The impact of visit-to-visit heart rate variability on all-cause mortality in atrial fibrillation.

OBJECTIVE: We aimed to investigate the association between visit-to-visit heart rate variability (VVHRV) and all-cause mortality in patients diagnosed with atrial fibrillation (AF). Previous studies have shown a positive correlation between VVHRV and several adverse outcomes. However, the relationship between VVHRV and the prognosis of AF remains uncertain. METHODS: In our study, we aimed to examine the relationship between VVHRV and mortality rates among 3983 participants with AF, who were part of the AFFIRM study (Atrial Fibrillation Follow-Up Investigation of Rhythm Management). We used the standard deviation of heart rate (HRSD) to measure VVHRV and divided the patients into four groups based on quartiles of HRSD (1st, <5.69; 2nd, 5.69-8.00; 3rd, 8.01-11.01; and 4th, ≥11.02). Our primary endpoint was all-cause death, and we estimated the hazard ratios for mortality using the Cox proportional hazard regressions. RESULTS: Our analysis included 3983 participants from the AFFIRM study and followed for an average of 3.5 years. During this period, 621 participants died from all causes. In multiple-adjustment models, we found that the lowest and highest quartiles of HRSD independently predicted an increased risk of all-cause mortality compared to the other two quartiles, presenting a U-shaped relationship (1st vs 2nd, hazard ratio = 2.28, 95% CI = 1.63-3.20, p < .01; 1st vs. 3rd, hazard ratio = 2.23, 95% CI = 1.60-3.11, p < .01; 4th vs. 2nd, hazard ratio = 1.82, 95% CI = 1.26-2.61, p < .01; and 4th vs. 3rd, hazard ratio = 1.78, 95% CI = 1.25-2.52, p < .01). CONCLUSION: In patients with AF, we found that both lower VVHRV and higher VVHRV increased the risk of all-cause mortality, indicating a U-shaped curve relationship.

Uncovering the transcriptional responses of tobacco (Nicotiana tabacum L.) roots to Ralstonia solanacearum infection: a comparative study of resistant and susceptible cultivars.

BACKGROUND: Tobacco bacterial wilt (TBW) caused by Ralstonia solanacearum is the most serious soil-borne disease of tobacco that significantly reduces crop yield. However, the limited availability of resistance in tobacco hinders breeding efforts for this disease. RESULTS: In this study, we conducted hydroponic experiments for the root expression profiles of D101 (resistant) and Honghuadajinyuan (susceptible) cultivars in response to BW infection at 0 h, 6 h, 1 d, 3 d, and 7d to explore the defense mechanisms of BW resistance in tobacco. As a result, 20,711 and 16,663 (total: 23,568) differentially expressed genes (DEGs) were identified in the resistant and susceptible cultivars, respectively. In brief, at 6 h, 1 d, 3 d, and 7 d, the resistant cultivar showed upregulation of 1553, 1124, 2583, and 7512 genes, while the susceptible cultivar showed downregulation of 1213, 1295, 813, and 7735 genes. Similarly, across these time points, the resistant cultivar had downregulation of 1034, 749, 1686, and 11,086 genes, whereas the susceptible cultivar had upregulation of 1953, 1790, 2334, and 6380 genes. The resistant cultivar had more up-regulated genes at 3 d and 7 d than the susceptible cultivar, indicating that the resistant cultivar has a more robust defense response against the pathogen. The GO and KEGG enrichment analysis showed that these genes are involved in responses to oxidative stress, plant-pathogen interactions, cell walls, glutathione and phenylalanine metabolism, and plant hormone signal transduction. Among the DEGs, 239 potential candidate genes were detected, including 49 phenylpropane/flavonoids pathway-associated, 45 glutathione metabolic pathway-associated, 47 WRKY, 48 ERFs, eight ARFs, 26 pathogenesis-related genes (PRs), and 14 short-chain dehydrogenase/reductase genes. In addition, two highly expressed novel genes (MSTRG.61386-R1B-17 and MSTRG.61568) encoding nucleotide-binding site leucine-rich repeat (NBS-LRR) proteins were identified in both cultivars at 7 d. CONCLUSIONS: This study revealed significant enrichment of DEGs in GO and KEGG terms linked to glutathione, flavonoids, and phenylpropane pathways, indicating the potential role of glutathione and flavonoids in early BW resistance in tobacco roots. These findings offer fundamental insight for further exploration of the genetic architecture and molecular mechanisms of BW resistance in tobacco and solanaceous plants at the molecular level.

