Site-specific delivery of therapeutic drugs to their target cells is a major scientific challenge for the pharmaceutical sciences. It offers a number of advantages over conventional drug administration. With drug targeting, high local concentrations of the drug can be achieved, thus circumventing many unwanted side effects. Various carriers have been suggested for the delivery of drugs, including liposomes[1 - 5] and (neo ) glycoproteins[6-8]. The asialoglycoprotein receptor (ASGP-R) has frequently been utilized for targeting drugs to the parenchymal liver cell[6- 12]. Liposomes have several advantageous characteristics as drug carrier, and particularly, ligandtacked liposomes achieve a highly effective targeting[13]. Hara et al reported that asialofetuin (AF)-tacked liposomes distributed to rat hepatocytes selectively in vivo[14], and ASGP-R mediated the uptake of AF-liposomes encapsulating IFN-γ by isolated rat hepatocytes in vitro[15]. Lactosaminated human serum albumin (L-HSA) is a neoglycoprotein taking number of galactose residue as terminal sugar[6].

China is a country with a high incidence of liver cancer in some areas[1]. Liver cancer has a wide distribution and threatens human health seriously. A rough estimation shows that out of a population of 1.2 × 108 in liver cancer areas patients are more than 1.0 × 105. The environment of the liver cancer area is very complicated and has different characteristics in different regions. But the epidemic regularity of liver cancer is obvious, and the environment in the cancer areas has also distinct characteristics that contribute to the study on the environmental etiology of liver cancer[2-5].

The mites found in stored food and house comprise a large group of subclass Acari, belonging to the suborder Acardida of the order Acarifornes. They can be found in dust and vacuum samples from floors, furniture, mattresses, Chinese herbal medicine, dry fruit, grain, flour, sugar, and bedding. These mites are nidicolous and feed on organic debris, including sloughed human skin, fungi, spilled food, pollen, etc. These mites are particularly prevalent in Chinese herbal medicine, dry fruit, grain, flour, sugar, beds, though carpeted floors near beds or couches may also have large numbers. The most common species are Acarus siro, Tyrophagus putrescentiae , Dermatophagoides farinae , D . pteronyssinus, Glycyphagus domesticus, G. Ornatus, Carpoglyphus lactis and Tarsonemus granarius, etc. The viability of mites in storage is quite strong and they can invade and parasitize the intestines of humans[1 -15]. They can cause pulmonary acariasis[16-25] , urinary acariasis[26-33] and so on. The dejecta of mites is a quite strong allergen and can cause different allergic diseases[34-44]. Intestinal acariasis can be caused by some mites related to the way of diet intake and invading against intestinal mucosa, intestinal muscle[45-5a]. The first report of intestinal acariasis caused by these mites was made by Hinman et al (1934)[45]. From then on, all kinds of studies on the disease have been reported gradually. In order to make an epidemiological survey of intestinal acariasis the investigation of the disease was taken in some areas of Anhui Province from 1989 to 1996.

Chronic gastritis ( CG ) and peptic ulcer ( PU ) are frequently-occurring diseases. It is now well recognized that Helicobacter pylori (Hp) is a major factor that leads to CG and PU[1-8] In order to study the relationship among T lymphocyte subsets, NO, Hexosamine and Hp infection in patients with chronic gastric diseases, the levelsof blood T lymphocyte subsets, plasma NO and hexosamine in gastric mucosa were measured respectively in 30 patients with CG and 32 patients of PU + CG.

Hepatitis G virus (HGV),also known as GB virus C, is a recently cloned virus which may be associated with human non A-E hepatitis[1，2] It is parenterally transmitted and usually coinfected or superinfected with hepatitis B or hepatitis C virus[3-5]. Some investigations have been reported on the seroprevalence and molecular prevalence of HGV infection in different areas and different population[6-15]. Current infection of HGV is diagnosed by detection of HGV RNA, and past infection with HGV is detectable by testing anti-HGV envelope protein (E2)[16-17]. To investigate the prevalence of HGV in Hubei Province, a central area of the People's Republic of China, ELISA and RT-PCR were employed to detect serum anti-HGV and HGV RNA in 1516 patients who were divided into 16 groups.

