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Chronic hepatitis B is one of the common infectious diseases in the world, with a wide epidemic range and strong contagiousness, which is difficult to completely eradicate. From July 2020 to April 2022, 142 patients with hepatitis B who were admitted to tertiary hospitals were selected and randomly divided into 2 cases, with 71 cases per case. The control group adopts a conventional model, and the observation group implements a nursing model based on the control group. The management capacity and quality of life before and after the two groups of care were compared. 94 patients with chronic hepatitis B who were admitted to the hospital from July 2020 to April 2022 were selected, and 47 cases were divided into the control group and observation group according to the admission time. The control group is given a conventional model, and the observation group is given a nursing model on the basis of the control group. Both groups of patients observed anxiety self-assessment scale (SAS), depression self-assessment scale (SDS), short life span scale (SF-36) scores, and treatment conditions before and after the intervention, to explore the application of nursing model in the management of hepatitis B patients in tertiary hospitals and its impact on patient quality of life. Based on study’s precare outcomes, there was no statistically significant difference between the self-administered scale (PIH) score and the quality of life measurement summary scale (QOL-BREF) score ( P > 0.05 ) between the two groups. After one month of care, both groups had lower PIH scores than before care, and QOL-BREF scores were higher than before care ( P < 0.05 ). After one month of treatment, the PIH score of the observation group was significantly reduced, and the QOL-BREF score after one month of treatment was significantly higher than that of the control group ( P < 0.05 ). The SAS and SDS scores in the observation group were lower than those in the control group, and the quality of life scores and treatment compliance were higher than those in the control group, and the difference was statistically significant ( P < 0.05 ). Conclusions. The nursing model can effectively improve the management and quality of life of hepatitis B patients. It also had a significant positive effect on the therapeutic capacity and quality of life of patients with hepatitis B and improved patient compliance behavior and quality of life.

Neurofibromatosis type 1 (NF1) is an autosomal dominant tumor predisposition syndrome that involves the central and peripheral nervous systems. Accurate detection and segmentation of neurofibromas are essential for assessing tumor burden and longitudinal tumor size changes. Automatic convolutional neural networks (CNNs) are sensitive and vulnerable as tumors' variable anatomical location and heterogeneous appearance on MRI. In this study, we propose deep interactive networks (DINs) to address the above limitations. User interactions guide the model to recognize complicated tumors and quickly adapt to heterogeneous tumors. We introduce a simple but effective Exponential Distance Transform (ExpDT) that converts user interactions into guide maps regarded as the spatial and appearance prior. Comparing with popular Euclidean and geodesic distances, ExpDT is more robust to various image sizes, which reserves the distribution of interactive inputs. Furthermore, to enhance the tumor-related features, we design a deep interactive module to propagate the guides into deeper layers. We train and evaluate DINs on three MRI data sets from NF1 patients. The experiment results yield significant improvements of 44% and 14% in DSC comparing with automated and other interactive methods, respectively. We also experimentally demonstrate the efficiency of DINs in reducing user burden when comparing with conventional interactive methods. The source code of our method is available at \url{https://github.com/Jarvis73/DINs}., Accepted by IEEE Journal of Biomedical and Health Informatics (JBHI)

Cellular senescence is a stress response that imposes a growth arrest on cancer and nonmalignant cells during cancer therapy. By secreting a plethora of proinflammatory factors collectively termed the senescence-associated secretory phenotype (SASP), therapy-induced senescent cells can promote tumorigenesis. Moreover, the SASP from senescent cells is also able to drive therapy resistance and mediate many adverse effects of cancer therapy. Because senescent cell production often occurs during cancer therapy, it is important to carefully consider these potential detrimental effects. Senotherapy, which refers to selective removal of senescent cells, has been proposed as a promising adjuvant approach to eliminate the adverse effects of senescent cells. Thus, in this review we summarize in detail the mechanisms by which senescent cells contribute to tumorigenesis and therapeutic resistance. Also, we thoroughly discuss the potential strategies regarding how to effectively circumvent the undesirable effects of therapy-induced senescent cells.

