Wai Keung Tam

Privatising Health Care in China: Problems and Reforms

Abstract This article examines the privatisation of Chinas health care, highlighting the adverse consequences on the accessibility and quality of health services within the public hospital sector and considering the recent governments efforts to de-privatise the health sector. It argues that the dramatic cutbacks in public financing for the health sector and the failure of the state to establish effective and strong regulatory institutions are two major reasons for the adverse consequences, particularly the declining service quality. The lack of effective regulatory institutions is in turn caused by the following factors: revenue-generation imperative, bureaucratic politics, poorly financed and unqualified regulators. Finally, this article discusses the weaknesses of the recent de-privatisation policy, including implementation problems, the difficulty of the government to reassert its ownership rights over public hospitals, and inadequate regulatory reform.

E-health in the East Asian tigers

Summary Objective: The article analyzes e-health progress in East Asias leading tiger economies: Japan, Hong Kong, Singapore, South Korea and Taiwan. It describes five main dimensions of e-health provision in the tigers: policymaking, regulation, provision, funding and physician-patient relations. Methods: We conducted a series of fieldwork interviews and analyzed key healthcare websites. Results and Conclusion: Our main finding is that the development of e-health in the region is less advanced than might be expected. Our explanation focuses on institutional, cultural and financial factors.

Extracellular matrix stability of primary mammalian chondrocytes and intervertebral disc cells cultured in alginate-based microbead hydrogels.

Three-dimensional alginate constructs are widely used as carrier systems for transplantable cells. In the present study, we evaluated the chondrogenic matrix stability of primary rat chondrocytes and intervertebral disc (IVD) cells cultured in three different alginate-based microbead matrices to determine the influence of microenvironment on the cellular and metabolic behaviors of chondrogenic cells confined in alginate microbeads. Cells entrapped in calcium, strontium, or barium ion gelled microbeads were monitored with the live/dead dual fluorescent cell viability assay kit and the 1,9-dimethylmethylene blue (DMB) assay designed to evaluate sulfated glycosaminoglycan (s-GAG) production. Expression of chondrogenic extracellular matrix (ECM) synthesis was further evaluated by semiquantitative RT-PCR of sox9, type II collagen, and aggrecan mRNAs. Results indicate that Ca and Sr alginate maintained significantly higher population of living cells compared to Ba alginate (p < 0.05). Production of s-GAG was similarly higher in Ca and Sr alginate microbead cultures compared to Ba alginate microbeads. Although there was no significant difference between strontium and calcium up to day 14 of culture, Sr alginate showed remarkably improved cellular and metabolic activities on long-term cultures, with chondrocytes expressing as much as 31% and 44% greater s-GAG compared to calcium and barium constructs, respectively, while IVD cells expressed 63% and 74% greater s-GAG compared to calcium and barium constructs, respectively, on day 28. These findings indicate that Sr alginate represent a significant improvement over Ca- and Ba alginate microbeads for the maintenance of chondrogenic phenotype of primary chondrocytes and IVD cells.

China's Debate on Health Care Reform, 2005-09

This commentary critically discusses China’s debate on health care reform during 2005-09 and analyses the politics involved. It examines a key point of contention – the financing of the health sector – given that the contention has been permeated with politics (who gets what, how and when) and that financing has an extremely critical impact on the performance of a health system. The debate on health care financing reflects two major changes brought by health care privatisation since the late 1980s, namely the changed incentives and behaviour of public hospitals and physicians, and the growing problem of effective management of the health workforces by the government. The commentary is organised as follows. First, it reviews the background of health care reform. Secondly, it studies the debate on how the government should finance the health sector. The third section discusses the changed incentives and behaviour of public hospitals and physicians and the growing problem of effective management of the health workforces and highlights how these two developments hinder health care reform. The final part concludes.

Fragmentation in the Hong Kong health care system : myth and reality

The Hong Kong health care system is often held to be excessively fragmented. However, little research has been undertaken to determine the extent of fragmentation. In this article we seek to separate myth from reality by reporting the results of a patient survey undertaken in the early months of 2000. Our analysis of these results enables us to contribute to current debates about fragmentation. Against the proposal of the 1999 Harvard Report for radical structural reform, we endorse the incremental strategy advanced by the Hospital Authority.

