Intensive insulin therapy effectively delays the onset and slows the progression of nephropathy in patients with IDDM. TGF- 0 has recently been implicated in the pathogenesis of diabetic nephropathy. We evaluated the effects of different level of glucose control with insulin therapy on the progression of diabetic nephropathy in age-matched control rats(C) and 3 groups of streptozotocininduced diabetic rats', high blood glucose diabetic rats without insulin therapy(HG), rnoderate glucose diabetic rats with insulin therapy(MG), and normal glucose diabetic rats with intensive insulin treatment (NG). Glomerular volume(VG) was measured using Image-Pro morphometric software, glomerular TGF- Bl mRNA expression by in situ hybridization, and glomerular expression of TGF-8 and type IV collagen proteins by immunohistochemical staining. VG was significantly higher in HG than in other groups in 12 weeks. Kidney weight(KW) was the highest while the body weight the lowest in HG of all groups in 12 weeks. Daily urine albumin excretion (UAE) increased with time in all groups but was significantly larger in HG than in all other groups in 12 weeks. MG also had significantly larger UAE than C in 12 weeks. There was no difference in VG, KW, and UAE between NG and C. Glomerular TGF-Bl mRNA expression was significantly higher in HG than in all the rest of the groups in 4 and 12 weeks. Glomerular expression of TGF-B and type IV collagen proteins was proportional to the levels of blood glucose, being the highest in HG in 12 weeks. There was little or no expression of TGF-0 1 mRNA and protein or type IV collagen protein in NG. Thus these results support the view that high blood glucose is the prerequisite for glomerular injury in diabetes mellitus and that the glomerular injury in diabetes mellitus is mediated, in part, by TGF-01 and suppressed by glucose control.
Animals ; Blood Glucose* ; Body Weight ; Collagen Type IV ; Diabetes Mellitus ; Diabetes Mellitus, Type 1 ; Diabetic Nephropathies* ; Glucose ; Humans ; In Situ Hybridization ; Insulin* ; Kidney ; Rats ; RNA, Messenger

No abstract available.
Low Back Pain*

PURPOSE: This study was designed to determine whether transabdominal ultrasound can detect different hepatic stiffness between patients with cirrhosis and control subjects. MATERIALS AND METHODS: Sevent-three patients (Child-Pugh class A stage) with liver cirrhosis and 57 control subjects were included in this study. All patients were subdivided arbitrarily into two groups: early cirrhosis (n = 53) and overt cirrhosis (n = 20). Two sagittal images of the left lobe of the liver were obtained in the left hepatic vein level during the resting state and at full inspiration while pushing their belly out, by abdominal US (i.e., resting and stress image). The length between the inferior hepatic angle and the midpoint of the liver dome was measured in all images for the evaluation of liver distortion. The elongation was calculated by a formula: (L2-L1/L1) x 100(%); where L1 and L2 are the length of the liver for both the resting and stress image. The calculated elongated length (L2-L1, EL) and elongation rate were compared between cirrhotic patients and control subjects. RESULTS: For the control subjects, early cirrhosis, and overt cirrhosis groups, the mean ELs (elongation rate) were 2.34+/-0.98 cm (30.2+/-13.2%), 1.18+/-0.73 cm (14.9+/-9.5%) and 0.53+/-0.54 cm (6.3+/-6.6%), respectively. This difference among the three groups was statistically significant (p < 0.05). A possible best cut-off value of liver elongation rate is 17% for the prediction of cirrhosis (sensitivity: 90%, specificity: 75.3%). CONCLUSION: The liver of patients with liver cirrhosis is stiffer than that of control subjects. Calculation of the elongation rate in the left lobe of the liver during a respiratory maneuver may be used as an ancillary method of US for the evaluation of liver cirrhosis.
Fibrosis ; Hepatic Veins ; Humans ; Liver ; Liver Cirrhosis ; Respiration

