Clinical characteristics of delirium in older patients with first-ever acute myocardial infarction who underwent percutaneous coronary intervention : A retrospective study.

OBJECTIVES: Delirium is a serious complication of cardiac surgery and a common clinical problem. The study aimed to identify the incidence, risk factors, and outcomes of delirium in older patients (≥ 65 years) with first-ever acute myocardial infarction (AMI) who underwent percutaneous coronary intervention (PCI). METHODS: A retrospective cohort study was performed in a hospital in northern China. A total of 1033 older patients with first-ever AMI who underwent PCI between January 2018 and April 2021 were screened for delirium using the CAM-ICU method. Clinical and laboratory data were collected. RESULTS: A total of 134 (12.97%) patients were diagnosed with delirium. Patients with delirium were older. The most common concomitant diseases were cardiac arrest, chronic renal failure, and a history of coronary artery bypass graft (CABG). Delirious patients experienced more times of mechanical ventilation, more intra-aortic balloon pump (IABP) support, high postoperative immediate pain score (VAS), more non-bedside cardiac rehabilitation, and longer total length of stay and cardiac care unit (CCU) time. Multivariable logistic regression showed that age, mechanical ventilation, postoperative immediate pain score, and non-bedside cardiac rehabilitation were independently associated with delirium. Delirium was an independent predictor of prolonged CCU stay, total length of stay, and 1­year mortality. CONCLUSION: Age, mechanical ventilation, postoperative immediate pain score, and non-bedside cardiac rehabilitation were independently closely related to delirium in older patients with first-ever AMI who underwent PCI. Delirium was associated with a higher 1­year all-cause mortality.

Differential expression of diacylglycerol kinase ζ is involved in inferior parietal lobule-related dysfunction in schizophrenia with cognitive impairments.

BACKGROUND: Cognitive impairment is the main factor in the poor prognosis of schizophrenia, but its mechanism remains unclear. The inferior parietal lobule (IPL) is related to various clinical symptoms and cognitive impairment in schizophrenia. We aimed to explore the relationship between IPL-related functions and cognitive impairment in schizophrenia. METHODS: 136 schizophrenia patients and 146 demographically matched healthy controls were enrolled for a cross-sectional study. High-spatial-resolution structural and resting-state functional images were acquired to demonstrate the alternations of brain structure and function. At the same time, the digit span and digit symbol coding tasks of the Chinese Wechsler Adult Intelligence Test Revised (WAIS-RC) were utilized in assessing the subjects' cognitive function. Patients were divided into cognitive impairment and normal cognitive groups according to their cognitive score and then compared whether there were differences between the three groups in fractional amplitude of low-frequency fluctuation (fALFF). In addition, we did a correlation analysis between cognitive function and the fALFF for the left IPL of patients and healthy controls. Based on the Allen Human Brain Atlas, we obtained genes expressed in the left IPL, which were then intersected with the transcriptome-wide association study results and differentially expressed genes in schizophrenia. RESULTS: Grouping of patients by the backward digit span task and the digit symbol coding task showed differences in fALFF values between healthy controls and cognitive impairment patients (P < 0.05). We found a negative correlation between the backward digit span task score and fALFF of the left IPL in healthy controls (r = - 0.388, P = 0.003), which was not seen in patients (r = 0.203, P = 0.020). In addition, none of the other analyses were statistically significant (P > 0.017). In addition, we found that diacylglycerol kinase ζ (DGKζ) is differentially expressed in the left IPL and associated with schizophrenia. CONCLUSION: Our study demonstrates that the left IPL plays a vital role in cognitive impairment in schizophrenia. DGKζ may act as an essential regulator in the left IPL of schizophrenia patients with cognitive impairment.

Bicyclol Alleviates Atherosclerosis by Manipulating Gut Microbiota.

