The ageing population is posing new challenges to Singapore's healthcare system. The rise of dual income and the decline of extended families, as well as an increase in age-related degenerative disorders due to increased longevity render it difficult for the family to remain the primary social safety net to care for our elderly in their own homes. Consequently, nursing homes may become increasingly relevant for resource and expertise-challenged families to cope with the burden of caring for a frail and dependent elderly. However, as the recent Nightingale Nursing Home elderly mistreatment incident attests, the standards of some have been found wanting. This paper will trace the history of nursing homes in Singapore and the evolution of government policies towards them, discuss the challenges and trade-offs of nursing home regulation, and provide suggestions for better care and governance.
Aged ; Forecasting ; Guidelines as Topic ; History, 20th Century ; History, 21st Century ; Humans ; Nursing Homes ; history ; legislation & jurisprudence ; standards ; trends ; Singapore

Persistent baculovirus infection is observed frequently in insect populations. Persistent infection can be transformed to a replicative and infective state caused by stress factors and plays an important role in regulating the size of insect population and in epizoology of baculoviruses. The aim of this study is to establish a persistently baculovirus-infected cell system to explore the molecular mechanisms of baculoviral persistence. Spodoptera exigua nucleopolyhedrovirus (SeMNPV) was serially undiluted passaged in Se301 cells to reduce virulence. Upon infection of Se301 cells with the SeMNPV up to passage 8, a few cells survived even if most of cells died due to virus infection. The surviving cells were passaged and designated as P8-Se301 cell strain. P8-Se301 cells had a population doubling time of 58-65 hours and grew slower than Se301 cells. Light microscopy and electron microscopy observation showed symptom of baculovirus infection, such as virogenic stroma, viral particles and occlusion bodies, in some of P8-Se301 cells. End-point dilution assay and infectious center assay showed that 4.14% +/- 0.99% cells continually released infectious progeny virus which replicated slower than SeMNPV in Se301 cells. The result indicated that P8-Se301 cells show a typical character trait of baculovirus persistent infection.
Animals ; Cells, Cultured ; Nucleopolyhedrovirus ; growth & development ; physiology ; Spodoptera ; virology ; Virus Cultivation ; methods

INTRODUCTIONWhile the readmission rate from community hospitals is known, the factors affecting it are not. Our aim was to determine the factors predicting unplanned readmissions from community hospitals (CHs) to acute hospitals (AHs).

MATERIALS AND METHODSThis was an observational prospective cohort study, involving 842 patients requiring post-acute rehabilitation in 2 CHs admitted from 3 AHs in Singapore. We studied the role of the Cumulative Illness Rating Scale (CIRS) organ impairment scores, the Mini-mental State Examination (MMSE) score, the Shah modified Barthel Index (BI) score, and the triceps skin fold thickness (TSFT) in predicting the rate of unplanned readmissions (UR), early unplanned readmissions (EUPR) and late unplanned readmissions (LUPR). We developed a clinical prediction rule to determine the risk of UR and EUPR.

RESULTSThe rates of EUPR and LUPR were 7.6% and 10.3% respectively. The factors that predicted UR were the CIRS-heart score, the CIRS-haemopoietic score, the CIRS-endocrine / metabolic score and the BI on admission. The MMSE was predictive of EUPR. The TSFT and CIRS-liver score were predictive of LUPR. Upon receiver operator characteristics analysis, the clinical prediction rules for the prediction of EUPR and UR had areas under the curve of 0.745 and 0.733 respectively. The likelihood ratios of the clinical prediction rules for EUPR and UR ranged from 0.42 to 5.69 and 0.34 to 3.16 respectively.

CONCLUSIONSPatients who have UR can be identified by the admission BI, the MMSE, the TSFT and CIRS scores in the cardiac, haemopoietic, liver and endocrine/metabolic systems.

