The progression of political censorship : Hong Kong cinema from colonial rule to Chinese-style socialist hegemony

Censorship is an important cultural regulatory instrument for the government of a society, or even a state. In certain socio-political settings, it can become a powerful administrative appartus (dispositif) and technique (techne) designed to render society governable. Censorship decisions often embody hegemonic views on social and political issues. No matter how virtuous the original intent maybe, the practice of censorship is inevitably geared to the social tensions surrounding issues of human rights and political dissent. The theory behind film censorship may once have been benign but banning or cutting a movie always involves an unnatural set of procedures and actions. This study examines this problem in the context of socio-political changes in Hong Kong. It is an enquiry into the evolution of political film censoship in its more conventional form to its full-fledged integration into other institutions and policies under today\u27s \u27on country, two systems\u27 policy. It also analyses the discourse surrounding the changes in film censorship practices from the days of early cinema to Hong Kong in the 21st century. By contextualizing Hong Kong cinema from a historical and political perspective, the study of the Hong Kong experience aims to shed light on censorship\u27s socio-political meanings for, and effects on, filmmakers and film production

Alternations of microRNAs, the microbiome, and gut-host interactions in gastrointestinal diseases

Over the past few decades, an ageing population combined with a shift towards a Western lifestyle has predisposed many individuals towards inter-connected gastrointestinal (GI) diseases, including inflammatory bowel disease (IBD), colorectal cancer (CRC), gastric cancer (GC) and Clostridioides difficile (C. difficile) infection (CDI). anti-TNF-α treatment for IBD patients has a high unresponsive rate, by using bioinformatics approaches, I identified neutrophil chemotaxis may contribute to the treatment resistance and IL13RA2 is the best predictor to identify treatment unresponsive patients. On the other hand, in the intestinal tract, colonocytes consistently exfoliate and shed into the lumen, affecting gut microbiota composition. These molecular/microbial changes involved in disease pathogenesis can be detected in faeces. By using Taqman probe-based real-time polymerase chain reaction (RT qPCR) assay, several non-coding microRNAs (such as miR-18a, miR-20a, miR-221 and miR 135b) and gut microbes (including Fusobacterium nucleatum, Parvimonas micra, Gemella morbillorum, Peptostreptococcus anaerobius, Clostridium hathewayi and Lachnoclostrium sp.) are highly expressed/enriched in faeces in CRC individuals compared to control subjects. The use of a faecal immunological test (FIT) in combination with these biomarkers may improve the non-invasive CRC screening accuracy. Furthermore, Epstein-Barr virus (EBV) is an oncogenic virus and EBV-driven GC accounts for roughly 10% of total GC cases. GC cells infected with EBV alter the molecular aspect at whole-genome, transcriptome, and epigenome levels. For instance, AKT2 activated by mutation in EBV-positive GC cells affecting downstream MAPK and focal adhesion signalling pathways; AKT2 mutation associates with poor patient survival in EBV-positive GC. Furthermore, once patients have received GI treatments, it may suppress/interfere with the patients’ immune system, disrupt the gut flora homeostasis and trigger CDI. Faecal microbiota transplantation (FMT) has been demonstrated as an effective and alternative treatment strategy for CDI patients. However, it is still in clinical trials due to safety concerns. My study revealed that serum miRNAs such as miR-23a-3p, miR-150-5p, miR-26b-5p and miR-28-5p could be used to monitor FMT treatment in CDI patients, and these markers inversely correlate with IL-12B, IL-18, FGF21 and TNFSRF9 at serum protein and mRNA levels, respectively. Furthermore, miR-23a and miR-150 showed cytoprotective effects against C. difficile Toxin B (TcdB)

PTEN underexpression was associated with more aggressive tumor behaviour in hepatocellular carcinoma and PTEN suppressed cell invasion by downregulating NF-κB signaling pathway

Top Scored Posters: P-006postprintThe 3rd Annual Conference of the International Liver Cancer Association (ILCA 2009), Milan, Italy, 4-6 September 2009. In Abstract Book of ILCA 2009, 2009, p. 20, abstract no. P-00

Intramuscular recurrence in a Hepatocellular carcinoma patient with indolent disease course

<p>Abstract</p> <p>Background</p> <p>Hepatocellular carcinoma (HCC) is a common malignancy worldwide and treatment options are depended on the stage of the tumour. In general, the prognosis of HCC patients with extra-hepatic metastasis is poor. The most common sites of extra-hepatic metastasis are the lung, abdominal lymph nodes and bone.</p> <p>Case presentation</p> <p>Here, we reported a 54-year-old man with an indolent clinical course of HCC. He had multiple extra-hepatic recurrences after initial hepatectomy for HCC and was benefited from repeated resections with prolonged survival. Eventually, he developed intramuscular recurrence in the thigh, which was initially mistaken as deep vein thrombosis.</p> <p>Conclusion</p> <p>Selected patients with indolent disease course of HCC may benefit from repeated resections of extra-hepatic metastases with prolonged survival.</p

