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Many sensors have to be used simultaneously for multipoint carbon dioxide (CO2) observation. All the sensors should be calibrated in advance, but this is a time-consuming process. To seek a simplified calibration method, we used four commercial CO2 sensor models and characterized their output tendencies against ambient temperature and length of use, in addition to offset characteristics. We used four samples of standard gas with different CO2 concentrations (0, 407, 1,110, and 1,810 ppm). The outputs of K30 and AN100 models showed linear relationships with temperature and length of use. Calibration coefficients for sensor models were determined using the data from three individual sensors of the same model to minimize the relative RMS error. When the correction was applied to the sensors, the accuracy of measurements improved significantly in the case of the K30 and AN100 units. In particular, in the case of K30 the relative RMS error decreased from 24% to 4%. Hence, we have chosen K30 for developing a portable CO2 measurement device (10 × 10 × 15 cm, 900 g). Data of CO2 concentration, measurement time and location, temperature, humidity, and atmospheric pressure can be recorded onto a Secure Digital (SD) memory card. The CO2 concentration in a high-school lecture room was monitored with this device. The CO2 data, when corrected for simultaneously measured temperature, water vapor partial pressure, and atmospheric pressure, showed a good agreement with the data measured by a highly accurate CO2 analyzer, LI-6262. This indicates that acceptable accuracy can be realized using the calibration method developed in this study.

Agrivoltaic systems, comprising photovoltaic panels placed over agricultural crops, have recently gained increasing attention. Emerging interest in these systems led us to investigate their influence on rice crops. Various factors affecting rice crop yield, including fertilizer application, temperature, and solar radiation, were directly observed, and measured to evaluate changes associated with the shading rates of photovoltaic systems installed above rice crops. The results suggest that the allowable upper limit of the shading rate for agrivoltaic installations ranges from 27 to 39%, which sustains at least 80% of the rice yield, a condition set by the Japanese Ministry of Agriculture, Forestry and Fisheries for these systems. If such systems are applied to rice paddies in Japan at 28% density, they could generate 284 million MWh/yr. This is equivalent to approximately 29% of the total Japanese electricity demand, based on 2018 calculations. This projection indicates the potential of agrivoltaic systems for efficient land use and sustainable energy generation.

Plant–insect interactions are basic components of biodiversity conservation. To attain the international Sustainable Development Goals (SDGs), the interactions in urban and in suburban systems should be better understood to maintain the health of green infrastructure. The role of ground-level ozone (O 3 ) as an environmental stress disrupting interaction webs is presented. Ozone mixing ratios in suburbs are usually higher than in the center of cities and may reduce photosynthetic productivity at a relatively higher degree. Consequently, carbon-based defense capacities of plants may be suppressed by elevated O 3 more in the suburbs. However, contrary to this expectation, grazing damages by leaf beetles have been severe in some urban centers in comparison with the suburbs. To explain differences in grazing damages between urban areas and suburbs, the disruption of atmospheric communication signals by elevated O 3 via changes in plant-regulated biogenic volatile organic compounds and long-chain fatty acids are considered. The ecological roles of plant volatiles and the effects of O 3 from both a chemical and a biological perspective are presented. Ozone-disrupted plant volatiles should be considered to explain herbivory phenomena in urban and suburban systems.

