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Rapid urbanization in China has led to the emergence of the 15-minute commercial circle, but more research is needed on its impact on residents' quality of life. This study aimed to propose construction plans and explore the circle's influence on residents' quality of life in Zhengzhou. Semi-structured interviews with 15 community residents were analyzed using NVivo software. Results indicated positive economic impacts but negative environmental and social impacts. The 15-minute commercial circle plays a dual role, requiring future sustainable and inclusive practices that address income inequality and environmental protection. Limitations include a small sample size and a focus on Zhengzhou. Keywords: 15-minute Commercial Circle; Resident Quality of Life; Urbanization; Zhengzhou eISSN: 2398-4287 © 2023. The Authors. Published for AMER ABRA cE-Bs by e-International Publishing House, Ltd., UK. This is an open-access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/). Peer–review under the responsibility of AMER (Association of Malaysian Environment-Behaviour Researchers), ABRA (Association of Behavioural Researchers on Asians/Africans/Arabians) and cE-Bs (Centre for Environment-Behaviour Studies), College of Built Environment, Universiti Teknologi MARA, Malaysia. DOI: https://doi.org/10.21834/ebpj.v8i24.4638

The caspase recruitment domain family member (CARD)11-Bcl10-Malt1 signalosome controls TGF-β–activated kinase 1 (TAK1) activation and regulates BCR-induced NF-κB activation. In this study, we discovered that CARD19 interacted with TAK1 and inhibited TAB2-mediated TAK1 ubiquitination and activation. Although CARD19 deficiency in mice did not affect B cell development, it enhanced clonal deletion, receptor editing, and anergy of self-reactive B cells, and it reduced autoantibody production. Mechanistically, CARD19 deficiency increased BCR/TAK1-mediated NF-κB activation, leading to increased expression of transcription factors Egr2/3, as well as the E3 ubiquitin ligases c-Cbl/Cbl-b, which are known inducers of B cell tolerance in self-reactive B cells. RNA sequencing analysis revealed that although CARD19 deficiency did not affect the overall Ag-induced gene expression in naive B cells, it suppressed BCR signaling and increased hyporesponsiveness of self-reactive B cells. As a result, CARD19 deficiency prevented Bm12-induced experimental systemic lupus erythematosus. In summary, CARD19 negatively regulates BCR/TAK1-induced NF-κB activation and its deficiency increases Egr2/3 and c-Cbl/Cbl-b expression in self-reactive B cells, thereby enhancing B cell tolerance.

A stoichiometric 2 : 1 complex of hydroxypropyl-β-cyclodextrin with fullerene was formed, and then a supramolecular hydrogel was constructed by carrying out a co-assembly of fullerene@hydroxypropyl-β-cyclodextrin, chitosan and bentonite.

The drug efflux by P-glycoprotein (P-gp) is the primary contributor of multidrug resistance (MDR), which eventually generates insufficient nuclear drug accumulation and chemotherapy failure. In this paper, reversible covalent nanoassemblies on the basis of catechol-functionalized methoxy poly (ethylene glycol) (mPEG-dop) and phenylboronic acid-modified cholesterol (Chol-PBA) are successfully synthesized for delivery of both doxorubicin (DOX, anti-cancer drug) and tariquidar (TQR, P-glycoprotein inhibitor), which shows efficient nuclear DOX accumulation for overcoming tumor MDR. Through naturally forming phenylboronate linkage in physiological circumstances, Chol-PBA is able to bond with mPEG-dop. The resulting conjugates (PC) could self-assemble into reversible covalent nanoassemblies by dialysis method, and transmission electron microscopy analysis reveals the PC distributes in nano-scaled spherical particles before and after drug encapsulation. Under the assistance of Chol, PC can enter into lysosome of tumor cells via low-density lipoprotein (LDL) receptor-mediated endocytosis. Then the loaded TQR and DOX are released in acidic lysosomal compartments, which inhibit P-gp mediated efflux and elevate nuclear accumulation of DOX, respectively. At last, this drug loaded PC nanoassemblies show significant tumor suppression efficacy in multidrug-resistant tumor models, which suggests great potential for addressing MDR in cancer therapy.