Nonalcoholic fatty liver disease (NAFLD) is a chronic disease caused by excessive fat accumulation in the liver in addition to alcohol consumption and other pathological factors. The incidence of NAFLD is rapidly growing, currently affecting 25% of the world population. Exosomes are extracellular vesicles containing a variety of biological molecules, including microRNAs (miRNAs). To monitor the expression of exosomal microRNAs in the NAFLD. In this study, five nonalcoholic fatty liver patients were included in the disease group, and five simple obesity patients were included in the control group. Exosomes from NAFLD patient serum were collected, and exosomal miRNAs were extracted. Exosomes were isolated and then confirmed by electron microscopy, nanoparticle tracking analysis (NTA) and western blotting. High-throughput sequencing methods were used to determine the expression profile of exosome-derived miRNAs. The sequencing results revealed that a total of 2588 miRNAs were identified. The expression of 80 miRNAs significantly differed between the NAFLD and control groups, including 30 upregulated and 50 downregulated miRNAs. miR-122-5p, miR‐27a, and miR‐335-5p may play an important role in NAFLD. Finally, GO and KEGG analyses were applied to explore the function of miRNA targets. Collectively, this study identified some key exosomal miRNAs and pathways in NAFLD that might be used as molecular targets or diagnostic biomarkers for NAFLD.

Context A high amount of red meat consumption has been associated with higher risks of coronary heart disease (CHD) and all-cause mortality in a single food-exposure model. However, this model may overlook the potentially differential influence of red meat on these outcomes depending on the foods replaced by red meat. Objective A PRISMA-compliant meta-analysis of prospective observational studies was performed to quantify the risks of CHD and all-cause mortality associated with the replacement of total, unprocessed, or processed red meat with fish/seafood, poultry, dairy, eggs, nuts, and legumes. Data sources The PubMed and Web of Science databases were searched to identify relevant articles published in any language from database inception to October 30, 2021. Data extraction The prospective observational studies were considered relevant if they reported relative risks (RRs) and 95%CIs for the associations of interest. Data analysis Thirteen articles were included. A random-effects model was used to estimate the summary RRs and 95%CIs for the associations of interest. Replacing total red meat with poultry (RR, 0.88, 95%CI, 0.82–0.96; I2 = 0%), dairy (RR, 0.90, 95%CI, 0.88–0.92; I2 = 0%), eggs (RR, 0.86, 95%CI, 0.79–0.94; I2 = 7.1%), nuts (RR, 0.84, 95%CI, 0.74–0.95; I2 = 66.8%), or legumes (RR, 0.84, 95%CI, 0.74–0.95; I2 = 7.3%) was associated with a lower risk of CHD, whereas substituting fish/seafood (RR, 0.91, 95%CI, 0.79–1.04; I2 = 69.5%) for total red meat was not associated with the risk of CHD. The replacement of total red meat with fish/seafood (RR, 0.92, 95%CI, 0.89–0.96; I2 = 86.9%), poultry (RR, 0.92, 95%CI, 0.90–0.95; I2 = 61.6%), eggs (RR, 0.91, 95%CI, 0.87–0.95; I2 = 33.8%), or nuts (RR, 0.92, 95%CI, 0.87–0.97; I2 = 81.9%) was associated with a lower risk of all-cause mortality, whereas the substitution of dairy (RR, 0.97, 95%CI, 0.93–1.01; I2 = 33.9%) or legumes (RR, 0.97, 95%CI, 0.93–1.01; I2 = 53.5%) for total red meat was not associated with the risk of all-cause mortality. Lower risks of CHD and all-cause mortality were more consistently observed for processed red meat replacements than for unprocessed red meat replacements. The results did not materially change when the analyses of total, processed, and unprocessed red meat were restricted to the studies that used a uniform substitution amount per unit of 1 serving/d. Conclusion Keeping red meat, particularly processed red meat, consumption to a minimum along with increasing healthier alternative protein sources to replace red meat in the diet may contribute to the prevention of CHD and premature death. Systematic review registration PROSPERO registration no. CRD42021259446.

