At the present there are no large-scale epidemiologic data on inflammatory bowel disease (IBD) in the Asia-Pacific region, but several studies have shown an increased incidence and prevalence of IBD in this region. Compared to the West, there appears to exist a time lag phenomenon. With regard to the two main forms of IBD, ulcerative colitis (UC) is more prevalent than Crohn's disease (CD). In addition to geographic differences, ethnic differences have been observed in the multiracial Asian countries. Moreover, the genetic backgrounds are different in the Asian compared to Western patients. For instance, NOD2/CARD15 variants have not been found in Asian CD patients. In general, the clinical course of IBD seems to be less severe in the Asia-Pacific region than in Western countries. Diagnosis of IBD in this region poses special problems. The lack of a gold standard for the diagnosis of IBD, and the existence of a variety of infectious enterocolitis with similar manifestations to those of IBD make the differential diagnosis particularly difficult. So far, Western diagnostic criteria have been introduced for the diagnosis of IBD. A stepwise approach to exclude non-IBD enterocolitis also must be introduced, and a definite diagnosis must include typical histological features. In some patients, follow up and therapeutic trials might be necessary to obtain a definitive diagnosis. A better understanding of the pathogenesis of IBD will allow the development of better diagnostic markers. The management of IBD also poses some special problems in the Asia-Pacific Region. There is often a delay in using proper medications for IBD, and alternative local remedies are still widely used. With a combination of Western guidelines and regional experiences, similar principles can be used for induction and maintenance of remission. A stepwise selection of medications is advocated depending on the extent, activity and severity of the disease. Comprehensive and individualized approaches are suggested for different IBD patients. Deeper understanding of disease pathogenesis and the unique characteristics of IBD in the Asia-Pacific region, combined with reasonable and practical guidelines for drug management and the future use of biological agents would improve the therapeutic outlook of IBD in this region.

This population-based intervention trial revealed that celecoxib treatment or H pylori eradication alone had beneficial effects on the regression of advanced gastric lesions. No favourable effects were seen for H pylori eradication followed by celecoxib treatment. Trial registration HARECCTR0500053 in accordance with WHO ICTRP requirements.

Triptolide, a major component in the extract of Chinese herbal plant Tripterygium wilfordii Hook f (TWHf), has potential anti-neoplastic eect. In the present study we investigated the potential therapeutic eects and mechanisms of triptolide against human gastric cancer cells. Four gastric cancer cell lines with dierent p53 status, AGS and MKN-45 (wild type p53); MKN-28 and SGC-7901 (mutant p53) were observed as to cell growth inhibition and induction of apoptosis in response to triptolide treatment. We showed that triptolide inhibited cell growth, induced apoptosis and suppressed NK-kB and AP-1 transactivation in AGS cells with wild-type p53. Triptolide induced apoptosis by stimulating the expressions of p53, p21 waf1/cip1 , bax protein, and increased the activity of caspases. In addition, it caused cell cycle arrest in the G 0 /G 1 phase. To examine the role of p53 in these functions, we showed that suppression of p53 level with antisense oligonucleotide abrogated triptolide-induced apoptosis and over-expression of dominant negative p53 abolished the inhibitory eect on NF-kB activation. Furthermore, we demonstrated that triptolide had dierential eects on gastric cancer cells with dierent p53 status. We showed that triptolide also inhibited cell growth and induced apoptosis in MKN-45 with wild-type p53, whereas it had no signi®cant growthinhibition and apoptosis induction eects on the MKN-28 and SGC-7901 cells with mutant p53. Our data suggest that triptolide exhibits anti-tumor and anti-in¯ammatory eects by inhibiting cell proliferation, inducing apoptosis and inhibiting NF-kB and AP-1 transcriptional activity. However, a functional p53 is required for these proapoptotic, anti-in¯ammatory and anti-tumor eects. Oncogene (2001) 20, 8009 ± 8018.

Chronic hepatitis B virus (HBV) infection is one of the most common viral infections in humans affecting over 300 million individuals, or 5% of the world's population. 1 It is of particular concern in the Asia-Pacific areas, where the infection is highly prevalent. Of the chronic HBV patients, around 25% to 40% will eventually die of liver disease (i.e., cirrhosis with or without hepatocellular carcinoma); the death rate is currently 50% for male patients and 15% for female patients. 2 To date, only interferon alfa and lamivudine ([-]-␤-L-2Ј,3Ј-dideoxy-3Ј-thiacytidine) monotherapy have been approved in many countries for the treatment of chronic HBV infection. The overall response to interferon in Asian patients is unsatisfactory: approximately 15% to 20% will clear hepatitis B e antigen (HBeAg), but less than 5% will clear hepatitis B surface antigen (HBsAg), 3 and its use is associated with a variety of side effects. 4 Recently, a number of nucleoside analogues such as lamivudine, 5,6 famciclovir, 7 adefovir dipivoxil, 8,9 entecavir, 10 and emtricitabine 11 have been shown to be effective in suppressing HBV replication. However, monotherapy with lamivudine is unlikely to be sufficient for eradication of HBV infection in the majority of patients who are chronically infected. 12 With prolonged therapy, a sustained HBeAg seroconversion rate is achieved in 22%, 29%, and 33% of Chinese patients at weeks 52, 104, and 156, respectively. 13 However, in the majority of patients who do not seroconvert, the use of lamivudine for more than 6 months is associated with the emergence of resistant YMDD variants, which may result in exacerbation of liver diseases. 14 In patients with human immunodeficiency virus (HIV), it has been found that combination therapy involving 2 or more reverse-transcriptase inhibitors or a reverse-transcriptase inhibitor and a protease inhibitor are more effective than monotherapy in reducing the viral load, improving the CD4 counts, and decreasing the emergence of resistance. 15,16 In primary duck hepatocyte cultures, the combination of penciclovir (9-[2-hydroxy-1-(hydroxymethyl)ethoxymethyl]guanine, the active metabolite of famciclovir) and lamivudine, has been shown to be at least additive and probably synergistic in reducing the duck HBV replication. In addition, penciclovir but not lamivudine was effective in decreasing the production of covalently closed circular DNA (cccDNA) and the expression of pre-S antigen. 17 However, it is unknown whether these synergistic or additive effects occur in humans and whether the use of combination therapy would have an effect on the rate of emergence of drug resistance.As in hepatitis C virus, 18-20 HIV, 21-23 and simian immunodeficiency virus, 24 the use of potent antiviral agents in chronic Abbreviations: HBV, hepatitis B virus; HBeAg, hepatitis B e antigen; HBsAg, hepatitis B surface antigen; HIV, human immunodeficiency virus; cccDNA, covalently closed circular DNA; ALT, alanine transaminase.From the