Effect of Oxygen-Glucose Deprivation of Microglia-Derived Exosomes on Hippocampal Neurons: A Study on miR-124 and Inflammatory Cytokines.

Stroke is a cerebrovascular disease that threatens human health. Developing safe and effective drugs and finding therapeutic targets has become an urgent scientific problem. The aim of this study was to investigate the effect of oxygen-glucose deprivation of the microglia-derived exosome on hippocampal neurons and its relationship to miR-124 in the exosome. We incubated hippocampal neurons with exosomes secreted by oxygen-glucose deprivation/ reoxygenation (OGD/R) microglia. The levels of glutamic acid (GLU) and gamma-aminobutyric acid (GABA) in the culture supernatant were detected by ELISA. CCK-8 was used to measure neuronal survival rates. The mRNA levels of TNF-α and IL-6 were detected by RT-qPCR to evaluate the effect of exosomes on neurons. RT-qPCR was then used to detect miR-124 in microglia and their secreted exosomes. Finally, potential targets of miR-124 were analyzed through database retrieval, gene detection with dual luciferase reporters, and western blotting experiments. The results showed that the contents of GLU, TNF-α and IL-6 mRNA increased in the supernatant of cultured hippocampal neurons, the content of GABA decreased, and the survival rate of neurons decreased. Oxygen-glucose deprivation increases miR-124 levels in microglia and their released exosomes. miR-124 acts as a target gene on cytokine signaling suppressor molecule 1(SOCS1), while miR-124 inhibitors reduce the expression of TNF-α and IL-6 mRNA in neurons. These results suggest that oxygen- and glucose-deprived microglia regulate inflammatory cytokines leading to reduced neuronal survival, which may be achieved by miR-124 using SOCS1 as a potential target.

Long-term benefits of hematopoietic stem cell-based macrophage/microglia delivery of GDNF to the CNS in a mouse model of Parkinson's disease.

Glial cell line-derived neurotrophic factor (GDNF) protects dopaminergic neurons in various models of Parkinson's disease (PD). Cell-based GDNF gene delivery mitigates neurodegeneration and improves both motor and non-motor functions in PD mice. As PD is a chronic condition, this study aims to investigate the long-lasting benefits of hematopoietic stem cell (HSC)-based macrophage/microglia-mediated CNS GDNF (MMC-GDNF) delivery in an MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) mouse model. The results indicate that GDNF treatment effectively ameliorated MPTP-induced motor deficits for up to 12 months, which coincided with the protection of nigral dopaminergic neurons and their striatal terminals. Also, the HSC-derived macrophages/microglia were recruited selectively to the neurodegenerative areas of the substantia nigra. The therapeutic benefits appear to involve two mechanisms: (1) macrophage/microglia release of GDNF-containing exosomes, which are transferred to target neurons, and (2) direct release of GDNF by macrophage/microglia, which diffuses to target neurons. Furthermore, the study found that plasma GDNF levels were significantly increased from baseline and remained stable over time, potentially serving as a convenient biomarker for future clinical trials. Notably, no weight loss, altered food intake, cerebellar pathology, or other adverse effects were observed. Overall, this study provides compelling evidence for the long-term therapeutic efficacy and safety of HSC-based MMC-GDNF delivery in the treatment of PD.

VEGF overexpression in transplanted NSCs promote recovery of neurological function in rats with cerebral ischemia by modulating the Wnt signal transduction pathway.

Neural stem cell transplantation is a good method to treat stroke, but the mechanism is still unclear. Therefore, this study aims to explore the regulatory mechanism of VEGF overexpression in transplanted NSCs to promote the recovery of neural function in ischemic rats by regulating Wnt signal transduction pathways. We amplified VEGF gene fragments by PCR and transfected them into NSCs with Ad5 adenovirus. Rat brain IRI model was established by MCAO method, and VEGF transfected NSCs (VEGF-NSCs) were transplanted 24 h after successful IRI model. One week after the transplant, cognitive function was assessed using a neurological deficit score; Brain injury was assessed by histopathology; Photochemical and ELISA methods were used to detect oxidative stress markers and inflammatory factors, respectively. Western blotting has been detected in molecules of the Wnt signaling pathway. The results showed that the transduced NSCs express VEGF at least for 14 days. VEGF-NSCs transplantation (VNT) improved spatial learning and memory in rats, and inhibited oxidative stress injury, inflammatory response, and histopathological injury. VNT also resulted in significant changes in the phosphorylation levels of ß-catenin and GSK-3ß proteins, ultimately triggering activation of the Wnt signal transduction pathway. These results suggest that the neuroprotective effects of VNT may be related to the regulation of the Wnt signal transduction pathway.

