Prior-free 3D tracking of a fast-moving object at 6667 frames per second with single-pixel detectors.

Real-time tracking and 3D trajectory computation of fast-moving objects is a promising technology, especially in the field of autonomous driving. However, existing image-based tracking methods face significant challenges when it comes to real-time tracking, primarily due to the limitation of storage space and computational resources. Here, we propose a novel approach that enables real-time 3D tracking of a fast-moving object without any prior motion information and at a very low computational cost. To enable 3D coordinate synthesis with a space-efficient optical setup, geometric moment patterns are projected on two non-orthogonal planes with a spatial resolution of 125 µm. Our experiment demonstrates an impressive tracking speed of 6667 frames per second (FPS) with a 20 kHz digital micromirror device (DMD), which is more than 200 times faster than the widely adopted video-based tracking methods. To the best of our knowledge, this is the highest tracking speed record in the field of single-pixel 3D trajectory tracking. This method promotes the development of real-time tracking techniques with single-pixel imaging (SPI).

Error-compensation network for ringing artifact reduction in holographic displays.

Recent advances in learning-based computer-generated holography (CGH) have unlocked novel possibilities for crafting phase-only holograms. However, existing approaches primarily focus on the learning ability of network modules, often neglecting the impact of diffraction propagation models. The resulting ringing artifacts, emanating from the Gibbs phenomenon in the propagation model, can degrade the quality of reconstructed holographic images. To this end, we explore a diffraction propagation error-compensation network that can be easily integrated into existing CGH methods. This network is designed to correct propagation errors by predicting residual values, thereby aligning the diffraction process closely with an ideal state and easing the learning burden of the network. Simulations and optical experiments demonstrate that our method, when applied to state-of-the-art HoloNet and CCNN, achieves PSNRs of up to 32.47 dB and 29.53 dB, respectively, surpassing baseline methods by 3.89 dB and 0.62 dB. Additionally, real-world experiments have confirmed a significant reduction in ringing artifacts. We envision this approach being applied to a variety of CGH algorithms, paving the way for improved holographic displays.

Image-free single-pixel keypoint detection for privacy preserving human pose estimation.

Computer vision technology has been applied in various fields such as identification, surveillance, and robot vision. However, computer vision algorithms used for human-related tasks operate on human images, which raises data security and privacy concerns. In this Letter, we propose an image-free human keypoint detection technique using a few coded illuminations and a single-pixel detector. Our proposed method can complete the keypoint detection task at an ultralow sampling rate on a measured one-dimensional sequence without image reconstruction, thus protecting privacy from the data collection stage and preventing the acquisition of detailed visual information from the source. The network is designed to optimize both the illumination patterns and the human keypoint predictor with an encoder-decoder framework. For model training and validation, we used 2000 images from Leeds Sport Dataset and COCO Dataset. By incorporating EfficientNet backbone, the inference time is reduced from 4 s to 0.10 s. In the simulation, the proposed network achieves 91.7% average precision. Our experimental results show an average precision of 88.4% at a remarkably low sampling rate of 0.015. In summary, our proposed method has the advantages of privacy protection and resource efficiency, which can be applied to many monitoring and healthcare tasks, such as clinical monitoring, construction site monitoring, and home service robots.

YY1: a key regulator inhibits gastric cancer ferroptosis and mediating apatinib-resistance.

OBJECTIVE: Gastric cancer (GC) stands as a prevalent and deadly global malignancy. Despite its role as a preoperative neoadjuvant therapy, Apatinib's effectiveness is curtailed among GC patients exhibiting elevated YY1 expression. YY1's connection to adverse prognosis, drug resistance, and GC metastasis is established, yet the precise underlying mechanisms remain elusive. This study aims to unravel potential pathogenic pathways attributed to YY1. DESIGN: Utilizing bioinformatics analysis, we conducted differentially expressed genes, functional annotation, and pathway enrichment analyses, and further validation through cellular and animal experiments. RESULTS: Higher YY1 expression correlated with diminished postoperative progression-free survival (PFS) and disease-specific survival (DSS) rates in TCGA analysis, identifying YY1 as an independent DSS indicator in gastric cancer (GC) patients. Notably, YY1 exhibited significantly elevated expression in tumor tissues compared to adjacent normal tissues. Bioinformatics analysis revealed noteworthy differentially expressed genes (DEGs), transcriptional targets, factors, and co-expressed genes associated with YY1. LASSO Cox analysis unveiled Transferrin as a prospective pivotal protein regulated by YY1, with heightened expression linked to adverse DSS and PFS outcomes. YY1's role in governing the p53 signaling pathway and ferroptosis in GC cells was further elucidated. Moreover, YY1 overexpression dampened immune cell infiltration within GC tumors. Additionally, YY1 overexpression hindered GC cell ferroptosis and mediated Apatinib resistance via the p53 pathway. Remarkably, IFN-a demonstrated efficacy in reversing Apatinib resistance and immune suppression in GC tissues. CONCLUSIONS: Our findings underscore the pivotal role of YY1 in driving GC progression and influencing prognosis, thus pinpointing it as a promising therapeutic target to enhance patient outcomes.

