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ABSTRACT: STUDY DESIGN:: In vitro experiment using degenerated human ligamentum flavum (LF) and various inflammatory cytokines. OBJECTIVES:: To examine the effect of inflammatory cytokines on LF cells and to identify their roles in the pathogenesis of LF hypertrophy and ossification. SUMMARY OF BACKGROUND DATA:: Spinal stenosis is caused, in part, by hypertrophy and ossification of the LF, which are induced by the degenerative processes (i.e., increased collagen synthesis and chondroid metaplasia) of ligament fibroblasts. Degenerated intervertebral disc (IVD) spontaneously produces inflammatory cytokines, which might affect the adjacent LF through local milieu of the spinal canal. METHODS:: The interlaminar portion of the LF was collected during surgical spinal procedures in 15 patients (age range: 49-78▒y) with lumbar spinal stenosis. LF fibroblasts were isolated by enzymatic digestion of LF tissue. LF cell cultures were treated with various inflammatory cytokines: interleukin-1α (IL-1α), IL-6, tumor necrosis factor-α (TNF-α), prostaglandin E2 (PGE2), and nitric oxide (NO). Cytotoxicity was analyzed by MTT assays. DNA synthesis was measured with 3H-thymidine incorporation, and mRNA expression of types I, III, V, and XI collagen and osteocalcin were performed by reverse transcription-polymerase chain reaction (RT-PCR). Histochemical stains such as Von Kossa were also performed to detect bone nodule formation. RESULTS:: There was no cytotoxicity in the LF cells treated with each cytokine. There were significant increases in DNA synthesis and upregulated mRNA expression of types I, V, XI collagen and osteocalcin in LF cultures treated with various cytokines. LF cultures treated with IL-6, TNF-α, PGE2, and NO showed positive Von Kossa staining, indicating bone nodule formation from LF cells. CONCLUSIONS:: Inflammatory cytokines (IL-6, TNF-α, PGE2, and NO) appear to play a crucial role in hypertrophy and ossification of LF. Degenerated, herniated IVDs, and facet arthrosis may influence LF via inflammatory cytokines and cause hypertrophy and ossification of LF.
Journal of spinal disorders & techniques 07/2012; · 1.21 Impact Factor
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Kwang-Il Lee,
Seong-Hwan Moon, Hyang Kim,
Un-Hye Kwon,
Ho-Joong Kim,
Si-Nae Park,
Hwal Suh,
Hwan-Mo Lee,
Hak-Sun Kim,
Heoung-Jae Chun,
Il-Keun Kwon,
Ju-Woong Jang
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ABSTRACT: In vitro experiment using rabbit nucleus pulposus (NP) cells seeded in atelocollagen scaffolds under the stimulation of growth factors.
To demonstrate the effect of anabolic growth factors in rabbit NP cells cultured in atelocollagen type I and type II.
Atelocollagen provides intervertebral disc (IVD) cells for a biocompatible environment to produce extracellular matrix. IVD cells with exogenous transforming growth factor-beta 1 (TGF-β1) and bone morphogenetic protein-2 (BMP-2) also render an increase in matrix synthesis. However, the effect of anabolic growth factors in NP cells cultured in atelocollagens was not elucidated before.
Rabbit NP cell was harvested, enzymatically digested, and cultured. The NP cells were seeded to atelocollagen type I and type II scaffolds, and then cultures were exposed to TGF-β1 (10 ng/mL) and/or BMP-2 (100 ng/mL). DNA synthesis was measured using [4H]-thymidine incorporation. Newly synthesized proteoglycan was measured using [35S]-sulfate incorporation. Reverse transcription-polymerase chain reactions (RT-PCRs) for mRNA expression of aggrecan, collagen type I, collagen type II, and osteocalcin were performed.
Rabbit NP cells cultured in atelocollagen type I scaffold showed an increase (1.7 to 2.4-fold) in DNA synthesis in response to TGF-β1 and/or BMP-2 (P < 0.05), whereas NP cultures in atelocollagen type II demonstrated a 30% increase in DNA synthesis only with combination of both growth factors compared with control (P < 0.05). Rabbit NP cells in atelocollagen type II scaffold with TGF-β1 and combination of both growth factors exhibited robust 5.3- and 5.4-fold increases in proteoglycan synthesis (P < 0.05), whereas any cultures in atelocollagen type I failed to show any significant increase compared with control. Rabbit NP cells in atelocollagen type I and type II scaffolds with TGF-β1 and/or BMP-2 demonstrated the upregulation of aggrecan, collagen type I, and collagen type II mRNA expression compared with saline control (P < 0.05). The response in transcriptional level was more robust in atelocollagen type II than in type I. In any event, there is no recognizable expression of osteocalcin (P < 0.05).
