• Childhood Kidney Diseases
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• v.9 no.1
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• pp.21-30
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• 2005

Purpose : Metabolic bone diseases have been mai or problems in children with renal diseases and steroid treatment is the main precipitating factor reducing bone mineral density(BMD). This study was performed to assess the prevalence of osteoporosis and to evaluate the clinical factors associated with decreased BMD in children with renal diseases. Methods : Forty-four children with renal diseases who were diagnosed at the Pediatric no phrology division of Ajou University hospital since Oct. 1994 were included. Using a new quantitative ultrasound device, BMD and the prevalence of osteoporosis were evaluated. The clinical and serological data were analyzed in association with decreased BMD. Results : A total of 44 patients were evaluated. The age at initial diagnosis was 6.7$\pm$4.2 years. At the time of evaluation, the chronological and bone age was 9.3$\pm$4.2 years and 8.2 $\pm$ 4.6 years, respectively. The renal diseases included nephrotic syndrome 24(54.5%), Henoch Schonlein purpura nephritis 7(15.9%), IgA nephropathy 6(13.9%), reflux nephropathy(RN) 2 (4.5%), and other renal disease 5(%). The prevalence of osteoporosis was 11%. There was no difference in the clinical factors between the long-term and the short-term treated steroid groups. Conclusion : The prevalence of osteoporosis was 12% in 44 children with renal diseases No significant factor was found in association with decreased BMD and there was no relationship between osteoporosis and steroid usage duration or cumulative dose. A new quantitative ultrasound, which is relatively easy to perform, especially in children, is expected to be in common use and will enable clinicians to evaluate metabolic bone disorders with ease.

• Korean Journal of Head & Neck Oncology
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• v.17 no.2
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• pp.169-173
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• 2001

Objectives: The p53 tumor suppressor gene encodes a nuclear transcription factor that is critical regulator of cell growth and proliferation through its action in cell-cycle checkpoint control. The wide variety of stressful stmuli which include DNA damage, hypoxia, heat shock, metabolic changes activate the p53 protein, which in turn drives a series of events that culminate either in cell cycle arrest or apoptosis. Mutations of the p53 gene is the most common genetic alteration in human cancer. This gene is altered in approximately 40-60% of head and neck cancers. Whereas the wild-type form of the p53 protein plays a central role in cell-cycle control in response to DNA damage, most of the mutant forms are unable to do so. The high levels of p53 protein expression in tissues are related to the increased cellular proliferative activity and may be associated with the poor clinical outcome. To determine whether the expression of the p53 protein has prognostic significance and is associated with patterns of treatment failure in head and neck squamous cell carcinoma (HNSCC), We analyzed p53 overexpression in 40 cases of HNSCC. Materials and Methods: Immunohistochemical analysis with a monoclonal antibody (DO7) specific for p53 protein was used to detect expression of the protein in formalin-fixed, paraffin-embedded tumor samples from 40 HNSCC. We evaluated p53 protein expression and analyzed the relationship between the p53 overexpression and age, sex, primary tumor site, stage, survival rate, recurrence. All reported P values resulted from two-sided statistical tests. Results: Overexpression of p53 was detected in 20 cases(50%) among 40 cases of HNSCC. The p53 overexpression was not associated with age, sex, primary tumor site, stage, recurrence and survival rate. Conclusions: In our results, p53 was not significant prognostic factor in HNSCC. Based on many previous studies, It is evident that p53 has a certain role in tumorigenesis of HNSCC. So, the further study is needed to evaluate the prognostic significance of p53 in HNSCC.

• Asian-Australasian Journal of Animal Sciences
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• v.23 no.9
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• pp.1213-1220
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• 2010

