Environmental risks of mask wastes binding pollutants: Phytotoxicity, microbial community, nitrogen and carbon cycles.

The increasing contamination of mask wastes presents a significant global challenge to ecological health. However, there is a lack of comprehensive understanding regarding the environmental risks that mask wastes pose to soil. In this study, a total of 12 mask wastes were collected from landfills. Mask wastes exhibited negligible morphological changes, and bound eight metals and four types of organic pollutants. Masks combined with pollutants inhibited the growth of alfalfa and Elymus nutans, reducing underground biomass by 84.6 %. Mask wastes decreased the Chao1 index and the relative abundances (RAs) of functional bacteria (Micrococcales, Gemmatimonadales, and Sphingomonadales). Metagenomic analysis showed that mask wastes diminished the RAs of functional genes associated with nitrification (amoABC and HAO), denitrification (nirKS and nosZ), glycolysis (gap2), and TCA cycle (aclAB and mdh), thereby inhibiting the nitrogen transformation and ATP production. Furthermore, some pathogenic viruses (Herpesviridae and Tunggulvirus) were also found on the mask wastes. Structural equation models demonstrated that mask wastes restrained soil enzyme activities, ultimately affecting nitrogen and carbon cycles. Collectively, these evidences indicate that mask wastes contribute to soil health and metabolic function disturbances. This study offers a new perspective on the potential environmental risks associated with the improper disposal of masks.

Combined effects of genetic predisposition and sleep quality on acceleration of biological ageing: Findings from the UK biobank cohort.

OBJECTIVE: Genetic risks can accelerate ageing, yet better quality sleep may slow down it. We thus examined the interaction and combined effects of genetic predisposition and sleep quality on the risk of accelerate aging. METHODS: This study included 407,027 participants from the UK Biobank. Sleep index of each participant was retrieved from the following seven sleep behaviors: snoring, chronotype, daytime sleepiness, sleep duration, insomnia, nap and difficulties in getting up. The biological age (PhenoAge) were estimated by corresponding algorithms based on clinical traits, and their residual discrepancies with chronological age were defined as the age accelerations (PhenoAgeaccel). We explored the interaction and combined effects of genetic risk and sleep quality on accelerated ageing by constructing a linear model. RESULTS: Compared with participants in low sleep quality group, those in medium and high sleep quality group decreased 0.727 (95%CI, 0.653 to 0.801) and 1.056 (95%CI, 0.982 to 1.130) years of PhenoAgeaccel, respectively. Compared with participants in low genetic risk group, those in medium and high genetic risk group increased 0.833 (95%CI, 0.792 to 0.874) and 1.543 (95%CI, 1.494 to 1.592) years of PhenoAgeaccel, respectively. There was interaction between the genetic risk and sleep quality (P-interaction<0.001). For combined effect, compared to the group with high sleep quality and lower genetic risk, people with low sleep quality and high genetic risk had 2.747 (95%CI, 2.602 to 2.892) years higher PhenoAgeaccel. CONCLUSION: Our findings elucidate that better sleep quality could lessen accelerated biological ageing especially among population with high genetic risk.

Biochar immobilized hydrolase degrades PET microplastics and alleviates the disturbance of soil microbial function via modulating nitrogen and phosphorus cycles.

Microplastics (MPs) pose an emerging threat to soil ecological function, yet effective solutions remain limited. This study introduces a novel approach using magnetic biochar immobilized PET hydrolase (MB-LCC-FDS) to degrade soil polyethylene terephthalate microplastics (PET-MPs). MB-LCC-FDS exhibited a 1.68-fold increase in relative activity in aquatic solutions and maintained 58.5 % residual activity after five consecutive cycles. Soil microcosm experiment amended with MB-LCC-FDS observed a 29.6 % weight loss of PET-MPs, converting PET into mono(2-hydroxyethyl) terephthalate (MHET). The generated MHET can subsequently be metabolized by soil microbiota to release terephthalic acid. The introduction of MB-LCC-FDS shifted the functional composition of soil microbiota, increasing the relative abundances of Microbacteriaceae and Skermanella while reducing Arthobacter and Vicinamibacteraceae. Metagenomic analysis revealed that MB-LCC-FDS enhanced nitrogen fixation, P-uptake and transport, and organic-P mineralization in PET-MPs contaminated soil, while weakening the denitrification and nitrification. Structural equation model indicated that changes in soil total carbon and Simpson index, induced by MB-LCC-FDS, were the driving factors for soil carbon and nitrogen transformation. Overall, this study highlights the synergistic role of magnetic biochar-immobilized PET hydrolase and soil microbiota in degrading soil PET-MPs, and enhances our understanding of the microbiome and functional gene responses to PET-MPs and MB-LCC-FDS in soil systems.

