Value of deep-learning image reconstruction at submillisievert CT for evaluation of the female pelvis.

AIM: To assess the value of deep-learning reconstruction (DLR) at submillisievert computed tomography (CT) for the evaluation of the female pelvis, with standard dose (SD) hybrid iterative reconstruction (IR) images as reference. MATERIALS AND METHODS: The present study enrolled 50 female patients consecutively who underwent contrast-enhanced abdominopelvic CT for clinically indicated reasons. Submillisievert pelvic images were acquired using a noise index of 15 for low-dose (LD) scans, which were reconstructed with DLR (body and body sharp), hybrid-IR, and model-based IR (MBIR). Additionally, SD scans were reconstructed with a noise index of 7.5 using hybrid-IR. Radiation dose, quantitative image quality, overall image quality, image appearance using a five-point Likert scale (1-5: worst to best), and lesion evaluation in both SD and LD images were analysed and compared. RESULTS: The submillisievert pelvic CT examinations showed a 61.09 ± 4.13% reduction in the CT dose index volume compared to SD examinations. Among the LD images, DLR (body sharp) had the highest quantitative quality, followed by DLR (body), MBIR, and hybrid-IR. LD DLR (body) had overall image quality comparable to the reference (p=0.084) and favourable image appearance (p=0.209). In total, 40 pelvic lesions were detected in both SD and LD images. LD DLR (body and body sharp) exhibited similar diagnostic confidence (p=0.317 and 0.096) compared with SD hybrid-IR. CONCLUSION: DLR algorithms, providing comparable image quality and diagnostic confidence, are feasible in submillisievert abdominopelvic CT. The DLR (body) algorithm with favourable image appearance is recommended in clinical settings.

Author Correction: Experimental study on thioredoxin redox inhibitor 1-methylpropyl 2-imidazolyl disulfide promoting apoptosis of multiple myeloma cells in vitro and in vivo.

Correction to: European Review for Medical and Pharmacological Sciences 2022; 26 (4): 1283-1292. DOI: 10.26355/eurrev_202202_28121-PMID: 35253185-published online on December 15, 2022. After publication, the authors corrected the order of the author's affiliations as follows: Q.-D. Lin1,2,3,4, L.-N. Liu1,2,3,4, X.-Y. Liu1,2, Y. Yan1,2, B.-J. Fang1,2,3,4, Y.-L. Zhang1,2,3,4, J. Zhou1,2,3,4, Y.-F. Li1,2,3,4, W.-L. Zuo1,2,3,4, Y.-P. Song1,2,3,4 1Affiliated Cancer Hospital of Zhengzhou University, Zhengzhou City, Henan Province, China 2Henan Cancer Hospital, Zhengzhou City, Henan Province, China 3Henan Key Lab of Experimental Hematology, Zhengzhou City, Henan Province, China 4Henan Institute of Hematology, Zhengzhou City, Henan Province, China There are amendments to this paper. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/28121.

Association between the Lymphocyte-to-C-Reactive Protein Ratio and Survival Outcomes in Cancer Patients with GLIM-Defined Malnutrition: A Multicenter Study.

BACKGROUND AND AIMS: This study assessed the prognostic value of LCR in patients with cancer-associated malnutrition (CAM). Systemic inflammatory markers, particularly the lymphocyte-to-C-reactive protein ratio (LCR), are related to the survival of patients with CAM. The present retrospective analysis based on a prospective multicenter cohort study, which involved 1,437 hospitalized patients with CAM. METHODS: The area under the receiver operating characteristic curve (AUC) of ten inflammatory indicators-LCR, advanced lung cancer inflammation index, neutrophil-to-lymphocyte ratio, prognostic nutritional index, modified Glasgow prognostic score, systemic immune-inflammation index, albumin-to-globulin ratio, LCR score, glucose-to-lymphocyte ratio, and platelet-to-lymphocyte ratio-were constructed. Nutritional status, blood markers, and quality of life (QoL) were evaluated within 48 h of admission. The overall survival (OS) was evaluated from September 1 to December 29, 2021. RESULTS: A total of 1,431 cancer patients diagnosed with malnutrition based on the Global Leadership Initiative on Malnutrition (GLIM) criteria. Male patients were 62.8% of all, and the mean age was 60.66 years old. The AUC of LCR was higher than that of other inflammatory markers. The restricted cubic spline (RCS) of the Hazard ratios (HRs) showed an inverse L-shaped relationship with LCR. In addition, patients with low LCR had significantly poorer OS than those with high LCR. The addition of LCR to the model increased the predictive ability of 1-year mortality (AUC increase of 0.036), 3-year mortality (AUC increase of 0.038), and 5-year mortality (AUC increase of 0.031). CONCLUSIONS: Assessing the LCR can help the medical staff identify cancer patients with nutritional deficiency at high risk of oncological outcomes and develop individualized therapeutic strategies.

