Effects of Camellia oleifera seed shell polyphenols and 1,3,6-tri-O-galloylglucose on androgenic alopecia via inhibiting 5a-reductase and regulating Wnt/ß-catenin pathway.

Androgenetic alopecia (AGA) is the leading cause of hair loss in adults. Its pathogenesis remains unclear, but studies have shown that the androgen-mediated 5α-reductase-AR receptor pathway and the Wnt/ß-catenin signaling pathway play significant roles. Camellia oleifera is an oil plant, and its fruits have been documented in folklore as having a hair cleansing effect and preventing hair loss. In this study, we used UPLC-Q-TOF-MS/MS to identify the structure of the substances contained in the polyphenols of Camellia oleifera seed shell. These polyphenols are mainly used for shampooing and anti-hair loss purposes. Next, we used molecular docking technology to dock 41 polyphenols and steroidal 5 alpha reductase 2 (SRD5A2). We found that the docking scores and docking sites of 1,3,6-tri-O-galloylglucose (TGG) and finasteride were similar. We constructed a mouse model of DHT-induced AGA to evaluate the effects of Camellia oleifera seed shell polyphenols (CSSP) and TGG in vivo. Treatment with CSSP and TGG alleviated alopecia symptoms and reduced DHT levels. Additionally, CSSP and TGG were able to reduce androgen levels by inhibiting the SRD5A2-AR receptor signaling pathway. Furthermore, by regulating the secretion of growth factors and activating the Wnt/ß-catenin signaling pathway, CSSP and TGG were able to extend the duration of hair growth. In conclusion, our study showed that CSSP and TGG can improve AGA in C57BL/6 J mice and reduce the effect of androgen on hair follicle through the two signaling pathways mentioned above. This provides new insights into the material basis and mechanism of the treatment of AGA by CSSP.

Differences in clinical characteristics of early-onset and late-onset severe acute respiratory syndrome coronavirus 2 infections in neonates.

Differences in clinical characteristics of early-onset and late-onset severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections in neonates remain unclear. This study aimed to determine whether there are differences in the main clinical, radiological, and laboratory features of early-onset and late-onset SARS-CoV-2 infections in neonates. This single-center, prospective cohort study enrolled neonates with SARS-CoV-2 infection from December 7, 2022, to January 3, 2023, and evaluated their clinical characteristics during hospitalization. All neonates (N = 58) infected with SARS-CoV-2 within 28 days of birth who were admitted to the neonatal intensive care unit of Taizhou Hospital were included. These neonates were classified into the early-onset (diagnosed within 7 days of birth) and late-onset (diagnosed more than 7 days after birth) groups. The symptoms, treatment, and prognosis of SARS-CoV-2 infection were the main study outcomes. The incidence of hospitalization attributable to SARS-CoV-2 infection was 10.6% (58 of 546 neonates) in Linhai. Sixteen (28%) of the 58 SARS-CoV-2 infections were early-onset cases, and 42 (72%) were late-onset cases. The common symptoms among the late-onset group were fever (p < 0.001) and cough (p < 0.001). Neonates with late-onset SARS-CoV-2 infection (p < 0.001) were significantly more likely to develop pneumonia.  Conclusion: The clinical symptoms and rates of pneumonia caused by SARS-CoV-2 infection in neonates differed between the early-onset and late-onset groups. Different clinical management is necessary for neonates with early-onset and late-onset SARS-CoV-2 infections. What is Known: • Neonates are susceptible to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). • Differences in clinical characteristics of early-onset and late-onset SARS-CoV-2 infections in neonates remain unclear. What is New: • Fever and cough were the most common symptoms among neonates with late-onset infection. • Neonates with late-onset SARS-CoV-2 infection were more likely to develop pneumonia.

Insulin reverses impaired alveolar fluid clearance in ARDS by inhibiting LPS-induced autophagy and inflammatory.