This experiment evaluated the effects of dietary lysine restriction and energy density on growth performance, nutrient digestibility and meat quality of finishing pigs. A $2{\times}2$ factorial arrangement of treatments was utilized in a randomized complete block (RCB) design, and factor 1 was lysine restriction and factor 2 was energy density. The control diet was formulated to contain 3.265 Mcal of ME/kg, 0.75% lysine in the early-finishing phase and 3.265 Mcal of ME/kg, 0.60% lysine in the late-finishing phase and other nutrients met or exceeded NRC (1998) standards. Compared to the control diet (CON), lysine levels of experimental diets were restricted to 15% (treatment EL, EEL) or 30% (treatment ELL, EELL), whereas energy level of experimental diets was increased by 0.100 or 0.200 Mcal of ME/kg. A total of 100 crossbred pigs ([Yorkshire${\times}$Landrace]${\times}$Duroc), with average initial body weight of $58.47{\pm}1.42\;kg$, were allotted to 5 dietary treatments based on sex and body weight. Each treatment had 5 replicates with 4 pigs (two barrows and two gilts) per pen. ADG, ADFI and feed efficiency were calculated in an 8-week growth trial. In the late finishing period (5-8 weeks), pigs fed ELL or EELL diets had decreased ADG and feed efficiency (p<0.01), however, when the EEL diet was provided, a similar growth performance was observed compared to those fed the CON diet during the whole experimental period (p>0.05). In a metabolic trial, 15 pigs were used to evaluate the effect of dietary lysine restriction and energy density on nutrient digestibility. The digestibility of dry matter, crude fat and crude ash was not improved by restricting dietary lysine or energy density. However, crude protein digestibility was decreased (p<0.05) as dietary lysine was restricted. When dietary lysine was restricted, fecal nitrogen was increased whereas nitrogen retention was decreased. BUN concentration was affected by dietary lysine restriction; treatments ELL and EELL had higher BUN values than other treatments (p<0.01). Carcass characteristics and meat quality were measured when average body weight of pigs reached $107.83{\pm}1.50\;kg$. Treatment ELL had higher last rib backfat depth (p<0.05) than treatment CON, but ELL and EEL did not differ significantly. The ELL and EEL treatments had higher (p<0.05) subjective marbling score than treatment CON. Treatment EEL showed higher longissimus fat content than treatment EL and CON (p<0.01). The results indicated that finishing pigs fed a diet with 15% lysine restriction and 3.465 Mcal of ME/kg energy density had no detrimental effects on growth performance and N utilization, and could achieve substantial increases in marbling and longissimus fat content of pork.

• Asian-Australasian Journal of Animal Sciences
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• v.10 no.4
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• pp.335-356
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• 1997

Injection of bovine growth hormone (bGH) to lactating dairy cows increases milk yield and yields of milk components including fat. It is generally believed that most of the anabolic effects derived from bGH in animal tissues are primarily mediated by IGF-1. IGF-1 is a strong anabolic peptide in the plasma of animals and exerts mitogenic and metabolic effects on target cells. Contrary to most protein hormones, the majority of IGF-1 in circulation is bound to the binding proteins (IGFBPs) which are known to be responsible for modifying the biological actions of IGF-1, thus making determinations of IGF-1 actions more difficult. On the other hand, fat is a major milk component and the greatest energy source in milk. Currently, the fat content of milk is one of the major criteria used in determining milk prices. It has been known that flavor and texture of dairy products are mainly affected by milk fat and its composition. Acetyl-CoA carboxylase (ACC) is the rate limiting enzyme which catalyzes the conversion of acetyl-CoA to malonyl-CoA for fatty acid synthesis in 1ipogenic tissues of animals including bovine lactating mammary glands. In addition to the short-tenn hormonal regulation of ACC by changes in the catalytic efficiency per enzyme molecule brought about by phosphorylation and dephosphorylation of the enzyme, the long-term hormonal regulation of ACC by changes in the number of enzyme molecules plays an essential role in control of ACC and lipogenesis. Insulin, at supraphysiological concentrations, binds to IGF-1 receptors, thereby mimicking the biological effects of IGF-1. The receptors for insulin and IGF-1 share structural and functional homology. Furthermore, epidermal growth factor increased ACC activity in rat hepatocytes and adipocytes. Therefore, it can be assumed that IGF-1 mediating bGH action may increase milk fat production by stimulation ACC with phosphorylation (short term) and/or increasing amounts of the enzyme proteins (long term). Consequently, the main purpose of this paper is to give the readers not only the galactopoietic effects of bGH, but also the insight of bGH action with regard to stimulating milk fat synthesis from the whole body to the molecular levels.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.6
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• pp.2495-2500
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• 2014

