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Dou Zhang,1,2,* Xuyi Liu,1,2,* Xiong Li,3,* Xinyi Cai,1,2 Zhenying Diao,1,2 Long Qiu,1,2 Xuelin Chen,1,2 Yuyu Liu,1,2 Jianbo Sun,1 Daxiang Cui,1,4 Qiaoyuan Ye,5 Ting Yin1,2 1Research Center of Nano Technology and Application Engineering, The First Dongguan Affiliated Hospital, School of Pharmacy, Guangdong Medical University, Dongguan, Guangdong, 523808, People’s Republic of China; 2Dongguan Biomedical Nano Engineering Technology Research Center, Guangdong Medical University, Dongguan, Guangdong, 523808, People’s Republic of China; 3Department of Pharmacy, Zhuhai People’s Hospital (Zhuhai Hospital Affiliated with Jinan University), Zhuhai, Guangdong, 519000, People’s Republic of China; 4School of Sensing Science and Engineering, School of Electronic Information and Electrical Engineering, Shanghai Jiao Tong University, Shanghai, 200240, People’s Republic of China; 5Department of Dermatology and Venereology, Second Clinical Medical College of Guangdong Medical University, Dongguan, Guangdong, 523808, People’s Republic of China*These authors contributed equally to this workCorrespondence: Qiaoyuan Ye, Department of Dermatology and Venereology, Second Clinical Medical College of Guangdong Medical University, Dongguan, Guangdong, 523808, People’s Republic of China, Email 13650248189@163.com Ting Yin, Research Center of Nano Technology and Application Engineering, School of Pharmacy, Guangdong Medical University, Dongguan, Guangdong, 523808, People’s Republic of China, Email wsyt132@163.comPurpose: Melanoma is a highly aggressive and dangerous malignant skin tumor and there is an urgent need to develop effective therapeutic approaches against melanoma. The main objective of this study was to construct a multifunctional nanomedicine (GNR@PEG-Qu) to investigate its therapeutic effect on melanoma from the oxidative stress pathway.Methods: First, the nanomedicine GNR@PEG-Qu was synthesized and characterized, and its photothermal and antioxidant properties were confirmed. In addition, in vivo imaging capabilities were observed. Finally, the tumor inhibitory effects of GNR@PEG-Qu in vivo and in vitro as well as its biosafety were observed.Results: GNR@PEG-Qu shows good photothermal and anti-oxidation properties. Following exposure to 1064 nm laser irradiation in the second near-infrared II (NIR-II) window, GNR@PEG-Qu shows anti-tumor ability through low-temperature photothermal therapy (PTT) adjuvant drug chemotherapy. GNR@PEG-Qu makes full use of the antioxidant capacity of quercetin, reduces ROS levels in melanoma, alleviates oxidative stress state, and achieves “oxidative stress avoidance” at the tumor site. Quercetin can also downregulate the expression of the heat shock protein Hsp70, which will improve the thermal sensitivity of the tumor site and enhance the efficacy of low-temperature PTT.Conclusion: GNR@PEG-Qu nanoagent exhibits synergistic treatment and high tumor inhibition effects, which is a promising strategy developed to achieve oxidative stress avoidance and synergistic therapy of melanoma using quercetin (Qu)-coated gold nanorod (GNR@PEG).Keywords: melanoma, gold nanorods, quercetin, chemo-photothermal therapy, oxidative stress

