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In recent years, biodegradable polymers have gained the attention of many researchers for their promising applications, especially in drug delivery, due to their good biocompatibility and designable degradation time. Poly (lactic-co-glycolic acid) (PLGA) is a biodegradable functional polymer made from the polymerization of lactic acid (LA) and glycolic acid (GA) and is widely used in pharmaceuticals and medical engineering materials because of its biocompatibility, non-toxicity, and good plasticity. The aim of this review is to illustrate the progress of research on PLGA in biomedical applications, as well as its shortcomings, to provide some assistance for its future research development.

The composition and concentration of amino acids and their derivatives in Polygonatum are crucial factors that indicate its nutritional value and have a substantial impact on its potential for market development as a medicinal and edible plant. This study utilized comprehensive targeted metabolomics detection, transcriptome analysis, and weighted gene co-expression network analysis (WGCNA) to assess the quality characteristics of amino acids and their derivatives. Additionally, it aimed to investigate the pivotal genes that influence the synthesis of these compounds. The analysis revealed that there was a total of 72 distinct amino acids and their derivatives present in both forms of Polygonatum . Furthermore, there were notable variations in the content of 37 of these amino acids. A total of 271 genes are responsible for encoding 37 enzymes that are involved in the production of amino acids and their derivatives. The WGCNA clustering analysis, along with the metabolic profile of amino acids and their derivatives and transcriptome analysis, categorized the transcripts into six modules. Among these modules, the active components of amino acids and their derivatives showed a positive correlation with the MEturquoise and MEblue modules. This correlation helped identify 10 key genes that are highly likely to influence the synthesis of amino acids and their derivatives. Therefore, we validated these results using qRT-PCR. The modulation of the expression patterns of these crucial genes can establish a theoretical foundation for the subsequent breeding of Polygonatum germplasm with abundant amino acid content and diversity.

Sweet potatoes are rich in amino acids, organic acids, and lipids, offering exceptional nutritional value. To accurately select varieties with higher nutritional value, we employed liquid chromatography–tandem mass spectrometry (LC-MS/MS) to analyze the metabolic profiles of three types of sweet potatoes (white sweet potato flesh, BS; orange sweet potato flesh, CS; and purple sweet potato flesh, ZS). When comparing CS vs. BS, ZS vs. BS, and ZS vs. CS, we found differences in 527 types of amino acids and their derivatives, 556 kinds of organic acids, and 39 types of lipids. After excluding the derivatives, we found 6 amino acids essential for humans across the three sweet potatoes, with 1 amino acid, 11 organic acids, and 2 lipids being detected for the first time. CS had a higher content of essential amino acids, while ZS had a lower content. Succinic acid served as a characteristic metabolite for ZS, helping to distinguish it from the other two varieties. These findings provide a theoretical basis for assessing the nutritional value of sweet potatoes and setting breeding targets while facilitating the selection of optimal varieties for food processing, medicine, and plant breeding.

Liver cancer remains a smajor cause of mortality worldwide, underscoring the urgent need for novel natural therapeutics. Polygonatum kingianum var. grandifolium (PK) and Polygonatum sibiricum Redouté (PS) are rice in terpenoids, yet their anti-liver cancer mechanisms remain poorly understood. This study used metabolism, network analysis, molecular docking, and molecular dynamics simulations to investigate their therapeutic potential. Metabolomic analysis identified nine differential terpenoid metabolites, with Maslinic acid and Alphitolic acid being species-specific. Network analysis revealed 23 liver cancer-related targets, including five key proteins: HMGCR, PTGS2, ESR1, PPARG, and PGR. Functional enrichment analysis identified 126 GO terms and 11 KEGG pathways ( P  < 0.05). Molecular docking suggested strong binding affinities between core compounds and targets, while molecular dynamics simulations confirmed the stability of maslinic acid and alphitolic acid with their respective targets. This study enhances the pharmacological understanding of Polygonatum species and offers promising insights for the development of novel liver cancer treatments.

Chronic pain represents a major clinical burden, with its intensity being a key measure of its severity. However, the genetic and neural underpinnings of chronic pain intensity remain unraveled. Here, we identified six genetic loci (including a novel discovery) significantly associated with chronic pain intensity using a genome-wide association study in the UK Biobank ( n  = 134,627). We then systematically investigate its relationship with 3924 brain imaging-derived phenotypes. Phenotypic correlation analyses revealed 29 imaging-derived phenotypes predictive of future chronic pain intensity. Genetic correlation and polygenic risk score analyses showed 13 of these imaging-derived phenotypes share a genetic basis with chronic pain intensity. Mediation analyses indicated that 12 imaging-derived phenotypes mediate genetic effects on chronic pain intensity. Mendelian randomization further supported a causal influence of three imaging-derived phenotypes, including brain structure and functional network connectivity, on chronic pain intensity. Our findings elucidate the genetic architecture and neurobiological pathways of chronic pain intensity, highlighting the brain’s central role in chronic pain pathophysiology. Chronic pain severity is influenced by genetics and brain structure, but mechanisms remain unclear. Here, the authors identify genetic loci linked to pain intensity and show that specific brain imaging traits mediate and causally influence chronic pain.