Subarachnoid hemorrhage (SAH) is a catastrophic form of stroke responsible for significant morbidity and mortality. Oxidative stress, inflammation, and neuronal apoptosis are important in the pathogenesis of early brain injury (EBI) following SAH. Preconditioning exercise confers neuroprotective effects, mitigating EBI; however, the basis for such protection is unknown. We investigated the effects of preconditioning exercise on brain damage and sensorimotor function after SAH. Male rats were assigned to either a sham-operated (Sham) group, exercise (Ex) group, or no-exercise (No-Ex) group. After a 3-week exercise program, they underwent SAH by endovascular perforation. Consciousness level, neurological score, and sensorimotor function were studied. The expression of nuclear factor erythroid 2 p45-related factor 2 (Nrf2), heme oxygenase 1 (HO-1), 4-hydroxynonenal (4HNE), nitrotyrosine (NT), ionized calcium-binding adaptor molecule 1 (Iba1), tumor necrosis factor alpha (TNF-α), interleukin 6 (IL-6), interleukin 1β (IL-1β), 14–3-3γ, p -β-catenin Ser37, Bax, and caspase-3 were evaluated by immunohistochemistry or western blotting. The terminal deoxynucleotidyl transferase-mediated biotinylated dUTP nick end labeling (TUNEL) assay was also performed. After SAH, the Ex group had significantly reduced neurological deficits, sensorimotor dysfunction, and consciousness disorder compared with the No-Ex group. Nrf2, HO-1, and 14–3-3γ were significantly higher in the Ex group, while 4HNE, NT, Iba1, TNF-α, IL-6, IL-1β, Bax, caspase-3, and TUNEL-positive cells were significantly lower. Our findings suggest that preconditioning exercise ameliorates EBI after SAH. The expression of 4HNE and NT was reduced by Nrf2/HO-1 pathway activation; additionally, both oxidative stress and inflammation were reduced. Furthermore, preconditioning exercise reduced apoptosis, likely via the 14–3-3γ/ p -β-catenin Ser37/Bax/caspase-3 pathway.

Background Midkine (MK) is a multifunctional cytokine found upregulated in the brain in the presence of different disorders characterized by neuroinflammation, including neurodegenerative disorders and ischemia. The neuroinflammatory response to traumatic brain injury (TBI) represents a key secondary injury factor that can result in further neuronal injury. In the present study, we investigated the role of endogenous MK in secondary injury, including neuroinflammation, immune response, and neuronal apoptosis activity, after TBI. Methods Wild type (Mdk +/+ ) and MK gene deficient (Mdk −/− ) mice were subjected to fluid percussion injury for TBI models and compared at 3, 7, and 14 days after TBI, in terms of the following: brain tissue loss, neurological deficits, microglia response, astrocytosis, expression of proinflammatory M1 and anti-inflammatory M2 microglia/macrophage phenotype markers, and apoptotic activity. Results As opposed to Mdk +/+ mice, Mdk −/− mice reported a significantly reduced area of brain tissue loss and an improvement in their neurological deficits. The ratios of the Iba1-immunoreactive microglia/macrophages in the perilesional site were significantly decreased in Mdk −/− than in the Mdk +/+ mice at 3 days after TBI. However, the ratios of the glial fibrillary acidic protein immunoreactive area were similar between the two groups. The M1 phenotype marker (CD16/32) immunoreactive areas were significantly reduced in Mdk −/− than in the Mdk +/+ mice. Likewise, the mRNA levels of the M1 phenotype markers (TNF-α, CD11b) were significantly decreased in Mdk −/− mice than in Mdk +/+ mice. Furthermore, flow cytometry analysis identified the M2 markers, i.e., CD163 + macrophages cells and arginase-1 + microglia cells, to be significantly higher in Mdk −/− than in Mdk +/+ mice. Finally, the ratios of apoptotic neurons were significantly decreased in the area surrounding the lesion in Mdk −/− than in Mdk +/+ mice following TBI. Conclusion Our findings suggest that MK-deficiency reduced tissue infiltration of microglia/macrophages and altered their polarization status thereby reducing neuroinflammation, neuronal apoptosis, and tissue loss and improving neurological outcomes after TBI. Therefore, targeting MK to modulate neuroinflammation may represent a potential therapeutic strategy for TBI management.

