Towards Sustainable Municipal Solid Waste Management in Malaysia

This work is part of the SYNERGORS project (“A Systems Approach to Synergistic Utilisation of Secondary Organic Streams”) funded by the UKRI Natural Environment Research Council (NE/R012938/1) through the UKRI/NERC Industrial Innovation Fellowship Programme (2018-2021). This project was led by Dr Kok Siew Ng at University of Oxford. Website: https://eng.ox.ac.uk/synergorsProject summary report: https://eng.ox.ac.uk/media/10670/synergors-final-report.pdfEXECUTIVE SUMMARY: The increasing amount of municipal solid waste (MSW) generation and the lack of strategic improvements on solid waste management in Malaysia require urgently the attention of the government and the public.It has been estimated that 1.17 kg/capita/day of MSW is generated in Malaysia, 65% of which is household solid waste that has doubled over the past 20 years due to population growth and urbanisation. Without a sufficient waste treatment and recycling infrastructure in place, most of the MSW is destined to continue to be landfilled. Not only it can cause pollution and health hazards, MSW is also one of the major sources of global methane emissions accounting for 11%. As methane is the second largest contributor of global greenhouse gas emissions after carbon dioxide, it is critical that Malaysia develops systemic sound solid waste management as part of its climate actions guided by the Paris agreement. Also, by treating waste as resource, the recent shift in the government strategy to move towards the circular economy should be aligned with SDG 12 targets (Responsible Consumption and Production). Although the quantity of recyclable waste collected tripled between 2018 and 2021, the officially reported recycling rate of 31.5% in 2021 remains questionable as the recycling infrastructure in Malaysia is not yet well established. This points to the significant efforts Malaysia needs to make to move towards a sustainable waste management regime, and to achieve its ambition for reaching a recycling target of 40% by 2025. Malaysia started implementing a plan for moving towards sustainable waste management in the early 1990s. However, the recycling programmes were not well received by the public at that time, and it was only in 2001, that policy goals for sustainable waste management have been included in the regulatory landscape through the 8th Malaysia Plan (2001-2005). In 2005, the National Strategic Plan for Solid Waste Management was developed to guide solid waste policy planning and resource allocation. Two years after, the Solid Waste and Public Cleansing Management Act 2007 (Act 672) was created that came into enforcement in September 2011 in six out of the thirteen states (Perlis, Kedah, Pahang, Negeri Sembilan, Melaka, Johor) and two out of the three federal territories (i.e. Kuala Lumpur and Putrajaya). This partial adoption of the Act has created inconsistency in waste management and planning as well as incomplete waste data gathering. This,has led to ineffective waste management practices, that, in turn, resulted in long-term environmental, economic and social consequences. Even though sustainable waste management goals continue to be included in the recent 12th Malaysia Plan (2021-2025), the lack of public awareness on the importance of source separation of waste and recycling prevents progress in this field. The infrastructure for waste collection and treatment is also insufficient to serve the needs. All these factors have created significant barriers for Malaysia to realise sustainable waste management.UK Natural Environment Research Council (NE/R012938/1

Diabetes with poor-control HbA1c is cardiovascular disease 'risk equivalent' for mortality: UK Biobank and Hong Kong population-based cohort study

