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We found differences in the structure and abundance of the three mosquito assemblages. The species assemblage of the highly anthropized site was significantly different from the other sites, and the relative abundance of the assemblages increased with landscape anthropization. Our results suggest that landscape anthropization alters the composition and structure of mosquito assemblages, modifying the abundance and species richness of mosquitoes associated with sylvatic ecosystems. This could support the hypothesis of intermediate disturbance that suggests the diversity is maximized when late and early successional species coexist in these ecosystems. This information is essential to understand the ecology of potential sylvatic vectors and the environmental factors that are involved in the emergence and re-emergence of mosquito-borne diseases.Schistosomiasis is a severe chronic disease caused by parasitic worms of the genus Schistosoma. Recent studies indicate that schistosomes can secrete extracellular vesicles (EVs), which play important regulatory roles in many biological processes. However, the mechanisms underlying EV biogenesis in schistosomes are poorly understood. In this study, we performed bioinformatic analyses and identified several genes putatively involved in EV biogenesis in Schistosoma japonicum, which were then confirmed by PCR. Quantitative transcriptional profiles of the selected genes indicated that they were differentially expressed in male and female worms as well as in the different developmental stages of S. japonicum. Thus, the highest expression of VAMP3 was detected in cercariae, whereas that of ARF6 was detected in eggs. RAB11A and the Syntenin-encoding gene SDCBP were highly expressed in 14-day schistosomula and VPS4A and RAB27A were highly expressed in 35-day-old adult schistosomes. The expression of RAB11A, CHMP4C, VPS4A, and SDCBP was higher in male worms, whereas that of ARF6, VAMP3, and RAB27A was higher in female worms. Our results are expected to provide important clues for understanding the role of EV biogenesis in S. japonicum development.Chagas disease is caused by Trypanosoma cruzi, and it is an important cause of morbidity and mortality in Latin America. There are no vaccines, and the chemotherapy available to treat this infection has serious side effects. In a search for alternative treatments, we determined the in vitro susceptibility of epimastigote and trypomastigote forms of T. cruzi and the cytotoxic effects on peripheral blood mononuclear cells (PBMCs) of ethanolic extracts obtained from six different plant species. The ethanolic extracts of Ageratina vacciniaefolia, Clethra fimbriata and Siparuna sessiliflora showed antiprotozoal activity against epimastigotes and low cytotoxicity in mammalian cells. However, only the ethanolic extract of C. fimbriata showed activity against T. cruzi trypomastigotes, and it had low cytotoxicity in PBMCs. An analysis on the phytochemical composition of C. fimbriata extract showed that its metabolites were primarily represented by two families of compounds flavonoids and terpenoids. Lastly, we analyzed whether the A. vacciniaefolia, C. fimbriata, or S. sessiliflora ethanolic extracts induced IFN-γ or TNF-α production. Significantly, ethanolic extracts of C. fimbriata induced TNF-α production and S. sessiliflora induced both cytokines. In addition, C. fimbriata and S. sessiliflora induced the simultaneous secretion of IFN-γ and TNF-α in CD8+ T cells. The antiprotozoal and immunomodulatory activity of C. fimbriata may be related to the presence of flavonoid and triterpene compounds in the extract. Thus, these findings suggest that C. fimbriata may represent a valuable source of new bioactive compounds for the therapeutic treatment of Chagas disease that combines trypanocidal activity with the capacity to boost the immune response.Current treatment options for Parkinson's disease (PD) typically aim to replace dopamine, and hence only provide symptomatic relief. However, in the long run, this approach alone loses its efficacy as it is associated with debilitating side effects. Hence there is an unmet clinical need for addressing levodopa resistant symptoms, and an urgency to develop therapies that can halt or prevent the course of PD. The premise that α-syn can transmit from cell-to-cell in a prion like manner has opened up the possibility for the use of immunotherapy in PD. There is evidence for inflammation in PD as is evidenced by microglial activation, as well as the involvement of the peripheral immune system in PD, and peripheral inflammation can exacerbate dopaminergic degeneration as seen in animal models of the disease. However, mechanisms that link the immune system with PD are not clear, and the sequence of immune responses with respect to PD are still unknown. Nevertheless, our present knowledge offers avenues for the development of immune-based therapies for PD. In order to successfully employ such strategies, we must comprehend the state of the peripheral immune system during the course of PD. This review describes the developments in the field of both active and passive immunotherapies in the treatment of PD, and highlights the crucial need for future research for clarifying the role of inflammation and immunity in this debilitating disease.Receptor-interacting protein kinase 1 (RIPK1) is up-regulated in patients with neurodegenerative diseases. Our study aimed to explore the underlying mechanisms that involved in the neurotoxic function of RIPK1 in Parkinson's disease (PD). MPP+/MPTP-induced PD cellular and mice models were used in this study. The results showed