A scoring system to predict the technical difficulty of endoscopic resection for cardial submucosal tumors.

BACKGROUND AND AIM: Endoscopic resection has been successfully used for the removal of digestive submucosal tumors (SMTs). However, the cardia has been considered a challenging location for endoscopic resection due to its narrow lumen and sharp angle. The objective of this study was to establish a clinical scoring model to grade the technical difficulty of endoscopic resection for cardial SMTs. METHODS: A total of 246 patients who suffered cardial SMTs and received endoscopic resection were included in this retrospective study. All of them were randomized into the training cohort (n = 123) or internal validation cohort (n = 123). Potential predictors were analyzed using univariate analysis. Then, covariates with P < 0.05 were selected for the multivariate logistic regression model. The ß coefficients from the logistic regression model were used to create a scoring system for technical difficulty prediction by rounding the score to the nearest integer of the absolute ß coefficient value. RESULTS: The clinical score consisted of the following factors: male gender (2 points), extraluminal growth (3 points), and maximum diameter ≥3 cm (3 points). The scoring model demonstrated good discriminatory power, with an area under the receiver operating characteristic curve of 0.860 and a 95% confidence interval of 0.763-0.958. The model also showed a good goodness of fit in the Hosmer-Lemeshow test (P = 0.979). In the training cohort, the probability of encountering technical difficulty in the easy (score = 0), intermediate (score = 1-3), difficult (score = 4-6), and very difficult (score >6) categories was 0, 6.8%, 33.3%, and 100.0%, respectively; similarly, in the validation cohort, it was 0, 5.6%, 22.2%, and 50.0%, respectively. CONCLUSIONS: This scoring system could serve as a valuable tool for clinicians in predicting the technical difficulty of endoscopic resection for cardial SMTs.

Non B Cell-Derived Immunoglobulins in Intestinal Tract.

Intestinal epithelium constitutes a barrier to the unrestricted movement of pathogens, and other detrimental substances from the external world (gut lumen) into the interstitial environment. Intestinal epithelial cells obstruct harmful substances passing through the epithelium as a physical and chemical barrier; Moreover, the epithelial cells can express Toll-like receptors (TLRs) and cytokines to exert innate immune function. In addition, high levels of immunoglobulin A (IgA) and other antibodies exist in the intestinal mucosa, maintaining intestinal immune homeostasis in conjunction with intestinal probiotics. Traditionally, these antibodies have been deemed to be secreted by submucosal plasma cells. Nonetheless, in recent years, it has been demonstrated that intestinal epithelial cells produce a substantial amount of Igs, especially IgA or free Ig light chains, which are involved in intestinal immune homeostasis and the survival of normal epithelial cells. Furthermore, mounting evidence affirms that many human carcinoma cells, including colorectal cancer (CRC), can overexpress Igs, particularly IgG. Cancer-derived Igs exhibit a unique V(D)J rearrangement pattern distinct from B cell-derived Ig; moreover, this cancer cell-derived IgG also has a unique sialic acid modification on the 162 site of CH1 domain (SIA-IgG). The SIA-IgG plays a crucial role in promoting cancer initiation, progression, metastasis, and tumour immune escape. Simultaneously, CRC cells can also express free Ig light chains, which promote colitis, colitis-associated colon carcinogenesis, and CRC progression. Therefore, Igs expressed by CRC cells could be a potential target for diagnosing and preventing the transformation of inflammation into cancer, as well as treating CRC.

End-to-end compression-aware computer-generated holography.

