BackgroundSleep deprivation (SD) leads to cognitive impairment. Neuroinflammation could be a significant contributing factor in the same. An increase in regional brain pro-inflammatory cytokines induces cognitive deficits, however, the magnitude of the effect under SD is not apparent. It is plausible that microglia activation could be involved in the SD-induced cognitive impairment by modulation of neuronal cell proliferation, differentiation, and brain-derived neuronal factor (BDNF) level. The present study aimed to evaluate the possible beneficial effect of minocycline in amelioration of spatial memory decline during SD by its anti-inflammatory and neuroprotective actions. We scrutinized the effect of minocycline on the inflammatory cytokine levels associated with glial cells (microglia and astrocytes) activity and neurogenesis markers crucial for behavioral functions during SD.MethodsMale Sprague-Dawley rats weighing 230–250 g were sleep deprived for 48 h using automated cage shaking apparatus. The spatial memory was tested using MWM apparatus immediately after completion of SD with and without minocycline. The animals were euthanized, blood was collected, and brain was extracted for neuroinflammation and neurogenesis studies. The set of experiments were also conducted with use of temozolomide, a neurogenesis blocker.ResultsMinocycline treatment increased the body weight, food intake, and spatial memory performance which declined during SD. It reduced the pro-inflammatory and increased the anti-inflammatory cytokine levels in hippocampus and plasma and inhibited the reactive gliosis in the hippocampus evidenced by improved cell count, morphology, and immunoreactivity. Additionally, minocycline administration promoted neurogenesis at different stages: proliferation (BrdU, Ki-67), differentiation (DCX) cells and growth factor (BDNF). However, no significant change was observed in maturation (NeuN) during SD. In addition, molecules related to behavior, inflammation, and neurogenesis were shown to be more affected after temozolomide administration during SD, and changes were restored with minocycline treatment. We observed a significant correlation of neurogenesis with microglial activation, cytokine levels, and spatial memory during SD.ConclusionThe present study demonstrated that the SD-induced decline in spatial memory, neuronal cells proliferation, differentiation, and BDNF level could be attributed to upregulation of neuroinflammatory molecules, and minocycline may be an effective intervention to counteract these changes.Graphical abstractMicroglial activation is involved in SD-induced changes in inflammatory molecules, neurogenesis, and spatial memory. Electronic supplementary materialThe online version of this article (10.1186/s12974-017-0998-z) contains supplementary material, which is available to authorized users.

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The United States Environmental Protection Agency held an international two-day workshop in June 2018 to deliberate possible performance targets for non-regulatory fine particulate matter (PM 2.5 ) and ozone (O 3 ) air sensors. The need for a workshop arose from the lack of any market-wide manufacturer requirement for Ozone documented sensor performance evaluations, the lack of any independent third party or government-based sensor performance certification program, and uncertainty among all users as to the general usability of air sensor data. A multi-sector subject matter expert panel was assembled to facilitate an open discussion on these issues with multiple stakeholders. This summary provides an overview of the workshop purpose, key findings from the deliberations, and considerations for future actions specific to sensors. Important findings concerning PM 2.5 and O 3 sensors included the lack of consistent performance indicators and statistical metrics as well as highly variable data quality requirements depending on the intended use. While the workshop did not attempt to yield consensus on any topic, a key message was that a number of possible future actions would be beneficial to all stakeholders regarding sensor technologies. These included documentation of best practices, sharing quality assurance results along with sensor data, and the development of a common performance target lexicon, performance targets, and test protocols.

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bPlasmodium vivax malaria, though benign, has now become a matter of concern due to recent reports of life-threatening severity and development of parasite resistance to different antimalarial drugs. The magnitude of the problem is still undetermined. The present study was undertaken to determine the in vivo efficacy of chloroquine (CQ) and chloroquine plus primaquine in P. vivax malaria in Kolkata and polymorphisms in the pvmdr1 and pvcrt-o genes. A total of 250 patients with P. vivax monoinfection were recruited and randomized into two groups, A and B; treated with chloroquine and chloroquine plus primaquine, respectively; and followed up for 42 days according to the WHO protocol of 2009. Data were analyzed using per-protocol analyses. T he burden of malaria caused by Plasmodium vivax has been greatly underappreciated in terms of both its clinical spectrum and incidence of disease (1, 2). P. vivax is the most widely distributed cause of malaria in the world; approximately 2.6 billion people are at risk, and 10 countries, including India, are at the highest risk of infection (3,4,5,6).P. vivax infections have been associated with mild symptoms, such as fever, headache, fatigue, chills, and musculoskeletal pain, and, in particular, paroxysms. Recently, however, severe complications, including renal failure, jaundice, acute respiratory distress syndrome, cerebral malaria, seizures, anemia, hyperparasitemia, thrombocytopenia, pulmonary edema, splenic rupture, and death, have been reported in exclusive association with P. vivax (7,8). The situation is further complicated by the emergence of resistance of the parasite to chloroquine (CQ).In most of the world, CQ remains the first-line treatment for patients with vivax malaria. In India, CQ was replaced by artemisinin combination therapy (ACT), a combination of artesunate and sulfadoxine-pyrimethamine, in 2010 for Plasmodium falciparum malaria, but for P. vivax malaria, CQ remains the first-line agent, along with primaquine (PQ) (0.25-mg/kg base) for 14 days under supervision or by detecting the glucose-6-phosphate dehydrogenase (G6PD) level. The first case of P. vivax resistance to CQ was reported in 1989 from Papua New Guinea (9). A higher rate of CQ-resistant P. vivax malaria, which exceeded 50%, was reported from different regions of Indonesia (10,11,12,13,14). Further sporadic cases were subsequently observed in the Philippines, Myanmar, Vietnam, Colombia, Guyana, and Turkey (15). Similar reports are also available from Madagascar (16) and Ethiopia (17). Despite these reports, it remains difficult to estimate the worldwide prevalence of P. vivax resistance to CQ. In India, the first case of CQ-resistant P. vivax malaria was reported from Assam in 1995 (18) and then in Mumbai (19) and Gujarat (20).The molecular mechanisms underlying CQ resistance in P. vivax malaria remain unknown and may involve multigenic loci, but two genes orthologous to the pfmdr1 and pfcrt genes that encode putative transporters, pvmdr1 (21) and pvcrt-o (22), have been suspected as possi...

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