Yuan Cheng,1 Qingqing Wang,2 Chuanxi Sun,3 Di Cui1 1Fuyang Medical College, Fuyang Normal University, Fuyang, Anhui, People’s Republic of China; 2Department of Neurology, The Affiliated Fuyang People’s Hospital of Anhui Medical University, Fuyang, Anhui, People’s Republic of China; 3Clinical Laboratory, The Second Hospital Affiliated to Fuyang Normal University, Fuyang, Anhui, People’s Republic of ChinaCorrespondence: Di Cui, Fuyang Medical College, Fuyang Normal University, Fuyang, Anhui, 236000, People’s Republic of China, Email fycuidi1990@163.comBackground: The atherogenic index of plasma (AIP) is a biomarker for coronary heart disease, atherosclerosis, and metabolic syndrome. However, the mechanism of its action in the acute phase of acute pontine infarction remains unclear. This study investigated the association between the AIP and the short-term prognosis of acute pontine infarction.Methods: Clinical and laboratory index data of patients admitted to the hospital for acute pontine infarction were continuously included, and these patients were followed up for 90 days after disease onset. The modified Rankin Scale (mRS) was used to evaluate the 90-day clinical outcomes of the patients, and an mRS score ≥ 3 was used to define adverse functional outcomes. Univariate analysis was used to detect differences in the indicators between the two groups. Patients were then divided into three groups according to the quantile of the AIP (T1: AIP ≤ 0.029; T2, 0.029 < AIP ≤ 0.248; T3, AIP > 0.248), and a binary logistic regression model was used to assess risk factors for prognosis shortly after acute pontine infarction.Results: A total of 260 patients with acute pontine infarction (mean age=64.5± 11.8 years) were included during the study period, and 68 (26.2%) patients had a poor 90-day prognosis. The AIP in the poor 90-day prognosis group was significantly greater (P < 0.05) than that in the good 90-day prognosis group. The multivariate logistic regression analysis revealed that the AIP (OR=9.829; 95% CI: 2.837– 34.051; p < 0.001), baseline NIHSS score (OR=1.663; 95% CI: 1.400– 1.975; p < 0.001) and infarct volume (OR=1.762; 95% CI: 1.013– 3.062; p=0.045) were significantly associated with poor 90-day prognosis in patients with acute pontine infarction.Conclusion: In patients with acute pontine infarction, the AIP may serve as an important biological marker of poor clinical prognosis and is independently associated with poor 90-day prognosis.Keywords: lipid metabolism, atherogenic index of plasma, pontine infarction, risk factors, outcome

Zhiying Yang,1,&ast; Shun Yao,1,2,&ast; Yichong Xu,1 Xiaoqing Zhang,1,2 Yuan Shi,1,2 Lijun Wang,1,2 Donghong Cui1,2 1Shanghai Mental Health Center, Shanghai Jiao Tong University School of Medicine, Shanghai, People’s Republic of China; 2Shanghai Key Laboratory of Psychotic Disorders, Shanghai Jiao Tong University School of Medicine, Shanghai, People’s Republic of China&ast;These authors contributed equally to this workCorrespondence: Donghong Cui, Email manyucc@126.comBackground: Schizophrenia is a devastating mental disease with high heritability. A growing number of susceptibility genes associated with schizophrenia, as well as their corresponding SNPs loci, have been revealed by genome-wide association studies. However, using SNPs as predictors of disease and diagnosis remains difficult. Here, we aimed to uncover susceptibility SNPs in a Chinese population and to construct a prediction model for schizophrenia.Methods: A total of 210 participants, including 70 patients with schizophrenia, 70 patients with bipolar disorder, and 70 healthy controls, were enrolled in this study. We estimated 14 SNPs using published risk loci of schizophrenia, and used these SNPs to build a model for predicting schizophrenia via comparison of genotype frequencies and regression. We evaluated the efficacy of the diagnostic model in schizophrenia and control patients using ROC curves and then used the 70 patients with bipolar disorder to evaluate the model’s differential diagnostic efficacy.Results: 5 SNPs were selected to construct the model: rs148415900, rs71428218, rs4666990, rs112222723 and rs1716180. Correlation analysis results suggested that, compared with the risk SNP of 0, the risk SNP of 3 was associated with an increased risk of schizophrenia (OR = 13.00, 95% CI: 2.35– 71.84, p = 0.003). The ROC-AUC of this prediction model for schizophrenia was 0.719 (95% CI: 0.634– 0.804), with the greatest sensitivity and specificity being 60% and 80%, respectively. The ROC-AUC of the model in distinguishing between schizophrenia and bipolar disorder was 0.591 (95% CI: 0.497– 0.686), with the greatest sensitivity and specificity being 60% and 55.7%, respectively.Conclusion: The SNP risk score prediction model had good performance in predicting schizophrenia. To the best of our knowledge, previous studies have not applied SNP-based models to differentiate between cases of schizophrenia and other mental illnesses. It could have several potential clinical applications, including shaping disease diagnosis, treatment, and outcomes.Keywords: schizophrenia, SNP, diagnostic model, bipolar disorder, differential diagnosis

