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"Tan, K. B."
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50 years of science in Singapore
\"As part of the commemorative book series on Singapore's 50 years of nation-building, this important compendium traces the history and development of the various sectors of Singapore science in the last 50 years or so. The book covers the government agencies responsible for science funding and research policy, the academic institutions and departments who have been in the forefront of the development of the nation's scientific manpower and research, the research centres and institutes which have been breaking new ground in both basic and applied science research, science museums and education, and the academic and professional institutions which the scientific community has set up to enable Singapore scientists to serve the nation more effectively. Each article is chronicled by eminent authors who have played important roles and made significant contributions in shaping today's achievement of science in Singapore\"-- Provided by publisher.
Book
Green synthesized CaO decorated ternary CaO/g-C3N4/PVA nanocomposite modified glassy carbon electrode for enhanced electrochemical detection of caffeic acid
A highly selective, sensitive caffeic acid (CA) detection based on calcium oxide nanoparticles (CaO NPs) derived from extract of
Moringa oleifera
leaves decorated graphitic carbon nitride covalently grafted poly vinyl alcohol (CaO/g-C
3
N
4
/PVA) nanocomposite modified glassy carbon electrode (GCE) was studied. A facile sonochemical method was adapted to synthesis nanomaterials and characterized by HR-TEM (High resolution transmission electron microscopy), FT-IR (Fourier transform infrared spectroscopy), XRD (X-ray diffraction), FE-SEM (Field emission scanning electron microscopy), EDX (Energy dispersive X-ray analysis), Mapping and BET (Brunauer-Emmett-Teller) analysis, and electrochemical techniques. The nanocomposite modified GCE exhibited an excellent catalytic performance to the oxidation of CA under optimized conditions owing to better electron transfer efficiency, conductivity and high surface area of the electrode material. The present electrochemical sensor showed high selectivity towards the determination of 10 µM CA in the presence of 100-fold higher concentrations of interferents. The modified CA sensor exhibited a wide sensing linear range from 0.01 µM to 70 µM and the detection limit (LOD) was found to be 0.0024 µM (S/
N
= 3) in 0.1 M phosphate buffer saline (PBS) as a supporting electrolyte at pH 7.0. The fabricated CA sensor provides an excellent stability, reproducibility and selectivity for the determination of CA. The modified CA sensor was applied to real blood plasma samples and obtained good recovery (97.6-100.1%) results.
Journal Article
Gain-of-function cardiomyopathic mutations in RBM20 rewire splicing regulation and re-distribute ribonucleoprotein granules within processing bodies
Mutations in the cardiac splicing factor RBM20 lead to malignant dilated cardiomyopathy (DCM). To understand the mechanism of RBM20-associated DCM, we engineered isogenic iPSCs with DCM-associated missense mutations in RBM20 as well as RBM20 knockout (KO) iPSCs. iPSC-derived engineered heart tissues made from these cell lines recapitulate contractile dysfunction of RBM20-associated DCM and reveal greater dysfunction with missense mutations than KO. Analysis of RBM20 RNA binding by eCLIP reveals a gain-of-function preference of mutant RBM20 for 3′ UTR sequences that are shared with amyotrophic lateral sclerosis (ALS) and processing-body associated RNA binding proteins (FUS, DDX6). Deep RNA sequencing reveals that the RBM20 R636S mutant has unique gene, splicing, polyadenylation and circular RNA defects that differ from RBM20 KO. Super-resolution microscopy verifies that mutant RBM20 maintains very limited nuclear localization potential; rather, the mutant protein associates with cytoplasmic processing bodies (DDX6) under basal conditions, and with stress granules (G3BP1) following acute stress. Taken together, our results highlight a pathogenic mechanism in cardiac disease through splicing-dependent and -independent pathways.
Mutations in the splicing factor RBM20 cause aggressive Dilated Cardiomyopathy. Here the authors generated RBM20 R636S mutants and knockout in human iPSC-derived cardiomyocytes. Mutant RBM20 showed different target RNA binding, altered splicing and localization to cytoplasmic processing bodies.