Until now, acute respiratory distress syndrome (ARDS) has been a difficult clinical condition with a high mortality and morbidity rate, and is characterized by a build-up of alveolar fluid and impaired clearance. The underlying mechanism is not yet fully understood and no effective medications available. Autophagy activation is associated with ARDS caused by different pathogenic factors. It represents a new direction of prevention and treatment of ARDS to restrain autophagy to a reasonable level through pharmacological and molecular genetic methods. Na, K-ATPase is the main gradient driver of pulmonary water clearance in ARDS and could be degraded by the autophagy-lysosome pathway to affect its abundance and enzyme activity. As a normal growth hormone in human body, insulin has been widely used in clinical for a long time. To investigate the association of insulin with Na, K-ATPase, autophagy and inflammatory markers in LPS-treated C57BL/6 mice by survival assessment, proteomic analysis, histologic examination, inflammatory cell counting, myeloperoxidase, TNF-α and IL-1ß activity analysis etc. This was also verified on mouse alveolar epithelial type II (AT II) and A549 cells by transmission electron microscopy. We found that insulin restored the expression of Na, K-ATPase, inhibited the activation of autophagy and reduced the release of inflammatory factors caused by alveolar epithelial damage. The regulation mechanism of insulin on Na, K-ATPase by inhibiting autophagy function may provide new drug targets for the treatment of ARDS.

Ingenane-type diterpenoids inhibit non-small cell lung cancer cells by regulating SRC/PI3K/Akt pathway.

Ingenane-type diterpenoids (ITDs) are distinct components of plants belonging to the genus Euphorbia. These compounds have significant cytotoxic effects on non-small cell lung cancer (NSCLC) cells. However, the underlying molecular mechanism has yet to be reported. To explore the mechanism of the anticancer effect of ITDs, we carried out a network pharmacology prediction study. PPI network suggested that SRC and PI3K had high levels of interaction. In addition, KEGG analysis revealed that these common targets were significantly enriched in the PI3K/Akt signalling pathway. 13-oxyingenol-dodecanoate (13OD) was used for validation after the biological evaluation of some ITDs against NSCLC cells. It demonstrated that 13OD could significantly inhibit the growth of NSCLC cells by inducing apoptosis. The results from molecular docking and Western blotting showed that 13OD interacted with SRC and PI3K and down-regulated the SRC/PI3K/Akt signalling pathway in NSCLC cells. This study provided the underlying mechanism of ITDs against NSCLC.

Bioinformatics Tools for Bulk Gene Expression Deconvolution in Diabetic Retinopathy.

Retinal neovascularization is one of the leading causes of vision loss and a hallmark of proliferative diabetic retinopathy (PDR). The immune system is observed to be involved in the pathogenesis of diabetic retinopathy (DR). The specific immune cell type that contributes to retinal neovascularization can be identified via a bioinformatics analysis of RNA sequencing (RNA-seq) data, known as deconvolution analysis. Previous study has identified the infiltration of macrophages in the retina of rats with hypoxia-induced retinal neovascularization and patients with PDR through a deconvolution algorithm, known as CIBERSORTx. Here, we describe the protocols of using CIBERSORTx to perform the deconvolution analysis and downstream analysis of RNA-seq data.

IL-26 modulates T cell function in autoimmune hepatitis.

OBJECTIVES: Autoimmune hepatitis (AIH) is an aberrant autoimmune condition mediated by T cell abnormality, which may cause fulminant liver failure and persistent liver injury. This study aimed to disclose the histopathological and functional engagement of interleukin (IL)-26, a potent inflammation mediator, in AIH disease progression. METHODS: We conducted immunohistochemical staining on liver biopsy samples to evaluate intrahepatic expression of IL-26. Cellular sources of hepatic IL-26 were detected by confocal microscopy. Flow cytometry was employed to determine the immunological alterations of CD4+ and CD8+ T cells following in vitro IL-26 treatment on primary peripheral blood mononuclear cells from healthy controls. RESULTS: Statistically significant increase in IL-26 level was observed in AIH (n = 48) liver samples in comparison with patients having chronic hepatitis B (n = 25), nonalcoholic fatty liver disease (n = 18), and healthy donors for living donor liver transplantation (n = 10). The number of intrahepatic IL-26+ cells was positively correlated with histological and serological severity. An immunofluorescence staining indicated that liver-infiltrating CD4+ T cells, CD8+ T cells, and CD68+ macrophages orchestrated IL-26 secretion in AIH. Both CD4+ and CD8+ T cells demonstrated effective activation, lytic, and proinflammatory functions upon IL-26 stimulation. CONCLUSION: We observed elevated IL-26 in AIH liver which promoted T cell activation and cytotoxic capacity, indicating a therapeutic potential of IL-26 intervention in AIH.

