The eukaryotic translation initiation factor eIF4E regulates flowering and circadian rhythm in Arabidopsis.

Translation initiation is a critical, rate-limiting step in protein synthesis. The eukaryotic translation initiation factor 4E (eIF4E) plays an essential role in this process. However, the mechanisms by which eIF4E-dependent translation initiation regulates plant growth and development remain not fully understood. In this study, we found that Arabidopsis eIF4E proteins are distributed in both the nucleus and cytoplasm, with only the cytoplasmic eIF4E being involved in the control of photoperiodic flowering. Genome-wide translation profiling using Ribo-tag sequencing reveals that eIF4E may regulate plant flowering by maintaining the homeostatic translation of components in the photoperiodic flowering pathway. eIF4E not only regulates the translation of flowering genes such as FLOWERING LOCUS T (FT) and FLOWERING LOCUS D (FLD) but also influences the translation of circadian genes like CIRCADIAN CLOCK ASSOCIATED 1 (CCA1) and PSEUDO-RESPONSE REGULATOR 9 (PRR9). Consistently, our results show that the eIF4E modulates the rhythmic oscillation of the circadian clock. Together, our study provides mechanistic insights into how the protein translation regulates multiple developmental processes in Arabidopsis, including the circadian clock and photoperiodic flowering.

Short working hours and perceived stress: Findings from a population-based nationwide study.

Background: Evidence on the potential negative health effects of short working hours remains limited. This study aimed to investigate the association between short working hours and perceived stress in a population-based sample from China. Methods: This cross-sectional study included 4368 participants aged 18-65 years from the China Health and Nutrition Surveys (CHNS) 2015. Working hours were categorized into <35, 35-40, 41-54, and ≥55 h/week. Perceived stress was assessed using the Perceived Stress Scale-14 (PSS-14). Results: Of the 4368 participants, 817 (18.7 %) reported short working hours (<35 h/week) and 1817 (41.6 %) reported perceived stress. Short working hours were associated with higher perceived stress compared to standard working hours (35-40 h/week) (Adjusted odds ratios (AOR) = 1.25, 95 % confidential intervals (CI): 1.04-1.51). Stratified analysis showed that short working hours were significantly associated with more perceived stress in subjects aged 36-50 years (AOR = 1.43, 95 % CI: 1.16-1.70), while long working hours (≥55 h/week) were significantly related to less perceived stress among low-income subjects (AOR = 0.56, 95 % CI: 0.33-0.94). Reduced income partially mediated the effects of short working hours on perceived stress (indirect effects = -0.002, 95 % CI: -0.007∼-0.001). Conclusion: Reduced working hours may be associated with increased risk of perceived stress in China, particularly among people aged 36-50 years and those with low income. Reduced income may be a possible reason for the increased perceived stress caused by short working hours. Future longitudinal studies are needed to examine these relationships and to explore mechanisms.

Polydatin alleviates mycoplasma pneumoniae-induced injury via inhibition of Caspase-1/GSDMD-dependent pyroptosis.

Mycoplasma pneumoniae (MP) is one of the main pathogens causing community acquired pneumonia (CAP) in children and adults. Previous pharmacological and clinical studies have shown that Polydatin (PD) exerts anti-inflammatory action by conferring protective benefit in MP pneumonia. However, the mechanism underlying the of PD on MP infection remains unclear. It was found that PD alleviated MP-induced injury by inhibiting caspase-1/gasdermin D (GSDMD)-mediated epithelial pyroptosis. The results demonstrated that PD inhibited the transformation of GSDMD to N-terminal gasdermin-N (GSDMD-N) by decreasing caspase-1 activation, as well as suppressed the formation and secretion of interleukin-1ß (IL-1ß) and interleukin-18 (IL-18), reversed Na, K-ATPase reduction, and suppressed LDH release both in vitro and vivo. Taken together, epithelial pyroptosis in BEAS-2B cells and lung injury in mice were prevented by PD. In conclusion, PD suppressed pulmonary injury triggered by MP infection, by inhibiting the caspase-1/GSDMD-mediated epithelial pyroptosis signaling pathway. Thus, PD may be regarded as a potential therapy for MP-induced inflammation.

