The Association of Metabolic Risk Factors with Advanced Adenomas in Hispanic Patients.

BACKGROUND: Obesity and metabolic syndrome (MetS) have been implicated as rising risk factors for the development of colorectal cancers. A rapid increase in the prevalence of obesity and severe obesity among Hispanic patients in the United States may present substantially increased risk for advanced colorectal neoplasia in this population. Currently, there is very little research in this area. AIMS: We sought to identify metabolic risk factors for advanced adenomas (AA) in Hispanic Americans. METHODS: We retrospectively reviewed data from the Los Angeles General (LAG) Medical Center of asymptomatic Hispanic patients above 45 years of age who underwent their first colonoscopies following a positive screening FBT. Patient demographics, metabolic characteristics, as well as colon polyp size and histology were recorded. Polyps were classified as adenomas or AA (including both high-risk adenomas and high-risk serrated polyps). Relative risk for AA was assessed by multivariate logistical regression analyses. RESULTS: Of the 672 patients in our study, 41.4% were male, 67% had adenomas, and 16% had AA. The mean BMI was 31.2 kg/m2. The mean HDL-C was 49.5 mg/dL (1.28 mmol/L) and the mean triglyceride level was 151 mg/dL. 44.6% had diabetes and 64.1% had hypertension. When comparing patients with AA to patients with no adenoma, male sex, BMI > 34.9 kg/m2, and elevated fasting triglyceride levels were associated with an increased risk of AA. FIB-4 ≥1.45 was also associated with an increased risk of AA in males. There was no significant difference in the risk of AA with diabetes, hypertension, FIB-4 score, LDL-C level, and HDL-C level. CONCLUSIONS: Hispanic patients with a positive FBT were observed to have a high incidence of AA. Class II obesity (BMI ≥ 35 kg/m2), elevated triglyceride levels were identified as risk factors among males in our study. Early interventions to address these modifiable risk factors in at-risk populations, such as multi-disciplinary weight management programs for the treatment of obesity and related co-morbidities, could potentially lead to risk reduction and CRC prevention.

Comparative analysis of IOL power calculations in postoperative refractive surgery patients: a theoretical surgical model for FS-LASIK and SMILE procedures.

BACKGROUND: As the two most prevalent refractive surgeries in China, there is a substantial number of patients who have undergone Femtosecond Laser-assisted In Situ Keratomileusis (FS-LASIK) and Small Incision Lenticule Extraction (SMILE) procedures. However, there is still limited knowledge regarding the selection of intraocular lens (IOL) power calculation formulas for these patients with a history of FS-LASIK or SMILE. METHODS: A total of 100 eyes from 50 postoperative refractive surgery patients were included in this prospective cohort study, with 25 individuals (50 eyes) having undergone FS-LASIK and 25 individuals (50 eyes) having undergone SMILE. We utilized a theoretical surgical model to simulate the IOL implantation process in postoperative FS-LASIK and SMILE patients. Subsequently, we performed comprehensive biological measurements both before and after the surgeries, encompassing demographic information, corneal biometric parameters, and axial length. Various formulas, including the Barrett Universal II (BUII) formula, as a baseline, were employed to calculate IOL power for the patients. RESULTS: The Barrett True K (BTK) formula, demonstrated an mean absolute error (AE) within 0.5 D for both FS-LASIK and SMILE groups (0.28 ± 0.25 D and 0.36 ± 0.24 D, respectively). Notably, the FS-LASIK group showed 82% of results differing by less than 0.25 D compared to preoperative BUII results. The Barrett True K No History (BTKNH) formula, which also incorporates measured posterior corneal curvature, performed similarly to BTK in both groups. Additionally, the Masket formula, relying on refractive changes based on empirical experience, displayed promising potential for IOL calculations in SMILE patients compared with BTK (p = 0.411). CONCLUSION: The study reveals the accuracy and stability of the BTK and BTKNH formulas for IOL power calculations in myopic FS-LASIK/SMILE patients. Moreover, the Masket formula shows encouraging results in SMILE patients. These findings contribute to enhancing the predictability and success of IOL power calculations in patients with a history of refractive surgery, providing valuable insights for clinical practice. Further research and larger sample sizes are warranted to validate and optimize the identified formulas for better patient outcomes.

