The transport impedance disparity indicator: A case study of Xi'an, China

This research proposes a transport mobility disparity indicator which identifies the accessibility by urban points of interest (PoI) (e.g. distribution of working place, park, school, hospital, supermarket, bus, and metro stations, etc.),community/hukou (household registration) policy types (local hukou/city residents vs non-local hukou/migrant residents), and their average transport cost to income ratios to describe the gap between traffic demand and accessibility of different communities.The lower the ratio of the average transport costs to average incomes of a community and the more PoI factors in the surrounding areas, the lower the transport impedance indicator of the community, and vice versa. Greater transport impedance disparity indicators between different communities in the same city indicate a larger gap in transport impedance, helping urban planners identify the severity of the unequal relationship between different areas and the decision-making support provided future urban planning and administrative policies. Xi'an, the capital city of Shaanxi province in China, is chosen as the research subject in this study to calculate the transport impedance disparity indicator between local and non-local hukou residents' communities. The transport impedance disparity indicator effectively reveals the different treatments between local and non-local hukou residents' communities in the same city. Compared to local hukou residents, non-local hukou residents experience clear disadvantages in terms of accessibility

Urban models: Progress and perspective

Urban modelling is an important branch of land use science. It integrates geography, surveying and mapping, information science, system science, economics, sociology and other disciplines to establish urban models, which have been used to provide support for urban policymaking or analyses. Urban models are used to understand, analyse, evaluate and reproduce the process of urban development, and predict the consequence of urban planning scenarios. In this paper, we provide a systematic review of urban models, including the evaluation, classification, application of urban models, and the timeline of urban models’ development. According to their modelling styles and applications, urban models can be classified into three categories: aggregate static models of economic and spatial interaction, urban dynamics models, and behavioural models of individual agents which linked to spatial location. According to the different modelling methods, urban models can be classified into two categories: top-down and bottom-up. Nowadays, emerging technologies, especially Information and Communication Technologies (ICT), are gradually but significantly changing the organization form of urban economic activities. It enables regions to break the location limitation and join in the national even global industry division, and that triggers a new bottom-up rural urbanization process, which formed a significant challenge for urban models. Based on above discussion, we proposed two perspectives for improvements of urban models, inculding the integration of ICT with tradtional urban models and integaration of top-down and bottom-up models

Association between matched chronotype and poor mental health among shift workers: a systematic review and meta-analysis

BACKGROUND: Nearly 0.7 billion workers are involved in the shift work system, leading to concerns about its potential impacts on the large-scale population mental health. This study aimed to synthesise evidence of the associations between matched chronotype and the risk of poor mental health among shift workers. METHODS: Six computerised databases were searched from inception to September 2022. Observational studies were selected if they reported any association between common mental health parameters and chronotype scores/types of shift workers. The Preferred Reporting Items for Systematic Reviews and Meta-analyses checklist was followed. We extracted adjusted risk estimates to calculate pooled effect sizes and explore sources of heterogeneity. The study was registered in PROSPERO: CRD42022357437. RESULTS: Fourteen studies including 49 909 workers were identified. Ever shift workers had a higher risk of poor mental health than the day workers (pooled OR 1.15, 95% CI 1.03 to 1.28; I 2=14%, p=0.29), with the evening chronotype ever shift workers having a 1.47 times higher risk than those who worked during the day (pooled OR 1.47, 95% CI 1.13 to 1.91; I 2=42%, p=0.16). Sensitivity analysis excluding studies with the highest risk of bias of each group demonstrated consistent findings. CONCLUSIONS: Evening chronotype ever shift workers have poorer mental health than shift workers with other chronotypes. Chronotype remains unrecognised in the contemporary rostering system, making it a hidden contributor to occupational mental health. Work-related physical and mental stresses may be prevented/mitigated with further investigation on optimising shift work schedule combined with individual chronotype preference

Transferred BCR/ABL DNA from K562 extracellular vesicles causes chronic myeloid leukemia in immunodeficient mice.

Our previous study showed that besides mRNAs and microRNAs, there are DNA fragments within extracellular vesicles (EVs). The BCR/ABL hybrid gene, involved in the pathogenesis of chronic myeloid leukemia (CML), could be transferred from K562 EVs to neutrophils and decrease their phagocytic activity in vitro. Our present study provides evidence that BCR/ABL DNAs transferred from EVs have pathophysiological significance in vivo. Two months after injection of K562 EVs into the tail vein of Sprague-Dawley (SD) rats, they showed some characteristics of CML, e.g., feeble, febrile, and thin, with splenomegaly and neutrophilia but with reduced neutrophil phagocytic activity. These findings were also observed in immunodeficient NOD/SCID mice treated with K562 EVs; BCR/ABL mRNA and protein were found in their neutrophils. The administration of actinomycin D, an inhibitor of de novo mRNA synthesis, prevented the abnormalities caused by K562 EVs in NOD/SCID mice related to CML, including neutrophilia and bone marrow hyperplasia. As a specific inhibitor of tyrosine kinases, imatinib blocked the activity of tyrosine kinases and the expression of phospho-Crkl, induced by the de novo BCR/ABL protein caused by K562 EVs bearing BCR/ABL DNA. Our current study shows the pathophysiological significance of transferred tumor gene from EVs in vivo, which may represent an important mechanism for tumorigenesis, tumor progression, and metastasis

