Analysis of the correlation mechanism between geometric parameters and the thermal environment of Xi'an's summer outdoor commercial pedestrian streets.

Intensive urban development has resulted in the degradation of the urban thermal environment in most regions. There is a growing consensus on the need to enhance urban thermal comfort through well-designed forms, especially in open spaces like urban canyons. To address this, our study focuses on Xi'an's commercial pedestrian streets, employing K-means clustering analysis to create 32 representative models based on actual scenes, capturing their textural characteristics. Simultaneously, 11 geometric indicators (2D/3D) were chosen to quantify the canyon's geometric form. We assessed the spatial and temporal distribution differences in the thermal environment across these models using Envi-met simulation. Finally, Spearman correlation analysis was employed to examine the correlation and significance of the two sets of indicators, culminating in formulating an ideal model. The findings reveal that (1) wind conditions are predominantly influenced by the canyon's geometric form, followed by solar radiation and temperature, with the lowest relative humidity change amplitude among the assessed thermal parameters. (2) Among the 11 geometric form indicators, 3D indicators correlate more significantly with thermal environment parameters than 2D indicators. Specifically, street orientation significantly impacts the thermal environment, Build-To-Line Rat holds greater significance than interface density, and both building shape coefficient and block surface ratio are significantly correlated with air temperature and wind speed, with a weaker correlation to solar radiation. (3) In the Xi'an region, courtyards oriented north-south demonstrate a more favorable trend in the thermal environment.

Early salvage therapy with anti-PD-1 antibody Camrelizumab in patients with advanced cervical cancer: a retrospective study.

OBJECTIVE: To observe the clinical efficacy of Camrelizumab in patients with advanced cervical cancer who presented with resistance to initial therapy. METHODS: We retrieved data from 25 patients with advanced (stage IIA2-IV) cervical cancer who were administered a combination salvage therapy with Camrelizumab due to the poor response to initial chemotherapy. The primary outcome was objective response rate (ORR) and disease control rate (DCR), the secondary endpoints included progression-free survival (PFS) and the occurrence of adverse events. To evaluate its long-term effect on PFS, we included 64 patients diagnosed with stage IIA2-IV during the study period, who were responsive to initial radiotherapy or chemotherapy and received conventional therapy as control. RESULTS: Camrelizumab exhibits a high salvage treatment efficacy, with ORR of 80.0% (20/25) and DCR of 88.0% (22/25) in Camrelizumab salvage group (CS group). The PFS in CS group was significantly longer than that in control group. The median follow-up time were 18.1 and 18.3 months in the CS group and the control group, respectively, and neither achieved median PFS. The adverse event (AEs) rates in the CS and control groups were 52.0% (13/25) and 51.6% (33/64), in which the most common adverse events were myelosuppression, cutaneous capillary endothelial proliferation (CCEP), and elevated liver enzymes, and the grade of AEs was less than grade 3 in all patients. CONCLUSION: Camrelizumab demonstrated promising efficacy and safety as the early salvage treatment for patients with advanced cervical cancer.

Proteomic detection of COX-2 pathway-related factors in patients with adenomyosis.

Background: Investigating the relationship between cyclooxygenase-2 (COX-2) pathway-related factors and clinical features in patients with adenomyosis by proteomics could provide potential therapeutic targets. Methods: This study recruited 40 patients undergoing surgical hysterectomy and pathological diagnosis of adenomyosis, collected ectopic endometrial specimens, and recorded clinical data. The expression levels of COX-2 in ectopic uterus lesions were detected using the immunohistochemical (IHC) SP method. The 40 samples were then divided into a COX-2 low or high expression group. Five samples with the most typical expression levels were selected from each of the two groups and the differential proteins between the two groups were identified using label-free quantitative proteomics. WW domain-binding protein 2 (WBP2), interferon induced transmembrane protein 3 (IFITM3), and secreted frizzled-related protein 4 (SFRP4) were selected for further verification, and their relationships with COX-2 and clinical characteristics were analyzed. Results: There were statistically significant differences in the expression of WBP2, IFITM3, and SFRP4 between the COX-2 low and high expression groups (P < 0.01). The expressions of COX-2, IFITM3, and SFRP4 were significantly correlated with dysmenorrhea between the two groups (P < 0.05), but not with uterine size or menstrual volume (P > 0.05). However, there was no significant correlation between the expression of WBP2 and dysmenorrhea, uterine size, and menstruation volume in both the high expression and low expression groups (P > 0.05). Conclusions: COX-2, IFITM3, SFRP4, and WBP2 may be involved in the pathogenesis of adenomyosis. COX-2, IFITM3, and SFRP4 may serve as potential molecular biomarkers or therapeutic targets in dysmenorrhea in patients with early adenomyosis.