Otoacoustic emission and its application in anesthesia.

OBJECTIVE: An otoacoustic emission (OAE) is a low-level sound emitted by the cochlea. OAEs are able to objectively evaluate the auditory perception and reflect the functional status of the auditory system. With the characteristics of non-invasiveness, high reliability, and easy manipulation, OAEs have gained wide popularity in clinical audiology and anesthesiology. This review aims to summarize the application of OAE in anesthesia. MATERIALS AND METHODS: This study collected data from the databases Web of Science-Clarivate Analytics, PubMed, and Google Scholar in English, covering research in the last 40 years. The keywords were defined as anesthesia, cochlea, OAEs, distortion product otoacoustic emissions, transient evoked otoacoustic emissions, bispectral index, auditory evoked potentials, and depth of anesthesia. Documents that matched defined keywords were selected and reviewed. RESULTS: Research showed that the types and doses of anesthetic drugs impacted OAEs. Ketamine-based anesthesia has a greater effect on OAE sensitivity over time compared to isoflurane. A higher dose of ketamine-xylazine significantly reduced the amplitude of OAEs. According to those characteristics, OAEs could be used as an objective evaluation method for the effect of anesthetics and have great potential to be applied for anesthetic drug dose control during surgery. OAEs also have been used to detect the cochlear function during anesthesia, which may cause irreversible damage to the cochlea. CONCLUSIONS: Studies reported that OAEs have been used in anesthesia. However, the existing studies have mainly focused on the influence of anesthetic types or dosages on OAEs. Considering the characteristics of OAEs, such as a convenient measurement, less susceptibility to interference, and fast detection speed, the application of OAE has a great potential in the anesthesia field.

Experimental study on thioredoxin redox inhibitor 1-methylpropyl 2-imidazolyl disulfide promoting apoptosis of multiple myeloma cells in vitro and in vivo.

OBJECTIVE:   To explore the in vitro and in vivo experimental study of thioredoxin-1(Trx1) inhibitor 1-methylpropyl 2-imidazolyl disulfide (PX-12) promoting multiple myeloma H929 cell apoptosis, investigate the relationship between the inhibitory effect of PX-12 on H929 cells and reactive oxygen species (ROS). MATERIALS AND METHODS: Inhibition of PX-12 on H929 cells in relation to reactive oxygen species (ROS), cell cycle, and apoptosis were assessed by flow cytometry. ELISA kit, IVIS Imaging, Hematoxylin and eosin (H&E) staining and immunohistochemical staining assessment were applied to assess the anti-myeloma effect in the SCID mice model established by H929EL cells. RESULTS: PX-12 inhibited proliferation of H929 cells performed time and dose dependent style. Furthermore, it significantly induced a G2/M phase arrest of the cell cycle in H929 cells. It also increased intracellular ROS and caspase-3 activity in H929 cells indicating that cells have undergone apoptosis. There was an almost 3-5-fold decrease in tumor viability measured by the Living-Imaging system after 21 and 28 days after PX-12 injection compared with the control group. Importantly, PX-12 caused significant decrease in expression of Kappa chain in vivo assessed by immunohistochemical staining. CONCLUSIONS: The results suggest that PX-12 may be a potential strategy for the treatment of MM, and the inhibition of TRX-1 in the treatment of myeloma deserves further research.

Skeletal muscle-secreted myokine interleukin-6 induces white adipose tissue conversion into beige adipose tissue in myostatin gene knockout pigs.