Diagnosis of asthmatic pneumonia in children by lung ultrasound vs. chest X-ray: an updated systematic review and meta-analysis.

Introduction: Chest X-ray (CXR) is used as the standard diagnostic method in lung diseases, especially in pneumonia, but unfortunately, despite the high risk of receiving radiation, it also has a high false negative rate. Therefore, some researchers recommend ultrasound to diagnose pneumonia. Aim: To investigate the accuracy of lung ultrasound compared to CXR for the diagnosis of pneumonia children by meta-analysis method. Material and methods: Original articles which evaluated accuracy of lung ultrasound compared to chest X-ray for the diagnosis of pneumonia in children, published between 1 January 2010 and 20 March 2021, were identified in the PubMed, Web of Science, Embase, Scopus and Cochrane Library databases. Data synthesis and statistical analysis were carried out using STATA software. Odds ratios with 95% confidence interval (CI), fixed effect model and mean difference with 95% CI, random effect model (REM) were calculated. Results: At the first step, 1016 potentially important research abstracts and titles were discovered in our electronic searches, 8 papers were in agreement with our inclusion criteria. The statistical analysis showed sensitivity of 95.5% (95% CI: 93.6-97.1%) and specificity of 96.3% (95% CI: 92.1-98.4%) for the lung ultrasound, and CXR sensitivity and specificity were 87.4% (95% CI: 84.3-90.0%) and 98.6% (95% CI: 95.8-99.6%), respectively. Conclusions: The present study showed that ultrasound can be useful in diagnosing pneumonia in children, and due to the lack of risk of receiving radiation, this method is even more preferred.

Establishment and validation of a nomogram to predict structural incomplete response in papillary thyroid carcinoma patients: a retrospective study.

OBJECTIVE: To identify risk factors related to structural incomplete response (SIR) in papillary thyroid carcinoma (PTC) and develop a nomogram for PTC patients. METHODS: In this respective study, clinical, ultrasonic, and pathological data of PTC patients treated at our institute between 2016 and 2020 were analyzed. Patients were randomly split into training and validation sets at a ratio of 7:3. Multivariate Cox regression analysis was conducted to determine independent prognostic factors. On the basis of these factors, a nomogram was built to predict SIR. P value, concordance index, calibration plots and decision curve analysis were used to evaluate the model. RESULTS: Multivariate Cox regression analysis showed that BRAF V600E status, lymph node metastasis, sex, tumor size, margin, and surgical procedure were independent prognostic factors. In the validation set, the concordance index of the nomogram was 0.774 (95% confidence interval: 0.703-0.845). Calibration plots at 3 and 5 years showed no apparent difference between predicted SIR probability and the actual SIR proportion. Additionally, the nomogram had good net clinical benefit according to the decision curve analysis compared with cases that were treat-all or treat-none. CONCLUSION: We build a nomogram to predict individualized outcomes and help postoperative surveillance in PTC patients.

Cell cycle kinases (AUKA, CDK1, PLK1) are prognostic biomarkers and correlated with tumor-infiltrating leukocytes in HBV related HCC.

Hepatocellular carcinoma (HCC) is one of the high incidence cancers and third leading cause of cancer-related mortality. HBV is the top most risk factor accounting for 50-80% of the HCC cases. Kinases: Aurora kinase A (AURKA), cyclin-dependent kinase (CDK1) and Polo-like kinase 1 (PLK1), the key regulators of cell mitosis are overexpressed in varieties of cancers including HCC. However, the exact role of these genes in prognosis of HCC is not fully unveiled. In addition, there is no such an accurate prognostic biomarker for HBV-related HCC. To address this issue, we performed a multidimensional analysis of AURKA, CDK1 and PLK1 with a series of publicly available databases in multiple cancers and with experimental validation in HBV-related HCC tissues. Overexpression of AURKA, CDK1 and PLK1 was found in multiple cancers including HCC. Elevated expression of these genes could result from lowered DNA methylation and genomic alterations. Transcriptional overexpression was significantly correlated with poor prognosis of HCC patients. The expression levels were also significantly positively associated with tumor grades and stages. Furthermore, the expression levels of these genes had a strong correlation with infiltration of immune cells. Our analysis shows that AURKA, CDK1 and PLK1 are correlated with immune infiltration and are the prognostic biomarkers for HBV-induced HCC.Communicated by Ramaswamy H. Sarma.