Modulation of miR-146b by N6-methyladenosine modification remodels tumor-associated macrophages and enhances anti-PD-1 therapy in colorectal cancer.

PURPOSE: MicroRNA-146b (miR-146b) alleviates experimental colitis in mice by mediating macrophage polarization and the release of inflammatory factors. Our goals were to evaluate the antitumor efficacy of miR-146b in colorectal cancer (CRC) and to investigate the underlying mechanisms. METHODS: We used murine models of CRC to evaluate whether miR-146b influenced the progression of tumors independent of tumor-associated macrophages (TAMs). RNA immunoprecipitation, N6-methyladenosine (m6A) RNA immunoprecipitation and in vitro pri-miRNA processing assays were conducted to examine whether m6A mediates the maturation of pri-miR-146b/miR-146b. In a series of in vitro and in vivo experiments, we further defined the molecular mechanisms of methyltransferase-like 3 (METTL3)/miR-146b-mediated antitumor immunity and its efficacy in combination with anti-PD-1 immunotherapy. RESULTS: We found that miR-146b deletion supported tumor progression by increasing the number of alternatively activated (M2) TAMs. Mechanistically, the m6A-related "writer" protein METTL3 and "reader" protein HNRNPA2B1 controlled miR-146b maturation by regulating the m6A modification region of pri-miR-146b. Furthermore, miR-146b deletion promoted the polarization of M2-TAMs by enhancing phosphoinositide 3-kinase (PI3K)/AKT signaling, and this effect was mediated by the class IA PI3K catalytic subunit p110ß, which reduced T cell infiltration, aggravated immunosuppression and ultimately promoted tumor progression. METTL3 knockdown or miR-146b deletion induced programmed death ligand 1 (PD-L1) production via the p110ß/PI3K/AKT pathway in TAMs and consequently augmented the antitumor activity of anti-PD-1 immunotherapy. CONCLUSIONS: The maturation of pri-miR-146b is m6A-dependent, and miR-146b deletion-mediated TAM differentiation promotes the development of CRC by activating the PI3K/AKT pathway, which induces upregulation of PD-L1 expression, inhibits T cell infiltration into the TME and enhances the antitumor activity of anti-PD-1 immunotherapy. The findings reveal that targeting miR-146b can serve as an adjuvant to anti-PD-1 immunotherapy.

Insulin alleviates murine colitis through microbiome alterations and bile acid metabolism.

BACKGROUND: Insulin has been reported to exhibit anti-inflammatory activities in the context of bowel inflammation. However, the role of the interaction between insulin and the microbiota in gut health is unclear. Our goal was to investigate the mechanism of action of insulin in bowel inflammation and the relationship between insulin and the gut microbiota. METHODS: We used acute and chronic murine models of inflammatory bowel disease (IBD) to evaluate whether insulin influences the progression of colitis. Colonic tissues, the host metabolome and the gut microbiome were analyzed to investigate the relationship among insulin treatment, the microbiome, and disease. Experiments involving antibiotic (Abx) treatment and fecal microbiota transplantation (FMT) confirmed the association among the gut microbiota, insulin and IBD. In a series of experiments, we further defined the mechanisms underlying the anti-inflammatory effects of insulin. RESULTS: We found that low-dose insulin treatment alleviated intestinal inflammation but did not cause death. These effects were dependent on the gut microbiota, as confirmed by experiments involving Abx treatment and FMT. Using untargeted metabolomic profiling and 16S rRNA sequencing, we discovered that the level of the secondary bile acid lithocholic acid (LCA) was notably increased and the LCA levels were significantly associated with the abundance of Blautia, Enterorhadus and Rumi-NK4A214_group. Furthermore, LCA exerted anti-inflammatory effects by activating a G-protein-coupled bile acid receptor (TGR5), which inhibited the polarization of classically activated (M1) macrophages. CONCLUSION: Together, these data suggest that insulin alters the gut microbiota and affects LCA production, ultimately delaying the progression of IBD.

Correlation of R2* with fat fraction and bone mineral density and its role in quantitative assessment of osteoporosis.

