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This study aims to investigate the potential factors affecting hydraulic fracturing of inter-salt oil shale reservoirs in the Qianjiang Depression, China. Using the inter-salt shale samples, the re-crystallization seepage tests, rock mechanical tests under high temperature and pressure, salt rock creep tests, and direct shear tests were conducted. The testing results suggest several major factors that affect hydraulic fracturing effects in the end. First, the seepage of reservoir and fracturing fluid through hydraulic fractures leads to salt dissolution and crystallization, reducing the effective seepage area of fractures. Second, the salt crystal may block the pore throats or micro fractures after brine invades the shale, decreasing the overall permeability. Third, the low strength and obvious plasticity of inter-salt shale and the strong creep characteristics of salt rock raise difficulties for proppant to effectively support fracture walls, thereby sharply narrowing the hydraulic fracture width. Lastly, the weak interfaces (bedding planes and lithology interfaces) in inter-salt oil shale reservoirs restrict the height of hydraulic fractures, resulting in the disconnection of seepage channels between multiple inter-salt shale reservoirs. Thus, several factors together reduce reservoir permeability, weaken the fluid flow capacity in the fracture, narrow the fracture width, and limit the effective stimulation volume, resulting in weaken the effect hydraulic fracturing. [ABSTRACT FROM AUTHOR]

In China, most normal BMI (body mass index of ≥18.5 to <25 kg/m2) adults with type 2 diabetes (T2DM) exhibit visceral adiposity. This study compared the effects of exenatide and humalog Mix25 on normal BMI patients with T2DM and visceral adiposity. A total of 95 patients were randomized to receive either exenatide or humalog Mix25 treatment for 24 weeks. Subcutaneous adipose tissue (SAT) and visceral adipose tissue (VAT) were quantified by magnetic resonance imaging (MRI) and liver fat content (LFC) by liver proton magnetic resonance spectroscopy (1H MRS). Each patient's weight, waist circumference, BMI, blood glucose, insulin sensitivity, pancreatic β-cell function, and fibroblast growth factor 21 (FGF-21) levels were measured. Data from 81 patients who completed the study (40 and 41 in the exenatide and humalog Mix25 groups, respectively) were analysed. The change in 2 h plasma blood glucose was greater in the exenatide group (P = 0.039). HOMA-IR and MBCI improved significantly after exenatide therapy (P < 0.01 , P = 0.045). VAT and LFC decreased in both groups (P < 0.01 for all) but to a greater extent in the exenatide group, while SAT only decreased with exenatide therapy (P < 0.01). FGF-21 levels declined more in the exenatide group (P < 0.01), but were positively correlated with VAT in the entire cohort before (r = 0.244 , P = 0.043) and after (r = 0.290 , P = 0.016) the intervention. The effects of exenatide on glycaemic metabolism, insulin resistance, pancreatic β-cell function, and fat deposition support its administration to normal BMI patients with T2DM and visceral adiposity. [ABSTRACT FROM AUTHOR]