NP cells in atelocollagens under the stimulation of TGF-β1 and BMP-2 exhibited anabolic responses in transcriptional and translational levels. Hence, such an approach can provide a suitable engineered tissue for IVD regeneration with potential for robust refurbishment of matrix.
Spine 10/2011; 37(6):452-8. · 2.08 Impact Factor
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ABSTRACT: The purpose of this study is to investigate the mechanism of cellular proliferation of electromagnetic field (EMF) on human intervertebral disc (IVD) cells.
Human IVD cells were cultured three-dimensionally in alginate beads. EMF was exposed to IVD cells with 650 Ω, 1.8 millitesla magnetic flux density, 60 Hz sinusoidal wave. Cultures were divided into a control and EMF group. Cytotoxicity, DNA synthesis and proteoglycan synthesis were measured by MTT assay, [(3)H]-thymidine, and [(35)S]-sulfate incorporation. To detect phenotypical expression, reverse transcription-polymerase chain reactions (RT-PCR) were performed for aggrecan, collagen type I, and type II mRNA expression. To assess action mechanism of EMF, IVD cells were exposed to EMF with N(G)-Monomethyl-L-arginine (NMMA) and acetylsalicylic acid (ASA).
There was no cytotoxicity in IVD cells with the EMF group in MTT assay. Cellular proliferation was observed in the EMF group (p < 0.05). There was no difference in newly synthesized proteoglycan normalized by DNA synthesis between the EMF group and the control. Cultures with EMF showed no significant change in the expression of aggrecan, type I, and type II collagen mRNA compared to the control group. Cultures with NMMA (blocker of nitric oxide) or ASA (blocker of prostaglandin E2) exposed to EMF demonstrated decreased DNA synthesis compared to control cultures without NMMA or ASA (p < 0.05).
EMF stimulated DNA synthesis in human IVD cells while no significant effect on proteoglycan synthesis and chondrogenic phenotype expressions. DNA synthesis was partially mediated by nitric oxide and prostaglandin E2. EMF can be utilized to stimulate proliferation of IVD cells, which may provide efficient cell amplification in cell therapy to degenerative disc disease.
Yonsei medical journal 11/2010; 51(6):954-9. · 0.77 Impact Factor
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ABSTRACT: Many patients with end-stage renal disease have additional comorbidities that are important to clinical study and impact the patient's outcome. The Charlson Comorbidity Index (CCI) is a popular tool and a strong predictor of outcome in end-stage renal disease patients. We obtained comorbidity data from the hospital discharge database using the International Classification of Disease, 10th revision (ICD-10) and analyzed the mortality rate in incident patients undergoing maintenance hemodialysis (HD).
We evaluated the medical records of a total of 456 patients on HD (58 ± 14 years of age, 56% males). We calculated CCI scores at the start of HD with information from the hospital discharge summary according to the ICD-10 code. We then analyzed patient mortality according to these CCI scores.
The percentages of patients that had diabetes with end-organ damage (51.1%), congestive heart failure (9.9%), coronary artery disease (8.1%) and stroke (6.8%) were identified. CCI scores were 5.09 ± 2.01 (range 2-11). Four comorbidity groups were established by quartile ranking of the CCI scores: low, moderate, high and very high. The mortality rates were: 0.83, 7.70, 14.09 and 18.69 deaths/100 patient-years, respectively (p = 0.001). Compared with the low comorbidity group, the hazard ratios for mortality were 9.22 (95% CI 3.29-25.84) for the moderate group, 16.77 (95% CI 5.97-47.11) for the high group, and 22.37 (95% CI 8.08-61.93) for the very high group.
The CCI scores using the ICD-10 database information were significant predictors of mortality in incident patients undergoing maintenance HD.
Nephron Clinical Practice 11/2010; 117(4):c379-84. · 2.04 Impact Factor
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ABSTRACT: This study evaluated the relationship between hyperuricemia and nonalcoholic fatty liver disease (NAFLD) by comparing the incidence rates of NAFLD in relation to serum uric acid levels in apparently healthy subjects during a 5-year period.