A 48-year-old man presented to our facility with debilitating motor and sensory symptoms due to advanced T10-11 thoracic spinal stenosis secondary to diffuse idiopathic skeletal hyperostosis (DISH). The patient's condition was addressed with endoscopic spine surgery through a yet-to-be-reported interlaminar approach, and at the 12-month follow-up, his neurologic function was significantly improved.Select patients with symptomatic thoracic spinal stenosis secondary to DISH can be effectively managed with endoscopic spine surgery through an interlaminar approach by clinicians with extensive endoscopic spine experience.

To observe the effects of electroacupuncture (EA) on reproductive outcomes in women with Shen (Kidndy) deficiency syndrome after in vitro fertilization-embryo transfer (IVF-ET), and explore the underlying molecular mechanism. Sixty-six infertile patients with Shen deficiency syndrome undergoing IVF-ET were divided into EA or control groups according to a random table, 33 cases in each group. Before undergoing IVF, patients in the EA and control groups received EA therapy and placebo needle puncture, respectively, for 3 menstrual cycles. Shen deficiency syndrome scores were assessed. Other outcome measures included the number of retrieved oocytes and fertilization, high-quality embryo and clinical pregnancy rates. Follicular fluid was collected on the day of oocyte retrieval, and granulosa cell expression of phosphatidylinositide 3-kinases (PI3K), serine-threonine kinase (Akt) and forkhead box O3 (Foxo3a) mRNA were measured by reverse transcribed and quantitative real-time polymerase chain reaction. Syndrome scores for pre- versus post-treatments decreased significantly (16.53±1.75 to 8.67±1.61) in the EA group (P

Emerging evidence suggests that cancer metabolism is closely associated to the serine biosynthesis pathway (SSP), in which glycolytic intermediate 3-phosphoglycerate is converted to serine through a three-step enzymatic transformation. As the rate-limiting enzyme in the first step of SSP, phosphoglycerate dehydrogenase (PHGDH) is overexpressed in various diseases, especially in cancer. Genetic knockdown or silencing of PHGDH exhibits obvious anti-tumor response both in vitro and in vivo, demonstrating that PHGDH is a promising drug target for cancer therapy. So far, several types of PHGDH inhibitors have been identified as a significant and newly emerging option for anticancer treatment. Herein, this comprehensive review summarizes the recent achievements of PHGDH, especially its critical role in cancer and the development of PHGDH inhibitors in drug discovery.

Magnetoencephalography (MEG) is a persuasive tool to study the human brain in physiology and psychology. It can be employed to obtain the inference of change between the external environment and the internal psychology, which requires us to recognize different single trial event-related magnetic fields (ERFs) originated from different functional areas of the brain. Current recognition methods for the single trial data are mainly used for event-related potentials (ERPs) in the electroencephalography (EEG). Although the MEG shares the same signal sources with the EEG, much less interference from the other brain tissues may give the MEG an edge in recognition of the ERFs. In this work, we propose a new recognition method for the single trial auditory evoked magnetic fields (AEFs) through enhancing the signal. We find that the signal strength of the single trial AEFs is concentrated in the primary auditory cortex of the temporal lobe, which can be clearly displayed in the 2D images. These 2D images are then recognized by an artificial neural network (ANN) with 100% accuracy, which realizes the automatic recognition for the single trial AEFs. The method not only may be combined with the source estimation algorithm to improve its accuracy but also paves the way for the implementation of the brain-computer interface (BCI) with the MEG.

To observe the clinical effect of needle-knife at cervical spine area as adjunctive therapy on dry eye syndrome.A total of 84 patients with dry eye syndrome were randomized into 3 groups, named group A, group B and group C, 28 cases in each one (1 case dropped off in the group A, 2 cases dropped off in both group B and C). In the group A, needle-knife was applied at the margo inferior of external occipital protuberance, the range of 4 cm bilateral to external occipital protuberance, the spinous process of CSⅠT was increased, BUT was prolonged, scores of CFS and eye symptom were reduced after treatment in the group A and group B (Needle-knife at cervical spine area as adjunctive therapy can relieve the clinical symptoms and improve the function of lacrimal gland in patients with dry eye syndrome.

