The impact of rivers and lakes on urban transportation expansion: A case study of the century-long evolution of the road network in Wuhan, China.

Throughout history, rivers and lakes have wielded a profound influence on the dynamics of urban transportation expansion. To illustrate this phenomenon, we turn to the century-long evolution of the road network in Wuhan, China, as a case study. The study aims to explore the relationship framework between water bodies and urban transportation, characterized by the sequence of "strong connection" to "weakened connection", then to "mutual restriction", and ultimately to "mutual benefit". Additionally, the analysis of the impact mechanisms of rivers and lakes on urban transportation at different stages of development is also a key research objective. To facilitate our exploration, we select the road networks in Wuhan from four years of 1922, 1969, 1995, and 2023 as the primary research subjects. By establishing water buffers, we scrutinize the evolving characteristics of riverside and lakeside transportation amidst the city's expansion. Based on the modified shortest path model, we introduce the innovative concepts of "Detour Index" and "Weighted Detour Index" to assess the road accessibility of each node in the city based on its inherent environmental conditions. This allows for the effective analysis of the potential impact of water bodies as "obstacles" on the road network at different stages of urban development. The study found that in the areas adjacent to the rivers and lakes in Wuhan, there is insufficient road accessibility based on their inherent environmental conditions. Particularly, some areas along the rivers may become "terminals" in the urban road network. Furthermore, during the process of urban expansion, the correlation between the urban road network and rivers continues to weaken, while the correlation with lakes continues to strengthen. These conclusions can provide valuable insights for the planning of urban roads near water bodies.

Association Between Albumin-Corrected Anion Gap and In-Hospital Mortality and Sepsis-Associated Acute Kidney Injury.

BACKGROUND This study aimed to investigate the association between albumin-corrected anion gap (ACAG) and in-hospital mortality in sepsis-associated acute kidney injury (S-AKI). MATERIAL AND METHODS We conducted this retrospective study based on data from the Medical Information Mart for Intensive Care IV database, and assessed the prognostic capabilities of ACAG in comparison with albumin (ALB) and anion gap (AG) to predict in-hospital mortality of patients with S-AKI. Binomial logistic regression analysis was performed to identify whether ACAG was an independent risk factor for in-hospital mortality for the patients, and receiver operating characteristic (ROC) curves were plotted to clarify its efficacy in predicting in-hospital mortality. We also performed a decision curve analysis (DCA) to determine whether there were net clinical benefits for patients when ACAG was used to predict in-hospital mortality. RESULTS Binary logistic regression analysis showed that ACAG was an independent risk factor for in-hospital mortality in patients with S-AKI, with an area under the ROC (AUC) curve of 0.675 (moderate predictive value) for the prediction of in-hospital mortality, higher than that of ALB or AG alone, with the highest Youden's index (0.2675). The DCA substantiated the superiority of ACAG in net clinical benefits at various threshold probability, enhancing its clinical applicability. CONCLUSIONS The research emphasizes the potential of ACAG as a valuable predictive tool for in-hospital mortality in S-AKI patients, which is better than albumin and AG, encouraging its consideration in clinical practice.

Erratum: "Baicalin prevents pulmonary arterial remodeling in vivo via the AKT/ERK/NF-κB signaling pathways".

[This corrects the article DOI: 10.1177/2045894019878599.].

Heart­lung crosstalk in pulmonary arterial hypertension following myocardial infarction (Review).

Left heart disease is the main cause of clinical pulmonary arterial hypertension (PAH). Common types of left heart disease that result in PAH include heart failure, left ventricular systolic dysfunction, left ventricular diastolic dysfunction and valvular disease. It is currently believed that mechanical pressure caused by high pulmonary venous pressure is the main cause of myocardial infarction (MI) in individuals with ischemic cardiomyopathy and left ventricular systolic dysfunction. In the presence of decreased cardiac function, vascular remodeling of pulmonary vessels in response to long­term stimulation by high pressure in turn leads to exacerbation of PAH. However, the underlying pathological mechanisms remain unclear. Elucidating the association between the development of MI and PAH may lead to a better understanding of potential risk factors and better disease treatment. In this article, the pathophysiological effects of multiple systems in individuals with MI and PAH were reviewed in order to provide a general perspective on various potential interactions between cardiomyocytes and pulmonary vascular cells.

Baicalin prevents pulmonary arterial remodeling in vivo via the AKT/ERK/NF-κB signaling pathways.

Pulmonary arterial hypertension is a rapidly progressive and often fatal disease. As the pathogenesis of pulmonary arterial hypertension remains unclear, there is currently no good drug for pulmonary arterial hypertension and new therapy is desperately needed. This study investigated the effects and mechanism of baicalin on vascular remodeling in rats with pulmonary arterial hypertension. A rat pulmonary arterial hypertension model was constructed using intraperitoneal injection of monocrotaline, and different doses of baicalin were used to treat these rats. The mean pulmonary arterial pressure (mPAP) and right ventricular systolic pressure (RVSP) were measured with a right heart catheter. Moreover, the hearts were dissected to determine the right ventricular hypertrophy index (RVHI). The lung tissues were stained with H&E and Masson's staining to estimate the pulmonary vascular remodeling and collagen fibrosis, and the expression of proteins in the AKT, ERK, and NF-κB p65 phosphorylation (p-AKT, p-ERK, p-p65) was examined by Western blot analysis. We found that compared with untreated pulmonary arterial hypertension rats, baicalin ameliorated pulmonary vascular remodeling and cardiorespiratory injury, inhibited p-p65 and p-ERK expression, and promoted p-AKT and p-eNOS expression. In conclusion, baicalin interfered with pulmonary vascular remodeling and pulmonary arterial hypertension development in rats through the AKT/eNOS, ERK and NF-κB signaling pathways.

ITE promotes hypoxia-induced transdifferentiation of human pulmonary arterial endothelial cells possibly by activating transforming growth factor-ß/Smads and MAPK/ERK pathways.

This study aimed to investigate the transdifferentiation of human pulmonary arterial endothelial cells (HPAECs) into smooth muscle like (SM-like) cells under hypoxic conditions and reveal the role of endogenous small molecular compound 2-(1'H-indole-3'-carbonyl)-thiazole-4-carboxylicacid methyl ester (ITE) in this process. HPAECs were treated by hypoxia and hypoxia + ITE with different durations. The endothelial markers (CD31 and VE-cad) and smooth muscle markers (α-SMA, SM22α, and OPN) were investigated by immunofluorescence double staining, and their expressions, along with the differentiation regulators transforming growth factor-ß (TGF-ß) ligands and downstream signals including TGF-ß1, bone morphogenetic protein (BMP2), BMP9, Samd2/3, ERK, and p38 MAPK, were determined by Western blot analysis. The viability and proliferation of HPAECs were detected by Cell Counting Kit-8 (CCK-8) method and bromodeoxyuridine (BrdU) assays. As a result, hypoxia induced HPAECs transdifferentiation from paving-stone-like into polygonal or spindle cells, whose number increased greatly after additional ITE stimulation for 7 days. Compared with the normoxic HPAECs, the expression of endothelial markers reduced and smooth muscle markers were enhanced with the extension of hypoxia + ITE treatment, and meanwhile the cell viability increased significantly. Hypoxia could promote expression of TGF-ß1 protein rather than BMP2 and BMP9, and regulate phosphorylation levels of Samd2/3, ERK and p38 MAPK in different manners. In conclusion, ITE can promote the hypoxia-induced transdifferentiation of HPAECs into SM-like cells via TGF-ß/Smads and MAPK/ERK pathways.