INTRODUCTION: Type 2 diabetes mellitus (T2DM) has traditionally been considered a coronary heart disease 'risk equivalent' for future mortality, but significant heterogeneity exists across people with T2DM. This study aims to determine the risk of all-cause mortality of patients with cardiovascular disease (CVD) and T2DM in UK and Hong Kong, with stratifications for hemoglobin A1 (HbA1c) concentrations, compared with those without CVD and diabetes mellitus. RESEARCH DESIGN AND METHODS: This is a retrospective cohort study of 3 839 391 adults from Hong Kong and a prospective cohort study of 497 779 adults from the UK Biobank. Individuals were divided into seven disease groups: (1) no T2DM and CVD, (2) T2DM only with HbA1c <7%, (3) T2DM only with HbA1c 7%-7.9%, (4) T2DM only with HbA1c 8%-8.9%, (5) T2DM only with HbA1c ≥9%, (6) CVD only, and (7) T2DM and CVD. Differences in all-cause mortality between groups were examined using Cox regression. RESULTS: After around 10 years of median follow-up, 423 818 and 19 844 deaths were identified in the Hong Kong cohort and UK Biobank, respectively. Compared with individuals without T2DM and CVD, the adjusted HR for all-cause mortality in the other six disease groups for the Hong Kong cohort was 1.25 (95% CI 1.23 to 1.27) for T2DM only with HbA1c <7%, 1.21 (95% CI 1.19 to 1.23) for T2DM only with HbA1c 7%-7.9%, 1.36 (95% CI 1.33 to 1.39) for T2DM only with HbA1c 8%-8.9%, 1.82 (95% CI 1.78 to 1.85) for T2DM only with HbA1c ≥9%, 1.37 (95% CI 1.36 to 1.38) for CVD only, and 1.83 (95% CI 1.81 to 1.85) for T2DM and CVD, and for the UK Biobank the HR was 1.45 (95% CI 1.33 to 1.58), 1.50 (95% CI 1.32 to 1.70), 1.72 (95% CI 1.43 to 2.08), 2.51 (95% CI 2.05 to 3.08), 1.67 (95% CI 1.59 to 1.75) and 2.62 (95% CI 2.42 to 2.83), respectively. This indicates that patients with T2DM had an increased risk of mortality compared with those without T2DM and CVD, and in those with HbA1c ≥9% an even higher risk than people with CVD. CONCLUSIONS: Patients with T2DM with poor HbA1c control (8%-8.9% and ≥9%) were associated with similar and higher risk of mortality compared with patients with CVD, respectively. Optimal HbA1c, controlled for risk reduction and prevention of mortality and complications in diabetes management, remains important

Two-dimensional amine and hydroxy functionalized fused aromatic covalent organic framework

Ordered two-dimensional covalent organic frameworks (COFs) have generally been synthesized using reversible reactions. It has been difficult to synthesize a similar degree of ordered COFs using irreversible reactions. Developing COFs with a fused aromatic ring system via an irreversible reaction is highly desirable but has remained a significant challenge. Here we demonstrate a COF that can be synthesized from organic building blocks via irreversible condensation (aromatization). The as-synthesized robust fused aromatic COF (F-COF) exhibits high crystallinity. Its lattice structure is characterized by scanning tunneling microscopy and X-ray diffraction pattern. Because of its fused aromatic ring system, the F-COF structure possesses high physiochemical stability, due to the absence of hydrolysable weak covalent bonds

Ultra-strong Adhesion of Graphene Membranes

As mechanical structures enter the nanoscale regime, the influence of van der Waals forces increases. Graphene is attractive for nanomechanical systems because its Young's modulus and strength are both intrinsically high, but the mechanical behavior of graphene is also strongly influenced by the van der Waals force. For example, this force clamps graphene samples to substrates, and also holds together the individual graphene sheets in multilayer samples. Here we use a pressurized blister test to directly measure the adhesion energy of graphene sheets with a silicon oxide substrate. We find an adhesion energy of 0.45 \pm 0.02 J/m2 for monolayer graphene and 0.31 \pm 0.03 J/m2 for samples containing 2-5 graphene sheets. These values are larger than the adhesion energies measured in typical micromechanical structures and are comparable to solid/liquid adhesion energies. We attribute this to the extreme flexibility of graphene, which allows it to conform to the topography of even the smoothest substrates, thus making its interaction with the substrate more liquid-like than solid-like.Comment: to appear in Nature Nanotechnolog

Spatiotemporal Structure of Molecular Evolution of H5N1 Highly Pathogenic Avian Influenza Viruses in Vietnam

BackgroundVietnam is one of the countries most affected by outbreaks of H5N1 highly pathogenic avian influenza viruses. First identified in Vietnam in poultry in 2001 and in humans in 2004, the virus has since caused 111 cases and 56 deaths in humans. In 2003/2004 H5N1 outbreaks, nearly the entire poultry population of Vietnam was culled. Our earlier study (Wan et al., 2008, PLoS ONE, 3(10): e3462) demonstrated that there have been at least six independent H5N1 introductions into Vietnam and there were nine newly emerged reassortants from 2001 to 2007 in Vietnam. H5N1 viruses in Vietnam cluster distinctly around Hanoi and Ho Chi Minh City. However, the nature of the relationship between genetic divergence and geographic patterns is still unclear.Methodology/Principal FindingsIn this study, we hypothesized that genetic distances between H5N1 viruses in Vietnam are correlated with geographic distances, as the result of distinct population and environment patterns along Vietnam's long north to south longitudinal extent. Based on this hypothesis, we combined spatial statistical methods with genetic analytic techniques and explicitly used geographic space to explore genetic evolution of H5N1 highly pathogenic avian influenza viruses at the sub-national scale in Vietnam. Our dataset consisted of 125 influenza viruses (with whole genome sets) isolated in Vietnam from 2003 to 2007. Our results document the significant effect of space and time on genetic evolution and the rise of two regional centers of genetic mixing by 2007. These findings give insight into processes underlying viral evolution and suggest that genetic differentiation is associated with the distance between concentrations of human and poultry populations around Hanoi and Ho Chi Minh City.Conclusions/SignificanceThe results show that genetic evolution of H5N1 viruses in Vietnamese domestic poultry is highly correlated with the location and spread of those viruses in geographic space. This correlation varies by scale, time, and gene, though a classic isolation by distance pattern is observed. This study is the first to characterize the geographic structure of influenza viral evolution at the sub-national scale in Vietnam and can shed light on how H5N1 HPAIVs evolve in certain geographic settings