Owing to the special configurations of the culvert–frame combined underground structure, discrepant responses at different portions of the structure arise when earthquakes strike in the longitudinal direction. This paper presents other experiments when shaking along the lateral direction and comparing structural dynamic responses between these two cases. Data on accelerations and culvert joint displacements were presented under a series of 1 g shaking tests, that is, five synthetic earthquake motions between white noise cases. Comparing the seismic responses of the culvert–frame structure under varying intensities of excitations gave findings that, with respect to longitudinal excitation, the acceleration responses of the model soil were increased under transverse excitations. For the model structure, the acceleration responses under longitudinal excitations were larger than those of transverse excitations. A significant difference in the displacement of the culvert joint was observed.

Chronic pain is a prevalent and debilitating condition that imposes substantial personal and societal burdens. Despite its significance, the neural mechanisms underlying individual susceptibility to chronic pain remain inadequately understood. In this study, we examined the prospective associations between 1325 brain structural imaging phenotypes and the future risk of developing chronic pain in a UK Biobank cohort of 5754–5756 participants. These phenotypes encompassed regional and tissue volume, cortical surface area and thickness. General linear models (GLMs) were employed to identify brain structural variations associated with the risk of developing chronic pain, and then Mendelian randomization (MR) was employed to explore potential causal relationships between brain structure and chronic pain development. GLMs identified three significant associations between imaging phenotypes and the future development of chronic pain. All three imaging phenotypes pertained to the cortical surface area of the frontal operculum, albeit derived from three different brain atlases. Specifically, reduced cortical surface area in the frontal operculum was significantly associated with an increased risk of developing chronic pain: BA atlas area 44 ( T = −4.10, p = 4.24 × 10 −5 ), Desikan atlas pars opercularis ( T = −4.21, p = 2.55 × 10 −5 ), and DKT atlas pars opercularis ( T = −3.96, p = 7.47 × 10 −5 ). Subsequent MR analysis further demonstrated a causally protective effect of larger cortical area in the prefrontal operculum against the risk of developing chronic pain (OR = 0.91, p = 1.91 × 10 −2 ). These results indicate a critical role of the surface area of frontal operculum in individual chronic pain susceptibility and provide a potential risk predictor for chronic pain development.

Sarcopenia is considered to be a new complication of type 2 diabetes (T2DM) leading to increased risk of adverse outcome. We performed a survey to evaluate glucose metabolism and nutritional status in sarcopenia patients with T2DM. Diabetic participants aged ≥50 years were grouped into a probable sarcopenia group with low muscle strength (n=405) and a nonsarcopenia group with normal muscle strength (n=720) according to the revised recommendations from EWGSOP2 (2018). Compared to the controls, the probable sarcopenia participants were older and had lower waist-to-hip ratio and BMI, longer diabetes duration, higher fasting plasma glucose level and glycosylated hemoglobin (HbA1c), decreased estimated glomerular filtration rate and lower bone mineral content, lower fatless upper arm circumference, lower appendicular skeletal muscle mass index (ASMI), and muscle quality in both genders. Multivariable logistic regression analysis showed increased age, male, low BMI, and increased HbA1c, combined with diabetic nephropathy and decreased serum albumin levels, were risk factors associated with low muscle strength in diabetes patients. In conclusion, diabetic patients with sarcopenia had worse glucose metabolism and nutritional status, decreased renal function and reduced muscle quality ,and muscle mass with a greater likelihood of osteoporosis, who need an overall health management to improve outcomes. This clinical trial registration is registered with the Chinese Clinical Trial Registry, ChiCTR-EOC-15006901.

Urbanization significantly reduced natural habitats and biodiversity, creating challenges for sustainable urban development. Urban parks, as essential green spaces, help mitigate these impacts by promoting biodiversity and enhancing urban resilience. This review synthesizes current knowledge on landscape factors that influence biodiversity in urban parks, emphasizing how these parks contribute to biodiversity conservation and urban sustainable development. A comprehensive literature search identified key landscape factors that affect biodiversity, categorized into five groups: park size and shape, vegetation composition, artificial components, landscape patterns, and surrounding land use. The findings reveal that larger park areas, simplified boundaries, diverse vegetation structures, reduced human interference, and improved habitat connectivity are crucial for boosting biodiversity. The review also suggests practical design strategies, such as enhancing green space networks and preserving old trees, to foster biodiversity in urban parks. Overall, this review provides valuable insights for urban planners and landscape designers aiming to create resilient, biodiversity-rich urban spaces that support sustainable development.

In a multicenter randomized double-blind study we demonstrated that Qiliqiangxin (QLQX), a traditional Chinese medicine, had a protective effect in heart failure patients. However, whether and via which mechanism QLQX attenuates cardiac remodeling after acute myocardial infarction (AMI) is still unclear. AMI was created by ligating the left anterior descending coronary artery in mice. Treating the mice in the initial 3 days after AMI with QLQX did not change infarct size. However, QLQX treatment ameliorated adverse cardiac remodeling 3 weeks after AMI including better preservation of cardiac function, decreased apoptosis and reduced fibrosis. Peroxisome proliferator-activated receptor-γ (PPARγ) was down-regulated in control animals after AMI and up-regulated by QLQX administration. Interestingly, expression of AKT, SAPK/JNK and ERK was not altered by QLQX treatment. Inhibition of PPARγ reduced the beneficial effects of QLQX in AMI remodeling, whereas activation of PPARγ failed to provide additional improvement in the presence of QLQX, suggesting a key role for PPARγ in the effects of QLQX during cardiac remodeling after AMI. This study indicates that QLQX attenuates cardiac remodeling after AMI by increasing PPARγ levels. Taken together, QLQX warrants further investigation as as a therapeutic intervention to mitigate remodeling and heart failure after AMI.