Atherosclerosis (AS) is associated with high morbidity and mortality, thus imposing a growing burden on modern society. Herb-derived bicyclol (BIC) is a versatile bioactive compound that can be used to treat AS. However, its efficacy in AS is not yet described. Here, it is shown that BIC normalizes gut microflora dysbiosis induced by a high fat diet in Apoe(-/-) mice. Metagenome-wide association study analysis verifies that the modulation on carbohydrate-active enzymes and short-chain fatty acid generating genes in gut flora is among the mechanisms. The gut healthiness, especially the gut immunity and integrity, is restored by BIC intervention, leading to improved systemic immune cell dynamic and liver functions. Accordingly, the endothelial activation, macrophage infiltration, and cholesterol ester accumulation in the aortic arch are alleviated by BIC to lessen the plaque onset. Moreover, it is proved that the therapeutic effect of BIC on AS is transmissible by fecal microbiota transplantation. The current study, for the first time, demonstrates the antiatherosclerotic effects of BIC and shows that its therapeutic value can at least partially be attributed to its manipulation of gut microbiota.

The MAP-Kinase HOG1 Controls Cold Adaptation in Rhodosporidium kratochvilovae by Promoting Biosynthesis of Polyunsaturated Fatty Acids and Glycerol.

The aim of this study was to investigate the role of RKHog1 in the cold adaptation of Rhodosporidium kratochvilovae strain YM25235 and elucidate the correlation of biosynthesis of polyunsaturated fatty acids (PUFAs) and glycerol with its cold adaptation. The YM25235 strain was subjected to salt, osmotic, and cold stress tolerance analyses. mRNA levels of RKhog1, Δ12/15-fatty acid desaturase gene (RKD12), RKMsn4, HisK2301, and RKGPD1 in YM25235 were detected by reverse transcription quantitative real-time PCR. The contents of PUFAs, such as linoleic acid (LA) and linolenic acid (ALA) was measured using a gas chromatography-mass spectrometer, followed by determination of the growth rate of YM25235 and its glycerol content at low temperature. The RKHog1 overexpression, knockout, and remediation strains were constructed. Stress resistance analysis showed that overexpression of RKHog1 gene increased the biosynthesis of glycerol and enhanced the tolerance of YM25235 to cold, salt, and osmotic stresses, respectively. Inversely, the knockout of RKHog1 gene decreased the biosynthesis of glycerol and inhibited the tolerance of YM25235 to different stresses. Fatty acid analysis showed that the overexpression of RKHog1 gene in YM25235 significantly increased the content of LA and ALA, but RKHog1 gene knockout YM25235 strain had decreased content of LA and ALA. In addition, the mRNA expression level of RKD12, RKMsn4, RKHisK2301, and RKGPD1 showed an increase at 15 °C after RKHog1 gene overexpression but were unchanged at 30 °C. RKHog1 could regulate the growth adaptability and PUFA content of YM25235 at low temperature and this could be helpful for the cold adaptation of YM25235.

Arterial Wall Stress Induces Phenotypic Switching of Arterial Smooth Muscle Cells in Vascular Remodeling by Activating the YAP/TAZ Signaling Pathway.

