Zika virus infection: a review of available techniques towards early detection

Zika virus belongs to the family Flaviviridae as do other viruses like Dengue, West Nile and Yellow Fever. They are arboviruses transmitted by the Aedes species of mosquito. Zika virus was first isolated in rhesus monkeys in Uganda in 1947. Human infections of the virus were found between the 1960s and 1980s in Africa, the Americas, Asia and the Pacific. The similarity in clinical presentation in Zika-infected patients compared with Dengue caused infections to be previously misdiagnosed as Dengue infection. The Zika virus pandemic in 2015 created a lot of concern globally because of little information about available techniques, samples as well as no available antiviral and vaccines for treatment and vaccination against infection. In addition, the vectors identified for transmission, Aedes aegypti and Aedes albopictus, were of great concern due to their ability to survive both temperate and tropical climatic conditions, hence indicating the possible global spread of Zika virus infection. Almost two years after the report of infection in pregnant women in Brazil resulting in microcephalic babies, Zika virus was identified as a public health problem. Thus, a lot of research into early detection and prevention has been conducted to control the spread of the virus. This review paper highlights available information on techniques currently available for diagnosis of infection caused by Zika virus.  

Family Businesses and Adaptation: A Dynamic Capabilities Approach

The main objective of this research was to propose a framework centred on the dynamic capabilities approach, and to be applied in the context of family businesses’ adaption to their changing business environment. Data were gathered through interviews with ten FBs operating in Western Australia. Based on the findings, the clusters of activities, sensing, seizing, and transforming emerged as key factors for firms’ adaptation, and were reinforced by firms’ open culture, signature processes, idiosyncratic knowledge, and valuable, rare, inimitable and non-substitutable attributes. Thus, the usefulness of the proposed framework was confirmed. Implications and future research opportunities are presented. © 2018, The Author(s)

Cytosolic phospholipase A₂alpha amplifies early cyclooxygenase-2 expression, oxidative stress and MAP kinase phosphorylation after cerebral ischemia in mice

<p>Abstract</p> <p>Background</p> <p>The enzyme cytosolic phospholipase A₂alpha (cPLA₂α) has been implicated in the progression of cerebral injury following ischemia and reperfusion. Previous studies in rodents suggest that cPLA₂α enhances delayed injury extension and disruption of the blood brain barrier many hours after reperfusion. In this study we investigated the role of cPLA₂α in early ischemic cerebral injury.</p> <p>Methods</p> <p>Middle cerebral artery occlusion (MCAO) was performed on cPLA₂α^+/+and cPLA₂α^-/-mice for 2 hours followed by 0, 2, or 6 hours of reperfusion. The levels of cPLA₂α, cyclooxygenase-2, neuronal morphology and reactive oxygen species in the ischemic and contralateral hemispheres were evaluated by light and fluorescent microscopy. PGE₂content was compared between genotypes and hemispheres after MCAO and MCAO and 6 hours reperfusion. Regional cerebral blood flow was measured during MCAO and phosphorylation of relevant MAPKs in brain protein homogenates was measured by Western analysis after 6 hours of reperfusion.</p> <p>Results</p> <p>Neuronal cPLA₂α protein increased by 2-fold immediately after MCAO and returned to pre-MCAO levels after 2 hours reperfusion. Neuronal cyclooxygenase-2 induction and PGE₂concentration were greater in cPLA₂α^+/+compared to cPLA₂α^-/-ischemic cortex. Neuronal swelling in ischemic regions was significantly greater in the cPLA₂α^+/+than in cPLA₂α^-/-brains (+/+: 2.2 ± 0.3 fold vs. -/-: 1.7 ± 0.4 fold increase; <it>P </it>< 0.01). The increase in reactive oxygen species following 2 hours of ischemia was also significantly greater in the cPLA₂α^+/+ischemic core than in cPLA₂α^-/-(+/+: 7.12 ± 1.2 fold vs. -/-: 3.1 ± 1.4 fold; <it>P </it>< 0.01). After 6 hours of reperfusion ischemic cortex of cPLA₂α^+/+, but not cPLA₂α^-/-, had disruption of neuron morphology and decreased PGE₂content. Phosphorylation of the MAPKs-p38, ERK 1/2, and MEK 1/2-was significantly greater in cPLA₂a^+/+than in cPLA₂α^-/-ischemic cortex 6 hours after reperfusion.</p> <p>Conclusions</p> <p>These results indicate that cPLA₂α modulates the earliest molecular and injury responses after cerebral ischemia and have implications for the potential clinical use of cPLA₂α inhibitors.</p