Effects of plant diversity, soil microbial diversity, and network complexity on ecosystem multifunctionality in a tropical rainforest.

Introduction: Plant diversity and soil microbial diversity are important driving factors in sustaining ecosystem multifunctionality (EMF) in terrestrial ecosystems. However, little is known about the relative importance of plant diversity, soil microbial diversity, and soil microbial network complexity to EMF in tropical rainforests. Methods: This study took the tropical rainforest in Xishuangbanna, Yunnan Province, China as the research object, and quantified various ecosystem functions such as soil organic carbon stock, soil nutrient cycling, biomass production, and water regulation in the tropical rainforest to explore the relationship and effect of plant diversity, soil microbial diversity, soil microbial network complexity and EMF. Results: Our results exhibited that EMF decreased with increasing liana species richness, soil fungal diversity, and soil fungal network complexity, which followed a trend of initially increasing and then decreasing with soil bacterial diversity while increasing with soil bacterial network complexity. Soil microbial diversity and plant diversity primarily affected soil nutrient cycling. Additionally, liana species richness had a significant negative effect on soil organic carbon stocks. The random forest model suggested that liana species richness, soil bacterial network complexity, and soil fungal network complexity indicated more relative importance in sustaining EMF. The structural equation model revealed that soil bacterial network complexity and tree species richness displayed the significantly positive effects on EMF, while liana species richness significantly affected EMF via negative pathway. We also observed that soil microbial diversity indirectly affected EMF through soil microbial network complexity. Soil bulk density had a significant and negative effect on liana species richness, thus indirectly influencing EMF. Simultaneously, we further found that liana species richness was the main indicator of sustaining EMF in a tropical rainforest, while soil bacterial diversity was the primary driving factor. Discussion: Our findings provide new insight into the relationship between biodiversity and EMF in a tropical rainforest ecosystem and the relative contribution of plant and soil microibal diversity to ecosystem function with increasing global climate change.

Correlation of ultrasound features with Bcl-2 protein expression in basal cell carcinomas (BCCs).

BACKGROUND: The expression of the Bcl-2 protein is frequently observed in basal cell carcinomas (BCCs), making it a significant biological marker and potential therapeutic target. Skin ultrasonography offers a noninvasive means of obtaining anatomical information about cutaneous tumors. OBJECTIVES: The purpose of this study was to investigate the correlation between ultrasound features and Bcl-2 expression in BCCs, to provide a reference for developing pharmacological treatment plans. METHODS: According to the Bcl-2 protein expression, 74 BCCs confirmed by surgical pathology were divided into high Bcl-2 expression BCCs (HB-BCCs) and low Bcl-2 expression BCCs (LB-BCCs). Preoperative lesion ultrasound features were analyzed retrospectively based on Liang's criteria, which included the following features: shape, surface, keratinization, base, infiltration level, internal echogenicity, distribution of hyperechoic spots, posterior echogenic changes, internal Doppler signal, and lesion size (maximum diameter and infiltration depth). The differences of two groups were compared using a chi-square test or a paired t-test. RESULTS: Based on ultrasound features, cystic areas were more frequent in LB-BCCs (χ2 = 7.015, P = .008). Furthermore, LB-BCCs exhibited greater infiltration depth than HB-BCCs (4.86 ± 2.12 mm vs. 2.72 ± 1.40 mm, P = .000), had a higher propensity to infiltrate the subcutaneous tissue (χ2 = 12.422, P = .002), and displayed a more abundant internal Doppler signal within the lesions (χ2 = 24.696, P = .000). Conversely, maximum diameter of the lesions, shape, surface, keratinization, base, hyperechoic spots distribution, and posterior echogenic changes of the lesions did not differ significantly between the two groups. CONCLUSIONS: Ultrasound features are correlated with Bcl-2 protein expression level in BCCs. LB-BCCs show greater infiltration depth, subcutaneous infiltration, more cystic changes and more abundant internal Doppler signal than HB-BCCs, which may suggest a potential basis for drug selection in BCC chemotherapy.

Genome-Wide Integration of Genetic and Genomic Studies of Atopic Dermatitis: Insights into Genetic Architecture and Pathogenesis.

Atopic dermatitis (AD) is a common heterogeneous, chronic, itching, and inflammatory skin disease. Genetic studies have identified multiple AD susceptibility genes. However, the genetic architecture of AD has not been elucidated. In this study, we conducted a large-scale meta-analysis of AD (35,647 cases and 1,013,885 controls) to characterize the genetic basis of AD. The heritability of AD in different datasets varied from 0.6 to 7.1%. We identified 31 previously unreported genes by integrating multiomics data. Among the 31 genes, MCL1 was identified as a potential treatment target for AD by mediating gene‒drug interactions. Tissue enrichment analyses and phenome-wide association study provided strong support for the role of the hemic and immune systems in AD. Across 1,207 complex traits and diseases, genetic correlations indicated that AD shared links with multiple respiratory phenotypes. The phenome-wide Mendelian randomization analysis (Mendelian randomization‒phenome-wide association study) revealed that the age of onset of diabetes exhibited a positive causal effect on AD (inverse-variance weighted ß = 0.39, SEM = 0.09, P = 2.77 × 10-5). Overall, these results provide important insights into the genetic architecture of AD and will lead to a more thorough and complete understanding of the molecular mechanisms underlying AD.