that RIPK1 was high expressed and activated in MPP+-treated SH-SY5Y cells and MPTP-induced PD mice. Overexpression of RIPK1 facilitated cell apoptosis, necrosis, inflammation response, ROS production and mitochondrial dysfunction in MPP+- treated SH-SY5Y cells, while the RIPK1 inhibitor Nec-1s has an opposite effect. In addition, the Apoptosis-signaling kinase-1 (ASK1)/c-Jun N-terminal kinase (JNK) signalling pathway was activated during the overexpression of RIPK1, and inhibiting the ASK1/JNK signal by the ASK1 inhibitor partially reversed the decline of cell viability, the increase of cell apoptosis, necrosis and inflammation induced by RIPK1 overexpression in MPP+-treated SH-SY5Y cells. Further studies suggested that the inhibition of RIPK1 by Nec-1s largely alleviated the behavioural impairment in PD mice. Hence, our study indicated that the RIPK1 inhibitor Nec-1s has neuroprotective effects against PD through inactivating the ASK1/JNK signalling pathway.The present study aimed to investigate the alterations of the GABAergic system in the laterodorsal nucleus (LDN) of the thalamus and the somatosensory cortex (SC) in an experimental model of absence seizure. HPK1-IN-2 cost The effects of pharmacological manipulation of both GABAA and GABAB receptor subunits in the LDN on the generation of spike-wave discharges (SWD) were evaluated. The experiments were carried out in four groups of both WAG/Rij and Wistar rats with 2 and 6 months of age. The expressions of various GABA receptor subunits were studied in the LDN and SC. Furthermore, recordings of unit activity from the LDN and electrocorticography were simultaneously monitored before, during, and after the application of GABAA and GABAB antagonists in the LDN. The generation of SWD in the older WAG/Rij rats was associated with significant alterations in the expression of GABAARα1, GABAARβ3, and GABABR2 subunits in the LDN as well as GABAARα1, GABAARβ3, GABAARγ2, and GABABR2 subunits in the SC. Furthermore, the occurrence of SWD was associated with a significant reduction of gene expression of GABAARα1 and increase of GABAARβ3 in the LDN as well as reduction of GABAARα1, GABAARβ3, GABAARγ2, and GABABR2 in the SC. The microionthophoretic application of the GABAA antagonist bicuculline resulted in a significant increase in the population firing rate of LDN neurons as well as the mean number and duration of SWD. The application of the GABAB antagonist CGP35348 significantly increased the population firing rate of LDN neurons but decreased the mean number of SWD. Our data indicate the regulatory effect of the GABAergic system of the LDN and SC in absence seizures.With increasing prevalence of lifestyle-related chronic diseases worldwide, understanding health behavior change and the development of successful interventions to support lifestyle modification is gaining increasing interest among politicians, scientists, therapists and patients alike. A number of health behavior change theories have been developed aiming at explaining health behavior change and understanding the domains that make change more likely. Until now, only few studies have taken into account automatic, implicit or non-cognitive aspects of behavior, including emotion and positive affect. Recent progress in the neuroscience of motivation and reward systems can provide further insights into the relevance of such domains. In this integrative review, we present a description of the possible motivation and reward systems (approach/wanting = pleasure; aversion/avoiding = relief; assertion/non-wanting = quiescence) involved in behavior change. Therefore, based on established theories encompassing both initiation and maintenance of behavior change, we create a flexible seven-stage behavior change process with three engagement phases (non-engagement, motivational engagement, executive engagement) and relate the motivation and reward systems to each of these stages. We propose that either appetitive (preferably) or aversive motivational salience is activated during motivational engagement, that learning leads to continued behavior and that assertive salience prevails when the new behavior has become habitual. We discuss under which circumstances these mechanisms and reward-motivation pathways are likely to occur and address potential shortcomings of our proposed theoretical framework. We highlight implications for future interventions aiming at lifestyle modification.Lysophosphatidic acid (LPA) is a potent signaling lipid, and state-dependent alterations in plasma LPA make it a promising diagnostic marker for various diseases. However, plasma LPA concentrations vary widely among reports, even under normal conditions. These variations can be attributed, at least in part, to the artificial metabolism of LPA after blood collection. Here, we aimed to develop an optimized plasma preparation method that reflects the concentration of LPA in the circulating blood. The main features of the devised method were suppression of both LPA production and degradation after blood collection by keeping whole blood samples at low temperature followed by the addition of an autotaxin inhibitor to plasma samples. Using this devised method, the LPA level did not change for 30 min after blood collection. Also, human and mouse LPA levels were found to be much lower than those previously reported, ranging from 40 to 50 nM with minimal variation across the individual. Finally, the increased accuracy made it possible to detect circadian rhythms in the levels of certain LPA species in mouse plasma. These results demonstrate the usefulness of the devised plasma preparation method to determine accurate plasma LPA concentrations.