of osteoporosis induced-ovariectomized rats and has a great potential as an alternative tool for the treatment of osteoporosis.

Exercise has beneficial effect on cancer apoptosis and benign prostatic hyperplasia (BPH). The BH3 interacting domain death agonist (BID) gene expression is associated with apoptosis or cell proliferation. In this study, we investigated the association between BID single nucleotide polymorphisms (SNPs) and the development, prostate volume, and international prostate symptom score (IPSS) of BPH. In 222 BPH males and 214 controls, two SNPs in BID [rs8190315 (Ser56Gly), and rs2072392 (Asp106Asp)] were genotyped and analyzed using multiple logistic regression models. In the result, the genotype and allele frequencies of rs8190315 and rs2072392 were not associated with BPH development or IPSS, however, the allele frequencies [odd ratio (OR)= 1.90, 95% confidence interval (CI)= 1.07–3.41, P= 0.03] and genotype frequencies (in dominant model, OR= 1.94, 95% CI= 1.01–3.74, P= 0.42) of rs8190315, and the genotype frequencies of rs2072392 (in dominant model, OR= 1.94, 95% CI= 1.01–3.74, P= 0.42) were associated with increased prostate volume. We propose that rs8190315 and rs2072392 of BID may contribute to the disease severity of BPH.

In traditional Korean and Chinese medicine, safflower (Carthamus tinctorius L.) for the treatment of central nervous system-related symptoms such as tremor, seizure, stroke and epilepsy. We investigated the effects of safflower could influence cerebral ischemia-induced neuronal and cognitive impairments. Administration of safflower for 1 day (200 ㎎/㎏ body weight, p.o.) increased the survival of hippocampal CA1 pyramidal neurons after transient global brain ischemia. And neurological functions measured as short term memory. Post-treatment with safflower for 2 times decreased the induction/reduction - induced production of neuronal cell loss from global cerebral ischemia. Safflower markedly decreased neuronal cell death and also caused a decrease in the content of thiobarbituric acid-reacting substances (TBARS) (55.2 ± 9.4 µmol mg -1 ) and significant improvement of activities of glutathione (GSH) (27.2 ± 5.0 µmol mg -1 ) in hippocampus. We conclude that treatment with safflower attenuated learning and memory deficits, and neuronal cell loss induced by global cerebral ischemia. These results suggest that safflower may be a potential candidate for the treatment of vascular dementia.

Monoamine oxidase A (MAOA) catalyzes monoamine neurotransmitters including dopamine, 5-hydroxytryptamine (5-HT, serotonin), and norepinephrine. MAOA also plays a key role in emotional regulation. The aim of this study was to investigate the associations between the exonic single nucleotide polymorphisms (SNPs) of the MAOA gene located on the X chromosome and schizophrenia. We also analyzed the relationships between these SNPs and the common clinical symptoms of schizophrenia such as persecutory delusion, auditory hallucinations, affective disturbances, and poor concentration. Two hundred seventy five Korean schizophrenia patients and 289 control subjects were recruited. Three SNPs [rs6323 (Arg294Arg), rs1137070 (Asp470Asp), and rs3027407 (3′-untranslated region)] of the MAOA gene were selected and genotyped by direct sequencing. The common clinical symptoms of schizophrenia according to the Operation Criteria Checklist were analyzed. Three examined SNPs showed no associations with male and female schizophrenia, respectively (p > 0.05). In the analysis of the common clinical symptoms of schizophrenia patients, three examined SNPs were associated with affective disturbances, especially restricted affect and blunted affect in male schizophrenia, respectively (restricted affect, p = 0.002, OR = 2.71, 95 % CI 1.45–5.00; blunted affect, p = 0.009, OR 2.25, 95 % CI 1.22–4.12). The SNPs were not associated with other clinical symptoms of schizophrenia (persecutory delusion, auditory hallucinations, and poor concentration). These results suggest that exonic SNPs (rs6323, rs1137070, and rs3027407) of the MAOA gene may be contributed to affective disturbances of Korean males schizophrenia, especially restricted affect and blunted affect.