Helicobacter pylori (H. pylori ) is a major causativebacterium of chronic gastritis, peptic ulcer and mucosaassociated lymphoid tissue lymphoma in humans, and associated with an increased risk of gastric cancer[1 -8]. An important virulant factor of H. pylori is the vacuolating cytotoxin ( VacA ) encoded by vacA that induces cytoplasmic vacuolation in target cells both in vitro and in vivo[9-11]. VacA is produced as a 140 kDa precursor which contains an N-terminal signal peptide and an approximately 33 kDa C-terminal outer membrance exporter. The precursor is cleaved at both N-terminal and C-terminal and secreted into the extracellular milieu as a 95 kDa mature protein. The mature protein futher undergoes specific cleavage to yield 37 kDa and 58 kDa subunits[12-14] Although vacA is present in all H. pylori strains, only about 50% to 60% of strains can induce vacuolation of epithelial cells as assessed by the HeLa cell assay. vacA shows considerable genetic variation in H. pylori isolated from all over the world and contains at least two variable regions. The s region exists as sl or s2 allelic types. Among type sl strains, subtypes sla and slb have been identified. The m region occurs as ml or m2 allelic types. Specific vacA genotype of H. pylori strains are associated with the production of the cytotoxin in vitro, epithelial damage in vivo, and clinical consequences[15-27]. The other virulant factor is the cytotoxin-associated protein (CagA) encoded by the cytotoxin-associated gene (cagA). The cagA gene is present in about 60% to 70% of strains and all of these strains express the cagA. The presence of cagA is also associated with the production of the cytotoxin in vitro, and clinical outcome[24-30]. The aim of this study was (i) to identify vacA genotypes and cagA status of H. pylori isolated from Chinese patients; (ii) to evaluation the relatioship beween vacA genotypes, cagA status and related gastroenterological disorders.

The principle of surgical treatment for gastric cancer is the radical resectioning although the suitable resecting range for different cases of gastric cancer is still being argued upon[1-9]. However, the diagnostic accuracy of early gastric cancer (EGC) without lymphatic metastasis has obviously improved with an improvement in the diagnostic technique and due to the accumulation of knowledge on the biological profiles of EG C[10-17]. The D2 lymph node excision was used as a regular operation to treat the EGC previously. But the concept for the EGC without lymphatic metastasis has gradually changed and the less invasive resections has been applied in some cases[18-20]. This study aimed at investigating the risk factors of lymphatic metastasis in EGC in order to find out the proofs for the suitable indications for less invasive operations such as endoscopic mucosal resectioning (EMR), laparoscopic and laparotomic resectioning.

The last two decades of the twentieth century have witnessed increasingly successful rates of liver transplantation. The number of liver transplantations has increased steadily while the number of organ donors has remained relatively constant. Thus a great disparity has developed between the demand and supply of donor organs and remains a major limiting factor for further expansion of liver transplantation. Although many procedures, such as split liver[1] , living-related transplantation[2] , and xenotransplantation[3], have been attempted clinically to overcome the shortage, it is hoped that livers harvested from non-heart-beating donors (NHBDs) would alleviatethe problem of organ shortage, which again becomes the focus of attention[4-9]. However, sensitivity of the liver to warm ischemia remains a major worry for use of theNHBDs. The aim of this animal study was to assess if murine liver could tolerate prolonged period of warm ischemia and to determine the optimum timing of intervention in the cadaver donor in order to preserve liver viability.

Calmodulin (CaM), widely distributed in almost all eukaryotic cells, is a major intracellular calcium receptor responsible for mediating the Ca2 + signal to a multitude of different enzyme systems and is thought to play a vital role in the regulation of cell proliferative cycle[1，2]. Recently, many studies showed that CaM is also present in extracellular fluid such as cell culture media and normal body fluid and has been reported to stimulate proliferation in a range of normal and neoplastic cells, apparently acting as an autocrine growth factor[3-11]. In 1988, Crocker et al reported for the first time that addition of extracellular pure pig brain CaM could promote DNA synthesis and cell [7]proliferation in K562 human leukaemic lymphocytes[7].After that, more and more research was done on extracellular CaM and evidences demonstrated that extracellular CaM could also stimulate cell proliferation in normal human umbilical vein endothelial cells[5], keratinocytes[4], suspension-cultured cells of Angelica Dahurica, etc[6]. CaM is a monomeric protein of 148 amino acids that contains four homologous Ca2 + -binding domains. CaM has been highly conserved throughout the evolution. Only 1 out of 148 amino acids of human CaM is different from that of fish CaM. Complementary DNAs encoding rat, eel, chicken, human, and trypanosome CaM have been cloned.

