Evidence for Topological Magnon-Phonon Hybridization in a 2D Antiferromagnet down to the Monolayer Limit.

Topological phonons and magnons potentially enable low-loss, quantum coherent, and chiral transport of information and energy at the atomic scale. Van der Waals magnetic materials are promising to realize such states due to their recently discovered strong interactions among the electronic, spin, and lattice degrees of freedom. Here, we report the first observation of coherent hybridization of magnons and phonons in monolayer antiferromagnet FePSe3 by cavity-enhanced magneto-Raman spectroscopy. The robust magnon-phonon cooperativity in the 2D limit occurs even in zero magnetic field, which enables nontrivial band inversion between longitudinal and transverse optical phonons caused by the strong coupling with magnons. The spin and lattice symmetry theoretically guarantee magnetic-field-controlled topological phase transition, verified by nonzero Chern numbers calculated from the coupled spin-lattice model. The 2D topological magnon-phonon hybridization potentially offers a new route toward quantum phononics and magnonics with an ultrasmall footprint.

Effect of Hypoxia-Ischemia on the Expression of Iron-Related Proteins in Neonatal Rat Brains.

Hypoxic-ischemic white matter injury (WMI) pathogenesis in preterm infants is not well established, and iron-related proteins in the brain may play an important role in imbalanced iron metabolism. We aimed to investigate the iron-related protein changes in neonatal rats after hypoxia-ischemia (HI), clarify the role of iron-related proteins in hypoxic-ischemic WMI, and potentially provide a new target for the clinical treatment of hypoxic-ischemic WMI in preterm infants. We adopted a WMI animal model of bilateral common carotid artery electrocoagulation combined with hypoxia in neonatal 3-day-old Sprague-Dawley rats. We observed basic myelin protein (MBP) and iron-related protein expression in the brain (ferritin, transferrin receptor [TfR], and membrane iron transporter 1 [FPN1]) via Western blot and double immunofluorescence staining. The expression of MBP in the WMI group was significantly downregulated on postoperative days (PODs) 14, 28, and 56. Ferritin levels were significantly increased on PODs 3, 7, 14, and 28 and were most significant on POD 28, returning to the sham group level on POD 56. FPN1 levels were significantly increased on PODs 7, 28, and 56 and were still higher than those in the sham group on POD 56. TfR expression was significantly upregulated on PODs 1, 7, and 28 and returned to the sham group level on POD 56. Immunofluorescence staining showed that ferritin, TfR, and FPN1 were expressed in neurons, blood vessels, and oligodendrocytes in the cortex and corpus callosum on POD 28. Compared with the sham group, the immune-positive markers of three proteins in the WMI group were significantly increased. The expression of iron-related proteins in the brain (ferritin, FPN1, and TfR) showed spatiotemporal dynamic changes and may play an important role in hypoxic-ischemic WMI.

Notch is an alternative splicing gene in brown planthopper, Nilaparvata lugens.

Much research has assumed that Notch codes one protein. Then the protein will be cleaved into two parts and regenerates a heterodimers receptor to construct Notch signal pathways to regulate development in the past three decades. Here, we show that Notch in brown planthopper is a complex alternatively spliced gene has at least three transcriptional start sites, four exon skips, and 21 transcriptional endpoints that uses these to form variants and codes a series of proteins. When used dsRNAs to suppression different regions of the full-length variant NlNF resulted in a similar phenotype. Insects were molting after treatment, sensation circles on antennas near to root decayed, bristles on wings shortened, thickened or disappeared, accompanied by thickening veins and blades of fore-wing apex regions thickened. These results suggested that Notch influenced developmental of sensation circles, bristles, veins, and blades in nymph late periods. This study has deepened our understanding of Notch.

Dynamic Changes in Brain Iron Metabolism in Neonatal Rats after Hypoxia-Ischemia.