Association of MLL3 and TGF-ß signaling gene polymorphisms with the susceptibility and prognostic outcomes of Stanford type B aortic dissection : MLL3 with TGF-ß signal pathway association with Stanford type B AD.

OBJECTIVE: This study aims to investigate the association of lysine methyltransferase 2 C (MLL3) and transforming growth factor ß (TGF-ß) signaling-related gene polymorphisms with the susceptibility of Stanford type B aortic dissection (AD) and its clinical prognostic outcomes. The methods involved investigating the MLL3 (rs10244604, rs6963460, rs1137721), TGFß1 (rs1800469), TGFß2 (rs900), TGFR1 (rs1626340) and TGFR2 (rs4522809) gene polymorphisms. Logistic regression was performed to investigate the association between 7 single nucleotide gene polymorphisms (SNPs) and Stanford type B aortic dissection. The GMDR software was used to analyze gene-gene and gene-environment interactions. The odds ratio (OR) with a 95% confidence interval (CI) was employed to evaluate the association of genes and Stanford type B AD risk. RESULTS: Genotypes and allele distributions in the case and control groups showed significant differences (P < 0.05). Logistic regression has shown that the Stanford Type B AD risk was highest in individuals with the rs1137721 CT genotype (OR = 4.33, 95% CI = 1.51-12.40). Additionally, WBC, drinking, hypertension, triglycerides (TG), and low-density lipoprotein (LDL-C) were independent risk factors for Stanford Type B AD. Logistic regression showed that the Stanford Type B AD risk was highest in individuals with the MLL3 (rs1137721)-TT + CT and TGFß1 (rs4522809)-AA genotype (OR = 6.72, 95% CI = 1.56-29.84), and lowest in those with the MLL3 (rs1137721)-CC and TGFß1 (rs4522809)-AA + GG genotype (OR = 4.38, 95% CI = 0.92-20.83). However, the 55-month median long-term follow-up did not show statistical significance. CONCLUSION: Carriers of both TT + CT of MLL3 (rs1137721) and AA of TGFß1 (rs4522809) polymorphisms may be closely related to the development of Stanford type B AD. MLL3 (rs1137721), WBC, and TG/TC were found to be associated with the morbidity of Stanford type B AD. MLL3 (KMT2C) is associated with the TGF-ß signaling pathway protein. The risk of Stanford type B AD is related to the interactions of gene-gene and gene-environment.

Association of gene polymorphisms in MYH11 and TGF-ß signaling with the susceptibility and clinical outcomes of DeBakey type III aortic dissection.

To investigate the association of myosin heavy chain protein 11 (MYH11) and transforming growth factor ß signaling-related gene polymorphisms with the susceptibility of DeBakey type III aortic dissection (AD) and its clinical outcomes. Four single-nucleotide polymorphism (SNPs) (MYH11 rs115364997, rs117593370, TGFB1 rs1800469, and TGFBR1 rs1626340) were analyzed in patients with DeBakey III AD (173) and healthy participants (335). Gene-gene and gene-environment interactions were evaluated using generalized multifactor dimensionality reduction. The patients were followed up for a median of 55.7 months. MYH11 rs115364997 G or TGFBR1 rs1626340 A carriers had an increased risk of DeBakey type III AD. MYH11, TGFB1, TGFBR1, and environment interactions contributed to the risk of DeBakey type III AD (cross-validation consistency = 10/10, P = 0.001). Dominant models of MYH11 rs115364997 AG + GG genotype (HR = 2.443; 95%CI: 1.096-5.445, P = 0.029), TGFB1 rs1800469 AG + GG (HR = 2.303; 95%CI: 1.069-4.96, P = 0.033) were associated with an increased risk of mortality in DeBakey type III AD. The dominant model of TGFB1 rs1800469 AG + GG genotype was associated with an increased risk of recurrence of chest pain in DeBakey type III AD (HR = 1.566; 95%CI: 1.018-2.378, P = 0.041). In conclusions, G carriers of MYH11 rs115364997 or TGFB1 rs1800469 may be the poor prognostic indicators of mortality and recurrent chest pain in DeBakey type III AD. The interactions of gene-gene and gene-environment are associated with the risk of DeBakey type III AD.