Background: Lung cancer is one of the most commonly diagnosed cancers and the most frequent cause of cancer-related death worldwide. In Iran, it ranks second and third as the cancer-causing death in men and women, respectively. We carried out this study to find out the demographic, clinical, and histological characteristics and risk factors of lung cancer in a referral tertiary center in Iran. Materials and Methods: A retrospective study was conducted on cases of primary lung cancer based on the results of registered cancer reports of cytological and pathological specimens between March 2001 and March 2012. Demographic variables, clinical manifestations, histology and location of tumors were determined based on the data found in the medical records of each patient. Definite or probable etiologic factors were identified. Data analysis was performed with SPSS version 16 and a p-value ${\leq}0.05$ was considered as significant. Results: A total of 203 patients, with a mean age of 65.7 years (SD=11.2), with primary lung cancer were identified, 81.3% being men. Of the total, 110 cases (54.2%) were living in urban areas. In 53.2% of cases, the site of tumor was on the right side and in 72.9% of cases the lesion was centrally located. The histological types of lung cancer were squamous cell carcinoma (SCC) in 107 cases (52.7%), adenocarcinoma (AC) in 30 cases (14.8%), and small cell carcinoma (SC) in 27 cases (13.3%). Significant correlations between the gender and residence, smoking, and the histological type and location (central or peripheral) of tumor were found. The percentage of smokers was 75.2% in men and 15.8% in women. Conclusions: Smoking was the most important risk factor and squamous cell carcinoma the most common histological type of lung cancer in our study. Male sex and being a smoker was associated with histological types of SCC while being nonsmoker had relationship with adenocarcinoma.

• Journal of Nutrition and Health
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• v.44 no.4
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• pp.292-302
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• 2011

Adipocytokines (adiponectin, leptin and resistin) are known to play a major role in development of cardiovascular disease (CVD) and intervention program is effective in reducing CVD risk factors. However, intervention program to improve the CVD risk factors including adipocytokines has been less studied. This study investigated the effects of 12-weeks worksite intervention program on cardiovascular risk factors, adipocytokines and nutrients intakes in industrial workers. 157 industrial male workers (32 metabolic syndrome (MS) subjects, 125 healthy subjects using age-matched stratified random sampling) received 5 face-to-face counseling based on their health profiles. Anthropometry, biochemical parameters and nutrients intakes were measured. The diagnosis of MS was adapted from modified NCEP-ATP III criteria (2001) and Asia-Pacific definition criteria (2000) for waist circumference (WC). After the intervention program, WC, BMI, SBP, insulin, leptin and intakes of total energy and fiber were significantly decreased (p < 0.05), while adiponectin was significantly increased (p < 0.05) in MS subjects. The WC, BMI, SBP, total cholesterol, LDL and HDL-cholesterol, HbA1c, leptin and intakes of total energy, protein and fat were significantly decreased (p < 0.05) and adiponectin was significantly increased (p < 0.05) in normal subjects. Multiple linear regression revealed that adiponectin was positively correlated with HDL-cholesterol (p < 0.01). Leptin was positively correlated with WC (p < 0.01), and resistin was positively correlated with HbA1c (p < 0.05) and intakes of total energy (p < 0.05), and negatively correlated with HDL-cholesterol (p < 0.05). The results of the 12 weeks intervention showed a positive impact on adipocytokines and nutrients intakes of industrial workers to reduce cardiovascular risk factors. Further research is needed to verify a tailored long-term worksite intervention program including adipocytokines as a protective factor for the CVD.

• Molecules and Cells
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• v.41 no.3
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• pp.244-255
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• 2018