BACKGROUND/AIMS: Increasing wall stress or biomechanical stretch experienced by arteries influences the initiation of atherosclerotic lesions. This initiation is mediated by Yes-associated protein (YAP) and transcriptional co-activator with PDZ-binding motif (TAZ), which are both effectors of the Hippo pathway. In this study, the functional roles of YAP/TAZ proteins in the regulation of the stretch-mediated programing of human umbilical arterial smooth muscle cells (HUASMCs) to a proliferative phenotype were examined. METHODS: HUASMCs were seeded on a Matrigel-coated silicone chamber and subjected to biomechanical stretch for 24 h after 48 h of growth. YAP/TAZ small interfering RNA was used to specifically knockdown YAP/ TAZ expression in HUASMCs. RESULTS: We observed that YAP/TAZ activation via biomechanical stretching is involved in the regulation of critical aspects of the HUASMC phenotypic switch. YAP/TAZ knockdown significantly attenuated the stretch-induced proliferative and pro-inflammatory phenotypes in HUASMCs. Furthermore, treatment with atorvastatin, an anti-atherosclerotic drug, attenuated the stretch-induced phenotypic switch of HUASMCs from the contractile to synthetic state by suppressing YAP/TAZ expression. Additional investigations demonstrated the role of stretch in inhibiting the Hippo pathway, leading to the activation of PI3-kinase (PI3K) and phosphoinositide dependent kinase (PDK1); the key molecule for the regulation of the PDK1 and Hippo complex interaction was Sav1. These results showed the importance of YAP/TAZ activation, induced by biomechanical stretch, in promoting atheroprone phenotypes in HUASMCs. CONCLUSION: Taken together, our findings revealed a mechanism by which YAP/TAZ activation contributes to the pathogenesis of atherosclerosis.

Cables1 Inhibits Proliferation and Induces Senescence by Angiotensin II via a p21-Dependent Pathway in Human Umbilical Vein Endothelial Cells.

Cables1 (Cdk5 and Abl enzyme substrate 1) is a vital cell cycle regulator and a candidate tumor suppressor that negatively regulates cell growth by inhibiting cyclin-dependent kinases. Here, we report on the critical role of the Cables1/p21 pathway, which inhibits cell proliferation and induces cell senescence in human umbilical vein endothelial cells. Moreover, we confirmed that silencing of Cables1 promoted cell proliferation as well as increased resistance to angiotensin II-induced senescence, at least in part, by altering Cables1 activation. We further demonstrated that knockdown of p21 reverses Cables1-mediated cell growth inhibition and cell senescence. Taken together, these results suggest that the Cables1/p21 pathway has a strong effect on the induction of cell senescence and inhibition of cell growth, and acts as a novel regulatory mechanism in which p21 is probably one of several downstream effector molecules to mediate Cables1.

A novel swine model for evaluation of dyslipidemia and atherosclerosis induced by human CETP overexpression.

BACKGROUND: The mechanism of cholesteryl ester transfer protein (CETP) in lipid metabolism is still unclear. Furthermore, the relationship of CETP and atherosclerosis (AS) has been controversial. As pigs are a good model for both lipid and AS research, we investigated the lipid metabolism of human CETP (hCETP) transgenic pigs and explored the mechanism of CETP in lipid modulation. METHODS: Plasmids expressing the hCETP gene were designed, successfully constructed, and transfected into porcine fetal fibroblasts by liposomes. Using somatic cell nuclear transfer technology and embryonic transfer, hCETP transgenic pigs were generated. After the DNA, RNA, and protein levels were identified, positive hCETP transgenic pigs were selected. Blood samples were collected at different ages to evaluate the phenotypes of biochemical markers, and the metabolomes of plasma samples were analyzed by liquid mass spectrometry. RESULTS: Eight positive hCETP transgenic pigs and five negative cloned pigs were generated by transgenic technology. Finally, five hCETP transgenic and five cloned pigs were grown healthily. After feeding with a normal diet, hCETP transgenic pigs compared with unmodified pigs had no significant differences in body weight, liver function, kidney function, or plasma ions, while total cholesterol and low-density lipoprotein were higher than in unmodified pigs, and high-density lipoprotein was significantly decreased. Metabolomics analysis showed that there were differences in metabolic components between hCETP transgenic pigs, cloned pigs, and unmodified pigs. CONCLUSIONS: In this study, we created hCETP transgenic pigs that could serve as an excellent model for lipid disorders and atherosclerosis.

Identification and characterization of a novel bifunctional Δ(12)/Δ(15)-fatty acid desaturase gene from Rhodosporidium kratochvilovae.