OBJECTIVES: The pathogenesis of hypoxic-ischemic white matter injury (WMI) in premature infants is still unclear, and the imbalance of cerebral iron metabolism may play an important role. Our study set out to investigate the changes in iron distribution, iron content and malondialdehyde (MDA) in disparate brain regions (parietal cortex, corpus callosum, hippocampus) within 84 days after hypoxia-ischemia (HI) in neonatal rats and to clarify the role of iron metabolism in WMI. MATERIALS AND METHODS: We adopted a rat model of hypoxic-ischemic WMI. Alterations in iron metabolism were detected by iron staining and iron assay kits, and the degree of brain injury was determined by MDA assays. RESULTS: Our results showed that different degrees of brain iron deposition occurred within 28 days after HI, and iron staining was the most obvious 3 days after HI. The iron content increased remarkably at 1-7 d after HI in the mixed tissues, especially at 3 d after HI. While the iron content in the parietal cortex and corpus callosum elevated obviously 14 days after HI. And the change trend of MDA was almost consistent with that of the iron content. CONCLUSIONS: Our findings revealed that brain iron metabolism changed dynamically in 3-day-old neonatal rats suffering from HI, which may cause lipid peroxidation damage to brain tissues. This process may be one of the pathogeneses of hypoxic-ischemic WMI.

Polycystic ovary syndrome and the risk of endometrial, ovarian and breast cancer: An updated meta-analysis.

BACKGROUND AND AIMS: This updated meta-analysis aimed to further quantify the risk of endometrial, ovarian, and breast cancer in patients with polycystic ovary syndrome (PCOS), thus providing updated and more reliable estimates. METHODS AND RESULTS: We identified relevant articles by searching electronic databases of PubMed, Embase, Web of Science, and Chinese Biological Medical Literature (CBM) published up to March 20, 2021. The pooled effect estimates and their 95% confidence intervals (CIs) were calculated using the random-effect model or the fixed-effect model. A total of 26 eligible studies were included. We found that PCOS was significantly associated with endometrial cancer (odds ratios [OR]: 3.66, 95%CI: 2.05-6.54, P < 0.001), but not with ovarian or breast cancer (OR: 1.23, 95%CI: 0.99-1.53, P = 0.059; OR: 0.94, 95%CI: 0.78-1.14, P = 0.551, respectively). However, in subgroups of high-quality studies, cohort studies, younger women (54 years or less or premenopausal), and studies with unadjusted body mass index (BMI), PCOS patients had a significantly higher risk of ovarian cancer. CONCLUSION: These results indicated that PCOS is a significant risk factor for endometrial cancer independent of BMI, but not for breast cancer. PCOS may increase the risk of ovarian cancer in younger women.

Individual vs household: How do different calculation patterns of catastrophic health expenditure matter? New evidence from China's critical illness insurance programme.

Reducing the incidence and severity of catastrophic health expenditure (CHE) has been considered to be one of the most fundamental goals of the global health care financing system. China, the second largest economy and the most populous country in the world, established a critical illness insurance (CII) programme in 2012 in an effort to protect Chinese residents from CHE shocks. This paper attempts to address whether the different calculation patterns (namely, individuals vs household) of CHE matter under China's CII programme. We compare two CII models built with the World Health Organization's (WHO's) standard and the Chinese standard. Exploiting the latest China family panel studies (CFPS) dataset, we demonstrate that using household as the calculation pattern is more effective in alleviating CHE under a tight premium budget, which is consistent with the international view. This finding raises concerns about the appropriate calculation pattern of CHE in policy making.

Unconventional Antiferromagnetic Quantum Critical Point in Ba(Fe_{0.97}Cr_{0.03})_{2}(As_{1-x}P_{x})_{2}.