Fibrillin-1 Gene Polymorphisms (rs145233125, rs11070646, rs201170905) Are Associated With the Susceptibility and Clinical Prognosis of DeBakey Type III Aortic Dissection in Chinese Han Population.

ABSTRACT: We aim to investigate whether genetic variants of the Fibrillin-1 (FBN1) gene were associated with DeBakey type III aortic dissection (AD) and its clinical prognosis in Chinese Han population. Three single-nucleotide polymorphisms (SNPs) (rs145233125, rs11070646, rs201170905) in FBN1 were analyzed in patients with DeBakey type III AD (159) and healthy subjects (216). Gene-environment interactions were evaluated to use generalized multifactor dimensionality reduction. Haplotype analysis of the 3 SNPs in the FBN1 gene was performed by Haploview software. Patients were followed up for average 4 years. G carriers of rs11070646 and rs201170905 in FBN1 have an increased risk of DeBakey type III AD. The interaction of FBN1 and environmental factors facilitated to the increased risk of DeBakey type III AD (cross-validation consistency = 10/10, P = 0.001). One of the most common haplotypes revealed an increased risk of DeBakey type III AD (CGG, P = 0.009). Recessive models of rs145233125 CC genotype ( P < 0.05) and rs201170905 GG genotype ( P < 0.001) were associated with an increased risk of death and recurrent chest pain of DeBakey type III AD. In conclusions, FBN1 gene polymorphisms contribute to DeBakey type III AD susceptibility. The interactions of gene and environment are related with the risk of DeBakey type III AD. C carriers of rs145233125 and G carriers of rs201170905 may be the adverse prognostic indicators of death and recurrent chest pain in DeBakey type III AD.

Genome-wide identification and development of InDel markers in tobacco (Nicotiana tabacum L.) using RAD-seq.

Insertions and deletions (InDels) can be used as molecular markers in genetic studies and marker-assisted selection breeding. However, genetic improvement in tobacco has been hindered by limited genetic diversity information and relatedness within available germplasm. A Chinese tobacco variety, Yueyan-98, was resequenced using restriction-site associated DNA (RAD-seq) approach to develop InDel markers. In total, 32,884 InDel loci were detected between Yueyan-98 and the K326 reference sequence [18,598 (56.55%) deletions and 14,288 (43.45%) insertions], ranging from 1 to 62 bp in length. Of the 6,733 InDels (> 4 bp) that were suitable for polyacrylamide gel electrophoresis, 150 were randomly selected. These 150 InDels were unevenly distributed on 23 chromosomes, and the highest numbers of InDels were observed on chromosomes Nt05, Nt13, and Nt23. The average density of adjacent InDels was 19.36 Mb. Thirty-seven InDels were located in genic regions. Polymerase chain reaction (PCR)-based markers were developed to validate polymorphism; 113 (79.80%) of the 150 InDel markers showed polymorphism and were further used for genetic diversity analysis of 50 tobacco accessions (13 from China, 1 from Mexico, and 36 from the USA). The average expected heterozygosity (He) and polymorphism information content (PIC) values were 0.28 ± 0.16 and 0.38 ± 0.10, respectively. The average Shannon diversity index (I) was 0.34 ± 0.18, with genetic diversity ranging from 0.13-0.57. The 50 accessions were classified into two groups with a genetic similarity coefficient of 0.68. Principal coordinate analysis (PCoA) and population structure analysis showed similar results and divided the population into two groups unrelated to their geographical origins. AMOVA showed 4% variance among the population and the remaining 96% within the population, suggesting low genetic differentiation between two subpopulations. Furthermore, 10 InDels (19 alleles) were significantly identified for tobacco plant height using GLM+Q model at P < 0.005. Among these, three markers (Nt-I-26, Nt-I-41, and Nt-I-44) were detected in at least two environments, with phenotypic variance explained (PVE) ranging from 14.03 to 32.68%. The polymorphic InDel markers developed can be used for hybrid identification, genetic diversity, genetic linkage map construction, gene mapping, and MAS breeding programs of tobacco. Supplementary Information: The online version contains supplementary material available at 10.1007/s12298-022-01187-3.

