PITX2 transcription factor is overexpressed and involved in the tumorigenicity of ovarian cancer

Free Paper Session - Biomedicine: abstract no. A2

Anti-inflammatory effects of lutein in retinal ischemic injury: in vivo and in vitro studies

postprin

Prevalence of occult hepatitis B infection in a highly endemic area for chronic hepatitis B: A study of a large blood donor population

Background and aims: The aim of the present study was to determine the population prevalence of occult hepatitis B (OHB) infection and its clinical profile in a highly endemic area of chronic hepatitis B virus disease. Methods: OHB was first identified by individual sample testing for hepatitis B surface antigen (HBsAg) followed by nucleic acid testing (NAT) and vice versa for 3044 (cohort 1, stored sera from donation within 1 year) and 9990 (cohort 2, prospective study) blood donors, respectively. OHB was confirmed meticulously by ≥2 out of 3 tests with detectable hepatitis B virus (HBV) DNA using a sensitive standardised assay. Detailed serology and viral load in the serum and liver were studied. Results: The prevalence of OHB was 0.13% (4/3044) and 0.11% (11/9967) for cohort 1 and 2, respectively. In cohort 2, 10 out of 11 OHB samples were positive for anti-HBc (hepatitis B core antigen) antibody (all were immunoglobulin G). Seven had detectable anti-HBs. The serum HBV DNA levels were extremely low (highest 14.1 IU/ml). Of the six donors who underwent liver biopsies, all had normal liver biochemistry, extremely low liver HBV DNA (highest 6.21 copies/cell) and nearly normal liver histology. For those with viral sequence generation, none had the common HBsAg mutant G145R. Conclusions: The prevalence of OHB in a highly endemic area of chronic HBV was very low, thus implying a low impact on transfusion services. To implement universal screening, the high cost of NAT should be taken into account. OHB blood donors had very low HBV replication, and normal liver biochemistry and histology, conferring a favourable prognosis.published_or_final_versio

Anti-autophagic effects of lutein in retinal ischemia

The Symposium was jointly organized by the Hong Kong Ophthalmological Society and the College of Ophthalmologists of Hong KongFree Paper - VitreoretinaObjective: Lutein protects the retina from ischemia/reperfusion (I/R) injuries through anti-oxidative, anti-apoptotic and anti-inflammatory properties. The role of lutein and autophagy in I/R-mediated retinal cell death is unknown. We further investigated the anti-autophagic effects of lutein-mediated protection in in vitro and in vivo models. Method: Cultured rat Müller cells (rMC-1) were exposed to cobalt(II) chloride (CoCl2) with or without lutein treatment. Cell viability (MTS assay), cell death (LDH assay), autophagy (Western blot of microtubule-associated protein light chain 3 LC3) and autophagic vesicle formation (immunohistochemistry) were assessed. Mice with middle cerebral artery occlusion-induced retinal I/R injury received lutein or vehicle treatment. Immunohistochemical detection of LC3 was performed on retinal sections. Results: Lutein treatment was able to improve cell viability, reduce LDH release and protect rMC-1 cells from CoCl2-induced autophagic cell death. It can also reduce I/R-induced autophagic activity in the retina

PITX2 transcription factor is overexpressed and involved in the tumorigenicity of ovarian cancer

The 22nd Lorne Cancer Conference, Lorne, Victoria, Australia, 11-13 February 2010

Upregulation of PITX2 transcription factor is associated with ovarian tumorigenesis

Poster Presentation - Theme 6: Cancer: 6.08The 15th Research Postgraduate Symposium (RPS 2010), the University of Hong Kong, Hong Kong, China, 1-2 December 2010

Association of hepatitis B virus Pre-S mutations with the risk of hepatocellular carcinoma development

Introduction: Recent studies suggest that hepatitis B virus (HBV) Pre-S/S mutations are associated with the development of hepatocellular carcinoma (HCC). However, in these case-control studies, the patients were not matched for age, gender and hepatitis B e-antigen (HBeAg) status. We aimed to investigate the association between PreS deletions and HCC using (1) a matched case-control approach and (2) a longitudinal approach. Methods: HBV PreS deletions were determined by DNA sequencing in sera collected from 105 HCC and 105 non-HCC patients matched with age, gender and HBeAg status, as well as in sera collected before the development of HCC. Results: PreS deletions were detected in 27 of 105 HCC cases (25.7%). At the time of writing, nucleotide sequence analysis in 68 HCC/non-HCC­–matched pairs showed that 20 HCC (29.4%) and 9 non-HCC (13.2%) patients acquired PreS2 deletions (P=0.035). In the longitudinal study, serum samples collected 1 to 7 years before HCC development were assessed in 12 HCC cases with PreS deletions. PreS deletions were absent in seven cases before HCC development (58.3%). Conclusion: The findings from this preliminary study suggested that PreS deletions, especially PreS2 deletions, were associated with HCC development. These results are being validated by our on-going studies with a larger number of patients