We have systematically studied physical properties of Ba(Fe_{0.97}Cr_{0.03})_{2}(As_{1-x}P_{x})_{2}, where superconductivity in BaFe_{2}(As_{1-x}P_{x})_{2} is fully suppressed by just 3% of Cr substitution of Fe. A quantum critical point is revealed at x∼0.42, where non-Fermi-liquid behaviors similar to those in BaFe_{2}(As_{1-x}P_{x})_{2} are observed. Neutron diffraction and inelastic neutron scattering measurements suggest that the quantum critical point is associated with the antiferromagnetic order, which is not of conventional spin-density-wave type as evidenced by the ω/T scaling of spin excitations. On the other hand, no divergence of low-temperature nematic susceptibility is observed when x is decreased to 0.42 from higher doping level, demonstrating that there are no nematic quantum critical fluctuations. Our results suggest that non-Fermi-liquid behaviors in iron-based superconductors can be solely resulted from the antiferromagnetic quantum critical fluctuations, which cast doubts on the role of nematic fluctuations played in the normal-state properties in iron-based superconductors.

Templated Self-Assembly of a Covalent Polymer Network for Intracellular Protein Delivery and Traceless Release.

Trafficking proteins inside cells is an emerging field with potential utility in basic cell biology and biological therapeutics. A robust and sustainable delivery strategy demands not only good protection of the cargo but also reversibility in conjugation and activity. We report a protein-templated polymer self-assembly strategy for forming a sheath around the proteins and then tracelessly releasing them in the cytosol. The versatility of the approach, demonstrated here, suggests that the strategy is compatible with a wide array of biologics.

Unified Phase Diagram for Iron-Based Superconductors.

High-temperature superconductivity is closely adjacent to a long-range antiferromagnet, which is called a parent compound. In cuprates, all parent compounds are alike and carrier doping leads to superconductivity, so a unified phase diagram can be drawn. However, the properties of parent compounds for iron-based superconductors show significant diversity and both carrier and isovalent dopings can cause superconductivity, which casts doubt on the idea that there exists a unified phase diagram for them. Here we show that the ordered moments in a variety of iron pnictides are inversely proportional to the effective Curie constants of their nematic susceptibility. This unexpected scaling behavior suggests that the magnetic ground states of iron pnictides can be achieved by tuning the strength of nematic fluctuations. Therefore, a unified phase diagram can be established where superconductivity emerges from a hypothetical parent compound with a large ordered moment but weak nematic fluctuations, which suggests that iron-based superconductors are strongly correlated electron systems.

Association of vitamin D receptor gene polymorphisms with the susceptibility to ulcerative colitis in patients from Southeast China.

The association studies from different ethnic groups showed that vitamin D receptor (VDR) gene polymorphisms might be connected with the susceptibility to ulcerative colitis (UC); however, the conclusions were less consistent. Our study aimed to analyze the associations of UC with common mutations of VDR in Chinese patients. A total of 382 UC patients and 489 healthy controls were recruited. The genotypes of VDR FokI (rs2228570), BsmI (rs1544410), ApaI (rs7975232) and TaqI (rs731236) were examined by SNaPshot assays. Haplotype analysis was performed in all study subjects. After Bonferroni correction, the mutant alleles and genotypes of VDR FokI, BsmI, ApaI and TaqI did not statistically differ between UC patients and the controls (all p > 0.0125). However, the mutant allele C and genotype TC + CC of FokI gene were significantly increased in patients with mild and moderate UC compared to those with severe UC (C allele: 54.1% versus 39.3%, OR = 1.83, 95% CI: 1.21-2.75, p = 0.004; TC + CC genotype: 81.6% versus 57.1%, OR = 3.32, 95% CI: 1.83-6.06, p < 0.001, respectively). Haplotype analysis showed that the VDR BsmI, ApaI and TaqI polymorphic loci were in a strong linkage disequilibrium. Furthermore, the frequency of AAC haplotype was statistically lower in UC patients than that in the controls (3.8 versus 5.9%, OR = 0.63, 95% CI: 0.39-1.01, p = 0.039). In conclusion, the mutation of FokI gene influenced severity of the disease in UC patients. Moreover, the AAC haplotype formed by the VDR BsmI, ApaI and TaqI gene might engender a reduced risk of UC attack.

Structural and Magnetic Phase Transitions near Optimal Superconductivity in BaFe2(As(1-x)Px)2.