Uric acid and its correlation with hypertension in postmenopausal women: A multi-ethnic study (Observational study).

We investigate the association of uric acid with hypertension among Han, Uygur, and Kazakh populations in the Xinjiang Province of Western China. Our study aims to evaluate the relationships of serum uric acid (SUA) with hypertension in the Chinese population according to the menopausal status. Medical data of 1684 Han, 1895 Uygur, and 294 Kazakh people was examined. The prevalence of hypertension was calculated by the quartiles of SUA. Correlation between hypertension-related risk factors calculated and compared between men and women. SUA was higher in men than in women. The level was significantly higher in postmenopausal than premenopausal women (4.40 ± 1.75 v.s 4.06 ± 1.63 mg/dl, P < .01). Logistic regression analysis showed Body mass index (BMI) [OR = 1.08, P < .01]; and eGFR<60 vs.≥60 [OR = 1.22, P = .04] were independent risk factors for hypertension in women. Age and diabetes were independent risk factors for the participants with hypertension [OR = 1.04, P < .01] and [OR = 2.24, P < .01]. High quartile SUA group has increased the risk for hypertension in postmenopausal women [OR = 1.34, P = .048]. We found that postmenopausal women have high SUA compared to premenopausal women. The high SUA quartiles uric acid may be an independent risk for hypertension in postmenopausal women.

Identification and characterization of NPC1L1 variants in Uygur and Kazakh with extreme low-density lipoprotein cholesterol.

BACKGROUND: Plasma levels of low-density lipoprotein cholesterol (LDL-C) are a major risk factor for cardiovascular disease and are influenced by both heredity and dietary habits. The Niemann-Pick C1 like 1 (NPC1L1) protein mediates efficient dietary cholesterol absorption and contributes to variations in human LDL-C levels. METHODS: In the present study, using high throughput sequencing we identified three non-synonymous (NS) variations and 64 synonymous variations in the NPC1L1 gene from subsets of Chinese Han, Uygur and Kazakh populations with high or low LDL-C. Subsequently, three NS variations encoding R174H, V177I and V1284L substitutions were observed only in Uygur and Kazakh individuals with limited maximal plasma LDL-C levels. RESULTS: In further experiments, we investigated cholesterol-regulated recycling and glycosylation and stability of these NS NPC1L1 variants. However, no significant differences between WT and variant NPC1L1 proteins were observed using in vivo assays in mouse livers with adenovirus-mediated expression, demonstrating that none of the three NPC1L1 NS variants caused decreased uptake of biliary cholesterol. CONCLUSIONS: Simultaneously, these data indicate that R174H, V177I and V1284L NPC1L1 variations in high or low LDL-C individuals may not directly influence cholesterol absorption by NPC1L1.

Upregulation of miR-184 enhances the malignant biological behavior of human glioma cell line A172 by targeting FIH-1.

BACKGROUND: In recent years, miRNAs have been suggested to play key roles in the formation and development of human glioma. The aim of this study is to investigate the effect and mechanism of miR-184 expression on the malignant behavior of human glioma cells. METHODS: The relative quantity of miR-184 was determined in human glioma cell lines, and the expression of hypoxia-inducible factor-1 alpha (HIF-1α) was explored using western blotting. The effects of miR-184 inhibition on cell viability and apoptosis were explored, and the miR-184 target gene was determined using a luciferase assay and western blotting. Flow cytometry and Hoechst staining were used to evaluate cell growth and apoptosis. Matrigel invasion and scratch assays were performed to measure the ability of cell invasion and migration. RESULTS: miR-184 and HIF-1α protein levels were significantly upregulated in human glioma cells. Downregulation of miR-184 inhibited cell viability and increased the HEB cell apoptotic rate. Luciferase and western blot assays verified that FIH-1 was the target gene of miR-184 and negatively controlled the protein level of HIF-1α. Inhibition of HIF-1α by siRNA facilitated the apoptosis of HEB cells and suppressed A172 cell invasion and migration. CONCLUSION: miR-184 upregulation enhanced the malignant phenotype of human glioma cancer cells by reducing FIH-1 protein expression.