Esomeprazole Alleviates Cisplatin Resistance by Inhibiting the AKT/mTOR Pathway in Ovarian Cancer Cells.

Purpose: Ovarian cancer is the most lethal malignancy in gynecology. Due to limited treatment strategies and platinum resistance, newer drugs and therapeutic options are needed. Esomeprazole (ESO) has been reported to have multiple anticancer activities in preclinical and clinical research. Therefore, this study aimed to explore the anticancer effects of esomeprazole on ovarian cancer and its underlying molecular mechanisms. Methods: CCK-8 and 5-ethynyl-2'-deoxyuridine (EdU) assays were used to detect cell viability and proliferation. The Transwell assay was used to evaluate cell migration and invasion capacity. Flow cytometry was used to detect cell apoptosis. Western blotting and immunofluorescence were used to detect protein expression. Results: ESO effectively inhibited the cell viability, proliferation, invasion, migration, and induced apoptosis of ovarian cancer cells in a concentration-dependent manner. Treatment with ESO decreased the expression of c-MYC, SKP2, E2F1, N-cadherin, vimentin, and matrix metalloproteinase 2 (MMP2), while it increased E-cadherin, caspase3, p53, BAX, and cleaved poly (ADP-ribose) polymerase (PARP) expression, and downregulated the PI3K/AKT/mTOR signaling pathway. Furthermore, ESO combined with cisplatin showed synergistic effects in inhibiting proliferation, invasion, and migration of cisplatin-resistant ovarian cancer cells. The mechanism may be related to the increased inhibition of c-MYC, epithelial-mesenchymal transition (EMT), and the AKT/mTOR signaling pathway and enhanced the upregulation of the pro-apoptotic protein BAX and cleaved PARP levels. Moreover, ESO combined with cisplatin synergistically upregulated the expression of the DNA damage marker γH2A.X. Conclusion: ESO exerts multiple anticancer activities and has a synergistic effect in combination with cisplatin on cisplatin-resistant ovarian cancer cells. This study provides a promising strategy to improve chemosensitivity and overcome resistance to cisplatin in ovarian cancer.

Celecoxib reduces inflammation and angiogenesis in mice with adenomyosis.

OBJECTIVE: This study aimed to explore the effect of COX-2 selective inhibitor (celecoxib) on adenomyosis and its mechanism. METHODS: By establishing a mouse model of adenomyosis and using celecoxib to treat adenomyosis, newly born female mice were randomly divided into a control group, adenomyosis model group, and celecoxib group. Hematoxylin-eosin (H&E) staining was used to observe the depth of endometrial infiltration of mouse adenomyosis. RT-PCR (reverse transcription PCR) and western blot were used to detect the expression of Cyclooxygenase-2 (COX-2), Vascular growth factor (VEGF), Nerve growth factor (NGF), and Corticotropin-releasing hormone (CRH) mRNA and protein in mice before and after celecoxib treatment. RESULTS: After treatment with celecoxib, the depth of endometrial infiltration of mouse adenomyosis was reduced. COX-2 and VEGF decreased significantly after celecoxib inhibited expression of COX-2 (P<0.001), but there was no significant difference in the expression of NGF or CRH (P>0.05). CONCLUSION: This study indicated that COX-2 may be an important factor related to the pathogenesis of adenomyosis, and it may become an important molecular target for the treatment of adenomyosis.