Elaiophylin triggers paraptosis and preferentially kills ovarian cancer drug-resistant cells by inducing MAPK hyperactivation.

Finely tuned mitogen-activated protein kinase (MAPK) signaling is important for cancer cell survival. Perturbations that push cells out of the MAPK fitness zone result in cell death. Previously, in a screen of the North China Pharmaceutical Group Corporation's pure compound library of microbial origin, we identified elaiophylin as an autophagy inhibitor. Here, we demonstrated a new role for elaiophylin in inducing excessive endoplasmic reticulum (ER) stress, ER-derived cytoplasmic vacuolization, and consequent paraptosis by hyperactivating the MAPK pathway in multiple cancer cells. Genome-wide CRISPR/Cas9 knockout library screening identified SHP2, an upstream intermediary of the MAPK pathway, as a critical target in elaiophylin-induced paraptosis. The cellular thermal shift assay (CETSA) and surface plasmon resonance (SPR) assay further confirmed the direct binding between the SHP2 and elaiophylin. Inhibition of the SHP2/SOS1/MAPK pathway through SHP2 knockdown or pharmacological inhibitors distinctly attenuated elaiophylin-induced paraptosis and autophagy inhibition. Interestingly, elaiophylin markedly increased the already-elevated MAPK levels and preferentially killed drug-resistant cells with enhanced basal MAPK levels. Elaiophylin overcame drug resistance by triggering paraptosis in multiple tumor-bearing mouse models resistant to platinum, taxane, or PARPi, suggesting that elaiophylin might offer a reasonable therapeutic strategy for refractory ovarian cancer.

SNORA70E promotes the occurrence and development of ovarian cancer through pseudouridylation modification of RAP1B and alternative splicing of PARPBP.

The present study demonstrated for the first time that SNORA70E, which belongs to box H/ACA small nucleolar noncoding RNAs (snoRNAs) who could bind and induce pseudouridylation of RNAs, was significantly elevated in ovarian cancer tissues and was an unfavourable prognostic factor of ovarian cancer. The over-expression of SNORA70E showed increased cell proliferation, invasion and migration in vitro and induced tumour growth in vivo. Further research found that SNORA70E regulates RAS-Related Protein 1B (RAP1B) mRNA through pseudouracil modification by combing with the pyrimidine synthase Dyskerin Pseudouridine Synthase 1 (DKC1) and increase RAP1B protein level. What's more, the silencing of DKC1/RAP1B in SNORA70E overexpression cells both inhibited cell proliferation, migration and invasion through reducing ß-catenin, PI3K, AKT1, mTOR, and MMP9 protein levels. Besides, RNA-Seq results revealed that SNORA70E regulates the alternative splicing of PARP-1 binding protein (PARPBP), leading to the 4th exon-skipping in PARPBP-88, forming a new transcript PARPBP-15, which promoted cell invasion, migration and proliferation. Finally, ASO-mediated silencing of SNORA70E could inhibit ovarian cancer cell proliferation, invasion, migration ability in vitro and inhibit tumorigenicity in vivo. In conclusion, SNORA70E promotes the occurrence and development of ovarian cancer through pseudouridylation modification of RAP1B and alternative splicing of PARPBP. Our results demonstrated that SNORA70E may be a new diagnostic and therapeutic target for ovarian cancer.

Autophagy in glaucoma pathogenesis: Therapeutic potential and future perspectives.