OBJECTIVES: To investigate the correlation of R2* with vertebral fat fraction (FF) and bone mineral density (BMD), and to explore its role in the quantitative assessment of osteoporosis (OP). METHODS: A total of 83 patients with low back pain (59.77 ± 7.46 years, 30 males) were enrolled, which underwent lumbar MRI in IDEAL-IQ sequences and quantitative computed tomography (QCT) scanning within 48h. The FF, R2*, and BMD of all 415 lumbar vertebrae were respectively measured. According to BMD, all vertebrae were divided into BMD normal, osteopenia, and OP groups, and the difference of FF and R2* among groups was analyzed by one-way ANOVA. The correlation between R2*, FF, and BMD was analyzed by Pearson's test. Taking BMD as the gold standard, the efficacies for FF and R2* in diagnosis of OP and osteopenia were assessed by receiver operating characteristic curve, and their area under the curve (AUC) was compared with DeLong's test. RESULTS: The FF and R2* were statistically different among groups (F values of 102.521 and 11.323, both p < 0.05), and R2* were significantly correlated with FF and BMD, respectively (r values of -0.219 and 0.290, both p < 0.05). In diagnosis of OP and osteopenia, the AUCs were 0.776 and 0.778 for FF and 0.638 and 0.560 for R2*, and the AUCs of R2* were lower than those of FF, with Z values of 4.030 and 4.087, both p < 0.001. CONCLUSION: R2* is significantly correlated with FF and BMD and can be used as a complement to FF and BMD for quantitative assessment of OP. KEY POINTS: • R2* based on IDEAL-IQ sequences has a definite but weak linear relationship with FF and BMD. • FF is significantly correlated with BMD and can effectively evaluate BMAT. • R2* can be used as a complement to FF and BMD for fine quantification of bone mineral loss and bone marrow fat conversion.

Quantitative Study of Vertebral Body and Paravertebral Muscle Degeneration Based on Dual-Energy Computed Tomography: Correlation With Bone Mineral Density.

OBJECTIVES: This study aimed to quantify the degeneration of the vertebral body and paravertebral muscles using dual-energy computed tomography (DECT) and study its relationship with osteoporosis. METHODS: A total of 130 patients with chronic low back pain were included in this study, and DECT scanning of the lumbar region was undertaken prospectively. By placing a standard quantitative computed tomography corrected phantom under the waist during the DECT procedure, bone mineral density (BMD) and the following quantitative parameters were obtained: calcium density (CaD), vertebral fat fraction (VFF), psoas major area, psoas major fat fraction, erector spinalis area, and erector spinalis fat fraction (ESFF). Independent sample t test and 1-way analysis of variance were used between different age-BMD groups. Pearson test was applied to determine correlations for all measurements, and a mathematical model of BMD was established through regression analysis. RESULTS: Calcium density, VFF, psoas major area, psoas major fat fraction, erector spinalis area, and ESFF were significantly different among the age-BMD groups (P < 0.05), and BMD was significantly correlated with these parameters (P < 0.05). Calcium density, VFF, and ESFF were included in the BMD regression equation: BMD = 69.062 + 11.637 × CaD - 1.018 × VFF - 0.726 × ESFF (R2 = 0.860, F = 125.979, P < 0.001). CONCLUSIONS: Degeneration of the vertebral body and paravertebral muscles can be quantitatively analyzed using DECT, and CaD, VFF, and ESFF were independent influencing factors of BMD.

Inulin intervention attenuates hepatic steatosis in rats via modulating gut microbiota and maintaining intestinal barrier function.