Among 15,638 healthy Korean subjects who participated in a health-screening program in 2003 and 2008, respectively, 4954 subjects without other risk factors were enrolled in this study. We compared the incidence rates of NAFLD in 2008 with respect to baseline uric acid levels.
In 2003, serum uric acid levels were categorized into the following quartiles: 0.6-3.9, 3.9-4.8, 4.8-5.9, and 5.9-12.6 mg/dL. The incidence of NAFLD in 2008 increased with the level of baseline uric acid (5.6%, 9.8%, 16.2%, and 20.9%, respectively; p<0.05). Multiple logistic regression analysis demonstrated that hyperuricemia was associated with the development of NAFLD. When compared to the subjects in quartile 1, the odds ratio (OR) for the incidence of NAFLD for quartiles 2, 3, and 4 were 1.53 (95% confidence interval [CI], 1.09-2.16; p=0.014], 1.69 (95% CI, 1.17-2.44; p=0.005), and 1.84 (95% CI, 1.25-2.71; p=0.002), respectively.
High serum uric acid levels appear to be associated with an increased risk of the development of NAFLD.
Gut and liver 09/2010; 4(3):378-83. · 0.83 Impact Factor
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Hak-Sun Kim,
Kwang-Il Lee, Hyang Kim,
Un-Hye Kwon,
Mi-Ran Nam,
M D Ju-Woong,
M D Jang,
In-Je Cho,
Boram Kim,
Hwan-Mo Lee,
Seong-Hwan Moon
J Korean Soc Spine Surg. 04/2010; 17:49-56.
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Hyang Kim,
Jeong-Uk Lee,
Seong-Hwan Moon,
Hyung-Chan Kim,
Un-Hae Kwon,
Nam-Hun Seol,
Ho-Joong Kim,
Jin-Oh Park,
Heoung-Jae Chun,
Il-Keun Kwon,
Hwan-Mo Lee
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ABSTRACT: In vitro experiment using bone morphogenetic protein-2 (BMP-2) and cells from the nucleus pulposus (NP), transitional zone (TZ), and anulus fibrosus (AF) of the human intervertebral disc (IVD).
To demonstrate the differential effect of BMP-2 on DNA synthesis, proteoglycan synthesis, and osteocalcin mRNA expression in human IVD cells from the NP, TZ, and AF, respectively.
BMP-2 has been proven to be effective in stimulating proteoglycan synthesis in articular chondrocytes and IVD cells from the NP. Nevertheless, the effect of BMP-2 on cells from different regions of the IVD has not yet been thoroughly elucidated.
Human IVDs were harvested from surgical disc procedures and tissue from the NP, TZ, and AF was obtained. Disc tissue was enzymatically digested, and IVD cells were cultured three-dimensionally in alginate beads. Then IVD cell cultures from the NP, TZ, and AF were exposed to BMP-2. DNA synthesis and newly synthesized proteoglycan were measured. Reverse transcription-polymerase chain reaction for mRNA expression of bone sialoprotein, DLX5, osteocalcin, and collagen type I, was performed.
Cells from the AF responded to BMP-2 with mitogenesis. There was no significant increase in DNA synthesis in cultures from the NP and TZ treated with BMP-2. Only cells from the NP showed a significant increase in newly synthesized proteoglycan in response to BMP-2. IVD cells from all zones demonstrated no significant expression of bone sialoprotein, DLX5, osteocalcin mRNA after treatment with BMP-2.
BMP-2 clearly exerted a mitogenic effect on AF cells, and stimulated proteoglycan synthesis in NP cells. However, BMP-2 did not have an osteogenic effect in any IVD region. Taken together, these results confirm that BMP-2 can be used as an anabolic agent for mitogenesis in AF cells and NP cell matrix regeneration without the possibility of osteogenesis.
Spine 09/2009; 34(17):1834-8. · 2.08 Impact Factor
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ABSTRACT: Several studies have reported the role of N-acetylcysteine on the prevention of contrast induced nephropathy (CIN) with conflicting results. To date, the effect of acetylcysteine on cystatin C-based CIN has not been described. This study was designed to examine the incidence of cystatin C-based CIN and investigate the effect of N-acetylcysteine on the prevention of CIN after coronary angiography (CAG).