We use nuclear magnetic resonance (NMR), high-resolution x-ray, and neutron scattering studies to study structural and magnetic phase transitions in phosphorus-doped BaFe2(As(1-x)P(x)2. Previous transport, NMR, specific heat, and magnetic penetration depth measurements have provided compelling evidence for the presence of a quantum critical point (QCP) near optimal superconductivity at x=0.3. However, we show that the tetragonal-to-orthorhombic structural (T{s}) and paramagnetic to antiferromagnetic (AF, TN) transitions in BaFe2(As(1-x)Px)2 are always coupled and approach T{N}≈T{s}≥T{c} (≈29 K) for x=0.29 before vanishing abruptly for x≥0.3. These results suggest that AF order in BaFe_{2}(As(1-x)Px)2 disappears in a weakly first-order fashion near optimal superconductivity, much like the electron-doped iron pnictides with an avoided QCP.

Associations of FUT2 and FUT3 gene polymorphisms with Crohn's disease in Chinese patients.

BACKGROUND AND AIM: FUT2 and FUT3 genes are responsible for the formation of histo-blood group antigens, which act as binding sites for some intestinal microbes. Several studies suggested that FUT2 gene might affect the intestinal microbiota composition and modulate innate immune responses. However, the effect of FUT2 polymorphisms on Crohn's disease (CD) is uncertain. Our study aimed to analyze associations of CD with FUT2 and FUT3 polymorphisms in Chinese population. METHODS: A total of 273 CD patients and 479 controls were recruited. The genotypes of FUT2 (rs281377, rs1047781, and rs601338) and FUT3 (rs28362459, rs3745635, and rs3894326) were detected by SNaPshot analysis. RESULTS: Compared with controls, homozygote TT of FUT2 (rs1047781) was significantly increased in CD patients (TT vs others; P = 0.002, odds ratio [OR] = 1.767, 95% confidence interval [CI] = 1.235-2.528). The haplotype TT formed with FUT2 (rs281377) and (rs1047781) was more prevalent in CD patients than in controls (48.9% vs 43.5%, P = 0.046). Mutant T allele and homozygote TT of FUT2 (rs1047781) were increased in colonic CD patients compared with controls (P < 0.001, OR = 1.843, 95% CI = 1.353-2.512; P < 0.001, OR = 2.607, 95% CI = 1.622-4.191, respectively). Although allele and genotypic distributions of FUT3 were not statistically different between CD patients and controls, mutant allele and genotype of FUT3 (rs28362459) and (rs3745635) were significantly discrepant in three subgroups of CD patients according to lesion locations (all P < 0.05). CONCLUSIONS: Our study strongly implicates the polymorphic locus of FUT2 (rs1047781) in CD susceptibility in Chinese population. Mutations of FUT3 (rs28362459) and (rs3745635) might influence the lesion locations in CD patients.

A novel method of identifying Mycobacterium tuberculosis Beijing strains by detecting SNPs in Rv0444c and Rv2629.

A particular genotype of tuberculosis, named Beijing strain, is strongly associated with drug resistance and high virulence. Therefore, rapid prospective identification of Mycobacterium tuberculosis Beijing strains is very important for identifying and controlling tuberculosis of Beijing genotype. In the present study, we found that the co-mutation, A191C in Rv2629 and G243C in Rv0444c, is closely related to Beijing genotype. Gene Rv2629 and Rv0444c of 139 clinical isolates of M. tuberculosis were analyzed by PCR amplification and sequencing. Among 99 Beijing strains, 86 % (n = 85) isolates had the mutation G243C in Rv0444c and 92.93 % (n = 92) isolates had the mutation A191C in Rv2629. Among 40 non-Beijing isolates, only six isolates carried the mutation G243C in Rv0444c and eight isolates carried the mutation A191C in Rv2629. The co-mutation existed in 84.85 % (n = 84) of 99 clinical genome samples of W-Beijing strains and in only 12.5 % (n = 5) of the 40 non-Beijing strains, and the positive predictive value of 94.38 %, obtained in our experiment with a designed ratio of Beijing isolates, is similar to that in China at present. This result suggested that the detection method of the co-mutation, A191C in Rv2629 and G243C in Rv0444c, proposed in this study was a rapid, reliable, and sensitive one for identifying tuberculosis with Beijing genotype.