Increasing evidence has suggested the mitigatory efficacy of prebiotic inulin on nonalcoholic fatty liver disease (NAFLD), nevertheless, its action mechanisms remain elusive. Herein, inulin consumption effectively ameliorated high-sucrose diet-induced hepatic steatosis and inflammation, and rehabilitated liver lipogenesis regulators, including carbohydrate response element-binding protein, stearoyl-CoA desaturase-1 and peroxisome proliferator-activated receptor alpha. Furthermore, inulin supplementation restored the intestinal barrier integrity and function by up-regulating expressions of tight junction proteins (zonula occludens-1, claudin-1 and occludin). High-throughput sequencing demonstrated that inulin administration regulated the gut microbiota composition, wherein abundance of short-chain fatty acid (SCFA)-producers, including Bifidobacterium, Phascolarctobacterium and Blautia, was significantly enhanced in the inulin-treated rats, conversely, opportunistic pathogens, such as Acinetobacter and Corynebacterium_1, were suppressed. SCFA quantitative analysis showed that dietary inulin suppressed faecal acetate levels, but improved propionate and butyrate concentrations in rats with NAFLD. Functional prediction showed that tryptophan metabolism was one of the key metabolic pathways affected by gut microbiota changes. A targeted metabolomics profiling of tryptophan metabolism demonstrated that inulin intervention up-regulated faecal contents of indole-3-acetic acid and kynurenic acid, whereas down-regulated levels of kynurenine and 5-hydoxyindoleacetic acid in NAFLD rats. Therefore, this study demonstrated that inulin intake alleviated hepatic steatosis likely by regulating the gut microbiota composition and function and restoring the intestinal barrier integrity, which may provide a novel notion for the prevention and treatment of NAFLD in future.

Accuracy and applicability of dual-energy computed tomography in quantifying vertebral bone marrow adipose tissue compared with magnetic resonance imaging.

OBJECTIVES: To evaluate the accuracy of dual-energy computed tomography (DECT) in quantifying bone marrow adipose tissue (BMAT) and its applicability in the study of osteoporosis (OP). METHODS: A total of 83 patients with low back pain (59.77 ± 7.46 years, 30 males) were enrolled. All patients underwent lumbar DECT and magnetic resonance imaging (MRI) scanning within 48 h, and the vertebral fat fraction (FF) was quantitatively measured, recorded as DECT-FF and MRI-FF. A standard quantitative computed tomography (QCT) phantom was positioned under the waist during DECT procedure to realize the quantization of bone mineral density (BMD). The intraclass correlation coefficient (ICC) and Bland-Altman method was used to evaluate the agreement between DECT-FF and MRI-FF. The Pearson test was used to study the correlation between DECT-FF, MRI-FF, and BMD. With BMD as a gold standard, the diagnostic efficacy of DECT-FF and MRI-FF in different OP degrees was compared by receiver operating characteristic (ROC) curve and DeLong test. RESULTS: The values of DECT-FF and MRI-FF agreed well (ICC = 0.918). DECT-FF and MRI-FF correlated with BMD, with r values of -0.660 and -0.669, respectively (p < 0.05). In the diagnosis of OP and osteopenia, the areas under curve (AUC) of DECT-FF was, respectively, 0.791 and 0.710, and that of MRI-FF was 0.807 and 0.708, and there was no significant difference between AUCs of two FF values (with Z values of 0.503 and 0.066, all p > 0.05). CONCLUSION: DECT can accurately quantify the BMAT of vertebrae and has the same applicability as MRI in the study of OP.

Retraction: application of hybrid particle swarm and ant colony optimization algorithms to obtain the optimum homomorphic wavelet image fusion.

[This retracts the article DOI: 10.21037/atm-20-5997.].

Use the right kidney contour as a landmark in adrenal vein sampling.

Adrenal Vein Sampling (AVS) is the gold standard for categorizing primary aldosteronism (PA). However, catheterization of the right adrenal vein (RAV) is challenging due the small size and variable location. This study aims to explore the relationship between the RAV orifice and the right kidney contour (RKC) on fluoroscopy, thus evaluating the potential of use the RKC as an anatomic marker for localizing RAV. Imaging data of 107 PA patients with successful bilateral AVS were retrospectively analyzed. Based on the body mass index (BMI), all patients were divided into the Normal Group (BMI < 24 kg/m2), Overweight Group (24 kg/m2 ≤ BMI < 28 kg/m2) and Obese Group (BMI ≥ 28 kg/m2). At the anterior view, the height level of RAV orifice was determined relative to vertebral bodies and disks. The distance from the RAV orifice to the upper edge of RKC was measured manually. The RAV orifice height level was mainly distributed from vertebral T11 to T12 (90.6%), and tended to be higher in patients with a larger BMI. The mean distance from the RAV orifice to the upper edge of RKC was 13.9±7.8mm, and had no difference among Normal group (n = 53, 14.1±8.2mm), Overweight group (n = 39, 13.7±8.0mm), and Obese group (n = 15, 13.9±5.5mm) (p = 0.981). Based on these findings, the RKC might be used as a landmark for localizing RAV on fluoroscopy, which is conductive to narrow down the exploration range and increase the success rate of RAV catheterization.