Objective To determine whether ACE insertion/deletion (I/D) polymorphism is associated with the ossification of the posterior longitudinal ligament (OPLL) of the spine in the Korean population. Methods A case-control study was conducted to investigate the association between I/D polymorphism of the angiotensin I converting enzyme (peptidyl-dipeptidase A) 1 (ACE) gene and OPLL. The 95 OPLL patients and 274 control subjects were recruited. Polymerase chain reaction for the genotyping of ACE I/D polymorphism was performed. The difference between the OPLL patients and the control subjects was compared using the contingency χ 2 test and the logistic regression analysis. For statistical analysis, SPSS, SNPStats, SNPAnalyzer, and Helixtree programs were used. Results The genotype and allele frequencies of ACE I/D polymorphism showed significant differences between the OPLL patients and the control subjects (genotype, p

Background We investigated whether single nucleotide polymorphisms (SNPs) of integrin beta 1 (ITGB1) and integrin beta 2 (ITGB2) contribute to the development of papillary thyroid cancer (PTC). Methods Two synonymous SNPs (rs2230396 and rs2298141) of ITGB1 and 1 synonymous SNP (rs2352326), 1 5′ URT-region SNP (rs2070947), and 1 promoter SNP (rs2070946) of ITGB2 SNPs were genotyped using direct sequencing in 94 patients with PTC and 213 healthy controls. Genetic data were analyzed using SNPStats (http://bioinfo.iconcologia.net/SNPstats), Helix Tree (Golden Helix Inc, Bozeman, MT), and SNPAnalyzer (ISTECH Corp, Goyang City, Republic of Korea). Results The promoter SNP (rs2070946) of ITGB2 was significantly associated with the development of PTC (dominant model, log-additive model). The G allele frequencies of the promoter SNP (rs2070946) of ITBG2 in patients with PTC (19.9%) were increased by about 2-fold compared with controls (10.2%). Conclusions Our results suggest that a promoter SNP (rs2070946) of ITGB2 might be associated with a risk of PTC.

Extracellular matrix (ECM) abnormality is implicated in the pathogenesis of schizophrenia. Matrix metalloproteinases (MMPs) mediate the proteolysis of ECM and may play a crucial role in neuronal plasticity. We investigated whether single nucleotide polymorphisms (SNPs) of MMP1 and MMP8 are associated with the development of schizophrenia. We also assessed the relationships between MMP1, MMP8 SNPs and the core symptoms of schizophrenia such as persecutory delusion, auditory hallucinations, affective disturbances, and poor concentration according to the Operation Criteria Checklist for Psychotic Illness (OPCRIT). Three coding SNPs (rs470558, Ala216Ala in MMP1; rs3740938, Leu291Leu and rs1940475, Lys87Glu in MMP8) were selected, and 263 patients and 283 controls were evaluated. SNPStats was used to obtain the odds ratio (OR), 95% confidence intervals (CI), and P value adjusted for age and gender as covariables. Multiple logistic regression models (codominant1, codominant2, dominant, recessive, and log-additive) were employed to analyze genetic data. As a result, the three examined SNPs were not associated with the development of schizophrenia. In the analysis of clinical symptoms, the genotype frequency of rs470558 in MMP1 was associated with auditory hallucinations (P=0.04 in the codominant1 model, P=0.014 in the dominant1 model, and P=0.0066 in the log-additive model). The allele frequency of rs470558 also showed a significant difference between schizophrenia without auditory hallucinations [the auditory hallucination (−) group] and schizophrenia with auditory hallucinations [the auditory hallucination (+) group] (P=0.009, OR= 1.94, 95% CI=1.19-3.28). The A allele frequency of rs470558 was higher in the auditory hallucination (+) group (19.2%) than that in the auditory hallucination (−) group (10.8%). Two MMP8 SNPs (rs3740938 and rs1940475) were not associated with the development and core symptoms of schizophrenia, respectively. These results suggest that the A allele of rs470558 (Ala216Ala) in MMP1 may contribute to the susceptibility to auditory hallucinations of schizophrenia.

