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Astronomical seeing is important for monitoring the atmospheric environment, observation scheduling and management, and selecting astronomical sites. This study first attempts to establish a near-global astronomical seeing map by employing the fifth European Centre for Medium-Range Weather Forecasts Reanalysis (ERA5) data combined with the estimated model. Then, some example sites’ results from ERA5 were compared against the astronomical seeing results from the balloon-borne microthermal measurements and the differential image motion monitor (DIMM) instrument. The global astronomical seeing variations exhibit large spatial dependence. The best seeing areas are generally discerned over the mid-latitude regions, consistent with the regions of the European Southern Observatory and Tibetan Plateau. In addition, the astronomical seeing values of the Tibetan Plateau in spring are better than in the other seasons. The site results from ERA5 show that the astronomical seeing values of some example sites are generally consistent with the measurements. Overall, the global astronomical seeing map presented in this study can provide a reference and basis to further understand the astronomy site selection and optoelectronics equipment observation path selection.

Optical turbulence strongly affects different types of optoelectronic and adaptive optics systems. Systematic direct measurements of optical turbulence profiles [Cn2(h)] are lacking for many climates and seasons, particularly in marine environments, because it is impractical and expensive to deploy instrumentation. Here, a backpropagation neural network optimized using a genetic algorithm (GA-BP) is developed to estimate atmospheric turbulence profiles in marine environments which is validated against corresponding [Cn2(h)] profile datasets from a field campaign of balloon-borne microthermal measurements at the Haikou marine environment site. Overall, the trend and magnitude of the GA-BP model and measurements agree. The [Cn2(h)] profiles from the GA-BP model are generally superior to those obtained by BP and the physically-based (HMNSP99) models. Several statistical operators were used to quantify the GA-BP model performance on reconstructing the optical turbulence profiles in marine environments. The characterization of vertical distributions of optical turbulence profiles and the main integral parameters derived from [Cn2(h)] profiles are presented. The median Fried parameter, isoplanatic angle, and coherence time are 9.94 cm, 0.69″, and 2.85 ms, respectively, providing independent optical turbulence parameters for adaptive optics systems. The proposed approach exhibits potential for implementation in ground-based optical applications in marine environments.

Hypercholesterolemia is a disease associated with numerous health problems. Growing evidence indicates that hypercholesterolemia, hyperlipidemia is closely linked to chronic inflammation, which can lead to cardiovascular disease, fatty liver disease, and type 2 diabetes. The purpose of this study was to investigate the protective effect of Nostoc sphaeroids Kütz (NO) on diet-induced hyperlipidemia in mice. At first, experimental animals received a high-fat diet (HFD) for 4 weeks, and then received a HFD supplemented with 2.5% or 7.5% NO for 6 weeks. In the current study, results show that treatment with NO decreases weight gain and liver index induced by HFD. In addition, the serum levels of TC, TG and LDL are significantly decreased in NO treatment groups. From the results of Oil Red staining and Hematoxylin and eosin staining (HE), treatment with NO significantly reduces liver lipid accumulation and protect liver structure. Further analysis reveals that NO has positive effects on liver lipid metabolism and inflammation, as showed by the lower protein expressions of FAS and SREBP-1, the lower concentrations of TNF-α, IL-1β, IL-6, and the lower gene expressions of TNF-α, IL-1β, IL-6 and NF-kB. Our results indicate that NO may significantly ameliorate diet-induced hyperlipidemia, which is possibly associated with improving liver lipid metabolism and reducing chronic inflammation.

Hyperlipidemia is associated with chronic inflammation and intestinal dysbiosis. The purpose of this study was to investigate the protective effect of Nostoc sphaeroids Kütz (NO) on diet‐induced hyperlipidemia in mice. Experimental animals received a high‐fat diet (HFD) for 4 weeks, then an HFD supplemented with 2.5% or 7.5% NO for 6 weeks. HFD‐fed mice exhibited a significant increase in serum total cholesterol, triglycerides, and low‐density lipid cholesterol, and a decrease in high‐density lipid cholesterol. NO supplementation was associated with significantly lower dyslipidemia, decreased intestinal inflammation, and inhibition of toll‐like receptor 4 gene repression in HFD‐fed mice. Results suggest that NO treatment protected the integrity of the intestinal barrier. NO treatment was also associated with significant changes in the intestinal microbiota induced by HFD and an increase in the Firmicutes‐to‐Bacteroidetes ratio. Furthermore, NO treatment was also inversely correlated with mice obesity and hyperlipidemia NO and was associated with no significant in fecal short‐chain fatty acids. In conclusion, NO significantly ameliorated hyperlipidemia induced by a HFD in mice, potentially via a decrease intestinal inflammation, increase in intestinal barrier integrity, and amelioration in the gut microbiota. Nostoc sphaeroids Kütz ameliorates hyperlipidemia. Nostoc sphaeroids Kütz protects intestinal barrier. Nostoc sphaeroids Kütz ameliorates intestinal barrier.