Kukoamine A Improves Mycoplasma pneumoniae Pneumonia by Regulating miR-222-3p/Superoxide Dismutase 2.

Mycoplasma pneumoniae pneumonia (MPP) represents a common respiratory disease in children patients. Kukoamine A (KuA) is a spermine alkaloid found in the Chinese herb Cortex Lycii radices, which has a variety of pharmacological properties. However, no study has been reported on the role of KuA in MPP. Exosomes, a type of lipid bilayer-enclosed extracellular vesicles, can be delivered to the target cells, where they regulate function and physiology. With the use of human alveolar basal epithelial cells (HABECs) as an in vitro model, in this study, we sought to characterize the changes in levels of superoxide dismutase 2 (SOD2) and proinflammatory cytokines including IL-6 and TNF-α in HABECs in response to exosomes, which were isolated from peripheral blood serum of MPP patients. We found that, compared to normal, MPP patients exhibited a significant up-regulated miR-222-3p. Further, exosomal miR-222-3p downregulated SOD2 activity but promoted nuclear NF-κB activity and expression of IL-6 and TNF-α in HABECs, ultimately leading to an oxidative stress condition. Interestingly, such stimulating effects were attenuated by the pretreatment of KuA. This study suggests a critical role possessed by KuA in MPP by regulating the miR-222-3p/SOD2 axis, which represents a promising strategy for the treatment of MPP.

Kukoamine A inhibits C-C motif chemokine receptor 5 to attenuate lipopolysaccharide-induced lung injury.

The aim of this study was to elucidate the mechanism underlying the effects of Kukoamine A (KuA) treatment on endotoxin-induced lung injury/inflammation. The study was performed in lipopolysaccharide (LPS)-exposed mouse models of lung injury and LPS-induced alveolar epithelial cell model. Relevant kits were used to detect levels of inflammation-related indicators, oxidative stress indicators, and mitochondrial function. Hematoxylin and eosin staining was to detect lung injury. Then, C-C motif chemokine receptor 5 (CCR5) overexpression plasmid was transfected into alveolar epithelial cells to investigate the mechanism of KuA in lung injury. The results showed that LPS induction increased the expression of inflammatory factors, oxidative stress markers, and mitochondrial dysfunction in both animal and cellular models. In the mouse model, KuA treatment improved lung tissue injury, decreased wet-to-dry ratio and MPO levels, reduced the expression of inflammatory factors, and ameliorated oxidative stress and mitochondrial dysfunction. The protective effect of KuA in the cell model remained whereas was markedly reversed after CCR5 overexpression. Taken together, KuA might improve LPS-induced lung injury by inhibiting CCR5. This might also provide a novel theory for KuA in the treatment of lung injury.

Intestinal bacteria flora changes in patients with Mycoplasma pneumoniae pneumonia with or without wheezing.