Objectives: Management of chronic coronary syndrome (CCS) encompasses a broad spectrum of practices, posing considerable complexity and variability. While guidelines have been established to augment the management quality of CCS, notable disparities persist across their recommendations. This study strives to scrutinize, compare, and reconcile these guideline recommendations pertaining to the diagnosis, treatment, and management of CCS patients. Our goal is to align these recommendations with contemporary clinical practices, thus laying a robust foundation for their pragmatic application in clinical settings., Methods: A comprehensive systematic search was conducted across multiple databases, including PubMed, EMBASE, China National Knowledge Infrastructure, Wanfang Database, China Science and Technology Journal Database, Chinese Biomedical Literature Service System, Chinese Science and Technology Periodical Database, and Chinese Biological Medicine Database. The timeframe for this search spanned from their inception up to May 30, 2022, aiming to collate all published guidelines relevant to CCS. Subsequently, two independent reviewers undertook the task of appraising the quality of these guidelines by utilizing the Appraisal of Guidelines for Research and Evaluation II instrument., Results: The search yielded a total of 10,699 citations. Following a thorough evaluation, fourteen clinical practice guidelines and four consensus statements, each offering specific recommendations for CCS, were selected. The quality of these guidelines showcased a broad spectrum of variation. The domain of "presentation clarity" received the highest accolades, while "applicability" languished at the lower end of the scoring spectrum. On average, the guidelines attained a quality score denoting sufficiency. Furthermore, recommendations across different guidelines for the diagnosis, treatment, and management of CCS displayed a striking level of divergence., Conclusion: The landscape of published CCS guidelines is marked by extensive variations in scope, quality, and recommendations. Hence, there is a compelling need for collaborative efforts amongst multidisciplinary professionals to forge comprehensive, higher-quality evidence-based guidelines; such a concerted approach is paramount to enhance treatment efficacy and health outcomes for patients grappling with CCS., Competing Interests: The authors declare that they have no conflicts of interest with respect to the research, authorship, and/or publication of this article., (Copyright © 2023 Tianyue Jing et al.)

Background: Even though presenting with similar clinical manifestations, necrotizing enterocolitis (NEC) and food protein-induced allergic protocolitis (FPIAP) have completely different treatments and prognosis. Our study aimed to quantify and evaluate differences in gut microbiota and short chain fatty acids (SCFAs) between infants with NEC and FPIAP to better identify these two diseases in clinical settings., Methods: A total of 43 infants with NEC or FPIAP in Children's Hospital of Chongqing Medical University, China between December 2020 and December 2021 were enrolled. Stool samples were prospectively collected and froze. Infants defined as NEC were those who presented with clinical courses consistent with NEC and whose radiographs fulfilled criteria for Bell's stage 2 or 3 NEC, while those who were healthy in appearance and had blood in the stool (visible or may be microscopic), had normal bowel sounds in physical examination, were resolved after eliminating the causative food, and/or had recurrence of symptoms after oral food challenge (OFC) were defined as FPIAP. Primers specific for bacterial 16S rRNA genes were used to amplify and pyrosequence fecal DNA from stool samples. Gas chromatography-mass spectrometry (GC-MS) technology was used to determine the concentrations of SCFAs., Results: Among the 43 infants, 22 were diagnosed with NEC and 21 were diagnosed with FPIAP. The microbial community structure in NEC infant stools differed significantly from those in FPIAP infant stools. NEC infants had significantly higher proportion of Actinobacteria and reduced proportion of Bacteroidetes compared with FPIAP infants, and the proportions of Halomonas, Acinetobacter, Bifidobacterium , and Stenotrophomonas in NEC infants were significantly higher than that of FPIAP infants. In addition, infants with NEC had significantly lower levels of acetic acid, propionic acid, butyric acid, isovaleric acid, and total SCFAs, and higher level of hexanoic acid as compared to the infants of the FPIAP group., Conclusions: The differences of gut microbiota composition and concentrations of SCFAs might represent suitable biomarker targets for early identification of NEC and FPIAP., 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 © 2022 Xiong, Liao, Yin, Liu, Bao and Li.)