Myostatin (MSTN) is primarily expressed in skeletal muscle and plays an important role in the regulation of muscle growth and development as well as fat deposition; however, little is known about the molecular mechanism through which MSTN regulates body fat deposition. Therefore, in this study, we sought to identify the signaling pathways through which MSTN regulates fat accumulation in pigs. MSTN knockout (MSTN-/-) pigs showed increased muscle mass, decreased fat mass, and a leaner body composition. In this study, we found that the adipose tissue of MSTN-/- pigs exhibits the characteristics of beige adipose tissue, and the mRNA expression levels of beige adipose marker genes, including UCP3, Cidea, and CD137, were significantly increased. Remarkably, the observed beige phenotype was not adipocyte autonomous but rather caused by muscle-secreted myokine interleukin (IL)-6. This occurrence results in increased AMP-activated protein kinase (AMPK) phosphorylation in adipose tissue, which subsequently activates peroxisome proliferator-activated receptor gamma coactivator 1α and the conversion of white adipocytes to beige in pigs. Therefore, we concluded that MSTN deficiency leads to increased IL-6 secretion in skeletal muscle and activates AMPK in adipocytes, thereby increasing the beige adipose tissue in MSTN-/- pigs.

Bioinformatic analysis for the identification of potential gene interactions and therapeutic targets in atrial fibrillation.

OBJECTIVE: Atrial fibrillation (AF) is the most common type of tachycardia. The major injury caused by AF is a systemic embolism. Although AF therapies have evolved substantially, the success rate of sinus rhythm maintenance is relatively low. The reason is the incomplete understanding of the AF mechanisms. MATERIALS AND METHODS: A Gene Expression Omnibus (GEO) dataset (GSE79768) was downloaded. Differentially expressed genes (DEGs) were identified by bioinformatic analysis. Enriched terms and pathways were identified by gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses. A protein-protein interaction (PPI) network was constructed to determine regulatory genes. CytoHubba and the Molecular Complex Detection (MCODE) algorithm were used to identify potential hub genes and important modules. The Predicting Associated Transcription Factors From Annotated Affinities (PASTAA) method was used to predict transcription factors (TFs). RESULTS: Two hundred thirty-five upregulated DEGs and seventy-seven downregulated DEGs were identified. In the GO biological process, cellular component, and molecular function analyses, positive regulation of cell migration, anchoring junctions, and cell adhesion molecule binding were enriched significantly. The Hippo signalling pathway was the most significantly enriched pathway. In the PPI network analysis, we found that Class A/1 (rhodopsin-like receptors) may be the critical module. Ten hub genes were extracted, including 6 upregulated genes and 4 downregulated genes. CXCR2, TLR4, and CXCR4 may play critical roles in AF. In the TF prediction, we found that Irf-1 may be implicated in AF. CONCLUSIONS: We found that the CXCR4, TLR4, CXCR2 genes, the Hippo signalling pathway and the class A/1 (rhodopsin-like receptors) module may play critical roles in AF occurrence and maintenance, which may provide novel targets for AF treatment.

Different effects of probiotics and antibiotics on the composition of microbiota, SCFAs concentrations and FFAR2/3 mRNA expression in broiler chickens.

AIMS: The aims of this study were to investigate the effects of probiotics and antibiotics on microbial composition, short chain fatty acids (SCFAs) concentration and free fatty acid receptor 2/3 (FFAR2/3) expression in boiler chickens. METHODS AND RESULTS: A total of 150 1-day-old male broilers were randomly allocated into three groups, control (CON) group, probiotics (PB) group and antibiotics (ATB) group. Results indicated that PB improved the average body weight from 1 to 21 days and feed intake from 21 to 42 days (P < 0·05), while ATB improved the feed efficiency from 1 to 42 days (P < 0·05). Based on 16s rRNA sequencing, PB treatment increased the amount of kingdom bacteria, and the relative abundance of the main bacteria including acetate and butyrate producing bacteria of phylum Firmicutes, family Ruminococcaceae and genus Faecalibacterium. ATB treatment also increased the relative abundance of phylum Firmicutes, family Ruminococcaceae and Lachnospiraceae, however, it introduced some pathogenic bacteria, such as bacteria of family Rikenellaceae and Enterobacteriaceae. Gas chromatography and mass spectrometry (GC-MS) assay revealed that PB increased acetate and butyrate concentrations at both 21 and 42 days, and propionate at 42 days in the colorectum. Moreover qRT-PCR analysis showed PB treatment significantly activated the FFAR2/3 mRNA expressions. On the contrast, ATB treatment lowered the colorectal propionate at 21 days, and decreased acetate, propionate and butyrate concentrations at 42 days, accompanied with decreased FFAR2/3 mRNA expressions. CONCLUSIONS: Compared to the CON birds, an enriched SCFAs producing bacteria with higher SCFAs contents and activated FFAR2/3 expressions are prominent features of PB birds. However, antibiotics treatment plays the reverse effect compared to PB treatment. SIGNIFICANCE AND IMPACT OF THE STUDY: This study brings a significant idea that less SCFAs concentration may be another reason why the antibiotics inhibit the immune system development and immunity of the body.