Hepatocellular carcinoma (HCC) is one of the most common malignancies in China. To date, surgery is still the best solution to it. However, metastatic recurrences after curative hepatic resections are very common. Tang et al have reported that recurrence rate within 5 years of curative hepatic resection is 61.5% [1]. As curative hepatic resection has a high tendency for metastatic recurrence, therapeutic interventions such as transarterial embolization and antiangiogenesis have been tried to further improve prognosis of HCC patients. Therefore, establishing a dependable, sensitive, easy, and economical method to predict metastatic recurrence following curative hepatic resection is of clinical urgency.

The endoplasmic reticulum (ER) consists of a complex system of tubules, lamellae, and flattened vesicles, and has a variety of morphologies in different cells. It is believed to play a central role in the biosynthesis of cholesterol, phospholipids, steroids, prostaglandins, membrane and secretory proteins[1]. Cancer cells have different functions and ultrastmcture from their original cells[2-4]. The studies on ER membrane system of cancer cells are of great significance in understanding their malignant behavior. In the present work, the ultrastructural characteristics of ER in human colorectal carcinoma cell lines with different differentiation degrees were investigated.

The use of laser energy to weld biological tissues and produce sutureless anastomosis has its advantages over conventional silk-sutured anastomosis since it was reported in small vessels[1] and fallopian tubes[2], in the late 1970s. Since then, more investigators have welded a larger variety of tissues[3-13] and have expanded its application to welding trials of entertomies of rabbit and rat small intestine[14-17] Sauer et al[18] reported results from Nd: YAG laser in reconstruction of end-to-end welding in rabbit small intestine. Recently, controlled temperature during YAG and argon laser-assisted welding of entertomies of rabbit and rat was implemented to eliminate exponential increases in the rate of denaturation associated with rapidly increasing temperature[19，20]. Yet there was no report of sutureless end-to-end bowel anastomosis using low-power CO2 laser. This is a report of a circumferential end-to-end laser welding bowel anastomosis in rabbit by using 3 different CO2 laser powers to explore the feasibility of CO2 laser welding of a circumferential intestinal tissue and to determine the optimal laser-welding parameter. Then the appropriate CO2 laser power was chosen to weld bowels in rabbit and its long-term healing effect was evaluated.

It has been reported in many studies that electroacupuncture (EA) can positively regulate erythrocytic immunity and T-lymphocytic subgroups[1-8].Nevertheless, its mechanism remains to be explored. In the present study, a multi-group, multi-stepped and multiindexed observation was conducted on the effects of EA on erythyrocytic immunity and T-lymphocytic subgroups. A simultaneous assay of the changes in immunoreactivesubstance-P (ir-SP) content in the pituitary gland and peripheral blood was also carried out. The objective of the study was to investigate the regulatory effects of the immune system and their possible mechanism in the treatment of relevant diseases with EA.

The main reason for the death of the patient with acute hemorrhage necrosis pancreatitis (AHNP) is pancreatic infection and multi-organ failure caused by endotoxemia and intestinal bacterial translocation[1-7]. However, the pathogenesis of endotoxemia and intestinal bacterial translocation remains a question[8-10]; moreover, no effective method of prevention and cure for it has been found till now[11 -15] In the present study, we infused low dose dopamine and low molecular weight dextran through the catheters to abdominal aorta and portal vein, and observed its influence on the endotoxin concentration in plasma and the rate of translocation of intestinal bacteria in AHNP rats.

AIM Several triggering receptors have been described to be involved in natural killer (NK) cellmediated target cytotoxicity. In these studies, NK cells derived from blood or spleen were used. Pit cells are liver-specific NK cells that possess a higher level of natural cytotoxicity and a different morphology when compared to blood NK cells. The aim of this study was to characterize the role of the NK-triggering molecules NKR-P1A, ANK61 antigen, and CD45 in pit cell-mediated killing of target cells. METHODS 51 Cr-release and DNA fragmentation were used to quantify target cell lysis and apoptosis, respectively. RESULTS Flow cytometric analysis showed that pit cells expressed CD45, NKR-P1A, and ANK61 antigen. Treatment of pit cells with monoclonal antibody ( mAb ) to CD45 ( ANK74 ) not only inhibited CC531s or YAC-1 target lysis but also apoptosis induced by pit cells. The mAbs to NKRP1A (3.2.3) and ANK61 antigen (ANK61) had no effect on pit cell-mediated CC531s or YAC-1 target cytolysis or apoptosis, while they did increase the Fcγ receptor positive (FcγR+) P815 cytolysis and apoptosis. This enhanced cytotoxicity could he inhibited by 3,4-dichloroisocoumarin, an inhibitor of granzymes. CONCLUSION These results indicate that CD45 participates in pit cell-mediated CC531s and YAC-1 target cytolysis and apoptosis. NKR-P1A and ANK61 antigen on pit cells function as activation structures against FcγR+ P815 cells, which was mediated by the perforin/granzyme pathway.

