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The Middle Jurassic Walloon Subgroup of Daandine gas field contains numerous coal seams with abundant coalbed methane (CBM) resources. However, the vertical gas content distribution of these coal seams is unclear currently, as well as its influencing factors, affecting the formulation of CBM exploration and exploitation strategy. For this purpose, using diverse geologic, experimental, and engineering data from recent exploration and development, this article ascertains the vertical coalbed gas content distribution in the Daandine gas field and discusses how the geological factors affect it. The results show that the coalbed gas contents have two basic trends as the depth increases: (1) increase, and then decrease; (2) increase. The former trend is dominant, and the inflection point occurs in the coal groups within or close to the Tangalooma Sandstone Formation. The correlation analysis shows that the macerals have little influence on the vertical coalbed gas content distribution. The moisture contents affect the adsorption capacity of coalbeds and show a negative correlation with the gas contents, and coal groups with higher moisture contents generally have lower gas contents. Three sets of independent gas-bearing systems exist in the Walloon Subgroup, and the coalbed gas content-depth relationship is relatively independent among different gas-bearing systems. The better the caprock condition, the higher the gas content, which is particularly evident in the coals of Condamine group. The permeabilities show a significant effect on the coalbed gas contents of Daandine coals. The coal groups within or close to the Tangalooma Sandstone Formation have higher permeabilities, as well as higher gas contents, and they are positively correlated. The reason is that the CBM in the study area is dominantly microbial in origin, and the higher permeability coals are conducive to the introduction of more microbial consortia into the coal seams, enhancing the generation of secondary biogenesis methane. [ABSTRACT FROM AUTHOR]

Cold stress is a major abiotic factor plants face during their life cycle. Although plants often exhibit phenotypic variation in cold tolerance, the underlying mechanism remains poorly understood. In the present study, the 50% lethal temperature (LT50) values of 37 Arabidopsis thaliana accessions at latitudes from 15° to 58° ranged from –13.2°C to –4.9°C and were closely correlated with the cold climates of the collection sites. According to a methylation analysis of all C-repeat (CRT)-binding factor (CBF) pathway genes, the coding and promoter regions of AtICE1, a regulator of CBF genes, exhibited the greatest variability in methylation levels among the accessions and included 5–122 methylated cytosine residues. In contrast, unmethylated or only slightly methylated genes in the CBF pathway showed little variation among the accessions. According to a gene expression analysis of four selected A. thaliana populations with distinct methylation patterns, except for the down-regulated gene AtCBF2, the expression levels of all members of the CBF pathway were negatively correlated with AtICE1 gene methylation levels. Treatment of the four A. thaliana populations with the DNA methylation inhibitory reagent 5-azacytidine resulted in a 30.0–78.3% enhancement of freezing tolerance and decreases in LT50 values of approximately 1.9–3.6°C. Similar effects were observed in drm2 mutants, including 30.0–48.3% increases in freezing tolerance and decreases in LT50 values of approximately 0.7–3.4°C. Thus, the AtICE1 methylation-regulated transcription of CBF pathway genes is responsible for the phenotypic variation in the freezing tolerance observed in A. thaliana. [ABSTRACT FROM AUTHOR]

Abstract: Fast protein liquid chromatography has been developed for purification of high-molecular-weight glutenin subunits HMW-GSs from wheat flour. Flour samples from four wheat cultivars with different HMW-GS alleles at Glu-A1, Glu-B1 and Glu-D1 loci were used to establish the method. The column material used was Resource™ Phe, and the optimal elution was with a gradient formed with buffer A [0.05M Tris–HCl containing 4M urea and 0.25M (NH4)2SO4, pH 8.0] and buffer B [0.05M Tris–HCl containing 4M urea (pH 8.0)] at a flow rate of 0.5ml/min. A pure single 1Dx-, 1Bx- HMW-GS, and all the y-type HMW-GSs present in one genotype can be reliably separated in a single step. [Copyright &y& Elsevier]