Targeting lysine demethylase 6B ameliorates ASXL1 truncation-mediated myeloid malignancies in preclinical models.

ASXL1 mutation frequently occurs in all forms of myeloid malignancies and is associated with aggressive disease and poor prognosis. ASXL1 recruits Polycomb repressive complex 2 (PRC2) to specific gene loci to repress transcription through trimethylation of histone H3 on lysine 27 (H3K27me3). ASXL1 alterations reduce H3K27me3 levels, which results in leukemogenic gene expression and the development of myeloid malignancies. Standard therapies for myeloid malignancies have limited efficacy when mutated ASXL1 is present. We discovered upregulation of lysine demethylase 6B (KDM6B), a demethylase for H3K27me3, in ASXL1-mutant leukemic cells, which further reduces H3K27me3 levels and facilitates myeloid transformation. Here, we demonstrated that heterozygous deletion of Kdm6b restored H3K27me3 levels and normalized dysregulated gene expression in Asxl1Y588XTg hematopoietic stem/progenitor cells (HSPCs). Furthermore, heterozygous deletion of Kdm6b decreased the HSPC pool, restored their self-renewal capacity, prevented biased myeloid differentiation, and abrogated progression to myeloid malignancies in Asxl1Y588XTg mice. Importantly, administration of GSK-J4, a KDM6B inhibitor, not only restored H3K27me3 levels but also reduced the disease burden in NSG mice xenografted with human ASXL1-mutant leukemic cells in vivo. This preclinical finding provides compelling evidence that targeting KDM6B may be a therapeutic strategy for myeloid malignancies with ASXL1 mutations.

Acupoint thread-embedding for children with tic disorders of spleen deficiency and liver hyperactivity and its effect on serum level of NSE. / ç©´ä½åŸ‹çº¿æ²»ç–—å„¿ç«¥è„¾è™šè‚æ—ºåž‹æŠ½åŠ¨éšœç¢çš„ä¸´åºŠç–—æ•ˆåŠå¯¹è¡€æ¸ NSE水平的影响.

OBJECTIVES: To observe the clinical efficacy of acupoint thread-embedding for children with tic disorders of spleen deficiency and liver hyperactivity and its effect on serum level of neuron-specific enolase (NSE). METHODS: A total of 68 children with tic disorders of spleen deficiency and liver hyperactivity were randomized into an observation group (34 cases, 1 case dropped out) and a control group (34 cases, 3 cases dropped out, 1 case was eliminated). In the observation group, acupoint thread-embedding was applied at Baihui (GV 20) and bilateral Hegu (LI 4), Taichong (LR 3), Pishu (BL 20), Ganshu (BL 18), Quchi (LI 11), Zusanli (ST 36),etc., once every 4 weeks. In the control group, tiapride hydrochloride tablet was given orally, twice a day. Both groups were treated for 12 weeks. Before and after treatment, the Yale global tic severity scale (YGTSS) score and serum level of NSE were observed in the two groups, and the clinical efficacy was evaluated. RESULTS: After treatment, except for vocal tic score of YGTSS in the control group, the each-item scores and total scores of YGTSS and serum levels of NSE in the two groups were decreased compared with those before treatment (P<0.05); the each-item scores and total score of YGTSS and serum level of NSE in the observation group were lower than those in the control group (P<0.05). The total effective rate in the observation group was 87.9% (29/33), which was higher than 76.7% (23/30) in the control group (P<0.05). CONCLUSIONS: Acupoint thread-embedding has a good effect in the treatment of children with tic disorders of spleen deficiency and liver hyperactivity, could reduce the YGTSS score and serum level of NSE.

