Zika virus (ZIKV) is a mosquito-borne flavivirus. Infection results in a dengue-like illness with fever, headache, malaise, and a maculopapular rash. Nearly all cases are mild and self-limiting but in 2007, a large outbreak of ZIKV was reported from the island of Yap (in Micronesia, northwest of Indonesia). Singapore is already endemic for dengue, and its impact on public health and economic burden is significant. Other dengue-like infections (e.g., Chikungunya virus) are present. Yet only 10% of reported dengue cases have laboratory confirmation. The identification and control of other dengue-like, mosquito-transmitted infections is thus important for the health of Singapore's population, as well as its economy. Given that ZIKV shares the same Aedes mosquito vector with both dengue and Chikungunya, it is possible that this virus is present in Singapore and causing some of the mild dengue-like illness. A specific and sensitive one-step, reverse transcription polymerase chain reaction (RT-PCR) with an internal control (IC) was designed and tested on 88 archived samples of dengue-negative, Chikungunya-negative sera from patients presenting to our hospital with a dengue-like illness, to determine the presence of ZIKV in Singapore. The assay was specific for detection of ZIKV and displayed a lower limit of detection (LoD) of 140 copies viral RNA/reaction when tested on synthetic RNA standards prepared using pooled negative patient plasma. Of the 88 samples tested, none were positive for ZIKV RNA, however, the vast majority of these were from patients admitted to hospital and further study may be warranted in community-based environments.

Although inhibition of the ubiquitin proteasome system has been postulated to play a key role in the pathogenesis of neurodegenerative diseases, studies have also shown that proteasome inhibition can induce increased expression of neuroprotective heat-shock proteins (HSPs). The global gene expression of primary neurons in response to treatment with the proteasome inhibitor lactacystin was studied to identify the widest range of possible pathways affected. Our results showed changes in mRNA abundance, both at different time points after lactacystin treatment and at different lactacystin concentrations. Genes that were differentially up-regulated at the early time point but not when most cells were undergoing apoptosis might be involved in an attempt to reverse proteasome inhibitor-mediated apoptosis and include HSP70, HSP22 and cell cycle inhibitors. The up-regulation of HSP70 and HSP22 appeared specific towards proteasome inhibitormediated cell death. Overexpression of HSP22 was found to protect against proteasome inhibitor-mediated loss of viability by up to 25%. Genes involved in oxidative stress and the inflammatory response were also up-regulated. These data suggest an initial neuroprotective pathway involving HSPs, antioxidants and cell cycle inhibitors, followed by a proapoptotic response possibly mediated by inflammation, oxidative stress and aberrant activation of cell cycle proteins. Keywords: apoptosis, heat-shock proteins, lactacystin, neurons, proteasome inhibition. A common feature of neurodegenerative diseases such as Alzheimer's disease (AD) and Parkinson's disease (PD) is the accumulation of abnormal proteins. However, despite the clear association between abnormal proteins and neurodegenerative diseases, the mechanism of neuronal death in these cases is still undetermined. Studies now suggest that protein aggregation directly impairs the function of the ubiquitin proteasome system (UPS) (Bence et al. 2001) and that dysfunction of the UPS is a possible primary mechanism leading to the pathogenesis of various neurodegenerative disorders .The UPS is the main machinery involved in the nonlysosomal degradation of short-lived, damaged and misfolded intracellular proteins in eukaryotic cells . This pathway involves attachment of multiple ubiquitin molecules to the substrate as a signal for degradation, Abbreviations used: AD, Alzheimer's disease; COX-2, cyclo-oxygenase-2; Cdk, cyclin-dependent kinase; CT, threshold cycle; DMEM, Dulbecco's modified Eagle's medium; EGFP, enhanced green fluorescent protein; GFAP, glial fibrillary acidic protein; HSP, heat-shock protein; LSD, least significant difference; MAP2, microtubule-associated protein 2; MT, metallothionein; MTT, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide; PD, Parkinson's disease; ROS, reactive oxygen species; STS, staurosporine; UPS, ubiquitin proteasome system; TBS, Tris-buffered saline.Journal of Neurochemistry, 2005Neurochemistry, , 94, 943-956 doi:10.1111Neurochemistry, /j.1471Neurochemistry, -4159.2005

From this large prospective study, there was a lower incidence of fever and dyspnea in patients with pandemic influenza A(H1N1/2009) infection. Similar to reports from elsewhere, it was also found that this pandemic virus tends to infect younger people, though with fewer symptoms, on average, than seasonal influenza. Early pandemic influenza A(H1N1/2009) infections appeared to be slightly milder than seasonal influenza as indicated by different symptom patterns in the presentation of more than 500 cases of influenza A(H1N1/2009) during April through July to a large teaching hospital in Singapore.

Mean viral loads for patients with pandemic (H1N1) 2009 were ≈1 log10 times lower than those for patients with seasonal influenza within the first week after symptom onset. Neither pandemic nor seasonal influenza viral loads correlated with clinical severity of illness. No correlation was found between viral loads and concurrent illness.

A simple model for the linewidth enhancement factor α and its frequency dependence in semiconductor lasers is presented. Calculations based on this model are in reasonable agreement with experimental results.