Background: Dual antiplatelet therapy (DAPT) after percutaneous coronary intervention (PCI) prevents ischemic events while increasing bleeding risk. Real-world-based metrics to accurately predict postdischarge bleeding (PDB) occurrence and its potential impact on postdischarge major cardiovascular event (MACE) remain undefined. This study sought to evaluate the impact of PDB on MACE occurrence, and to develop a score to predict PDB risk among Chinese acute coronary syndrome (ACS) patients after PCI., Methods and Results: From May 2014 to January 2016, 2496 ACS patients who underwent PCI were recruited consecutively from 29 nationally representative Chinese tertiary hospitals. Among 2,381 patients (95.4%, 2,381/2,496) who completed 1-year follow-up, the cumulative incidence of PDB (bleeding academic research consortium type [BARC] ≥2) and postdischarge MACE (a composite of all-cause death, nonfatal myocardial infarction, ischemic stroke, or urgent revascularization) was 4.9% (n = 117) and 3.3% (n = 79), respectively. The association between PDB and MACE during 1-year follow-up, as well as the impact of DAPT with ticagrelor or clopidogrel on PDB were evaluated. PDB was associated with higher risk of postdischarge MACE (7.7 vs. 3.1%; adjusted hazard ratio: 2.59 [95% confidence interval: 1.17-5.74]; p = .02). For ticagrelor versus clopidogrel, PDB risk was higher (8.0 vs. 4.4%; 2.05 [1.17-3.60]; p = .01), while MACE risk was similar (2.0 vs. 3.4%; 0.70 [0.25-1.93]; p = .49). Based on identified PDB predictors, the constructed bleeding risk in real world Chinese acute coronary syndrome patients (BRIC-ACS) score for PDB was established. C-statistic for the score for PDB was 0.67 (95% CI: 0.62-0.73) in the overall cohort, and >0.70 in subgroups with non-ST- and ST-segment elevation myocardial infarction, diabetes and receiving more than two drug eluting stents., Conclusions: In Chinese ACS patients, PDB with BARC ≥2 was associated with higher risk for MACE after PCI. The constructed BRIC-ACS risk score provides a useful tool for PDB discrimination, particularly among high ischemic and bleeding risk patients., (© 2019 Wiley Periodicals, Inc.)

This study aims to explore the dynamic changes of pulmonary arterial pressure (PAP) and its clinical significance in prenatal neonates with pulmonary and extra-pulmonary acute lung injury/respiratory distress syndrome (ALI/ARDS).A prospective study was conducted in the Neonate Intensive Care Unit (NICU) between May 2015 and April 2017. A total of 78 prenatal neonates with ALI/ARDS were selected and divided into 2 groups: pulmonary group (n = 37) and extra-pulmonary group (n = 41). These neonates were further divided into 3 groups according to the OSI index: mild, moderate, and severe groups. The dynamic changes of PAP were observed in these neonates. In the moderate and severe groups, PAP was significantly higher in neonates with pulmonary ALI/ADDS (ALI/ARDSp) than in neonates with extrapulmonary ALI/ARDS(ALI/ARDSexp) (62.5 ± 5.4 vs 68.0 ± 6.5, 54.7 ± 5.9 vs 64.2 ± 4.9; t = 3.264, 3.123; P = .004,.039). Furthermore, PAP was higher in neonates with ALI/ADDSp in the severe group, compared with those in the moderate group (t = 2.420, P < .05). There was significant difference among the 3 subgroups of neonates with ALI/ADDSexp (F = 60.100, P = .000). PAP was positively correlated with the OSI index (r = 0.823). The overall dynamic PAP monitoring results revealed that PAP was higher in the pulmonary group than that in the extrapulmonary group, and this exhibited a gradually decreasing trend as the condition of the subject improved.PAP in perinatal neonates with ALI/ARDS increases in varying degrees, and its extent was related to the severity of the illness. PAP was significantly higher in neonates with ALI/ADDSp than in neonates with ALI/ADDSexp. This can be used as a monitoring indicator for the severity of illness.

