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Previous research on how unemployment influences house prices is limited by employing a symmetric approach to cointegration. The symmetric method masks the underlying link between unemployment and housing prices. This study examines the impact of unemployment on house prices across 20 Organisation for Economic Co-operation and Development (OECD) economies by using an asymmetric approach to cointegration. The current research additionally leverages Hatemi-J causality to bolster the asymmetric causation between unemployment and house prices. According to the symmetric approach, 13 of the 20 OECD economies in the short run and 9 economies in the long run have at least one lagged significant coefficient associated with the LnUN variable. The asymmetric effects demonstrate a significant short- and long-term asymmetric association between unemployment and house prices in the instance of 16 OECD nations. The Hatemi-J causality results demonstrate that in each of the selected economies, there is evidence of an asymmetric bidirectional causal relationship between unemployment and house prices, as shown by at least one significant variable that runs either from unemployment to house prices or from house prices to unemployment. [ABSTRACT FROM AUTHOR]

Escalating with rapid population growth and urban sprawl, unregulated Municipal Solid Waste (MSW) poses serious threats to public health and environmental safety. The current study examines the performance and physiological features of MSW and evaluates its potential as a renewable energy source in the Bannu region of Khyber Pakhtunkhwa (KPK) province, Pakistan. Depending on the average MSW generation of 0.439 kg/capita/day, the daily production of MSW in the city can reach up to 2000 tons/day. However, its safe treatment is inhibited by the lack of planning, public services, political determination, and public awareness. Various samples of MSW were collected for characterization/segregation purposes. Amounts of MSW in Bannu have been found to be declining through the use of decaying material, plastic bags of nylon, cloth, nappy, and paper. A close assessment of the recycling potential of MSW was performed by obtaining temperature values from combustion. The maximum energy output from MSW combustion was found to be 13369.935 kJ/kg. The power output of 44.29 MW is continuously tested from 2000 ton-of-MSW/day. The results of this study are expected to help policymakers develop management strategies for MSW in order to utilize these wastes for power generation. [ABSTRACT FROM AUTHOR]

Borders in the globalized world are the converging points of not only the globalizing forces of security, trade and migration but also the related conflicting identities, ideologies and civilizations. Just like its spatial connotations that relate to territorial zones, borderlands can also mean phenomena that create psychological borders by means by the enactment of social policy, and ideology. In that case, people of either sides of the border may struggle with the question of identity. Using the psychological borders-related theoretical underpinnings, provided by Gloria Anzaldua, the current study attempts to trace the contribution of border-crossing and globalization in the treatment of such people by the host societies, as depicted in H. M. Naqvi's novel Home Boy. Since physical as well as psychological borders are created for the security of a nation, the outsiders are often thought of as a threat to the security of that very nation. The study finds that the host societies question the identities and cultures of these people in the name of the so-called human welfare and security. [ABSTRACT FROM AUTHOR]

The current study was undertaken to unveil the protective effects of Luteolin, a natural flavonoid, against amyloid-beta (Aβ1–42)-induced neuroinflammation, amyloidogenesis, and synaptic dysfunction in mice. For the development of an AD mouse model, amyloid-beta (Aβ1–42, 5 μL/5 min/mouse) oligomers were injected intracerebroventricularly (i.c.v.) into mice's brain by using a stereotaxic frame. After that, the mice were treated with Luteolin for two weeks at a dose of 80 mg/kg/day. To monitor the biochemical changes, we conducted western blotting and immunofluorescence analysis. According to our findings, the infusion of amyloid-beta activated c-Jun N-terminal kinases (p-JNK), p38 mitogen-activated protein kinases, glial fibrillary acidic protein (GFAP), and ionized calcium adaptor molecule 1 (Iba-1) in the cortex and hippocampus of the experimental mice; these changes were significantly inhibited in Aβ1–42 + Luteolin-treated mice. Likewise, we also checked the expression of inflammatory markers, such as p-nuclear factor-kB p65 (p-NF-kB p65 (Ser536), tissue necrosis factor (TNF-α), and Interleukin1-β (IL-1β), in Aβ1–42-injected mice brain, which was attenuated in Aβ1–42 + Luteolin-treated mice brains. Further, we investigated the expression of pro- and anti-apoptotic cell death markers such as Bax, Bcl-2, Caspase-3, and Cox-2, which was significantly reduced in Aβ1–42 + Lut-treated mice brains compared to the brains of the Aβ-injected group. The results also indicated that with the administration of Aβ1–42, the expression levels of β-site amyloid precursor protein cleaving enzyme (BACE-1) and amyloid-beta (Aβ1–42) were significantly enhanced, while they were reduced in Aβ1–42 + Luteolin-treated mice. We also checked the expression of synaptic markers such as PSD-95 and SNAP-25, which was significantly enhanced in Aβ1–42 + Lut-treated mice. To unveil the underlying factors responsible for the protective effects of Luteolin against AD, we used a specific JNK inhibitor, which suggested that Luteolin reduced Aβ-associated neuroinflammation and neurodegeneration via inhibition of JNK. Collectively, our results indicate that Luteolin could serve as a novel therapeutic agent against AD-like pathological changes in mice. [ABSTRACT FROM AUTHOR]