Low-grade pro-inflammatory state and leptin resistance are important underlying mechanisms that contribute to obesity-associated hypertension. We tested the hypothesis that Astragaloside IV (As IV), known to counteract obesity and hypertension, could prevent obesity-associated hypertension by inhibiting pro-inflammatory reaction and leptin resistance. High-fat diet (HFD) induced obese rats were randomly assigned to three groups: the HFD control group (HF con group), As IV group, and the As IV + ${\alpha}$-bungaratoxin (${\alpha}-BGT$) group (As IV+${\alpha}-BGT$ group). As IV ($20mg{\cdot}Kg^{-1}{\cdot}d^{-1}$) was administrated to rats for 6 weeks via daily oral gavage. Body weight and blood pressure were continuously measured, and NE levels in the plasma and renal cortex was evaluated to reflect the sympathetic activity. The expressions of leptin receptor (LepRb) mRNA, phosphorylated signal transducer and activator of transcription-3 (p-STAT3), phosphorylated phosphatidylinositol 3-kinase (p-PI3K), suppressor of cytokine signaling 3 (SOCS3) mRNA, and protein-tyrosine phosphatase 1B (PTP1B) mRNA, pro-opiomelanocortin (POMC) mRNA and neuropeptide Y (NPY) mRNA were measured by Western blot or qRT-PCR to evaluate the hypothalamic leptin sensitivity. Additionally, we measured the protein or mRNA levels of ${\alpha}7nAChR$, inhibitor of nuclear factor ${\kappa}B$ kinase subunit ${\beta}/nuclear$ factor ${\kappa}B$ ($IKK{\beta}/NF-KB$) and pro-inflammatory cytokines ($IL-1{\beta}$ and $TNF-{\alpha}$) in hypothalamus and adipose tissue to reflect the anti-inflammatory effects of As IV through upregulating expression of ${\alpha}7nAChR$. We found that As IV prevented body weight gain and adipose accumulation, and also improved metabolic disorders in HFD rats. Furthermore, As IV decreased BP and HR, as well as NE levels in blood and renal tissue. In the hypothalamus, As IV alleviated leptin resistance as evidenced by the increased p-STAT3, LepRb mRNA and POMC mRNA, and decreased p-PI3K, SOCS3 mRNA, and PTP1B mRNA. The effects of As IV on leptin sensitivity were related in part to the up-regulated ${\alpha}7nAchR$ and suppressed $IKK{\beta}/NF-KB$ signaling and pro-inflammatory cytokines in the hypothalamus and adipose tissue, since co-administration of ${\alpha}7nAChR$ selective antagonist ${\alpha}-BGT$ could weaken the improved effect of As IV on central leptin resistance. Our study suggested that As IV could efficiently prevent obesityassociated hypertension through inhibiting inflammatory reaction and improving leptin resistance; furthermore, these effects of As IV was partly related to the increased ${\alpha}7nAchR$ expression.

• Asian-Australasian Journal of Animal Sciences
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• v.31 no.4
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• pp.595-606
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• 2018

Objective: The Fusarium mycotoxins of deoxynivalenol (DON) and zerolenone (ZEN) cause health hazards for both humans and farm animals. Therefore, the main intention of this study was to reveal DON and ZEN effects on the mRNA expression of pro-inflammatory cytokines and other immune related genes in the liver of piglets. Methods: In the present study, 15 six-week-old piglets were randomly assigned to the following three different dietary treatments for 4 weeks: control diet, diet containing 8 mg DON/kg feed, and diet containing 0.8 mg ZEN/kg feed. After 4 weeks, liver samples were collected and sequenced using RNA-Seq to investigate the effects of the mycotoxins on genes and gene networks associated with the immune systems of the piglets. Results: Our analysis identified a total of 249 differentially expressed genes (DEGs), which included 99 upregulated and 150 downregulated genes in both the DON and ZEN dietary treatment groups. After biological pathway analysis, the DEGs were determined to be significantly enriched in gene ontology terms associated with many biological pathways, including immune response and cellular and metabolic processes. Consistent with inflammatory stimulation due to the mycotoxin-contaminated diet, the following Kyoto encyclopedia of genes and genomes pathways, which were related to disease and immune responses, were found to be enriched in the DEGs: allograft rejection pathway, cell adhesion molecules, graft-versus-host disease, autoimmune thyroid disease (AITD), type I diabetes mellitus, human T-cell leukemia lymphoma virus infection, and viral carcinogenesis. Genome-wide expression analysis revealed that DON and ZEN treatments downregulated the expression of the majority of the DEGs that were associated with inflammatory cytokines (interleukin 10 receptor, beta, chemokine [C-X-C motif] ligand 9), proliferation (insulin-like growth factor 1, major facilitator superfamily domain containing 2A, insulin-like growth factor binding protein 2, lipase G, and salt inducible kinase 1), and other immune response networks (paired immunoglobulin-like type 2 receptor beta, Src-like-adaptor-1 [SLA1], SLA3, SLA5, SLA7, claudin 4, nicotinamide N-methyltransferase, thyrotropin-releasing hormone degrading enzyme, ubiquitin D, histone $H_2B$ type 1, and serum amyloid A). Conclusion: In summary, our results demonstrated that high concentrations DON and ZEN disrupt immune-related processes in the liver.