BACKGROUND: High glucose upregulates MCP-1 expression in rat glomerular mesangial cells and in human peritoneal mesothelial cells. However, the role of high glucose-induced MCP-1 on the development and progression of diabetic renal injury and peritoneal injury during peritoneal dialysis(PD) using high glucose PD solutions are not clear. Since MCP-1 was shown to upregulate transforming growth factor-beta1(TGF-beta1) and collagen expression in lung fibroblasts, the present study investigated the effects of MCP-1 on fibronectin secretion by mouse mesangial cells(MMC), human peritoneal mesothelial cells (HPMC), and human peritoneal fibroblasts(HPFB). METHODS: Synchronized cells were stimulated by different concentrations of MCP-1(0.1-100 ng/mL) or TGF-beta1(0.1-10 ng/mL) for 48 hours. Fibronectin protein secreted into the media was analyzed by Western blot analysis. RESULTS: MCP-1 up to 100 ng/mL did not affect fibronectin secretion by MMC. TGF-beta1 10 ng/mL, however, increased fibronectin secretion by MMC 2.8 fold that of control. MCP-1 up to 100 ng/mL did not affect fibronectin secretion by HPMC. But, TGF-beta1 0.1 ng/mL increased fibronectin secretion by HPMC 1.8 fold compared to control. On the other hand, MCP-1 increased fibronectin secretion by HPFB in a dose-dependent manner. MCP-1 at 1-10 ng/mL significantly increased fibronectin when compared to M199 control. 100 ng/mL MCP-1 further increased fibronectin secretion by HPFB compared to 0.1-10 ng/mL MCP-1. CONCLUSION: These results suggest a possible role for MCP-1 in the development and progression of peritoneal fibrosis and support the view that in addition to recruiting inflammatory cells MCP-1 may play a role in tissue fibrosis in other organs.
Animals ; Blotting, Western ; Chemokine CCL2* ; Collagen ; Fibroblasts* ; Fibronectins* ; Fibrosis ; Glucose ; Hand ; Humans* ; Lung ; Mesangial Cells ; Mice ; Monocytes* ; Peritoneal Fibrosis ; Rats ; Transforming Growth Factor beta1

OBJECTIVE: The purpose of this retrospective study was to report the outcome of the endovascular treatment of eight patients with eight saccular posterior inferior cerebellar artery (PICA) aneurysms. MATERIALS AND METHODS: Over the last seven years (1999-2006), eight consecutive patients with saccular PICA aneurysms were treated by endovascular methods. Five of the aneurysms were presented with subarachnoid hemorrhaging, whereas three were discovered incidentally. Four of the aneurysms (3 ruptured and 1 incidental) were treated by intrasaccular coiling, whereas the remaining four (1 ruptured and 3 incidental) were treated by vertebral artery (VA) occlusion. RESULTS: Of the four aneurysms treated by intrasaccular coiling, three were completely packed with coils and one was partially packed. In three of four patients who underwent vertebral artery occlusions, follow-up digital subtraction angiographies demonstrated thrombosed aneurysms and PICA. No procedure-related morbidity occurred and no re-bleed was encountered during a follow-up examination (mean; 31 months). CONCLUSION: As a result of this study, we found that the endovascular management of saccular PICA aneurysms should be considered as safe and effective.
Adult ; Aged ; Aneurysm, Ruptured/radiography/*therapy ; Cerebellum/blood supply/*radiography ; Cerebral Angiography ; Embolization, Therapeutic/*methods ; Female ; Humans ; Incidental Findings ; Intracranial Aneurysm/radiography/*therapy ; Male ; Middle Aged ; Retrospective Studies ; Subarachnoid Hemorrhage/radiography/*therapy ; Treatment Outcome

No abstract available.
Brain Stem Infarctions*

A retrospective analysis of 60 patients with traumatic subdural hygroma who had been managed and followed up at least 6 months, was done in relation to time of development and associated intracranial lesion, initial Glasgow Coma Scale(GCS), sequeritial changes of subdural hygroma, and Glasgow Outcome Scale(GOS). The incidence of traumatic subdural hygroma was 8.4%, 131 cases among 1,563 head-injured cases. And most of them was subacute from(55%, 33 cases among 60 cases), complex subdural hygroma was 65%(39 cases among 60 cases). The conversion rate of traumatic subdural hygroma into chronic subdural hematoma was 15%(9 cases among 60 cases). There was no statistically significant relation between initial GCS score and time of development and also intial GCS score and development of complex subdural hygroma and time of development and GOS of 6 months follow-up(P>0.05). There noted only highly significant relation between initial GCS score and GOS of 6 months follow-up(P<0.001).
Coma ; Craniocerebral Trauma ; Hematoma, Subdural, Chronic ; Humans ; Incidence ; Retrospective Studies ; Subdural Effusion*