Metabolic score and its components are associated with carotid plaque prevalence in young adults.

PURPOSE: No study has comprehensively assessed the relationship of metabolic factors including insulin resistance, hypertension, hyperuricemia, and hypercholesterolemia with the development of carotid plaque. Therefore, we constructed metabolic scores based on the above metabolic factors and examined its association with carotid plaque in young and older Chinese adults. METHODS: This study included 17,396 participants who underwent carotid ultrasound examinations, including 14,173 young adults (<65 years) and 3,223 older adults (≥65 years). Individual metabolic score was calculated using triglyceride-glucose (TyG) index, mean arterial pressure (MAP), uric acid, and total cholesterol (TC). Logistic regression models were conducted to examine the role of metabolic score and its components in the prevalence of carotid plaque. The nonlinear relationship was examined using restricted cubic spline regression. Meanwhile, subgroup, interaction, and sensitivity analyses were conducted. RESULTS: The multivariate logistic regression analysis showed that TyG (OR: 1.088; 95%CI: 1.046-1.132), MAP (OR: 1.121; 95%CI: 1.077-1.168), TC (OR: 1.137; 95%CI: 1.094-1.182) and metabolic score (OR: 1.064; 95%CI: 1.046-1.082) were associated with carotid plaque prevalence in young adults rather than older adults. The nonlinear association was not observed for metabolic scores and carotid plaque. Subgroup analyses showed significant associations between metabolic scores and carotid plaque prevalence in men, women, normal-weight, and overweight young adults. No interaction of metabolic score with sex and BMI were observed. CONCLUSIONS: The results support that control of TyG, MAP, TC, and metabolic scores is a key point in preventing the prevalence of carotid plaque in the young adults.

Imaging Transcriptomics of the Brain for Schizophrenia.

Schizophrenia is a severe mental disorder with a neurodevelopmental origin. Although schizophrenia results from changes in the brain, the underlying biological mechanisms are unknown. Transcriptomics studies quantitative expression changes or qualitative changes of all genes and isoforms, providing a more meaningful biological insight. Magnetic resonance imaging (MRI) techniques play roles in revealing brain structure and function. We give a narrative focused review on the current transcriptome combined with MRI studies related to schizophrenia and summarize the research methodology and content of these studies to identify the research commonalities as well as the implications for future research, in an attempt to provide new insights into the mechanism, clinical diagnosis, and treatments of schizophrenia.

Lithium Bromide-Promoted Formal C(sp3)-H Bond Insertion Reactions of ß-Carbonyl Esters with Sulfoxonium Ylides to Synthesize 1,4-Dicarbonyl Compounds.

A LiBr-promoted formal C(sp3)-H bond insertion reaction between ß-carbonyl esters and sulfoxonium ylides is established. This practical reaction has a wide range of substrate scope for both ß-carbonyl esters and sulfoxonium ylides to give a variety of 1,4-dicarbonyl compounds with 43-94% yields. The reaction features transition-metal-free reaction conditions and exclusive C-alkylation chemselectivity. The use of bench-stable sulfoxonium ylides overcomes previous methods that require transition metal as catalysts and unstable diazo compounds or toxic haloketones as alkylation reagents.

Associations of Dietary Diversity Trajectories with Frailty among Chinese Older Adults: A Latent Class Trajectory Analysis Based on a CLHLS Cohort.