KLF13 loss-of-function variation contributes to familial congenital heart defects.

OBJECTIVE: Congenital heart defect (CHD) represents the most common form of human developmental abnormality and contributes to substantial morbidity, mortality, and socioeconomic burden worldwide. Accumulating evidence underscores the strong genetic basis of CHD. Nevertheless, CHD is of pronounced genetic heterogeneity, and the genetic determinants underlying CHD in most patients are still unclear. This study was mainly sought to identify the causative gene for CHD in a consanguineous Chinese family. PATIENTS AND METHODS: Whole-exosome sequencing and bioinformatics analyses were performed in a Chinese family with CHD (double-outlet right ventricle and ventricular septal defect), which was transmitted in an autosomal dominant pattern. A total of 312 unrelated healthy individuals were then genotyped for the identified genetic variation. The functional effect of the identified variation was characterized by utilizing a Dual-Luciferase reporter assay system. RESULTS: A novel heterozygous variation, NM_015995.3: c.370G>T; p.(Glu124*), was identified in the KLF13 gene, which encodes Kruppel-like factor 13 key to proper heart development. Genetic analysis of the pedigree unveiled that the variation co-segregated with CHD, with complete penetrance. The variation was absent from 624 control chromosomes. The biological analysis revealed that the Glu124*-mutant KLF13 protein failed to transactivate its cardiac target genes ACTC1 and ANP. Furthermore, the variation disrupted the synergistic transactivation between KLF13 and GATA4, as well as GATA6, two other genes that have been recognized to cause CHD. CONCLUSIONS: These findings firstly indicate that genetically defective KLF13 predisposes to familial CHD, implying potential implications for genetic counseling and an improved prophylactic strategy in a subset of CHD patients.

Caprin1 targeted by circular circ_0000885 in the tumor progression of osteosarcoma.

Since this article has been suspected of research misconduct and the corresponding authors did not respond to our request to prove originality of data and figures, "Caprin1 targeted by circular circ_0000885 in the tumor progression of osteosarcoma, by X.-Y. Liu, M. Li, B. Dong, Q. Feng, published in Eur Rev Med Pharmacol Sci 2020; 24 (9): 4665-4670-DOI: 10.26355/eurrev_202005_21152-PMID: 32432729" has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/21152.

Caprin1 targeted by circular circ_0000885 in the tumor progression of osteosarcoma.

OBJECTIVE: Recent studies have revealed that circular RNAs (circRNAs) participate in the progression and development of many human diseases. Therefore, the purpose of this study was to uncover the role of circ_0000885 in the development of osteosarcoma and to explore the possible underlying mechanism. PATIENTS AND METHODS: Circ_0000885 expression in osteosarcoma tissues and cells was detected by Real Time-quantitative Polymerase Chain Reaction (RT-qPCR). The knockdown of circ_0000885 was conducted in osteosarcoma cells. Subsequently, its function in the progression of osteosarcoma was determined by cell proliferation assay, colony formation assay, and cell cycle assay, respectively. Furthermore, the underlying mechanism was explored by RT-qPCR and Western blot. RESULTS: Circ_0000885 was highly expressed in osteosarcoma tissues than that of adjacent tissues. Cell growth was significantly suppressed, and the distribution of cell cycle was regulated after circ_0000885 knock-down in vitro. Besides, both the mRNA and protein expressions of Caprin1 were significantly downregulated via silence of circ_0000885. Furthermore, Caprin1 was positively correlated with circ_0000885 in osteosarcoma tissues. CONCLUSIONS: Circ_0000885 could enhance osteosarcoma cell proliferation and regulate cell cycle by upregulating Caprin1, which might contribute to the therapy for osteosarcoma.