Objective: Type 2 diabetes mellitus is increasing in young adults, and greater adiposity is considered a major risk factor. However, whether there is an association between obesity and diabetes and how this might be impacted by age is not clear. Therefore, we investigated the association between body mass index (BMI) and diabetes across a wide range of age groups (20-30, 30-40, 40-50, 50-60, 60-70 and ≥70 years old)., Design: We performed a retrospective cohort study using healthy screening programme data., Setting: A total of 211 833 adult Chinese persons >20 years old across 32 sites and 11 cities in China (Shanghai, Beijing, Nanjing, Suzhou, Shenzhen, Changzhou, Chengdu, Guangzhou, Hefei, Wuhan, Nantong) were selected for the study; these persons were free of diabetes at baseline., Primary and Secondary Outcome Measures: Fasting plasma glucose levels were measured and information regarding the history of diabetes was collected at each visit. Diabetes was diagnosed as fasting plasma glucose ≥7.00 mmol/L and/or self-reported diabetes. Patients were censored at the date of diagnosis or the final visit, whichever came first., Results: With a median follow-up of 3.1 years, 4174 of the 211 833 participants developed diabetes, with an age-adjusted incidence rate of 7.35 per 1000 persons. The risk of incident diabetes increased proportionally with increasing baseline BMI values, with a 23% increased risk of incident diabetes with each kg/m 2 increase in BMI (95% CI 1.22 to 1.24). Across all age groups, there was a linear association between BMI and the risk of incident diabetes, although there was a stronger association between BMI and incident diabetes in the younger age groups (age×BMI interaction, p<0.0001)., Conclusions: An increased BMI is also independently associated with a higher risk of developing diabetes in young adults and the effects of BMI on incident diabetes were accentuated in younger adults., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2018. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.)

Purpose: Hypertension is a very important risk factor for cardiac vascular disease. The previous studies showed that mitochondrial DNA mutations are associated with cardiovascular disease, including hypertension., Methods: In this study we did systematical analysis on the total 22 mitochondrial tRNAs and the clinical, genetic and molecular changes of 140 Chinese hypertension and 124 controls., Results: This analysis identified 22 nucleotide changes among 15 different tRNA genes. There are 15 mutations with CI (Conservation index) larger than 75%. Of these, there are 26 patients with CI larger than 75% in the HTN group, higher than the 6 subjects in the control group (P=0.00). The tRNA(Phe) G586A, tRNA(Lys) G8313A and tRNA(His) G12147A mutations create highly conservative base-pairings on the D-stem, tRNA(Lys) G8342A on the T-stem, tRNA(Phe) T616C, tRNA(Ala) T5628C, tRNA(Tyr) G5856A and tRNA(Thr) A15924G on the AC stem, tRNA(Leu(CUN)) G12300A on the AC loop, tRNA(Met) C4467T, tRNA(Trp) T5578C, tRNA(Lys) A8296G, tRNA(Arg) T10463C and tRNA(Thr) C15891T on ACC stem, and tRNA(Ser(UCN)) C7492T on D-A junction, while the other tRNA variants were polymorphisms. The pedigrees of PLAH78 carrying the T5578C, PLAH84 carrying the C4467T, PLAH60 carrying the T5628C and PLAH118 carrying the C7492T mutation exhibited maternal transmission of essential hypertension. Sequence analysis of their mitochondrial genomes revealed the presence of T5578C, C4467T, T5628C or C7492T mutations but the absence of other functionally significant mutations in all matrilineal relatives of these families., Conclusions: These tRNAs mutations, associated with altered structures of tRNAs and mitochondrial dysfunction, may contribute to the hypertension in Chinese population. A lot of work still should be done for the mechanism and functional effect of the mtDNA mutation on hypertension., (Copyright © 2016 Elsevier B.V. and Mitochondria Research Society. All rights reserved.)