Bibliometric analysis of the Vogt‒Koyanagi‒Harada disease literature.

PURPOSE: As an autoimmune disease, Vogt‒Koyanagi‒Harada disease (VKHD) is a main type of uveitis in many countries and regions, significantly impacting patient vision. At present, information regarding VKHD is still limited, and further research is needed. We conducted a bibliometric analysis to characterize the overall status, current trends, and current focus of VKHD research. METHOD: Literature published from 1975 to 2022 was obtained from the Web of Science core collection and analysed with the R-language packages Bibliometrix, VOSviewer, and CiteSpace software. RESULTS: A total of 1050 papers on VKHD were retrieved from 261 journals, and 16,084 references were obtained from the papers in the original search. The average annual number of published articles was approximately 21.9, and the number of publications rapidly increased after 2004. The journal Ocular Immunology and Inflammation published the most papers on VKHD, while the American Journal of Ophthalmology has the highest citation frequency. The leading countries were Japan, China (PRC), and the United States of America (USA). Yang PZ from Chongqing Medical University was the most prolific and cited author. The most frequently cited study discussed revision of VKHD diagnostic criteria. An analysis of the highest frequency keywords showed that most research focused on the treatment, diagnosis, and pathogenesis of VKHD and its relationship with other related diseases. At present, the most urgent research direction is in the relationship between COVID-19 or COVID-19 vaccines and VKHD and the corresponding mechanisms underlying it. CONCLUSION: Utilizing dynamic and visualization tools, bibliometrics provides a clear depiction of the research history, development trends, and research hotspots in VKHD It serves as a valuable tool for identifying research gaps and areas that necessitate further exploration. Our study revealed potential directions for future VKHD research, including investigating specific molecular mechanisms underlying the disease, exploring the clinical utility of optical coherence tomography angiography and other diagnostic techniques, and conducting clinical research on novel therapeutic drugs.

Portrait of Regional Trends in Liver Transplantation for Nonalcoholic Steatohepatitis in the United States.

INTRODUCTION: Nonalcoholic steatohepatitis (NASH) is one of the most common etiologies of liver transplantation (LT) in the United States. We investigated regional trends in waitlist candidates, LT rates, and recipient survival among patients with NASH. METHODS: Using the United Network for Organ Sharing database by Organ Procurement and Transplantation Network regions, we investigated waitlist registration, LT rates, and survival for NASH between January 2004 and December 2019. RESULTS: The absolute number and percentage of total LT performed for NASH increased substantially in all Organ Procurement and Transplantation Network regions. In 2019, region 11 had the highest percentage of NASH-related LT with 31.4% followed by region 10 (25.3%) and region 8 (23.1%). Between 2015 and 2019, region 5 had the highest rising percentage in LT for NASH at 208%, followed by region 1 (194%) and region 4 (183%). The proportion of NASH hepatocellular carcinoma (NASH-HCC) was the highest in region 9 at 37.7% and lowest in region 10 (19.2%), region 3 (20.6%), and region 11 (20.8%). In multivariate analysis, diabetes (HR 1.18, P < 0.001), dialysis before LT (hazard ratio [HR] 1.53, P < 0.001), HCC (HR 1.19, P < 0.00), portal vein thrombosis (HR 1.24, P < 0.001), donor age (HR 1.026, P = 0.03), and recipient age (HR 1.24, P = <0.001) were associated with worse survival. DISCUSSION: LT for patients with NASH has dramatically increased across all regions since 2004, but with substantial heterogeneity among regions in the proportion with HCC and post-LT survival. Identifying contributing factors to these regional differences is warranted.

Metabolic Risk Profiles for Hepatic Steatosis Differ by Race/Ethnicity: An Elastography-Based Study of US Adults.