Joint photographic experts group (JPEG) compression standard is widely adopted for digital images. However, as JPEG encoding is not designed for holograms, applying it typically leads to severe distortions in holographic projections. In this work, we overcome this problem by taking into account the influence of JPEG compression on hologram generation in an end-to-end fashion. To this end, we introduce a novel approach to merge the process of hologram generation and JPEG compression with one differentiable model, enabling joint optimization via efficient first-order solvers. Our JPEG-aware end-to-end optimized holograms show significant improvements compared to conventional holograms compressed using JPEG standard both in simulation and on experimental display prototype. Specifically, the proposed algorithm shows improvements of 4 dB in peak signal-to-noise ratio (PSNR) and 0.27 in structural similarity (SSIM) metrics, under the same compression rate. When maintained with the same reconstruction quality, our method reduces the size of compressed holograms by about 35% compared to conventional JPEG-compressed holograms. Consistent with simulations, the experimental results further demonstrate that our method is robust to JPEG compression loss. Moreover, our method generates holograms compatible with the JPEG standard, making it friendly to a wide range of commercial software and edge devices.

Muscular injury as an independent risk factor for esophageal stenosis after endoscopic submucosal dissection of esophageal squamous cell cancer.

BACKGROUND AND AIMS: Stenosis after esophageal endoscopic submucosal dissection (ESD) has a high incidence, and muscular injury is an important risk factor for esophageal stenosis. Hence, this study aimed to classify muscular injury degrees and investigate their association with postoperative stenosis. METHODS: This retrospective study included 1033 patients with esophageal mucosal lesions treated with ESD between August 2015 and March 2021. Demographic and clinical parameters were analyzed, and stenosis risk factors were identified using multivariate logistic regression. A novel muscular injury classification system was proposed and used to investigate the association between different muscular injury degrees and postoperative stenosis. Finally, a scoring system was established to predict muscular injury. RESULTS: Of 1033 patients, 118 (11.4%) had esophageal stenosis. The multivariate analysis demonstrated that the history of endoscopic esophageal treatment, circumferential range, and muscular injury were significant risk factors for esophageal stenosis. Patients with type II muscular injuries tended to develop complex stenosis (n = 13 [36.1%], P < .05), and type II muscular injuries were more likely to predispose patients to severe stenosis than type I (73.3% and 92.3%, respectively). The scoring system showed that patients with high scores (3-6) were more likely to have muscular injury. The score model presented good discriminatory power in the internal validation (area under the receiver-operating characteristic curve, .706; 95% confidence interval, .645-.767) and goodness-of-fit in the Hosmer-Lemeshow test (P = .865). CONCLUSIONS: Muscular injury was an independent risk factor for esophageal stenosis. The scoring system demonstrated good performance in predicting muscular injury during ESD.

Risk factors for complications and incomplete resection after endoscopic resection for duodenal submucosal tumors.

BACKGROUND AND AIM: Endoscopic resection (ER) has been used to remove submucosal tumors (SMTs) in recent years; however, duodenal ER is associated with high rates of immediate or delayed bleeding and perforation. Whether ER can be recommended for the treatment of duodenal SMTs remains controversial. Therefore, we aimed to investigate the clinical outcomes associated with the ER of duodenal SMTs and to assess possible predictive factors for complications and incomplete resection. METHODS: This retrospective study included 141 patients with duodenal SMTs. The therapeutic outcomes from ER and procedure-related complications were analyzed. RESULTS: Of the 141 patients, 78.7% achieved complete resection and nine (6.4%) developed complications. The multivariate analysis suggested that location near the duodenal papilla (P = 0.010) and diameter exceeding 15 mm (P = 0.091) of duodenal SMTs were independent risk factors for complications in ER. Besides, submucosal fibrosis (P = 0.042), location near the duodenal papilla (P = 0.049), and irregular morphology (P = 0.067) were independent risk factors for incomplete resection. CONCLUSIONS: ER can be recommended as an effective and minimally invasive treatment for duodenal SMTs.

A prediction model and nomogram for technical difficulty of peroral endoscopic myotomy.