Diagnosis of hypertrophic cardiomyopathy accompanied with primary aldosteronism-Case report.

Hypertrophic cardiomyopathy (HCM) is known to be the most prevalent genetic cardiac condition. However, there have been limited reports on the diagnosis of HCM accompanied by secondary hypertension and the subsequent systematic therapy. In this case report, we present the case of a 65-year-old male patient who presented with recurring chest discomfort during physical activity, along with refractory hypertension. Cardiac magnetic resonance imaging (MRI) and transthoracic echocardiogram(TTE) revealed the presence of HCM in this individual. Further investigation revealed hypokalemia, elevated aldosterone levels, decreased plasma renin activity, and an aldosterone-to-renin ratio above 30. These findings strongly indicated primary aldosteronism (PA) as an additional condition affecting this patient. Through the utilization of whole exome sequencing, we successfully identified a suspected pathogenic gene TTN as the underlying cause of the patient's condition. The presence of HCM accompanied by secondary hypertension due to PA resulted in significant enlargement of the left ventricle, particularly the ventricular septum. While certain genetic mutations may suggest a potential link to cardiomyopathy development, they cannot definitively establish a direct association between HCM and PA.

Partial desensitization of MYC2 transcription factor alters the interaction with jasmonate signaling components and affects specialized metabolism.

The activity of bHLH transcription factor MYC2, a key regulator in jasmonate signaling and plant specialized metabolism, is sensitive to repression by JASMONATE-ZIM-domain (JAZ) proteins and co-activation by the mediator subunit MED25. The substitution of a conserved aspartic acid (D) to asparagine (N) in the JAZ-interacting domain (JID) of Arabidopsis MYC2 affects interaction with JAZ, although the mechanism remained unclear. The effects of the conserved residue MYC2D128 on interaction with MED25 have not been investigated. Using tobacco as a model, we generated all possible substitutions of aspartic acid 128 (D128) in NtMYC2a. NtMYC2aD128N partially desensitized the repression by JAZ proteins, while strongly interacting with MED25, resulting in increased expression of nicotine pathway genes and nicotine accumulation in tobacco hairy roots overexpressing NtMYC2aD128N compared to those overexpressing NtMYC2a. The proline substitution, NtMYC2aD128P, negatively affected transactivation and abolished the interaction with JAZ proteins and MED25. Structural modeling and simulation suggest that the overall stability of the JID binding pocket is a predominant cause for the observed effects of substitutions at D128. The D128N substitution has an overall stabilizing effect on the binding pocket, which is destabilized by D128P. Our study offers an innovative tool to increase the production of plant natural products.

Incorporation of functionalized gold nanoparticles into nanofibers for enhanced attachment and differentiation of mammalian cells.

BACKGROUND: Electrospun nanofibers have been widely used as substrata for mammalian cell culture owing to their structural similarity to natural extracellular matrices. Structurally consistent electrospun nanofibers can be produced with synthetic polymers but require chemical modification to graft cell-adhesive molecules to make the nanofibers functional. Development of a facile method of grafting functional molecules on the nanofibers will contribute to the production of diverse cell type-specific nanofiber substrata. RESULTS: Small molecules, peptides, and functionalized gold nanoparticles were successfully incorporated with polymethylglutarimide (PMGI) nanofibers through electrospinning. The PMGI nanofibers functionalized by the grafted AuNPs, which were labeled with cell-adhesive peptides, enhanced HeLa cell attachment and potentiated cardiomyocyte differentiation of human pluripotent stem cells. CONCLUSIONS: PMGI nanofibers can be functionalized simply by co-electrospinning with the grafting materials. In addition, grafting functionalized AuNPs enable high-density localization of the cell-adhesive peptides on the nanofiber. The results of the present study suggest that more cell type-specific synthetic substrata can be fabricated with molecule-doped nanofibers, in which diverse functional molecules are grafted alone or in combination with other molecules at different concentrations.

