No abstract available.
Pregnancy*

BACKGROUND/AIMS: Although interferon-a(IFNa) is currently the most effective antiviral agent for treating patients with chronic hepatitis C, its efficacy is not always reliable. Factors suggested to infruence outcome of IFN-a therapy for chronic hepatitis C are histological activity, level of viremia and HCV genotype, etc. The aim of this study was to determine the relationship between several pretreatment factors and response to IFN-a therapy in patients with chronic HCV infection. METHODS: Fifty-four patients with chronic HCV infection(47 with chronic hepatitis and 7 with liver cirrhosis) who received IFN-a(2a or 2b) therapy(3 6 MU, three times a week, for 3 12 months) were included. Level of serum HCV RNA(50 patients), HCV genotype(27 patients) and IgM anti- HCV(21 patients) during pretreatment period were assayed. RESULTS: Overall, 19(35%) subjects achieved sustained response(SR), 12(22%) had transient response(TR) and 23(43%) did not respond (nonresponse;NR). Mean age of patients with SR, TR and NR was 46+ 10, 51+ 7.5 and 54+ 9.7 years, respectively(p<0.05 between SR and NR). Among 30 patients with biopsy-proven chronic hepatitis, 13(43%) achieved SR;but only one(14%) in 7 patients with liver cirrhosis. Mean serum HCV RNA level(X10' copies/ml) was higher in nonresponders(7,7+ 13.0) compared with SR(2.3+ 2. 7) or TR(3.1+ 4.9), although statistically insignificant HCV genotyping in 27 patients revealed type la in 5(18.5%), 1b in 14(52%), 2a in 5(18.5%), 2b in 1(3.7%) and 4 in 2(7%), respectively. In non-1b patients, SR rate was significantly higher than 1b patients(69.2% vs. 21.4%, p=0.03). Although IgM anti-HCV was positive in 12(57%) among 21 patients studied, the positive rate and the titer of IgM anti-HCV was not significantly different in three groups. CONCLUSION: Our results suggest that in patients with chronic hepatitis C, infection with genotype 1b, old age, high serum HCV RNA level and the presence of cirrhosis would predict poor response to IFN therapy.
Fibrosis ; Genotype ; Hepatitis C, Chronic ; Hepatitis, Chronic ; Humans ; Immunoglobulin M ; Interferons* ; Liver ; Liver Cirrhosis ; RNA ; Viremia

No abstract available.
Humans ; Pulmonary Atresia* ; Siblings* ; Ventricular Septum*

No abstract available.
Thanatophoric Dysplasia*

No abstract available.
Thanatophoric Dysplasia*

No abstract available.
Chondrogenesis* ; Ear*

No abstract available.
Ascites* ; Hernia, Umbilical* ; Leiomyoma*

No abstract available.
Animals ; Dogs* ; Facial Bones* ; Periosteum* ; Silicone Elastomers* ; Transplants*

Mesangial cell proliferation contributes to the development of glomerulonephritis and is associated with glomerulosclerosis. It has been reported that IL-6 is a pluri-potent cytokine which is involved in the mesangial inflammation and the activation of IL-6 is related to the recruitment of transcriptional factors or cytokines such as IL-1beta. It has been known that bacterial infection sometimes precedes the exacerbation of glomerulonephritis and bacterial LPS, a potent activator of IL-6, is presumed to be one of the mediators of this inflammatory process. To understand the underlying mechanisms of how IL-6 is activated by LPS, we examined the serial changes of the expression of IL-1beta, IL-6 and NF IL-6(nuclear factor for IL-6) using the growth arrested human mesangial cells at 0, 2, 4, 8, and 18 hours after LPS stimulation. Exposure of serum-free mesangial cells to LPS resulted in the production and the expression of IL-1beta and IL-6. However, there was a steady increase of IL-1b expression throughout the 18 hours, while the peak expression of IL-6 was around 4 hours after LPS stimulation and this peak expression of IL-6 was preceded by NF IL-6. Interestingly, the NF IL-6 expression was not observed in the IL-6 stimulation by r-IL-1beta stimulation. Furthermore, the addition of anti-IL-1beta prior to the LPS stimulation reduced the IL-6 expression partially, but, it did not affect the NF IL-6 expression. These results demonstrated that the mesangial IL-6 expression by LPS is mediated by NF IL-6 as well as IL-1beta in a separate pathways. The capacity of LPS to express IL-6 by these mechanisms may play a role in the mesangial inflammatory process.
Bacterial Infections ; Cytokines ; Glomerulonephritis ; Humans* ; Inflammation ; Interleukin-6* ; Mesangial Cells

No abstract available.
Methylation*