Glaucoma is a common blinding eye disease characterized by progressive loss of retinal ganglion cells (RGCs) and their axons, progressive loss of visual field, and optic nerve atrophy. Autophagy plays a pivotal role in the pathophysiology of glaucoma and is closely related to its pathogenesis. Targeting autophagy and blocking the apoptosis of RGCs provides emerging guidance for the treatment of glaucoma. Here, we provide a systematic review of the mechanisms and targets of interventions related to autophagy in glaucoma and discuss the outlook of emerging ideas, techniques, and multidisciplinary combinations to provide a new basis for further research and the prevention of glaucomatous visual impairment.

[Effect of Gegen Qinlian Decoction on gut microbiota of irritable bowel syndrome with diarrhea rats].

This study aims to explore the effect of Gegen Qinlian Decoction on gut microbiota of irritable bowel syndrome with diarrhea(IBS-D) rats. A total of 36 male SD rats were randomly classified into the control group, model group, rifaximin group(150 mg·kg~(-1)), and high-dose(8.125 g·kg~(-1)), medium-dose(4.062 5 g·kg~(-1)) and low-dose(2.031 3 g·kg~(-1)) Gegen Qinlian Decoction groups with the random number table method, 6 in each group. After modeling, rats were treated for 8 days. The general state, bristol stool chart(BSC) score, and the minimum volume threshold for abdominal withdrawal reflex were recorded. Pathological changes of colon tissues were observed based on hematoxylin and eosin(HE) staining, and gut microbiota was analyzed based on 16 S rRNA sequencing. Compared with the model group, rifaximin group and high-dose and medium-dose Gegen Qinlian Decoction groups showed low BSC score(P<0.01) and high minimum volume threshold for abdominal lifting(P<0.05). HE staining showed that Gegen Qinlian Decoction could relieve intestinal inflammation. 16 S rRNA sequencing suggested obvious variation of gut microbiota in IBS-D rats. Gegen Qinlian Decoction significantly raised the richness index and diversity index of gut microbiota, regulated the number of the flora, and improved alpha diversity and beta diversity. Species composition of gut microbiota and LEfSe analysis showed that Gegen Qinlian Decoction could significantly increase the ratio of Bacteroidota to Firmicutes, elevate the abundance of probiotics such as Clostridia and Lachnospirales, and reduce the abundance of conditional pathogens such as Bacteroidales, and Prevotellaceae. PICRUSt2 analysis indicated that Gegen Qinlian Decoction was mainly related to multiple metabolic pathways such as carbohydrate metabolism and amino acid metabolism. In summary, Gegen Qinlian Decoction can significantly reduce visceral hypersensitivity of IBS-D rats, alleviate intestinal inflammation, and relieve clinical symptoms such as diarrhea. The mechanism is the likelihood that it regulates the composition and structure of gut microbiota and improves its metabolic pathway as well.

Resveratrol Inhibits DEN-induced Malignant Proliferation of Rat Hepatocellular Precancerous Stage Through Reprogramming of Glucose Metabolism / 中国生物化学与分子生物学报

Resveratrol (RES) can inhibit the growth and proliferation of liver cancer cells. However, its role in the precancerous stage is still unclear. This paper aims to study the effect and mechanism of RES on the precancerous stage of liver cancer in rats induced by diethylinitrosamine (DEN). SD rats were divided into normal control group, RES treatment group, DEN treatment group and RES-DEN treatment group. The results showed that after the rats were treated with DEN for 8 weeks, the total expression level of proliferating cell nuclear antigen (PCNA) of hepatocytes increased to 2-fold (P<0.05), and the expression level of PCNA protein in the nucleus increased to 3-fold (P<0.001). However, the expression levels of total PCNA (P<0.05) and nuclear PCNA protein (P<0.001) in hepatocytes of rats treated with RES-DEN decreased, suggesting that RES could significantly inhibit the liver malignant proliferation of cells. Through non-targeted metabolomics and KEGG metabolic pathway enrichment analysis, the results showed that the level of glycolysis did not increase significantly in the hepatocytes of RES-DEN-treated rats, although the transition from the pentose phosphate pathway to the glycolysis pathway was enhanced when compared with the DEN group rats. This finding suggested that the metabolic pathway of phosphoenolpyruvate-pyruvate-lactate was inhibited. Further verification found that the protein expression levels of key enzymes M2-type pyruvate kinase (PKM2) and lactate dehydrogenase (LDHA) in this metabolic pathway were inhibited (P<0.05). RES can reprogram glucose metabolism and inhibit DEN-induced excessive proliferation of rat hepatocytes in the precancerous stage of liver cancer, providing an experimental basis for RES to prevent liver cancer.