Journal Article
SMARTphone and social media-based Cardiac Rehabilitation and Secondary Prevention (SMART-CR/SP) for patients with coronary heart disease in China: a randomised controlled trial protocol
IntroductionThe burden of cardiovascular disease (CVD) is rapidly increasing in developing countries, however access to cardiac rehabilitation and secondary prevention (CR/SP) in these countries is limited. Alternative delivery models that are low-cost and easy to access are urgently needed to address this service gap. The objective of this study is to investigate whether a smartphone and social media-based (WeChat) home CR/SP programme can facilitate risk factor monitoring and modification to improve disease self-management and health outcomes in patients with coronary heart disease (CHD), after percutaneous coronary intervention (PCI) therapy.Methods and analysisWe propose a single-blind, randomised controlled trial of 300 patients post-PCI with follow-up over 12 months. The intervention group will receive a smartphone-based and WeChat-based CR/SP programme providing education and support for risk factor monitoring and modification. SMART-CR/SP incorporates core components of modern CR/SP: physical activity tracking with interactive feedback and goal setting; education modules addressing CHD understanding and self-management; remote blood pressure monitoring and strategies to improve medication adherence. Furthermore, a dedicated data portal and a CR/SP coach will facilitate individualised supervision and counselling. The control group will receive usual care but no formal CR/SP programme. The primary outcome is change in exercise capacity measured by 6 minute walk test distance. Secondary outcomes include knowledge and awareness of CHD, risk factor status, medication adherence, psychological well-being and quality of life, major cardiovascular events, re-hospitalisations and all-cause mortality. To assess the feasibility and patients’ acceptance of the intervention, a process evaluation will be performed at the conclusion of the study.Ethics and disseminationEthics approval was granted by both the Human Research Ethics Committee of Fudan University Zhongshan Hospital (HREC B2016-058) and Curtin University Human Research Ethics Office (HRE2016-0120). Results will be disseminated via peer-reviewed publications and presentations at conferences.Clinical trial registration numberChiCTR-INR-16009598; Pre-results.
Journal Article
QSHS: an axion dark matter resonant search apparatus
We describe a resonant cavity search apparatus for axion dark matter constructed by the quantum sensors for the hidden sector collaboration. The apparatus is configured to search for QCD axion dark matter, though also has the capability to detect axion-like particles, dark photons, and some other forms of wave-like dark matter. Initially, a tuneable cylindrical oxygen-free copper cavity is read out using a low noise microwave amplifier feeding a heterodyne receiver. The cavity is housed in a dilution refrigerator (DF) and threaded by a solenoidal magnetic field, nominally 8 T. The apparatus also houses a magnetic field shield for housing superconducting electronics, and several other fixed-frequency resonators for use in testing and commissioning various prototype quantum electronic devices sensitive at a range of axion masses in the range 2.0– 40μeVc−2. The apparatus as currently configured is intended as a test stand for electronics over the relatively wide frequency band attainable with the TM010 cavity mode used for axion searches. We present performance data for the resonator, DF, and magnet, and plans for the first science run.
Journal Article
Electrolyte imbalances as poor prognostic markers in COVID-19: a systemic review and meta-analysis
Purpose
Serum electrolyte imbalances are highly prevalent in COVID-19 patients. However, their associations with COVID-19 outcomes are inconsistent, and of unknown prognostic value. We aim to systematically clarify the associations and prognostic accuracy of electrolyte imbalances (sodium, calcium, potassium, magnesium, chloride and phosphate) in predicting poor COVID-19 clinical outcome.
Methods
PubMed, Embase and Cochrane Library were searched. Odds of poor clinical outcome (a composite of mortality, intensive-care unit (ICU) admission, need for respiratory support and acute respiratory distress syndrome) were pooled using mixed-effects models. The associated prognostic sensitivity, positive and negative likelihood ratios (LR + , LR-) and predictive values (PPV, NPV; assuming 25% pre-test probability), and area under the curve (AUC) were computed.
Results
We included 28 observational studies from 953 records with low to moderate risk-of-bias. Hyponatremia (OR = 2.08, 95% CI = 1.48–2.94,
I
2
= 93%,
N
= 8), hypernatremia (OR = 4.32, 95% CI = 3.17–5.88,
I
2
= 45%,
N
= 7) and hypocalcemia (OR = 3.31, 95% CI = 2.24–4.88,
I
2
= 25%,
N
= 6) were associated with poor COVID-19 outcome. These associations remained significant on adjustment for covariates such as demographics and comorbidities. Hypernatremia was 97% specific in predicting poor outcome (LR + 4.0, PPV = 55%, AUC = 0.80) despite no differences in CRP and IL-6 levels between hypernatremic and normonatremic patients. Hypocalcemia was 76% sensitive in predicting poor outcome (LR- 0.44, NPV = 87%, AUC = 0.71). Overall quality of evidence ranged from very low to moderate.
Conclusion
Hyponatremia, hypernatremia and hypocalcemia are associated with poor COVID-19 clinical outcome. Hypernatremia is 97% specific for a poor outcome, and the association is independent of inflammatory marker levels. Further studies should evaluate if correcting these imbalances help improve clinical outcome.