Background: Mitochondrial DNA mutations may be associated with cardiovascular disease, including the common cardiac vascular disease, hypertension., Methods: In this study we performed segregation analysis and systematically evaluated the entire mitochondrial genome in nine maternally inherited hypertension probands from Chinese Han families. We also performed clinical, genetic and molecular characterization of 74 maternally inherited members from these families and 216 healthy controls., Results: In the maternally inherited members, 12 had coronary heart disease (CHD), six had cerebrovascular disease, five had diabetes, nine had hyperlipidemia and three had renal disease. Laboratory tests showed that the sodium and potassium levels in blood of the maternally inherited members were higher than those of the control group (P < 0.01), while no differences were observed in fasting blood glucose (FBG), total cholesterol (TC), triglyceride, low density lipoprotein cholesterol (LDL-c) and creatinine levels (P > 0.05). The high density lipoprotein cholesterol (HDL-c) level of the maternally inherited members was lower than that of the control group (P = 0.04). The whole mitochondrial DNA sequence analysis revealed a total of 172 base changes, including 17 in ribosomal RNA (rRNA) genes, four in transfer RNA (tRNA) genes, and 22 amino acid substitutions. The remainder were synonymous changes or were located in non-coding regions. We identified seven amino acid changes in the nine maternally inherited hypertension families, including four mutations in ATPase6 and three in Cytb. More interestingly, tRNA(Ser(UCN)) 7492 T > C was absent in controls and was present in <1% of 2704 mtDNAs, indicating potential functional significance., Conclusions: This study showed that mutations in mtDNA may contribute to the pathogenesis of hypertension in these Chinese Han families. In the near future, identification of additional mtDNA mutations may indicate further candidate genes for hypertension.

This study was designed to evaluate the effect of the warfarin dose-associated genotypes, CYP2C9*3 (rs1057910), VKORC1 -1639 G/A (rs9923231), and CYP4F2 1347 C/T (rs2108622), on hemorrhagic complications in Han Chinese patients. Consecutively recruited patients requiring more than 1 year of warfarin treatment were followed from the initiation of warfarin anticoagulation for at least 3 months. CYP2C9*3, VKORC1 -1639 G/A, and CYP4F2 1347 C/T were genotyped by sequencing. The association between genotypes and warfarin hemorrhagic complications was evaluated using Cox proportional hazard regression, adjusted for demographic and clinical factors. Of 312 eligible patients obtaining stable warfarin anticoagulation in 3 months, 11 major and 69 minor hemorrhages occurred over 147 person-years. The CYP2C9*3 genotype conferred an increased risk of all [hazard ratio (HR) 3.07, 95 % confidence interval (CI) 1.57-6.01] and minor hemorrhage (HR 3.28, 95 % CI 1.62-6.65), but not major hemorrhage (HR 0.44, 95 % CI 0.04-4.72). CYP2C9*3 also conferred an increased risk of over-anticoagulation with international normalization ratio (INR) ≥4 (HR 2.92, 95 % CI 1.08-7.85). VKORC1 -1639 G/A, and CYP4F2 rs2108622 did not confer significant increase in risk for hemorrhage or over-anticoagulation. Kaplan-Meier curves showed that time to all hemorrhagic events was significantly shorter for patients with CYP2C9*3 genotype than non-carriers (P = 0.001), but not for patients with VKORC1 -1639 G/A or CYP4F2 rs2108622 genotype (P = 0.3 and 0.2). CYP2C9*3 may be the main genetic factor in hemorrhagic complications in Chinese patients under warfarin anticoagulation.

Pharmacogenetic (PG) dosing algorithms have been confirmed to predict warfarin therapeutic dose more accurately; however, most of them are based on standard intensity of warfarin anticoagulation, and their utility outside this range is limited. This study was designed to develop and validate a PG refinement algorithm in Chinese patients mainly under low-intensity warfarin anticoagulation. Consented Chinese-Han patients (n=310) under stable warfarin treatment were randomly divided into a derivation (n=207) and a validation cohort (n=103), with 83% and 80% of the patients under low-intensity anticoagulation, respectively. In the derivation cohort, a PG algorithm was constructed on the basis of genotypes (CYP2C9*3 and VKORC1-1639A/G) and clinical data. After integrating additional covariates of international normalised ratio (INR) values (INR on day 4 of therapy and target INR) and genotype of CYP4F2 (rs2108622), a PG refinement algorithm was established and explained 54% of warfarin dose variability. In the validation cohort, warfarin dose prediction was more accurate (p < 0.01) with the PG refinement algorithm than with the PG algorithm and the fixed dose approach (3 mg/day). In the entire cohort, the PG refinement algorithm could accurately identify larger proportions of patients with lower dose requirement (≤2 mg/day) and higher dose requirement (≥4 mg/day) than did the PG algorithm. In conclusion, PG refinement algorithm integrating early INR response and three genotypes (CYP2C9*3, VKORC1-1639A/G, CYP4F2 rs2108622) improves the accuracy of warfarin dose prediction in Chinese patients mainly under low-intensity anticoagulation.