Yushan Xu, Miaomiao Li, Mengjiao Lin, Dawei Cui, Jue Xie Department of Blood Transfusion, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, 310003, People’s Republic of ChinaCorrespondence: Jue Xie; Dawei Cui, Tel +86571-87236391 ; +86571-87236390, Email zyyyxj2011@zju.edu.cn; daweicui@zju.edu.cnAbstract: CD4+ T cells play a critical role in the pathogenesis of viral diseases, which are activated by the internal metabolic pathways encountering with viral antigens. Glutaminolysis converts glutamine into tricarboxylic acid (TCA) circulating metabolites by α-ketoglutaric acid, which is essential for the proliferation and differentiation of CD4+ T cells and plays a central role in providing the energy and structural components needed for viral replication after the virus hijacks the host cell. Changes in glutaminolysis in CD4+ T cells are accompanied by changes in the viral status of the host cell due to competition for glutamine between immune cells and host cells. More recently, attempts have been made to treat tumours, autoimmune diseases, and viral diseases by altering the breakdown of glutamine in T cells. In this review, we will discuss the current knowledge of glutaminolysis in the CD4+ T cell subsets from viral diseases, not only increasing our understanding of immunometabolism but also providing a new perspective for therapeutic target in viral diseases.Keywords: CD4+ T cells, viral diseases, glutamine, glutaminolysis, immune response

Luxinyi Xu,1,2 Xiaotong Wen,1,2 Ying Yang,1,2 Dan Cui1,2 1School of Public Health, Wuhan University, Wuhan, 430071, People’s Republic of China; 2Global Health Institute, Wuhan University, Wuhan, 430071, People’s Republic of ChinaCorrespondence: Dan Cui, School of Public Health, Wuhan University, 115&num; Donghu Road, Wuhan, 430071, People’s Republic of China, Tel +86 133 1715 0755, Email 00008766@whu.edu.cnBackground: Patients with both diabetes and hypertension could face more health risks than those with either condition alone, and less attention has been paid to their management outcomes, so this study may be the first to specifically address this problem. We aimed to examine the management outcomes of blood pressure (BP) in hypertensive patients with/without diabetes and fasting plasma glucose (FPG) in diabetic patients with/without hypertension.Methods: Follow-up data were obtained from the National Basic Public Health Service Project in Sanming (2017– 2021). A total of 25,795 adults with hypertension only, 4111 adults with diabetes only, and 5729 comorbid adults (namely, hypertensive patients with diabetes) were included. Generalized estimating equations were applied.Results: Systolic blood pressure (SBP) and diastolic blood pressure (DBP) in patients with hypertension only both dropped significantly (Coef. = − 0.00088, P < 0.001; Coef. = − 0.00081, P < 0.001). DBP in comorbid patients decreased considerably (Coef. = − 0.00033, P < 0.001). Pulse pressure in comorbid patients grew rapidly (Coef. = 0.00044, P < 0.001). BP control rate in patients with hypertension only increased significantly (OR = 1.00039, P < 0.001). FPG control rates in diabetic patients with/without hypertension grew markedly (OR = 1.00013, P < 0.001; OR = 1.00020, P < 0.001). Comorbid patients had lower baseline SBP and DBP but higher latest SBP than patients with hypertension only (Coef. = − 1.18872, P < 0.001; Coef. = − 1.16049, P < 0.001; Coef. = 1.0634, P < 0.001). Comorbid patients had lower baseline BP and FPG control rates than those with either condition alone, and differences were greater at the latest follow-up (OR = 0.28086, P < 0.001; OR = 0.91012, P = 0.049; OR = 0.04020, P < 0.001; OR = 0.69465, P < 0.001).Conclusion: BP and FPG management outcomes have achieved progress. Comorbid patients have poorer performance than patients with either disease alone in BP levels especially the SBP level and control rates of SBP, DBP, and FPG. Future studies should be conducted using national data and include more confounding factors.Keywords: hypertension, diabetes mellitus, comorbidity, blood pressure, fasting plasma glucose, longitudinal studies