Journal Article
In vivo and in vitro studies on the roles of neutrophil extracellular traps during secondary pneumococcal pneumonia after primary pulmonary influenza infection
Seasonal influenza virus infections may lead to debilitating disease, and account for significant fatalities annually worldwide. Most of these deaths are attributed to the complications of secondary bacterial pneumonia. Evidence is accumulating to support the notion that neutrophil extracellular traps (NETs) harbor several antibacterial proteins, and trap and kill bacteria. We have previously demonstrated the induction of NETs that contribute to lung tissue injury in severe influenza pneumonia. However, the role of these NETs in secondary bacterial pneumonia is unclear. In this study, we explored whether NETs induced during pulmonary influenza infection have functional significance against infections with Streptococcus pneumoniae and other bacterial and fungal species. Our findings revealed that NETs do not participate in killing of Streptococcus pneumoniae in vivo and in vitro. Dual viral and bacterial infection elevated the bacterial load compared to animals infected with bacteria alone. Concurrently, enhanced lung pathogenesis was observed in dual-infected mice compared to those challenged with influenza virus or bacteria alone. The intensified NETs in dual-infected mice often appeared as clusters that were frequently filled with partially degraded DNA, as evidenced by punctate histone protein staining. The severe pulmonary pathology and excessive NETs generation in dual infection correlated with exaggerated inflammation and damage to the alveolar-capillary barrier. NETs stimulation in vitro did not significantly alter the gene expression of several antimicrobial proteins, and these NETs did not exhibit any bactericidal activity. Fungicidal activity against Candida albicans was observed at similar levels both in presence or absence of NETs. These results substantiate that the NETs released by primary influenza infection do not protect against secondary bacterial infection, but may compromise lung function.
Journal Article
Inhibition of hepatic fibrosis with artificial microRNA using ultrasound and cationic liposome-bearing microbubbles
We sought to investigate the antifibrotic effects of an artificial microRNA (miRNA) targeting connective tissue growth factor (CTGF) using the ultrasound-targeted cationic liposome-bearing microbubble destruction gene delivery system. Cationic liposomes were conjugated with microbubbles using a biotin–avidin system. Plasmids carrying the most effective artificial miRNA sequences were delivered by ultrasound-targeted cationic liposome-bearing microbubble destruction gene delivery system to rats with hepatic fibrosis. The results show that this method of gene delivery effectively transported the plasmids to the rat liver. The artificial miRNA reduced hepatic fibrosis pathological alterations as well as the protein and mRNA expressions of CTGF and transforming growth factor β1. Furthermore, the CTGF gene silencing decreased the levels of type I collagen and α-smooth muscle actin (
P
<0.01). These data suggest that delivery of an artificial miRNA targeted against CTGF using ultrasound-targeted cationic liposome-bearing microbubble destruction may be an efficacious therapeutic method to ameliorate hepatic fibrosis.
Journal Article
Doping mechanisms and electrical properties of bismuth tantalate fluorites
Phase-pure bismuth tantalate fluorites were successfully prepared via conventional solid-state method at 900 °C in 24–48 h. The subsolidus solution was proposed with the general formula of Bi
3+
x
Ta
1−
x
O
7−
x
(0 ≤
x
≤ 0.184), wherein the formation mechanism involved a one-to-one replacement of Ta
5+
cation by Bi
3+
cation within ~4.6 mol% difference. These samples crystallised in a cubic symmetry, space group Fm-3 m with lattice constants,
a
=
b
=
c
in the range 5.4477(± 0.0037)–5.4580(± 0.0039) Å. A slight increment in the unit cell was discernible with increasing Bi
2
O
3
content, and this may attribute to the incorporation of relatively larger Bi
3+
cation in the host structure. The linear correlation between lattice parameter and composition variable showed that the Vegard’s law was obeyed. Both TGA and DTA analyses showed Bi
3+
x
Ta
1−
x
O
7−
x
samples to be thermally stable as neither phase transition nor weight loss was observed within ~28–1000 °C. The AC impedance study of Bi
3
TaO
7
samples was performed over the frequency range 5–13 MHz. At intermediate temperatures, ~350–850 °C, Bi
3+
x
Ta
1−
x
O
7−
x
solid solution was a modest oxide ion conductor with conductivity, ~10
−6
–10
−3
S cm
−1
; the activation energy was in the range 0.98–1.08 eV.
Journal Article
The role of reactive oxygen species and autophagy in safingol-induced cell death
Safingol is a sphingolipid with promising anticancer potential, which is currently in phase I clinical trial. Yet, the underlying mechanisms of its action remain largely unknown. We reported here that safingol-induced primarily accidental necrotic cell death in MDA-MB-231 and HT-29 cells, as shown by the increase in the percentage of cells stained positive for 7-aminoactinomycin
D
, collapse of mitochondria membrane potential and depletion of intracellular ATP. Importantly, safingol treatment produced time- and concentration-dependent reactive oxygen species (ROS) generation. Autophagy was triggered following safingol treatment, as reflected by the formation of autophagosomes, acidic vacuoles, increased light chain 3-II and Atg biomarkers expression. Interestingly, scavenging ROS with
N
-acetyl-
L
-cysteine could prevent the autophagic features and reverse safingol-induced necrosis. Our data also suggested that autophagy was a cell repair mechanism, as suppression of autophagy by 3-methyladenine or bafilomycin A1 significantly augmented cell death on 2-5
μ
M
safingol treatment. In addition, Bcl-xL and Bax might be involved in the regulation of safingol-induced autophagy. Finally, glucose uptake was shown to be inhibited by safingol treatment, which was associated with an increase in p-AMPK expression. Taken together, our data suggested that ROS was the mediator of safingol-induced cancer cell death, and autophagy is likely to be a mechanism triggered to repair damages from ROS generation on safingol treatment.
Journal Article