Introduction: Multiple warfarin pharmacogenetic algorithms have been confirmed to predict warfarin dose more accurately than clinical algorithm or the fixed-dose approach. However, their performance has never been objectively evaluated in patients under low intensity warfarin anticoagulation, which is optimal for prevention of thromboembolism in Asian patients., Material and Methods: We sought to compare the performances of 8 eligible pharmacogenetic algorithms in a cohort of Chinese patients (n=282) under low intensity warfarin anticoagulation with target international normalized ratio (INR) ranged from 1.6 to 2.5. The performance of each algorithm was evaluated by calculating the percentage of patients whose predicted dose fell within 20% of their actual therapeutic dose (percentage within 20%), and the mean absolute error (MAE) between each predicted dose and actual stable dose., Results: In the entire cohort, the pharmacogenetic algorithms could predict warfarin dose with the average MAE of 0.87 ± 0.17 mg/day (0.73-1.17 mg/day), and the average percentage within 20% of 43.8% ± 8.1% (29.1% - 52.1%). By pairwise comparison, warfarin dose prediction was significantly more accurate with the algorithms derived from Asian patients (48.6% - 50.0%) than those from Caucasian patients (29.1% - 39.7%; odds ratio [OR]: 1.61-3.36, p ≤ 0.02). Algorithms with additional covariates of INR values or CYP4F2*3 performed better than those without the covariates (adding INR: OR: 1.71 (1.08-2.72), p =0.029; adding CYP4F2*3: OR: 2.67(1.41-5.05), p =0.004). When the patients were stratified according to the dose range, the algorithms from Caucasian and racially mixed populations tended to perform better in higher dose group (≥ 4.5mg/day), and algorithms from Asian populations performed better in intermediate dose group (1.5-4.5mg/day). None of the algorithms performed well in lower dose group (≤ 1.5mg/day)., Conclusions: No eligible pharmacogenetic algorithm could perform the best for all dosing range in the Chinese patients under low intensity warfarin anticoagulation. Construction of a refinement pharmacogenetic algorithm integrating 3 genotypes (CYP2C9, VKORC1 and CYP4F2) and INR data should be warranted to improve the warfarin dose prediction in such patients., (Copyright © 2012 Elsevier Ltd. All rights reserved.)

Hypertension induced by obstructive sleep apnea (OSA) may be multifactorial in origin, and systemic inflammation is one of the major factors. However, OSA patients do not always have the identical probability with hypertension even in patients with the same history and degree of OSA. The aim of this study was to compare the levels of inflammation and insulin resistance in two groups of patients who had the same degree as well as the same long history of OSA, but with/without hypertension. OSA patients (Apnea Hyponea Index, AHI ≥ 40/h, n = 70) were examined by polysomnography and blood analysis for the measurements of fasting plasma glucose, serum insulin (FINS), high-sensitivity C-reactive protein (CRP), peptide C,TNF-α, IL-6, and IL-10. Patients with hypertension (n = 40) had higher level of LDL-C and lower HDL-C levels than patients without hypertension. Almost half (16/40) of OSA patients with hypertension had family history of hypertension. Moreover in OSA patients with hypertension, the levels of TNF-α, IL-6, and CRP were higher, but IL-10 was lower than those without hypertension. FINS, peptide C, HOMA-IR, and HOMA-islet were also higher in OSA patients with hypertension. OSA patients with hypertension have higher level of inflammation and insulin resistance. Systemic inflammation and insulin resistance are both important factors for the development of hypertension in OSA patients.