No studies have examined endogenous insulin secretion in pediatric patients with type 1 diabetes in China using the gold-standard mixed-meal tolerance test. Because the latter is labor-intensive, we examined simpler surrogate markers of endogenous insulin secretion in Chinese youth, as previously reported for a European population.Participants were 57 children and adolescents with type 1 diabetes aged 4.4-16.8 years (56% females). We performed 120-minute mixed-meal tolerance tests with serum C-peptide (CP) measurements every 30 minutes. Severe insulin deficiency (SID) was defined as CP peak 0.2 nmol/L. Urine CP and creatinine levels were measured at 0 and 120 minutes.Twenty-five (44%) patients had SID. Fasting CP levels missed one case (96% sensitivity) with no false positives (100% specificity). While the 120-minute urine CP/creatinine had 100% sensitivity, it yielded markedly lower specificity (63%). Every 1-year increase in diabetes duration and 1-year decrease in age at diagnosis were associated with 37% (P 0.001) and 20% (P = 0.005) reductions in serum CP area-under-the-curve, respectively. Thus, 86% of children aged 5 years had SID compared to none among patients aged ≥ 11 years.Simple fasting CP measurements could be used to detect most SID cases in Chinese youth with type 1 diabetes. Fasting CP is a far more reliable measure of endogenous insulin secretion than the more commonly used insulin dose. Therefore, it could more precisely determine insulin secretory capacity to target those who could benefit, if treatments to preserve residual insulin secretion are developed.

The epidemic coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has now spread worldwide and efficacious therapeutics are urgently needed. 3-Chymotrypsin-like cysteine protease (3CLpro) is an indispensable protein in viral replication and represents an attractive drug target for fighting COVID-19. Herein, we report the discovery of 9,10-dihydrophenanthrene derivatives as non-peptidomimetic and non-covalent inhibitors of the SARS-CoV-2 3CLpro. The structure-activity relationships of 9,10-dihydrophenanthrenes as SARS-CoV-2 3CLpro inhibitors have carefully been investigated and discussed in this study. Among all tested 9,10-dihydrophenanthrene derivatives, C1 and C2 display the most potent SARS-CoV-2 3CLpro inhibition activity, with IC50 values of 1.55 ± 0.21 μM and 1.81 ± 0.17 μM, respectively. Further enzyme kinetics assays show that these two compounds dose-dependently inhibit SARS-CoV-2 3CLprovia a mixed-inhibition manner. Molecular docking simulations reveal the binding modes of C1 in the dimer interface and substrate-binding pocket of the target. In addition, C1 shows outstanding metabolic stability in the gastrointestinal tract, human plasma, and human liver microsome, suggesting that this agent has the potential to be developed as an orally administrated SARS-CoV-2 3CLpro inhibitor., Graphical abstract Image 1

Background The long-term efficacy of mesoatrial shunt (MAS) for Budd-Chiari syndrome (BCS) is not well studied. The purpose of our study was to investigate the long-term outcome and efficacy of MAS for BCS. Methods We retrospectively evaluated 11 patients who underwent MAS for BCS from April 1986 to November 1995. Records of patients’ clinical presentations, laboratorial investigation, Doppler duplex ultrasonography, radiologic image, and treatment outcomes were all retrieved and analyzed. Results Follow-up intervals ranged from 1 year and 2 months to 30 years and 2 months (mean, 17 years and 8 months). Portal pressure decreased significantly from 35.72 ± 3.52 cm H2O to 27.86 ± 5.83 cm H2O post-MAS (P = 0.001). The 5-year, 10-year, and 20-year patency were 72.7%, 54.5%, 36.4%, respectively; 63.3% of patients had survived for more than 10 years and 45.5% for more than 20 years. A male has been alive with patent shunt for 28 years and 1 month. Conclusions The MAS with enforced rings is an effective therapeutic modality for BCS with cautious perioperative management.