RBMS3 delays disc degeneration by inhibiting Wnt/ß-catenin signaling pathway.

OBJECTIVE: To study the effect of RBMS3 on nucleus pulposus cells and its effect on the Wnt/ß-catenin signaling pathway. PATIENTS AND METHODS: We measured the expression of RBMS3 in human nucleus pulposus tissues with different degrees of degeneration. Recombinant human IL-1ß is used to stimulate the degeneration of human nucleus pulposus cells. We used Wnt/ß-catenin signaling pathway inhibitors and cell transfection to study the effect of RBMS3 on nucleus pulposus cells and its mechanism. RESULTS: RBMS3 was less expressed in the nucleus pulposus tissue of people with higher degeneration degree. IL-1ß reduced the expression of RBMS3 in nucleus pulposus cells. Overexpression of RBMS3 can promote the proliferation of nucleus pulposus cells and reduce the apoptosis and inflammation of cells. In addition, RBMS3 can reduce the expression of ß-catenin and c-myc in nucleus pulposus cells, and inhibit the activity of the Wnt/ß-catenin signaling pathway. CONCLUSIONS: RBMS3 inhibits the Wnt/ß-catenin signaling pathway, improves the proliferation ability of nucleus pulposus cells, inhibits their apoptosis and inflammation, and thus delays the degeneration of the intervertebral disc.

The expression of TRPM7 in serum of patients with sepsis, its influences on inflammatory factors and prognosis, and its diagnostic value.

OBJECTIVE: This study aimed to investigate the expression of TRPM7 in the serum of patients with sepsis and its influences on inflammatory factors and prognosis. PATIENTS AND METHODS: A prospective analysis was performed. 78 patients with sepsis were enrolled in the experimental group and treated from May 2015 to April 2017 in the Emergency Department of The Second Hospital of Dalian Medical University, and 75 healthy people were collected in the control group and received physical examinations during the same period. Real-time quantitative PCR was used to detect the relative expression of TRPM7, and sandwich enzyme-linked immunosorbent assay (ELISA) was applied to measure the serum expression levels of TNF-α, IL-6, and IL-10 in patients. Besides, the receiver operating characteristic (ROC) curve was drawn to analyze the diagnostic value of TRPM7. RESULTS: The serum level of TRPM7 mRNA in the experimental group was higher than that in the control group (p<0.05). The serum levels of TNF-α, IL-6, and IL-10 in the experimental group were significantly higher than those in the control group (p<0.05). The optimal cut-off point value for the diagnosis of sepsis was 0.841; the specificity was 86%, and the sensitivity was 99%. Based on the survival data of the experimental group and the average expression level of TRPM7 which was 1.38, patients with a TRPM7 expression level less than 1.38 were divided into the low expression group, while those with a TRPM7 expression level equal or more than 1.38 were divided into the high expression group. The survival rate of the high expression group was significantly lower than that of the low expression group (p<0.05). CONCLUSIONS: In summary, TRPM7, with high expression level in the serum of patients with sepsis is expected to be a potential prognostic indicator for sepsis.

MEG3 promotes liver cancer by activating PI3K/AKT pathway through regulating AP1G1.