This study presents a methodology for developing a high-resolution (2 m) urban tree canopy leaf area inventory in different tree phenological seasons and a subsequent application of the methodology to a 625 km2 urban area in Tokyo. Satellite remote sensing has the advantage of imaging large areas simultaneously. However, mapping the tree canopy cover and leaf area accurately is still difficult in a highly heterogeneous urban landscape. The WorldView-2/3 satellite imagery at the individual tree level (2 m resolution) was used to map urban trees based on a simple pixel-based classification method. The comparison of our mapping results with the tree canopy cover derived from aerial photography shows that the error margin is within an acceptable range of 5.5% at the 3.0 km2 small district level, 5.0% at the 60.9 km2 municipality level, and 1.2% at the 625 km2 city level. Furthermore, we investigated the relationship between the satellite data (vegetation index) and in situ tree-measurement data (leaf area index) to develop a simple model to directly map the tree leaf area from the WorldView-2/3 imagery. The estimated total leaf area in Tokyo urban area in the leaf-on season (633 km2) was twice that of the leaf-off season (319 km2). Our results also showed that the estimated total leaf area in Tokyo urban area was 1.9–6.2 times higher than the results of the moderate-resolution (30 m) satellite imagery.

Background Osteoarthritis (OA) is a degenerative joint disease associated with aging, which often leads to joint stiffness and disability. Exercise is one of the most important non-pharmacological treatments and is prescribed as an indispensable treatment for OA. However, whether physical exercise is beneficial for preventing the progression of OA symptoms with age is poorly understood. We investigated the effects of exercise on spontaneously developed knee OA using male senescence-accelerated mouse prone 8 (SAMP8). Methods To examine age-related changes in the knee joints of SAMP8, knee articular cartilage changes, synovitis, knee joint flexion and extension angles, swelling, walking ability, and quadriceps muscle atrophy were analyzed at 3, 5, 7, and 9 months. SAMP8 were required to run at a speed of 10 m/min for 15 min/day from 7 to 9 months of age. The knee joint pathologies and symptoms of exercising and non-exercising mice were compared by histological, immunohistochemical, and morphometrical analyses. Results The mice presented with various histological changes, including cartilage destruction, osteocyte formation, synovitis, declined joint angles, and swelling. Notably, medial and posterior cartilage destruction was more severe than that of the lateral and anterior cartilage. Knee joint angles were significantly correlated with the histological scores (modified Mankin and OARSI, osteophyte formation and synovial lining cell layer). Exercise did not attenuate cartilage degeneration in the medial and posterior tibial plateau, although the articular cartilage of the anterior and lateral tibial plateau and its histological scores was remained and significantly improved, respectively, by exercise. Exercise suppressed the age-related decline of collagen type II-positive areas in the remaining articular cartilage and improved the OA symptoms. Exercise reduced the expression of monocyte chemoattractant protein (MCP)-1 and tumor necrosis factor (TNF)-α positive macrophages in the synovium. Conclusion This study revealed that SAMP8 developed spontaneous knee OA with age, which resembled the disease symptoms in humans. Low-intensity exercise temporarily alleviated degeneration of the remaining cartilage, synovitis, and age-related decreases in knee flexion angle, stride length, and muscle atrophy in SAMP8. However, exercise during OA progression with age may cause mechanical stress that could be both beneficial and detrimental to joint health.

Preconditioning exercise prior to stroke exerts neuroprotection, which is an endogenous strategy that leads the brain cells to express several intrinsic factors and inhibits their apoptosis. However, it is unclear how long these benefits last after exercise cessation. The aim of this study was to investigate the effects of detraining on preconditioning exercise-induced neuroprotective potential after stroke. Rats were trained using a treadmill for aerobic exercise 5 days each week for 3 weeks, and their neuroprotective effects were examined until 3 weeks after exercise cessation. Stroke was induced by 60 min of left middle cerebral artery occlusion at 3 days, 1, 2, and 3 weeks after exercise cessation. Infarct volume, neurological deficits, sensorimotor function, expression levels of brain-derived neurotrophic factor (BDNF), hypoxia-induced factor-1α (HIF-1α), glial fibrillary acidic protein (GFAP), and P2X7 receptors, and apoptosis activity were examined using immunohistochemical and western blot analyses. Preconditioning exercise significantly reduced infarct volume and ameliorated sensorimotor function after stroke, and its beneficial effects were observed until 2 weeks after exercise cessation. The expression level of BDNF in the ischemic brain was significantly upregulated at 3 days after exercise cessation; however, the expression levels of HIF-1α, GFAP, and P2X7 receptor were significantly increased until 2 weeks after exercise cessation; thereby, significant anti-apoptotic effects were lost at 3 weeks of detraining. Our findings suggest that preconditioning exercise-induced neuroprotective potential may be lost shortly after exercise cessation. Neuroprotection through intrinsic protective factors, such as BDNF and HIF-1α, may provide different neuroprotective mechanisms in a time-dependent manner during detraining.