OBJECTIVES: To elucidate the biosynthesis pathway of linoleic acid and α-linolenic acid in Rhodosporidium kratochvilovae YM25235 and investigate the correlation of polyunsaturated fatty acids with its cold adaptation. RESULTS: A 1341 bp cDNA sequence, designated as RKD12, putatively encoding a Δ(12)-desaturase was isolated from YM25235. Sequence analysis indicated that this sequence comprised a complete ORF encoding 446 amino acids of 50.6 kDa. The encoded amino acid sequence shared higher similarity to known fungal Δ(12)-desaturases that are characteristic of three conserved histidine-rich motifs. RKD12 was further transformed into Saccharomyces cerevisiae INVScl for functional characterization. Fatty acid analysis showed the yeast transformants accumulated two new fatty acids: linoleic acid and α-linolenic acid. Furthermore, mRNA expression level of RKD12 and the content of linoleic acid and α-linolenic acid were increased significantly with the culture temperature downshift from 30 to 15 °C, which might be helpful for the cold adaptation of YM25235. CONCLUSION: RKD12 is a novel bifunctional ∆(12)/∆(15)-desaturase gene, and the increased RKD12 mRNA expression level and PUFAs content at low temperature might be helpful for the cold adaptation of YM25235.

The association between cadmium exposure and the risk of chronic obstructive pulmonary disease: A systematic review and meta-analysis.

According to the World Health Organization, chronic obstructive pulmonary disease (COPD) was one of the top ten causes of death worldwide in 2019. The ratio of forced expiratory volume in the first second to forced vital capacity (FEV1/FVC) provides a useful indicator for the diagnosis of COPD. Existing data have demonstrated that cadmium (Cd) exposure is associated with COPD. However, data concerning the incidence and progression of cadmium-induced COPD is inconsistent. To explore the relationship between cadmium exposure and the risk of COPD in humans, through January 12, 2023, we conducted a thorough search of the PubMed, Cochrane, Web of Science, Embase and Scopus databases for relevant material. In this study, a meta-analysis was conducted to evaluate the association between cadmium and COPD. This meta-analysis indicated that exposure to cadmium (per 1 µg/L increase) was associated with reduced FEV1/FVC (% change = -47.54%, 95% CI: -54.99% to -40.09%). Subgroup analysis showed that the combined effect estimates were significantly higher in the COPD patient group (% change = -54.66%, 95% CI: -83.32% to -26.00%) than in the general population (% change = -52.11%, 95%CI: -60.53% to -43.70%). Therefore, we conclude that cadmium exposure is associated with reduced FEV1/FVC, which suggests a risk for COPD.

Cancer Differentiation Inducer Chlorogenic Acid Suppresses PD-L1 Expression and Boosts Antitumor Immunity of PD-1 Antibody.

As immune checkpoint inhibitors have shown good clinical efficacy, immune checkpoint blockade has become a vital strategy in cancer therapy. However, approximately only 12.5% patients experience benefits from immunotherapy. Herein, we identified the cancer differentiation inducer chlorogenic acid (CGA, now in the phase II clinical trial in China for glioma treatment) to be a small-molecular immune checkpoint inhibitor that boosted the antitumor effects of the anti-PD-1 antibody. CGA suppressed the expression of PD-L1 induced by interferon-γ in tumor cell culture through inhibition of the p-STAT1-IRF1 pathway and enhanced activity of activated T-cells. In two murine tumor xenografts, combination therapy of CGA with anti-PD-1 antibody decreased the expression of PD-L1 and IRF1 and increased the inhibitory effect of the anti-PD-1 antibody on tumor growth. Particularly, the activity of tumor infiltrated T cells was enhanced by CGA. CGA improved the gene expression of granzymes in tumor-infiltrated immune cells. In conclusion, through induction of differentiation, CGA appeared to suppress the expression of PD-L1 on cancer cells, effectively promoting infiltrated T cells in the tumor and boosting the antitumor effect of the anti-PD-1 antibody. Thus, CGA might serve as a promising agent to enhance anticancer immunotherapy if combined with anti-PD-1 antibodies.