OBJECTIVE: This study aims to explore the biological function of maternally expressed gene 3 (MEG3) in liver cancer and the potential mechanism of phosphatidylinositide 3-kinases/protein kinase B (PI3K/AKT) pathway in regulating proliferation and invasion of hepatoma cells. PATIENTS AND METHODS: Quantitative Real-time polymerase chain reaction (qRT-PCR) was applied to examine the level of MEG3 in 72 pairs of liver cancer tissues and corresponding adjacent tissues. Expression levels of MEG3 and AP1G1 in hepatocellular carcinoma cell lines including SMMC-7721 and BEL-7402 were detected. After transfection of MEG3-siRNA or AP1G1 overexpression plasmid, the proliferative and invasive abilities of hepatoma cells were detected through cell counting kit-8 (CCK-8) and cell invasion assay. The effects of MEG3 and AP1G1 on the cell cycle of hepatoma cell lines were examined using flow cytometry. Western blot was conducted to estimate the changes in the protein levels of AP1G1, p-PI3K, p-AKT and VEGF before and after transfection. RESULTS: The level of MEG3 in hepatoma cancer tissues and cell lines was significantly reduced, especially in patients with advanced liver cancer. Knockdown of MEG3 significantly promoted proliferation and invasion of hepatoma cells, but accelerated cell cycle. Western blot analysis revealed that knockdown of MEG3 reduced the level of AP1G1 and activated the PI3K/AKT pathway. In addition, rescue experiments demonstrated that overexpression of AP1G1 partially reversed the promotive effect of lowly-expressed MEG3 on cell proliferation and invasion, suggesting that low expression of MEG3 may activate PI3K/AKT pathway by inhibiting AP1G1 expression. CONCLUSIONS: Low expression of MEG3 could promote the proliferative and invasive abilities of hepatoma cells and accelerate cell cycle. The mechanism may be related to the inhibition of AP1G1 expression and activation of PI3K/AKT pathway.

Influence of roflumilast on sepsis mice through the JAK/STAT signaling pathway.

OBJECTIVE: The aim of this study was to explore the influence of roflumilast on sepsis mice through the Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling pathway. MATERIALS AND METHODS: A total of 36 Sprague-Dawley mice were randomly divided into normal group (n=12), model group (n=12) and roflumilast group (n=12). Mice in the normal group were fed normally. However, mice in the model group and roflumilast group were intraperitoneally injected with endotoxin to establish the sepsis mouse model. Furthermore, mice in the model group and roflumilast group were intraperitoneally injected with 0.9% sodium chloride and roflumilast once a day, respectively. After 7 d of intervention, mice were sampled. Lung tissue morphology was observed via hematoxylin-eosin (HE) staining, and the pathological score was given. The protein expression levels of JAK and STAT-3 were detected via Western blotting. The expression levels of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were detected via enzyme-linked immunosorbent assay (ELISA). Meanwhile, the mRNA expression levels of JAK, STAT-3, IL-6 and TNF-α were detected via quantitative Polymerase Chain Reaction (qPCR). The number of inflammatory cells in the lavage fluid was counted by a biochemical detector. RESULTS: The survival rate of mice in the roflumilast group was significantly higher than that of the model group (p<0.05). The results of HE staining revealed that lung tissue morphology in roflumilast group was significantly improved when compared with the model group. Meanwhile, the pathological score in the roflumilast group was significantly lower than that of the model group (p<0.05). Western blotting showed that the protein expression levels of JAK and STAT-3 in the roflumilast group were markedly lower than those of the model group (p<0.05). According to the results of ELISA, the expression levels of IL-6 and TNF-α in the roflumilast group were remarkably lower than the model group (p<0.05). Further qPCR results manifested that the mRNA expression levels of JAK, STAT-3, IL-6 and TNF-α in the roflumilast group were significantly lower than those of the model group (p<0.05). Moreover, the number of neutrophils, monocytes and lymphocytes in the roflumilast group was significantly smaller than the model group. CONCLUSIONS: Roflumilast can improve lung tissue morphology of sepsis mice by inhibiting the JAK/STAT signaling pathway.

A modified approach from the edge of the tragus in the surgical treatment of mandibular condyle fractures.

Introduction We present our experiences using a modified surgical approach from the edge of the tragus for mandibular condyle fractures, to reduce the risk of postoperative complications and visible scars. Materials and methods Thirty-two patients presenting with mandibular condyle fractures were treated through a modified approach on the edge of the tragus. The age of the patients ranged from 6 to 62 years. All mandibular condyle fractures were fixed. The patients were asked to start open-mouth training one week postoperatively, undergoing a cone-beam computed tomography examination and clinical follow-up. Postoperative complications were evaluated after surgery. Results Mouth opening was normal (average 39.5 mm) in all the patients during the operation and the occlusion improved significantly compared with preoperatively. No cases of damaged facial nerves were observed during the final follow-up at six months and postoperative scars were less noticeable. Conclusions The modified surgical approach from the edge of the tragus for mandibular condyle fractures provides a good view of the operative field, reduces the risk of facial nerve damage and produces a less noticeable postoperative scar.