BACKGROUND: High dietary diversity has been found to be associated with frailty. However, the trajectory of dietary diversity intake in relation to frailty is unclear. METHODS: Using the latent class trajectory modeling approach, we identified distinctive dietary variety trajectory groups among 2017 participants based on the Chinese Longitudinal Healthy Longevity Survey acquired at four time points within a 10-year period. Frailty status was assessed using a frailty index comprising 37 health deficits. Dietary diversity was quantified using the dietary variety score (DVS), based on food category consumption frequency. Logistic regression analyses were employed to explore the association between DVS change trajectories and frailty. RESULTS: This study identified two distinct DVS trajectories: "Moderate-Slow decline-Slow growth", encompassing 810 (40.16%) individuals, and "Moderate-Slow growth-Accelerated decline", including 1207 (59.84%) individuals. After adjusting for covariates, the odds ratio for DVS in the "Moderate-Slow decline-Slow growth" group was 1.326 (95% confidence interval: 1.075-1.636) compared to the "Moderate-Slow growth-Accelerated decline" group. The "Moderate-Slow decline-Slow growth" trajectory continued to decrease and was maintained at a low level in the early stages of aging. CONCLUSION: Sustaining a high dietary diversity trajectory over time, particularly in the early stages of aging, could potentially decrease the risk of frailty among older Chinese adults.

Investigating the shared genetic architecture between breast and ovarian cancers.

High heritability and strong correlation have been observed in breast and ovarian cancers. However, their shared genetic architecture remained unclear. Linkage disequilibrium score regression (LDSC) and heritability estimation from summary statistics (ρ-HESS) were applied to estimate heritability and genetic correlations. Bivariate causal mixture model (MiXeR) was used to qualify the polygenic overlap. Then, stratified-LDSC (S-LDSC) was used to identify tissue and cell type specificity. Meanwhile, the adaptive association test called MTaSPUsSet was performed to identify potential pleiotropic genes. The Single Nucleotide Polymorphisms (SNP) heritability was 13% for breast cancer and 5% for ovarian cancer. There was a significant genetic correlation between breast and ovarian cancers (rg=0.21). Breast and ovarian cancers exhibited polygenic overlap, sharing 0.4 K out 2.8 K of causal variants. Tissue and cell type specificity displayed significant enrichment in female breast mammary, uterus, kidney tissues, and adipose cell. Moreover, the 74 potential pleiotropic genes were identified between breast and ovarian cancers, which were related to the regulation of cell cycle and cell death. We quantified the shared genetic architecture between breast and ovarian cancers and shed light on the biological basis of the co-morbidity. Ultimately, these findings facilitated the understanding of disease etiology.

Causal effects of sleep traits on metabolic syndrome and its components: a Mendelian randomization study.

PURPOSE: Previous observational studies have suggested an association between sleep disturbance and metabolic syndrome (MetS). However, it remains unclear whether this association is causal. This study aims to investigate the causal effects of sleep-related traits on MetS using Mendelian randomization (MR). METHODS: Single-nucleotide polymorphisms strongly associated with daytime napping, insomnia, chronotype, short sleep, and long sleep were selected as genetic instruments from the corresponding genome-wide association studies (GWAS). Summary-level data for MetS were obtained from two independent GWAS datasets. Univariable and multivariable MR analyses were conducted to investigate and verify the causal effects of sleep traits on MetS. RESULTS: The univariable MR analysis demonstrated that genetically predicted daytime napping and insomnia were associated with increased risk of MetS in both discovery dataset (OR daytime napping = 1.630, 95% CI 1.273, 2.086; OR insomnia = 1.155, 95% CI 1.108, 1.204) and replication dataset (OR daytime napping = 1.325, 95% CI 1.131, 1.551; OR insomnia = 1.072, 95% CI 1.046, 1.099). For components, daytime napping was positively associated with triglycerides (beta = 0.383, 95% CI 0.160, 0.607) and waist circumference (beta = 0.383, 95% CI 0.184, 0.583). Insomnia was positively associated with hypertension (OR = 1.101, 95% CI 1.042, 1.162) and waist circumference (beta = 0.067, 95% CI 0.031, 0.104). The multivariable MR analysis indicated that the adverse effect of daytime napping and insomnia on MetS persisted after adjusting for BMI, smoking, drinking, and another sleep trait. CONCLUSION: Our study supported daytime napping and insomnia were potential causal factors for MetS characterized by central obesity, hypertension, or elevated triglycerides.

Endogenous stimuli-responsive separating microneedles to inhibit hypertrophic scar through remodeling the pathological microenvironment.