Chemically-defined scaffolds created with electrospun synthetic nanofibers to maintain mouse embryonic stem cell culture under feeder-free conditions.

Embryonic stem cells (ESCs) are useful resources for drug discovery, developmental biology and disease studies. Cellular microenvironmental cues play critical roles in regulating ESC functions, but it is challenging to control them with synthetic components. Nanofibers hold a potential to create artificial cellular cues for controlling cell adhesion and cell-cell interactions. Mouse ESC (mESC) were cultured on electrospun nanofibers made from polymethylglutarimide (PMGI), which is a synthetic thermoplastic polymer stable under culture conditions. Both topology and the density of PMGI nanofibers were key factors. mESCs on nanofibers had a growth rate comparable to those cultured conventionally and retained their pluripotency. Furthermore, self-renewed ESCs differentiated into all three germ layers thereby providing a reliable way to expand mESCs without feeder cells.

[Efficacy comparison between endovascular aneurysm repair versus open surgery for patients with abdominal aortic aneurysms: a meta-analysis].

OBJECTIVE: To compare the efficacy between endovascular aneurysm repair versus open surgery in patients with abdominal aortic aneurysms (AAA). METHODS: A systematic review was performed to identify clinical outcomes of randomized controlled trials for AAA patients receiving endovascular aneurysm repair or open surgery. The Cochrane Library (issue 7 of 2011), MEDLINE (1996 to 2011), EMBASE (1974 to 2011), CBM (1989 to 2011), CNKI (1997 to 2011), Wanfang data (1989 to 2011) were searched. Randomized trials that compared open or endovascular AAA repair and published clinical outcomes were selected. The outcome included all-cause mortality, aneurysm-related mortality, technical complications and re-open surgery. Data analyses were performed with the RevMan5.1 software. Publication bias was assessed by STATA software. A meta-regression model was used to describe between study variability. A total of 123 trials were excluded according to criteria. Four randomized controlled trials with 2607 patients met the inclusion criteria. RESULTS: There were no publication bias (Begg's test, Z = 1.02, P > 0.05; Egger's test, t = 0.98, P > 0.05). The meta-analysis showed that the incidence of all-cause mortality of endovascular repair was significantly lower than that of open repair up to 30 days post procedures [ RR = 0.32, 95%CI (0.18 - 0.56), P < 0.01] while long-term all-cause mortality was similar: DREAM study: [RR = 1.18, 95%CI (0.88 - 1.58), P > 0.05], EVAR study: [RR = 1.04, 95%CI (0.88 - 1.22), P > 0.05]. The incidence of aneurysm-related mortality of endovascular repair was lower than that of open repair in two studies [RR = 0.53, 95%CI (0.33 - 0.85), P < 0.01]. Technical complication between open repair group and endovascular repair group was similar [RR = 1.43, 95%CI (0.68 - 2.98), P > 0.05]. Incidence of re-open surgery was higher in endovascular repair group than in open surgery group [RR = 2.03, 95%CI (1.14 - 3.62), P < 0.05]. CONCLUSION: Compared with open surgery, endovascular repair is associated with lower 30-day all-cause mortality and aneurysm-related mortality, similar technical complication and long-term all-cause mortality, but higher risk for re-open surgery.

Tobacco Stalk Flour/Magnesium Oxysulfate Whiskers Reinforced Hybrid Composites of Recycled Polypropylene: Mechanical and Thermal and Antibacterial Properties.