ASXL1 mutations are associated with a response to alvocidib and 5-azacytidine combination in myelodysplastic neoplasms.

Inhibitors of anti-apoptotic BCL-2 family proteins in combination with chemotherapy and hypomethylating agents (HMAs) are promising therapeutic approaches in acute myeloid leukemia (AML) and high-risk myelodysplastic syndromes (MDS). Alvocidib, a cyclin-dependent kinase 9 (CDK9) inhibitor and indirect transcriptional repressor of the anti-apoptotic factor MCL-1, has previously shown clinical activity in AML. Availability of biomarkers for response to the alvocidib + 5- AZA could also extend the rationale of this treatment concept to high-risk MDS. In this study, we performed a comprehensive in vitro assessment of alvocidib and 5-AZA effects in n=45 high-risk MDS patients. Our data revealed additive cytotoxic effects of the combination treatment. Mutational profiling of MDS samples identified ASXL1 mutations as predictors of response. Further, increased response rates were associated with higher gene-expression of the pro-apoptotic factor NOXA in ASXL1 mutated samples. The higher sensitivity of ASXL1 mutant cells to the combination treatment was confirmed in vivo in ASXL1Y588X transgenic mice. Overall, our study demonstrated augmented activity for the alvocidib + 5-AZA combination in higher-risk MDS and identified ASXL1 mutations as a biomarker of response for potential stratification studies.

Loss of BRD4 induces cell senescence in HSC/HPCs by deregulating histone H3 clipping.

Bromodomain-containing protein 4 (BRD4) is overexpressed and functionally implicated in various myeloid malignancies. However, the role of BRD4 in normal hematopoiesis remains largely unknown. Here, utilizing an inducible Brd4 knockout mouse model, we find that deletion of Brd4 (Brd4Δ/Δ ) in the hematopoietic system impairs hematopoietic stem cell (HSC) self-renewal and differentiation, which associates with cell cycle arrest and senescence. ATAC-seq analysis shows increased chromatin accessibility in Brd4Δ/Δ hematopoietic stem/progenitor cells (HSC/HPCs). Genome-wide mapping with cleavage under target and release using nuclease (CUT&RUN) assays demonstrate that increased global enrichment of H3K122ac and H3K4me3 in Brd4Δ/Δ HSC/HPCs is associated with the upregulation of senescence-specific genes. Interestingly, Brd4 deletion increases clipped H3 (cH3) which correlates with the upregulation of senescence-specific genes and results in a higher frequency of senescent HSC/HPCs. Re-expression of BRD4 reduces cH3 levels and rescues the senescence rate in Brd4Δ/Δ HSC/HPCs. This study unveils an important role of BRD4 in HSC/HPC function by preventing H3 clipping and suppressing senescence gene expression.

A self-assembled DNA double-crossover-based fluorescent aptasensor for highly sensitivity and selectivity in the simultaneous detection of aflatoxin M1 and aflatoxin B1.

Realizing the simultaneous speedy detection of multiple mycotoxins in contaminated food and feed is of great practical importance in the domain of food manufacturing and security. Herein, a fluorescent aptamer sensor based on self-assembled DNA double-crossover was developed and used for effective simultaneous quantitative detection of aflatoxins M1 and B1 by fluorescence resonance energy transfer (FRET). Fluorescent dye-modified aflatoxin M1 and B1 aptamers are selected as recognition elements and signal probes, and DNA double crosses are consistently locked by the aflatoxin aptamers, which results in a "turn-off" of the fluorescent signal. In the presence of AFM1 and AFB1, the aptamer sequences are more inclined to form Apt-AFM1 and Apt-AFB1 complexes, and the fluorescent probes are released from the DNA double-crossing platform, leading to an enhanced fluorescent signal (Cy3: 568 nm; Cy5: 660 nm). Under the optimal conditions, the signal response of the constructed fluorescent aptamer sensor showed good linearity with the logarithm of AFM1 and AFB1 concentrations, with detection limits of 6.24 pg/mL and 9.0 pg/mL, and a wide linear range of 0.01-200 ng/mL and 0.01-150 ng/mL, respectively. In addition, the effect of potential interfering substances in real samples was analyzed, and the aptasensor presented a good interference immunity. Moreover, by modifying and designing aptamer probes, the sensor can be applied to high-throughput simultaneous screening of other analytes, providing a new approach for the development of fluorescent aptamer sensors.

