As interest in natural capital grows and society increasingly recognizes the value of biodiversity, we must discuss how ecosystem observations to detect changes in biodiversity can be sustained ...through collaboration across regions and sectors. However, there are many barriers to establishing and sustaining large-scale, fine-resolution ecosystem observations. First, comprehensive monitoring data on both biodiversity and possible anthropogenic factors are lacking. Second, some
ecosystem observations cannot be systematically established and maintained across locations. Third, equitable solutions across sectors and countries are needed to build a global network. Here, by examining individual cases and emerging frameworks, mainly from (but not limited to) Japan, we illustrate how ecological science relies on long-term data and how neglecting basic monitoring of our home planet further reduces our chances of overcoming the environmental crisis. We also discuss emerging techniques and opportunities, such as environmental DNA and citizen science as well as using the existing and forgotten sites of monitoring, that can help overcome some of the difficulties in establishing and sustaining ecosystem observations at a large scale with fine resolution. Overall, this paper presents a call to action for joint monitoring of biodiversity and anthropogenic factors, the systematic establishment and maintenance of
observations, and equitable solutions across sectors and countries to build a global network, beyond cultures, languages, and economic status. We hope that our proposed framework and the examples from Japan can serve as a starting point for further discussions and collaborations among stakeholders across multiple sectors of society. It is time to take the next step in detecting changes in socio-ecological systems, and if monitoring and observation can be made more equitable and feasible, they will play an even more important role in ensuring global sustainability for future generations. This article is part of the theme issue 'Detecting and attributing the causes of biodiversity change: needs, gaps and solutions'.
Increasing evidence has demonstrated that emotional states and intestinal conditions are inter-connected in so-called “brain–gut interactions.” Indeed, many psychiatric disorders are accompanied by ...gastrointestinal symptoms, such as the irritable bowel syndrome (IBS). However, the functional connection remains elusive, partly because there are few useful experimental animal models. Here, we focused on a highly validated animal model of stress-induced psychiatric disorders, such as depression, known as the chronic vicarious social defeat stress (cVSDS) model mice, which we prepared using exposure to repeated psychological stress, thereafter examining their intestinal conditions. In the charcoal meal test and the capsaicin-induced hyperalgesia test, cVSDS model mice showed a significantly higher intestinal transit ratio and increased visceral pain-related behaviors, respectively. These changes persisted over one month after the stress session. On the other hand, the pathological evaluations of the histological and inflammatory scores of naive and cVSDS model mice did not differ. Furthermore, keishikashakuyakuto—a kampo medicine clinically used for the treatment of IBS—normalized the intestinal motility change in cVSDS model mice. Our results indicate that cVSDS model mice present IBS-like symptoms such as chronic intestinal peristaltic changes and abdominal hyperalgesia without organic lesion. We therefore propose the cVSDS paradigm as a novel animal model of IBS with wide validity, elucidating the correlation between depressive states and intestinal abnormalities.
Disulfiram is an FDA approved drug for the treatment of alcoholism. The drug acts by inhibiting aldehyde dehydrogenase, an enzyme essential to alcohol metabolism. However, a recent study has ...demonstrated that disulfiram also potently inhibits the cytoplasmic protein FROUNT, a common regulator of chemokine receptor CCR2 and CCR5 signaling. Several studies have reported that chemokine receptors are associated with the regulation of emotional behaviors in rodents, such as anxiety. Therefore, this study was performed to clarify the effect of disulfiram on emotional behavior in rodents. The anxiolytic-like effects of disulfiram were investigated using an elevated plus-maze (EPM) test, a typical screening model for anxiolytics. Disulfiram (40 or 80 mg/kg) significantly increased the amount of time spent in the open arms of the maze and the number of open arm entries without affecting the total open arms entries. Similar results were obtained in mice treated with a selective FROUNT inhibitor, disulfiram-41 (10 mg/kg). These disulfiram-associated behavioral changes were similar to those observed following treatment with the benzodiazepine anxiolytic diazepam (1.5 mg/kg). Moreover, disulfiram (40 mg/kg) significantly and completely attenuated increased extracellular glutamate levels in the prelimbic-prefrontal cortex (PL-PFC) during stress exposure on the elevated open-platform. However, no effect in the EPM test was seen following administration of the selective aldehyde dehydrogenase inhibitor cyanamide (40 mg/kg). In contrast to diazepam, disulfiram caused no sedation effects in the open-field, coordination disorder on a rotarod, or amnesia in a Y-maze. This is the first report suggesting that disulfiram produces anxiolytic-like effects in rodents. We found that the presynaptic inhibitory effects on glutaminergic neurons in the PL-PFC may be involved in its underlying mechanism. Disulfiram could therefore be an effective and novel anxiolytic drug that does not produce benzodiazepine-related adverse effects, such as amnesia, coordination disorder, or sedation, as found with diazepam. We propose that the inhibitory activity of disulfiram against FROUNT function provides an effective therapeutic option in anxiety.