The role of Parkin protein in cardiac function and ventricular remodeling in myocardial infarction rats.

OBJECTIVE: This study aims to explore the role and the mechanism of Parkin protein in cardiac function and ventricular remodeling in myocardial infarction (MI) rats, and to provide a new sight for the treatment of myocardial infarction. MATERIALS AND METHODS: Fifty Sprague- Dawley (SD) male rats were randomly divided into 5 groups: sham operation group (Sham group), model group (MI group), low-dose Parkin group (L-Parkin group), middle-dose Parkin group (M-Parkin group) and high-dose Parkin group (H-Parkin group). The rat model of myocardial infarction was established by ligation of the anterior descending branch. Small animal ultrasound was used to measure cardiac function. The myocardial infarct size was observed by triphenyltetrazolium chloride (TTC) staining. The pathological changes of myocardial tissues were observed by hematoxylin-eosin (HE) staining. The myocardial cell apoptosis was detected by TUNEL assay. The mRNA expression of matrix metalloproteinase 2 (MMP2), matrix metalloproteinase 9 (MMP9), tissue inhibitor of matrix metalloproteinase 1 (TIMP1), tissue inhibitor of matrix metalloproteinase 2 (TIMP2) were detected by qRT-PCR. The expression of Parkin protein in myocardial tissue of rats was detected by Western-blot. RESULTS: Compared with MI group, left ventricular end-systolic volume (LVESV) and left ventricular end-diastolic volume (LVEDV) in Parkin overexpressing group were significantly decreased (p<0.05), while the value of left ventricular short axis shortening (FS) and left ventricular ejection fraction (EF %) in Parkin overexpression group were significantly increased (p<0.05). Overexpression of Parkin improved abnormal structure of myocardial tissue, reduced the size of myocardial infarct, made the arrangement of myocardium fibers more neatly and made the stain of myocardial cells more uniformly. Apoptosis index (AI) values were significantly decreased (p<0.05), and MMP2, MMP9, TIMP1 and TIMP2 mRNA levels were significantly decreased (p<0.05), while Parkin protein expression was significantly elevated in a dose-dependent manner (p<0.05). CONCLUSIONS: After treatment with Parkin in myocardial infarction rats, the relevant mRNA levels decreased, the number of apoptotic cells decreased, the myocardial fiber morphology returned to normal, the myocardial infarct size decreased, and the cardiac function of rats improved. Therefore, Parkin therapy plays an active role in cardiac function and ventricular remodeling in myocardial infarction rats.

LncRNA CASC9 promotes tumorigenesis by affecting EMT and predicts poor prognosis in esophageal squamous cell cancer.

OBJECTIVE: The purpose of this study was to explore the clinical significance and biological function of long noncoding RNA CASC9 (CASC9) in esophageal squamous cell carcinoma (ESCC). PATIENTS AND METHODS: Quantitative Real-time PCR (qRT-PCR) was used to determine the expression of CASC9 in ESCC tissues and cell lines. Receiver operating characteristic curves were used to evaluate the sensitivity and specificity of CASC9. The correlation between the CASC9 levels and the clinicopathological factors of the patients was also analyzed. Then, the survival was assessed by the Kaplan-Meier method and proportional hazards model. The effects of CASC9 on ESCC cells were evaluated by Cell Counting Kit-8 (CCK-8), migration and invasion. Finally, several EMT markers expression was detected by Western blot. RESULTS: We found that CASC9 was significantly upregulated in ESCC cell lines and clinical tissues. The CASC9 levels discriminated ESCC tissues from normal tissues with an area under the ROC curve (AUC) of 0.813. In addition, there is statistical significance between CASC9 expression level and tumor stage, lymph nodes metastasis, and clinical stage. Kaplan-Meier analysis indicated that high CASC9 expression had a significant impact on overall survival (p = 0.014) and disease-free survival (p = 0.0025). Moreover, CASC9 expression was an independent prognostic marker of overall survival and disease-free survival in a multivariate analysis. In vitro assay indicated that inhibition of CASC9 could suppress proliferation, migration, and invasion in ESCC. Further mechanistic studies found that aberrant CASC9 expression could modulate the expression levels of markers of EMT. CONCLUSIONS: Our data highlight the pivotal role of CASC9 as a novel diagnostic, prognostic biomarker and a potential therapeutic target of ESCC.