Circ_002363 is regulated by the RNA binding protein BCAS2 and inhibits neodymium oxide nanoparticle-induced DNA damage by non-homologous end-joining repair.

Neodymium oxide nanoparticles (NPs-Nd2O3) are increasingly being used in industry and biomedicine, causing adverse health effects such as lung disease. However, the underlying molecular mechanisms controlling these adverse consequences are unknown at present. In this study, a human bronchial epithelial cell line (16HBE) was exposed to increasing concentrations of NPs-Nd2O3, and Sprague-Dawley rats were treated with NPs-Nd2O3 by intratracheal instillation. We found that NPs-Nd2O3 exposure induced DNA damage and down-regulated levels of circular RNA (circRNA) circ_002363 in 16HBE cells as well as in rat lung tissue. We also observed that circ_002363 levels in the serum of workers employed in the production of NPs-Nd2O3 diminished as the work time progressed, suggesting that circ_002363 may be a potential biomarker of lung injury. Functional experiments showed that circ_002363 significantly inhibited DNA damage induced by NPs-Nd2O3. RNA pull-down and western blot assays found that circ_002363 interacted with proteins PARP1/Ku70/Ku80/Rad50, which are critical participants in non-homologous end-joining (NHEJ) DNA repair. Moreover, we found that formation of circ_002363 was regulated by the RNA binding protein Breast Carcinoma Amplified Sequence 2 (BCAS2). The BCAS2 protein affected circ_002363 expression through interaction with Pre-DNA2, the host gene of circ_002363, in NPs-Nd2O3-exposed 16HBE cells. In conclusion, our findings show first that circ_002363, which is regulated by BCAS2, acts as regulator of DNA damage via the NHEJ pathway. These results enhance our understanding of the regulatory mechanisms controlling the actions of circular RNAs and highlight the relationship between genetics and epigenetics in the development of diseases following exposure to environmental chemicals.

Transcription factor TP63 mediates LncRNA CNTFR-AS1 to promote DNA damage induced by neodymium oxide nanoparticles via homologous recombination repair.

The widespread use of neodymium oxide nanoparticles (NPs-Nd2O3) has caused environmental pollution and human health problems, thus attracting significant attention. Understanding the mechanisms of NPs- Nd2O3-induced genetic damage is of great significance for identifying early markers for NPs- Nd2O3-induced lung injury. At present, the mechanisms underlying DNA damage induced by NPs- Nd2O3 remain unclear. In this study, we performed functional assays on human bronchial epithelial cells (16HBEs) exposed to various concentrations of NPs-Nd2O3 and SD rats administered with a single intratracheal instillation with NPs-Nd2O3. Exposure to NPs-Nd2O3 could lead to DNA damage in 16HBE cells and rat lung tissue cells. We found a novel long non-coding RNA, named CNTFR-AS1, which was highly expressed after exposure to NPs-Nd2O3. Our data verified that transcription factor TP63 mediates the high expression levels of CNTFR-AS1, which in turn regulates NPs-Nd2O3-induced DNA damage in cells by inhibiting HR repair. Moreover, the levels of CNTFR-AS1 were correlated with the number of years worked by occupational workers. Collectively, these results demonstrate that CNTFR-AS1 acts as a novel DNA damage regulator in bronchial epithelial cells exposed to NPs-Nd2O3. Hence, our data provide a basis for the identification of lncRNAs as early diagnostic markers for rare earth lung injury.

Induction of RIPK3/MLKL-mediated necroptosis by Erigeron breviscapus injection exhibits potent antitumor effect.