Investigating the Efficacy of Hydrocolloid Dressing for Preventing Nasotracheal Tube-Related Pressure Injury in the PICU.

OBJECTIVES: To investigate the efficacy of hydrocolloid dressing in reducing the occurrence rate and severity of nasotracheal tube-related pressure injury. DESIGN: Randomized controlled trial. SETTING: A PICU in a tertiary medical center in southern China. PATIENTS: Pediatric patients received invasive mechanical ventilation via nasotracheal tubes. INTERVENTIONS: The hydrocolloid dressing was cut into an optimal square size, which should cover the area from the nasal columella to the ala. MEASUREMENTS AND MAIN RESULTS: Eligible participants were randomly allocated to the control group and the experimental group. The participants in the experimental group received hydrocolloid dressing to protect nasal skin from the beginning of nasotracheal intubation, while the participants in the control group received the current care procedure (without hydrocolloid dressing) unless pressure injuries occurred. The hydrocolloid dressing was changed daily to assess the nasal skin. The pressure injury staging system that was redefined and updated by the National Pressure Ulcer Advisory Panel in 2016 was used. The mean duration of nasotracheal intubation was 150.10 ± 117.09 hours in the experimental group and 161.75 ± 120.72 hours in the control group. Forty-five participants had nasotracheal tube-related pressure injuries in control group, whereas 26 patients had in experimental group (72.6% vs 43.3%; absolute difference, 29.3%, 95% CI, 12.5-46%; p = 0.001). The median survival times of the nasal skin integrity were 95.5 hours in the control group and 219.5 hours in the experimental group (p < 0.001). CONCLUSIONS: Hydrocolloid dressing can not only reduce the occurrence rate of nasotracheal tube-related pressure injury in the child with long-term nasotracheal intubation but also improve the endurance of the nasal skin significantly.

Interaction between tissue factor pathway inhibitor-2 gene polymorphisms and environmental factors associated with coronary atherosclerosis in a Chinese Han.

To investigate the association of single nucleotide polymorphisms (SNPs) within tissue factor pathway inhibitor-2 (TFPI-2) gene polymorphisms and additional gene-environment interaction with coronary atherosclerosis risk. Generalized multifactor dimensionality reduction (GMDR) was used to screen the best interaction combination among 4 SNPs, smoking and alcohol drinking. Logistic regression was performed to investigate association between 4 SNPs within TFPI-2 gene and coronary atherosclerosis risk. Coronary atherosclerosis risk was significantly higher in carriers with the A allele of rs34489123 within TFPI-2 gene than those with GG genotype (GA+AA versus GG), adjusted OR (95% CI) = 1.70 (1.20-2.31), and was also higher in carriers with the G allele of rs4264 within TFPI-2 gene than those with AA genotype (AG+GG versus AA), adjusted OR (95% CI) = 1.62 (1.21-2.11). GMDR model shown the best models for gene-environment interaction were rs34489123 and smoking after adjusting the covariates, which scored 10 out of 10 for cross-validation consistency and 0.0010 for the sign test. Heavy LD was found for SNPs rs34489123 and rs59805398 (D' value was more than 0.8). Compared to control individuals, the AG haplotypes appeared to be significantly associated with increased coronary atherosclerosis risk, OR (95% CI) = 1.73 (1.22-2.32). We found that the A allele of rs34489123 and the G allele of rs4264 within TFPI-2 gene, interaction between rs34489123 and smoking and AG haplotypes were all associated with increased coronary atherosclerosis risk.

Aldehyde dehydrogenase 1A1 up-regulates stem cell markers in benzo[a]pyrene-induced malignant transformation of BEAS-2B cells.

Recently, Aldehyde dehydrogenase 1A1 (ALDH1A1) has been proposed to be a common marker of cancer stem cells and can be induced by benzo[a]pyrene (B[a]P) exposure. However, the underlying mechanism of how ALDH1A1 contributes to B[a]P-induced carcinogenesis in human bronchial epithelial cells remains unclear. Here, we found that B[a]P up-regulated expression levels of stem cell markers (ABCG2, SOX2, c-Myc and Klf4), epithelial-mesenchymal transition (EMT) associated genes (SNAIL1, ZEB1, TWIST and ß-CATENIN) and cancer-related long non-coding RNAs (lncRNAs; HOTAIR and MALAT-1) in malignant B[a]P-transformed human bronchial epithelial cells (BEAS-2B-T cells), and these up-regulations were dependent on increased expression of ALDH1A1. The inhibition of endogenous ALDH1A1 expression down-regulated expression levels of stem cell markers and reversed the malignant phenotype as well as reduced the chemoresistance of BEAS-2B-T cells. In contrast, the overexpression of ALDH1A1 in BEAS-2B cells increased the expression of stem cell markers, facilitated cell transformation, promoted migratory ability and enhanced the drug resistance of BEAS-2B cells. Overall, our data indicates that ALDH1A1 promotes a stemness phenotype and plays a critical role in the BEAS-2B cell malignant transformation induced by B[a]P.