OBJECTIVE The aim of this study was to investigate whether single nucleotide polymorphisms (SNPs) of dopamine receptor D2 (DRD2) are associated with schizophrenia in Korean population. METHODS Four SNPs (rs4648317, rs7131056, rs4936270, and rs1076562) of DRD2 were selected and genotyped by direct sequencing in 197 schizophrenia patients and 370 control subjects. SNPAnalyzer, SNPStats, and Haploview version 4.2 programs were performed to analyze the genetic data. Multiple logistic regression models (codominant1, codominant2, dominant, recessive, overdominant, and log-additive) were used to evaluate the odds ratios (ORs), 95% confidence intervals (CIs), and p values. For multiple testing, p values (p(c)) were re-evaluated by Bonferroni's correction. RESULTS The genotype frequency of DRD2 rs4936270 SNP was associated with the development of schizophrenia (p=0.0007, OR=1.71, 95% CI=1.16-2.52 in the codominant1 model; p=0.011, OR=1.63, 95% CI=1.12-2.37 in the dominant model; p=0.035, OR=1.41, 95% CI=1.03-1.95 in the log-additive model). The allele frequency of rs4936270 was also associated with the development of schizophrenia (p=0.024, OR=1.45, 95% CI=1.05-1.98). After Bonferroni's correction, the genotype distribution of rs4936270 was still related to the development of schizophrenia (p(c)=0.0028 in the codominant1 model; p(c)=0.044 in the dominant model). A linkage disequilibrium block consisted of rs4648317, rs7131056, and rs4936270. The CAT haplotype frequency was different between schizophrenia and controls (p=0.039). CONCLUSION These results suggest that DRD2 SNPs may be associated with the development of schizophrenia in Korean population.

The incidence of thyroid cancer has been on the increase in a number of countries, and certain genetic factors associated with the increased incidence of the papillary thyroid cancer (PTC) have been identified. However, little is known about the effect of mutations of the cystic fibrosis trans - membrane conductance regulator (CFTR) gene, expressed in the thyroid. We hypothesized and investigated that CFTR single nucleotide polymorphisms (SNPs) may be associated with the risk and/or progression of PTC. A total of 105 PTC patients, confirmed by pathological tests, and 323 controls, without any thyroidal disease, were recruited. One promoter SNP (rs4148682) and one coding SNP (rs213950, Val470Met) in the CFTR gene were analyzed, using direct sequencing. The PTC patients were sub-grouped and compared by their clinical and pathological characteristics of PTC. The results showed that the association between SNPs in the CFTR gene and the development of PTC was statistically insignificant. However, in the clinical and pathological features, rs4148682 was found to be correlated with multifocal tumors, location and cervical node metastasis of PTC. rs231950 was also correlated with multifocal tumors, location and nodal metastasis of PTC. The G allele of rs213950 was correlated with increased risk of multifocal tumors and bilateral lobe location. However, in cervical lymph node metastasis, the A allele of rs213950 was found to reflect high risk. Our study suggests that the CFTR gene polymorphisms studied may not be associated with the development of PTC, but that rs4148682 and rs213950 may be associated with clinical features and prognosis, such as multi- focality, location of cancer and cervical lymph node metastasis of PTC.

Purpose: Integrins play crucial roles in the pathogenesis of papillary thyroid carcinoma (PTC). The aim of this study was to investigate whether two single nucleotide polymorphisms (SNPs) (rs2141698, -1687A/G; rs11895564, Ala380Thr) of the integrin alpha 6 (ITGA6) gene are associated with the development and clinicopathologic characteristics of PTC such as the size (＜1 cm and ≥1 cm), number (unifocality and multifocality), location (one lobe and both lobes), extrathyroid invasion, and cervical lymph node metastasis. Methods: We enrolled 104 PTC patients and 318 control subjects. Genotypes of each SNP were determined by direct sequencing. SNPStats, SNPAnalyzer, and Helixtree programs were used to evaluate odds ratios (ORs), 95% confidence intervals (CIs), and P-values. Multiple logistic regression models were performed to analyze genetic data. Results: A missense SNP rs11895564 was associated with the development of PTC. The A allele frequency of rs11895564 was higher in PTC patients than in controls (13.5% vs. 7.1%; P = 0.005; OR, 2.04; 95% CI, 1.24 to 3.37). In the clinicopathologic characteristics, the A allele frequency of rs11895564 showed difference in the size (19.6% in ＜1 cm vs. 6.9% in ≥1 cm; P = 0.010; OR, 0.30; 95% CI, 0.12 to 0.75) and number (8.5% in unifocality vs. 20.8% in multifocality; P = 0.015; OR, 2.85; 95% CI, 1.23 to 6.59) of PTC. Conclusion: These results suggest that the A allele of rs11895564 (Ala380Thr) in ITGA6 may be a risk factor of PTC, and also contribute to the progression of PTC in the Korean population.