Cancer stem cells (CSCs), which comprise a small proportion of total cancer cells, have special capacities for self-renewal, differentiation and tumor formation. Currently, CSCs are regarded as the major cause of the failure in anticancer therapy, such as chemoresistance and/or radioresistance, tumor recurrence and metastasis. Autophagy, a process of cellular self-digestion and response to stress, has a role in tumor formation and progression, and it may play a dual role in CSCs-related resistance to anticancer therapy. Most researchers believe that autophagy contributes to stemness maintenance of CSCs and is responsible for the failure of anticancer therapy. Unexpectedly, several studies have also suggested that loss of stemness in CSCs could be mediated by autophagy. Here, we review the recent advances in CSCs and autophagy, especially analyze the complex relationship between them, and hope to apply this new knowledge to the strategies for anticancer therapy.

Epithelial-mesenchymal transition (EMT) is implicated in the metastasis of human prostate cancer (PCa). Notch signaling has been established as a regulator of EMT. Notch-4 has emerged as a mammary proto-oncogene and a target in several cancers. However, the role and the mechanism of action of Notch-4 in PCa are still unclear. In the present study, we first observed a marked increase in Notch-4 expression in the PCa cell lines DU145, PC3 and LnCAP compared with the non-malignant prostate epithelial cell line RWPE1. Knocking down the expression of Notch-4 suppressed the viability and proliferation in the PCa cell lines DU145 and PC3. Also, further study showed that a decline in Notch-4 significantly promoted apoptosis in PC3 cells. Notch-4 silencing also resulted in decreased cell migration and invasion and affected the expression of EMT markers. We hypothesized that Notch-4 ablation suppresses the activity of NF-κB, so we used PMA to stimulate NF-κB p50 and p65 activation in PC3 cells. The results indicate that PMA treatment impaired the action of Notch-4 ablation in the biology of PC3 cells including cell growth, apoptosis, migration, invasion and EMT. The results of the present study show that RNAi targeting against Notch-4 expression suppresses PCa progression.

To explore how long noncoding RNA-ROR (lncRNA-ROR) affects the tamoxifen resistance of breast cancer cells. Breast epithelial (MCF10A), breast cancer (MCF7), and natural tamoxifen-resistant breast cancer (MDA-MB-231) cell lines were selected, and the relative lncRNA-ROR expressions were detected using quantitative real-time polymerase chain reaction (qRT-PCR). In vitro induction of TR5 cell line was performed. There were six groups: MCF7, MCF7/TR5, MDA-MB-231, MCF7-ROR, MCF7/TR5 ROR-siRNA, and the MDA-MB-231 ROR-siRNA groups. CCK-8 assay was conducted to assess the changes in drug resistance of each group. The expression of the epithelial mesenchymal transition (EMT) marker was detected using Western blotting. Transwell was selected to test the invasive ability of the cells. Expressions of microRNA-205 (miR-205) and ZEB1/2 were detected using qRT-PCR . Compared with the MCF7 cells, the proliferation rates of the MCF7/TR5 and MDA-MB-231 cells were significantly increased. Compared with the MCF7 cells, the MCF7-ROR cells had remarkably higher proliferation rates, down-regulated E-cadherin and miR-205 expressions, as well as increased vimentin, invasive ability, and mRNA expression of ZEB1 and ZEB2. Compared with the MCF7/TR5 and MDA-MB-231 cells, up-regulated E-cadherin and miR-205 expression, down-regulated expression of vimentin, ZEB1, and ZEB2 mRNA, and decreased invasive ability were observed in the MCF7/TR5 ROR-siRNA and MDA-MB-231 ROR-siRNA cells. In MDA-MB-231 cells, down-regulated lncRNA-ROR could inhibit the EMT of breast cancer cells and enhance the sensibility of breast cancer cells to tamoxifen by increasing miR-205 expression and suppressing the expressions of ZEB1 and ZEB2.