Endoplasmic reticulum stress (ERS) is involved in the pathological process of vascular dementia (VD). GJ-4 is extracted from Gardenia jasminoides J. Ellis and has been reported to have protective roles in ischemia-related brain damage. However, the role of GJ-4 in ERS has not been elucidated. We established a VD rat model through bilateral common carotid arteries occlusion (2-VO). The rats were intragastrically administrated with GJ-4 (10, 25, and 50[Formula: see text]mg/kg) and nimodipine (10[Formula: see text]mg/kg). Data from a Morris water maze test showed that GJ-4 could significantly alleviate learning and memory deficits in VD rats. Nissl and cleaved caspase-3 staining revealed that GJ-4 can inhibit apoptosis and thus exert a protective role in the brain of 2-VO rats. Western blot results suggested that GJ-4 significantly reduced ERS-related protein expression and inhibited apoptosis through suppression of the PERK/eIF2[Formula: see text]/ATF4/CHOP signaling pathway. For in vitro studies, the oxygen-glucose deprivation (OGD) SH-SY5Y model was employed. Western blot and Hoechst 33342/PI double staining were utilized to explore the effects of crocetin, the main active metabolite of GJ-4. Like GJ-4 in vivo, crocetin in vitro also decreased ERS-related protein expression and inhibited the activation of the PERK/eIF2[Formula: see text]/ATF4/CHOP signaling pathway. Thus, crocetin exerted similar protective roles on OGD challenged SH-SY5Y cells in vitro. In summary, GJ-4 and crocetin reduce the ERS in the brain of VD rats and SY5Y cells subjected to OGD and inhibit neuronal apoptosis through suppression of the PERK/eIF2[Formula: see text]/ATF4/CHOP pathway, suggesting that GJ-4 may be useful for the treatment of VD.

The photosynthetic mechanism of crop yields in fluctuating light environments in the field remains controversial. To further elucidate this mechanism, we conducted field and simulation experiments using maize (Zea mays) plants. Increased planting density enhanced the light fluctuation frequency and reduced the duration of daily high light, as well as the light-saturated photosynthetic rate, biomass, and yield per plant. Further analysis confirmed a highly significant positive correlation between biomass and yield per plant and the duration of photosynthesis related to daily high light. The simulation experiment indicated that leaf area and photosynthetic rate of maize leaves decreased gradually and considerably when shortening the daily duration of high light, while the quantum yield of regulatory energy dissipation decreased slightly. Under an identical duration of high light exposure, increasing the fluctuation frequency decreased leaf area and the light-saturated photosynthetic rate slightly and increased the quantum yield of regulatory energy dissipation distinctly. Proteomic data also demonstrated that photosynthesis was mainly affected by the duration of high light, not the light fluctuation frequency. Consequently, the current study proposes that an appropriate duration of daily high light under fluctuating light environments is the key factor for greatly improving photosynthesis while the regulatory energy dissipation changes slightly in maize plans. This is a promising mechanism through which to enhance the photosynthetic productivity and yield of maize under complex light environments in the field.

In brief Transforming the endometrial luminal epithelium (LE) into a receptive state is a requisite event for successful embryo implantation. This study suggests the role of a transcription factor in regulating endometrial LE receptivity. Abstract The endometrial luminal epithelium (LE) undergoes extensive remodeling during implantation to establish receptivity of the uterus in response to the conceptus signals, such as interleukin 1β (IL1B). But the mechanisms remain to be fully understood. This study investigated the role of CCAAT/enhancer-binding protein β (C/EBP-β) in regulating pig endometrial LE receptivity. Our results showed that C/EBP-β was expressed and activated only in the endometrial LE in an implantation-dependent manner. In addition, C/EBP-β was highly activated at the pre-attachment stage compared to the attachment stage, and its activation was correlated with the expression of IL1B-dependent extracellular signal-regulated kinases1/2-p90 ribosomal S6 kinase signaling axis. Subsequent chromatin immunoprecipitation (ChIP)-sequencing analysis revealed that the binding of C/EBP-β within the promoter was positively associated with the transcription of genes related to cell remodeling. One such gene is matrix metalloproteinase 8 (MMP8), which is responsible for extracellular matrix degradation. The expression of MMP8 was abundant at the pre-attachment stage but dramatically declined at the attachment stage in the endometrial LE. Consistent with C/EBP-β, the expression and activation of MMP8 were limited to the endometrial LE in an implantation-dependent manner. Using ChIP-qPCR and electrophoresis mobility shift assay approaches, we demonstrated that C/EBP-β regulated the expression of the MMP8 gene during implantation. Furthermore, we detected that MMP8 and one of its substrates, type II collagen, showed a mutually exclusive expression pattern in pig endometrial LE during implantation. Our findings indicate that C/EBP-β plays a role in pig endometrial LE receptivity by regulating cell remodeling-related genes, such as MMP8, in response to conceptus signals during implantation.