BACKGROUND AND AIMS: Peroral endoscopic myotomy (POEM) is a promising endoscopic technique for achalasia. We aimed to establish a regression model and develop a simple nomogram to predict the technical difficulty of POEM in a single center with large volume cases. METHODS: 3385 achalasia patients treated with POEM were included, and the technical difficulty was systemically evaluated. All of them were randomized into the training cohort (n = 1693) or internal validation cohort (n = 1692). Then, the prediction model and nomogram were proposed based on multivariate logistic regression analysis in the training cohort and assessed in the validation cohort. RESULTS: Of 3385 patients, technical difficulty happened in 417 (12.32%) cases. In the training stage, six factors were weighted based on the ß coefficient from the regression model, including age, disease duration, sigmoid esophagus, mucosal edema, submucosal fibrosis, and tunnel length. The patients were categorized into low-risk (< 0.1), medium-risk (0.1-0.25), and high-risk (> = 0.25) groups. Our score model performed satisfying discrimination with the areas under the receiver-operating characteristic curve (AUC) of 0.743 (95% confidence interval (CI), 0.701-0.785) and calibration with goodness of fit in the Hosmer-Lemeshow test (P = 0.088) in internal validation. CONCLUSIONS: The prediction model and nomogram demonstrated good performance in predicting the technical difficulty of POEM.

Dementia and the history of disease in older adults in community.

INTRODUCTION: Many studies have revealed the effect of medical history on dementia. The aim of this study was to explore the relationship between the history of disease and onset of dementia. METHODS: This was a multi-center, cross-sectional study, with 2595 older adults enrolled. The onset of dementia was evaluated with Revised Hasegawa Dementia Scale (HDS-R). The diagnosed diseases after the age of 40 of the participants were investigated, including respiratory system diseases, digestive system diseases, cardiovascular diseases, endocrine disorders, genitourinary system diseases, nervous system disease, sensory system diseases, dental/oral diseases, bone/joint diseases and mental illnesses. RESULTS: Data of 2458 older adults were analyzed. Univariate analysis showed that diabetes, thyroid disease, mental illness, hearing loss, stroke, dental/oral disease, Denture use, fracture/osteoporosis, kidney disease and number of diseases were risk factors for dementia. After controlling for demographic sociological variables, diabetes, dental/oral disease, and denture use were independent risk factors for dementia. Thyroid disease (P = 0.313), mental illnesses (P = 0.067), hearing loss (P = 0.595), stroke (P = 0.538), fractures/osteoporosis (P = 0.069), kidney disease (P = 0.168) were no longer significant to dementia. CONCLUSION: Diabetes, dental/oral disease and denture use were main risk factors for dementia.

FDX1 regulates leydig cell ferroptosis mediates PM2.5-induced testicular dysfunction of mice.

Epidemiological studies have established an association between chronic exposure to PM2.5 and male infertility. However, the underlying mechanisms were not fully revealed. In this study, we established mice models exposed to PM2.5 for 16 weeks, and a significant decrease in sperm quality accompanied by an increase in testosterone levels were observed after PM2.5 exposure. Moreover, treatment with ferrostatin-1 (Fer-1), a specific ferroptosis inhibitor, effectively mitigated PM2.5-induced testicular dysfunction in mice. And lipid peroxidation and ferritin accumulation were found to be significantly increased in Leydig cells of testes with a PM2.5-dose dependent manner. Further investigations revealed that TM-3 cells, a mouse Leydig cell line, were prone to ferroptosis after PM2.5 exposure, and the cell viability was partly rescued after the intervention of Fer-1. Furthermore, our results supported that the ferroptosis of TM-3 cells was attributed to the upregulation of ferredoxin 1 (FDX1), which was the protein transferring electrons to cytochrome P450 family 11 subfamily A member 1 to aid lysing cholesterol to pregnenolone at initial of steroidogenesis. Mechanically, PM2.5-induced FDX1 upregulation resulted in cellular ROS elevation and ferrous iron overload, which together initiated an autoxidation process of polyunsaturated fatty acids in the cell membrane of Leydig cells until the accumulated lipid peroxides triggered ferroptotic cell death. Simultaneously, upregulation of FDX1 promoted steroidogenesis and let to an increased level of testosterone. In summary, our work suggested that FDX1, a mediator involving steroidogenesis, was a key regulator in PM2.5-induced Leydig cells ferroptosis.

MicroRNA-205-5p: A potential therapeutic target for influenza A.