We conducted a prospective, randomized trial on 166 patients (80 patients in N-acetylcysteine group and 86 patients in control group) that underwent elective CAG with apparently normal renal function. Serum cystatin C and creatinine concentrations were measured before, and at 24 and 48 h after CAG.
The overall incidence of cystatin C-based CIN among all study subjects was 10.2% (5.0% in N-acetylcysteine group and 15.1% in control group, p<0.05) and that of serum creatinine-based CIN was 6% (3.8% in N-acetylcysteine group and 8.1% in control group, p=NS). Kappa analysis between cystatin C-based CIN and serum creatinine-based CIN showed a substantial agreement (k=0.64). Multivariate logistic regression analysis showed that N-acetylcysteine administration was independently protective against the development of cystatin C-based CIN (Odd ratio[95% confidence interval] 0.255[0.066 to 0.994]) but there was a trend toward protection against that of serum creatinine-based CIN.
This study suggests that in patients with apparently normal renal function, prophylactic oral N-acetylcysteine administration is effective at preventing cystatin C-based CIN development after elective coronary angiography and/or intervention, and that serum cystatin C might be a more sensitive marker of the early CIN than serum creatinine.
International journal of cardiology 09/2008; 138(3):239-45. · 7.08 Impact Factor
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ABSTRACT: In vitro experiment using human intervertebral disc (IVD) cells and adenovirus-therapeutic gene constructs.
To examine the biologic effect of "cocktail" therapeutic gene transfer to human IVD cells in three-dimensional cultures.
Gene therapy is regarded as a potential option for the treatment of degenerative disc disease. Although various anabolic genes have previously been introduced for this purpose, cocktail gene transfer of anabolic genes to IVD cells has never been attempted.
Human IVDs were harvested during surgical disc procedures and cultured. We prepared recombinant adenovirus constructs bearing the TGF-beta1 gene (Ad/TGF-beta1), the IGF-1 gene (Ad/IGF-1), and the BMP-2 gene (Ad/BMP-2). Transgene expression was detected by luciferase assays, enzyme linked immunosorbent assays, and Western blot analysis. Newly synthesized proteoglycan was measured by S-sulfate incorporation on Sephadex G-25 M in PD 10 columns. Human IVD cells were transduced by single, double, and triple combination of Ad/TGF-beta1, Ad/IGF-1, Ad/BMP-2 with an MOI of 75, then cultured three-dimensionally in alginate beads.
Transgene expression was detected at 18 hours after viral transduction. IVD cultures with Ad/TGF-beta1, Ad/IGF-1, Ad/BMP-2 (MOI of 75) showed 2.9, 1.8, and 1.9 fold increases, respectively, in proteoglycan synthesis compared to control. Human IVD cultures with double gene combination (MOI of 75) showed 3.2 to 3.9 fold increases of proteoglycan synthesis. Lastly, Human IVD cultures with triple gene combination (TGF-beta1+IGF-1+BMP-2 genes with an MOI of 75) transfer demonstrated 4.7 fold increase in proteoglycan synthesis compared control.
Combination or "cocktail" gene therapy offers a promising mechanism for maximizing matrixsynthesis with low dose of adenoviral mixtures, circumventing systemic, local toxic effect, and immune response.
Spine 08/2008; 33(17):1850-5. · 2.08 Impact Factor
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ABSTRACT: The effects of luminal ATP between rabbit pulmonary (PAs) and coronary arteries (CAs) were compared to understand the role of purinoceptors in the regulation of pulmonary arterial pressure (PAP) under hypoxia. Diameters of vessels were video analyzed under luminal perfusion. ATP-induced membrane currents and intracellular Ca(2+) signals ([Ca(2+)](i)) were compared in pulmonary (PASMCs) and coronary myocytes (CASMCs) using patch clamp and spectrofluorimetry. PAP was measured in perfused lungs under ventilation. Luminal ATP induced constriction of rabbit PAs in the presence of endothelium. In contrast, CAs showed dilating responses to luminal ATP even in the absence of endothelium. In PASMCs, both P2X-mediated inward current and P2Y-mediated store Ca(2+) release were consistently observed. In contrast, CASMCs showed neither P2X nor P2Y responses. In the perfused lungs, hypoxia-induced PAP increase was decreased by suramin, a purinergic antagonist. A luminal application of alpha,beta-meATP largely increased PAP, whereas UTP decreased PAP. The combined application of P2X- and P2Y-selective agonists (alpha,beta-meATP and UTP) increased PAP. However, the perfusion of ATP alone decreased PAP, and the ATP-induced PAP decrease was affected neither by adenosine receptor antagonist nor by nitric oxide synthase inhibitor. In summary, although the luminal ATP constricts isolated PAs and suramin attenuated the HPV of perfused lungs, the bimodal responses of PAP to purinergic agonists indicate that the luminal ATP regulates pulmonary circulation via complex signaling interactions in situ.