Fatigue can lead to several health issues and is particularly prevalent among elderly individuals with chronic inflammatory conditions. Ninjin’yoeito, a traditional Japanese herbal medicine, is used to address fatigue and malaise, anorexia, and anemia. This study aimed to examine whether relieving inflammation in the brain and skeletal muscle of senescence-accelerated mice prone 8 (SAMP8) could reduce fatigue-like conditions associated with aging. First, SAMP8 mice were divided into two groups, with and without ninjin’yoeito treatment. The ninjin’yoeito-treated group received a diet containing 3% ninjin’yoeito for a period of 4 months starting at 3 months of age. At 7 months of age, all mice underwent motor function, treadmill fatigue, and behavioral tests. They were then euthanized and the skeletal muscle weight, muscle cross-sectional area, and concentration of interleukin (IL)-1β and IL-1 receptor antagonist (IL-1RA) in both the brain and skeletal muscle were measured. The results showed that the ninjin’yoeito-treated group had higher motor function and spontaneous locomotor activity than the untreated group did and ran for significantly longer in the treadmill fatigue test. Moreover, larger muscle cross-sectional area, lower IL-1β concentrations, and higher IL-1RA concentrations were observed in both the brain and skeletal muscle tissues of the ninjin’yoeito-treated group than in the untreated group. The results suggest that ninjin’yoeito improves age-related inflammatory conditions in both the central and peripheral tissues and reduces fatigue.

Type 2 diabetes significantly increases cardiovascular risk. Glucagon-like peptide-1 receptor agonists (GLP-1 RA) reduce major adverse cardiovascular events, heart failure hospitalizations, and death. However, the comparison among GLP-1 RAs on cardiovascular outcomes is limited. We compared all-cause death and cardiovascular events in patients using semaglutide or dulaglutide in patients with type 2 diabetes. This retrospective observational study used the TriNetX database of deidentified electronic medical records from January 1, 2018, to December 31, 2020. We identified 4,691,652 patients with type 2 diabetes, among whom 231,075 initiated semaglutide and 189,103 initiated dulaglutide. After propensity score matching, 171,105 patients were included in each group. The primary outcome measure was all-cause death during the 3-year follow-up period.; secondary outcomes were acute myocardial infarction, stroke, and acute heart failure.Over 3 years, the risk for all-cause death in patients who received semaglutide relative to those who received dulaglutide was significantly lower (4.2% vs. 5.6%, p  < 0.001; hazard ratio [HR] 0.75; 95% confidence interval [CI] 0.72–0.78). Similarly, patients who received semaglutide were less likely to have acute myocardial infarction (5.2% vs. 5.6%; HR, 0.94; 95% CI, 0.91–0.97; p  < 0.001), stroke (5.8% vs. 6.4%; HR, 0.90; 95% CI, 0.87–0.93; p  < 0.001), and acute heart failure (5.3% vs. 6.1%; HR, 0.88; 95% CI, 0.85–0.91; p  < 0.001).In this multicenter, retrospective, observational study, semaglutide was associated with lower 3-year risks of all-cause death, acute myocardial infarction, stroke, and acute heart failure compared with dulaglutide in patients with type 2 diabetes.