BACKGROUND AND AIMS: Most population-based studies of risk profiles for liver steatosis have relied upon serum markers (e.g., ALT or FIB-4) or ultrasound steatosis index to define cases. We sought to examine racial/ethnic differences in metabolic risk factors associated with liver steatosis and fibrosis at the population level using elastography-based measures. METHODS: In total, 4509 adults completed vibration-controlled transient elastography (VCTE) with controlled attenuated parameter (CAP) examinations in the 2017-2018 National Health and Nutrition Examinations Survey. Race/ethnicity was self-identified; metabolic parameters included waist circumference, obesity, diabetes, hypertension, and hyperlipidemia. Primary outcome was steatosis defined by CAP score ≥ 280 decibels per meter and secondary outcome significant fibrosis by VCTE median stiffness ≥ 8 kilopascals. Race-specific logistic regression models were performed to assess the relationship between metabolic parameters and hepatic steatosis and fibrosis. RESULTS: Prevalence of elastography-based hepatic steatosis was > 30% for all race/ethnicities. Steatosis was associated with increasing waist circumference for all race/ethnicities (OR ranging 1.7-2.3, p < 0.01). Steatosis was associated with diabetes for Whites (OR 2.4, 95% CI 1.2-4.7), Asians (OR 3.0, 1.4-6.3), and Hispanics (OR 2.2, 1.3-3.6), but not Blacks (OR 1.3, 0.8-2.2); hypertension for Whites (OR 1.7, 1.3-4.7) and Asians (OR 2.1, 1.1-3.8); and hyperlipidemia for Blacks only (OR 2.2, 1.3-3.7). Of metabolic risk factors, higher odds of fibrosis were demonstrated with higher waist circumference per 10 cm increase (OR 2.1, 1.8-2.4) and diabetes (OR 2.5, 1.6-3.7), but the effect of diabetes was present in all racial/ethnic groups except Blacks (p-interaction < 0.05). CONCLUSION: Blacks have a distinct metabolic phenotype for steatosis, while Asians, Whites, and Hispanics are more similar. Racial/ethnic differences in risk profiles are important to consider in prevention, screening strategies, and interventions for fatty liver disease.

PGG.Han: the Han Chinese genome database and analysis platform.

As the largest ethnic group in the world, the Han Chinese population is nonetheless underrepresented in global efforts to catalogue the genomic variability of natural populations. Here, we developed the PGG.Han, a population genome database to serve as the central repository for the genomic data of the Han Chinese Genome Initiative (Phase I). In its current version, the PGG.Han archives whole-genome sequences or high-density genome-wide single-nucleotide variants (SNVs) of 114 783 Han Chinese individuals (a.k.a. the Han100K), representing geographical sub-populations covering 33 of the 34 administrative divisions of China, as well as Singapore. The PGG.Han provides: (i) an interactive interface for visualization of the fine-scale genetic structure of the Han Chinese population; (ii) genome-wide allele frequencies of hierarchical sub-populations; (iii) ancestry inference for individual samples and controlling population stratification based on nested ancestry informative markers (AIMs) panels; (iv) population-structure-aware shared control data for genotype-phenotype association studies (e.g. GWASs) and (v) a Han-Chinese-specific reference panel for genotype imputation. Computational tools are implemented into the PGG.Han, and an online user-friendly interface is provided for data analysis and results visualization. The PGG.Han database is freely accessible via http://www.pgghan.org or https://www.hanchinesegenomes.org.

IgG:IgM Ratios of Liver Plasma Cells Reveal Similar Phenotypes of Primary Biliary Cholangitis With and Without Features of Autoimmune Hepatitis.

Within the spectrum of autoimmune liver diseases, there are patients who manifest features of more than one disease, which was previously identified as having overlap syndrome1,2 and is now referred to as variant syndromes. The most common variant syndrome is between primary biliary cholangitis (PBC) and autoimmune hepatitis (AIH). Typically, AIH presents with elevated serum immunoglobulin (Ig) G, whereas PBC is associated with elevated serum IgM.3,4 Previous studies have suggested that plasma cells in liver biopsies of AIH patients are predominantly IgG+, whereas in PBC, there is an abundance of IgM+ cells.5,6 We wanted to determine the immunostaining pattern for IgG and IgM of liver plasma cells among Hispanic patients in Los Angeles with features of both PBC-AIH compared with those with PBC or AIH alone.

Dynamic alterations of genome and transcriptome in KRAS G13D mutant CRC PDX model treated with cetuximab.