Chemodivergent Tandem Radical Cyclization of Alkene-Substituted Quinazolinones: Rapid Access to Mono- and Di-Alkylated Ring-Fused Quinazolinones.

Chemodivergent tandem radical cyclization offers exciting possibilities for the synthesis of structurally diverse cyclic compounds. Herein, we revealed a chemodivergent tandem cyclization of alkene-substituted quinazolinones under metal- and base-free conditions, this transformation is initiated by alkyl radicals produced from oxidant-induced α-C(sp3 )-H functionalization of alkyl nitriles or esters. The reaction resulted in the selective synthesis of a series of mono- and di-alkylated ring-fused quinazolinones by modulating the loading of oxidant, reaction temperature, and reaction time. Mechanistic investigations show that the mono-alkylated ring-fused quinazolinones is constructed by the key process of 1,2-hydrogen shift, whereas the di-alkylated ring-fused quinazolinones is mainly achieved through crucial steps of resonance and proton transfer. This protocol is the first example of remote second alkylation on the aromatic ring via α-C(sp3 )-H functionalization and difunctionalization achieved by association of two unsaturated bonds in radical cyclization.

Impact of sinonasal anatomic changes after endoscopic anterior skull base surgery on nasal airflow and air conditioning: a computational fluid dynamics study / 中华耳鼻咽喉头颈外科杂志

Objective: To analyze the impact of the sinonasal anatomic changes after endonasal endoscopic anterior skull base surgery on the nasal airflow and heating and humidification by computational fluid dynamics (CFD), and to explore the correlation between the postoperative CFD parameters and the subjective symptoms of the patients. Methods: The clinical data in the Rhinology Department of the First Affiliated Hospital of Zhengzhou University from 2016 to 2021 were retrospectively analyzed. The patients received the endoscopic resection of the anterior skull base tumor were selected as the case group, and the adults whose CT scans had no sinonasal abnormalities were chosen as the control group. The CFD simulation was performed on the sinonasal models after reconstructed from the patients' sinus CT images during the post-surgical follow-up. All the patients were asked to complete the Empty Nose Syndrome 6-Item Questionnaire (ENS6Q) to assess the subjective symptoms. The comparison between two independent groups and the correlation analysis were carried out by using the Mann-Whitney U test and the Spearman correlation test in the SPSS 26.0 software. Results: Nineteen patients (including 8 males and 11 females, from 22 to 67 years old) in the case group and 2 patients (a male of 38 years old and a female of 45 years old) in the control group were enrolled in this study. After the anterior skull base surgery, the high-speed airflow moved to the upper part of the nasal cavity, and the lowest temperature shifted upwards on the choana. Comparing with the control group, the ratio of nasal mucosal surface area to nasal ventilation volume in the case group decreased [0.41 (0.40, 0.41) mm-1 vs 0.32 (0.30, 0.38) mm-1; Z=-2.04, P=0.041], the air flow in the upper and middle part of the nasal cavity increased [61.14 (59.78, 62.51)% vs 78.07 (76.22, 94.43)%; Z=-2.28, P=0.023], the nasal resistance decreased [0.024 (0.022, 0.026) Pa·s/ml vs 0.016 (0.009, 0.018) Pa·s/ml; Z=-2.29, P=0.022], the lowest temperature in the middle of the nasal cavity decreased [28.29 (27.23, 29.35)℃ vs 25.06 (24.07, 25.50)℃; Z=-2.28, P=0.023], the nasal heating efficiency decreased [98.74 (97.95, 99.52)% vs 82.16 (80.24, 86.91)%; Z=-2.28, P=0.023], the lowest relative humidity decreased [(79.62 (76.55, 82.69)% vs 73.28 (71.27, 75.05)%; Z=-2.28, P=0.023], and the nasal humidification efficiency decreased [99.50 (97.69, 101.30)% vs 86.09 (79.33, 87.16)%; Z=-2.28, P=0.023]. The ENS6Q total scores of all patients in the case group were less than 11 points. There was a moderate negative correlation between the proportion of the inferior airflow in the post-surgical nasal cavity negatively and the ENS6Q total scores (rs=-0.50, P=0.029). Conclusions: The sinonasal anatomic changes after the endoscopic anterior skull base surgery alter the nasal airflow patterns, reducing the efficiency of nasal heating and humidification. However, the post-surgical occurrence tendency of the empty nose syndrome is weak.