Auto/cross-regulation of Hoxb3 expression in posterior hindbrain and spinal cord

The complex and dynamic pattern of Hoxb3 expression in the developing hindbrain and the associated neural crest of mouse embryos is controlled by three separate cis-regulatory elements: element I (region A), element IIIa, and the r5 enhancer (element IVa). We have examined the cis-regulatory element IIIa by transgenic and mutational analysis to determine the upstream trans-acting factors and mechanisms that are involved in controlling the expression of the mouse Hoxb3 gene in the anterior spinal cord and hindbrain up to the r5/r6 boundary, as well as the associated neural crest which migrate to the third and posterior branchial arches and to the gut. By deletion analysis, we have identified the sequence requirements within a 482-bp element III482. Two Hox binding sites are identified in element III482 and we have shown that in vitro both Hoxb3 and Hoxb4 proteins can interact with these Hox binding sites, suggesting that auto/cross-regulation is required for establishing the expression of Hoxb3 in the neural tube domain. Interestingly, we have identified a novel GCCAGGC sequence motif within element III482, which is also required to direct gene expression to a subset of the expression domains except for rhombomere 6 and the associated neural crest migrating to the third and posterior branchial arches. Element III482 can direct a higher level of reporter gene expression in r6, which led us to investigate whether kreisler is involved in regulating Hoxb3 expression in r6 through this element. However, our transgenic and mutational analysis has demonstrated that, although kreisler binding sites are present, they are not required for the establishment or maintenance of reporter gene expression in r6. Our results have provided evidence that the expression of Hoxb3 in the neural tube up to the r5/r6 boundary is auto/cross-regulated by Hox genes and expression of Hoxb3 in r6 does not require kreisler. © 2002 Elsevier Science (USA).published_or_final_versio

Rho GTPase-activating protein deleted in liver cancer suppresses cell proliferation and invasion in hepatocellular carcinoma

Deleted in liver cancer (DLC1) is a candidate tumor suppressor gene recently isolated from human hepatocellular carcinoma. Structurally, DLC1 protein contains a conserved GTPase-activating protein for Rho family protein (RhoGAP) domain, which has been thought to regulate the activity of Rho family proteins. Previous studies indicated that DLC1 was frequently inactivated in cancer cells. In the present study, we aimed to characterize the tumor suppressor roles of DLC1 in hepatocellular carcinoma. We showed that DLC1 significantly inhibited cell proliferation, anchorage-independent growth, and in vivo tumorigenicity when stably expressed in hepatocellular carcinoma cells. Moreover, DLC1 expression greatly reduced the motility and invasiveness of hepatocellular carcinoma cells. With RhoGAP-deficient DLC1 mutant (DLC1-K714E), we showed that the RhoGAP activity was essential for DLC1-mediated tumor suppressor function. Furthermore, the 292- to 648-amino acid region and the steroidogenic acute regulatory related lipid transfer domain played an auxiliary role to RhoGAP and tumor suppressor function of DLC1. Taken together, our findings showed that DLC1 functions as a tumor suppressor in hepatocellular carcinoma and provide the first evidence to support the hypothesis that DLC1 suppresses cancer cell growth by negatively regulating the activity of Rho proteins. ©2005 American Association for Cancer Research.postprin

Two Years versus One Year of Tianjiu Therapy in Sanfu Days for Chronic Asthma: A Clinical Efficacy Observation Trial

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Hepatocyte-specific activation of NF-κB does not aggravate chemical hepatocarcinogenesis in transgenic mice

The NF-κB signalling pathway plays important roles in liver organogenesis and cardnogenesis. Mouse embryos deficient in IKKβ die in mid-gestation, due to excessive apoptosis of hepatoblasts. Although activation of the NF-κB signalling pathway has been demonstrated in human hepatocellular carcinoma, the role of NF-κB is controversial. Here, we have generated transgenic mice in which a constitutively active form of IKKβ was expressed in a hepatocyte-specific manner. Using electrophoretic mobility shift assay, we documented increased NF-κB activities and up-regulated levels of NF-κB downstream target genes, Bcl-xL and STAT5, in the transgenic mouse livers. These results confirmed that the NF-κB pathway was activated in the livers of the transgenic mice. However, there was no significant difference in tumour formation between transgenic and wild-type mice up to an age of 50 weeks. When we treated the transgenic mice with the chemical carcinogen diethylnitrosamine (DEN), we observed no significant differences in the incidence and size of liver tumours formed in these mice with and without DEN treatment at 35 weeks of age, suggesting that the activated NF-κB pathway in the livers of the transgenic mice did not enhance hepatocarcinogenesis. Interestingly, some of the transient transgenic embryos (E12.5) had abnormal excessive accumulation of nucleated red blood cells in their developing livers. In summary, NF-κB activation in hepatocytes did not significantly affect chemical hepatocarcinogenesis. In addition, the TTR/IKKCA transgenic mice may serve as a useful model for studying the role of NF-κB activation in hepatocarcinogenesis as well as inflammatory and metabolic diseases. Copyright © 2008 Pathological Society of Great Britain and Ireland.postprin

Randomized trial of acupoints herbal patching in Sanfu Days for asthma in clinical remission stage

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