AIM To study relationship of injury induced by nitric oxide, oxidation, peroxidation, lipoperoxidation with chronic cholecystitis. METHODS The values of plasma nitric oxide (PNO), plasma vitamin C (P-VC), plasma vitamin E ( P-VE ), plasma β-carotene ( P-β-CAR ), plasma lipoperoxides (P-LPO), erythrocyte superoxide dismutase (E-SOD), erythrocyte catalase (ECAT), erythrocyte glutathione peroxidase (E-GSHPx) activities and erythrocyte lipoperoxides (ELPO) level in 77 patients with chronic cholecystitis and 80 healthy control subjects were determined, differences of the above average values between the patient group and the control group and differences of the average values between preoperative and postoperative patients were analyzed and compared, linear regression and correlation of the disease course with the above determination values as well as the stepwise regression and correlation of the course with the values were analyzed. RESULTS Compared with the control group, the average values of P-NO, P-LPO, E-LPO were significantly increased ( P < 0.01 ), and of P-VC, P-VE, P-β-CAR, E-SOD, E-CAT and E-GSH-Px decreased ( P < O. 01 ) in the patient group. The analysis of the linear regression and correlation showed that with prolonging of the course, the values of P-NO, P-LPO and E-LPO in the patients were gradually ascended and the values of P-VC, P-VE, P-β-CAR, E-SOD, E-CAT and E-GSH-Px descended (P < 0. 01 ). The analysis of the stepwise regression and correlation indicated that the correlation of the course with P-NO, P-VE and P-β-CAR values was the closest. Compared with the preoperative patients, the average values of PNO, P-LPO and E-LPO were significantly decreased (P < 0.01 ) and the average values of PVC, E-SOD, E-CAT and E-GSH-Px in postoperative patients increased ( P < 0.01) in postoperative patients. But there was no significant difference in the average values of P-VE, P-W-CAR preoperative and postoperative patients. CONCLUSION Chronic cholecystitis could induce the increase of nitric oxide, oxidation, peroxidation and lipoperoxidation.

AIM To evaluate a culture system for bile acid formation in primary human hepatocytes in comparison with HepG2 cells. METHODS Hepatocytes were isolated from normal human liver tissue and were cultured in serum-free William's E medium. The medium was collected and renewed every 24 h. Bile acids and their precursors in media were finally analysed by gas chromatography-mass spectrometry. RESULTS Cholic acid ( CA ) andchenodeoxycholic acid (CDCA) conjugated with glycine or taurine accounted for 70% and 25% of total steroids. A third of CDCA was also conjugated with sulphuric acid. Dexamathasone and thyroid hormorm alone or in combination did not significantly effect bile acid formation. The addition of cyclosporin A (10 μmol/L) inhibited the synthesis of CA and CDCA by about 13% and 30%, respectively. CONCLUSION Isolated human hepatocytes in primary culture behave as in the intact liver by converting cholesterol to conjugated CA and CDCA. This is in contrast to cultured HepG2 cells, which release large amounts of bile acid precursors and unconjugated bile acids into the medium.

AIM We have previously reported that inducible over-expresaion of Bak may prolong cell cycle in G1 phase and lead to apoptosis in HCC-9204 cells. This study is to investigate whether p27KIP1 plays an important role in this process. MEHODS In order to elucidate the exact function of p27KIP1 in this process, a zinc inducible p27KIP1 stable transfectant and transient p27KIP1- GFP fusion transfectant were constructed. The effects of inducible p27KIP1 on cell growth, cell cycle arrest and apoptosis were examined in the mock, control pMD vector, and pMD-KIP1 transfected HCC-9204 cells. RESULTS This p27KIP1-GFP transfectant may transiently express the fusion gene. The cell growth was reduced by 35% at 48 h of p27KIP1 induction with zinc treatment as determined by trypan blue exclusion assay. These differences remained the same after 72 h of p27KIP1 expression, p27KIP1 caused cell cycle arrest after 24 h of induction, with 40% increase in G1 population. Prolonged p27KIP1 expression in this cell line induced apoptotic cell death reflected by TUNEL assay. Fourty-eight h and 72 h of p27KIP1 expression showed a characteristic DNA ladder on agarose gel electrophoresis.