Direct and indirect control of the initiation of meiotic recombination by DNA damage checkpoint mechanisms in budding yeast

Meiotic recombination plays an essential role in the proper segregation of chromosomes at meiosis I in many sexually reproducing organisms. Meiotic recombination is initiated by the scheduled formation of genome-wide DNA double-strand breaks (DSBs). The timing of DSB formation is strictly controlled because unscheduled DSB formation is detrimental to genome integrity. Here, we investigated the role of DNA damage checkpoint mechanisms in the control of meiotic DSB formation using budding yeast. By using recombination defective mutants in which meiotic DSBs are not repaired, the effect of DNA damage checkpoint mutations on DSB formation was evaluated. The Tel1 (ATM) pathway mainly responds to unresected DSB ends, thus the sae2 mutant background in which DSB ends remain intact was employed. On the other hand, the Mec1 (ATR) pathway is primarily used when DSB ends are resected, thus the rad51 dmc1 double mutant background was employed in which highly resected DSBs accumulate. In order to separate the effect caused by unscheduled cell cycle progression, which is often associated with DNA damage checkpoint defects, we also employed the ndt80 mutation which permanently arrests the meiotic cell cycle at prophase I. In the absence of Tel1, DSB formation was reduced in larger chromosomes (IV, VII, II and XI) whereas no significant reduction was found in smaller chromosomes (III and VI). On the other hand, the absence of Rad17 (a critical component of the ATR pathway) lead to an increase in DSB formation (chromosomes VII and II were tested). We propose that, within prophase I, the Tel1 pathway facilitates DSB formation, especially in bigger chromosomes, while the Mec1 pathway negatively regulates DSB formation. We also identified prophase I exit, which is under the control of the DNA damage checkpoint machinery, to be a critical event associated with down-regulating meiotic DSB formation

Gene set of nuclear-encoded mitochondrial regulators is enriched for common inherited variation in obesity

There are hints of an altered mitochondrial function in obesity. Nuclear-encoded genes are relevant for mitochondrial function (3 gene sets of known relevant pathways: (1) 16 nuclear regulators of mitochondrial genes, (2) 91 genes for oxidative phosphorylation and (3) 966 nuclear-encoded mitochondrial genes). Gene set enrichment analysis (GSEA) showed no association with type 2 diabetes mellitus in these gene sets. Here we performed a GSEA for the same gene sets for obesity. Genome wide association study (GWAS) data from a case-control approach on 453 extremely obese children and adolescents and 435 lean adult controls were used for GSEA. For independent confirmation, we analyzed 705 obesity GWAS trios (extremely obese child and both biological parents) and a population-based GWAS sample (KORA F4, n = 1,743). A meta-analysis was performed on all three samples. In each sample, the distribution of significance levels between the respective gene set and those of all genes was compared using the leading-edge-fraction-comparison test (cut-offs between the 50(th) and 95(th) percentile of the set of all gene-wise corrected p-values) as implemented in the MAGENTA software. In the case-control sample, significant enrichment of associations with obesity was observed above the 50(th) percentile for the set of the 16 nuclear regulators of mitochondrial genes (p(GSEA,50) = 0.0103). This finding was not confirmed in the trios (p(GSEA,50) = 0.5991), but in KORA (p(GSEA,50) = 0.0398). The meta-analysis again indicated a trend for enrichment (p(MAGENTA,50) = 0.1052, p(MAGENTA,75) = 0.0251). The GSEA revealed that weak association signals for obesity might be enriched in the gene set of 16 nuclear regulators of mitochondrial genes

