Recipients of organ transplantation are subjected to lifelong immunosuppression. Thus an increased incidence of developing cancer is expected in recipients with longer follow-up. The longer transplant recipients survive, the greater the risk of cancer accumulates. This was supported by the results in our series. We noted, as expected, that the number of 
de novo cancers increased as further Procyanidin-B2 follow-up accrued. Moreover, though receiving aggressive treatments after diagnosis, poor survival of those patients with de novo cancers was noted in our series. All the patients who died after the diagnosis had a direct relationship with the de novo cancers. Indeed, the causes of patient later death after LTx are multifactorial including chronic rejection, primary disease recurrence and others. Recent studies have currently considered de novo cancer as the second leading cause of death following cardiovascular complications. It has been clear that tumor recurrence is the major cause of death after LTx for recipients of malignant liver disease. However, after excluding the patients who died of tumor recurrence, our single center study showed that the survival of patients with de novo cancers was significantly lower than those without de novo cancers, suggesting that compared with nontumor factors de novo cancer has contributed more to the later mortality after LTx in Chinese population. Although the incidence and mortality rates in developed countries have been decreasing during the past 25 years, both rates have been increasing in many developing countries. In China, breast cancer is the most prevalent cancer and is ranked the sixth leading cause of death in Chinese women. Except for ill-fitted environmental exposures, lifestyle and behavioral factors, many studies have also suggested that genetic factors are usually associated with the risk of breast cancer. In recent years, the use of genome-wide association studies to screen disease-associated genetic variants, has led to the successful identification of Praeruptorin-B numerous breast cancer susceptibility regions, supporting a polygenic model of breast cancer susceptibility. However, such loci explain only a small percentage of the total risk, and important regions harboring genetic variants associated with breast cancer risk still remain to be identified. It is well accepted that biofilm formation in aquatic ecosystems both enhances survival and persistence of V. cholerae, by providing nutrients and protection from protozoan grazing and phage predation, and that it plays a critical role in the transmission of the pathogen. V. cholerae also forms biofilms while inside infected individuals. Stool samples from cholera patients contain V. cholerae both in biofilm-like clumps and in a planktonic form. The average infectivity of biofilm-like clumps is higher than that of planktonic cells, and growth in biofilm induces a hyper-infectious phenotype, suggesting that V. cholerae biofilms are important in the disease process. Biofilm formation depends on production of a biofilm matrix i.e., exopolysaccharides, proteins, and nucleic acids. In many bacteria exopolysaccharides represent a major portion of the biofilm matrix; and mutants unable to produce exopolysaccharides are impaired in biofilm formation. We have previously isolated VPS, performed initial glycosyl composition and linkage analyses, and identified the gene clusters required for VPS biosynthesis. However, chemical structure of VPS has remained elusive due to difficulties in obtaining its NMR spectra. In this study, we report the chemical structure of VPS, and describe a reliable method for the isolation of VPS from the extracellular material produced by V. cholerae.