BACKGROUND: KRAS mutations have been characterized as the major predictive biomarkers for resistance to cetuximab treatment. However, studies indicate that not all KRAS mutations are associated with equivalent treatment outcomes. KRAS G13D mutations were observed to account for approximately 16% of all KRAS mutations in advanced colorectal cancer patients, and whether these patients can benefit from cetuximab has not been determined. METHODS: An established KRAS G13D mutant colorectal cancer (CRC) patient-derived xenograft (PDX) model was treated with cetuximab. After repeated use of cetuximab, treatment-resistant PDX models were established. Tissue samples were collected before and during treatment, and multiomics data were subsequently sequenced and processed, including whole-exome, mRNA and miRNA data, to explore potential dynamic changes. RESULTS: Cetuximab treatment initially slowed tumor growth, but resistance developed not long after treatment. WES (whole-exome sequencing) and RNA sequencing found that 145 genes had low P values (< 0.01) when analyzed between the locus genotype and its related gene expression level. Among these genes, SWAP70 was believed to be a probable cause of acquired resistance. JAK2, PRKAA1, FGFR2 and RALBP1, as well as 10 filtered immune-related genes, also exhibited dynamic changes during the treatment. CONCLUSIONS: Cetuximab may be effective in KRAS G13D mutation patients. Dynamic changes in transcription, as determined by WES and RNA sequencing, occurred after repeated drug exposure, and these changes were believed to be the most likely cause of drug resistance.

Involvement of NEAT1/miR-133a axis in promoting cervical cancer progression via targeting SOX4.

NEAT1 is an important tumor oncogenic gene in various tumors. Nevertheless, its involvement remains poorly studied in cervical cancer. Our study explored the functional mechanism of NEAT1 in cervical cancer. NEAT1 level in several cervical cancer cells was quantified and we found NEAT1 was greatly upregulated in vitro. NEAT1 knockdown inhibited cervical cancer development through repressing cell proliferation, colony formation, capacity of migration, and invasion and also inducing the apoptosis. For another, microRNA (miR)-133a was downregulated in cervical cancer cells and NEAT1 negatively modulated miR-133a expression. Subsequently, we validated that miR-133a functioned as a potential target of NEAT1. Meanwhile, SOX4 is abnormally expressed in various cancers. SOX4 was able to act as a downstream target of miR-133a and silencing of SOX4 can restrain cervical cancer progression. In addition, in vivo assays were conducted to prove the role of NEAT1/miR-133a/SOX4 axis in cervical cancer. These findings implied that NEAT1 served as a competing endogenous RNA to sponge miR-133a and regulate SOX4 in cervical cancer pathogenesis. To sum up, it was implied that NEAT1/miR-133a/SOX4 axis was involved in cervical cancer development.

The transcriptome profiles and methylation status revealed the potential cancer-related lncRNAs in patients with cervical cancer.

Cervical cancer continues to be a major public health problem. Although long noncoding RNAs (lncRNAs) were involved in the initiation and progression of cancer, few studies focus on the lncRNAs in the cervical cancer. Here, we systematically studied the clinical information, transcriptome profiling, and methylation array data of cervical squamous cell carcinoma and endocervical adenocarcinoma that retrieved from genomic data commons (GDC). Compared with protein-coding genes, the expression levels of pseudogenes and lncRNAs were much lower. A total of 190 differentially expressed lncRNAs and 2,326 protein-coding genes were identified. Meanwhile, 269 differentially methylation regions (DMRs), where 16 lncRNAs were located, were figured out. Only one lncRNA, LINC00592, which was located in the DMRs, was also found differentially expressed. Several transcriptional regulation genes, such as ZNF20, ZNF441, ZNF573, and TMF1, were highly correlated with the expression of LINC00592, which illustrated its possible function on the transcription. Two microRNAs, which were both associated with tumor progression, can bind to LINC00592. Moreover, LINC00592 were also differentially expressed in other tumors. We proposed, with the help of various databases, that LINC00592 is a potential cancer-related lncRNA in cervical cancer and might activate the cancer progression through the regulation of transcription or structural integrity.

Overexpression of LINC00037 represses cervical cancer progression by activating mTOR signaling pathway.