Pflügers Archiv - European Journal of Physiology 07/2008; 457(2):281-91. · 4.46 Impact Factor
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ABSTRACT: The development of a perirenal hematoma is rare and primarily the result of trauma, malignancy, or a connective tissue disease. Infrequently, a continuous or even mild trauma can cause a perirenal hematoma. Here, we report a case involving the development of a perirenal hematoma after excessive hula-hooping in the absence of a major trauma history.
Yonsei Medical Journal 11/2007; 48(5):868-70. · 1.14 Impact Factor
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Seung Ha Park,
Byung Ik Kim,
Sang Hoon Kim,
Hong Joo Kim,
Dong Il Park,
Yong Kyun Cho,
In Kyung Sung,
Chong Il Sohn, Hyang Kim,
Dong Keuk Keum,
Heung Dae Kim,
Jung Ho Park,
Jin Ho Kang,
Woo Kyu Jeon
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ABSTRACT: The aim of this study was to characterize the relationship between nonalcoholic fatty liver disease (NAFLD) and body fat distribution and insulin resistance in a sample of non-diabetic overweight men.
We conducted a cross-sectional survey of 117 overweight men with NAFLD, as well as 117 controls, who were matched with regard to age and body mass index. None of the study subjects exhibited signs of alcohol abuse, hepatitis B or C, diabetes or fasting hyperglycemia, or hypertension. The diagnosis of NAFLD was based on dual findings of elevated alanine aminotransferase levels and sonographically-determined fatty liver. Body fat distribution was assessed via bioelectrical impedance. Insulin resistance was evaluated via homeostasis model assessment (HOMA-IR).
The risk of developing NAFLD was found to be profoundly associated with elevated measurements of waist circumference, fat mass, percentage of body fat and abdominal fat, iron, triglycerides, apolipoprotein B, and results of HOMA-IR. Multivariate analysis revealed that NAFLD was significantly associated with elevated measurements of waist circumference, iron, apolipoprotein B, and HOMA-IR.
Our study provides evidence for a profound and dose-dependent association of NAFLD with central adiposity, insulin resistance in overweight men lacking complications of metabolic syndrome. Overweight subjects with insulin resistance or central adiposity were at more risk of NAFLD than were those subjects with less insulin resistance or central adiposity, even those with a similar degree of obesity.
Journal of the American College of Nutrition 09/2007; 26(4):321-6. · 2.29 Impact Factor
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ABSTRACT: Recent studies of the distribution of PKC isoenzymes in the mouse kidney demonstrated that PKC-alpha, -beta(I), and -delta are expressed in intercalated cells. The purpose of this study was to identify the intercalated cell subtypes that express the different PKC isoenzymes and determine the location of the PKC isoenzymes within these cells. Adult C57BL/6 mice kidney tissues were processed for multiple-labeling immunohistochemistry. Antibodies against the vacuolar H(+)-ATPase and pendrin were used to identify intercalated cell subtypes, whereas antibodies against calbindin D(28K) and aquaporin-2 (AQP2) were used to identify connecting tubule cells and principal cells of the collecting duct, respectively. Within type A intercalated cells, PKC-delta was highly expressed in the apical part of the cells, whereas immunoreactivity for both PKC-alpha and PKC-beta(I) was weak. Type B intercalated cells exhibited strong expression of PKC-alpha, -beta(I), and -delta. PKC-alpha and -beta(I) were localized throughout the cytoplasm, whereas PKC-delta was restricted to the basal domain. Within non-A-non-B cells, immunoreactivity for both PKC-alpha and PKC-beta(I) was high in intensity and localized diffusely in the cytoplasm, whereas PKC-delta was localized in the apical part of the cells. None of the PKC isoenzymes (PKC-alpha, -beta(I), or -delta) were expressed in the calbindin D(28K)-positive connecting tubule cells. Within AQP2-positive principal cells of the collecting duct, PKC-alpha was expressed on the basolateral plasma membrane, but no significant staining was detected for PKC-beta(I) and -delta. In summary, this study demonstrates distinct and differential expression patterns of PKC-alpha, -beta(I), and -delta in the three subtypes of intercalated cells in the mouse kidney.
