Detection of anti-ENA antibodies (Ab) in systemic lupus erythematosus (SLE): advantages of supplementing countercurrent immunoelectrophoresis with Western blotting (WB)

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Serum lipid and apolipoprotein distributions in Hong Kong Chinese

STUDY OBJECTIVE--The aim was to describe the distribution of lipids and apolipoproteins in the Chinese population in Hong Kong. DESIGN--This was a prospective, cross sectional, population based survey. SETTINGS--The study was conducted in a single, self referred, out patient screening centre. PARTICIPANTS--Altogether 825 Chinese adults aged > or = 20 years were screened. One hundred subjects who had previously had lipid measurement and 29 who were taking lipid modifying drugs were excluded but 289 men and 407 women remained for further analysis. MAIN RESULTS--Age standardised mean (SEM) lipids concentrations for Hong Kong Chinese were total cholesterol: men, 5.48 (0.05) mmol/l and women, 5.46 (0.06) mmol/l; triglycerides: men, 1.22 (1.03) mmol/l and women, 1.00 (1.03) mmol/l; high density lipoprotein (HDL) cholesterol: men, 1.25 (0.02) mmol/l and women, 1.42 (0.02) mmol/l; low density lipoprotein (LDL) cholesterol: men, 3.56 (0.05) mmol/l and women, 3.50 (0.06) mmol/l; apolipoprotein A-I (apo A-I): men, 1.34 (0.01) g/l and women, 1.46 (0.01) g/l; and apolipoprotein B (apo B): men, 1.15 (0.02) g/l and women, 1.06 (0.02) g/l. The total to HDL cholesterol ratios were men, 4.62 (0.07) and women, 4.10 (0.08); and apo B to apo A-I ratios (apo B/A) were men, 0.88 (0.02) and women, 0.75 (0.02). While levels of total cholesterol, LDL cholesterol, apo B, triglycerides, total/HDL cholesterol, and apo B/A were positively associated with age in both sexes and were higher in men before the age 50-59 years, they rose steeply thereafter in women to cross over the levels in men. In contrast, HDL cholesterol decreased with age while apo A-I remained constant, and both were consistently higher in women than in men in all age groups. CONCLUSIONS--Hong Kong Chinese have attained lipid profiles similar to those in other developed western populations. Environmental factors seem influential in this regard. Faced with the increasing coronary mortality of recent years, there should be a major effort to reduce the cholesterol concentrations in this population.published_or_final_versio

C-terminal truncated hepatitis B virus X protein regulates tumorigenicity, self-renewal and drug resistance via STAT3/Nanog signaling pathway

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The feasibility of age-specific travel restrictions during influenza pandemics

<p>Abstract</p> <p>Background</p> <p>Epidemiological studies have shown that imposing travel restrictions to prevent or delay an influenza pandemic may not be feasible. To delay an epidemic substantially, an extremely high proportion of trips (~99%) would have to be restricted in a homogeneously mixing population. Influenza is, however, strongly influenced by age-dependent transmission dynamics, and the effectiveness of age-specific travel restrictions, such as the selective restriction of travel by children, has yet to be examined.</p> <p>Methods</p> <p>A simple stochastic model was developed to describe the importation of infectious cases into a population and to model local chains of transmission seeded by imported cases. The probability of a local epidemic, and the time period until a major epidemic takes off, were used as outcome measures, and travel restriction policies in which children or adults were preferentially restricted were compared to age-blind restriction policies using an age-dependent next generation matrix parameterized for influenza H1N1-2009.</p> <p>Results</p> <p>Restricting children from travelling would yield greater reductions to the short-term risk of the epidemic being established locally than other policy options considered, and potentially could delay an epidemic for a few weeks. However, given a scenario with a total of 500 imported cases over a period of a few months, a substantial reduction in the probability of an epidemic in this time period is possible only if the transmission potential were low and assortativity (i.e. the proportion of contacts within-group) were unrealistically high. In all other scenarios considered, age-structured travel restrictions would not prevent an epidemic and would not delay the epidemic for longer than a few weeks.</p> <p>Conclusions</p> <p>Selectively restricting children from traveling overseas during a pandemic may potentially delay its arrival for a few weeks, depending on the characteristics of the pandemic strain, but could have less of an impact on the economy compared to restricting adult travelers. However, as long as adults have at least a moderate potential to trigger an epidemic, selectively restricting the higher risk group (children) may not be a practical option to delay the arrival of an epidemic substantially.</p

Phosphorylation of nucleophosmin at threonine 234/237 is associated with HCC metastasis