Long non-coding RNAs have been reported to play crucial roles in tumorigenesis including cervical cancer. LINC00037 has been identified as a significant regulator in several cancers. Our study was aimed to investigate the function of LINC00037 in cervical cancer progression. LINC00037 was significantly downregulated in human cervical cancer cells (HeLa, HCC94, HT-3, Caski, and SiHa cells) compared with the ectocervical epithelial cells (End1/E6E7 cells). Overexpression of LINC00037 was able to inhibit cervical cancer cell proliferation, induce cell apoptosis, and restrain the cell migration/invasion capacity. Reversely, knockdown of LINC00037 exhibited an opposite process in vitro. mTOR has been recognized as an atypical serine/threonine kinase that is involved in regulating significant cellular functions. In our present study, we observed that the mTOR signaling pathway was strongly activated in human cervical cancer cells. Meanwhile, upregulation of LINC00037 contributed to the inactivation of mTOR signaling whereas downregulation of LINC00037 activated the pathway. Subsequently, in vivo animal models using SiHa cells were established and we proved that LINC00037 repressed cervical cancer progression via targeting the mTOR signaling pathway. All these findings implied that LINC00037 could regulate cervical cancer pathogenesis via mTOR signaling. In conclusion, a novel role of LINC00037 was manifested in cervical cancer progression.

A 15-long non-coding RNA signature to improve prognosis prediction of cervical squamous cell carcinoma.

Long non-coding RNAs (lncRNAs), which have little or no protein-coding capacity, caught a particular interest since their potential roles in the cancer paradigm. As the most common cancer in women, cervical squamous cell carcinoma remains one of the leading causes of deaths from cancer. However, limited evidence is available to determine the role of lncRNAs in the prognosis of cervical squamous cell carcinoma. In this study, we collected lncRNA expression profiling to identify prognosis related lncRNAs for cervical squamous cell carcinoma from TCGA database. In addition, we developed a 15-lncRNA signature based risk score to comprehensively assess the prognostic function of lncRNA. Furthermore, we performed a ROC analysis to identify the optimal cut-off point for classification risk level of the patients. Univariate Cox regression models were used to assess the association between lncRNAs and prognosis of patients with cervical squamous cell carcinoma. A 15-lncRNA based risk score was developed based on the Cox co-efficient of the individual lncRNAs. The prognostic value of this risk score was validated in the complete set and internal testing set. In summary, a 15-lncRNA expression signature (BAIAP2-AS1, RP11-203J24.8, LINC01133, RP1-7G5.6, RP11-147L13.15, SERHL, CTC-537E7.3, RP11-440L14.1, RP11-131N11.4, ILF3-AS1, RP11-80H18.4, RP11-1096G20.5, CTD-2192J16.26, RP11-621L6.3, and RP11-571M6.18) were identified and validated which can predict cervical cancer patient survival. The potential functions of this 15-lncRNA expression signature and individual lncRNAs as prognostic targets of cervical cancer were revealed by this study. Furthermore, these findings may have important implications in the understanding of the potential therapeutic method for the cervical squamous cell carcinoma patients.

Arsanilic acid causes apoptosis and oxidative stress in rat kidney epithelial cells (NRK-52e cells) by the activation of the caspase-9 and -3 signaling pathway.

Arsenic exists widely in rock, water and air, and arsanilic acid (also known as aminophenyl arsenic acid) is an organoarsenic compound and has been used as feed additives. Organoarsenic compounds in foodstuff cause adverse effects, including acute and chronic toxicity, in animals and humans. However, little is known about the cellular toxicity and mechanisms of organic arsenic on the kidney. In this study, we explored the toxicity and molecular mechanisms of arsanilic acid on rat kidney epithelial cells (NRK-52e cells). The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay showed that arsanilic acid inhibited the proliferation of rat NRK-52e cells in a dose-dependent manner, and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling assay and flow cytometry revealed that arsanilic acid induced cellular apoptosis in NRK-52e cells. Fluorescence spectrophotometer displayed that arsanilic acid caused a loss of mitochondrial transmembrane potential (MMP) of NRK-52e cells, but enhanced reactive oxygen species level of these cells. Notably, trolox, a water-soluble derivative of vitamin E, protected NRK-52e cells against MMP loss and apoptosis caused by arsanilic acid. Western blots with caspase inhibitors further indicated that arsanilic acid increased expression of active caspase-3 and -9 in NRK-52e cells. Collectively, these results suggest that arsanilic acid causes apoptosis and oxidative stress in rat kidney epithelial cells through activation of the caspase-9 and -3 signaling pathway. This study thus provides a novel insight into molecular mechanisms by which arsanilic acid has adverse cytotoxicity on renal tubular epithelial cells.

Evaluating coverage of exons by HapMap SNPs.