We are committed to finding host targets for influenza A therapeutics. The nucleoprotein (NP) plays an important role in influenza A virus replication and is an indispensable part of viral transcription and replication. Exploring endogenous substances that can modulate NP is critical for finding host targets. MicroRNAs (miRNAs, miR) are a novel class of powerful, endogenous gene expression regulators. Herein, we used miRanda to analyse the base complementarity between the NP gene and the 14 host miRNAs reported previously by us. MiRanda predicted that miR-431-5p, miR-744-3p and miR-205-5p could complement the NP gene. To understand the effect of these miRNAs on NP expression, we co-transfected 293 T cells with NP gene sequence containing above miRNAs binding site or full sequence of NP gene (transfected into pmirGlo or pcDNA3.1 vectors, respectively), and mimics of miR-205-5p, miR-431-5p and miR-744-3p. Dual luciferase reporter gene or Western blotting assays confirmed that miR-205-5p and miR-431-5p inhibit NP expression by binding with the miRNA binding site of NP gene. Further, we infected Mouse Lung Epithelial (MLE-12) cells overexpressing miR-205-5p and miR-431-5p with influenza A virus and performed Western blotting to examine NP expression. We found that NP expression was significantly reduced in MLE-12 cells overexpressing miR-205-5p during influenza A infection. The miR-205-5p overexpression-induced inhibition of influenza A replication could be attributed to the inhibition of NP expression. Further, we administered oseltamivir and Jinchai Antiviral Capsules (JC, an anti-influenza Chinese medicine) to influenza A virus-infected MLE-12 cells and mice. We found that miR-205-5p was significantly decreased increased in infected cells and lung tissues, and oseltamivir and JC could up-regulate miR-205-5p. In conclusion, we provide new evidence that miR-205-5p plays a role in regulating viral NP protein expression in combating influenza A and may be a potential target for influenza A therapy.

NEK2 promotes the migration and proliferation of ESCC via stabilization of YAP1 by phosphorylation at Thr-143.

BACKGROUND: Esophageal Squamous Cell Carcinoma (ESCC) was characterized as a regional-prevalent and aggressive tumor with high morbidity and mortality. NIMA-related kinase 2 (NEK2) is an interesting oncogene, the alteration of which leads to patients-beneficial outcomes. We aimed to explore the role of NEK2 in ESCC and excavate its mechanism. METHODS: RNA-seq data were downloaded from TCGA and GEO and analyzed by R software. The protein levels were detected by immunohistochemistry (IHC) or western blot (WB), and mRNA expression was detected by qRT-PCR. The in vitro role of proliferation and migration was detected by Transwell migration assay and by colony formation assay, respectively. The in vivo roles were explored using a subcutaneous xenograft tumor model, where immunofluorescence (IF) and IHC were employed to investigate expression and localization. The interaction between proteins was detected by immunoprecipitation. The stability of proteins was measured by WB in the presence of cycloheximide. RESULTS: A higher level of NEK2 was found in ESCC than normal esophageal epithelia in GEO, TCGA, and tissue microarray, which was associated with worse prognoses. The NEK2 knockdown impaired the proliferation and migration of ESCC, which also downregulated YAP1 and EMT markers like N-cadherin and Vimentin in vitro. On the contrary, NEK2 overexpression enhanced the migration of ESCC and elevated the levels of YAP1, N-cadherin, and Vimentin. Additionally, the overexpression of YAP1 in NEK2 knocked down ESCCs partly rescued the corresponding decrease in migration. The knockdown of NEK2 played an anti-tumor role in vivo and was accompanied by a lower level and nucleus shuffling of YAP1. In mechanism, NEK2 interacted with YAP1 and increased the stability of both endogenous and exogenous YAP1 by preventing ubiquitination. Moreover, the computer-predicted phosphorylation site of YAP1, Thr-143, reduced the ubiquitination of HA-YAP1, strengthened its stability, and thus influenced the migration in vitro. CONCLUSIONS: NEK2 is a prognostic oncogene highly expressed in ESCC and promotes the progression of ESCC in vitro and in vivo. Mechanistically, NEK2-mediated phosphorylation of YAP1 at Thr-143 protects it from proteasome degradation and might serve as a promising therapeutic target in ESCC. Video Abstract.

Endoscopic submucosal dissection for giant esophageal lipomatous tumors.