Introduction 5-aminolevulinic acid (ALA) is a precursor of heme and is involved in mitochondrial activation. It has been suggested that mitochondrial dysfunction in the brain is associated with ...chronic fatigue. To clarify the anti-fatigue effect of ALA, we used the established chronic fatigue model mice and examined the effects of ALA on fatigue and noradrenaline (NA) level in the frontal cortex (FCX).Methods Female C57BL/6N mice were orally given ALA hydrochloride or DW for 8 weeks. The fatigue model mice were developed by housing them in a cage filled with water to a height of 1.5 cm for 4 days. The fatigue was evaluated using the running distance in the treadmill test. After the test, their brains were quickly dissected and NA in the FCX were quantified by HPLC.Results and Discussion The running distance in the treadmill test were significantly reduced in the fatigue group. In addition, the running distance in the ALA-treated fatigue group was significantly increased as compared with DW-treated fatigue group. In the fatigue group, NA contents in the FCX were significantly decreased and ALA treatment canceled it. These results suggested that chronic ALA treatment produced the anti-fatigue effect and the protective effects on NA neurons in the FCX which may be involved in the mechanisms of the effect of ALA.
Recent study has demonstrated that anti-alcoholism drug disulfiram (DSF) inhibits chemokine receptor-mediated migration signals. Several studies have reported that the chemokine receptors are ...associated with emotion regulation. Therefore, this study was performed to clarify the effect of DSF on emotional behavior in rodents.Male ICR mice were used. In the elevated plus-maze test, a screening model for anxiolytics, DSF (40 mg/kg, i.p.) significantly produced the increases in the percentage of time spent on the open-arms without any effects on the total open arms entries. These behavioral changes were similar to that observed for the benzodiazepine anxiolytics diazepam (1.5 mg/kg, s.c.). In contrast to diazepam, DSF produced no effects on the spontaneous locomotor activity in mice. On the other hand, in the rotarod test, diazepam significantly increased the number of falls, suggesting the coordination disorder, whereas DSF produced no effects. Furthermore, DSF decreased noradrenaline content and increased dopamine content in mice amygdala.This is the first report suggesting that DSF produced the anxiolytic-like effects in rodents. We proposed that DSF could be an effective novel anxiolytic drug without the coordination disorder found in diazepam, and that the monoamine content changes in amygdala may be involved in its underlying mechanism.
Introduction 5-aminolevulinic acid (ALA) is a precursor of heme and is involved in mitochondrial activation. It has been suggested that mitochondrial dysfunction in the brain is associated with ...chronic fatigue. To clarify the anti-fatigue effect of ALA, we used the established chronic fatigue model mice and examined the effects of ALA on fatigue and noradrenaline (NA) level in the frontal cortex (FCX).Methods Female C57BL/6N mice were orally given ALA hydrochloride or DW for 8 weeks. The fatigue model mice were developed by housing them in a cage filled with water to a height of 1.5 cm for 4 days. The fatigue was evaluated using the running distance in the treadmill test. After the test, their brains were quickly dissected and NA in the FCX were quantified by HPLC.Results and Discussion The running distance in the treadmill test were significantly reduced in the fatigue group. In addition, the running distance in the ALA-treated fatigue group was significantly increased as compared with DW-treated fatigue group. In the fatigue group, NA contents in the FCX were significantly decreased and ALA treatment canceled it. These results suggested that chronic ALA treatment produced the anti-fatigue effect and the protective effects on NA neurons in the FCX which may be involved in the mechanisms of the effect of ALA.