Do female legislators have different policy priorities than their male colleagues in an undemocratic/semi-democratic legislature?: The case of Hong Kong

ABSTRACT This article investigates the impacts of democratic transition on gender outcomes in Hong Kong, which has a unique path of transition. The author studies whether democratic transition in Hong Kong since the mid-1980s has brought positive gender outcomes. Specifically, this article examines the extent to which Hong Kong’s female legislators acted for women’s interests from 1970 to 2012. The study finds that after the introduction of legislative elections, female legislators were more likely to represent women’s interests than male legislators. Apart from gender, the study also finds that political orientation of a legislator significantly affected legislator policy priorities and/or gender outcome. Liberal legislators proposed significantly more motions related to women’s interests than conservative legislators. Finally, the study highlights that as the legislature was transited from an undemocratic to a semi-democratic body, legislators were significantly more likely to propose motions related to women’s interests.

Women Representing Women? Evidence from Hong Kong’s Semi-Democratic Legislature

Using Hong Kong as a case study, this article examines whether female legislators are more likely to represent womens interests than their male colleagues in a semi-democratic legislature. We address this question through conducting content analyses of the questions asked by legislators at the plenary meetings during the 2008–12 and 2012–16 legislative sessions. Our results show that female legislators in Hong Kong were significantly more likely to advance womens rights. However, except in the arena of education, there was no significant gender difference regarding traditional womens concerns. This study also finds that political orientation of legislators and the path through which legislators were elected significantly affected their likelihood of representing womens interests.

Hif-αs Modulation of Sox9-Dependent Extracellular Matrix Production: Insight into Intervertebral Disc Cell Activity under Hypoxia

