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This systematic review and meta-analysis examines the associations of allergic rhinitis with sleep duration and sleep impairment. Observational studies published before August 2019 were obtained through English language literature searches in the PubMed, Embase, and CINAHL databases. Mean differences and odds ratios with 95% confidence intervals were extracted and used for meta-analysis. Heterogeneity was confirmed by the I2-heterogeneity test. Subgroup analysis was conducted to evaluate the influence of study design. The Grading of Recommendations Assessment, Development, and Evaluation approach was used to determine the level of evidence. In total, 2544 records were identified through database searches; 914 duplicate records were excluded, 1452 records were removed after screening of titles and abstracts, 151 records were excluded after full-text screening, and 27 articles were included in the final meta-analyses. A total of 240,706,026 patients (19,444,043 with allergic rhinitis) were considered. No significant difference in sleep duration between the allergic rhinitis and the control groups was found. Patients with allergic rhinitis presented with significantly higher sleep quality scores, sleep disturbances scores, and sleep latency scores; more frequent use of sleep medications; and lower sleep efficiency as measured by the Pittsburgh Sleep Quality Index and polysomnography. Meta-analyses for adjusted odds ratios showed that allergic rhinitis was also associated with higher risks of nocturnal dysfunctions, including insomnia, nocturnal enuresis, restless sleep, sleep-disordered breathing, obstructive sleep apnea, and snoring. Meta-analysis for adjusted odds ratio also showed that allergic rhinitis was associated with daytime dysfunction, including difficulty waking up, daytime sleepiness, morning headache, and the use of sleep medications. The overall quality of evidence ranged from low to very low, indicating that caution is required when interpreting these results. This study demonstrates that there is a significant association of AR with sleep characteristics.

ObjectivesTo determine the clinical features and course of thyroid-associated ophthalmopathy (TAO) in a large sample of Chinese patients.Design and methodsWe retrospectively identified a cohort of consecutive patients diagnosed with TAO at the West China Hospital from October 1, 2009 to October 1, 2019. We analysed clinical data from 3620 patients, including demographic data, clinical manifestations, ophthalmology examinations, and prognosis.ResultsTAO most frequently occurred with hyperthyroidism, with most patients developing TAO after thyroid disease (TD). The TAO phenotype was asymmetric in 375 (50.7%) euthyroid patients, 25 (27.8%) hypothyroid patients, and 314 (12.1%) hyperthyroid patients (p < 0.0001). The most frequent symptom was lid lag and the most commonly involved extraocular muscle was the inferior rectus. Severity assessment (NOSPECS score) and clinical activity assessment (Clinical Activity Scores, CAS) differed significantly between male and female patients (P < 0.000). The majority (88.8%) of patients had clinically inactive TAO, and only 3.2% of cases were sight-threatening. Regarding the clinical process, 75.5% of patients had an active phase time less than 12 months and 2.1% showed complete remission.ConclusionsTAO most commonly develops in females and is closely related to hyperthyroidism. Euthyroid TAO often has an asymmetric clinical phenotype. CAS combined with magnetic resonance imaging can improve the detection of TAO. NOSPECS scores should be slightly refined regarding the criteria for corneal involvement. Clinical management of TAO should be individualized according to CAS or NOSPECS assessments and a multidisciplinary approach is paramount. A minority of patients showed complete remission.

Protein tyrosine kinases (PTKs) are a class of proteins with tyrosine kinase activity that phosphorylate tyrosine residues of critical molecules in signaling pathways. Their basal function is essential for maintaining normal cell growth and differentiation. However, aberrant activation of PTKs caused by various factors can deviate cell function from the expected trajectory to an abnormal growth state, leading to carcinogenesis. Inhibiting the aberrant PTK function could inhibit tumor growth. Therefore, tyrosine kinase inhibitors (TKIs), target-specific inhibitors of PTKs, have been used in treating malignant tumors and play a significant role in targeted therapy of cancer. Currently, drug resistance is the main reason for limiting TKIs efficacy of cancer. The increasing studies indicated that tumor microenvironment, cell death resistance, tumor metabolism, epigenetic modification and abnormal metabolism of TKIs were deeply involved in tumor development and TKI resistance, besides the abnormal activation of PTK-related signaling pathways involved in gene mutations. Accordingly, it is of great significance to study the underlying mechanisms of TKIs resistance and find solutions to reverse TKIs resistance for improving TKIs efficacy of cancer. Herein, we reviewed the drug resistance mechanisms of TKIs and the potential approaches to overcome TKI resistance, aiming to provide a theoretical basis for improving the efficacy of TKIs.