BACKGROUND AND AIM: Thoracotomy is the foremost choice of giant esophageal lipomatous tumors in previous studies, but it is highly traumatic and possibly diminishes the quality of patients' lives. To minimize such impacts, a minimally invasive method without loss of curability is desirable for giant lipomatous tumors of the esophagus. With recent progress in endoscopic techniques and devices, endoscopic submucosal dissection (ESD) has been successfully used to remove esophageal or gastric submucosal tumors. In our study, we aimed to evaluate the clinical impact of ESD for giant esophageal lipomatous tumors. METHODS: Design, single-center, retrospective study; setting, academic medical center; patients, six patients with six giant lipomatous tumors of the esophagus between February 2013 and December 2020; interventions, ESD; and main outcome measurements, procedure duration, en bloc resection rate, complications, local recurrence, and distant metastases. RESULTS: Endoscopic en bloc resections of esophageal lipomatous tumors were successfully performed in all patients, with a mean duration of 56.5 ± 26.0 min. All en bloc resection lesions showed both lateral and deep tumor-free margins. The average maximum diameter of the esophageal lipomatous tumors was 171.7 ± 66.2 mm. No complications such as bleeding and perforations happened during hospitalization with 4.0 ± 1.6 days. Besides, local recurrence and distant metastasis have not occurred during the follow-up period. CONCLUSIONS: Endoscopic submucosal dissection is a safe and effective way to dissect giant lipomatous tumors of the esophagus thoroughly.

Informational support for depression and quality of life improvements in older patients with cancer: a systematic review and meta-analysis.

PURPOSE: To assess and summarize the effects of informational support on depression and quality of life of older patients with cancer. METHODS: PubMed, MEDLINE, and Web of Science were searched to identify articles written in English and published until March 2021. Studies within 10 years period (2010-2021) were included. Randomized controlled trials were included if they evaluated the impact of informational support on depression and quality of life. All analyses were performed with Review Manager 5.3. RESULTS: Twelve studies with a total of 2374 participants met the inclusion criteria. Our primary outcomes included depression and quality of life. (1) Depression: results indicated no statistically significant difference and low heterogeneity [SMD = 0.28, 95% CI (- 0.24,0.80), p = 0.45; I2 = 0%], (2) Quality of life: in the subgroup analyses of EORTC QLQ-C30, results indicated a significant effect of informational support on quality of life [SMD = 2.84, 95% CI (0.63, 5.05), p = 0.03; I2 = 79%]; in the subgroup analyses of FACT and SF-36, there were no significance. CONCLUSIONS: Informational support could reduce depression and did improve the quality of life in older cancer patients with statistical significance. The findings suggested that informational support was an effective approach to improve depression and quality of life in older patients with cancer.

Attenuated T cell activation and rearrangement of T cell receptor ß repertoire in silica nanoparticle-induced pulmonary fibrosis of mice.

Silica nanoparticles (SiNPs) cause pulmonary fibrosis through a complex immune response, but the underlying mechanisms by which SiNPs interact with T cells and affect their functions remain unclear. The T cell receptor (TCR) repertoire is closely related to T cell activation and proliferation and mediates innate and adaptive immunity. High-throughput sequencing of the TCR enables comprehensive monitoring of the immune microenvironment. Here, the role of the TCRß repertoire was explored using a mouse model of SiNP-induced pulmonary fibrosis and a co-culture of RAW264.7 and CD4+ T cells. Our results demonstrated increased TCRß expression and decreased CD25 and CD69 expression in CD4+ T cells from peripheral blood and lung collected 14 days after the induction of pulmonary fibrosis by SiNPs. Simultaneously, SiNPs significantly decreased CD25 and CD69 expression in CD4+ T cells in vitro via RAW264.7 cell presentation. Mechanistically, pLCK and pZap70 expression, involved in mediating T cell activation, were also decreased in the lung of mice with SiNP-induced pulmonary fibrosis. Furthermore, the profile of the TCRß repertoire in mice with SiNP-induced pulmonary fibrosis showed that SiNPs markedly altered the usage of V genes, VJ gene combinations, and CDR3 amino acids in lung tissue. Collectively, our data suggested that SiNPs could interfere with T cell activation by macrophage presentation via the LCK/Zap70 pathway and rearrange the TCRß repertoire for adaptive immunity and the pulmonary microenvironment.

Multidimensional measure of instrumental support in transitional care - design and pilot test of a questionnaire assessing instrumental support among older adults with chronic diseases.