Recent progress in the radical α-C(sp3)-H functionalization of ketones.

The direct use structurally simple ketones as α-ketone radical sources for α-C(sp3)-H functionalization is a sustainable and powerful approach for constructing complex and multifunctional chemical scaffolds with diverse applications. The reactions of α-ketone radicals with alkenes, alkynes, enynes, imides, and imidazo[1,2-a]pyridines have broadened the structural diversity and complexity of ketones. Through chosen illustrative examples, we outline the recent progress in the development of methods that enable the radical α-C(sp3)-H functionalization of ketones, with an emphasis on radical initiation systems and possible mechanisms of the transformations. The application of these strategies is illustrated by the synthesis of several biologically active molecules and drug molecules. Further subdivision is based on substrate type and reaction type.

Selective divergent radical cyclization of 1,6-dienes with alkyl nitriles.

An efficient, selective, and step economical radical cyclization of 1,6-dienes with alkyl nitriles initiated by α-C(sp3)-H functionalization under the Sc(OTf)3 and Ag2CO3 system is described here. The selective divergent cyclization relies on the substitution effect at the α-position of the acrylamide moiety and nitriles, which is terminated by hydrogen abstraction, direct cyclization with the aryl ring, or further cyclization with the CN bond and hydrolysis, respectively.

The construction of benzimidazo[2,1-a]isoquinolin-6(5H)-ones from N-methacryloyl-2-phenylbenzoimidazoles through radical strategies.

Benzimidazo[2,1-a]isoquinolin-6(5H)-one constitutes a structurally unique class of tetracyclic N-heterocycles that are found throughout a myriad of biologically active natural products, pharmaceutical compounds, and functional materials. Various synthetic routes for the preparation of benzimidazo[2,1-a]isoquinolin-6(5H)-ones have been reported. In particular, the use of N-methacryloyl-2-phenylbenzoimidazoles to construct benzimidazo[2,1-a]isoquinolin-6(5H)-ones through various radical strategies have attracted widespread attention due to the versatility and simple preparation of raw materials, as well as the step-economy and mild reaction conditions. Using representative examples, we highlight significant progress in the synthesis of benzimidazo[2,1-a]isoquinolin-6(5H)-ones, including the selection of the catalytic system, substrate scope, mechanistic understanding, and applications. The contents of this review focus on the development of C-, S-, P-, and Si-centered radical addition-intramolecular cyclization strategies.

INTS11 regulates hematopoiesis by promoting PRC2 function.

INTS11, the catalytic subunit of the Integrator (INT) complex, is crucial for the biogenesis of small nuclear RNAs and enhancer RNAs. However, the role of INTS11 in hematopoietic stem and progenitor cell (HSPC) biology is unknown. Here, we report that INTS11 is required for normal hematopoiesis and hematopoietic-specific genetic deletion of Ints11 leads to cell cycle arrest and impairment of fetal and adult HSPCs. We identified a novel INTS11-interacting protein complex, Polycomb repressive complex 2 (PRC2), that maintains HSPC functions. Loss of INTS11 destabilizes the PRC2 complex, decreases the level of histone H3 lysine 27 trimethylation (H3K27me3), and derepresses PRC2 target genes. Reexpression of INTS11 or PRC2 proteins in Ints11-deficient HSPCs restores the levels of PRC2 and H3K27me3 as well as HSPC functions. Collectively, our data demonstrate that INTS11 is an essential regulator of HSPC homeostasis through the INTS11-PRC2 axis.