Introduction Intervertebral disc (IVD) degeneration leads to loss of mechanical function of motion segment and is attributed to deregulated extracellular matrix components in the nucleus pulposus (NP). The NP is rich in type II collagen (encoded by COL2A1) and aggrecan (encoded by AGC1), which are known to be regulated by the master chondrogenic transcription factor, Sox9.1 In situ studies of human degenerated NP illustrated a reduction of COL2A1 and absence of AGC1 expression, whereas SOX9 expression level remained high.2 This indicates that there may be other factors in the IVD that can regulate the Sox9-dependent matrix expression. Recent studies in aged rabbit IVD suggest that the abnormal NP cells may be contributed by a migration of the Sox9-expressing prechondrocytic cells from the annulus fibrosus (AF) adjacent to the endplate (EP).3, 4 Among the hypoxia inducible factor-α subunits (Hif-α), Hif-1α and Hif-2α (EPAS1) have been illustrated as important transcription factors in maintaining disc cell and matrix homeostasis, particularly in the hypoxic NP region.5-7 We hypothesized that Hif-αs may regulate the Sox9-dependent transcription of the extracellular matrix genes in response to IVD degeneration. First, we aimed at identification of Sox9 and Hif-αs co-expression in cells of non-degenerated and degenerated IVD. Second, we tested the modulatory effects of Hif-1α/Hif-2α on the expression of Col2a1 and Agc1 using Sox9-expressing mouse prechondrocytic cells as a model. Materials and Methods IVD were harvested from wild-type C57BL/6N mice at 3 and 6 month old. Disc degeneration was induced by an insertion of 25G needle into contralateral AF of 4-month old Lewis rat and discs were harvested post 2 to 4 weeks of operation. Lumbar IVD of scoliosis patients and degenerative disc disease patient were collected. All animal and human works were approved by local ethical committee. Comparative immunohistochemistry staining of Hif-1α, Hif-2α and Sox9 were studied in parrafilm sections of IVD. Luciferase-based promoter assays based on specific Col2a1 or Agc1 cis-acting elements via the overexpression for each of the HIF-α subunits and/or for Sox9 in ATDC5 cells were performed. Results Relative co-expression patterns of Hif-1α, Hif-2α and Sox9 were detected in AF, NP and EP of the mouse, rat and human IVD. Intracellular expression of Hif-1α, Hif-2α, and Sox9 were confirmed by immunofluorescence, indicating a possible role for Hif-αs-Sox9 tonic activity in the IVD. By luciferase-based promoter assay, Sox9 is demonstrated as a dominant transcription factor in the activation of transcription of Col2a1 and Agc1 in mouse chondroprogenitor cells. Overt additive transcriptional upregulation of Col2a1 and Agc1 was observed with a co-expression of HIF-1α and Sox9. Strikingly, Hif-2α inhibited the Sox9-dependent transcriptional upregulation of Col2a1 and Agc1. Conclusion Our findings indicate the presence of Hif-αs/Sox9 expressing cells in IVD. In addition, our data suggest that Hif-αs can modulate Sox9-mediated transcriptional regulation of Col2a1 and Agc1 in prechondrocytic cells, implicating a possible role of dynamic Hif-αs-Sox9 interaction in the IVD degeneration process. Further investigations of the orchestration mechanisms of Hif-αs/Sox9 in the IVD may provide insights in potential strategies to alleviate disc degeneration. Disclosure of Interest None declared References Richardson SM, Hoyland JA, Mobasheri R, Csaki C, Shakibaei M, Mobasheri A. Mesenchymal stem cells in regenerative medicine: opportunities and challenges for articular cartilage and intervertebral disc tissue engineering. J Cell Physiol 2010;222(1):23–32 Sive JI, Baird P, Jeziorsk M, Watkins A, Hoyland JA, Freemont AJ. Expression of chondrocyte markers by cells of normal and degenerate intervertebral discs. Mol Pathol 2002;55(2):91–97 Henriksson H, Thornemo M, Karlsson C, et al. Identification of cell proliferation zones, progenitor cells and a potential stem cell niche in the intervertebral disc region: a study in four species. Spine 2009;34(21):2278–2287 Henriksson HB, Svala E, Skioldebrand E, Lindahl A, Brisby H. Support of concept that migrating progenitor cells from stem cell niches contribute to normal regeneration of the adult mammal intervertebral disc: a descriptive study in the New Zealand white rabbit. Spine 2012;37(9):722–732 Rajpurohit R, Risbud MV, Ducheyne P, Vresilovic EJ, Shapiro IM. Phenotypic characteristics of the nucleus pulposus: expression of hypoxia inducing factor-1, glucose transporter-1 and MMP-2. Cell Tissue Res 2002;308(3):401–407 Risbud MV, Guttapalli A, Stokes DG, et al. Nucleus pulposus cells express HIF-1 alpha under normoxic culture conditions: a metabolic adaptation to the intervertebral disc microenvironment. J Cell Biochem 2006;98(1):152–159 Agrawal A, Gajghate S, Smith H, et al. Cited2 modulates hypoxia-inducible factor-dependent expression of vascular endothelial growth factor in nucleus pulposus cells of the rat intervertebral disc. Arthritis Rheum 2008;58(12):3798–3808

Cadherin 2 Is Required for Intervertebral Disc Homeostasis and Maintenance of Vacuolated Phenotype in Nucleus Pulposus Cells