AIM To compare the effects of liposomes and glyco-poly-L-lysine on liver targeted uptake and expression of plasmid in rat liver. METHODS After binding with lipofectamine or galactose-terminal glyco-poly- L-lysine, the plasmid could be expressed in eukaryotic cells when injected into Wistar rats by intravenous route. At different time intervals after the injection, the distribution and expression of the plasmid in liver of rats were observed and compared using in situ hybridization and immunohistochemistry. RESULTS The expression of the plasmid binding to liposomes or G-PLL could be markedly observed 24 h later, and began to decrease one week later, but it still could be observed up to three weeks. Both liposomes and G-PLL could deliver the plasmid to the liver effectively, but the effect of the latter was better than the former concerning the distribution and expression of the plasmid targeted uptake in the liver. CONCLUSION G-PLL is better than liposome as the targeted carrier for delivering exogenous genes to the liver.

AIM To investigate effect of Iosartan, an AT1 receptor antagonist, on hepatic fibrosis induced by CCI4; and to determine whether or not AT1 receptors are expressed on hepatic stellate cells. M~THODS AND RESULTS Fifty male SpragueDawley rats, weighing (180 ± 20) g, were randomized into five groups (control group, model group, and three Iosartan treated groups ), in which all rats were given the subcutaneous injection of 40% CCl4 (every 3 days for 6 weeks) except for rats of control group. Rats of Iosartantreated groups were treated with Iosartan (20 mg/ kg, 10 mg/kg, 5 mg/kg, daily gavage). After 6 weeks liver tissue and serum samples of all rats were examined. Serum hyaluronic acid (HA), procollagen type Ⅲ (PC Ⅲ ) were detected by radioimmunoassays. van Giesion collagen staining was used to evaluate the extracellular matrix of rats with liver fibrosis. The expression of AT1 receptors, transforming growth factor-beta (TGFβ), and alpha-smooth muscle actin (α-SMA) in liver tissue were determined by immunohistochemical techniques. Compared with model group, serum ALT and AST of Iosartantreated groups were significantly reduced (t = 4.20, P < 0.01 and t = 4.57, P < 0.01 ). Serum HA and PC Ⅲ also had significant differences (t = 3.53, P<0.01 and t=2.20, P<0.05). The degree of fibrosis was improved by Iosartan and correlated with the expressions of AT1 receptors, TGF-β, and α-SMA in liver tissue. CONCLUSION AT1 receptor antagonist, Iosartan, could limit the progression of the hepatic fibrosis induced by CCl4. The mechanism may be related to the decrease in the expression of AT1 receptors and TGF-β, ameliorating the injury of hepatocytes; activation of local renin-angiotensin system might relate to hepatic fibrosis; and during progression of fibrosis, activated hepatic stellate cells might express AT1 receptors.

AIM To compare the effects of intravenous routeand peritoneal route on liver targeted uptake and expression of plasmid delivered by galactoseterminal glyco-poly-L-Iysine (G-PLL). METHOTS The plasmid pTM/MMP-1 which could be expressed in eukaryotic cells was bound to GPLL, and wes then transferred into Wistar rats by intravenous and intraperitoneal injection. The expression and distribution of the plasmid were observed at different time periods by in situ hybridization and immunohistochemistry. RESULTS The plasmid could be expressed significantly within 24 h after being transferred in vivo by both intravenous and intraperitoneal routes. One week later the expression began to decrease, and could still be observed three weeks later. Although both the intravenous and intraperitoneal route could target-specifically deliver the plasmid to the liver, the effect of the former was better as compared to that of the latter. CONCLUSION Intravenous route is better for liver targeted uptake and expression of G-PLL-bound plasmids than the peritoneal route.