Mycoplasma pneumoniae (MP) infection is a common cause of community-acquired pneumonia in children. Furthermore, many children with Mycoplasma pneumoniae pneumonia (MPP) have recurrent wheezing and reduced small airway function after their clinical symptoms have resolved, eventually leading to asthma. MPP can trigger immune disorders and systemic inflammatory responses. Hence, the intestine is the largest immune organ of the body. Therefore, we sought to investigate whether the alteration of intestinal flora is correlated with the development of wheezing in children with MPP. We collected 30 healthy children as group A, 50 children with nonwheezing MPP as group B, and 50 children with wheezing MPP as group C. We found that the percentage of eosinophil cells (EC) was significantly higher in group C than that in group B for routine blood tests and serum inflammatory factors. The serum cytokines, including IL-4, IL-17, TNF-α, and TGF-ß, were significantly higher in group C than in group B. In addition, the level of IL-10 was significantly lower in group C than in group B. The distribution characteristics of intestinal flora strains in children with MPP were detected by sequencing of 16S rRNA gene amplicon sequencing. There were differences in the abundance of intestinal flora between children with MPP and healthy children, with lower abundance of Ruminococcus flavefaciens, Clostridium butyricum, Lactobacillus, and Bifidobacterium in the intestine of children with MPP compared to healthy children. The abundance of Ruminococcus flavefaciens and Clostridium butyricum was significantly lower in the intestine of children with wheezing MPP compared to children without wheezing MPP. In the correlation analysis between children with MPP and inflammatory factors, Ruminococcus flavefaciens was found to be negatively correlated with IL-17. Clostridium butyricum was negatively correlated with L-4, IL-17, TNF-α, and TGF-ß; however, it positively correlated with IL-10. Thus, it was concluded that alterations in intestinal flora play a crucial role in the immune response to MPP, where a significant decline in intestinal Ruminococcus flavefaciens and Clostridium butyricum leads to an exacerbation of the inflammatory responses, which may promote the development of children with wheezing MPP.

Interleukin-17 Weakens the NAFLD/NASH Process by Facilitating Intestinal Barrier Restoration Depending on the Gut Microbiota.

Interleukin-17 (IL-17) is associated with nonalcoholic fatty liver disease (NAFLD) and gut microbiota, and how IL-17 mediates the NAFLD/nonalcoholic steatohepatitis (NASH) process depending on the gut microbiota is unclear. We found that T helper 17 (TH17) cells were decreased in the small intestine in a methionine choline-deficient (MCD) diet-induced NASH model. IL-17-deficient (Il17-/-) mice showed alterations in intestinal microbiota, including the inhibition of probiotic growth and the overgrowth of certain pathogenic bacteria, and were prone to higher endotoxemia levels and more severe gastrointestinal barrier defects than wild-type (WT) mice. Furthermore, TH17 cells were responsible for restoring the intestinal barrier after administration of recombinant IL-17 to Il17-/- mice or injection of CD4+ T cells into a Rag1-/- mouse model. Additionally, transplantation of the microbiota from WT mice to Il17-/- mice restored the intestinal barrier. Notably, microbiota-depleted Il17-/- mice were resistant to MCD diet-induced intestinal barrier impairment. Fecal microbiota transplantation from Il17-/- mice to microbiota-depleted mice aggravated intestinal barrier impairment and then promoted the development of NASH. Collectively, this study showed that host IL-17 could strengthen intestinal mucosal barrier integrity and reduce dysbiosis-induced intestinal injury and secondary extraintestinal organ injury induced by a special diet. IMPORTANCE The morbidity of NASH has increased, with limited effective treatment options. IL-17 plays a protective role in the gut mucosa in high-fat-diet (HFD)-related metabolic disorders, and HFD-related microbiota dysbiosis is responsible for a decreased number of T helper 17 (TH17) cells in the lamina propria. The mechanism by which IL-17 mediates the NAFLD/NASH process depending on the gut microbiota is unclear. In our study, IL-17 originating from TH17 cells maintained intestinal barrier integrity and determined the outcomes of diet-related disease, which may be a target strategy for NAFLD/NASH.

Nonlinear dependence between China's carbon market and stock market: new evidence from quantile coherency and causality-in-quantiles.

This study examines the nonlinear dependence between carbon market and stock market in China under normal and extreme market conditions by employing two novel nonlinear approaches, namely, quantile coherency and causality-in-quantiles methods. Given our results on the overall and sector level of stock market, we find that there is a negative dependence between the two markets under bearish and normal market states in the short- and medium-term respectively, while the dependence becomes positive under bearish and bullish market states in the long-term. Furthermore, we also prove that the Granger causality from carbon market to stock market exists. However, no evident impacts from stock market to carbon market have been found. Additionally, at sector stock market, we discover heterogeneity across market conditions. And emission-intensive sector stock indices are more affected by carbon prices.

Hepatic Steatosis: CT-Based Prevalence in Adults in China and the United States and Associations With Age, Sex, and Body Mass Index.

