Terminal Index: A New Way for Precise Description of Topologic Structure of Highly Branched Polymers Derived from A₂ + B₃ Stepwise Polymerization

Terminal index (TI) was presented as a new characteristic parameter for quantitative description of branched and cyclic topology of highly branched soluble polymers derived from A₂ + B₃ stepwise polymerization. TI is defined as the ratio of terminal units of an A₂ + B₃ type highly branched polymer to those in its perfect hyperbranched counterpart. TI is concisely represented as T/(D + L), which can be conveniently calculated from a quantitative NMR spectrum. The model of soluble A₂ + B₃ type polymers is suggested as an intermediate between multicyclic polymers and perfect hyperbranched polymers. The TI ranges between 0 and 1 where a higher TI indicates a perfect hyperbranched topology while a low TI indicates a multicyclic structure. The analysis of soluble A₂ + B₃ type polyesters and polycarbosilanes as model polymers demonstrates that TI as a more precise parameter, along with degree of branching, can be generally applied to understand the fine topology of highly branched polymers derived from A₂ + B₃ polymerization

Additional file 2 of Genetic liability to obesity and peptic ulcer disease: a Mendelian randomization study

Additional file 2. Figure S1. Scatter plots for MR estimates of BMI (A) and WHR (B) on PUD; Figure S2. Scatter plots for MR estimates of BMI (A) and WHR (B) on PUD in the replication analysis; Figure S3. Scatter plots for MR estimates of PUD on BMI (A) and WHR (B); Figure S4. Scatter plots for MR estimates of PUD on BMI (A) and WHR (B) in the replication analysis

Additional file 1 of Genetic liability to obesity and peptic ulcer disease: a Mendelian randomization study

Additional file 1. Tabel S1. Proxies for SNPs not found in the outcome dataset (Forward MR); Tabel S2. Characteristics of the genetic variants associated with body mass index; Tabel S3. Characteristics of the genetic variants associated with waist-to-hip ratio; Tabel S4. Characteristics of the genetic variants associated with body mass index in replication analyses; Tabel S5. Characteristics of the genetic variants associated with waist-to-hip ratio in replication analyses; Tabel S6. Proxies for SNPs not found in the outcome dataset (Reverse MR); Tabel S7. Characteristics of the genetic variants associated with peptic ulcer disease; Tabel S8. Evaluation of heterogeneity and directional pleiotropy using different methods (Forward MR); Tabel S9. Evaluation of heterogeneity and directional pleiotropy in replication analyses (Forward MR); Table S10. Associations of genetic predisposition to PUD with risk of obesity in complementary Mendelian Randomization analyses (Reverse MR); Tabel S11. Evaluation of heterogeneity and directional pleiotropy using different methods (Reverse MR); Tabel S12. Evaluation of heterogeneity and directional pleiotropy in replication analyses (Reverse MR)

How does language change as a lexical network? An investigation based on written Chinese word co-occurrence networks

<div><p>Language is a complex adaptive system, but how does it change? For investigating this process, four diachronic Chinese word co-occurrence networks have been built based on texts that were written during the last 2,000 years. By comparing the network indicators that are associated with the hierarchical features in language networks, we learn that the hierarchy of Chinese lexical networks has indeed evolved over time at three different levels. The connections of words at the micro level are continually weakening; the number of words in the meso-level communities has increased significantly; and the network is expanding at the macro level. This means that more and more words tend to be connected to medium-central words and form different communities. Meanwhile, fewer high-central words link these communities into a highly efficient small-world network. Understanding this process may be crucial for understanding the increasing structural complexity of the language system.</p></div

DataSheet1_Genetic liability to asthma and risk of cardiovascular diseases: A Mendelian randomization study.docx

Background and Aims: Epidemiological studies have suggested positive associations between asthma and the risk of cardiovascular diseases (CVDs). However, causality remains inconclusive. We aim to explore the causal associations between asthma and CVDs risk using the Mendelian Randomization (MR) approach.Methods: We obtained summary-level data for eight CVDs [including atrial fibrillation (AF), coronary artery disease (CAD), heart failure (HF), stroke, ischemic stroke, large artery stroke, small vessel stroke, and cardioembolic stroke] from several large genome-wide association studies (GWASs) and the FinnGen consortium. Nine lead single-nucleotide polymorphisms associated with asthma (p −8) were identified from the GWAS conducted by the Trans-National Asthma Genetic Consortium. MR analyses were performed using the inverse variance weighted method, supplemented by the weighted median and MR-Egger methods.Results: Inverse variance weighted method showed suggestive effects of genetically determined asthma on AF (odds ratio (OR), 1.08; 95% confidence interval (CI), 1.02, 1.14; p = 0.009) and HF (OR, 1.05; 95% CI, 1.01, 1.09; p = 0.029). We found no causal associations between asthma and other CVDs. No horizontal pleiotropy was observed.Conclusion: This MR study provides genetic evidence suggesting a causal association between asthma and the risk of AF and HF, although not at the level of significance after multiple testing correction. Programs aimed at treating asthma among asthmatics might help prevent the adverse health effects inflicted by CVDs.</p

Power-law fitting (dual-log) of degree distributions of four diachronic Chinese networks.

<p>Power-law fitting (dual-log) of degree distributions of four diachronic Chinese networks.</p

MUL distributions (TP1 corresponds to Network 1 text).

MUL distributions (TP1 corresponds to Network 1 text).</p

DataSheet2_Genetic liability to asthma and risk of cardiovascular diseases: A Mendelian randomization study.xlsx

Background and Aims: Epidemiological studies have suggested positive associations between asthma and the risk of cardiovascular diseases (CVDs). However, causality remains inconclusive. We aim to explore the causal associations between asthma and CVDs risk using the Mendelian Randomization (MR) approach.Methods: We obtained summary-level data for eight CVDs [including atrial fibrillation (AF), coronary artery disease (CAD), heart failure (HF), stroke, ischemic stroke, large artery stroke, small vessel stroke, and cardioembolic stroke] from several large genome-wide association studies (GWASs) and the FinnGen consortium. Nine lead single-nucleotide polymorphisms associated with asthma (p −8) were identified from the GWAS conducted by the Trans-National Asthma Genetic Consortium. MR analyses were performed using the inverse variance weighted method, supplemented by the weighted median and MR-Egger methods.Results: Inverse variance weighted method showed suggestive effects of genetically determined asthma on AF (odds ratio (OR), 1.08; 95% confidence interval (CI), 1.02, 1.14; p = 0.009) and HF (OR, 1.05; 95% CI, 1.01, 1.09; p = 0.029). We found no causal associations between asthma and other CVDs. No horizontal pleiotropy was observed.Conclusion: This MR study provides genetic evidence suggesting a causal association between asthma and the risk of AF and HF, although not at the level of significance after multiple testing correction. Programs aimed at treating asthma among asthmatics might help prevent the adverse health effects inflicted by CVDs.</p

The means of the top 10, the middle 10, and the final 10 degree-dependent clustering coefficients.

The means of the top 10, the middle 10, and the final 10 degree-dependent clustering coefficients.</p

Power-law fitting (dual-log) of average degree of nearest neighbors of four diachronic Chinese networks.

Power-law fitting (dual-log) of average degree of nearest neighbors of four diachronic Chinese networks.</p