Background: New-onset atrial fibrillation (NOAF) is the most common arrhythmia in critically ill patients admitted to intensive care and is associated with poor prognosis and disease burden. Identifying high-risk individuals early is crucial. This study aims to create and validate a NOAF prediction model for critically ill patients using machine learning (ML)., Methods: The data came from two non-overlapping datasets from the Medical Information Mart for Intensive Care (MIMIC), with MIMIC-IV used for training and subset of MIMIC-III used as external validation. LASSO regression was used for feature selection. Eight ML algorithms were employed to construct the prediction model. Model performance was evaluated based on identification, calibration, and clinical application. The SHapley Additive exPlanations (SHAP) method was used for visualizing model characteristics and individual case predictions., Results: Among 16,528 MIMIC-IV patients, 1520 (9.2%) developed AF post-ICU admission. A model with 23 variables was built, with XGBoost performing best, achieving an AUC of 0.891 (0.873-0.888) in validation and 0.769 (0.756-0.782) in external validation. Key predictors included age, mechanical ventilation, urine output, sepsis, blood urea nitrogen, percutaneous arterial oxygen saturation, continuous renal replacement therapy and weight. A risk probability greater than 0.6 was defined as high risk. A friendly user interface had been developed for clinician use., Conclusion: We developed a ML model to predict the risk of NOAF in critically ill patients without cardiac surgery and validated its potential as a clinically reliable tool. SHAP improves the interpretability of the model, enables clinicians to better understand the causes of NOAF, helps clinicians to prevent it in advance and improves patient outcomes., (© 2024. The Author(s).)

Background: Coronary heart disease (CHD) is the leading cause of death in both developed and many developing countries. Exercise training is a fundamental component of cardiac rehabilitation programs for patients with CHD. This study aims to investigate the effects of a Tai Chi rehabilitation program, which is provided through a hybrid online and offline mode, on oxidative stress and inflammatory responses in patients with CHD., Methods: A total of 34 patients with coronary heart disease were randomly assigned to two groups: an experiment group ( n  = 14, age 62.07 ± 9.076 years) and a control group ( n  = 20, age 61.90 ± 9.700 years). The experiment group underwent a 12-week Tai Chi cardiac rehabilitation program (TCCRP), while the control group followed a conventional exercise rehabilitation program (CERP) consisting of 1-h sessions, 3 times per week, for a total of 36 sessions. Participants were studied at baseline and post-intervention. The main assessments include the levels of Malondialdehyde (MDA), Superoxide dismutase (SOD), Tumor necrosis factor (TNF-α) and Interleukin-10 (IL - 10) in blood samples. Pearson correlation analysis was used, and the differences between the two groups were subsequently tested using two-way repeated ANOVA. Statistical significance was defined as a two-sided p -value of <0.05., Results: The key finding of the study reveals that MDA was significantly reduced by 1.027 nmoL/mL. Additionally, the TCCRP showed significant improvements in SOD and IL-10, with values of 10.110 U/mL and 2.441 pg./mL, respectively. Notably, a significant positive correlation was found between SOD and IL-10 ( r  = 0.689, p  = 0.006), while MDA showed a significant positive correlation with TNF-a ( r  = 0.542, p  = 0.045). In contrast, the ECRP group only showed a significant improvement in SOD., Conclusion: The study conducted a 12-week program on TCCRP, which utilized a hybrid online and offline model for individuals with coronary heart disease. The program showed promising results in alleviating oxidative stress and inflammation, possibly by regulating the balance between oxidative and antioxidative factors, as well as pro-inflammatory and anti-inflammatory factors., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Cui, Wei, Li, Liu, Sun, Liu, Chen, Fang, Liu, Fu, Li, Li, Ma, Zhang, Huang, Li, Lyu and Zhang.)

Transition metal zinc sulfide (ZnS) is a promising anode material for potassium ion batteries due to its rich abundance and high capacity (conversion/alloy dual mechanism), while still suffering the drawbacks of sluggish kinetics process and structural degradation, which restrict its practical application. Herein, ZnS spheres assembled from nanoparticles embedded in carbon nanosheets (ZnS/C@C) were synthesized with alkali-activated agricultural waste bagasse as the carbon precursor. The removal of lignin and hemicellulose by pre-treatment of bagasse with alkali solutions opens ionic diffusion channels and promotes adsorption of Zn 2+ by bagasse, which is crucial for the growth of ZnS in bagasse sheets and the suppression of ZnS particle size during hydrothermal processes. Benefiting from the synergistic effects between robust embedded structure, carbon conductive network and the nanoscale nature of ZnS, the ZnS/C@C exhibited enhanced performance with high capacity (374.7 mA h g -1 at 0.2 A g -1 ) and rate performance (195.9 mA h g -1 at 2.0 A g -1 ). Kinetic studies further demonstrate that ZnS/C@C electrodes possess faster K + transport kinetics and lower interfacial impedance. This work provides a reference for the construction of robust embedded carbon composite structures based on surface control of agricultural waste., (© 2023 IOP Publishing Ltd.)

