In China, hepatocellular carcinoma (HCC) is the second most common cancer in urban areas and first most common in rural areas. It ranks as the second leading cause of cancer-related deaths in males and the third leading cause of cancer-related deaths in females, with the total mortality rate of 26.26 per 100,000. Currently, people with hepatitis B virus (HBV) infection are a major population at risk of developing HCC in China. In fact, there are 93 million Chinese who are HBV carriers, and about 20 million of them have chronic HBV- infection. Several cohort studies have shown that screening high-risk patients with HBV- or HCV-related chronic liver disease may improve the rate of early HCC detection and the rate of curative treatment. However, a government-funded national program to screen for high-risk patients with HBV-related chronic liver disease has yet to be established in China. Although several remarkable advances in HCC management have been made during the past few decades, most patients with HCC still present with advanced-stage disease, thus reducing the chance of curative treatment. Based on firsthand experience in Japan and other countries or areas, this work examined the current status, challenges, and prospects for the future of early detection of HCC in China. Findings suggested the need for a systematic guideline for the standardized management of HCC, a government-funded nationwide screening and surveillance program for high-risk patients with HBV-related chronic liver disease, and extensive use of des-γ-carboxyprothrombin (DCP) as a screening tool in China in order to facilitate the early detection of HCC in China.
China has one of the world's highest rates of hepatitis B infection. Over the past 20 years, a series of strategies have been implemented to prevent infection with the hepatitis B virus (HBV) in China. These strategies include hepatitis B (hepB) immunization for susceptible populations such as infants and young children and for high-risk populations such as health care workers and patients, premarital health care for couples of childbearing age, and standard medical practices. A series of measures implemented by the Chinese government caused the HBV infection rate in China to decrease from 9.75% in 1992 to 7.2% in 2006. However, a report on infectious diseases indicated that more than 1 million people in China were infected with hepB in 2011. There is room for improvement. The current work analyzed the current status of and challenges for strategies to prevent HBV infection in China. This work also recommends clear guidance regarding hepB immunization for parents in rural areas, more flexible premarital health care, health education for both patients and health care workers, and routine HBV screening for high-risk health care workers.
As ~75% of the Werner syndrome (WS) patients recognized between 1904 and 2008 all over the world are of Japanese origin, the most case reports and clinical studies on WS has been published in Japanese journals. Thus, the detailed English-written clinical review on the recent WS case reports has been warranted. Although WS has been characterized by a variety of clinical manifestations mimicking premature aging, the recent longevity and delayed age-associated manifestations observed both from Japanese WS and general population may suggest a common environmental effect on some gene(s) other than WRN and may give us a newer pathophysiological look at WS and also natural aging through the molecular dysfunction of WRN.
Environmental factors during fetal life program the health outcomes regarding many diseases in future life. This idea has been supported by worldwide epidemiological studies, but the underlying mechanisms are still poorly understood. Three questions should be answered. (i) Does a common underlying cause of ordinary pathological fetal development exist? (ii) If such a cause exists, which mechanism might develop disease in later life? (iii) Is it possible to prevent this underlying cause and therefore the associated obstetric complications to primarily prevent future life diseases? The objective of this review is to attempt to answer these three questions by using PubMed (extending to October 2012) and other sources. Three data-based answers corresponding to these questions were found: (i) hypoxia, (ii) excessive stimulation of neurogenesis, and (iii) preconditioning/adaptation to hypoxia. The method for such preconditioning/adaptation is intermittent hypoxic training (IHT), in which air with low oxygen concentration is breathed through a mask to protect against subsequent strong adverse influences. Data are cited for IHT applications for the prevention/treatment of diseases in different fields, particularly in obstetrics. Data suggested that all common fetal origins of adult diseases are likely predetermined by changes in the fetal brain; therefore, early detection of these changes must be very important. The use of IHT may be a real means to primarily prevent obstetric complications and therefore, prevent future life diseases.