Insulin-like growth factor 1 (IFG1) is neuroprotective in animal models of focal brain ischemia and correlates with ischemic stroke (IS) outcome in the elderly. In this study, we investigated whether single nucleotide polymorphisms (SNPs) of the IFG1 gene are associated with the development and clinical features of IS in a Korean population. A total of 119 patients with IS and 289 control subjects were recruited. Stroke patients were classified into subgroups according to the scores of the National Institutes of Health Stroke Survey (NIHSS

Toll-like receptor 2 (TLR2) has been shown to have an important role in the postischemic inflammatory response and to contribute to ischemic brain damage. In this study, we investigated whether coding region single nucleotide polymorphisms (SNPs) of the TLR2 gene were associated with ischemic stroke (IS) and with clinical phenotypes in IS patients. We genotyped two SNPs (rs3804099 [Asn199Asn] and rs3804100 [Ser450Ser]) using direct sequencing in 202 IS patients and 291 control subjects. No SNPs of the TLR2 gene were found to be associated with IS. However, in analysis of clinical phenotypes, we found that rs3804099 was associated with the National Institute of Health Stroke Scale (NIHSS) scores of IS patients in codominant (TC vs. TT, p = 0.0005; CC vs. TT, p = 0.0007) and dominant models (TC/CC vs. TT, p = 0.0001). Also, rs3804100 revealed significant association in codominant (TC vs. TT, p = 0.0002; CC vs. TT, p = 0.008) and dominant models (TC/CC vs. TT, p

Glutamate toxicity plays a key role in neuronal cell death. The aim of this study was to investigate whether three single nucleotide polymorphisms (SNPs) (rs2073287, intron; rs2942, Lys931Lys; rs6923492, Ser993Pro) of glutamate receptor, metabotropic 1 (GRM1) were associated with the development and clinical features of stroke. We recruited 365 control subjects and 195 stroke patients consisted of 119 ischemic stroke (IS) and 76 intracerebral hemorrhage (ICH). All stroke patients were divided into clinical subgroups according to the scores of the National Institutes of Health Stroke Survey (NIHSS, < 6 and ≥ 6) and Modified Barthel Index (MBI, < 60 and ≥60). SNPStats and SPSS 18.0 were conducted to evaluate odds ratios (ORs), 95% confidence intervals (CIs), and P values. Multiple logistic regression models were performed to analyze the genetic data. A rs2073287 SNP of GRM1 was associated with the susceptibility of stroke (IS+ ICH) (P=0.002, OR=1.49, 95% CI=1.16-1.92 in allele frequencies). The rs2073287 was also associated with the development of IS (P=0.028, OR=1.40, 95% CI= 1.04-1.89 in allele frequencies) and ICH (P=0.006, OR=1.65, 95% CI=1.16–2.35 in allele frequencies). The G allele frequencies of rs2073287 in stroke (IS+ ICH), IS, and ICH were higher than in the control group, respectively. The rs2942 and rs6923492 were not related to stroke (IS+ICH), IS, and ICH, respectively. These results suggested that the G allele of rs2073287 could be a risk factor to the susceptibility of stroke in Korean population.

Objectives Among the apoptosis signals, B-cell CLL/lymphoma 2 (BCL2) is a well-known regulator of apoptosis with anti-apoptotic properties. We investigated here whether single nucleotide polymorphisms (SNPs) of the BCL2 were associated with host susceptibility of papillary thyroid cancer (PTC) occurrence and clinicopathologic parameters. Methods Ninety-two PTC patients and 222 control subjects were recruited. One promoter SNP (rs2279115, -938A/C) and one synonymous SNP (rs1801018, Thr7Thr) in the BCL2 gene were selected and genotyped using direct sequencing. Multiple logistic regression models were performed to evaluate odds ratios, 95% confidence intervals, and P-values. Results rs1801018 of the BCL2 gene was not associated with the development of PTC. In the clinicopathologic features, rs1801018 SNP was associated with the number and location. The G allele frequency of rs1801018 in PTC patients with multifocality (13.3%) was about four-fold higher than that in PTC patients with unifocality (3.4%). The G allele frequency of rs1801018 in PTC patients with both lobes (15.4%) was increased by about five-fold, compared to PTC patients with one lobe (3.2%). Conclusion The results suggest that synonymous SNP rs1801018 and the G allele of the BCL2 gene may be associated with the multifocality and bilaterality of PTC in Korean population.