Background: Previous studies have shown that levosimendan can reduce mortality and complications in patients undergoing cardiac surgery. The purpose of this study was to investigate the effect of levosimendan on the recovery of cardiac function, quality of life and prognosis in patients with heart disease after operation., Methods: From October 2017 to August 2019, 93 patients admitted to our hospital for cardiac surgery were retrospectively enrolled in this study. Fifty-three patients treated with levosimendan were included in the experimental group (EG) and 40 who did not receive levosimendan were recruited into the control group (CG). After operation, the length of ICU stay and hospitalization, mean arterial pressure, central venous pressure, heart rate, the changes of cardiac parameters (left ventricular end diastolic volume (LVEDV), end-systolic volume (LVESV), left ventricular ejection index (LVEF) and cardiac index (CI) at different time points), and the changes of high sensitive troponin I (hs-cTnI), creatine kinase isoenzyme (CK-MB) and N-terminal pro-brain natriuretic peptide (NT-proBNP) levels were compared between the two groups. The stroke volume index (SVI), left ventricular stroke work index (LVSWI), systemic vascular resistance index (SVRI) and other hemodynamic indexes were also compared., Results: The length of ICU stay and hospitalization time in the EG were shorter than those in the CG. After treatment, MAP (mean arterial pressure), CVP (central venous pressure), HR (heart rate), LVEDV, LVESV, HS CTN, NT proBNP and SVRI in the EG were lower than those in the CG group, while LVEF, CI, SVI and LVSWI were higher than those in the CG. The quality of life of patients in the EG was better than that of those in the CG one month after treatment. Logistics regression analysis revealed that the use of levosimendan can reduce the risk of death., Conclusion: Levosimendan can improve the cardiac function and prognosis of patients after cardiac surgery, which is worthy of clinical promotion., Competing Interests: None., (AJTR Copyright © 2022.)

Objective: To explore the genetic basis for a patient diagnosed with tuberous sclerosis complex (TSC)., Methods: Peripheral blood samples of the patient and his parents were collected for the extraction of genomic DNA. Next generation sequencing (NGS) was carried out to detect potential variant, and the result was verified by Sanger sequencing., Results: The patient was found to harbor a heterozygous c.1053delG (p.Glu352SerfsX10) frameshifting variant of the TSC2 gene. The same variant was not found in his unaffected parents and 100 unrelated healthy controls. Based on the American College of Medical Genetics and Genomics guidelines, the variant was predicted to be pathogenic (PVS1+PS2+PM2)., Conclusion: The novel c.1053delG (p.Glu352SerfsX10) frameshifting variant of the TSC2 gene probably underlay the TSC in this patient.

Objective: To identify pathogenic mutation of TSC1 and TSC2 genes in a patient with long-time misdiagnosis of epilepsy., Methods: Peripheral blood samples and clinical data of the patient and her 2 parents were collected. Potential mutation of TSC1 and TSC2 genes were detected by direct sequencing., Results: The patient had frequent episodes of epilepsy in addition with Shagreen patches for 10 years. A frame-shifting mutation c.2509&#95;2512delAACA was detected in exon 20 of the TSC1 gene. This same mutation was not found in her unaffected parents., Conclusion: The recurrent frame-shifting mutation c.2509&#95;2512delAACA (p.Asn837ValfsX11) of the TSC1 gene probably underlies the disease in this patient.

Objective: To detect pathogenic mutation of the SLC39A4 gene in a male patient with acrodermatitis enteropathica (AE)., Methods: Peripheral venous blood sample and clinical data from the patient and his parents were collected. One hundred unrelated healthy individuals were recruited as controls. All coding exons and flanking exon-intron sequences of the SLC39A4 gene were analyzed by PCR and direct sequencing., Results: The results revealed that the patient and his mother have both carried a novel frame-shift mutation c.1110InsG (p.Gly370GlyfsX47 to TGA) in exon 6. A novel nonsense mutation c.958C to T (p.Q320X) in exon 5 was also detected in the patient and his father and grandmother. This novel mutation was not detected in the unaffected family members and 100 unrelated healthy controls., Conclusion: The novel frame-shift mutation c.1110InsG (p.Gly370GlyfsX47 to TGA) derived from the mother and nonsense mutation c.958C to T (p.Q320X) of the SLC39A4 gene derived from the father may underlie the disease in the patient.