Sulfonyl radical triggered selective iodosulfonylation and bicyclization of 1,6-dienes.

A novel sulfonyl radical triggered selective iodosulfonylation and bicyclization of 1,6-dienes has been described for the first time. High selectivity and efficiency, mild reaction conditions, excellent functional group compatibility, and broad substrate scope are the attractive features of this synthetic protocol, which provides a unique platform for precise radical cyclization.

Pan-cancer analysis identifies ITIH1 as a novel prognostic indicator for hepatocellular carcinoma.

Although a previous pan-cancer study has reported the expression patterns of ITIHs in various tumors, their analyses have been restricted to limited cancer types. We thus comprehensively analyzed the expression profiles and clinical significances of ITIHs in a broader spectrum of cancers from TCGA. Our results showed that ITIHs were primarily down-regulated in tested cancers. The ITIH members were associated with either survival advantage or disadvantage, depending on the cancer type tested and the genes queried. Importantly, we for the first time demonstrated that ITIH1 had substantially decreased expression in liver hepatocellular carcinoma (LIHC) compared with corresponding normal tissue, and its down-regulation adversely impacted patient outcome. Moreover, ITIH1 expression was consistently declining during the progression of LIHC. Further analysis revealed that ITIH1 may be involved in cellular metabolic processes. Our findings established ITIH1 as a potential diagnostic and prognostic biomarker for LIHC, which awaits future experimental validation.

Assessment of heart's changes of elite Chinese male weightlifter by speckle tracking echocardiography / 北京大学学报(医学版)

OBJECTIVE@#To evaluate the changes of heart structure and function in elite Chinese weightlifters by spot tracking technique.@*METHODS@#Chinese elite male weightlifters (weightlifter group, n=16) and age-matched healthy men (control group, n=16) were included as subjects. Transthoracic echocardiography and speckle-tracking automatic functional imaging were used for two-dimensional myocardial strain measurements.@*RESULTS@#The thickness of septum and left ventricular (LV) posterior wall and the myocardial mass index of LV were all higher than those of the control group [(9.3±1.3) mm vs. (8.0±0.4) mm, (9.2±0.8) mm vs. (8.0±0.8) mm, (77.8±12.8) g/m2 vs. (67.8±11.2) g/m2, all P < 0.05]. Although the LV ejection fraction (LVEF) and global long axis strain value (LVGLS) were not significantly different from those in the control group, the LV mean Sm and Em reflecting the systolic and diastolic functions of the LV were lower than those in the control group (P < 0.05). Further myocardial strain analysis showed that the absolute value of the long axial strain of the basal anteroseptal and mid-inferoseptal segments of the weightlifters were significantly lower than those of the control group [|(-15.1±4.2)%|vs.|(-18.7±3.0)%|, |(-18.8±2.6)%|vs.|(-21.3±2.8)%|, all P < 0.05]. There was no significant difference in other segments. The athletes were divided into two groups according to their best performance in the National Youth Games. The athletes were divided into two sub-groups according to their performance in the National Youth Games. The thickness of the septum in the sub-group with better performance (who ranked the 1st to 8th) was larger [(10.2±1.1) mm vs. (8.5±1.0) mm, P < 0.05], and the absolute value of the long-axis strain in the mid-inferoseptal segment was lower [|(-17.1±2.1)%|vs.|(-20.4±2.1)%|, P < 0.05].@*CONCLUSION@#The thickening of septum is more obvious in the excellent weightlifters, accompanied by the decrease of myocardial systolic function. The speckle-tracking technique of echocardiography can identify the changes of the heart structure and function of elite athletes at an early stage, which may provide a basis for sports medicine supervision and the selection of excellent talents.