Factors that predict lymph node status in clinical stage T1aN0M0 lung adenocarcinomas.

BACKGROUND: To identify patients in whom systematic lymph node dissection would be suitable, preoperative diagnosis of the biological invasiveness of lung adenocarcinomas through the classification of these T1aN0M0 lung adenocarcinomas into several subgroups may be warranted. In this retrospective study, we sought to determine predictive factors of lymph node status in clinical stage T1aN0M0 lung adenocarcinomas. METHODS: We retrospectively reviewed the records of 273 consecutive patients undergone surgical resection of clinical stage T1aN0M0 lung adenocarcinomas at Shanghai Chest Hospital, from January 2011 to December 2012. Preoperative computed tomography findings of all 273 patients were reviewed and their tumors categorized as pure GGO, GGO with minimal solid components (<5 mm), part-solid (solid parts >5 mm), or purely solid. Relevant clinicopathologic features were investigated to identify predictors of hilar or mediastinal lymph node metastasis using univariate or multiple variable analysis. RESULTS: Among the 273 eligible clinical stage T1aN0M0 lung adenocarcinomas examined on thin-section CT, 103 (37.7%) were pure GGO, 118 (43.2%) GGO with minimal solid components, 13 (4.8%) part-solid (solid parts >5 mm, five GGO predominant and eight solid predominant), and 39 (14.3%) pure solid. There were 18 (6.6%) patients with lymph node metastasis. Incidence of N1 and N2 nodal involvement was 11 (6.6%) and seven (2.6%) patients, respectively. All patients with pure GGO and GGO with minimal solid components (<5 mm) tumors were pathologically staged N0. Multivariate analyses showed that the following factors significantly predicted lymph node metastasis for T1a lung adenocarcinomas: symptoms at presentation, GGO status, and abnormal carcinoembryonic antigen (CEA) titer. Multivariate analyses also showed that the following factors significantly predicted lymph node metastasis for pure solid tumors: air bronchogram sign, tumor size, symptoms at presentation, and abnormal CEA titer. CONCLUSIONS: The patients of clinical stage T1aN0M0 lung adenocarcinomas with pure GGO and GGO with minimal solid components tumors were pathologically staged N0 and systematic lymph node dissection should be avoided. But systematic lymph node dissection should be performed for pure solid tumors or part-solid, especially in patients with CEA greater than 5 ng/mL or symptoms at presentation, because of the high possibility of lymph node involvement.

Prevalence of unruptured cerebral aneurysms in Chinese adults aged 35 to 75 years: a cross-sectional study.

BACKGROUND: The reported prevalence of unruptured cerebral aneurysms (UCAs) varies widely. OBJECTIVE: To measure the prevalence of UCAs by using 3-dimensional time-of-flight magnetic resonance angiography in adults aged 35 to 75 years. DESIGN: Cross-sectional study done between June 2007 and June 2011. SETTING: Two communities chosen at random from 2 districts (1 urban and 1 suburban) in Shanghai, China. PARTICIPANTS: 4813 adults aged 35 to 75 years. MEASUREMENTS: Three-dimensional time-of-flight magnetic resonance angiography, interpreted by 3 observers blinded to the participants' information, was used to identify the location and size of UCAs and to estimate the overall, age-specific, and sex-specific prevalence. RESULTS: 369 UCAs were found in 336 participants (130 men and 206 women); 4477 participants had no evidence of UCAs. The prevalence was 7.0% overall (95% CI, 6.3% to 7.7%), with 5.5% for men (CI, 4.6% to 6.4%) and 8.4% for women (CI, 7.3% to 9.5%). The overall prevalence of UCAs was higher in women than in men (P < 0.001) and peaked at ages 55 to 64 years in men and women. The UCAs were mostly located in the internal carotid artery (81%), and 90.2% had a maximum diameter less than 5 mm. Mean diameter was larger in women than in men (3.7 mm vs. 3.2 mm; P < 0.009). LIMITATION: Participants were from 2 communities selected from 2 districts in Shanghai, and adults older than 75 years were not studied. CONCLUSION: The overall prevalence of UCAs was 7.0% in Chinese adults aged 35 to 75 years, and most lesions had a diameter less than 5 mm. PRIMARY FUNDING SOURCE: National Natural Science Foundation of China.