• Archives of Plastic Surgery
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• v.32 no.6
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• pp.699-705
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• 2005

Transgender is the severe type of gender identity disorder. The prevalence rate of transgender is reported to occur to about 1 out of 50,000 men, and about 1 out of 10,000 women. As for Korea, it is estimated to have about 1400 transgender patients. Lately, not only the numbers of them are increasing but also they are influencing our society increasingly. As for female transgender patients, they take female hormone for a long term before and even after the operation to maintain their physical identity of female. We have analyzed insulin like growth factor-1(IGF-1), insulin like growth factor protein binding-3(IGFBP-3), female hormone, male hormone and thyroid hormone in female transgender patients who have undergone the gender reassignment operation. We examined the changes of hormone level due to having female hormone steadily, and also examined how the steady use of the hormone could affect body organs. As for IGF-1, it showed significantly low in the female transgender group compared to control ($319.30{\pm}37.4$ vs $539{\pm}55.0$, p<0.05). As for IGFBP-3, there was no significant difference ($2859{\pm}200.3$ vs $2607{\pm}262.5$, p>0.05). As for female hormone, there was no significant differences in FSH($13.42{\pm}13.8$ vs $8.95{\pm}3.5$, p>0.05), estradiol($104.41{\pm}97.1$ vs $121.68{\pm}60.2$, p>0.05), and LH($7.62{\pm}5.6$ vs $7.4{\pm}3.3$, p>0.05). Even in comparison of testosterone, there was no significant differences($0.23{\pm}0.09$ vs $0.33{\pm}1.33$, p>0.05). As for thyroid hormone, there was no significant differences in TSH and free T4($1.34{\pm}0.94$ vs $1.71{\pm}0.12$, $1.4{\pm}0.37$ vs $1.46{\pm}0.17$, p>0.05). Therefore, this study concludes that apart from the decreased level of IGF-1, the possible endocrine side-effect problem due to female hormone seems to be low because there was no differences of female, male, and thyroid hormone level compared with normal female. Further study will be required in metabolic change including bone metabolism occurred by decrease level of IGF-I.

• Proceedings of the PSK Conference
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• 2001.10a
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• pp.109-113
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• 2001

Oxidized low-density lipoprotein (oxLDL) has been shown to modulate transactivations by the peroxisome proliferator activated receptor (PPAR)$\gamma$ and nuclear factor-kappa B (NF$\kappa$B). In this study, the oxLDL signaling pathways involved with the NF$\kappa$B transactivation were investigated by utilizing a reporter construct driven by three upstream NF$\kappa$B binding sites, and various pharmacological inhibitors. OxLDL and its constituent lysophophatidylcholine (lysoPC) induced a rapid and transient increase of intracellular calcium and stimulated the NF-KB transactivation in resting RAW264.7 macrophage cells in an oxidation-dependent manner. The NF$\kappa$B activation by oxLDL or lysoPC was inhibited by protein kinase C inhibitors or an intracellular calcium chelator. Tyrosine kinase or PI3 kinase inhibitors did not block the NF$\kappa$B transactivation. Furthermore, the oxLDL-induced NF$\kappa$B activity was abolished by the PPAR$\gamma$ ligands. When the endocytosis of oxLDL was blocked by cytochalasin B, the NF$\kappa$B transactivation by oxLDL was synergistically increased, while PPAR transactivation was blocked. These results suggest that oxLDL activates NF-$\kappa$B in resting macrophages via protein kinase C- and/or calcium-dependent pathways, which does not involve the endocytic processing of oxLDL. The endocytosis-dependent PPAR$\gamma$ activation by oxLDL may function as an inactivation route of the oxLDL induced NF$\kappa$B signal. Short heterodimer partner (SHP), specifically expressed in liver and a limited number of other tissues, is an unusual orphan nuclear receptor that lacks the conventional DNA-binding domain. In this work, we found that SHP expression is abundant in murine macrophage cell line RAW 264.7 but suppressed by oxLDL and its constituent I3-HODE, a ligand for peroxisome proliferator-activated receptor y. Furthermore, SHP acted as a transcription coactivator of nuclear factor-$\kappa$B (NF$\kappa$B) and was essential for the previously described NF$\kappa$B transactivation by lysoPC, one of the oxLDL constituents. Accordingly, NF$\kappa$B, transcriptionally active in the beginning, became progressively inert in oxLDL-treated RAW 264.7 cells, as oxLDL decreased the SHP expression. Thus, SHP appears to be an important modulatory component to regulate the transcriptional activities of NF$\kappa$B in oxLDL-treated, resting macrophage cells.