Osteoporosis is a common metabolic bone disease, influenced by genetic and environmental factors, that increases bone fragility and fracture risk and, therefore, has a serious adverse effect on the quality of life of patients. However, epigenetic mechanisms involved in the development of osteoporosis remain unclear. There is accumulating evidence that epigenetic modifications may represent mechanisms underlying the links of genetic and environmental factors with increased risk of osteoporosis and bone fracture. Some RNAs, such as microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs), have been shown to be epigenetic regulators with significant involvement in the control of gene expression, affecting multiple biological processes, including bone metabolism. This review summarizes the results of recent studies on the mechanisms of miRNA-, lncRNA-, and circRNA-mediated osteoporosis associated with osteoblasts and osteoclasts. Deeper insights into the roles of these three classes of RNA in osteoporosis could provide unique opportunities for developing novel diagnostic and therapeutic approaches to this disease.

This paper presents a highly efficient, low-power, fully integrated neural stimulation circuit implemented using solely low-voltage devices. The circuit primarily consists of a high-voltage-generation circuit, an output driver circuit, and a constant-current source, designed and simulated using a 180 nm low-voltage CMOS process. The high-voltage-generation circuit utilizes a negative-voltage-generation module together with a series–parallel capacitor charge pump circuit, which effectively reduces the number of charge pump stages by three, and saves 29% of the area compared to a conventional charge pump circuit. A bootstrap clock generation circuit was utilized to generate the control signal to ensure that all transistors work within their voltage limit. To realize the high-voltage output driver circuit using low-voltage devices, a stacked transistor structure with deep N-well (DNW) devices was utilized. The four different output voltage levels from the high-voltage-generation circuit were utilized to generate a different voltage domain of control signals and bias voltage for the stacked transistors, making sure that all transistors work within their voltage limit. Simulation results show that the high-voltage-generation circuit can generate an output of up to 12.69 V from a 1.65 V low input voltage, with a maximum output current of 1 mA, achieving 74.9% efficiency. The overall efficiency of the neural stimulation circuit, including the high-voltage-generation circuit, output driver circuit and constant-current source, reaches 74% under the voltage-controlled stimulation (VCS) mode and 59.5% under the current-controlled stimulation (CCS) mode, whereas the standby static power consumption is as low as 66 pW.

Background MYB transcription factors are a kind of DNA binding protein that can specifically interact with the promoter region. Members of MYB TFs are widely involved in plant growth and development, secondary metabolism, stress response, and hormone signal transduction. However, there is no report of comprehensive bioinformatics analysis on the MYB family of Casuarina equisetifolia . Results In this study, bioinformatics methods were used to screen out 182 MYB transcription factors from the Casuarina equisetifolia genome database, including 69 1R-MYB, 107 R2R3-MYB, 4 R1R2R3-MYB, and 2 4R-MYB. The C. equisetifolia R2R3-MYB genes were divided into 29 groups based on the phylogenetic topology and the classification of the MYB superfamily in Arabidopsis thaliana , while the remaining MYB genes (1R-MYB, R1R2R3-MYB, and 4R-MYB) was divided into 19 groups. Moreover, the conserved motif and gene structure analysis shown that the members of the CeqMYB s were divided into the same subgroups with mostly similar gene structures. In addition, many conserved amino acids in the R2 and R3 domains of CeqMYB s by WebLogo analysis, especially tryptophan residues (W), with 3 conserved W in R2 repeat and 2 conserved W in R3 repeat. Combining promoter and GO annotation analysis, speculated on the various biological functions of CeqMYB s, thus 32 MYB genes were selected to further explore its response to salt stress by using qPCR analysis technique. Most CeqMYB genes were differentially regulated following multiple salt treatments. Conclusions Seven genes ( CeqMYB164 , CeqMYB4 , CeqMYB53 , CeqMYB32 , CeqMYB114, CeqMYB71 and CeqMYB177 ) were assigned to the “response to salt stress” by GO annotation. Among them, the expression level of CeqMYB4 was up-regulated under various salt treatments, indicating CeqMYB4 might participated in the response to salt stress. Our results provide important information for the biological function of C. equisetifolia , as well as offer candidate genes for further study of salt stress mechanism.

Abstract Background: Spatiotemporal disparities exist in the disease burden of non-communicable diseases (NCDs) attributable to kidney dysfunction, which has been poorly assessed. The present study aimed to evaluate the spatiotemporal trends of the global burden of NCDs attributable to kidney dysfunction and to predict future trends. Methods: Data on NCDs attributable to kidney dysfunction, quantified using deaths and disability-adjusted life-years (DALYs), were extracted from the Global Burden of Diseases Injuries, and Risk Factors (GBD) Study in 2019. Estimated annual percentage change (EAPC) of age-standardized rate (ASR) was calculated with linear regression to assess the changing trend. Pearson’s correlation analysis was used to determine the association between ASR and sociodemographic index (SDI) for 21 GBD regions. A Bayesian age–period–cohort (BAPC) model was used to predict future trends up to 2040. Results: Between 1990 and 2019, the absolute number of deaths and DALYs from NCDs attributable to kidney dysfunction increased globally. The death cases increased from 1,571,720 (95% uncertainty interval [UI]: 1,344,420–1,805,598) in 1990 to 3,161,552 (95% UI: 2,723,363–3,623,814) in 2019 for both sexes combined. Both the ASR of death and DALYs increased in Andean Latin America, the Caribbean, Central Latin America, Southeast Asia, Oceania, and Southern Sub-Saharan Africa. In contrast, the age-standardized metrics decreased in the high-income Asia Pacific region. The relationship between SDI and ASR of death and DALYs was negatively correlated. The BAPC model indicated that there would be approximately 5,806,780 death cases and 119,013,659 DALY cases in 2040 that could be attributed to kidney dysfunction. Age-standardized death of cardiovascular diseases (CVDs) and CKD attributable to kidney dysfunction were predicted to decrease and increase from 2020 to 2040, respectively. Conclusion: NCDs attributable to kidney dysfunction remain a major public health concern worldwide. Efforts are required to attenuate the death and disability burden, particularly in low and low-to-middle SDI regions.