Molecular mechanism of resveratrol promoting differentiation of preosteoblastic MC3T3-E1 cells based on network pharmacology and experimental validation.

The purpose of this study was to investigate the mechanism by which resveratrol (Res) inhibits apoptosis and promotes proliferation and differentiation of pre-osteoblastic MC3T3-E1 cells, laying the groundwork for the treatment of osteoporosis (OP). The TCMSP database was used to find the gene targets for Res. The GeneCards database acquire the gene targets for OP. After discovering the potential target genes, GO, KEGG, and Reactome enrichment analysis were conducted. Verifying the major proteins involved in apoptosis can bind to Res using molecular docking. CCK8 measured the proliferative activity of mouse pre-osteoblasts in every group following Res intervention. Alkaline phosphatase staining (ALP) and alizarin red staining to measure the ability of osteogenic differentiation. RT-qPCR to determine the expression levels of Runx2 and OPG genes for osteogenic differentiation ability of cells. Western blot to measure the degree of apoptosis-related protein activity in each group following Res intervention. The biological processes investigated for GO of Res therapeutic OP involved in cytokine-mediated signaling pathway, negative regulation of apoptotic process, Aging, extrinsic apoptotic signaling pathway in absence of ligand, according to potential therapeutic target enrichment study. Apoptosis, FoxO signaling pathway, and TNF signaling pathway are the primary KEGG signaling pathways. Recactome pathways are primarily engaged in Programmed Cell Death, Apoptosis, Intrinsic Apoptotic Pathway, and Caspase activation via extrinsic apoptotic signaling pathways. This research established a new approach for Res treatment of OP by demonstrating how Res controls the apoptosis-related proteins TNF, IL6, and CASP3 to suppress osteoblast death and increase osteoclastogenesis.

N6-Methyladenosine enhances the translation of ENO1 to promote the progression of bladder cancer by inhibiting PCNA ubiquitination.

The mechanism underlying N6-methyladenosine (m6A) modification in bladder cancer (BC) remains elusive. We identified that the RBM15/METTL3 complex enhances m6A modification and promotes the ENO1 protein translation efficiency through its 359A site by depending on YTHDF1 in BC cells. In the tumor microenvironment, TGF-ß effectively stimulates RBM15/METTL3 expression to improve ENO1 mRNA m6A modification through the Smad2/3 pathway. Reduced ENO1 m6A levels hamper tumor proliferation both in vitro and in vivo. Mechanistically, ENO1 augments PCNA protein stability by reducing its K48-linked ubiquitination and thus prevents protein degradation through the endoplasmic reticulum-associated degradation pathway. According to the subsequent experiments, the ENO1 inhibitor significantly reduced tumor proliferation both in vitro and in vivo. Our study highlights the significance of RBM15/METTL3 complex-mediated ENO1 mRNA m6A modification in ENO1 expression. It also reveals a novel mechanism by which ENO1 promotes BC progression, thereby suggesting that ENO1 can be a therapeutic target for BC.

Identification and validation of a signature based on myofibroblastic cancer-associated fibroblast marker genes for predicting prognosis, immune infiltration, and therapeutic response in bladder cancer.