Hypertrophic scar (HS) considerably affects the appearance and causes tissue dysfunction in patients. The low bioavailability of 5-fluorouracil poses a challenge for HS treatment. Here we show a separating microneedle (MN) consisting of photo-crosslinked GelMA and 5-FuA-Pep-MA prodrug in response to high reactive oxygen species (ROS) levels and overexpression of matrix metalloproteinases (MMPs) in the HS pathological microenvironment. In vivo experiments in female mice demonstrate that the retention of MN tips in the tissue provides a slowly sustained drug release manner. Importantly, drug-loaded MNs could remodel the pathological microenvironment of female rabbit ear HS tissues by ROS scavenging and MMPs consumption. Bulk and single cell RNA sequencing analyses confirm that drug-loaded MNs could reverse skin fibrosis through down-regulation of BCL-2-associated death promoter (BAD), insulin-like growth factor 1 receptor (IGF1R) pathways, simultaneously regulate inflammatory response and keratinocyte differentiation via up-regulation of toll-like receptors (TOLL), interleukin-1 receptor (IL1R) and keratinocyte pathways, and promote the interactions between fibroblasts and keratinocytes via ligand-receptor pair of proteoglycans 2 (HSPG2)-dystroglycan 1(DAG1). This study reveals the potential therapeutic mechanism of drug-loaded MNs in HS treatment and presents a broad prospect for clinical application.

Causal association of rheumatoid arthritis with frailty and the mediation role of inflammatory cytokines: A Mendelian randomization study.

BACKGROUND: Previous observational studies have suggested the association between rheumatoid arthritis (RA) and frailty. However, it remains obscure whether this association is causal. This study aims to investigate the causal association of RA with frailty and the mediation effect of inflammatory cytokines using Mendelian randomization (MR) design. METHODS: Summary-level data for RA (N = 58,284), frailty index (FI) (N = 175,226), Fried frailty score (FFS) (N = 386,565), and 41 inflammatory cytokines (N = 8,293) were obtained from recent genome-wide association studies. Univariable and multivariable MR analyses were conducted to investigate and verify the causal association of RA with frailty. The potential mediation effects of inflammatory cytokines were estimated using two-step MR. RESULTS: Univariable inverse variance weighted MR analysis suggested that genetically determined RA was associated with increased FI (beta=0.021; 95 % CI: 0.012, 0.03; p = 2.2 × 10-6) and FFS (beta=0.011; 95 %CI: 0.007, 0.015; p = 8.811 × 10-8). The consistent results were observed in multivariable MR analysis after adjustment for asthma, smoking, BMI, physical activity, telomere length, and depression. Mediation analysis showed evidence of an indirect effect of RA on FI through monokine induced by interferon-gamma (MIG) with a mediated proportion of 9.8 % (95 %CI: 4.76 %, 19.05 %), on FFS via MIG and stromal cell-derived factor-1 alpha with a mediated proportion of 9.6 % (95 %CI: 0 %, 18.18 %) and 8.44 % (95 %CI: 0 %, 18.18 %), respectively. CONCLUSION: This study provided credible evidence that genetically predicted RA was associated with a higher risk of frailty. Additionally, inflammatory cytokines were involved in the mechanism of RA-induced frailty.

Large-scale mechanism hypothesis and research prospects of cognitive impairment in schizophrenia based on magnetic resonance imaging.

Cognitive impairments in schizophrenia are pivotal clinical issues that need to be solved urgently. However, the mechanism remains unknown. It has been suggested that cognitive impairments in schizophrenia are associated with connectome damage, and are especially relevant to the disrupted hub nodes in the frontal and parietal lobes. Activating the dorsolateral prefrontal cortex (DLPFC) via repetitive transcranial magnetic stimulation (rTMS) could result in improved cognition. Based on several previous magnetic resonance imaging (MRI) studies on schizophrenia, we found that the first-episode patients showed connectome damage, as well as abnormal activation and connectivity of the DLPFC and inferior parietal lobule (IPL). Accordingly, we proposed that DLPFC-IPL pathway destruction might mediate connectome damage of cognitive impairments in schizophrenia. In the meantime, with the help of multimodal MRI and noninvasive neuromodulation tool, we may not only validate the hypothesis, but also find IPL as the potential intervention target for cognitive impairments in schizophrenia.

Vitamin D deficiency increases the risk of diabetic peripheral neuropathy in elderly type 2 diabetes mellitus patients by predominantly increasing large-fiber lesions.