Association of hepatitis B virus pre-S deletions with the risk of development of hepatocellular carcinoma

Background and Aims: Recent studies suggest that hepatitis B virus (HBV) pre-S/S mutations are associated with hepatocellular carcinoma (HCC) development [1, 2]. However, in these case-control studies, patients were not matched for age, gender and hepatitis B e-antigen (HBeAg) status. We aimed to investigate the association between pre-S deletions and HCC using 1) a matched case-control approach and 2) a longitudinal approach. In addition, the association between pre-S deletions and HBeAg seroconversion was investigated. Methods: HBV pre-S deletions were determined by DNA sequencing in sera collected from 117 HCC and 117 non-HCC chronic hepatitis B (CHB) patients matched with age, gender and HBeAg status, as well as in sera collected before the development of HCC. HBV pre-S deletions were also determined in 76 non-HCC CHB patients before and after HBeAg seroconversion. Results: Pre-S deletions were detected in 33 out of 117 HCC cases (28.2%). At the time of writing, nucleotide sequence analysis in 78 HCC/non-HCC-matched pairs showed that 26 HCC (33.3%) and 15 nonHCC (19.2%) patients acquired pre-S deletions (P = 0.045). In the longitudinal study, serum samples collected 1−7 years before HCC development were assessed in 16 HCC cases with pre-S deletions. Pre-S deletions were absent in 4 cases before HCC development (25.0%). Pre-S deletions were also assessed in serum samples collected from 76 non-HCC CHB patients 1.4−8.3 months (median 5.6 months) before HBeAg seroconversion and 1.7−7.6 months (median 5.6 months) after seroconversion. Seven patients had newly emerged pre-S deletions after HBeAg seroconversion (9.2%) while 5 had pre-S deletions before HBeAg seroconversion (6.6%). Conclusions: These findings suggested that pre-S deletions were associated with HCC development. 25% of HCC patients had developed pre-S deletions within 1 year before the occurrence of HCC. However its association with HBeAg seroconversion was not clear. These results are being validated by our on-going studies with a larger number of patients. References [1] Choi M.S., Kim D.Y., Lee D.H., et al. (2007) J Viral Hepat. 14:161−8. [2] Lin C.L., Liu C.H., Chen W., et al. (2007) J Gastroenterol Hepatol. 22:1098– 103.link_to_subscribed_fulltex

Anti-inflammatory effects of lutein in retinal ischemic/hypoxic injury : in vivo and in vitro studies

2012-2013 > Academic research: refereed > Publication in refereed journalVersion of RecordRGCHKU 7732/10MPublishe

Anti-inflammatory effects of lutein in retinal ischemic/ hypoxic injury: In vivo and in vitro studies

PURPOSE: Lutein protects retinal neurons by its anti-oxidative and anti-apoptotic properties in ischemia/reperfusion (I/R) injury while its anti-inflammatory effects remain unknown. As Müller cells play a critical role in retinal inflammation, the effect of lutein on Müller cells was investigated in a murine model of I/R injury and a culture model of hypoxic damage. METHODS: Unilateral retinal I/R was induced by a blockade of internal carotid artery using the intraluminal method in mice. Ischemia was maintained for 2 hours followed by 22 hours of reperfusion, during which either lutein (0.2 mg/kg) or vehicle was administered. Flash electroretinogram (flash ERG) and glial fibrillary acidic protein (GFAP) activation were assessed. Lutein's effect on Müller cells was further evaluated in immortalized rat Müller cells (rMC-1) challenged with cobalt chloride-induced hypoxia. Levels of IL-1β, cyclooxygenase-2 (Cox-2), TNFoα and nuclear factor-NF-kappa-B (NF-κB) were examined by Western blot analysis. RESULTS: Lutein treatment minimized deterioration of b-wave/a-wave ratio and oscillatory potentials as well as inhibited upregulation of GFAP in retinal I/R injury. In cultured Müller cells, lutein treatment increased cell viability and reduced level of nuclear NF-κB, IL-1β, and Cox-2, but not TNFα after hypoxic injury. CONCLUSIONS: Reduced gliosis in I/R retina was observed with lutein treatment, which may contribute to preserved retinal function. Less production of pro-inflammatory factors from Müller cells suggested an anti-inflammatory role of lutein in retinal ischemic/hypoxic injury. Together with our previous studies, our results suggest that lutein protected the retina from ischemic/hypoxic damage by its anti-oxidative, antiapoptotic, and anti-inflammatory properties.link_to_OA_fulltex