CD8+ T cells actively penetrate hepatocytes via the CD44/p-ERM/F-actin pathway in autoimmune hepatitis.

OBJECTIVE: Emperipolesis is a pathological feature for the diagnosis of autoimmune hepatitis (AIH). We have previously found that CD8+ T cells participated in the emperipolesis in AIH. In this study we aimed to clarify the characteristics and molecular mechanisms of emperipolesis in patients with AIH in vitro and in mice with α-Galactosylceramide (α-GalCer)-induced acute hepatitis. METHODS: The peripheral blood mononuclear cells (PBMC) of patients with various chronic liver diseases and healthy controls were co-cultured with hepatic cell lines to induce emperipolesis in vitro. Confocal staining was performed to illustrate the cellular types and potential mechanisms of emperipolesis in AIH. In addition, a murine model of α-GalCer-induced acute hepatitis that mimics human AIH was used to confirm the role of CD44/p-ERM/F-actin in the emperipolesis process in vivo. RESULTS: In the co-cultured system of PBMC and hepatic cell line, emperipolesis was observed most commonly in patients with AIH. The main cells participating in emperipolesis were CD8+ T cells, and they penetrated hepatic cells actively via the CD44/p-ERM/F-actin pathway. As a result, most CD8+ T cells engulfed by hepatic cells underwent apoptosis. In the α-GalCer-induced acute hepatitis model, emperipolesis was observed around the inflammatory foci and was inhibited by the ezrin phosphorylation inhibitor NSC668394. Similarly, activated murine CD8+ T cells penetrated primary hepatocytes via the CD44/p-ERM/F-actin pathway in vitro. CONCLUSIONS: CD8+ T cells penetrate hepatic cells actively via the CD44/p-ERM/F-actin signaling pathway and undergo apoptosis. This may be a compensatory mechanism to attenuate the overwhelming immune attack in AIH.

The function and regulation mechanism of piRNAs in human cancers.

Piwi-interacting RNAs (piRNAs) are mainly expressed in mammalian germ cells, playing an important role in maintaining germ line DNA integrity, inhibiting transposon transcription and translation, participating in heterochromatin formation, epigenetic regulation, and germ cell genesis. They combine with P-element induced wimpy testis (PIWI) proteins to form effector complexes known as piRNA-induced silencing complexes (pi-RISC) to regulate the gene silencing pathway. Recent evidence suggests that numerous piRNAs, with tumor-promoting and tumor-suppressing functions in cancer development, are dysregulated in tumor tissues, and are related to clinical prognosis. In the present review, we summarize the current state of knowledge on the function and regulatory mechanisms of piRNAs in the tumorigenesis and progression of cancer, providing evidence for the potential use of piRNAs in the diagnosis and clinical treatment of cancer.

Four new lanostane triterpenoids from latex of Euphorbia resinifera / 中国中药杂志

Four new lanostane triterpenoids, 3β-hydroxy-12α-methoxylanosta-7,9(11),24-triene(1), 3β-hydroxy-12α-methoxy-24-methylene-lanost-7,9(11)-dien(2), 3,7-dioxo-lanosta-8,24-diene(3), and 3,7-dioxo-24-methylene-lanost-8-en(4), were isolated from the latex of Euphorbia resinifera with a variety of chromatography methods. Their structures were elucidated based on spectroscopic data and/or comparison with the data reported in previous research. Compounds 1, 2, and 4 showed moderate inhibition of LPS-induced NO production by RAW264.7, with IC_(50) of 30.4, 37.5, and 28.3 μmol·L~(-1), respectively.

The presence of joint predictors generates conjunctive predictions.