Weidong Zhang,1 Dong Cui,1 Yaqian Liu,2 Kefeng Shi,1 Xia Gao,3 Rulin Qian1 1Department of Thoracic Surgery, Henan Provincial Chest Hospital, Zhengzhou City, Henan Province, People’s Republic of China; 2Medical Records and Statistics Room, Henan Provincial Chest Hospital, Zhengzhou City, Henan Province, People’s Republic of China; 3Department of Cardiovascular Surgery, Henan Provincial Chest Hospital, Zhengzhou City, Henan Province, People’s Republic of ChinaCorrespondence: Rulin Qian; Xia Gao, Henan Provincial Chest Hospital, Room 1, Weiwu Road, Zhengzhou City, Henan Province, 450003, People’s Republic of China, Email qianrulin0371@163.com; gaoxia03712022@163.comObjective: To analyze the clinical characteristics of patients with malignant pulmonary sclerosing pneumocytoma (PSP) with metastasis, recurrence, and growth and to improve clinicians’ understanding of PSP in patients with malignant tumor characteristics.Methods: A total of 46 PSP patients with malignant tumor characteristics were identified in the literature search and compared with 38 patients with benign PSP diagnosed and treated in our hospital in the past 5 years. We explored the pathogenesis, clinical symptoms, diagnostic methods, treatment strategies and prognosis of PSP patients with malignant tumor.Results: The characteristics of young age (≤ 41 years old), larger tumor (≥ 36mm), lymph node metastasis and distribution in East Asians are indicative of PSP with malignant potential. Such patients should undergo segmental resection or lobectomy, combined with necessary lymph node dissection or biopsy. All patients with PSP should have an entire course of follow-up management, because they may have an adverse prognosis such as recurrence, growth, metastasis, and even death.Conclusion: PSP has the potential for malignancy. Anatomical lobectomy or segmental resection combined with lymph node dissection should be performed in PSP with some specific characteristics. Inappropriate diagnosis and treatment may lead to poor prognosis in PSP patients.Keywords: pulmonary sclerosing pneumocytoma, malignant tumor, metastasis, recurrence, growth, treatment and diagnosis

Jinjin Tong,1,&ast; Xintong Ji,1,&ast; Hua Zhang,1 Benhai Xiong,2 Defeng Cui,3 Linshu Jiang1 1Beijing Key Laboratory for Dairy Cow Nutrition, Beijing University of Agriculture, Beijing, People’s Republic of China; 2State Key Laboratory of Animal Nutrition, Institute of Animal Science, Chinese Academy of Agricultural Sciences, Beijing, People’s Republic of China; 3Beijing Key Laboratory of TCVM, Beijing University of Agriculture, Beijing, People’s Republic of China&ast;These authors contributed equally to this workCorrespondence: Defeng Cui, Beijing Key Laboratory of TCVM, Beijing University of Agriculture, Beijing, People’s Republic of China, Tel +86 (10)-81798091, Email cdfffff@163.com Linshu Jiang, Beijing Key Laboratory for Dairy Cow Nutrition, Beijing University of Agriculture, Beijing, People’s Republic of China, Tel +86 (10)-81798091, Email linshujiangbua@163.comPurpose: Streptococcus agalactiae is one of the primary pathogens responsible for subclinical mastitis, a significant economic burden for dairy farms. An essential component of the immune response to infection is ubiquitination, which plays important roles in the complex interactions between the pathogen and host.Materials and Methods: In the present study, quantitative ubiquitylomics was performed to profile changes in the global ubiquitinome of bovine mammary gland epithelial cells (BMECs) infected with S. agalactiae.Results: The most notable changes in the BMEC ubiquitinome were related to the adherens junction, ribosome, and tight junction pathways. Ubiquitination of CTNNB1, EGFR, ITGB1, CTNNA1, CTNNA2, CDH1, YES1, and SLC9A3R1 appears to be fundamental for regulating multiple cellular processes in BMECs in response to S. agalactiae infection. In addition, broad ubiquitination of various effectors and outer membrane proteins was observed. Ubiquitinated proteins in S. agalactiae-infected BMECs were associated with regulating cell junctions in the host, with potential implications for susceptibility to infection.Conclusion: The preliminary findings suggest that extensive ubiquitination of CTNNB1, CDH1 and SLC9A3R1 and proteins closely related to cell junctions might play an important role in mastitis progression in dairy cows. The results provide evidence that ubiquitin modification of certain proteins in S. agalactiae-infected BMECs could be a promising therapeutic strategy for reducing mammary gland injury and mastitis.Keywords: ubiquitination, protein degradation, mastitis, dairy cows

