BACKGROUND Development assistance for health (DAH) is one of the most important means for Japan to promote diplomacy with developing countries and contribute to the international community. This study, for the first time, estimated the gross disbursement of Japan's DAH from 2012 to 2016 and clarified its flows, including source, aid type, channel, target region, and target health focus area. METHODS Data on Japan Tracker, the first data platform of Japan's DAH, were used. The DAH definition was based on the Organisation for Economic Co-operation and Development's (OECD) sector classification. Regarding core funding to non-health-specific multilateral agencies, we estimated DAH and its flows based on the OECD methodology for calculating imputed multilateral official development assistance (ODA). RESULTS Japan's DAH was estimated at 1472.94 (2012), 823.15 (2013), 832.06 (2014), 701.98 (2015), and 894.57 million USD (2016) in constant prices of 2016. Multilateral agencies received the largest DAH share of 44.96-57.01% in these periods, followed by bilateral grants (34.59-53.08%) and bilateral loans (1.96-15.04%). Ministry of Foreign Affairs (MOFA) was the largest contributors to the DAH (76.26-82.68%), followed by Ministry of Finance (MOF) (10.86-16.25%). Japan's DAH was most heavily distributed in the African region with 41.64-53.48% share. The channel through which the most DAH went was Global Fund to Fight AIDS, Tuberculosis, and Malaria (20.04-34.89%). Between 2012 and 2016, approximately 70% was allocated to primary health care and the rest to health system strengthening. CONCLUSIONS With many major high-level health related meetings ahead, coming years will play a powerful opportunity to reevaluate DAH and shape the future of DAH for Japan. We hope that the results of this study will enhance the social debate for and contribute to the implementation of Japan's DAH with a more efficient and effective strategy.Neutrophil chemotaxis plays a vital role in human immune system. Compared with traditional cell migration assays, the emergence of microfluidics provides a new research platform of cell chemotaxis study due to the advantages of visualization, precise control of chemical gradient, and small consumption of reagents. A series of microfluidic devices have been fabricated to study the behavior of neutrophils exposed on controlled, stable, and complex profiles of chemical concentration gradients. In addition, microfluidic technology offers a promising way to integrate the other functions, such as cell culture, separation and analysis into a single chip. Therefore, an overview of recent developments in microfluidic-based neutrophil chemotaxis studies is presented. Meanwhile, the strength and drawbacks of these devices are compared.BACKGROUND Increased circulating levels of tumor necrosis factor (TNF) are associated with greater risk of impaired neurodevelopment after preterm birth. In this study, we tested the hypothesis that systemic TNF inhibition, using the soluble TNF receptor Etanercept, would attenuate neuroinflammation in preterm fetal sheep exposed to lipopolysaccharide (LPS). METHODS Chronically instrumented preterm fetal sheep at 0.7 of gestation were randomly assigned to receive saline (control; n = 7), LPS infusion (100 ng/kg i.v. over 24 h then 250 ng/kg/24 h for 96 h plus 1 μg LPS boluses at 48, 72, and 96 h, to induce inflammation; n = 8) or LPS plus two i.v. infusions of Etanercept (2 doses, 5 mg/kg infused over 30 min, 48 h apart) started immediately before LPS-exposure (n = 8). Sheep were killed 10 days after starting infusions, for histology. RESULTS LPS boluses were associated with increased circulating TNF, interleukin (IL)-6 and IL-10, electroencephalogram (EEG) suppression, hypotension, tachycardia, and increased carotid artery perfusion (P  less then  0.05 vs. control). In the periventricular and intragyral white matter, LPS exposure increased gliosis, TNF-positive cells, total oligodendrocytes, and cell proliferation (P  less then  0.05 vs control), but did not affect myelin expression or numbers of neurons in the cortex and subcortical regions. Etanercept delayed the rise in circulating IL-6, prolonged the increase in IL-10 (P  less then  0.05 vs. LPS), and attenuated EEG suppression, hypotension, and tachycardia after LPS boluses. Histologically, Etanercept normalized LPS-induced gliosis, and increase in TNF-positive cells, proliferation, and total oligodendrocytes. CONCLUSION TNF inhibition markedly attenuated white matter gliosis but did not affect mature oligodendrocytes after prolonged systemic inflammation in preterm fetal sheep. Further studies of long-term brain maturation are now needed.Traumatic brain injury (TBI) is one of the leading causes of fatality and disability worldwide. Despite its high prevalence, effective treatment strategies for TBI are limited. Traumatic brain injury induces structural and functional alterations of astrocytes, the most abundant cell type in the brain. As a way of coping with the trauma, astrocytes respond in diverse mechanisms that result in reactive astrogliosis. Astrocytes are involved in the physiopathologic mechanisms of TBI in an extensive and sophisticated manner.  https://www.selleckchem.com/products/AdipoRon.html  Notably, astrocytes have dual roles in TBI, and some astrocyte-derived factors have double and opposite properties. Thus, the suppression or promotion of reactive astrogliosis does not have a substantial curative effect. In contrast, selective stimulation of the beneficial astrocyte-derived molecules and simultaneous attenuation of the deleterious factors based on the spatiotemporal-environment can provide a promising astrocyte-targeting therapeutic strategy. In the current review, we describe for the first time the specific dual roles of astrocytes in neuronal plasticity and reconstruction, including neurogenesis, synaptogenesis, angiogenesis, repair of the blood-brain barrier, and glial scar formation after TBI. We have also classified astrocyte-derived factors depending on their neuroprotective and neurotoxic roles to design more appropriate targeted therapies. Video Abstract.