Lu-Jiao Fang (LJF), a traditional Chinese medicine prescription, can improve the cardiac function of chronic heart failure (CHF) patients; however, knowledge about the cardiac distribution of LJF, especially in CHF animal models, is rather limited. This work aimed to explore the cardiac distribution of LJF in pressure overload-induced CHF rats at the last gavage administration of LJF after 30 weeks of treatment. LC-MS/MS methods for analyzing nine active components (i.e. loganin, hesperidin, epimedin C, icariin, psoralen, isopsoralen, baohuoside I, morroniside and specnuezhenide) of LJF in cardiac tissue samples were established, and the components were then analyzed in left ventricular wall (LVW) and right ventricular wall (RVW) in parallel at same time point postdose for three dose groups. The results showed that most analytical component levels in LVW (hypertrophic myocardium) were only 39-74% of those in RVW (normal myocardium); however, psoralen and isopsoralen levels in LVW were equal to or even greater than the levels in RVW, suggesting that the hypertrophic myocardium tissue affinity of psoralen and isopsoralen might overcome the negative effect of decreased blood flow on distribution. This study indicated that the pathological state may influence drug distribution, and the efficacy of psoralen and isopsoralen for improving CHF deserves further investigation.

OBJECTIVES Lung ultrasound can reliably diagnose pulmonary atelectasis. The object of this study is to determine the most efficient region to assess changes in atelectasis in children with congenital heart disease under general anesthesia. DESIGN Randomized controlled trial. SETTING Operating room at university-affiliated children's hospital. PATIENTS Children between 3 months and 3 years old, scheduled for elective congenital heart disease surgery under general anesthesia. INTERVENTIONS Forty children with congenital heart disease were randomly allocated to either a 5 cm H2O positive end-expiratory pressure group or a standard therapy control group. MEASUREMENTS AND MAIN RESULTS Preoperative lung ultrasound was performed twice in each patient-after 1 and 15 minutes of mechanical ventilation. Atelectatic areas and B-lines were compared between two examinations. Different ultrasound regions were evaluated using Bland-Altman plots. The occurrence rate of atelectasis was much higher in inferoposterior lung regions (Scans 4-6) than in anterior and lateral regions (Scans 1-3). The median (interquartile range) lung ultrasound scores were lower in the positive end-expiratory pressure group than in the control group after treatment: 8 (3.3-9.8) versus 13 (8.3-17.5; p < 0.001). The atelectatic area was significantly decreased after treatment in the positive end-expiratory pressure group: 128 mm (34.5.5-213.3 mm) versus 49.5 mm (5.3-75.5 mm; p < 0.001). Bland-Altman plots revealed concordance between measurements in Scans 1-6 and those in Scans 4-6. In the posterior axillary line regions, changes in atelectatic area were significantly larger in the positive end-expiratory pressure group than in the control group (p = 0.03, 0.007, and 0.018). CONCLUSIONS Lung ultrasound in inferoposterior lung regions may be more likely to reflect changes in atelectasis and save examination time; 5 cm H2O positive end-expiratory pressure may be useful in lung reaeration and can reduce, but not eliminate, atelectasis in children with congenital heart disease.

Signal transducer and activator of transcription 3 (STAT3) is identified as a promising target for multiple cancer therapy and attracts widespread concern. Herein, we reported the discovery of a series of 2-acetyl-7-phenylamino benzofuran derivatives as STAT3 inhibitors using scaffold fusion strategy. Further structure activity relationship study led to the discovery of compound C6, which displayed the most potent anti-proliferation activities against MDA-MB-468 cells (IC50 = 0.16 μM). Western blot assay demonstrated that C6 inhibited the activation of STAT3 (Tyr705) without influencing the phosphorylation of STAT1 (Tyr701). Further mechanistic studies indicated that C6 caused a notable G2/M cycle-arresting and early apoptosis in a concentration-dependent manner in MDA-MB-468 cells. Finally, molecular modelling study elucidated the binding mode of C6 in STAT3 SH2 domain.

In the present study, a series of novel flavanone derivatives were designed and synthesized, and the antipsychotic activities of the target compounds were evaluated in vitro and in vivo. The results showed that synthesized compounds 7a-7g decreased the activity of dopamine D2 receptors in HEK293 cells co-transfected with D2 receptor/G protein α16a, with IC50 values of 0.051–0.35 μM. Compounds 7a-7g inhibited the over-production of nitric oxide stimulated by lipopolysaccharide/interferon-γ in BV-2 microglial cells. In mice, intragastric administration of 7d, 7e, and 7g reversed the increase in locomotor activity induced by MK-801 (an antagonist of NMDA receptors), and decreased the hyperactivity of climbing behavior induced by apomorphine (a dopamine receptor agonist). These results suggest that some of the novel flavanone derivatives have potential antipsychotic effects, and may be useful in the treatment of schizophrenia. This article is protected by copyright. All rights reserved.