American journal of physiology. Renal physiology 12/2006; 291(5):F1052-60. · 3.68 Impact Factor
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ABSTRACT: Neopterin is a pyrazino-pyrimidine compound, and is known to be a marker associated with cell-mediated immunity in various diseases. We hypothesized that the levels of serum and urine neopterin would be elevated in renal disease, and would correlate with certain clinical parameters. We evaluated serum and urinary neopterin levels in patients with several renal diseases, including nephrotic syndrome (NS, n=19), chronic renal failure (CRF, n=8), end stage renal disease (ESRD, n=64) and controls (n=22). Serum neopterin was elevated in patients with CRF and ESRD, as compared to controls. Urinary neopterin levels were also found to be elevated in patients with CRF and ESRD, as compared to controls. Serum neopterin levels showed significant positive correlation with age, serum BUN and creatinine levels, and inverse correlation with WBC, hemoglobin, hematocrit, serum albumin and total iron binding capacity. Urine neopterin levels exhibited positive correlation with age and serum creatinine levels, and inverse correlation with WBC, hemoglobin, hematocrit, BUN and serum albumin. In conclusion, increased serum and urinary neopterin levels were found in some patients with renal disease and were correlated with certain clinical parameters.
Journal of Korean Medical Science 09/2006; 21(4):678-82. · 0.99 Impact Factor
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ABSTRACT: In vitro and in vivo experiment using degenerated human ligamentum flavum (LF) and Type 5 adenovirus construct with bone morphogenetic protein-2 (BMP-2) cDNA.
To demonstrate in vitro and in vivo osteogenic effect of BMP-2 gene transfer to human LF and to propose genetically modified LF as a substitute for autogenous bone graft in spinal fusion.
Spinal fusion is still considered to be an important option for treating various spinal disorders. To induce solid spinal fusion, osteoinductive and/or osteoconductive agents have been widely adopted. Autogenous LF, however, has never been seriously considered as a carrier for ex vivo osteoinductive gene therapy for spinal fusion.
In vitro experiment: Degenerated human LF was harvested and cultured. Type 5 adenovirus lacZ (Ad/lacZ) and BMP-2 construct (Ad/BMP-2) were produced. LF cell cultures were then exposed to Ad/BMP-2. Expressions of osteocalcin and BMP-2 mRNA were analyzed by reverse transcriptase-polymerase chain reaction (RT-PCR). Western blot analysis was performed to detect osteocalcin protein. Alkaline phosphatase and von Kossa stains were used to detect osteogenic markers and bone nodule formation, respectively. In vivo experiment: Human LF tissues treated with Ad/lacZ, Ad/BMP-2, and saline were implanted into the subcutaneous tissue of nude mice. After 4 weeks, nude mice were radiographed and killed. Implanted LF tissues were harvested and histologically stained.
LF cell cultures with Ad/BMP-2 revealed strong expression of BMP-2 and osteocalcin mRNA in RT-PCR and osteocalcin protein in western blot analysis. LF cell culture with saline showed baseline expression of BMP-2, osteocalcin mRNA, and osteocalcin protein, respectively. Furthermore, LF cell culture with Ad/BMP-2 demonstrated the expression of alkaline phosphatase and bone nodule formation in the aforementioned histochemical stain. LF tissues with Ad/BMP-2 revealed de novo osteogenesis in nude mice, whereas LF with Ad/lacZ or saline showed only remaining LF tissue without sign of bone formation.
Human LF cells transduced with Ad/BMP-2 exhibited the expression of osteogenic phenotype and bone nodule formation. Additionally, genetically modified human LF with BMP-2 cDNA clearly demonstrated de novo osteogenesis, which supports the concept that biologically modified LF can be a substitute for autogenous bone graft in spinal fusion surgery.
Spine 01/2006; 30(24):2749-54. · 2.08 Impact Factor
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Tae Woo Yoo,
Ki Chul Sung,
Hun Sub Shin,
Byung Jin Kim,
Bum Soo Kim,
Jin Ho Kang,
Man Ho Lee,
Jung Ro Park, Hyang Kim,
Eun Jung Rhee,
Won Young Lee,
Sun Woo Kim,
Seung Ho Ryu,
Dong Geuk Keum
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ABSTRACT: Associations between hyperuricemia, cardiovascular diseases and diabetes have been reported, but few of the studies have been conducted in the Korean population. The present study examined a Korean adult population with respect to the relationships between serum uric acid concentrations and hypertension, insulin resistance, and the risk factors of metabolic syndrome.