To elucidate some DNA adducts as a biological marker for workers of chromate pigment, the effects of chromium exposure on the formation of 8-hydroxydeoxyguanosine(8-OH-dG) and sister chromatid exchanges(SCEs) frequency in 38 workers of a pigment plant in Bucheon which utilized lead chromates, were examined. The chromium contents of venous blood and urine were measured as working environmental exposure level. The concentrations of 8-OH-dG in DNA isolated from lymphocytes were determined with high performance liquid chromatography and electrochemical detector and denoted as a molar ratio of 8-OH-dG to deoxyguanosine(dG). The SCEs frequency were analyzed in DNA isolated from lymphocytes. A significant correlation was found between creatinine adjusted urine chromium concentration and the molar ratio of 8-OH-dG to dG(r=0.47, p<0.01). After adjusting the current smoking habit, the correlation coefficient was increased(r=0.62, p<0.05). However, there was no significant correlation between the SCE frequency and chromium exposure. This significant results between molar ratio of 8-OH-dG to dG and chromium exposure are in good agreement with in vitro studies that support the importance of DNA adduct formation for the carcinogenic effect of chromium.
Biomarkers ; Chromates ; Chromatids ; Chromatography, Liquid ; Chromium* ; Creatinine ; DNA ; DNA Adducts ; Environmental Exposure ; Gyeonggi-do ; Humans ; Lymphocytes ; Molar ; Plants ; Siblings* ; Sister Chromatid Exchange* ; Smoke ; Smoking

No abstract available.
Female ; Humans ; Pregnancy Trimester, First* ; Pregnancy*

BACKGROUND: Advanced glycation end products (AGE) are independent risk factors in the development and progression of diabetic nephropathy. Receptor for AGE(RAGE) is considered the main receptor involved in AGE-induced cell activation. Galectin-3, another AGE receptor, has recently been found upregulated in mesangial cells(MC) cultured under high glucose and in diabetic rat kidneys. N epsilon(carboxymethyl)lysine(CML) is a well characterized AGE but its role in MC activation is unknown. The present study examined the effects of CML on MC proliferation and extracellular matrix(ECM) secretion. METHODS: Synchronized rat MC were stimulated with different concentrations of CML-bovine serum albumin(BSA), control BSA, and transforming growth factor-beta(TGF-beta) for up to 72 hours. Cell proliferation was measured by [3H]-thymidine incorporation. Fibronectin, TGF-beta, plasminogen activator inhibitor(PAI)-1 secreted into the media and RAGE and galectin-3 expression in MC were measured by Western blot analysis and ELISA. RESULTS: 1,000 micro /mL of CML-BSA decreased [3H]-thymidine incorporation by MC at 48 hours and 10 ng/mL TGF-beta at 24 and 48 hours. CML-BSA 100 and 1,000 micro /mL, control BSA 1,000 micro /mL, and TGF-beta 10 ng/mL increased fibronectin secretion at 48 hours. CML-BSA up to 1,000 micro /mL did not affect TGF-beta or PAI-1 secretion. TGF-beta 10 ng/mL, however, significantly increased PAI-1 secretion. Cultured MC expressed both RAGE and galectin-3. CML-BSA 100 micro /mL upregulated galectin-3 expression. CONCLUSION: CML-BSA decreased MC proliferation and increased fibronectin secretion, suggesting that CML may lead to ECM accumulation and glomerulosclerosis in diabetic animals. MC express RAGE and galectin-3 constitutively and CML-induced galectin-3 upregulation may have a role in AGE-induced MC activation.
Animals ; Blotting, Western ; Cell Proliferation ; Diabetic Nephropathies ; Enzyme-Linked Immunosorbent Assay ; Fibronectins ; Galectin 3 ; Glucose ; Glycosylation End Products, Advanced ; Kidney ; Mesangial Cells* ; Plasminogen Activator Inhibitor 1 ; Plasminogen Activators ; Rage ; Rats ; Risk Factors ; Transforming Growth Factor beta ; Up-Regulation ; Advanced Glycosylation End Product-Specific Receptor