Effects of Bacillus fermentation on the protein microstructure and anti-nutritional factors of soybean meal.

This study evaluated the effects of Bacillus fermentation on soybean meal protein (SBMP) microstructure and major anti-nutritional factors (ANFs) in soybean meal (SBM). The Bacillus siamensis isolate JL8 producing high yield of protease at 519·1 U g-1 was selected for the laboratory production of fermented soybean meal (FSBM). After 24 h fermentation, the FSBM showed better properties compared with those of SBM, the ANFs such as glycinin, ß-conglycinin and trypsin inhibitor significantly decreased by 86·0, 70·3 and 95·01%, while in vitro digestibility and absorbability increased by 8·7 and 18·9% respectively. Scanning electron microscopy (SEM) image of fermented soybean meal protein showed smaller aggregates and looser network than that of SBMP. Secondary structure examination of proteins revealed fermentation significantly decreased the content of ß-sheet structure by 43·2% and increased the random coil structure by 59·9%. It is demonstrated that Bacillus fermentation improved the nutritional quality of SBM through degrading ANFs and changing the microstructure of SBMP. SIGNIFICANCE AND IMPACT OF THE STUDY: There is limited information about the structural property changes of soybean protein during fermentation. In this study, physicochemical analysis of soybean meal protein showed evidence that the increase in in vitro digestibility and absorbability of fermented soybean meal reflected the decrease in ß-conformation and destruction of original structure in soybean meal protein. The results directly gained the understanding of nutritional quality improvement of soybean meal by Bacillus fermentation, and supply the potential use of Bacillus siamensis for fermented soybean meal production.

Regulation of miR-92a on vascular endothelial aging via mediating Nrf2-KEAP1-ARE signal pathway.

OBJECTIVE: Various human aging-related diseases start with vascular aging, in which the aging of vascular endothelium is the first step to cause a structural and functional deficit of vascular endothelium, leading to vascular disorders. MicroRNA (miR) participates in various processes of body development and pathological processes via mediating cell proliferation, differentiation, and apoptosis. A previous study showed the correlation between cardiovascular disease and miR-92a, whose role and mechanism in vascular endothelial aging has not been reported. MATERIALS AND METHODS: In vitro, cultured human umbilical vein endothelial cells (HUVECs) were prepared for the vascular endothelial aging model by using 10-6 mM angiotensin II. MiR-92a expression was examined. After transfecting with the miR-92a inhibitor, 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-tetrazolium bromide (MTT) assay was employed to describe cell proliferation, and the Caspase 3 activity assay kit was used to evaluate apoptosis activity. Myeloid peroxidase (MPO) and superoxidase (SOD) activity, plus reactive oxygen species (ROS) content were measured. Nrf2, KEAP1 and ARE mRNA expressions were measured by real-time PCR. Nuclear factor erythroid 2 p45 related factor 2 (Nrf2) protein level, inflammatory factors tumor necrosis factor α (TNF-α) and interleukin-2 (IL-2) were tested by western blot or enzyme-linked immunosorbent assay (ELISA). RESULTS: In model group, miR-92a expression was elevated significantly compared to the control group (p < 0 .05). MiR-92a inhibitor transfection facilitated cell proliferation, decreased Caspase 3 activity, ROS or MPO, expressions of TNF-α, IL-2 and KEAP1, and enhanced SOD level and Nrf2, ARE expressions significantly compared to the model group (p < 0.05). CONCLUSIONS: In aged vascular endothelium, miR-92a was up-regulated. Through inhibiting miR-92a expression and regulating Nrf2-KEAP1-ARE signal pathway, the oxidative stress reaction or inflammation can be suppressed, thus inhibiting endothelial apoptosis and facilitating cell proliferation.