Anticancer drug discovery has yielded unprecedented progress in recent decades, resulting in the approval of innovative treatment options for patients and the successful implementation of personalized medicine in clinical practice. This remarkable progress has also reshaped the research scope of pharmacological research. This article, as a tribute to cancer research at Shanghai Institute of Materia Medica in celebration of the institute's 90th birthday, provides an overview of the conceptual revolution occurring in anticancer therapy, and summarizes our recent progress in the development of molecularly targeted therapeutics and exploration of new strategies in personalized medicine. With this review, we hope to provide a glimpse into how antitumor pharmacological researchers have embraced the new era of personalized medicine research and to propose a future path for anticancer drug discovery and pharmacological research.

Successful attachment of conceptus to the uterine luminal epithelium (LE) is crucial for establishing a functional placenta in pigs. However, the underlying mechanisms are yet to be elucidated. The uterine LE-conceptus interface is enriched in various glycoconjugates essential to implantation. Using MALDI-MS profiling, we identified for the first time the O-glycan repertoire of pig endometrium during the conceptus attachment stage. The expression pattern of blood group A, O(H), Lewis x, y, a, b (Lex, Ley, Lea, and Leb), the sialylated and sulfated Lex antigens in the uterine LE-conceptus interface was assessed using immunofluorescence assays. Notably, the Lex-carrying O-glycans exhibited a temporal–spatial expression pattern. They were absent in the endometrium on estrous cycle days but strongly and spatially presented in the conceptus and uterine LE to which the conceptus apposes during the early conceptus attachment stage. In addition, Lex-carrying O-glycans were co-localized with secreted phosphoprotein 1 (SPP1), a well-characterized factor that plays a role in promoting conceptus attachment through interacting with integrin αVβ3 and integrin αVβ6. Meanwhile, the immunoprecipitation assays revealed an interaction between the Lex-carrying O-glycans and SPP1, integrin αV, and integrin β6. Furthermore, we provided evidence that the β1,4-galactosyltransferase 1 (B4GALT1) gene is a potential regulator for Lex antigen expression in the uterine LE-conceptus interface during the early conceptus attachment stage. In conclusion, our findings show that Lex-carrying O-glycans, presumably dependent on B4GALT1 gene expression, might modulate conceptus attachment by interacting with the SPP1-integrin receptor complex in pigs.

ObjectiveTo evaluate the efficacy and safety of gonadotropin-releasing hormone agonist (GnRHa) combined with a levonorgestrel-releasing intrauterine device (LNG-IUD) or aromatase inhibitor (letrozole) in women with endometrial carcinoma or atypical endometrial hyperplasia who wished to preserve fertility.MethodsPatients at the Department of Obstetrics and Gynecology, Peking Union Medical College Hospital between January 2013 and December 2020 were retrospectively reviewed. A total of 179 patients who were unsuitable to undergo treatment with high-dose oral progestin, including those with progestin allergies, body mass index ≥30 kg/m2, liver and/or renal dysfunction, hypercoagulable state, and thrombosis were included. Patient data were retrieved from medical records and a prospectively maintained database that represented the standard protocol was followed for all patients. Clinical characteristics, treatment outcomes, adverse events, and reproductive outcomes were collected and analyzed. Logistic regression models were constructed to determine the associations between complete remission, recurrence, and fertility.ResultsOverall, 169 patients (94.4%) achieved complete remission; 58 (96.7%) had atypical endometrial hyperplasia and 111 (93.3%) had endometrial carcinoma. The complete remission rates for the GnRHa plus LNG-IUD and GnRHa plus letrozole groups were 93.5% and 95.8%, respectively. The median time to complete remission was 6 (range 3–18) months: 4 (range 3–10) months for atypical endometrial hyperplasia and 8 (range 3–18) months for endometrial carcinoma. After a median follow-up of 27.5 (range 3–92) months, 41 (24.3%) women developed recurrence, with a median recurrence time of 17 (range 6–77) months. Of the patients with complete remission, 134 patients desired to conceive and 42 (32.3%) became pregnant, 24 (17.9%) were successfully delivered, 5 (3.7%) were still pregnant, while 13 miscarried.ConclusionGnRHa combined treatment provides favorable oncological and reproductive outcomes. Larger multi-institutional studies are required to confirm these preliminary findings.