Objective: To identify pathogenic mutations of TSC1 and TSC2 genes in two familial and one sporadic cases with tuberous sclerosis complex (TSC)., Methods: For five patients and their family members, potential mutations of the TSC1 and TSC2 genes were detected by direct sequencing., Results: For one family, a novel missense mutation c.1964C>T (p.S655F) was detected in the exon 19 of the TSC2 gene. For the sporadic patient, a repeat substitution with deletion mutation c.5238-5255delCATCAAGCGGCTCCGCCA (p.His1746GlnfsX56) was detected in the exon 40 of the TSC2 gene, which led to a stop codon TGA after the 56th amino acids. No mutation was found in another family., Conclusion: The missense mutation c.1964C>T(P.S655F) and the substitution with deletion mutation 5238-5255delCATCAAGCGGCTCCGCCA(p.His1746GlnfsX56) of the TSC2 gene probably underlie the disease in the first family and the sporadic case.

Objective: To identify potential mutation of the ADAR1 gene in a Chinese family and a sporadic case affected with dyschromatosis symmetrica hereditaria(DSH)., Methods: Clinical data and peripheral blood samples from the pedigree and the sporadic patient were collected. Following extraction of genomic DNA, all 15 exons and exon-intron flanking sequences of the ADAR1 gene were amplified by polymerase chain reaction and subjected to direct sequencing., Results: A novel frame-shift mutation c.2638delG (p.Asp880ThrfsX15) from the patients of the pedigree was detected in exon 8 of the ADAR1 gene. And a novel nonsense mutation c.2867C>A (p.Ser956X) was detected in exon 10 of the ADAR1 gene from the sporadic case. Neither mutation was identified among the unaffected family members nor 100 unrelated healthy controls., Conclusion: The frame-shift mutation c.2638delG (p.Asp880ThrfsX15) and the nonsense mutation c.2867C>A (p.Ser956X) in the ADAR1 gene probably underlie the DSH in our patients.

Objective: To identify pathogenic mutation of the TSC1 and TSC2 genes in a patient with tuberous sclerosis., Methods: Peripheral venous blood samples and clinical data of a pregnant woman with tuberous sclerosis and 4 family members (parents, uncle and husband) were collected. Genomic DNA was extracted. All coding exons of the TSC1 and TSC2 genes and their flanking intronic sequences were amplified by polymerase chain reaction and subjected to direct sequencing., Results: The patient has presented facial angiofibroma and prefrons fibrous plaque for 20 years, and lumbar connective tissue nevus for 10 years. She also had mental retardation but no epilepsy. A novel frame-shift mutation c.4258-4261delTCAG was detected in exon 34 of the TSC2 gene, which had led to a premature stop codon TAG after the 55th amino acids. The same mutation was not found in the unaffected family members and 100 unrelated healthy controls., Conclusion: The novel frame-shifting mutation c.4258-4261delTCAG (p.Ser1420GlyfsX55) in the TSC2 gene may be responsible for the disease in the patient.

Background and Aim of the Study: The study aim was to evaluate whether individualized quantified selective tricuspid valve annuloplasty would be suitable for the treatment of Ebstein anomaly., Methods: Between March 1999 and February 2011, a total of 23 patients with Ebstein anomaly underwent individualized quantified selective tricuspid valve annuloplasty at the authors' institution. The annulus was reconstructed according to each patient's individual anatomic characteristics of their tricuspid valve. Echocardiography was used to assess the changes of tricuspid valve regurgitation and heart function perioperatively and also during the follow up period., Results: There was no hospital mortality. One patient died suddenly at 41 months after surgery, and two patients were lost to follow up; the remaining patients are still alive. During the follow up, tricuspid valve regurgitation and cardiac function were improved in all patients postoperatively, with no acquired tricuspid stenosis., Conclusion: The study results and analysis of follow up data suggested that an '...individualized quantified selective concept and technique of tricuspid valve reconstruction' is reasonable, suitable, and practical in the treatment of Ebstein anomaly.