AIMS: This study explores the link between Vitamin D deficiency (VDD) and diabetic peripheral neuropathy (DPN) in elderly type 2 diabetes mellitus (T2DM) patients. METHODS: Involving 257 elderly T2DM patients, the study utilized propensity score matching to balance age, sex, and diabetes duration. VDD was defined as serum 25-hydroxyvitamin D [25(OH)D] levels below 20 ng/ml. Large nerve fiber lesions were evaluated by electromyogram, while small nerve fiber lesions were assessed by measuring skin conductance. RESULTS: DPN patients had notably lower serum 25(OH)D levels than non-DPN patients [15.05 vs. 18.4 ng/ml, P = 0.018]. VDD was identified as an independent risk factor for DPN (odds ratio = 2.488, P = 0.008) in multivariate logistic regression analysis. Spearman's correlation showed negative correlations between serum 25(OH)D levels and specific nerve latencies, and positive correlations with specific nerve velocities and amplitudes. The VDD group exhibited longer median sensory nerve latencies and motor evoked potential latencies compared to the vitamin D-sufficient group. Further, VDD is associated with the prolongation of the median motor nerve latency (odds ratio = 1.362, P = 0.038). CONCLUSIONS: VDD is independently associated with a higher risk of DPN. VDD may promote the development of DPN by affecting large nerve fibers.

Acidity-activated aggregation and accumulation of self-complementary zwitterionic peptide-decorated gold nanoparticles for photothermal biofilm eradication.

Drug-resistant biofilm infection is an extremely serious clinical problem, that easily leads to failure of antibiotic treatment. Although gold nanoparticles (AuNPs) as photothermal agents have been widely used in biofilm eradication, there are still challenges to be addressed, such as insignificantly redshifted absorption and slow assembly process of aggregated AuNPs. Herein, we developed an acidity-activated dispersion-to-aggregation transition to enhance the accumulation of self-complementary zwitterionic peptide-decorated AuNPs for photothermal eradication of drug-resistant biofilm infections. AuNPs were decorated with self-complementary zwitterionic peptides (ZP1 and ZP2) coupled with pH-sensitive anhydride (DMA) and pH-insensitive anhydride (SA), respectively. ZP2-decorated AuNPs with DMA modification (AuNP@ZP2(DMA)) exhibited prolonged blood circulation and enhanced accumulation in acidic biofilm microenvironment. Moreover, the electrostatic attraction between self-complementary ligands drove AuNPs to form closely packed aggregates with strong near-infrared absorption, leading to in vivo photoacoustic imaging ability and photothermal effect against drug-resistant bacteria and fungus, as well as microbial biofilms. AuNP@ZP2(DMA) with longer charge domains and a polyethylene glycol oligomer spacer showed greater photothermal antimicrobial and biofilm resistance in vitro and in vivo. This study develops an innovative acidity-activated AuNP photothermal agent, which provides an effective approach for treatment of biofilm infections.

Transcriptional level of inflammation markers associates with short-term brain structural changes in first-episode schizophrenia.

BACKGROUND: Inflammation has been implicated in the pathology of schizophrenia and may cause neuronal cell death and dendrite loss. Neuroimaging studies have highlighted longitudinal brain structural changes in patients with schizophrenia, yet it is unclear whether this is related to inflammation. We aim to address this question, by relating brain structural changes with the transcriptional profile of inflammation markers in the early stage of schizophrenia. METHODS: Thirty-eight patients with first-episode schizophrenia and 51 healthy controls were included. High-resolution T1-weighted magnetic resonance imaging (MRI) and clinical assessments were performed at baseline and 2 ~ 6 months follow-up for all subjects. Changes in the brain structure were analyzed using surface-based morphological analysis and correlated with the expression of immune cells-related gene sets of interest reported by previous reviews. Transcriptional data were retrieved from the Allen Human Brain Atlas. Furthermore, we examined the brain structural changes and peripheral inflammation markers in association with behavioral symptoms and cognitive functioning in patients. RESULTS: Patients exhibited accelerated cortical thickness decrease in the left frontal cortices, less decrease or an increase in the superior parietal lobule and right lateral occipital lobe, and increased volume in the bilateral pallidum, compared with controls. Changes in cortical thickness correlated with the transcriptional level of monocyte across cortical regions in patients (r = 0.54, p < 0.01), but not in controls (r = - 0.05, p = 0.76). In addition, cortical thickness change in the left superior parietal lobule positively correlated with changes in digital span-backward test scores in patients. CONCLUSIONS: Patients with schizophrenia exhibit regional-specific cortical thickness changes in the prefrontal and parietooccipital cortices, which is related to their cognitive impairment. Inflammation may be an important factor contributing to cortical thinning in first-episode schizophrenia. Our findings suggest that the immunity-brain-behavior association may play a crucial role in the pathogenesis of schizophrenia.