Dan Cui, Caifang Ni Department of Interventional Radiology, The First Affiliated Hospital of Soochow University, Suzhou City, Jiangsu Province 215006, People’s Republic of ChinaCorrespondence: Caifang NiDepartment of Interventional Radiology, The First Affiliated Hospital of Soochow University, No.188 Shizi Street, Suzhou City, Jiangsu Province 215006, People’s Republic of ChinaTel +86-512-65223637Email np0973@163.comBackground: It is known that Lnc712 plays an important role in the pathogenesis of breast cancer. However, whether it is involved in hepatocellular carcinoma (HCC) remains unknown. In this study, we aimed to investigate the role and underlying mechanism of Lnc712 in HCC.Methods: Sixty-four HCC patients were enrolled and followed up for 5 years to analyze the prognostic value of Lnc712 for HCC. HCC cells were transfected with Lnc712 expression vector, Bach-1 expression vector (or siRNA) and miR-142-3p mimic (or inhibitor) to explore the interactions among Lnc712, miR-142-3p and Bach-1. Cell proliferation, migration, invasion and cell cycle were analyzed by CCK-8 assay, transwell assay, wound healing assay and flow cytometry assay, respectively.Results: The expression of Lnc712 was upregulated in HCC, and the upregulated Lnc712 expression was significantly related to poor overall survival in HCC patients. In HCC cells, Lnc712 interacted with miR-142-3p and upregulated Bach-1, a target of miR-142-3p. In addition, Lnc712 promoted HCC cell proliferation, migration, invasion and cell cycle, while its effects were abolished by miR-142-3p mimic. Moreover, miR-142-3p mimic enhanced HCC cell proliferation, migration, invasion and cell cycle, while its effects were abolished by Bach-1 overexpression. miR-142-3p inhibitor repressed cell proliferation, migration, invasion and cell cycle in HCC cells, while its effects were abolished by Bach-1 knockdown. Furthermore, Lnc712 knockdown remarkably inhibited HCC tumor growth in nude mice.Conclusion: Lnc712 may promote the development of HCC by targeting the miR-142-3p/Bach-1 axis.Keywords: hepatocellular carcinoma, Lnc712, Bach-1, miR-142-3p

Zhe Zhang,1,2 Di Cui,1,2 Tan Zhang,1,2 Yi Sun,1,2 Shuzhe Ding1,2 1Key Laboratory of Adolescent Health Assessment and Exercise Intervention of Ministry of Education, East China Normal University, Shanghai 200241, People’s Republic of China; 2College of Physical Education and Health, East China Normal University, Shanghai 200241, People’s Republic of ChinaCorrespondence: Shuzhe DingKey Laboratory of Adolescent Health Assessment and Exercise Intervention of Ministry of Education, East China Normal University, Shanghai 200241, People’s Republic of ChinaTel +86 13601798505Email szding@tyxx.ecnu.edu.cnPurpose: Mitochondrial dysfunction and endoplasmic reticulum stress (ERS) are associated with metabolic diseases such as obesity and Type 2 diabetes mellitus (T2DM). Mitochondria and ER are connected via mitochondria-associated membranes (MAM) that are involved in glucose homeostasis and insulin resistance. We postulated that exercise might positively benefit T2DM-induced ER and mitochondrial dysfunction that might be associated with MAM.Materials and Methods: Mice were fed a high-fat diet and injected with streptozotocin (STZ) to create T2DM models. Glucose tolerance, mitochondrial quality, MAM quality, and ERS were investigated in diabetic mice after six weeks of swimming.Results: Type 2 DM induced decreased MAM quantity, impaired mitochondrial quality, and deteriorated ERS in skeletal muscle that led to endoplasmic reticulum-associated degradation (ERAD). Swimming alleviated strong ERS caused by T2DM. Importantly, MAM quantity was positively associated with mitochondrial function and tended to negatively correlate with the ERS branch, ATF6. Moreover, both ATF6 branches of ERS and ERAD were positively associated with the pIRE1α branch of ERS.Conclusion: Type 2 DM induced glucose intolerance, powerful ERS, and mitochondrial dysfunction associated with decreased amounts of MAM. Swimming improved glucose intolerance and selectively mitigated the ERS in skeletal muscle. Therefore, MAM quality and ATF6 might be novel and important targets for T2DM treatment. Endoplasmic reticulum stress might be an effective target of swimming to improve diabetes.Keywords: T2DM, skeletal muscle, mitochondrial quality, ERS, MAM