A total of 53,477 subjects were divided into 4 groups according to serum uric acid quartiles. The incidence of hypertension in all subjects was higher in the first quartile than in the third plus fourth quartile (odds ratio (OR) 1.192, p < 0.001). Homeostasis model assessment index was found to be associated with serum uric acid concentration in all subjects (OR 1.193, p < 0.001), and the serum uric acid concentration was positively correlated with the risk factors of metabolic syndrome. In addition, the number of metabolic syndrome variables increased as serum uric acid concentration increased.
Serum uric acid concentration was found to be independently correlated with hypertension, insulin resistance and the risk factors of metabolic syndrome. In addition, even those with a serum uric acid concentration in the normal range showed an increased risk of metabolic syndrome as serum uric acid concentration increased.
Circulation Journal 08/2005; 69(8):928-33. · 3.77 Impact Factor
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ABSTRACT: Endothelium-derived nitric oxide (NO) is synthesized within the developing kidney and may play a crucial role in the regulation of renal hemodynamics. The purpose of this study was to establish the expression and intrarenal localization of the NO-synthesizing enzyme endothelial NO synthase (eNOS) during kidney development. Rat kidneys from 14 (E14)-, 16 (E16)-, 18 (E18)-, and 20-day-old (E20) fetuses and 1 (P1)-, 3 (P3)-, 7 (P7)-, 14 (P14)-, and 21-day-old (P21) pups were processed for immunocytochemical and immunoblot analysis. In fetal kidneys, expression of eNOS was first observed in the endothelial cells of the undifferentiated intrarenal capillary network at E14. At E16, strong eNOS immunoreactivity was observed in the endothelial cells of renal vesicles, S-shaped bodies (stage II glomeruli), and stage III glomeruli at the corticomedullary junction. At E18-20, early-stage developing glomeruli located in the subcapsular region showed less strong eNOS immunoreactivity than those of E16. The eNOS-positive immature glomeruli were observed in the nephrogenic zone until 7 days after birth. In fetal kidneys, eNOS was also expressed in the medulla in the endothelial cells of the capillaries surrounding medullary collecting ducts. After birth, eNOS immunostaining gradually increased in the developing vascular bundles and peritubular capillaries in the medulla and was highest at P21. Surprisingly, eNOS was also expressed in proximal tubules, in the endocytic vacuolar apparatus, only at P1. The strong expression of eNOS in the early stages of developing glomeruli and vasculature suggests that eNOS may play a role in regulating renal hemodynamics of the immature kidney.
American journal of physiology. Renal physiology 05/2005; 288(4):F694-702. · 3.68 Impact Factor
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Ki Chul Sung,
Byung Jin Kim,
Bum Su Kim,
Jin Ho Kang,
Man Ho Lee,
Jung Roe Park,
Eun Jung Rhee,
Won Young Lee,
Sun Woo Kim, Hyang Kim,
Kyu Beck Lee,
Seung Ho Ryu
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ABSTRACT: There is some controversy about the role of insulin resistance (IR) in the regulation of blood pressure (BP). Moreover, a large study of the association between BP and IR has not been conducted in normal glucose tolerance Asians. The present study investigated the relationships between IR, body mass index (BMI) and waist circumference and BP in normoglycemic Koreans.
Anthropometric indices of adiposity, metabolic variables (fasting serum insulin and a homeostasis model assessment (HOMA) index of insulin sensitivity), BP and several cardiovascular risk factors were measured during a cross-sectional survey of 49,076 normoglycemic Korean subjects. A high BP was defined as a systolic BP >/=140 mmHg or a diastolic BP >/=90 mmHg. The prevalence of high BP by HOMA grading was 0.985 (95% confidence interval (CI) 0.857-1.132, p=0.835), 1.180 (95% CI 1.032-1.350, p=0.016), 1.289 (95% CI 1.129-1.472, p<0.001), and 1.540 (95% CI 1.341-1.768, p<0.001) times higher in subjects in the second, third, fourth, and fifth quintiles, respectively, compared with those in the first quintile. In addition, age, sex, waist circumference and BMI were found to be significantly associated with a high BP.