The present investigation utilizes tobacco stalks flour and magnesium oxysulfate whiskers as fillers to enhancers the recycle polypropylene through melt blending and injection molding. Studied the microscopic morphology, mechanical, thermal, and antibacterial properties of recycled polypropylene (rPP) based composites with different weight ratios of tobacco stalks flour (TSF) and magnesium oxysulfate whiskers (MOSw). Composites' morphological studies indicated that tobacco stalks flour, and recycled polypropylene has good adhesion, improving composites' mechanical properties. The addition of TSF did not significantly change the tensile strength of rPP, but it can effectively increase the flexural strength and flexural modulus. Compared with rPP, adding 30 wt% tobacco stalks flour to rPP can increase the flexural strength by about 32.74%. Meanwhile, the addition of magnesium oxysulfate whiskers further improves the material's tensile strength. An increase in tobacco stalks flour content in the rPP enhances the crystallization temperature and degree of crystallinity of the polymer. In addition, attributed to the existence of tobacco stalks flour hydrophilic and antibacterial ability, the water absorption of the hybrid composites was increased and obtained antibacterial ability. Hence, this study provides a new development idea for tobacco stalks r recycling and applications.

Biomass Straw-Derived Porous Carbon Synthesized for Supercapacitor by Ball Milling.

A large amount of biomass straw waste is generated every year in the world, which can cause serious environmental pollution and resource waste if disposed of improperly. At present, biomass-derived porous carbon materials prepared from biomass waste as a carbon source have garnered attention due to their renewability, huge reserves, low cost, and environmental benevolence. In this work, high-performance carbon materials were prepared via a one-step carbonization-activation method and ball milling, with waste tobacco straw as precursor and nano-ZnO as template and activator. The specific surface area and porous structure of biomass-derived carbon could be controlled by carbonization temperature, which is closely related to the electrochemical performances of the carbon material. It was found that, when the carbonization temperature was 800 °C, the biochar possesses maximum specific surface area (1293.2 m2·g-1) and exhibits high capacitance of 220.7 F·g-1, at 1 A·g-1 current density in a three-electrode configuration with 6 M KOH aqueous solution. The capacitance retention maintained about 94.83% at 5 A·g-1 after 3000 cycles. This work proves the porous biochar derived from tobacco straws has a great potential prospect in the field of supercapacitors.

Nicotine in Inflammatory Diseases: Anti-Inflammatory and Pro-Inflammatory Effects.

As an anti-inflammatory alkaloid, nicotine plays dual roles in treating diseases. Here we reviewed the anti-inflammatory and pro-inflammatory effects of nicotine on inflammatory diseases, including inflammatory bowel disease, arthritis, multiple sclerosis, sepsis, endotoxemia, myocarditis, oral/skin/muscle inflammation, etc., mainly concerning the administration methods, different models, therapeutic concentration and duration, and relevant organs and tissues. According to the data analysis from recent studies in the past 20 years, nicotine exerts much more anti-inflammatory effects than pro-inflammatory ones, especially in ulcerative colitis, arthritis, sepsis, and endotoxemia. On the other hand, in oral inflammation, nicotine promotes and aggravates some diseases such as periodontitis and gingivitis, especially when there are harmful microorganisms in the oral cavity. We also carefully analyzed the nicotine dosage to determine its safe and effective range. Furthermore, we summarized the molecular mechanism of nicotine in these inflammatory diseases through regulating immune cells, immune factors, and the vagus and acetylcholinergic anti-inflammatory pathways. By balancing the "beneficial" and "harmful" effects of nicotine, it is meaningful to explore the effective medical value of nicotine and open up new horizons for remedying acute and chronic inflammation in humans.

Association of gene polymorphisms in FBN1 and TGF-ß signaling with the susceptibility and prognostic outcomes of Stanford type B aortic dissection.