Introduction Integrity of the nucleus pulposus (NP) has been implicated in the function and homeostasis of intervertebral disc (IVD). Understanding the regulation of NP cells would contribute to their engineering and development of therapeutics for treating IVD degeneration. Studies in mouse models indicate that early events of IVD degeneration involve segregation of the notochordal NP cell clusters,1 suggesting that disc degeneration may be associated with cell adhesion molecule activities. Cadherins are transmembrane glycoproteins that mediate calcium dependent cell adhesion.2 Based on microarray analysis, we have revealed specific expression of Cdh2 gene, encoding cadherin 2/N-cadherin, in rodent NP cells, suggesting a potential regulatory role of cadherins in IVD homeostasis. To date, the function of cadherin 2 in IVD and its relationship to IVD degeneration remain elusive. We hypothesize that cadherin 2 has a regulatory role in NP cells and that a deregulation of its activities has adverse effects on IVD homeostasis. We aimed to study the expression pattern of cadherin 2 in rodent discs during development, aging, and degeneration, and to investigate its function in the NP via a gene and protein ablation strategies. Materials and Methods Animal experiments were approved by local ethics committee. The vertebral columns of wild-type C57BL/6N mice were collected at different ages (n = 4): embryonic day (E) 12.5, E14.5, postnatal day 0 (P0), 3 months old, 6 months old, 1 year old, 1.5 and 2 years old. Progressive disc degeneration was induced by annulus puncture of 4-month-old inbred Lewis rats (n = 6) with 25G needle, and the discs were harvested after 2-, 4-, and 8-weeks of operation. Lumbar IVD of scoliosis patients and lower lumbar spine of the aborted fetus in the second trimester were used as controls. Immunohistochemistry was performed on paraffin sections to study the cadherin 2 expression pattern. For protein ablation study, 4-month-old inbred Lewis rats were anesthetized and the tail IVDs were exposed for injection of rabbit anti-cadherin 2 antibody or control rabbit IgG (n = 6) into the NP via 34G hypodermic needle. Cadherin 2 gene (Cdh2) was knocked out in the NP using notochord-specific Foxa2-Cre recombination strategy. Disc height was measured and expressed as disc height index (%DHI). The IVD were harvested by 2 and 8 weeks after operation (protein ablation) and from P0 and 1 month-old mutants (gene knockout) for histological analysis. Results By immunofluorescence, cadherin 2 was weakly detected in murine embryonic notochord and newborn NP. At 3- and 6-month old, strong cadherin 2 signals were specifically detected as foci along the cell-cell junctions of the vacuolated NP cells (notochordal cells). Annulus fibrosus showed no signals. In aged IVD, the notochordal cells were replaced by small chondrocyte-like cells with lower expression of cadherin 2. In puncture-induced degenerative rodent discs, the notochordal NP cells were replaced by rounded chondrocyte-like cells, showing reduced level of cadherin 2 expression. Human NP showed heterogeneous cadherin 2 expression. By injecting cadherin 2 antibody into rat NP to perturb its function in vivo, cadherin 2 expression was reduced along with reduction of disc height. Compared with the IgG injection control, cadherin 2 antibody ablation group showed a transformation of the notochordal NP cells into less vacuolated chondrocyte-like phenotype with upregulation of collagen II. Cdh2 conditional knockout mice (CKO) showed absence of cadherin 2 and a loss of vacuolated phenotype in the NP cells (Fig. 1A), displaying significantly smaller body size by 1-month old (Fig. 1B). Moreover, the mutant exhibited irregular annulus organization and reduced disc height in IVD (V). Conclusion Our study suggests cadherin 2 as a marker of notochordal NP cells. The lower expression of cadherin 2 in the aged and puncture-injured rodent IVD substantiates its association with IVD degeneration. The reduction of cadherin 2 positive NP cells in mature human IVD is consistent with gradual loss of notochordal cells after the first decade of life. Our parallel in vivo studies of gene/protein ablation support that cadherin 2 is essential to the maintenance of a vacuolated phenotype of the notochordal NP cells, and that a loss of cadherin 2 function may initiate degenerative changes in the IVD. In summary, our study implicates an important role of cadherin 2 in notochordal cell function and regulating IVD homeostasis. Acknowledgments This work is funded by the Area of Excellence grant (AoE/M-04/04) and the General Research Fund (HKU763712M) from the Research Grant Council of Hong Kong. Disclosure of Interest None declared References Yang F, Leung VY, Luk KD, Chan D, Cheung KM. Injury-induced sequential transformation of notochordal nucleus pulposus to chondrogenic and fibrocartilaginous phenotype in the mouse. J Pathol 2009;218(1):113–121 Leckband D, Prakasam A. Mechanism and dynamics of cadherin adhesion. Annu Rev Biomed Eng 2006;8:259–287