AIM To study the effects of arsenic trioxide and HCPT on different degrees of differentiated gastric cancer cells (SGC-7901, MKN-45, MKN-28)with respect to both cytotoxicity and induction of apoptosis in vitro. ~ODS The cytotoxicity of As2O3 and HCPT on gastric cancer cells was determined by MTTassay. Morphologic changes of apoptosis of gastric cancer cells were observed by light microscopy and transmission electron microscopy. Apoptosis and cell cycle changes of gastric cancer cells induced by HCPT and As2O3 were investigated by TUNEL method and flow cytometry. RESULTS As2O3 and HCPT had remarkable cytotoxic effects on different degrees of differentiated gastric cancer cells. The IC50 of As2O3 on well differentiated gastric cancer cell MKN-28, moderately differentiated gastric cancer cell SGC-7901, and poorly differentiated gastric cancer cell MKN-28 were 8. 91 μmol/L, 10. 57 μmol/L, and 11.65 μmol/L, respectively. The IC50 of HCPT on MKN-28, SGC-7901, and MKN-45 were 9. 35 rg/L, 10. 21 rg/L, and 12. 63 mg/L respectively after 48 h treatment. After 12 h of exposure to both drugs, gastric cancer cells exhibited morphologic features of apoptosis, including cell shrinkage, nuclear condensation,and formation of apoptotic bodies. A typical subdiploid peak before G0/G1 phase was observed by flow cytometry. The apoptotic rates of SGC7901, MKN-45, and MKN-28 were 13. 84%, 22.52%, and 9. 68%, respectively after 48 h exposure to 10 μmol/L As2O3. The apoptotic rates of SGC-7901, MKN-45, and MKN-28 were 21.88%, 12.35%, and 30. 26%, respectively after 48 h exposure to 10 mg/L HCPT. The apoptotic indice were 7% - 15% as assessed by TUNEL method. The effect of As2O3 on SGC-7901 showed remarkable cell cycle specificity, which induced cell death in G1 phase, and blocked G2/M phase. HCPT also showed a remarkable cell cycle specificity, by inducing cell death and apoptosis in G1 phase and arrest of proliferation at S phase. CONCLUSION AS2O3 and HCPT exhibit significant cytotoxicity on gastric cancer cells by induction of apoptosis. As2O3 and HCPT might have a promising prospect in the treatment of gastric cancer, which needs to be further studied.

DEFINITIONAcute diarrhoea is defined as passage of loose or watery stools at least three times in a 24 h period. When loose stools contain blood, it is called bloody diarrhoea (dysentery). It is the consistency of the stools which is most important rather than the frequency. Breast-fed babies often pass “pasty” stools frequently which is not diarrhoea. The mother can often tell accurately whether child has diarrhoea or not. MAGNITUDE OF THE PROBLEMAcute diarrhoea is an important cause of mortality and morbidity particularly in young children in the developing countries. Of the 11.6 million deaths among children less than five years old in all developing countries (1995) due to infectious diseases, 19% deaths are attributed to diarrhoeah]. In 1993, an estimated 3.2 million children below five years of age died from diarrhoea alone; 80 % of these deaths occurred in the first two years of life[2].

The 1990's have brought a significant promise and the hope for a better and brighter future in the new millennium for patients with inflammatory bowel disease (I3D). A better understanding of the pathophysiology of IBD symptoms has led to newer treatnent modalities and streamlining of therapy for specific subsets of patients. ULCERATIVE COUTISThe treatnent for ulcerative colitis (UC) is aimed at modulating the inflammatory response. The drugs which are found to be effective are sulfasalazine (Azulfidine, Salazopyrin) and its 5ASA derivatives, glucocorticosteroids, immunomodulators/immunosuppressants, and other new potential drugs (Table 1).

Of the three cardinal manifestations of chronic pancreatitispain, diabetes mellitus and steatorrhea, it is pain that brings the patient to the physician and is the most difficult to manage. The intractabale pain that is quite debilitating disrupts lifestyle and leads to functional incapacity, drug and alcohol dependency, and a drug-seeking behavior that occasionally might push the desperate patient to suicidal tendency. Painless CP is an exception that has been observed in nearly 5% to 10% of patients with all forms of chronic pancreatitis. Lack of pain is also a feature of the late onset idiopathic CP.