BACKGROUND: Previous studies indicated that poor quantity and quality of instrumental support are one of the main barriers in the application of transitional care. Instrumental support, as one common function of social support, is the provision of financial assistance, material goods, or services. The purpose of our study is to develop an Instrumental Support in Transitional Care Questionnaire (ISTCQ) and use this questionnaire to make an assessment among older adults with chronic diseases. METHODS: The draft questionnaire was examined by 18 experts from different professional fields performing three rounds of content validity testing with the Delphi method. Afterward, we conducted a pilot test recruiting 174 participants as a convenience sample in Nantong, China. The construct validity was confirmed via exploratory factor analysis and reliability was assessed using Cronbach's alpha. RESULTS: The authority coefficient of experts was 0.74-0.99 and Kendall harmony coefficient W was 0.381. The exploratory factor analysis indicated that the questionnaire can be interpreted by three factors: namely, anticipated support (items 1, 2, 3, 4), received support (items 5, 6, 7, 8) and support satisfaction (items 9, 10, 11, 12). These three factors (eigenvalues > 1 and factor loading > 0.4) explained 69.128% of the total variance. Furthermore, the calculation of Cronbach's alpha and test-retest reliability have shown good reliability among each dimension of the 12-item questionnaire (Cronbach's alpha 0.711-0.827, test-retest reliability 0.704-0.818). CONCLUSION: Results from the pilot test demonstrated excellent reliability and validity of ISTCQ through each dimension and as an entire.

Effects of ambient PM2.5 on development of psoriasiform inflammation through KRT17-dependent activation of AKT/mTOR/HIF-1α pathway.

Exposure to fine particulate matter (PM2.5) has significant effects on human skin health, mainly disrupting skin homeostasis and accelerating aging. To date, the effects of PM2.5 on psoriasis (PSO) have not been elucidated. An ambient particulate matter exposed and well characterized imiquimod (IMQ)-induced psoriasis mouse model was established. Thirty male C57BL/6 mice aged 8 weeks were randomly divided into three groups: filtered air (FA) group (Control group), PSO+ FA group and PSO + PM2.5 group. A KRT17 knockdown (KRT17-KD) mouse model was simultaneously established by subcutaneously injecting KRT17-KD lentivirus. Forty male C57BL/6 mice were randomly divided into four groups: PSO + FA + KRT17-RNAi negative control lentivirus (KRT17-NC) group, PSO+ FA+ KRT17-KD group, PSO + PM2.5 + KRT17-NC group and PSO + PM2.5 + KRT17-KD group. PM2.5 exposure continued for 8 weeks. Psoriasis was induced by topically applying IMQ on the dorsal skin of the mice for 6 days during week 8. Morphometric and histological analyses were performed to investigate the changes in psoriatic lesions. Differentially expressed genes and enriched pathways were explored using bioinformatics analysis and showed that KRT17 gene and the vascular endothelial growth factor receptor signaling pathway were associated with psoriasis. HaCaT cells were stimulated with interleukin-17A and infected with KRT17-KD lentivirus to establish an in vitro KRT17 knockdown psoriasis cell model. Notably, PM2.5 exposure increased the expression of KRT17 protein and activated AKT/mTOR/HIF-1α signaling pathway in vivo. Moreover, specific agonist of AKT (740Y-P) reversed the decreased neovascularization induced by KRT17 knockdown through AKT/mTOR/HIF-1α signaling pathway in vitro. Consequently, PM2.5 exposure could promote the development and progression of psoriasis through KRT17-dependent activation of AKT/mTOR/HIF-1α signaling pathway.

Relative contribution of multi-source water recharge to riparian wetlands along the lower Yellow River.

Rivers play a vital role in both the formation and maintenance of riparian wetland hydrology. However, few studies have focused on the response of water recharge of riparian wetlands to altered hydrological processes induced by water-sediment regulation practices. To fill this gap, our study investigated the contribution of multi-source water recharge of riparian wetlands in the lower Yellow River, as well as its influence both during and before the water-sediment regulation scheme of Xiaolangdi Dam. Our study is based on hydrochemistry and isotopic methods, using a Bayesian mixing model and artificial neutral network model. The results showed that riparian wetlands were fed by mixed sources, including groundwater, canals, the Yellow River, and precipitation. However, seasonal evaporation introduced additional variation, which affected the relative contribution of these sources across seasons. Among these sources, the Yellow River served as the main water source for recharging riparian wetlands, and its contribution varied both spatially and temporally (across seasons). Specifically, proximity of riparian wetlands was the primary factor explaining spatial variation in the contribution of Yellow River, while climatic (12.38%) and hydrological variabilities (87.62%) explained seasonal variation. Among these climatic and hydrological variables, suspended sediment content was the most important factor-with a relative contribution of 36.33%. By determining the contribution of the Yellow River to the recharge of riparian wetlands, our study has provided information which is beneficial to adaptive management of river-fed riparian wetlands, especially under the implementation of water-sediment regulation practices.