BACKGROUND: This study is aimed at investigating the association of Fibrillin-1 (FBN1) and transforming growth factor ß (TGF-ß) signaling-related gene polymorphisms with the susceptibility of Stanford type B aortic dissection (AD) and its clinical prognostic outcomes. METHODS: Five single-nucleotide polymorphism (SNPs) (FBN1rs 145233125, rs201170905, rs11070646, TGFB1rs1800469, and TGFB2rs900) were analyzed in patients with Stanford type B AD (164) and healthy controls (317). Gene-gene and gene-environment interactions were assessed by generalized multifactor dimensionality reduction. A 4-year follow-up was performed for all AD patients. RESULTS: G carriers of FBN1 rs201170905 and TGFB1 rs1800469 have an increased risk of Stanford type B AD. The interaction of FBN1, TGFB1, TGFB2 and environmental promoted to the increased risk of type B AD (cross-validation consistency = 10/10, P = 0.001). Dominant models of FBN1rs145233125 TC + CC genotype (P = 0.028), FBN1 rs201170905 AG + GG (P = 0.047) and TGFB1 rs1800469 AG + GG (P = 0.052) were associated with an increased risk of death of Stanford type B AD. The recessive model of FBN1 rs145233125 CC genotype (P < 0.001), FBN1rs201170905 GG (P < 0.001), TGFB1 rs1800469 AG + GG genotype (P = 0.011) was associated with an increased risk of recurrence of chest pain in Stanford type B AD. CONCLUSIONS: The interactions of gene-gene and gene-environment are related with the risk of Stanford type B AD. C carriers of rs145233125, G carriers of rs201170905 and G carriers of rs1800469 may be the poor clinical outcome indicators of mortality and recurrent chest pain in Stanford type B AD.

Identification of Novel Quantitative Trait Nucleotides and Candidate Genes for Bacterial Wilt Resistance in Tobacco (Nicotiana tabacum L.) Using Genotyping-by-Sequencing and Multi-Locus Genome-Wide Association Studies.

Tobacco bacterial wilt (TBW) is a devastating soil-borne disease threatening the yield and quality of tobacco. However, its genetic foundations are not fully understood. In this study, we identified 126,602 high-quality single-nucleotide polymorphisms (SNPs) in 94 tobacco accessions using genotyping-by-sequencing (GBS) and a 94.56 KB linkage disequilibrium (LD) decay rate for candidate gene selection. The population structure analysis revealed two subpopulations with 37 and 57 tobacco accessions. Four multi-locus genome-wide association study (ML-GWAS) approaches identified 142 quantitative trait nucleotides (QTNs) in E1-E4 and the best linear unbiased prediction (BLUP), explaining 0.49-22.52% phenotypic variance. Of these, 38 novel stable QTNs were identified across at least two environments/methods, and their alleles showed significant TBW-DI differences. The number of superior alleles associated with TBW resistance for each accession ranged from 4 to 24; eight accessions had more than 18 superior alleles. Based on TBW-resistant alleles, the five best cross combinations were predicted, including MC133 × Ruyuan No. 1 and CO258 × ROX28. We identified 52 candidate genes around 38 QTNs related to TBW resistance based on homologous functional annotation and KEGG enrichment analysis, e.g., CYCD3;2, BSK1, Nitab4.5_0000641g0050, Nitab4.5_0000929g0030. To the best of our knowledge, this is the first comprehensive study to identify QTNs, superior alleles, and their candidate genes for breeding TBW-resistant tobacco varieties. The results provide further insight into the genetic architecture, marker-assisted selection, and functional genomics of TBW resistance, improving future breeding efforts to increase crop productivity.

Research on High-Value Utilization of Carbon Derived from Tobacco Waste in Supercapacitors.

Large quantities of tobacco stalks residues are generated and discarded as crop waste or combusted directly every year. Thus, we need to find an appropriate way to dispose of this type of waste and recycle it. The conversion of biomass waste into electrode materials for supercapacitors is entirely in line with the concept of sustainability and green. In this paper, tobacco-stalk-based, porous activated carbon (TC) was successfully synthesized by high-temperature and high-pressure hydrothermal pre-carbonization and KOH activation. The synthesized TC had a high pore volume and a large surface area of 1875.5 m2 g-1, in which there were many mesopores and interconnected micro-/macropores. The electrochemical test demonstrated that TC-1 could reach a high specific capacitance of up to 356.4 F g-1 at a current density of 0.5 A g-1, which was carried in 6M KOH. Additionally, a symmetrical supercapacitor device was fabricated by using TC-1 as the electrode, which delivered a high energy density up to 10.4 Wh kg-1 at a power density of 300 W kg-1, and excellent long-term cycling stability (92.8% of the initial capacitance retention rate after 5000 cycles). Therefore, TC-1 is considered to be a promising candidate for high-performance supercapacitor electrode materials and is a good choice for converting tobacco biomass waste into a resource.