OBJECTIVE: Intervertebral disc degeneration (IVDD) is associated with the apoptosis of nucleus pulposus (NP) cells. Previous studies have shown that PTEN plays crucial roles in cell survival and apoptosis. The effect of PTEN inhibitors on cell survival following IVDD has been rarely examined. In this study, we investigated the protective effect of SF1670, as a specific PTEN inhibitor, on an in vitro NP cells degenerated model. PATIENTS AND METHODS: We collected human disc samples from IVDD patients and detected PTEN expression in them with different degenerated degrees. NP cells were isolated from the samples and exposed to IL-1β with or without SF1670. Then, cells viability was determined by CCK-8 assay. We also measured the levels of collagen II, p16, p53, PTEN, Akt, aggrecan, caspase 3/9, Bax, Bcl-2, and several inflammatory factors in NP cells. RESULTS: We found that the expression of PTEN markedly increased in severely degenerated disc tissues. The data showed that IL-1β upregulated the expressions of p16, p53, PTEN, caspase 3/9, and Bax, but decreased the expressions of collagen II, Akt, aggrecan, and Bcl-2. Surprisingly, the treatment with SF1670 could significantly reverse the regulatory effects of IL-1β. Moreover, relative levels of IL-6, IL-8, TNF-α, and MMP3/9/13 were significantly suppressed by SF1670 stimuli compared with IL-1β group. CONCLUSIONS: Overall, these results demonstrated that SF1670 prevented NP degradation via suppressing apoptosis and inflammation through inhibition of PTEN and activation of Akt. SF1670 may become a novel target for the therapy of IVDD in the future. [ABSTRACT FROM AUTHOR]

Background: Antimicrobial resistance (AMR) and healthcare-associated infections (HAIs) are among the biggest global public health challenges, and overlap widely. These infections cause significant morbidity and mortality, put pressure on health systems, and incur rising direct and indirect costs.Aim: This study analysed the direct medical burden attributable to AMR-HAIs in Chinese public tertiary hospitals, and aimed to inform both the medical regulators and hospital managers for better control of HAIs and containment of AMR.Methods: The propensity score matching method (γ= 0.25σ, nearest neighbor 1:1 matching) was applied to conduct a retrospective cohort study in five public tertiary hospitals in the Hubei province of China during 2013-2015. Descriptive analysis, Pearson's chi-squared test, Mann-Whitney U-test, Wilcoxon signed-rank test and paired/independent Z/T test were conducted. The statistically significant level was set at P<0.05.Findings: From 2013 to 2015 overall, the additional total medical expenditure per HAI-AMR inpatient was US$15,557.25 compared with that of the non-HAIs, and the additional length of per hospital stay of the HAI-AMR inpatient was 41 days compared with that of the non-HAIs (P<0.001).Conclusions: In combination with AMR, HAIs caused significant additional medical expenses and affected the turnover rate of hospital beds. Most of the increased medical costs fell to patients and their families. These findings call for more effective control of HAIs and containment of AMR. A national study is needed to estimate the medical, social and economic burden of HAIs in combination with AMR. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Primary hepatocellular carcinoma (HCC) is one of the most important malignant liver cancers in clinic. Serum alpha-fetoprotein (AFP) positive expression is an important examination index. However, there are some hepatocellular carcinoma patients show negative AFP expressions. Therefore, how to screen AFP-hepatocellular carcinoma patients is important and difficult. PATIENTS AND METHODS: Total of 80 cases of AFP- hepatocellular carcinoma patients with or without focal nodular hyperplasia (FNH) confirmed by surgery was enrolled. Clinical information was collected for correlation analysis. Real-time PCR (RT-PCR) and Western blot were applied for gene expression analysis, and the target gene includes CD34, proliferation cell nuclear antigen (PCNA) and cell keratin 19 (CK19). Their relationship was analyzed. RESULTS: CD34 positive rate in the 80 cases was 48%, of which patients with FNH showed higher expression level than those of patients without FNH. The PCNA positive rate was 38%, and there was no statistical difference between patients with and without FNH. The CK19 positive rate was 56%, while the patients with FNH presented a higher level than the patients without FNH. CD34, PCNA, and CK19 showed no evident difference on different gender, age, or tumor size. CD34 was negatively correlated with PCNA and positively correlated with CK19. CONCLUSIONS: AFP- hepatocellular carcinoma patients with FNH showed high CD34 and CK19, and low PCNA level. [ABSTRACT FROM AUTHOR]