Evolution of Highly Pathogenic H5N1 Avian Influenza Viruses in Vietnam between 2001 and 2007

Highly pathogenic avian influenza (HPAI) H5N1 viruses have caused dramatic economic losses to the poultry industry of Vietnam and continue to pose a serious threat to public health. As of June 2008, Vietnam had reported nearly one third of worldwide laboratory confirmed human H5N1 infections. To better understand the emergence, spread and evolution of H5N1 in Vietnam we studied over 300 H5N1 avian influenza viruses isolated from Vietnam since their first detection in 2001. Our phylogenetic analyses indicated that six genetically distinct H5N1 viruses were introduced into Vietnam during the past seven years. The H5N1 lineage that evolved following the introduction in 2003 of the A/duck/Hong Kong/821/2002-like viruses, with clade 1 hemagglutinin (HA), continued to predominate in southern Vietnam as of May 2007. A virus with a clade 2.3.4 HA newly introduced into northern Vietnam in 2007, reassorted with pre-existing clade 1 viruses, resulting in the emergence of novel genotypes with neuraminidase (NA) and/or internal gene segments from clade 1 viruses. A total of nine distinct genotypes have been present in Vietnam since 2001, including five that were circulating in 2007. At least four of these genotypes appear to have originated in Vietnam and represent novel H5N1 viruses not reported elsewhere. Geographic and temporal analyses of H5N1 infection dynamics in poultry suggest that the majority of viruses containing new genes were first detected in northern Vietnam and subsequently spread to southern Vietnam after reassorting with pre-existing local viruses in northern Vietnam. Although the routes of entry and spread of H5N1 in Vietnam remain speculative, enhanced poultry import controls and virologic surveillance efforts may help curb the entry and spread of new HPAI viral genes

Trends of public health research output from India during 2001-2008

BACKGROUND: An understanding of how public health research output from India is changing in relation to the disease burden and public health priorities is required in order to inform relevant research development. We therefore studied the trends in the public health research output from India during 2001-2008 that was readily available in the public domain. METHODS: The scope and type of the published research from India in 2007 that was included in the PubMed database was assessed and compared with a previous similar assessment for 2002. Papers were classified based on the review of abstracts and original public health research papers were assessed in detail. Impact factors for the journals were used to compute quality-adjusted research output. The websites of governmental organizations, academic and research institutions and international organizations were searched in order to identify and review reports on original public health research produced in India from 2001 to 2008. The reports were classified based on the topics covered and quality and their trends over time were assessed. RESULTS: The number of original health research papers from India in PubMed doubled from 4494 in 2002 to 9066 in 2007. This included a 3.1-fold increase in public health research papers, but these comprised only 5% of the total papers in 2007. Within public health, the increase was lowest for the health system and policy category. Several major causes of disease burden in India continued to be underrepresented in the quality-adjusted public health research output in 2007. The number of papers evaluating population health interventions increased from 2002 to 2007, but there were none on the leading non-communicable causes of disease burden or on road traffic injuries. The number of identified original public health research reports increased by 64.7% from 204 in 2001-2004 to 336 in 2005-2008. The proportion of reports on reproductive and child health was very high but decreased slightly from 38.7% of the total in 2001-2004 to 31.5% in 2005-2008 (P = 0.09); those on the leading chronic non-communicable conditions and injuries increased from 6.4% to 13.4% (P = 0.01) but this was still much lower than their contribution to the disease burden. Health system/policy issues were the topic in 27.4% reports but health information issues were covered in a miniscule 0.6% reports. The proportion of reports that were evaluations increased slightly from 26% in 2001-2004 to 31.5% in 2005-2008, with this proportion being higher among the reports commissioned by international organizations (P < 0.001). The proportion of reports commissioned by Indian governmental organizations alone, or in collaboration with international organizations, doubled from 2001-2004 to 2005-2008 (P < 0.001). Only 25% of the total 540 reports had a quality score of adequate or better. The quality of reports produced by collaborations between Indian and international organizations was higher than those produced by Indian or international organizations alone (P < 0.001). CONCLUSION: This is the first analysis from India that includes research reports in addition to published papers. It provides the most up-to-date understanding of public health research output from India. The increase in available public health research output and the increase in commissioning of this research by Indian governmental organizations are encouraging. However, the distribution of research topics and the quality of research reports continue to be unsatisfactory. It is necessary for health policy to address these continuing deficits in public health research in order to reduce the very large disease burden in India.13 page(s