PURPOSE: Myofibroblastic cancer-associated fibroblasts (myCAFs) are important components of the tumor microenvironment closely associated with tumor stromal remodeling and immunosuppression. This study aimed to explore myCAFs marker gene biomarkers for clinical diagnosis and therapy for patients with bladder cancer (BC). MATERIALS AND METHODS: BC single-cell RNA sequencing (scRNA-seq) data were obtained from the National Center for Biotechnology Information Sequence Read Archive. Transcriptome and clinical data were downloaded from The Cancer Genome Atlas and the Gene Expression Omnibus databases. Subsequently, univariate Cox and LASSO (Least Absolute Shrinkage and Selection Operator regression) regression analyses were performed to construct a prognostic signature. Immune cell activity was estimated using single-sample gene set enrichment analysis whilst the TIDE (tumor immune dysfunction and exclusion) method was employed to assess patient response to immunotherapy. The chemotherapy response of patients with BC was evaluated using genomics of drug sensitivity in cancer. Furthermore, Immunohistochemistry was used to verify the correlation between MAP1B expression and immunotherapy efficacy. The scRNA-seq data were analyzed to identify myCAFs marker genes. RESULTS: Combined with bulk RNA-sequencing data, we constructed a two-gene (COL6A1 and MAP1B) risk signature. In patients with BC, the signature demonstrated outstanding prognostic value, immune infiltration, and immunotherapy response. This signature served as a crucial guide for the selection of anti-tumor chemotherapy medications. Additionally, immunohistochemistry confirmed that MAP1B expression was significantly correlated with immunotherapy efficacy. CONCLUSIONS: Our findings revealed a typical prognostic signature based on myCAF marker genes, which offers patients with BC a novel treatment target alongside theoretical justification.

Exploration of a Predictive Model for Keloid and Potential Therapeutic Drugs based on Immune Infiltration and Cuproptosis-Related Genes.

The aim of this study was to investigate the correlation between CRGs and immunoinfiltration in keloid, develop a predictive model for keloid occurrence, and explore potential therapeutic drugs. The microarray datasets (GSE7890 and GSE145725) were obtained from Gene Expression Omnibus database to identify the differentially expressed genes (DEGs) between keloid and non-keloid samples. Key genes were identified through immunoinfiltration analysis and DEGs, then analyzed for Gene Ontology and Kyoto Encyclopedia of Genes and Genomes, followed by the identification of protein-protein interaction networks, transcription factors, and miRNAs associated with key genes. Additionally, a logistic regression analysis was performed to develop a predictive model for keloid occurrence, and potential candidate drugs for keloid treatment were identified. Three key genes (FDX1, PDHB, DBT) were identified, showing involvement in acetyl-CoA biosynthesis, mitochondrial matrix, oxidoreductase activity, and the tricarboxylic acid cycle. Immune infiltration analysis suggested the involvement of B cells, Th1 cells, DCs, T helper cells, APC co-inhibition, and T cell co-inhibition in keloid. These genes were used to develop a logistic regression-based nomogram for predicting keloid occurrence with an AUC of 0.859 and good calibration.We identified 32 potential drug molecules and extracted the top 10 compounds based on their P-values, showing promise in targeting key genes and potentially effective against keloid. Our study identified some genes in keloid pathogenesis and potential therapeutic drugs. The predictive model enhance early diagnosis and management. Further research is needed to validate and explore clinical implications.

Improved Thermoelectric Performance of p-Type PbTe by Entropy Engineering and Temperature-Dependent Precipitates.

Entropy engineering is aneffective scheme to reduce the thermal conductivity of thermoelectric materials, but it inevitably deteriorates the carrier mobility. Here, we report the optimization of thermoelectric performance of PbTe by combining entropy engineering and nanoprecipitates. In the continuously tuned compounds of Pb0.98Na0.02Te(1-2x)SxSex, we show that the x = 0.05 sample exhibits an exceptionally low thermal conductivity relative to its configuration entropy. By introducing Mn doping, the produced temperature-dependent nanoprecipitates of MnSe cause the high-temperature thermal conductivity to be further reduced. A very low lattice thermal conductivity of 0.38 W m-1 K-1 is achieved at 825 K. Meanwhile, the carrier mobility of the samples is only slightly influenced, owing to the well-controlled configuration entropy and the size of nanoprecipitates. Finally, a high peak zT of ∼2.1 at 825 K is obtained in the Pb0.9Na0.04Mn0.06Te0.9S0.05Se0.05 alloy.