The interfacial transition zone tends to be the weakest link in cement-based materials. This zone is widely believed to be less dense compared with the bulk hydrated cement matrix and is often the location where the failure first initiates. Because of its increased porosity, the interface also acts as a preferential path for transport of deleterious fluids. Understanding the microstructure of the interface, therefore, is of high importance. In this paper, a new technique is developed to calculate the width, as well as the average porosity, of the interface. The method relies on computer tomography (CT). Compared with the traditional porosity-measurement methods, the proposed dual-scan method is non-destructive, and, to a great extent, preserves the initial microstructure of the interface, thereby providing an undisturbed characterization. This article further attests that the dual-scan method can mitigate the deficiency of traditional CT scan in terms of its limited resolution. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To investigate the correlation between LeY glycan expression and embryo implantation. MATERIALS AND METHODS: Uterine epithelial cells before implantation were transfected with FUT1siRNA to inhibit FUT1 (the gene encoding the key enzyme of LeY synthesis) expression and treated with 10 ng/ml leukemia inhibitory factor (LIF). Murine embryo implantation model in vitro was prepared by late blastocysts with identical morphology and treated uterine epithelial cells co-culture. Using RT-PCR, dot blot and observation of embryo attachment to analyze FUT1 gene expression and LeY synthesis of uterine epithelial cells and studied further the correlation of LeY expression level and embryo implantation. RESULTS: FUT1 gene expression and LeY synthesis declined after cells were transfected with FUT1siRNA, and LIF promoted FUT1 expression and LeY synthesis. After expression of FUT1 gene was inhibited, attachment rate of embryos lowered, but LIF up-regulated FUT1 expression and increased the attachment rate of embryos. CONCLUSIONS: These results indicated regulating FUT1 expression affected LeY synthesis, and then LeY regulated the recognition and attachment of uterus-embryo and participates in embryo implantation further. [ABSTRACT FROM AUTHOR]

Zero-field cooling (ZFC) exchange bias (EB) was observed in antiperovskite compounds Ga1- xNMn3+ x ( x = 0.06 and 0.1). The existence of ferromagnetic (FM) clusters has been demonstrated in a spin glass (SG) matrix. The ZFC-EB is suggested to originate from the unidirectional anisotropy formed isothermally along the FM/SG interface. For this typical physical system, both ways including the initial magnetization process and FC process could result in the unidirectional anisotropy. In addition, the training effect after ZFC is similar to those observed in conventional FC-EB systems. [ABSTRACT FROM AUTHOR]

Zero-field cooling (ZFC) exchange bias (EB) was observed in antiperovskite compounds Ga1- xNMn3+ x ( x = 0.06 and 0.1). The existence of ferromagnetic (FM) clusters has been demonstrated in a spin glass (SG) matrix. The ZFC-EB is suggested to originate from the unidirectional anisotropy formed isothermally along the FM/SG interface. For this typical physical system, both ways including the initial magnetization process and FC process could result in the unidirectional anisotropy. In addition, the training effect after ZFC is similar to those observed in conventional FC-EB systems. [ABSTRACT FROM AUTHOR]