Persistently activated signal transducer and activator of transcription 3 (STAT3) plays an important role in the development of multiple cancers, and therefore is a potential therapeutic target for cancer prevention. Herein, we report the rational design, synthesis, and biological evaluation of novel potent STAT3 inhibitors based on BBI608. Among them, compound A11 exhibited the most potent in vitro tumor cell growth inhibitory activities toward MDA-MB-231, MDA-MB-468 and HepG2 cells with IC50 values as low as 0.67 ± 0.02 μM, 0.77 ± 0.01 μM and 1.24 ± 0.16 μM, respectively. Fluorescence polarization (FP) assay validated the binding of compound A11 in STAT3 SH2 domain with the IC50 value of 5.18 μM. Further mechanistic studies indicated that A11 inhibited the activation of STAT3 (Y705), and thus reduced the expression of STAT3 downstream genes CyclinD1 and C-Myc. Simultaneously, it induced cancer cell S phase arrest and apoptosis in a concentration-dependent manner. An additional in vivo study revealed that A11 suppressed the MDA-MB-231 xenograft tumor growth in mice at the dose of 10 mg/kg (i.p.) without obvious body-weight loss. Finally, molecular docking study further elucidated the binding mode of A11 in STAT3 SH2 domain.

Cisplatin (DDP) is the first-line drug for the treatment of gastric cancer (GC). However, DDP resistance is common. Autophagy, which is closely related to chemoresistance, is a process of resolving and recycling proteins and damaged cellular organs. Additionally, O-6-methylguanine-DNA methyltransferase (MGMT) is responsible for alkylating drug resistance. However, the relationship between autophagy and MGMT in response to DDP in GC is still unknown. In the present study, we determined that autophagy induced by DDP decreases chemosensitivity in GC cell lines. DDP may have induced autophagy in GC by inhibiting MGMT to increase autophagy-related gene (ATG) 4B. Inhibition of MGMT-mediated ATG4B suppression resulted in autophagy induction and DDP resistance. In vivo, combined DDP and autophagy inhibitor chloroquine (CQ) enhanced the anti-tumor effect of DDP; additionally, the negative correlation of MGMT and ATG4B was confirmed. High expression of MGMT and low expression of ATG4B were significantly correlated with favorable five-year survival rate (P

Background and aims Human telomerase reverse transcriptase (hTERT) plays an important role in cancer invasion, but the relevant mechanism is not well known. This study aims to investigate the role and mechanism of hTERT in gastric cancer metastasis. Design Proteomics analysis, qPCR and western blotting were used to screen for hTERT-regulated candidate molecules in gastric cancer invasion. Chromatin immunoprecipitation (ChIP) qPCR was performed to identify the binding sites of hTERT at the regulatory region of the integrin β1 ( ITGB1 ) gene. ChIP assays were further applied to elucidate the transcription factors that bound to the regulatory region. The interactions between hTERT and the transcription factors were tested by co-immunoprecipitation (Co-IP) and glutathione S-transferase (GST) pull-down experiments. Moreover, the revealed pathway was verified in tumour-bearing nude mice and human gastric cancer tissues. Results ITGB1 was identified as a downstream gene of hTERT, and there were two hTERT-binding regions within this gene. hTERT alleviated the binding of forkhead box O3 (FOXO3a) to FOXO3a binding element (+9972∼+9978), but it enhanced the binding of forkhead box M1 (FOXM1) to FOXM1 binding element (−1104∼−1109) in ITGB1 gene. Importantly, FOXO3a played a major role in hTERT-induced ITGB1 expression, and the hTERT/murine double minute 2 (MDM2) complex promoted the ubiquitin-mediated degradation of FOXO3a. Moreover, hTERT increased ITGB1 expression in xenograft gastric cancer, and the level of hTERT was positively correlated with that of ITGB1 in human gastric cancer tissues. Conclusions The hTERT/MDM2–FOXO3a–ITGB1 pathway markedly contributes to hTERT-promoted gastric cancer invasion, suggesting that this pathway might be a novel target for the prevention and treatment of gastric cancer metastasis.