Acute Disease ; therapy ; Aged ; Female ; Follow-Up Studies ; Hospitals, Community ; statistics & numerical data ; Hospitals, Special ; statistics & numerical data ; Humans ; Intensive Care Units ; statistics & numerical data ; Male ; Patient Readmission ; trends ; Prospective Studies ; Risk Factors ; Severity of Illness Index ; Singapore

Objective To investigate the effect of caveolin-1 scaffolding domain (CSD) peptides on heme oxygenase-1 (HO-1) activity increasing and M1/M2 phenotype polarization in rat alveolar macrophages (AMs) induced by lipopolysaccharide (LPS).Methods Bioinformatics was used to analyze the binding of full-length wild-type CSD polypeptide and 101 amino acid deleted truncated mutant CSD polypeptide (Δ101CSD) to HO-1. Primary AMs were isolated from rats, when cell fusion reached 80％, they were synchronized with serum-free medium and divided into five groups: no treatment was given to the blank control group; LPS group was treated with 100μg/L LPS for 16 hours;LPS+ hemin group was treated with 100μg/L LPS and 20μmol/L hemin for 16 hours; wild-type CSD polypeptide+ LPS+hemin group was pretreated with 10μmol/L wild-type CSD polypeptide 6 hours before LPS treatment; Δ101CSD+ LPS+hemin group was pretreated with 10μmol/L Δ101CSD polypeptide 6 hours before LPS treatment. After treatment for 16 hours, the co-localization between caveolin-1 (Cav-1) and HO-1 was displayed by confocal microscope; the mRNA expressions of inflammatory cytokines interleukin-1β (IL-1β) and monocyte chemoattractant protein-1 (MCP-1) and M1/M2 polarization cytokines tumor necrosis factor-α (TNF-α), inducible nitric oxide synthase (iNOS), leukocyte differentiation antigen 206 (CD206) and IL-10 were determined by real-time fluorescent quantitative reverse transcription-polymerase chain reaction (RT-qPCR); the HO-1 activity and nitric oxide (NO) production were determined by spectrophotometry.Results Bioinformatics analysis showed: both wild-type CSD and Δ101CSD peptides could bind to HO-1, and there was no significant difference in the binding ability between the two peptides, but the deletion of 101 Arg resulted in the disappearance of part of the binding region between Δ101CSD and HO-1. The results of laser confocal microscopy showed: the expressions of Cav-1 and HO-1 were lowed in the blank control group, and Cav-1 was bound to HO-1 in LPS group and LPS+ hemin group. Both wild-type CSD and Δ101CSD peptides pretreatment could significantly reduce the binding of HO-1 to Cav-1 induced by LPS. HO-1 activity analysis showed: after LPS stimulation, the activity of HO-1 was significantly higher than that of the blank control group; the activity of HO-1 induced by LPS was increased by hemin; after pretreatment with two kinds of CSD peptides, the activity of HO-1 was further increased, and the effect of wild-type CSD peptide was more significant, which showed a statistically significant difference as compared with that of LPS+ hemin group (pmol·mg-1·h-1: 3683±266 vs. 2408±132,P < 0.05). RT-qPCR results showed: LPS could induce elevation of cytokines and M1 markers and decrease of M2 markers, while hemin could inhibit LPS-induced inflammatory response and M1/M2 phenotypic polarization. Compared with LPS+ hemin group, after pretreatment with wild-type CSD peptide, the levels of inflammatory factors in AMs were decreased, and the mRNA expression levels of TNF-α and iNOS, M1 markers, were decreased [TNF-α mRNA (2-??Ct): 6.82±0.05 vs. 8.70±0.24, iNOS mRNA (2-??Ct): 331.50±32.05 vs. 506.70±0.10, bothP < 0.05], and IL-10 mRNA expression level was increased (2-??Ct: 269.09±6.54 vs. 119.05±3.30,P < 0.05). The deletion of 101 site partially weakened the inhibitory effect of CSD peptides on inflammatory factors and only reduced the expression of iNOS mRNA (2-??Ct: 429.11±8.92 vs. 506.70±0.10,P < 0.05), indicating that its ability to transform AMs from M1 phenotype to M2 phenotype was poor. The two peptides had no effect on the expression of CD206.Conclusion Wild-type CSD had beneficial effects of anti-inflammation by reducing Cav-1 binding to HO-1 induced by LPS, restoring the HO-1 activity and driving M2 phenotype in alveolar macrophages.