Re‐establishing extirpated wildlife—or “rewilding”—is touted as a way to restore biodiversity and ecosystem processes, but we lack real‐world examples of this process, particularly in Southeast Asia. Here, we use a decade of aggregated camera trap data, N‐mixture occupancy models, and input from local wildlife experts to describe the unassisted recolonization of two native large herbivores in Singapore. Sambar deer (Rusa unicolor) escaped from captivity (in private or public zoos) in the 1970s and contemporary camera trap data show they have only colonized nearby forest fragments and their abundance remains low. Wild pigs (Sus scrofa), in contrast, naturally recolonized by swimming from Malaysia in the 1990s and have rapidly expanded their range and abundance across Singapore. While wild pigs have not recolonized all viable green spaces yet, their trajectory indicates they soon will. We also note that a third ungulate, the muntjac deer (Muntiacus muntjak), was captured in camera trapping in 2014 and 2015 but was never recorded afterward despite increased sampling effort, and thus we do not focus on their presumably unsuccessful recolonization. The divergent rewilding trajectories between sambar deer and wild pigs suggest different conservation outcomes and management requirements. Sambar deer may restore lost plant–animal interactions such as herbivory and seed dispersal without requiring significant management. Wild pigs, in contrast, have reached high numbers rapidly and may require active management to avoid hyperabundance and negative ecological impacts in regions, such as Singapore that lack both hunting and large predators.
Consumption of a Western-style diet (WS-diet), high in saturated fat and added sugar, is associated with increased depression risk. However, the physiological mechanisms underlying the relationship requires elucidation. Diet can alter tryptophan metabolism along the kynurenine pathway (KP), potentially linking inflammation and depression. This study aimed to examine whether urinary inflammatory markers and KP metabolites differed according to WS-diet consumption and depression severity. Depression symptoms and habitual WS-diet consumption were assessed in 169 healthy adults aged 17–35 recruited from two experimental studies. Targeted metabolomics profiling of seven KP metabolites, ELISA-based assays of interleukin-6 (IL-6) and C-reactive protein (CRP) were performed using urine samples collected from the participants. Parametric tests were performed for group comparison and associations analysis. Multilevel mixed-effect modelling was applied to control for biases. Higher intake of WS-diet was associated with lower levels of neuroprotective kynurenic acid (KA; R = −0.17, p = 0.0236). There were no differences in IL-6 or CRP across diet groups (p > 0.05). Physical activity had negative associations with most KP metabolites. Mixed-effects regression analysis showed the glutamatergic inhibitor, KA, was the only biomarker to have a significant association with depression symptoms in a model adjusted for demographic and lifestyle variables: a unit increase in KA was associated with 0.21 unit decrease in Depression Anxiety and Stress Scale-21 depression score (p = 0.009). These findings suggest that urinary KA is associated with both habitual WS-diet intake, and levels of depression symptoms, independent of inflammation. Findings support the role of neuroprotection and glutamatergic modulation in depression. We propose that KA may act as endogenous glutamatergic inhibition in regulating depression severity in the absence of inflammation. Further comparison with blood-based markers will assist in validating the utility of non-invasive urine samples for measuring KP metabolites.
The metabolism of tryptophan through the kynurenine pathway (KP) has been increasingly recognised in contributing to disease progression in the autoimmune and inflammatory disease multiple sclerosis (MS). In this review, the roles of inflammation and the KP are recontextualised to better understand the aetiology of the neuropsychiatric symptoms (depression, postpartum depression, suicidality, fatigue and cognitive dysfunction) in MS. These symptoms will be discussed in the context of cytokine-induced sickness behaviours, KP activation and levels of neurotoxicity and neuroprotection in MS. In particular, there will be emphasis on how neuropsychiatric symptoms in MS occur against the shared background of inflammation and KP dysregulation. The discourse of this review aims to promote future research in elucidating KP mechanisms in MS that would inevitably lead to more targeted treatment options for neuropsychiatric symptoms and disease progression.
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