We have carried out a study with the aim of investigating the association between single nucleotide polymorphisms (SNPs) of the IL-1 gene cluster and childhood IgA nephropathy (IgAN). SNPs of the IL-1 alpha, IL-1 beta, and IL-1 receptor antagonist (RN) genes (IL1A, IL1B, and IL1RN, respectively) were analyzed in 182 patients with childhood IgAN and in 500 healthy controls. The IgAN patients were also dichotomized and compared with respect to proteinuria (4 mg andor=4 mg/m(2) per hour, respectively), the presence or absence of podocyte foot process effacement, and the presence of pathologically early and advanced disease markers, such as interstitial fibrosis, tubular atrophy, or global sclerosis. Significant differences in SNP frequencies were observed for the IL1B and IL1RN genes (rs1143627, rs3917356, and rs1143633 in the IL1B gene, and rs928940, rs439154, and rs315951 in the IL1RN gene). Moreover, rs1143627, rs3917356, and rs1143633 of IL1B were found to be significantly associated with the presence of podocyte foot process effacement. Our results suggest that the IL1B and IL1RN genes are associated with increased susceptibility to IgAN in children. They also suggest that the development of proteinuria in IgAN is related to IL1A and that podocyte foot process effacement is associated with IL1B.

Diabetic nephropathy (DN) has become the leading cause of end stage renal failure, and prevention or retardation of DN has become a major goal in biomedical research. In this study, Tanshinone IIA, a component extracted from Salvia miltiorrhiza, was studied in experimental rats in which DN was induced by streptozotocin (STZ) treatment. The DN rats were treated with 10 mg/kg of Tanshinone IIA for 12 weeks to analyze its reno-protective effect with different parameters. Renal hypertrophy and 24-h urinary protein excretion were ameliorated by Tanshinone IIA. Moreover, advanced glycation end-products (AGEs), angiotensin II (Ang II), transforming growth factor beta(1) (TGF-beta(1)), collagen IV, and monocyte/macrophage (ED-1) either in the serum or kidney were significantly reduced. These results suggest that Tanshinone IIA might have protective effects on several pharmacological targets during the progression of DN, and could be a potential drug for the prevention of DN.

SUMMARY The root of Astragalus membranaceous (AM) has been used to treat edema and arthritis in thetraditional Korean medicine. To elucidate the anti-inflammatory and anti-nociceptive effects ofethanol extract of AM, the carrageenan-induced paw edema using a plethysmometer and thermalhypersensitivity using the plantar test were measured. Ibuprofen was used as a control drug.Pretreatment with AM (400 mg/kg p.o.) significantly reduced paw edema, compared to thecarrageenan-treated rats. In the plantar test, the thermal withdrawal latency in AM-treated groupwas significantly increased than the carrageenan-treated group. The results indicate that AMcould have be the anti-inflammatory and anti-nociceptive properties.Key words: Astragalus membranaceous; Inflammation; Nociception; Paw edema INTRODUCTION Recently, complementary and alternative medicineis increasingly used for the treatment of immunediseases and inflammation (Luo et al., 2007).Astragalus membranaceous (AM) is a traditionalmedicinal plant, and it has been widely used as atonic to enhance the body’s natural defensemechanisms such as the immune reaction andcirculation (Ryu et al., 2008). AM may exhibit theimmunomodulating and immunorestorative effectsboth in vitro and in vivo (Cho and Leung, 2007).Shen et al. (2008) also found that AM administrationduring 28 days significantly decreased inflammatoryinfiltration and mucus secretion in the lung tissueof allergic mice. AM has been shown to have anti-allergic, anti-inflammatory, and anti-nociceptiveproperties (Kosuge et al., 1985; Luo et al., 2007). Inaddition, it seems to have an anti-oxidantproperty (Boucheny and Brum-Bousquet, 1990)and inhibit the aggregation of platelets (Yun-Choi et al., 1985; Lu et al., 2005). Luo et al. (2007)reported that AM can reduce the small intestinemucosal damage after hemorrhage shockreperfusion. However, the mechanism of actionof AM is not fully defined.The present study was aimed to investigate theanti-inflammatory and anti-nociceptive propertiesof AM in carrageenan-induced paw edema model.For the anti-inflammatory effect, the volume ofedema was measured using a plethysmometer. Totest the anti-nociceptive effect, the thermal withdrawallatency by the plantar test was estimated.