Herein, we assayed the antioxidant and anti-inflammatory potential of caffeine in a lipopolysaccharide (LPS)-injected mouse model of neurodegeneration and synaptic impairment. For this purpose, LPS was injected for two weeks on an alternate-day basis (250 µg/kg/i.p. for a total of seven doses), while caffeine was injected daily for four weeks (30 mg/kg/i.p/four weeks). According to our findings, there was a significant increase in the level of reactive oxygen species (ROS), as evaluated from the levels of lipid peroxidation (LPO) and ROS assays. Also, we evaluated the expression of nuclear factor erythroid-2-related factor 2 (Nrf2) and the enzyme hemeoxygenase 1 (HO-1) in the mouse groups and found reduced expression of Nrf2 and HO-1 in the LPS-treated mice brains, but they were markedly upregulated in the LPS + caffeine co-treated group. We also noted enhanced expression of toll-Like Receptor 4 (TLR4), phospho-nuclear factor kappa B (p-NF-kB), and phospho-c-Jun n-terminal kinase (p-JNK) in the LPS-treated mice brains, which was significantly reduced in the LPS + caffeine co-treated group. Moreover, we found enhanced expression of Bcl2-associated X, apoptosis regulator (Bax), and cleaved caspase-3, and reduced expression of B-cell lymphoma 2 (Bcl-2) in the LPS-treated group, which were markedly reversed in the LPS + caffeine co-treated group. Furthermore, we analyzed the expression of synaptic proteins in the treated groups and found a marked reduction in the expression of synaptic markers in the LPS-treated group; these were significantly upregulated in the LPS + caffeine co-treated group. In summary, we conclude that caffeine may inhibit LPS-induced oxidative stress, neuroinflammation, and synaptic dysfunction. [ABSTRACT FROM AUTHOR]

Cerebral ischemia is one of the leading causes of neurological disorders. The exact molecular mechanism related to chronic unilateral cerebral ischemia-induced neurodegeneration and memory deficit has not been precisely elucidated. In this study, we examined the effect of chronic ischemia on the induction of oxidative stress and c-Jun N-terminal kinase-associated detrimental effects and unveiled the inhibitory effect of specific JNK inhibitor (SP600125) on JNK-mediated brain degeneration in adult mice. Our behavioral, biochemical, and immunofluorescence studies revealed that chronic ischemic injuries sustained increased levels of oxidative stress-induced active JNK for a long time, whereas SP600125 significantly reduced the elevated level of active JNK and further regulated Nrf2/HO-1 and NF- κ B signaling, which have been confirmed in vivo. Neuroinflammatory mediators and loss of neuronal cells was significantly reduced with the administration of SP600125. Ischemic brain injury caused synaptic dysfunction and memory impairment in mice. However, these were significantly improved with SP600125. On the whole, these findings suggest that elevated ROS-mediated JNK is a key mediator in chronic ischemic conditions and has a crucial role in neuroinflammation, neurodegeneration, and memory dysfunction. Our findings suggest that chronic oxidative stress associated JNK would be a potential target in time-dependent studies of chronic ischemic conditions induced brain degeneration., Competing Interests: The authors declared no competing financial interests., (Copyright © 2020 Muhammad Sohail Khan et al.)