Hepatocellular carcinoma (HCC) is frequently complicated by the occurrence of intrahepatic and extrahepatic metastases, leading to poor prognosis. To improve the prognosis for HCC patients, there is an urgent need to understand the molecular mechanisms of metastasis in HCC. Since protein Serine/Threonine phosphorylation emerges to be an important posttranslational modification critical in signaling process associated with cell proliferation, survival and metastasis, we employed a pair of primary tumor-derived and corresponding lung-metastatic counterparts (PLC/PRF/5-PT and PLC/PRF/5-LM) and aimed to identify these changes using CelluSpot Serine/Threonine kinase peptide array. Upon analysis, we found phosphorylated level of nucleophosmin (NPM) at Threonine 234/237 (p-NPM-Thr234/237) had remarkably high level in metastatic HCC cells (PLC-LM) than the corresponding primary HCC cell line (PLC-PT). Similar observation was observed in another match primary and their metastatic counterparts (MHCC-97L and MHCC-97H). By immunohistochemical staining, p-NPM-Thr234/237 was consistently found to be preferentially expressed in metastatic HCCs when compared with primary HCC in 28 HCC cases (p < 0.0001). By overexpressing Flag-tagged NPM and its phosphorylation site mutant (Thr234/237A) into low p-NPM-Thr234/237 expressing cells (Hep3B and Huh7) using a lentiviral based approach, we demonstrated that p-NPM-Thr234/237 is critical in invasion and migration of HCC cells, and this effect was mediated by cyclin-dependent kinase 1 (CDK1). Wild-type NPM was found to physically interact with a metastatic gene, ROCK2, and defective in Thr234/237 phosphorylation decreased its binding affinity, resulting in decrease in ROCK2 mediated signaling pathway. Identification of CDK1/p-NPM/ROCK2 signaling pathway provides a novel target for molecular therapy against HCC metastasis.published_or_final_versio

Polysaccharopeptide enhanced the anti-cancer effect of gamma-tocotrienol through activation of AMPK

BACKGROUND: Prostate cancer (PCa) frequently relapses after hormone ablation therapy. Unfortunately, once progressed to the castration resistant stage, the disease is regarded as incurable as prostate cancer cells are highly resistant to conventional chemotherapy. METHOD: We recently reported that the two natural compounds polysaccharopeptide (PSP) and Gamma-tocotrienols (gamma-T3) possessed potent anti-cancer activities through targeting of CSCs. In the present study, using both prostate cancer cell line and xenograft models, we seek to investigate the therapeutic potential of combining gamma-T3 and PSP in the treatment of prostate cancer. RESULT: We showed that in the presence of PSP, gamma-T3 treatment induce a drastic activation of AMP-activated protein kinase (AMPK). This was accompanied with inactivation of acetyl-CoA carboxylase (ACC), as evidenced by the increased phosphorylation levels at Ser 79. In addition, PSP treatment also sensitized cancer cells toward gamma-T3-induced cytotoxicity. Furthermore, we demonstrated for the first time that combination of PSP and gamma-T3 treaments significantly reduced the growth of prostate tumor in vivo. CONCLUSION: Our results indicate that PSP and gamma-T3 treaments may have synergistic anti-cancer effect in vitro and in vivo, which warrants further investigation as a potential combination therapy for the treatment of cancer.published_or_final_versio

Infection fatality risk of the pandemic A(H1N1)2009 virus in Hong Kong

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Anti-CD47 antibody suppresses tumor growth and augments the effect of chemotherapy treatment in hepatocellular carcinoma

BACKGROUND & AIMS: Hepatocellular carcinoma (HCC) is often associated with metastasis and recurrence leading to a poor prognosis. Therefore, development of novel treatment regimens is urgently needed to improve the survival of HCC patients. In this study, we aimed to investigate the in vitro and in vivo effects of anti-CD47 antibody alone and in combination with chemotherapy in HCC. METHODS: In this study, we examined the functional effects of anti-CD47 antibody (B6H12) on cell proliferation, sphere formation, migration and invasion, chemosensitivity, macrophage-mediated phagocytosis, and tumorigenicity both in vitro and in vivo. The therapeutic efficacy of anti-CD47 antibody alone or in combination with doxorubicin was examined in patient-derived HCC xenograft. RESULTS: Blocking CD47 with anti-CD47 monoclonal antibody (B6H12) at 10mug/mL could suppress self-renewal, tumorigenicity and migration and invasion abilities of MHCC-97L and Huh-7 cells. Interestingly, anti-CD47 antibody synergized the effect of HCC cells to chemotherapeutic drugs including doxorubicin and cisplatin. Blockade of CD47 by anti-CD47 antibody induced macrophage-mediated phagocytosis. Using a patient-derived HCC xenograft mouse model, we found that anti-CD47 antibody (400mug/mouse) in combination with doxorubicin (2mg/kg) exerted maximal effects on tumor suppression, as compared with doxorubicin and anti-CD47 antibody alone. CONCLUSIONS: Anti-CD47 antibody treatment could complement chemotherapy which may be a promising therapeutic strategy for the treatment of HCC patients. This article is protected by copyright. All rights reserved.postprin

SENP1 promotes hypoxia-induced cancer stemness by HIF-1α deSUMOylation and SENP1/HIF-1α positive feedback loop

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