Genome-wide association (GWA) studies are currently one of the most powerful tools in identifying disease-associated genes or variants. In typical GWA studies, single-nucleotide polymorphisms (SNPs) are often used as genetic makers. Therefore, it is critical to estimate the percentage of genetic variations which can be covered by SNPs through linkage disequilibrium (LD). In this study, we use the concept of haplotype blocks to evaluate the coverage of five SNP sets including the HapMap and four commercial arrays, for every exon in the human genome. We show that although some Chips can reach similar coverage as the HapMap, only about 50% of exons are completely covered by haplotype blocks of HapMap SNPs. We suggest further high-resolution genotyping methods are required, to provide adequate genome-wide power for identifying variants.

Sarcopenia and metabolic dysfunction associated steatotic liver disease: Time to address both.

Sarcopenia and metabolic dysfunction associated steatotic liver disease (MASLD) are closely intertwined. Sarcopenia, traditionally a disease of the older adult and chronic disease population, has been closely studied as one of the pathophysiologic conditions at play in the development of MASLD. They share similar risk factors of insulin resistance and physical inactivity. Given similar pathophysiology along the liver-muscle axis, sarcopenia has been studied as a risk factor for MASLD, and vice versa. Current research suggests a bidirectional relationship. Given the chronicity of MASLD as a chronic inflammatory liver disease, it can break down muscle mass and lead to sarcopenia, while sarcopenia promotes intramuscular lipid accumulation that releases cytokines that can aggravate inflammation in the liver. However, for the longest time, a lack of consensus definition for MASLD and sarcopenia made it difficult to study their relationship and outcomes. A recent nomenclature update to diagnosing MASLD has made it easier for researchers to identify cohorts for study. However, no gold standard technique to measure muscle mass or consensus sarcopenia definition has been identified yet. Future studies are needed to reach a consensus and reduce diagnostic variation. With similar pathophysiology and shared risk factors between the two diseases, future research may also identify potential therapeutic targets along the liver-muscle axis that would benefit both sarcopenia and MASLD in order to maximize their outcomes.

Nano-revolution in hepatocellular carcinoma: A multidisciplinary odyssey - Are we there yet?

In this editorial we comment on the review by Zhou et al reviewing the landscape of nanomedicine in the treatment of hepatocellular carcinoma (HCC). We focus on the immense potential of nanotechnology, particularly ligand-receptor mediated nanotherapy, in revolutionizing the treatment landscape of HCC. Despite advancements in multidisciplinary treatment, HCC remains a significant global health challenge. Ligand-mediated nanotherapy offers the opportunity for precise drug delivery to tumor sites, targeting specific receptors overexpressed in HCC cells, thereby enhancing efficacy and minimizing side effects. Overcoming drug resistance and aggressive tumor biology is facilitated by nanomedicine, bypassing traditional hurdles encountered in chemotherapy. Examples include targeting glypican-3, asialoglycoprotein, transferrin receptor or folic acid receptors, capitalizing on their over-expression in tumor cells. The ability for multi-receptor targeting through dual-ligand nanoparticle modification holds the prospect of further enhancement in specificity and efficacy of directed therapy. However, challenges including immune responses, reproducibility in nanoparticle synthesis, and production scalability remain. Future directions involve refining targeting strategies, improving drug release mechanisms, and streamlining production processes to enable personalized and multifunctional nanotherapies. Overall, the integration of nanotherapy in HCC treatment holds immense promise, but continued partnership and effort are needed in offering hope for more effective, precise, and accessible clinical care in the management of HCC.

Effects of natural sound exposure on health recovery: A systematic review and meta-analysis.