The cognitive system readily detects statistical relationships where a cue predicts a specific outcome. What is less known is how the mind generates predictions when multiple cues are presented simultaneously that predict different outcomes. Here, we examine the nature of such predictions. Specifically, we examine whether the presence of joint cues leads to conjunctive predictions that represent the overlap between the outcomes associated with the cues, or disjunctive predictions that represent the total possible outcomes. To test this, we used a visual search paradigm where participants first viewed a cue and then searched for a target in an array. Each cue predicted where the target would appear in one of the four quadrants in the array. After learning the cue-location associations, two cues were presented simultaneously, and participants searched for the target where the target now appeared in each quadrant with equal probability. We found that participants were faster to find the target in conjunctive locations over disjunctive ones upon seeing two cues (Experiment 1). This attentional prioritization was not solely driven by the smaller spatial scope of conjunctive locations (Experiment 2), and was present when two cues were presented in two feature dimensions in a single object (Experiment 3). These results were consistent with a conjunctive account, where the presence of joint cues led to a conjunctive prediction that represented the overlap of the different outcomes associated with each cue. The study sheds a new light on how the mind makes predictions in novel contexts based on existing knowledge.

Influence of intravascular ultrasound on the prognosis of patients after rotational atherectomy / 医学研究生学报

ObjectiveThe development of new endovascular imaging techniques has optimized surgical treatment strategies. In this paper, we investigated the effect of rotational atherectomy (RA) guided by intravascular ultrasound (IVUS) on long-term postoperative follow-ups.MethodsClinical data of 211 patients who underwent RA in the Department of Cardiology, Nanjing Drum Tower Hospital from November 2011 to December 2018 were retrospectively analyzed, and they were divided into IVUS Group (116 patients) and Non-IVUS Group (95 patients) according to whether they underwent the guidance of intravascular ultrasound or not. Basic information of all patients, coronary artery lesions and details of operation and other clinical data were collected. The long-term prognosis of the patients was collected and compared by telephone or outpatient follow-ups.ResultsThe head diameter, average stent diameter and total hospitalization expenses of the IVUS Group were significantly higher than those of the Non-IVUS Group, and the differences were statistically significant [(1.53±0.19) mm vs (1.46±0.14) mm, P=0.001; (3.09±0.48) mm vs (2.87±0.30) mm, P0.05). Multivariate COX regression analysis showed that the cardiogenic mortality was significantly reduced in the IVUS Group (HR=0.10, 95%CI: 0.02~0.63, P=0.014), but there was no statistically significant difference between the two groups in the incidence of all-cause death and long-term MACE (P>0.05).ConclusionCompared with the Non-IVUS Group, IVUS-guided RA can significantly reduce the incidence of long-term cardiogenic death and total hospitalization expenses.

Influence of intravascular ultrasound on the prognosis of patients after rotational atherectomy / 医学研究生学报

ObjectiveThe development of new endovascular imaging techniques has optimized surgical treatment strategies. In this paper, we investigated the effect of rotational atherectomy (RA) guided by intravascular ultrasound (IVUS) on long-term postoperative follow-ups.MethodsClinical data of 211 patients who underwent RA in the Department of Cardiology, Nanjing Drum Tower Hospital from November 2011 to December 2018 were retrospectively analyzed, and they were divided into IVUS Group (116 patients) and Non-IVUS Group (95 patients) according to whether they underwent the guidance of intravascular ultrasound or not. Basic information of all patients, coronary artery lesions and details of operation and other clinical data were collected. The long-term prognosis of the patients was collected and compared by telephone or outpatient follow-ups.ResultsThe head diameter, average stent diameter and total hospitalization expenses of the IVUS Group were significantly higher than those of the Non-IVUS Group, and the differences were statistically significant [(1.53±0.19) mm vs (1.46±0.14) mm, P=0.001; (3.09±0.48) mm vs (2.87±0.30) mm, P0.05). Multivariate COX regression analysis showed that the cardiogenic mortality was significantly reduced in the IVUS Group (HR=0.10, 95%CI: 0.02~0.63, P=0.014), but there was no statistically significant difference between the two groups in the incidence of all-cause death and long-term MACE (P>0.05).ConclusionCompared with the Non-IVUS Group, IVUS-guided RA can significantly reduce the incidence of long-term cardiogenic death and total hospitalization expenses.