Colorectal cancer (CRC) is the second leading cause of tumor-related deaths worldwide. Resistance of tumor cells to drug-induced apoptosis highlights the need for safe and effective antitumor alternatives. Erigeron breviscapus (Dengzhanxixin in China) injection (EBI), extracted from the natural herb Erigeron breviscapus (Vant.) Hand.-Mazz (EHM), has been widely used in clinical practice for cardiovascular diseases. Recent studies have suggested that EBI's main active ingredients exhibit potential antitumor effects. This study aims to explore the anti-CRC effect of EBI and elucidate the underlying mechanism. The anti-CRC effect of EBI was evaluated in vitro using CCK-8, flow cytometry, and transwell analysis, and in vivo through a xenograft mice model. RNA sequencing was utilized to compare the differentially expressed genes, and the proposed mechanism was verified through in vitro and in vivo experiments. Our study demonstrates that EBI significantly inhibits the proliferation of three human CRC cell lines and effectively suppresses the migration and invasion of SW620 cells. Moreover, in the SW620 xenograft mice model, EBI markedly retards tumor growth and lung metastasis. RNA-seq analysis revealed that EBI might exert antitumor effects by inducing necroptosis of tumor cells. Additionally, EBI activates the RIPK3/MLKL signaling pathway, a classical pathway of necroptosis and greatly promotes the generation of intracellular ROS. Furthermore, the antitumor effect of EBI on SW620 is significantly alleviated after the pretreatment of GW806742X, the MLKL inhibitor. Our findings suggest that EBI is a safe and effective inducer of necroptosis for CRC treatment. Notably, necroptosis is a non-apoptotic programmed cell death pathway that can effectively circumvent resistance to apoptosis, which provides a novel approach for overcoming tumor drug resistance.

Corrigendum: Induction of RIPK3/MLKL-mediated necroptosis by Erigeron breviscapus injection exhibits potent antitumor effect.

[This corrects the article DOI: 10.3389/fphar.2023.1219362.].

Hepatic Stellate Cell- and Liver Microbiome-Specific Delivery System for Dihydrotanshinone I to Ameliorate Liver Fibrosis.

Liver fibrosis is a major contributor to the morbidity and mortality associated with liver diseases, yet effective treatment options remain limited. Hepatic stellate cells (HSCs) are a promising target for hepatic fibrogenesis due to their pivotal role in disease progression. Our previous research has demonstrated the potential of Dihydrotanshinone I (DHI), a lipophilic component derived from the natural herb Salvia miltiorrhiza Bunge, in treating liver fibrosis by inhibiting the YAP/TEAD2 interaction in HSCs. However, the clinical application of DHI faces challenges due to its poor aqueous solubility and lack of specificity for HSCs. Additionally, recent studies have implicated the impact of liver microbiota, distinct from gut microbiota, on the pathogenesis of liver diseases. In this study, we have developed an HSC- and microbiome-specific delivery system for DHI by conjugating prebiotic-like cyclodextrin (CD) with vitamin A, utilizing PEG2000 as a linker (VAP2000@CD). Our results demonstrate that VAP2000@CD markedly enhances the cellular uptake in human HSC line LX-2 and enhances the deposition of DHI in the fibrotic liver in vivo. Subsequently, intervention with DHI-VAP2000@CD has shown a notable reduction in bile duct-like structure proliferation, collagen accumulation, and the expression of fibrogenesis-associated genes in rats subjected to bile duct ligation. These effects may be attributed to the regulation of the YAP/TEAD2 interaction. Importantly, the DHI-VAP2000@CD intervention has also restored microbial homeostasis in the liver, promoting the amelioration of liver inflammation. Overall, our findings indicate that DHI-VAP2000@CD represents a promising therapeutic approach for liver fibrosis by specifically targeting HSCs and restoring the liver microbial balance.

circCIMT Silencing Promotes Cadmium-Induced Malignant Transformation of Lung Epithelial Cells Through the DNA Base Excision Repair Pathway.