Natural products and medicinal foods have attracted more and more attention because of their potential prevention and inhibition effect on constipation. Nostoc sphaeroides Kütz Polysaccharide (NSKP) polysaccharide is a natural product rich in polysaccharides. This work attempted to prove the effects of aqueous extracts of NSKP on STC treatment and to determine the possible mechanisms by a loperamide-induced slow transit constipation (STC) model. The results show that, in rats of the NSKP group, compared with the model group, the colon propulsion rate was improved, the time of the first grain of black stool was shortened, and the fecal wet weight was increased remarkably. The 5-HT levels were increased, but the VIP and NO levels were reduced dramatically. The number of interstitial cells of cajal (ICC) was increased by c-kit/SCF signal pathway, and the intestines were moisturized; then, constipation was relieved. It is interesting to note that NSKP appeared to be effective on constipation, so further experiments are necessary to clarify the exact mechanisms involved.

In this study, we investigated the effects of Nostoc sphaeroids Kütz polysaccharide (NSKP) on renal fibrosis in high‐fat mice. ApoE−/− male mice were randomly divided into four groups: control (Cont) group, high‐fat diet (HFD) group, HFD+0.4 g/kg BW NSKP, and HFD+0.8 g/kg BW NSKP (NSKP groups). The Cont was fed a standard diet. The HFD group was fed HFD. Every day, NSKP groups were fed HFD, as well as given 0.4 g/kg BW or 0.8 g/kg BW NSKP. After 22 weeks, the serum biochemical indices (TC, TG, LDL‐C, HDL‐C, GLU, BUN, and SCR) were measured. For the kidney, the histopathological sections were observed and analyzed, and inflammatory factors and markers of renal fibrosis were measured. For the NSKP groups, the serum TC, TG, LDL‐C, BUN, and SCR were decreased, HDL‐C significantly increased compared with the HFD group. The protein expressions of TNF‐α, IL‐1β, and TGF‐β1 were significantly downregulated. The α‐SMA in renal cortex was decreased, and the mRNA expression of Col‐I and Col‐IV in renal collagen fibers was downregulated. To sum up, NSKP reduced the blood lipid of HFD mice, downregulated the inflammation of kidney, inhibited the expression of collagen fiber, and improved the renal fibrosis caused by long‐term lipid metabolism disorder. Nostoc sphaeroids Kütz polysaccharide improved the lipid level of ApoE−/− mice, reduced the renal inflammatory response of high‐fat mice, reduced the expression of renal collagen fiber, and interfered with the development of renal fibrosis. This study provided more basis for the future study of chronic kidney disease caused by high fat diet.

Background Traumatic brain injury (TBI) is a critical public health and socioeconomic problem throughout the world. Inflammation-induced secondary injury is one of the vital pathogenic parameters of TBI. Molecular signaling cascades of pyroptosis, a specific type of cellular necrosis, are key drivers of TBI-induced inflammation. Methods In this study, mice with genetically ablated caspase-1 (caspase-1 −/− ) were subjected to controlled cortical impact injury in vivo, and primary neuron deficient in caspase-1 through siRNA knockdown and pharmacologic inhibition was stimulated by mechanical scratch, equiaxial stretch, and LPS/ATP in vitro. We evaluated the effects of caspase-1 deficiency on neurological deficits, inflammatory factors, histopathology, cell apoptosis, and pyroptosis. Results During the acute post-injury period (0–48 h) in vivo, motor deficits, anti-inflammatory cytokines (TGF-β and IL-10), pro-inflammatory cytokines (IFN-γ, IL-1β, and IL-18), and blood lactate dehydrogenase (LDH), as well as pyroptosis-related proteins (caspase-1, caspase-1 fragments, caspase-11 and GSDMD), were increased. Caspase-1 was activated in the cortex of TBI mice. Inflammatory activation was more profound in injured wild-type mice than in caspase-1 −/− mice. In vitro, mechanical scratch, equiaxial stretch, and LPS/ATP-induced neuron pyroptosis, apoptosis, LDH release, and increased expression of inflammatory factors. The effects of mechanical and inflammatory stress were reduced through inhibition of caspase-1 activity through siRNA knockdown and pharmacologic inhibition. Conclusion Collectively, these data demonstrate that pyroptosis is involved in neuroinflammation and neuronal injury after TBI, and ablation of caspase-1 inhibits TBI-induced pyroptosis. Our findings suggest that caspase-1 may be a potential target for TBI therapy.

Gastrointestinal (GI) cancers impose a substantial global health burden, highlighting the necessity for deeper understanding of their intricate pathogenesis and treatment strategies. This review explores the interplay between intratumoral microbiota, tumor metabolism, and major types of GI cancers (including esophageal, gastric, liver, pancreatic, and colorectal cancers), summarizing recent studies and elucidating their clinical implications and future directions. Recent research revealed altered microbial signatures within GI tumors, impacting tumor progression, immune responses, and treatment outcomes. Dysbiosis-induced alterations in tumor metabolism, including glycolysis, fatty acid metabolism, and amino acid metabolism, play critical roles in cancer progression and therapeutic resistance. The integration of molecular mechanisms and potential biomarkers into this understanding further enhances the prognostic significance of intratumoral microbiota composition and therapeutic opportunities targeting microbiota-mediated tumor metabolism. Despite advancements, challenges remain in understanding the dynamic interactions within the tumor microenvironment (TME). Future research directions, including advanced omics technologies and prospective clinical studies, offer promising avenues for precision oncology and personalized treatment interventions in GI cancer. Overall, integrating microbiota-based approaches and molecular biomarkers into GI cancer management holds promise for improving patient outcomes and survival.