BACKGROUND. Calibrated CT fat fraction (FFCT) measurements derived from un-enhanced abdominal CT reliably reflect liver fat content, allowing large-scale population-level investigations of steatosis prevalence and associations. OBJECTIVE. The purpose of this study was to compare the prevalence of hepatic steatosis, as assessed by calibrated CT measurements, between population-based Chinese and U.S. cohorts, and to investigate in these populations the relationship of steatosis with age, sex, and body mass index (BMI). METHODS. This retrospective study included 3176 adults (1985 women and 1191 men) from seven Chinese provinces and 8748 adults (4834 women and 3914 men) from a single U.S. medical center, all drawn from previous studies. All participants were at least 40 years old and had undergone unenhanced abdominal CT in previous studies. Liver fat content measurements on CT were cross-calibrated to MRI proton density fat fraction measurements using phantoms and expressed as adjusted FFCT measurements. Mild, moderate, and severe steatosis were defined as adjusted FFCT of 5.0-14.9%, 15.0-24.9%, and 25.0% or more, respectively. The two cohorts were compared. RESULTS. In the Chinese and U.S. cohorts, the median adjusted FFCT for women was 4.7% and 4.8%, respectively, and that for men was 5.8% and 6.2%, respectively. In the Chinese and U.S. cohorts, steatosis prevalence for women was 46.3% and 48.7%, respectively, whereas that for men was 58.9% and 61.9%, respectively. Severe steatosis prevalence was 0.9% and 1.8% for women and 0.2% and 2.6% for men in the Chinese and U.S. cohorts, respectively. Adjusted FFCT did not vary across age decades among women or men in the Chinese cohort, although it increased across age decades among women and men in the U.S. cohort. Adjusted FFCT and BMI exhibited weak correlation (r = 0.312-0.431). Among participants with normal BMI, 36.8% and 38.5% of those in the Chinese and U.S. cohorts, respectively, had mild steatosis, and 3.0% and 1.5% of those in the Chinese and U.S. cohorts, respectively, had moderate or severe steatosis. Among U.S. participants with a BMI of 40.0 or greater, 17.7% had normal liver content. CONCLUSION. Steatosis and severe steatosis had higher prevalence in the U.S. cohort than in the Chinese cohort in both women and men. BMI did not reliably predict steatosis. CLINICAL IMPACT. The findings provide new information on the dependence of hepatic steatosis on age, sex, and BMI.

The benefits of sacubitril-valsartan in patients with acute myocardial infarction: a systematic review and meta-analysis.

AIMS: We aimed to investigate whether sacubitril-valsartan could further improve the prognosis, cardiac function, and left ventricular (LV) remodelling in patients following acute myocardial infarction (AMI). METHODS AND RESULTS: We searched the PubMed, Embase, Cochrane Library, and China National Knowledge Infrastructure (CNKI) from inception to 10 May 2021 to identify potential articles. Randomized controlled trials (RCTs) meeting the inclusion criteria were included and analysed. Thirteen RCTs, covering 1358 patients, were analysed. Compared with angiotensin-converting enzyme inhibitors (ACEI)/angiotensin receptor blockers (ARB), sacubitril-valsartan did not significantly reduced the cardiovascular mortality [risk ratio (RR) 0.65, 95% confidence interval (CI) 0.22 to 1.93, P = 0.434] and the rate of myocardial reinfarction (RR 0.65, 95% CI 0.29 to 1.46, P = 0.295) of patients following AMI, but the rate of hospitalization for heart failure (HF) (RR 0.48, 95% CI 0.35 to 0.66, P < 0.001) and the change of LV ejection fraction (LVEF) [weighted mean difference (WMD) 5.49, 95% CI 3.62 to 7.36, P < 0.001] were obviously improved. The N-terminal pro-brain natriuretic peptide (NT-ProBNP) level (WMD -310.23, 95% CI -385.89 to -234.57, P < 0.001) and the LV end-diastolic dimension (LVEDD) (WMD -3.16, 95% CI -4.59 to -1.73, P < 0.001) were also significantly lower in sacubitril-valsartan group than in ACEI/ARB group. Regarding safety, sacubitril-valsartan did not increase the risk of hypotension, hyperkalaemia, angioedema, and cough. CONCLUSIONS: This meta-analysis suggests that early administration of sacubitril-valsartan may be superior to conventional ACEI/ARB to decrease the risk of hospitalization for HF, improve the cardiac function, and reverse the LV remodelling in patients following AMI.