Purpose This study aims to analyze how bed and breakfast (B&B) experience influences customer value cocreation (CVCC) through emotional psychological factors under the social servicescape (SSC). Design/methodology/approach A moderated chain mediation model was constructed based on the SSC framework. This study collected 722 valid questionnaires through convenience sampling in Xiamen, China, and tourists with B&B experiences were taken as samples. A structural equation model analysis was used to test relevant hypotheses. Findings Results reveal that B&B experience is the core factor to stimulate CVCC. In this process, the individual emotional psychological factors [pleasant arousal (PAL) and place attachment (PAT)] play the critical chain mediating role. In addition, localness positively moderates the reinforcing effect of B&B experience on PAL and strengthens the positive effect of PAL on PAT. Practical implications The findings can provide useful CVCC strategies for B&B operators. They can achieve CVCC by enhancing customer experiences, strengthening emotional interactions and building local culture, thereby improving the competitiveness of B&Bs. Originality/value Current research lacks an in-depth analysis on the internal relationship and logic between B&B experience and CVCC, especially from emotional psychological perspectives. To the best of the authors’ knowledge, this study is one of the first studies to reveal the mechanism of the CVCC process of B&Bs under the SSC from an emotional psychological perspective. It provides a new theoretical model for research on the CVCC of experience-dominant logic.

Recently, the ant colony algorithm has been widely used in the field of path planning, which is a key technology required for ship operations in offshore wind farms to improve navigation efficiency and power generation. However, the ant colony algorithm has the defects of a long search time and stagnation in the early stage of the operation and maintenance path planning of offshore wind farms, and it easily falls into the problem of local optima; furthermore, the ant colony algorithm uses incremental construction to build a complete itinerary path, it takes a lot of time to search the path, and only the suboptimal solution is obtained. To address the above problems, in this paper, we propose a multi-agent-based operation and maintenance model for offshore wind farms. Specifically, the introduction of the heuristic factor can optimize the local optimal solution and make the ant colony algorithm clearer when searching for the target. Based on this, increasing the pheromone adjustment factor can eliminate the invalid path from searching and select a high-quality path. In addition, by integrating the genetic algorithm, it is possible to select, cross, and mutate to simulate the natural evolution process to search for the optimal solution, reduce the similarity of the paths constructed by the ant colony, reduce the probability of algorithm stagnation, improve the convergence speed, and improve the time efficiency and solution accuracy of the algorithm. Simulation experiments on a series of benchmark datasets show that the proposed GA-PACO algorithm achieves better performance in global search and path planning than the existing three algorithms.

Renal impairment is affected by various mechanisms of oxidative stress, mitochondrial dysfunction, and basement membrane thickening, which are the major causes of renal dysfunction in diabetes. Of note, hyperglycemia-induced mitochondrial dysfunction has been identified as a common cause of diabetic nephropathy and renal impairment, and the decrease in PGC-1α expression brought on by hyperglycemia plays an immensurable role in both the reduction of mitochondrial biogenesis and the rise in oxidative stress. Reduced PGC-1α expression levels may occur with rising SGLT2-dependent increase of cytoplasmic sodium and protons in the renal cells of diabetes, even if the precise mechanism of hyperglycemia-induced disruption of PGC-1α expression has not been identified. Additionally, it has been observed that SGLT2 inhibitors enhance PGC-1α expression and activity and decrease cytoplasmic sodium and protons in many kidney cells, which may be helpful in reducing renal impairment brought on by diabetes. This review summarizes our and other recent studies on the function of PGC-1α in diabetic nephropathy, provides another potential mediator of the lower PGC-1α expression levels brought on by hyperglycemia in diabetics, and identifies a new pathogenesis of diabetes-related renal impairment. It also explains the mechanism underlying the protective effects of SGLT2 inhibitors on diabetic nephropathy. Therefore, it should be taken into account that SGLT2 inhibitors are an effective therapeutic strategy for reducing renal dysfunction caused by diabetes.