Spatial distribution and driving factors of the associations between temperature and influenza-like illness in the United States: a time-stratified case-crossover study.

BACKGROUND: Several previous studies investigated the associations between temperature and influenza in a single city or region without a national picture. The attributable risk of influenza due to temperature and the corresponding driving factors were unclear. This study aimed to evaluate the spatial distribution characteristics of attributable risk of Influenza-like illness (ILI) caused by adverse temperatures and explore the related driving factors in the United States. METHODS: ILI, meteorological factors, and PM2.5 of 48 states in the United States were collected during 2011-2019. The time-stratified case-crossover design with a distributed lag non-linear model was carried out to evaluate the association between temperature and ILI at the state level. The multivariate meta-analysis was performed to obtain the combined effects at the national level. The attributable fraction (AF) was calculated to assess the ILI burden ascribed to adverse temperatures. The ordinary least square model (OLS), spatial lag model (SLM), and spatial error model (SEM) were utilized to identify driving factors. RESULTS: A total of 7,716,115 ILI cases were included in this study. Overall, the temperature was negatively associated with ILI risk, and lower temperature gave rise to a higher risk of ILI. AF ascribed to adverse temperatures differed across states, from 49.44% (95% eCI: 36.47% ~ 58.68%) in Montana to 6.51% (95% eCI: -6.49% ~ 16.46%) in Wisconsin. At the national level, 29.08% (95% eCI: 27.60% ~ 30.24%) of ILI was attributable to cold. Per 10,000 dollars increase in per-capita income was associated with the increment in AF (OLS: ß = -6.110, P = 0.021; SLM: ß = -5.496, P = 0.022; SEM: ß = -6.150, P = 0.022). CONCLUSION: The cold could enhance the risk of ILI and result in a considerable proportion of ILI disease burden. The ILI burden attributed to cold varied across states and was higher in those states with lower economic status. Targeted prevention programs should be considered to lower the burden of influenza.

Differential expression of diacylglycerol kinase ζ is involved in inferior parietal lobule-related dysfunction in schizophrenia with cognitive impairments.

BACKGROUND: Cognitive impairment is the main factor in the poor prognosis of schizophrenia, but its mechanism remains unclear. The inferior parietal lobule (IPL) is related to various clinical symptoms and cognitive impairment in schizophrenia. We aimed to explore the relationship between IPL-related functions and cognitive impairment in schizophrenia. METHODS: 136 schizophrenia patients and 146 demographically matched healthy controls were enrolled for a cross-sectional study. High-spatial-resolution structural and resting-state functional images were acquired to demonstrate the alternations of brain structure and function. At the same time, the digit span and digit symbol coding tasks of the Chinese Wechsler Adult Intelligence Test Revised (WAIS-RC) were utilized in assessing the subjects' cognitive function. Patients were divided into cognitive impairment and normal cognitive groups according to their cognitive score and then compared whether there were differences between the three groups in fractional amplitude of low-frequency fluctuation (fALFF). In addition, we did a correlation analysis between cognitive function and the fALFF for the left IPL of patients and healthy controls. Based on the Allen Human Brain Atlas, we obtained genes expressed in the left IPL, which were then intersected with the transcriptome-wide association study results and differentially expressed genes in schizophrenia. RESULTS: Grouping of patients by the backward digit span task and the digit symbol coding task showed differences in fALFF values between healthy controls and cognitive impairment patients (P < 0.05). We found a negative correlation between the backward digit span task score and fALFF of the left IPL in healthy controls (r = - 0.388, P = 0.003), which was not seen in patients (r = 0.203, P = 0.020). In addition, none of the other analyses were statistically significant (P > 0.017). In addition, we found that diacylglycerol kinase ζ (DGKζ) is differentially expressed in the left IPL and associated with schizophrenia. CONCLUSION: Our study demonstrates that the left IPL plays a vital role in cognitive impairment in schizophrenia. DGKζ may act as an essential regulator in the left IPL of schizophrenia patients with cognitive impairment.