Listening to natural sounds, both live and recorded, in either a natural or built environment is considered natural sound exposure (NSE). Sound is closely related to daily life, and research on the restorative effects of natural sounds is expanding. However, there is a lack of quantitative and comprehensive analysis on the impact of NSE on health recovery. This study systematically reviewed and conducted a meta-analysis on the impact of NSE on health recovery. Fifteen studies (1285 participants) were selected for the meta-analysis out of the 1157 literatures about the recovery of the NSE, searched from the Web of Science and Science Direct. The results indicate that NSE has certain positive effects: (a) In terms of emotional changes, NSE significantly reduces anxiety as measured by both the Visual Analog Scale (VAS) -2.31 (95 % CI -2.83, -1.79) and the State Anxiety Inventory (SAI) -12.22 (95 % CI -22.46, -1.98). (b) In terms of physiological reaction, NSE resulted in reduced heart rate (HR) -5.46 (95 % CI -9.62, -1.31), systolic blood pressure (SBP) -11.74 (95 % CI -15.51, -7.97), diastolic blood pressure (DBP) -13.98 (95 % CI -24.96, -2.99) and respiratory rate (RR) -1.58 (95 % CI -3.06, -0.10). (c) While the potential for restoration of cognitive performance by NSE was found, no consistent conclusions have been reached yet. However, there was significant heterogeneity between studies, primarily attributed to variations in study populations and methodologies. Because of the limited literature, we did not conduct subgroup analysis and meta-regression analysis. It is recommended that future studies address this heterogeneity by including more and higher-quality literature and employing rigorous methodologies to establish a robust foundation for evidence-based medicine. This will be of great significance for the application natural sounds in landscape planning and medical rehabilitation environments, and has the potential to promote improvements in public health.

Systematic bibliometric analysis of research hotspots and trends on the application of premium IOLs in the past 2 decades.

AIM: To analysis of research hotspots and trends on the application of premium intraocular lens (PIOLs) in the past 2 decades. METHODS: The literature search was performed on the Web of Science and included PIOLs studies published between January 2000 and December 2022. The retrieved literature was collated and analyzed by R-tool's Bibliometrix package, CitNetExplorer, CiteSpace and other software. RESULTS: A total of 1801 articles about PIOLs were obtained, most of which were published in Spain and the United States. The organization that published the most articles was the University of Valencia in Spain. Alió JL, and Montés-Micó R, from Spain were the most influential authors in this field. The Journal of Cataract and Refractive Surgery and Journal of Refractive Surgery were the core journals for this field; the top 10 cited articles mainly focus on postoperative satisfaction with multifocal intraocular lens (IOLs) and postoperative results of toric IOLs. Through the keyword analysis, we found that trifocal IOLs, astigmatism and extended depth of focus (EDoF) IOLs are the most discussed topics at present, and the importance of astigmatism and the clinical application of the new generation of PIOLs are the emerging research trends. CONCLUSION: Bibliometric analysis can effectively help to identify multilevel concerns in PIOLs research and the prevailing research trends in the realm of PIOLs encompass the adoption of EDoF IOLs, trifocal IOLs, and their respective Toric models.

Association of Sleep Pattern and Genetic Susceptibility with Obstructive Sleep Apnea: A Prospective Analysis of the UK Biobank.

Purpose: The prevalence of obstructive sleep apnea (OSA) is high worldwide. This study aimed to quantify the relationship between the incidence of OSA and sleep patterns and genetic susceptibility. Methods: A total of 355,133 white British participants enrolled in the UK Biobank between 2006 and 2010 with follow-up data until September 2021 were recruited. We evaluated sleep patterns using a customized sleep scoring method based on the low-risk sleep phenotype, defined as follows: morning chronotype, 7-8 hours of sleep per day, never/rarely experience insomnia, no snoring, no frequent daytime sleepiness, never/rarely nap, and easily getting up early. The polygenic risk score was calculated to assess genetic susceptibility to OSA. Cox proportional hazard models were used to evaluate the associations between OSA and sleep patterns and genetic susceptibility. Results: During a mean follow-up of 12.57 years, 4618 participants were diagnosed with OSA (age: 56.83 ± 7.69 years, women: 31.3%). Compared with those with a poor sleep pattern, participants with a normal (HR: 0.42, 95% CI: 0.38-0.46), ideal (HR: 0.21, 95% CI: 0.19-0.24), or optimal (HR: 0.15, 95% CI: 0.12-0.18) sleep pattern were significantly more likely to have OSA. The genetic susceptibility of 173,239 participants was calculated, and the results showed that poor (HR: 3.67, 95% CI: 2.95-4.57) and normal (HR: 1.89, 95% CI: 1.66-2.16) sleep patterns with high genetic susceptibility can increase the risk for OSA. Conclusion: This large-scale prospective study provides evidence suggesting that sleep patterns across seven low-risk sleep phenotypes may protect against OSA in individuals with varying degrees of genetic susceptibility.