Development and Validation of Prediction Models for Hypertensive Nephropathy, the PANDORA Study

Importance: Hypertension is a leading cause of end-stage renal disease (ESRD), but currently, those at risk are poorly identified. Objective: To develop and validate a prediction model for the development of hypertensive nephropathy (HN). Design Setting and Participants: Individual data of cohorts of hypertensive patients from Kailuan, China served to derive and validate a multivariable prediction model of HN from 12, 656 individuals enrolled from January 2006 to August 2007, with a median follow-up of 6.5 years. The developed model was subsequently tested in both derivation and external validation cohorts. Variables: Demographics, physical examination, laboratory, and comorbidity variables. Main Outcomes and Measures: Hypertensive nephropathy was defined as hypertension with an estimated glomerular filtration rate (eGFR) \u3c 60 ml/min/1.73 m and/or proteinuria. Results: About 8.5% of patients in the derivation cohort developed HN after a median follow-up of 6.5 years that was similar in the validation cohort. Eight variables in the derivation cohort were found to contribute to the risk of HN: salt intake, diabetes mellitus, stroke, serum low-density lipoprotein, pulse pressure, age, hypertension duration, and serum uric acid. The discrimination by concordance statistics (C-statistics) was 0.785 (IQR, 0.770-0.800); the calibration slope was 1.129, the intercept was -0.117; and the overall accuracy by adjusted was 0.998 with similar results in the validation cohort. A simple points scale developed from these data (0, low to 40, high) detected a low morbidity of 7% in the low-risk group (0-10 points) compared with \u3e40% in the high-risk group (\u3e20 points). Conclusions and Relevance: A prediction model of HN over 8 years had high discrimination and calibration, but this model requires prospective evaluation in other cohorts, to confirm its potential to improve patient care

Prenatal Lipopolysaccharides Exposure Induces Transgenerational Inheritance of Hypertension

BACKGROUND: Adverse environmental exposure during the prenatal period can lead to diseases in the offspring, including hypertension. Whether or not the hypertensive phenotype can be transgenerationally transmitted is not known. METHODS: Pregnant Sprague Dawley rats were intraperitoneally injected with lipopolysaccharide (LPS) on gestation days 6, 8, 10, and 12 to generate the prenatal LPS exposure model. Blood pressure was monitored by both telemetry and tail-cuff method. RNA sequencing was performed to analyze transcriptome alteration in the kidney of the third generation. Tempol and spironolactone were used to test the potential prevention and therapeutic effect of targeting reactive oxygen species and mineralocorticoid receptor signaling, respectively. Molecular biological experiments were performed to illustrate the mechanism of epigenetic and transcription regulation. RESULTS: Prenatal LPS exposure can impair the ability to excrete a salt load and induce hypertension from the first to the third generations, with the fourth and fifth generations, inducing salt-sensitive hypertension. Compared with control pups, the transcriptome in the kidney of the hypertensive third-generation prenatal LPS-exposed offspring have upregulation of the Ras-related C3 botulinum toxin substrate 1 () gene and activation of mineralocorticoid receptor signaling. Furthermore, we found that LPS exposure during pregnancy triggered oxidative stress that upregulated KDM3B (histone lysine demethylase 3B) in the oocytes of first-generation female rats, leading to an inheritable low level of H3K9me2 (histone H3 lysine 9 dimethylation), resulting in the transgenerational upregulation of . Based on these findings, we treated the LPS-exposed pregnant rats with the reactive oxygen species scavenger, tempol, which successfully prevented hypertension in the first-generation offspring and the transgenerational inheritance of hypertension. CONCLUSIONS: These findings show that adverse prenatal exposure induces transgenerational hypertension through an epigenetic-regulated mechanism and identify potentially preventive and therapeutic strategies for hypertension

LncRNA PSR Regulates Vascular Remodeling Through Encoding a Novel Protein Arteridin.