Transcriptomics and magnetic resonance imaging in major psychiatric disorders.

Major psychiatric disorders create a significant public health burden, and mental disorders such as major depressive disorder, bipolar disorder, and schizophrenia are major contributors to the national disease burden. The search for biomarkers has been a leading endeavor in the field of biological psychiatry in recent decades. And the application of cross-scale and multi-omics approaches combining genes and imaging in major psychiatric studies has facilitated the elucidation of gene-related pathogenesis and the exploration of potential biomarkers. In this article, we summarize the results of using combined transcriptomics and magnetic resonance imaging to understand structural and functional brain changes associated with major psychiatric disorders in the last decade, demonstrating the neurobiological mechanisms of genetically related structural and functional brain alterations in multiple directions, and providing new avenues for the development of quantifiable objective biomarkers, as well as clinical diagnostic and prognostic indicators.

Birth Weight, Cardiometabolic Factors, and Coronary Heart Disease: A Mendelian Randomization Study.

CONTEXT: Observational studies have shown associations of birth weight (BW) with coronary heart disease (CHD), but results are inconsistent and do not distinguish the fetal or maternal effect of BW. OBJECTIVE: This study aims to explore the causal association between BW and CHD, analyze the fetal and maternal contribution, and quantify mediating effects of cardiometabolic factors. METHODS: Genetic variants from genome-wide association study summary-level data of own BW (N = 298 142), offspring BW (N = 210 267 mothers), and 16 cardiometabolic (anthropometric, glycemic, lipidemic, and blood pressure) factors were extracted as instrumental variables. We used two-sample Mendelian randomization study (MR) to estimate the causal effect of BW on CHD (60 801 cases and 123 504 controls from mixed ancestry) and explore the fetal and maternal contributions. Mediation analyses were conducted to analyze the potential mediating effects of 16 cardiometabolic factors using two-step MR. RESULTS: Inverse variance weighted analysis showed that lower BW raised the CHD risk (ß -.30; 95% CI: -0.40, -0.20) and consistent results were observed in fetal-specific/maternal-specific BW. We identified 5 mediators in the causal pathway from BW to CHD, including body mass index-adjusted hip circumference, triglycerides, fasting insulin, diastolic blood pressure, and systolic blood pressure (SBP), with mediated proportion ranging from 7.44% for triglycerides to 27.75% for SBP. Causality between fetal-specific and maternal-specific BW and CHD was mediated by glycemic factors and SBP, respectively. CONCLUSION: Our findings supported that lower BW increased CHD risk and revealed that fetal-specific and maternal-specific BW may both contribute to this effect. The causality between BW and CHD was mediated by several cardiometabolic factors.

Left compared with right thoracic approach thoracotomy in esophageal cancer: a retrospective cohort study.

BACKGROUND: Esophagectomy is regarded as one of the optimal treatments for resectable esophageal cancer. However, the impact of surgical approach on the long-term prognosis of esophageal cancer remains controversial. This study attempted to compare the long-term survival outcomes of patients receiving left and right thoracic esophagectomy for esophageal cancer. METHODS: A total of 985 patients underwent esophagectomy (including 453 left and 532 right thoracic approach) for esophageal cancer in Henan Cancer Hospital from January 2015 to December 2016 were enrolled. Their 5 year overall survival (OS) and disease-free survival (DFS) were retrospectively collected. Cox regression was performed to compare OS and DFS in patients who underwent left and right thoracic esophagectomy. Propensity score matching (PSM) analysis was used to balance confounding factors. RESULTS: The 5 year OS rates were 60.21% in the left and 51.60% in the right thoracic esophagectomy, respectively (P = 0.67). The 5 year DFS rates were 56.73% in the left and 47.93% and in the right thoracic esophagectomy, respectively (P = 0.36). Cox regression analysis showed there was no significant difference in long-term survival between patients with left and right surgical access (OS: HR = 0.95, 95% CI 0.77-1.18; DFS: HR = 0.91, 95% CI 0.74-1.12). In the cohort of patients obtained by PSM, Cox regression analysis yielded the similar results. CONCLUSION: For patients with resectable esophageal cancer, the surgical treatment through left thoracic approach can achieve the same long-term survival outcomes as the right thoracic approach.