Recent study has demonstrated that anti-alcoholism drug disulfiram (DSF) inhibits chemokine receptor-mediated migration signals. Several studies have reported that the chemokine receptors are ...associated with emotion regulation. Therefore, this study was performed to clarify the effect of DSF on emotional behavior in rodents.Male ICR mice were used. In the elevated plus-maze test, a screening model for anxiolytics, DSF (40 mg/kg, i.p.) significantly produced the increases in the percentage of time spent on the open-arms without any effects on the total open arms entries. These behavioral changes were similar to that observed for the benzodiazepine anxiolytics diazepam (1.5 mg/kg, s.c.). In contrast to diazepam, DSF produced no effects on the spontaneous locomotor activity in mice. On the other hand, in the rotarod test, diazepam significantly increased the number of falls, suggesting the coordination disorder, whereas DSF produced no effects. Furthermore, DSF decreased noradrenaline content and increased dopamine content in mice amygdala.This is the first report suggesting that DSF produced the anxiolytic-like effects in rodents. We proposed that DSF could be an effective novel anxiolytic drug without the coordination disorder found in diazepam, and that the monoamine content changes in amygdala may be involved in its underlying mechanism.
An optical phase shifter based on phase-change materials (PCMs) is a promising building block of quantum photonic integrated circuits (QPICs) operating at mid-infrared (MIR) wavelengths on a Si ...photonics platform. In this article, we propose a record low-loss non-volatile PCM phase shifter operating at MIR wavelengths based on Ge2Sb2Te3S2 (GSTS), which is a new Se-free widegap PCM. On the basis of the refractive index and extinction coefficient spectra measured by spectroscopic ellipsometry, we show that GSTS has excellent material properties for optical phase shifters. By using GSTS in the MIR range, the optical absorption of a PCM phase shifter can be considerably reduced. We achieved an optical loss of 0.29 dB for a <inline-formula> <tex-math notation="LaTeX">\pi </tex-math></inline-formula> phase shift, which is the lowest loss ever reported for a PCM phase shifter integrated with a Si waveguide. We also demonstrate the non-volatile resonance wavelength tuning of a microring resonator (MRR) with a GSTS phase shifter and the optically induced phase transition of a GSTS phase shifter based on laser irradiation.
Long-term infection of the stomach with Helicobacter pylori can cause gastric cancer. However, the mechanisms by which the bacteria adapt to the stomach environment are poorly understood. Here, we ...show that a small non-coding RNA of H. pylori (HPnc4160, also known as IsoB or NikS) regulates the pathogen's adaptation to the host environment as well as bacterial oncoprotein production. In a rodent model of H. pylori infection, the genomes of bacteria isolated from the stomach possess an increased number of T-repeats upstream of the HPnc4160-coding region, and this leads to reduced HPnc4160 expression. We use RNA-seq and iTRAQ analyses to identify eight targets of HPnc4160, including genes encoding outer membrane proteins and oncoprotein CagA. Mutant strains with HPnc4160 deficiency display increased colonization ability of the mouse stomach, in comparison with the wild-type strain. Furthermore, HPnc4160 expression is lower in clinical isolates from gastric cancer patients than in isolates derived from non-cancer patients, while the expression of HPnc4160's targets is higher in the isolates from gastric cancer patients. Therefore, the small RNA HPnc4160 regulates H. pylori adaptation to the host environment and, potentially, gastric carcinogenesis.
Group A Streptococcus (GAS) secretes deoxyribonucleases and evades neutrophil extracellular killing by degrading neutrophil extracellular traps (NETs). However, limited information is currently ...available on the interaction between GAS and NETs in the pathogenicity of GAS pharyngitis. In this study, we modified a mouse model of GAS pharyngitis and revealed an essential role for DNase in this model. After intranasal infection, the nasal mucosa was markedly damaged near the nasal cavity, at which GAS was surrounded by neutrophils. When neutrophils were depleted from mice, GAS colonization and damage to the nasal mucosa were significantly decreased. Furthermore, mice infected with deoxyribonuclease knockout GAS mutants (∆spd, ∆endA, and ∆sdaD2) survived significantly better than those infected with wild-type GAS. In addition, the supernatants of digested NETs enhanced GAS-induced cell death in vitro. Collectively, these results indicate that NET degradation products may contribute to the establishment of pharyngeal infection caused by GAS.
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