Neuroendocrine neoplasms (NENs) originate from neuroendocrine cells, and mainly occur in the gastrointestinal tract and lungs, rarely occurring in the orbit. Here, the clinicopathologic factors, treatments and prognosis of three cases of orbital NENs are described. The mean age of the three patients (two females and one male) was 59 years. Two cases exhibited ocular symptoms, including unilateral proptosis and eyelid mass, while the third case presented systemic symptoms exhibited as Cushing’s syndrome. The tumours were surgically resected in all three patients. Immunohistochemistry assays revealed positive expression for pan cytokeratin and epithelial membrane antigen in all cases. Additionally, neural cell adhesion molecule 1 (also known as CD56) and synaptophysin were positive in two cases. The pathological diagnosis for case 1 and 2 was ‘neuroendocrine carcinoma’ and both patients died three months after diagnosis. Case 3 was diagnosed with a neuroendocrine tumour and the symptoms of Cushing’s syndrome gradually improved following surgery. In addition, no recurrence was observed during the four-year follow-up period. These cases demonstrate that orbital neuroendocrine tumours show different clinical manifestations due to the different types. Pathology may clarify the diagnosis, classification and grading, and provide a reference value for treatment and prognosis.

The molecular pathogenesis of ocular adnexal mucosa-associated lymphoid tissue (MALT) lymphoma and IgG4-related ophthalmic disease (IgG4-ROD) remains incompletely understood. Differentiating between the two diseases is vital given that the diagnostic evaluation and treatment approaches can vary significantly; this difficulty in distinction is exacerbated by the absence of specific biomarkers. This study aimed to investigate the differences between these two diseases based on their cellular composition, transcriptional heterogeneity, and the immune microenvironment using single-cell RNA transcriptional sequencing (scRNA-seq) technology. We collected orbital lacrimal gland region tissue samples from three patients with MALT lymphoma and another three with IgG4-ROD and performed single-cell sequencing experiments. Subsequently, we conducted bioinformatics analyses, including cell subpopulation segmentation and inter-group comparison, tumor cell identification, functional enrichment analysis, and pseudotime trajectory analysis. Furthermore, we analyzed the cellular communication between tumor B-cell and T-cell subsets within the immune microenvironment of MALT lymphoma tissues. We performed immunofluorescence assays to verify the co-expression of receptor-ligand pairs. A total of six major cell subpopulations were identified, with B-cells and T-cells being the predominant cell types. All B-cell subpopulations in MALT lymphomas are malignant, exhibiting significant intratumoral and intertumoral heterogeneity. Reclustering of the T-cell subpopulation identified five major T-cell subpopulations. Pseudotime analysis revealed that CD4+ naive T-cells in MALT lymphoma patients were highly likely to differentiate into follicular helper T-cells, whereas, in IgG4-ROD patients, CD4+ naive T-cells were highly likely to differentiate into regulatory T-cells. Intercellular communication analysis revealed that the CD27-CD70 immune checkpoint receptor-ligand pair and CXCL13-CXCR5 chemokine receptor-ligand pair were significantly upregulated between malignant B-cells and T-cells subpopulations. This study is the first to conduct a comparative single-cell transcriptome sequencing analysis of ocular adnexal MALT lymphoma and IgG4-ROD. Our results reveal the cellular composition, key pathways, and critical immune microenvironment implicated in the development of these two diseases. These findings provide important insights into the pathogenesis of these two diseases and highlight the differences between them.

Chemosensors based on traditional fluorescent dyes have always contributed to the development of chemical sensor areas. In this review, the rhodamine-based chemosensors’ improvements and applications from 2018 to 2022 are discussed, mainly focusing on cations (metal ions and H+), anions (CN−, F−, etc.), and small bio-functional molecules’ (thiols, amino acids, etc.) detection. Specifically, this review highlights the detection target, detection limit, detection solution system, detection mechanism, and performance of the rhodamine-based sensors. Although these rhodamine-based sensors are well developed, their repeatability and sensitivity still need significant improvement. This review is expected to bring new clues and bright ideas to researchers for further advances in rhodamine-based chemosensors in the future.