The acidosis that accompanies many diseases and pathological conditions can promote osteoclast formation and activation. Acidosis mainly acts on the last phase of osteoclast formation to generate large osteoclasts and promote bone resorption. There are several acid-sensing mechanisms, among which transient receptor potential (TRP) channels and G protein-related receptors have been focused on. TRPV4 channels appear to be, at least partly, implicated in acidosis-promoted large osteoclast formation. Other TRP channels including TRPV1 and TRPV2 might be components of the acid-sensing machinery. Several reports suggest the involvement of ovarian cancer G protein-coupled receptor 1 (OGR1), a G-protein-related acid sensor, in receptor activator of nuclear factor kappa-B ligand (RANKL) expression via cyclooxygenase-2 (COX-2). On the other hand, acidosis impairs osteoblast differentiation, which is further impeded in the presence of inflammatory cytokines.
β-Catenin has been reported to play a crucial role in the invasion and metastasis of lung cancer. However, the value of β-catenin as a prognostic factor for non-small cell lung cancer (NSCLC) remains controversial. The present study systematically reviewed the evidence of predicting significance of β-catenin expression in NSCLC patients with meta-analysis. Twelve literatures were included by searching PubMed, Cochrane library, and EMBASE databases. Separate hazard ratio estimates and a 95% confidence interval (CI) for the prognostic value of β-catenin in NSCLC were extracted and merged from the included literatures. The summary hazard ratios were 1.91 (95% CI 1.60-2.28), indicating a worse overall survival for NSCLC patients with reduced β-catenin expression. There Publication bias was not statistically significant. Sensitivity analysis showed that omission of any single study had little effect on the combined risk estimates. This meta-study revealed that decreased β-catenin expression denoted a poor prognosis in NSCLC patients.
Immunological rejection induced by allogeneic Schwann cells remains a problem for construction of artificial nerves. Class II transactivator (CIITA) gene is a chief regulator of major histocompatibility complex class II (MHC II) molecules which contributes to the immunogenicity of Schwann cells. This study aimed to downregulate MHC II expression by suppressing CIITA expression, therefore reducing the immunogenicity of Schwann cells. Recombinant siRNA expression vectors targeting the CIITA gene were produced and subsequently transfected into rat RSC96 Schwann cells. Interferon (IFN)-γ was used to augment immunological rejection of RSC96 cells. The mRNA levels of CIITA and MHC II were assessed by fluorescence quantitative PCR. The protein levels of MHC II were determined using flow cytometry assays. Finally, the immunogenicity of RSC96 cells was analyzed using mixed lymphocytes reactions. Results indicated the expression of MHC II molecules was at a low level in cultured RSC96 cells, while significantly elevated after treatment with IFN-γ. Concurrent treatment with the constructed CIITA siRNAs efficiently downregulated the mRNA levels of CIITA and MHC II in RSC96 cells at 48 h post-transfection. MHC II protein levels were also significantly reduced after CIITA siRNAs transfection. Correspondingly, the immunogenicity of RSC96 cells was significantly downregulated post-transfection. These studies suggest suppressing CIITA gene was efficient in reducing MHC II expression and thus decreasing the immunogenicity of rat Schwann cells.
The current study aimed to examine the effects and underlying mechanisms of chronic psychological stress on the growth of ovarian carcinoma. Human ovarian carcinoma cells SKOV-3 were subcutaneously inoculated into nude mice to establish an ectopic mouse model. The animals were experimentally stressed 6 h daily for a total of 42 days with a physical restraint system. We examined the effects of stress on the growth of tumor cells that were inoculated 7 days after the initiation of stress. The growth of SKOV-3 xenografts in the stress group showed a more rapid trend than that in the control. The mean weight of tumors that were removed at the end of the experiment increased by 71.7% in the stress group as compared to the control. In order to explore the underlying mechanisms, we first determined the serum levels of norepinephrine (NE) and interleukin 10 (IL-10) in the mice using an enzyme-linked immunoabsorbent assay (ELISA) and then analyzed protein expression profiles of SKOV-3 xenografts using a proteomics-based approach combining two-dimensional electrophoresis with ultra performance liquid chromatography-electrospray tandem mass spectrometry (nanoUPLC-ESI-MS/MS). Results demonstrated that serum levels of NE and IL-10 were obviously increased in the mice receiving 6 h of immobilization daily for 42 days. In xenografts exposed to stress, a tumor promoting protein nm23 was significantly upregulated while a tumor suppressing protein NDRG1 was obviously downregulated, which were confirmed by subsequent Western blot analysis. Results obtained in the current study suggested that chronic stress promoted the growth of ovarian carcinoma in nude mice through increasing serum levels of NE and IL-10 and altering nm23 and NDRG1 expression in tumor tissues.