Dual-Energy Computed Tomography Virtual Noncalcium Technique in Diagnosing Osteoporosis: Correlation With Quantitative Computed Tomography.

OBJECTIVE: The aim of this study was to evaluate dual-energy computed tomography (CT) virtual noncalcium (VNCa) technique as a means of quantifying osteoporosis. METHODS: Dual-energy CT scans were obtained prospectively, targeting lumbar regions of 55 patients with chronic low back pain. A standard quantitative CT (QCT) phantom was positioned at the waist during each procedure, using proprietary software (QCT Pro; Mindways, Tex) to measure bone mineral density (BMD) in each vertebral body. Vendor dual-energy analytic software was altered with a specially modified configuration file to produce a "Virtual Non Calcium" or "VNCa" output, as such output variables were remapped to produce the following calcium values rather than iodine, yielding the following QCT parameters: CT value of calcium (originally "contrast media" [CM]), CT value of mixed energy imaging (regular CT value [rCT]), calcium density (originally "contrast agent density" [CaD]), and fat fraction (FF). Pearson test served to assess correlations between BMD and these parameters. Multiple linear regression analysis was applied to construct an equation for generating regressive BMD (rBMD) values. In gauging diagnostic accuracies, the criterion-standard BMD cutoff point (<80 mg/cm3) was adopted for QCT, whereas the rBMD threshold was defined by receiver operating characteristic curve. RESULTS: Contrast media, rCT, CaD, and FF values (reflecting CT value of calcium, regular CT value, calcium density, and fat fraction, respectively) significantly correlated with BMD (r values: 0.885, 0.947, 0.877, and 0.492, respectively; all P < 0.01). Contrast media, CaD, and FF showed independent associations with BMD; the regressive equation was formulated as follows: rBMD = 54.82 - 0.19 × CM + 20.03 × CaD - 1.24 × FF. The area under the curve of rBMD in diagnosing osteoporosis was 0.966 ± 0.009 (P < 0.01). At an rBMD threshold of less than 81.94 mg/cm3, sensitivity and specificity were 90.0% and 92.0%, respectively. CONCLUSIONS: Dual-energy CT VNCa technique may constitute a valid alternative method for quantifying the mineral content and marrow fat composition of bone in diagnostic assessments of osteoporosis.

Schisandrin B Attenuates Airway Inflammation and Airway Remodeling in Asthma by Inhibiting NLRP3 Inflammasome Activation and Reducing Pyroptosis.

Asthma is a chronic inflammatory disorder of the airways. Schisandrin B (SB) is the main effective component. This study investigated the effects of SB on airway inflammation and airway remodeling in asthma. The rat model of asthma was established. The rats were treated with SB to evaluate the effects of SB on airway inflammation, airway remodeling, NLRP3 inflammasome activation, and pyroptosis. Alveolar macrophages of rats were isolated, and the macrophage inflammatory model was established by lipopolysaccharide (LPS) induction. The LPS-induced macrophages were treated with SB. The binding relationship between miR-135a-5p and TPRC1 was analyzed. LPS + SB-treated macrophages were transfected with miR-135a-5p inhibitor. The expressions of key factors of the STAT3/NF-κB pathway were detected. SB reduced airway inflammation and airway remodeling in asthmatic rats. SB inhibited NLRP3 inflammasome activation and reduced pyroptosis in asthmatic rats and LPS-induced macrophages. SB reversely regulated the miR-135a-5p/TRPC1 axis. Downregulation of miR-135a-5p attenuated the inhibitory effect of SB on NLRP3 inflammasome activation. SB inhibited the STAT3/NF-κB pathway via the miR-135a-5p/TRPC1 axis. In conclusion, SB inhibited NLRP3 inflammasome activation and reduced pyroptosis via the miR-135a-5p/TRPC1/STAT3/NF-κB axis, thus alleviating airway inflammation and airway remodeling in asthma. This study may confer novel insights for the management of asthma.