Left ventricular function and remodeling assessed by echocardiography and cardiac magnetic resonance imaging in Chinese weightlifter athletes / 中华心血管病杂志

Objectives: To explore the impact of strength sport on heart structure by echocardiography (ECHO) and cardiac resonance imaging (CMR). Methods: This is a case control study. A total of 14 male weightlifter athletes who underwent physical examination in Peking University Third Hospital from January 16, 2019 to November 1, 2019 were included in this study. Fourteen age-matched healthy Chinese men served as the control group. ECHO and CMR were used to detect the heart structure and function of the participants. Results: The age of athlete group was (21±3) years, and the training time was (9±4) years. The weekly exercise time of athlete group was more than 15 hours, while that of control group was less than 3 hours. ECHO-derived interventricular septal (IVS) thickness value ((9.3±1.3) mm vs. (8.1±0.5) mm, P=0.006) and CMR-derived IVS value ((11.0±1.5) mm vs. (10.0±0.5) mm, P=0.003) was both significantly higher in the athlete group than in the control group. For the athlete group, the indicators of left ventricular volume measured by ECHO (left ventricular end diastolic volume (LVEDV), left ventricular end diastolic volume index (LVEDVI), left ventricular end systolic volume, left ventricular end systolic volume index) and IVS thickness were significantly lower than those measured by CMR (all P<0.05). Left ventricular ejection fraction ((67.0±3.8)% vs. (59.0±3.9)%, P<0.001) and left ventricular global longitudinal strain ((19.3±2.9)% vs. (11.2±1.2)%, P<0.001) values measured by ECHO were significantly higher than those measured by CMR. There was no significant difference in the proportion of subjects with the left ventricular end diastolic diameter, LVEDV and LVEDVI above the upper limit of normal as measured by ECHOs and CMR (all P>0.05). IVS values measured by ECHO were all within the normal range, and CMR showed that 9 (9/14) weightlifter athletes had IVS>11 mm with a maximum thickness of 13.8 mm, which occurred in the inferoseptum. Conclusion: Weightlifter sport could result in thickening of the left ventricular inferoseptum, and CMR is superior to ECHO in detecting the thickening of the left ventricular wall, which serves as a helpful tool for sports medicine supervision.

Predictive model for acute abdominal pain after transarterial chemoembolization for liver cancer.

BACKGROUND: Transarterial chemoembolization (TACE) is the first-line treatment for patients with unresectable liver cancer; however, TACE is associated with postembolization pain. AIM: To analyze the risk factors for acute abdominal pain after TACE and establish a predictive model for postembolization pain. METHODS: From January 2018 to September 2018, all patients with liver cancer who underwent TACE at our hospital were included. General characteristics; clinical, imaging, and procedural data; and postembolization pain were analyzed. Postembolization pain was defined as acute moderate-to-severe abdominal pain within 24 h after TACE. Logistic regression and a classification and regression tree were used to develop a predictive model. Receiver operating characteristic curve analysis was used to examine the efficacy of the predictive model. RESULTS: We analyzed 522 patients who underwent a total of 582 TACE procedures. Ninety-seven (16.70%) episodes of severe pain occurred. A predictive model built based on the dataset from classification and regression tree analysis identified known invasion of blood vessels as the strongest predictor of subsequent performance, followed by history of TACE, method of TACE, and history of abdominal pain after TACE. The area under the receiver operating characteristic curve was 0.736 [95% confidence interval (CI): 0.682-0.789], the sensitivity was 73.2%, the specificity was 65.6%, and the negative predictive value was 92.4%. Logistic regression produced similar results by identifying age [odds ratio (OR) = 0.971; 95%CI: 0.951-0.992; P = 0.007), history of TACE (OR = 0.378; 95%CI: 0.189-0.757; P = 0.007), history of abdominal pain after TACE (OR = 6.288; 95%CI: 2.963-13.342; P < 0.001), tumor size (OR = 1.978; 95%CI: 1.175-3.330; P = 0.01), multiple tumors (OR = 2.164; 95%CI: 1.243-3.769; P = 0.006), invasion of blood vessels (OR = 1.756; 95%CI: 1.045-2.950; P = 0.034), and TACE with drug-eluting beads (DEB-TACE) (OR = 2.05; 95%CI: 1.260-3.334; P = 0.004) as independent predictive factors for postembolization pain. CONCLUSION: Blood vessel invasion, TACE history, TACE with drug-eluting beads, and history of abdominal pain after TACE are predictors of acute moderate-to-severe pain. The predictive model may help medical staff to manage pain.