Molecular biology has made a tremendous impact on the diagnosis and treatment of liver diseases[1，2]. In particular, advances in molecular biology made possible the discovery of the virus that causes hepatitis C. In this review, we use hepatitis C as an example of the impact that molecular biology has made in the area of liver disorders. We emphasize how our growing understanding of the hepatitis C virus (HCV) has lead to the identification of targets for development of new treatments.

major function of the intestinal epithelium is to control the amount of fluid entering into and being absorbed from the lumen[1]. In healthy conditions, net fluid movement follows an absorptive vector, although significant secretion also takes place to subserve digestive function. Thus, the secretion of fluid, driven by the active secretion of electrolytes, is important for maintaining the fluidity of intestinal contents during various stages of digestion and thereby allowing for diffusion of enzymes and nutrients. In the setting of disease, dysregulation of intestinal transport mechanisms may alter the balance between absorptive and secretory processes such that secretion predominates, leading to the clinical consequence of diarrhea. However, under conditions of both health and disease, fluid secretion is driven largely by the active secretion of chloride ions. Thus, there are both basic and clinical reasons for wishing to gain a full understanding of the basis and regulation of this transport process. The goal of my article, therefore, will be to review our understanding of intestinal chloride secretion and the ways in which it is regulated. Recent insights in this area enhancing our ability to intervene in diseases where chloride secretion is over-expressed, such as infectious and inflammatory diarrheal illnesses will also be discussed. This article will also cover the implications of intestinal secretory mechanisms for a genetic disease where chloride secretion is under-expressed, namely cystic fibrosis, where significant intestinal dysfunction, including obstruction and malabsorption,may also ensue.

Helicobacter pylori is recognized as a cause of chronic active gastritis, gastric and duodenal ulcers, and gastric cancer, though the mechanisms of pathogenesis for H. pylori-associated diseases are not yet well understood[1 -4] The ecological niche to which H. pylori is well-adapted is the mucous layer of the human gastric antrum, which has mucin glycoproteins as major constituents. Mucins, highmolecular weight carbohydrate-rich glycoproteins that coat the surface of the stomach and are secreted into the lumen, function to protect the stomach and could be important in H. pylori colonization. For further understanding the pathogenesis of H. pylori-related diseases, it is important to consider whether H. pylori colonization of the surface epithelium is associated, as cause or effect, with changes in the gastric mucin synthesized by surface mucous cells.

Angiomyolipoma (AML) is a rare benign mesenchymal tumor of the liver, composed of a varying heterogeneous mixture of three tissue components: blood vessels, smooth muscle, and adipose cells. It has recently been proposed that the perivascular epithelial cell (PEC) is the common progenitor[1，2] Since its first description by Ishak in 1976[3], there have been more than 100 cases reported in the English literature[4-6]. With the advance of radiological techniques, many more tumors are being diagnosed by the means. But radiological findings of AML may only be suggestive of the lesion; its definitive diagnosis requires histological confirmation[9-19]. Some authors regard renal and hepatic AMLs, pulmonary and soft tissue lymphangiomyomatosis[2], pulmonary and pancreatic clear cell “sugar” tumor, and cardiac rhabdomyoma as closely related groups of tumors, based on their morphologic overlap and common immunoreactivity for HMB-45[l]. They show different microscopic appearances, however, according to their organ of origin. The goals of this study were to highlight more subtle morphology and to gain possible insights into the differential diagnosis that could provide important information about this disease.

Stomach carcinoma is still the leading cause of cancer death in China and the second one in the world. Its possible causes include: A) chemical factors such as intragastric formation of N-nitroso compounds (NOC) and high salt intake; B ) biological factors such as infection of Helicobacter pylori and biotoxins intake; and C ) nutritional factors such as deficiency of vitamin C, selenium, and other antioxidants. Nitrogenous precursors of NOC, e.g., alkylamines, alkylureas, alkylguanidines, and alkylamides, occur widely in nature and potential nitrosating agents, e.g., nitrite (NO2-) and NOx (the gaseous oxides of nitrogen ) are similarly widespread. Relationship between exposure to NOC and causes of human cancer was investigated extensively ten years ago. Results indicated that the exposures of NOC might contribute to the occurrences of malignancy in the upper digestive tracts including stomachs. It was also observed that both high salt intake and deficiency of some micronutrients enhanced NOC-induced carcinogenicity. Recent studies show that infection of H. pylori can lead to atrophic gastritis and achlorhydria, and promote endogenous formation of NOC indirectly[1] . Much attention has been paid to stomach cancer and NOC regarding the characterization of natural N-nitrosamides in human environment in the 1990s.