Changes in gene expression in lung epithelial cells are detected in cancer tissues during exposure to pollutants, highlighting the importance of gene-environmental interactions in disease. Here, a Cd-induced malignant transformation model in mouse lungs and bronchial epithelial cell lines is constructed, and differences in the expression of non-coding circRNAs are analyzed. The migratory and invasive abilities of Cd-transformed cells are suppressed by circCIMT. A significant DNA damage response is observed after exposure to Cd, which increased further following circCIMT-interference. It is found that APEX1 is significantly down-regulated following Cd exposure. Furthermore, it is demonstrated that circCIMT bound to APEX1 during Cd exposure to mediate the DNA base excision repair (BER) pathway, thereby reducing DNA damage. In addition, simultaneous knockdown of both circCIMT and APEX1 promotes the expression of cancer-related genes and malignant transformation after long-term Cd exposure. Overall, these findings emphasis the importance of genetic-epigenetic interactions in chemical-induced cancer transformation.

The regulation loop of MARVELD1 interacting with PARP1 in DNA damage response maintains genome stability and promotes therapy resistance of cancer cells.

The DNA damage response (DDR) plays crucial roles in cancer prevention and therapy. Poly(ADP-ribose) polymerase 1 (PARP1) mediates multiple signal transduction in the DDR as a master regulator. Uncovering the regulatory factors of PARP1 contributes to a more comprehensive view of tumorigenesis and treatment strategies. Here, we reveal that MARVELD1 acts as a mediator of DDR to perform early events and maintain genome stability. Mechanistically, PARP1 PARylates MARVELD1 at D102, D118 and D130, and in turn, MARVELD1 stabilizes PARP1 by enhancing NAA50-mediated acetylation, thus forming a positive feedback loop. MARVELD1 knockout mice and their embryo fibroblasts exhibit genomic instability and shorter half-life of PARP1. Moreover, MARVELD1 partnering with PARP1 facilitates resistance to genotoxic drugs and disrupts PARP inhibitor (PARPi) effect in PDX model of colorectal cancer (CRC). Overall, our results underline the link between MARVELD1 and PARP1 in therapeutic resistance based on DDR and provide new insights for clinical tumor therapy of PARPi.

Affected cortico-striatal-cerebellar network in schizophrenia with catatonia revealed by magnetic resonance imaging: indications for electroconvulsive therapy and repetitive transcranial magnetic stimulation.

Catatonia is a psychomotor syndrome that can occur in a broad spectrum of brain disorders, including schizophrenia. Current findings suggest that the neurobiological process underlying catatonia symptoms in schizophrenia is poorly understood. However, emerging neuroimaging studies in catatonia patients have indicated that a disruption in anatomical connectivity of the cortico-striatal-cerebellar system is part of the neurobiology of catatonia, which could serve as a target of neurostimulation such as electroconvulsive therapy and repetitive transcranial magnetic stimulation.

The Combination of Feature Tracking and Late Gadolinium Enhancement for Identification Between Hypertrophic Cardiomyopathy and Hypertensive Heart Disease.