IR, BMI and waist circumference are independently correlated with high BP in normoglycemic Koreans.
Circulation Journal 10/2004; 68(10):898-902. · 3.77 Impact Factor
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Seung Ha Park,
Byung Ik Kim,
Jung Won Yun,
Jeong Wook Kim,
Dong Il Park,
Yong Kyun Cho,
In Kyung Sung,
Chang Young Park,
Chong Il Sohn,
Woo Kyu Jeon, Hyang Kim,
Eun Jung Rhee,
Won Young Lee,
Sun Woo Kim
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ABSTRACT: Although insulin resistance is often considered the link between obesity and non-alcoholic fatty liver disease (NAFLD), the role of insulin resistance, independent of obesity, as a NAFLD risk factor in non-obese men has been less well established. Systemic inflammation may be accompanied by insulin resistance in healthy subjects. The goal of the present study was to examine if insulin resistance and systemic inflammatory markers are independent predictors of NAFLD in non-obese men.
The authors conducted a cross-sectional survey of 120 patients with NAFLD and 240 controls matched by age and body mass index. Controls had no evidence of alcohol abuse, hepatitis B or C, obesity, or previous history of diabetes, fasting hyperglycemia or hypertension. Diagnosis of NAFLD was based on an elevated alanine aminotransferase level and sonographic evidence of a fatty liver. Insulin resistance was determined using a homeostasis model assessment (HOMA-IR).
The age-adjusted risk of developing NAFLD was strongly associated with the elevated levels in measurements of uric acid, fasting blood sugar, triglycerides, apolipoprotein B, C-reactive protein (CRP) and HOMA-IR, and decreased levels of high density lipoprotein cholesterol and apolipoprotein A-I. Multivariate analysis based on univariate analysis indicated that an increase in CRP (odds ratio [OR] = 1.37; 95% confidence interval [CI]: 1.06-1.77) per 1 SD (1.48 mg/L) and HOMA-IR (OR = 2.28; 95% CI: 1.67-3.11) per 1 SD (0.63) were independent risk factors for NAFLD.
Insulin resistance and systemic inflammatory response are of key importance for inducing NAFLD, particularly in apparently healthy non-obese men.
Journal of Gastroenterology and Hepatology 07/2004; 19(6):694-8. · 2.87 Impact Factor
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ABSTRACT: Eosinophilic peritonitis is defined as when there are more than 100 eosinophils present per milliliter of peritoneal effluent, of which eosinophils constitute more than 10% of its total WBC count. Most cases occur within the first 4 weeks of peritoneal catheter insertion and they usually have a benign and self-limited course. We report a patient of eosinophilic peritonitis that was successfully resolved without special treatment. An 84-year-old man with end stage renal disease secondary to diabetic nephropathy was admitted for dyspnea and poor oral intake. Allergic history was negative. and physical examination was unremarkable. Complete blood count showed a hemoglobin level of 11.1 g/dL, WBC count was 24,500/mm3 (neutrophil, 93%; lymphocyte, 5%; monocyte, 2%), platelet count was 216,000/mm3, serum BUN was 143 mg/dL, Cr was 5.7 mg/dL and albumin was 3.5 g/dL. Creatinine clearance was 5.4 mL/min. Three weeks after peritoneal catheter insertion, he was started on peritoneal dialysis with a 6-hour exchange of 2L 1.5% peritoneal dialysate. After nine days, he developed turbid peritoneal effluents with fever (38.4 degrees C), abdominal pain and tenderness. Dialysate WBC count was 180/mm3 (neutrophil, 20%; lymphocyte, 4%; eosinophil, 76% [eosinophil count: 136/mm3]). Cultures of peritoneal fluid showed no growth of aerobic or anaerobic bacteria, or of fungus. Continuous ambulatory peritoneal dialysis (CAPD) was commenced, and he was started on intraperitoneal ceftazidime (1.0 g/day) and cefazolin (1.0 g/day). After two weeksr, the dialysate had cleared up and clinical symptoms were improved. Dialysate WBC count decreased to 8/mm3 and eosinophils were not detected in peritoneal fluid. There was no recurrence of eosinophilic peritonitis on follow-up evaluation, but he died of sepsis and pneumonia fifteen weeks after admission.
The Korean Journal of Internal Medicine 07/2004; 19(2):121-3.