RATIONALE: Vascular smooth muscle cells (VSMCs) phenotype switch from contractile to proliferative phenotype is a pathological hallmark in various cardiovascular diseases. Recently, a subset of long noncoding RNAs was identified to produce functional polypeptides. However, the functional impact and regulatory mechanisms of long noncoding RNAs in VSMCs phenotype switching remain to be fully elucidated. OBJECTIVES: To illustrate the biological function and mechanism of a VSMC-enriched long noncoding RNA and its encoded peptide in VSMC phenotype switching and vascular remodeling. RESULTS: We identified a VSMC-enriched transcript encoded by a previously uncharacterized gene, which we called phenotype switching regulator (PSR), which was markedly upregulated during vascular remodeling. Although PSR was annotated as a long noncoding RNA, we demonstrated that the lncPSR (PSR transcript) also encoded a protein, which we named arteridin. In VSMCs, both arteridin and lncPSR were necessary and sufficient to induce phenotype switching. Mechanistically, arteridin and lncPSR regulate downstream genes by directly interacting with a transcription factor YBX1 (Y-box binding protein 1) and modulating its nuclear translocation and chromatin targeting. Intriguingly, the PSR transcription was also robustly induced by arteridin. More importantly, the loss of PSR gene or arteridin protein significantly attenuated the vascular remodeling induced by carotid arterial injury. In addition, VSMC-specific inhibition of lncPSR using adeno-associated virus attenuated Ang II (angiotensin II)-induced hypertensive vascular remodeling. CONCLUSIONS: PSR is a VSMC-enriched gene, and its transcript IncPSR and encoded protein (arteridin) coordinately regulate transcriptional reprogramming through a shared interacting partner, YBX1. This is a previously uncharacterized regulatory circuit in VSMC phenotype switching during vascular remodeling, with lncPSR/arteridin as potential therapeutic targets for the treatment of VSMC phenotype switching-related vascular remodeling

Pathophysiological parameters in NOD/SCID mice injected with K562 EVs.

<p>NOD/SCID mice were injected with K562 EVs or K562 cells and/or actinomycin D via tail-vein, every three days for 2 months. Rectal temperature (<b>A</b>), body weight (<b>B</b>), and spleen weight (<b>C-a</b>) were measured and histologies (<b>C-b</b>) were examined (* <i>P</i><0.05 vs. control, n = 3). In <b>Figure C-b</b>, sections of spleen of NOD/SCID mouse stained with hematoxylin-eosin (HE) were examined under a microscope using 10×40 lens. Spleens of NOD/SCID mice treated with vehicle (PBS) (<b>1</b>), actinomycin D (7 µg/kg) (<b>2</b>), K562 EVs (2×10⁶) and actinomycin D (7 µg/kg) (<b>3</b>), K562 EVs (2×10⁶) (<b>4</b>), and K562 cells (2×10⁶) (<b>5</b>).</p

BCR/ABL expression in neutrophils from NOD/SCID mice.

<p>(<b>A</b>): BCR/ABL DNA expression in neutrophils from NOD/SCID mice. NOD/SCID mice were injected with K562 EVs or K562 cells and/or actinomycin D, via tail-vein every three days for 2 months. (<b>a</b>) The upper figure shows the BCR/ABL DNA detected by PCR that was resolved on precasted 2% agarose gel with ethidium bromide. (<b>b</b>): The lower figure shows the sequence of the PCR product of BCR/ABL DNA in the neutrophils from the NOD/SCID mice; the percentage sequence identity was more than 99.5%. The black arrow indicates the merge point of the BCR DNA and ABL DNA. (<b>B</b>): BCR/ABL mRNA expression in neutrophils from NOD/SCID mice. NOD/SCID mice were injected with K562 EVs or K562 cells and/or actinomycin D, via tail-vein every three days for 2 months. (<b>a</b>): The upper figures show the expression of BCR/ABL mRNA in neutrophils detected by RT-PCR on precasted 2% agarose gel with ethidium bromide. (<b>b</b>): The lower figures show the sequence of the RT-PCR product of BCR/ABL mRNA and β-actin mRNA in the neutrophils from the NOD/SCID mice; the percentage sequence identity is more than 99.5%. The black arrow indicates the merge point of the BCR mRNA and ABL mRNA. (<b>C</b>): BCR/ABL protein expression in neutrophils from NOD/SCID mice. NOD/SCID mice were injected with K562 EVs or K562 cells and/or actinomycin D, via tail-vein every three days for 2 months. The neutrophils were collected and the expression of BCR/ABL protein was detected by immunoblotting. <b>Lane M</b>, DNA marker; neutrophils from NOD/SCID mice treated with vehicle (PBS) (<b>lane 1</b>), actinomycin D (7 µg/kg) (<b>lane 2</b>), K562 EVs (2×10⁶) and actinomycin D (7 µg/kg) (<b>lane 3</b>), K562 EVs (2×10⁶) (<b>lane 4</b>), and K562 cells (2×10⁶) (<b>lane 5</b>); K562 cells and ddH₂O were taken as positive and negative controls, respectively (<b>lane 6 and 7</b>).</p