Background Benign prostatic hyperplasia (BPH) is one of the common male diseases, which is provoked by dihydrotestosterone (DHT) and androgen signals. Several studies showed that curcumin has various effects of prevention and treatment to diseases. We investigated whether curcumin may repress the development of BPH in male Wistar rats. Methods Seven weeks male Wistar rats were and divided into 4 groups (normal group, BPH group, finasteride group, curcumin group; n = 8 for each group). In order to induce BPH in rats, rats were castrated and testosterone was injected subcutaneously everyday (s.c., 20 mg/kg). Rats in the curcumin group were treated 50 mg/kg, administered orally for 4 weeks. After 4 weeks, all rats were sacrificed and their prostate and serum were analyzed. Results Compared to the finasteride group as positive group, the curcumin group showed similarly protective effect on BPH in histopathologic morphology, prostate volume. Results of immunohistochemistry and western-blot showed decreased expressions of VEGF, TGF-ß1, and IGF1 were also decreased in the curcumin group. Conclusions These results suggested that curcumin inhibited the development of BPH and might a useful herbal treatment or functional food for BPH.

Objective To investigate whether baculoviral inhibitor of apoptosis (IAP) repeat containing 5 gene (BIRC5) polymorphisms are associated with the development and clinical phenotypes of ischemic stroke in Korea population. Methods We enrolled 121 ischemic stroke patients and 291 control subjects. Ischemic stroke patients were divided into subgroups according to the scores of National Institutes of Health Stroke Survey (

The human paraoxonase (PON) gene family includes three members: PON1, PON2, and PON3. PON, which prevents the oxidative modification of lipoproteins, has been implicated as a potential risk factor of the cerebrovascular disease. In this study, we investigated associations between coding region single-nucleotide polymorphisms (cSNPs) of PON1, PON2, and PON3 genes and intracerebral hemorrhage (ICH) in a Korean population. Six cSNPs [rs13306698 and rs662 for PON1; rs12026 and rs7493 for PON2; rs13226149 and rs1053275 for PON3] were genotyped using direct sequencing in 145 ICH patients and 372 control subjects. Of the six cSNPs, rs12026 and rs7493, which were in complete linkage disequilibrium, were associated with ICH in log-additive (GC vs. CC vs. GG, p = 0.0008, OR = 0.53, 95 % CI = 0.36-0.78) and dominant models (GC/CC vs. GG, p = 0.0006, OR = 0.47, 95 % CI = 0.30-0.73). In addition, rs13226149 was associated with ICH in log-additive model (GA vs. AA vs. GG, p = 0.0033, OR = 0.58, 95 % CI = 0.39-0.84). In the allele frequency analysis, the C alleles of rs12026 and rs7493 and the A allele of rs13226149 were also shown to contribute to the decreased risk of ICH (p = 0.001, OR = 0.55, 95 % CI = 0.38-0.80 in rs12026 and rs7493; p = 0.003, OR = 0.58, 95 % CI = 0.40-0.83 in rs13226149). These results suggest that PON genes may be involved in the susceptibility of ICH.

Cytokines and their receptors are involved in the development of intracerebral hemorrhage (ICH). Interleukin 23 receptor (IL23R) has been implicated in numerous inflammatory and immune diseases. In this study, we investigated whether single nucleotide polymorphisms (SNPs) of IL23R were associated with the susceptibility of ICH in Korean population. Two coding region SNPs (cSNPs) [rs1884444 (Gln3His), and rs7530511 (Leu310Pro)] were selected, and genotyped in 167 ICH patients and 377 control subjects using direct sequencing. Of two cSNPs, only rs7530511 showed a significant association with ICH in codominant model (C/T vs. C/C, P = 0.017, odds ratio (OR) 4.15, 95 % confidential interval (CI) 1.27-13.58). Allele frequency analysis also revealed that rs7530511 was associated with ICH (P = 0.023, OR 3.68, 95 % CI 1.19-11.32). The frequency of the T allele was increased in the ICH patients, compared to the control subjects. These results suggest that IL23R may contribute to the development of ICH.

Autism spectrum disorder (ASD) is a neurodevelopmental syndrome associated with impairments of reciprocal communication and cognitive function. Associations between single-nucleotide polymorphisms (SNPs) and ASD were analysed by logistic regression. Polymorphisms in fibronectin type III domain-containing 3A (FNDC3A) exhibited significant associations in genotype and diplotype analyses. We conclude that FNDC3A influences the prevalence of ASD.