Background: The differentiation between hypertrophic cardiomyopathy (HCM) and hypertensive heart disease (HHD) is challenging due to similar myocardial hypertrophic phenotype. The purpose of this study is to evaluate the feasibility of cardiovascular magnetic resonance feature tracking (CMR-FT) and late gadolinium enhancement (LGE) to distinguish between HCM and HHD and the potential relationship between myocardial strain and cardiac functional parameters. Methods: One hundred and seventy subjects (57 HCM, 45 HHD, and 68 controls) underwent 3.0 T CMR, including steady-state free precession cines and LGE images. Global and segmental (basal, mid, and apical) analyses of myocardial radial, circumferential, longitudinal strain, and left ventricular (LV) torsion, as well as global and 16 segments of LGE were assessed. The multivariate analysis was used to predict the diagnostic ability by combining comprehensive myocardial strain parameters and LGE. Results: Global radial strain (GRS), global circumferential strain (GCS), and LV torsion were significantly higher in the HCM group than in the HHD group (GRS, 21.18 ± 7.52 vs. 14.56 ± 7.46%; GCS, -13.34 ± 3.52 vs. -10.11 ± 4.13%; torsion, 1.79 ± 0.69 vs. 1.23 ± 0.65 deg/cm, all P < 0.001). A similar trend was also seen in the corresponding strain rate. As for segmental strain analysis, basal radial strain (BRS), basal circumferential strain (BCS), basal longitudinal strain (BLS), mid-radial strain (MRS), and mid-circumferential strain (MCS) were higher in the HCM group than in the HHD group (all P < 0.001). The receiver operating characteristic (ROC) results showed that the area under the curve (AUC) of LGE in the mid-interventricular septum (mIVS) was the highest among global and segmental LGE analyses. On the multivariate regression analysis, a combined model of LGE (mIVS) with GRS obtained the highest AUC value, which was 0.835 with 88.89% sensitivity and 70.18% specificity, respectively. In addition, for patients with HCM, GRS, GCS, and global longitudinal strain had correlations with LV ejection fraction (LVEF), maximum interventricular septum thickness (IVST max), and left ventricular mass index (LVMi). Torsion was mildly associated with LVEF. Conclusion: CMR-FT-derived myocardial strain and torsion provided valuable methods for evaluation of HCM and HHD. In addition, the combination of GRS and LGE (mIVS) achieved the highest diagnostic value.

Prognostic significance of myocardial salvage assessed by cardiac magnetic resonance in reperfused ST-segment elevation myocardial infarction.

Aims: Myocardial salvage index (MSI) is attracting increasing attention for predicting prognosis in acute myocardial infarction (AMI); however, the evaluation of MSI is mainly based on contrast agent-dependent cardiac magnetic resonance (CMR) scanning sequences. This study aims to investigate the prognostic value of MSI in reperfused ST-segment elevation myocardial infarction (STEMI) through the contrast agent-free CMR technique. Methods and results: Nighty-two patients with acute STEMI, who underwent CMR after primary percutaneous coronary intervention (PPCI), were finally enrolled. Patients were subcategorized into two groups according to median MSI. T1 and T2 mapping were conducted for measuring infarct size (IS) and area at risk (AAR). IS was significantly larger in < median MSI group than ≥ median MSI group (P < 0.001). AAR between the two groups showed no obvious differences (P = 0.108). Left ventricular ejection fraction (LVEF) was lower in < median MSI group than ≥ median MSI group (P = 0.014). There was an obvious inverse correlation between MSI and reperfusion time (R = -0.440, P < 0.001) and a strong inverse correlation between MSI and IS (R = -0.716, P = 0.011). As for the relationship LVEF, MSI showed positive but weak correlation (R = 0.2265, P < 0.001). Over a median follow-up period of 263 (227-238) days, prevalence of MACEs was significantly higher in the < median MSI group [HR: 0.15 (0.04-0.62); Log-rank P = 0.008]. The univariate Cox regression analysis revealed that LVEF, IS, and MSI were significant predictors for major adverse cardiovascular events (MACEs) (all P < 0.05). In the stepwise multivariate Cox regression analysis, LVEF and MSI were identified as independent parameters for predicting MACEs (both P < 0.05). In the receiver-operating characteristic analysis, LVEF, IS, and MSI showed prognostic value in predicting MACEs with AUCs of 0.809, 0.779, and 0.896, respectively, all (P < 0.05). A combination of MSI with LVEF showed the strongest prognostic value of MACEs (AUC: 0.901, sensitivity: 77.78%, specificity: 98.80%, P < 0.001). Delong's test showed that the combination of LVEF with MSI had an incremental value than LVEF itself in predicting MACEs (P = 0.026). Conclusion: Contrast agent-free CMR technique provides a reliable evaluation of MSI, which contributes to assessing the efficacy of reperfusion therapy and predicting the occurrence of MACEs.