Myeloid cell leukemia-1 (Mcl-1) is an anti-apoptotic protein that belongs to the Bcl-2 family. The aberrant expression of Mcl-1 is important for sensitivity to chemotherapy drugs in gastric cancer. However, the regulatory mechanism of Mcl-1 in gastric cancer cells remains unclear. In this study, we first found that Forkhead box M1 (FOXM1) and Mcl-1 expression levels were positively correlated in human gastric cancer specimens and that both are associated with poor prognosis of patients treated with oxaliplatin. Second, we demonstrated that the expression level of Mcl-1 was correlated with FOXM1 expression in gastric cancer cells. Third, reporter assays showed that FOXM1 upregulated the promoter activity of the Mcl-1 gene. Electrophoretic mobility shift assays (EMSA) and chromatin immunoprecipitation (ChIP) assays further demonstrated that FOXM1 could bind to a particular site (-635acaaacaa-628) in the promoter region of the Mcl-1 gene. Moreover, CCK-8 assays and analyses of apoptosis revealed that the suppression of the FOXM1/Mcl-1 pathway induced apoptosis and thus increased sensitivity to oxaliplatin in gastric cancer cells, whereas the enhancement of the FOXM1/Mcl-1 pathway inhibited apoptosis and decreased sensitivity to oxaliplatin in gastric cancer cells. Taken together, this study is the first to not only show that Mcl-1 is a novel target gene of FOXM1 but also suggest that targeting FOXM1/Mcl-1 may be a novel strategy to enhance sensitivity to oxaliplatin in gastric cancer.

Disorders of sex development (DSD) is defined as a congenital condition or atypical development of the chromosomal, gonadal, or anatomic sex. The diagnosis, gender assignment, and treatment of DSD require the guidance from experienced multidisciplinary teams. So far there has been no consensus about it in China. Due to dysgenetic gonads, defects in sex steroid biosynthesis or action, or gonadectomy during the prepubertal years, those with DSD suffer from hypogonadism. The hormone replacement therapy of DSD aims at general physiological health and long-term prognosis as well as the avoidance of unnecessary genital and gonadal surgery. This review focuses on the advances in the studies of the diagnosis and hormone replacement therapy of 46,XY DSD.性发育异常（DSD）是指先天性的染色体、性腺和解剖性别不典型。DSD的明确诊断、性别分配和治疗，须在有经验的多学科团队（MDT）指导下进行。目前我国对此病尚无统一的诊治指南。过去DSD的治疗只注重男女生殖器外观的要求，由于性腺发育不良、生殖激素合成或作用缺陷、或性腺被切除，导致DSD患者性腺功能低下，现今激素替代治疗不仅提高性生理健康及长期预后，有时还可以避免不必要的生殖器和性腺的手术。本文将对46,XY DSD诊断及激素替代治疗的研究进展进行综述。.

The purpose of this study is to determine the possible preoperative predictors of spontaneous pregnancy (SPR) for infertile males with varicocele after microsurgical subinguinal varicocelectomy (MVL) performed in two medical centers in a prospective cohort study. A total of 120 males with varicocele that underwent MVL between June 2013 and June 2014 in two medical centers were documented. Related data, including male and female partner age, male body mass index (BMI), female BMI, preoperative semen parameters, hormone levels, testicular volume, grade and side of varicocele, were collected and analyzed. The follow-up assessment was also conducted within a 2-year period after the surgery. The outcome measure was SPR within the 2-year follow-up reported. The possible determinants of SPR were also analyzed and indentified using Cox regression analysis. Of the 110 patients that accomplished the 2-year follow-up, 42 patients reported pregnancy outcome. Using Cox regression analysis, total motile sperm count [TMC; RR (95% CI) = 1.362 (1.120–1.560), p = 0.003] and follicle-stimulating hormone [FSH; RR (95% CI) = 0.726 (0.541–0.980), p = 0.020] levels posed significant determinants for SPR. Our study indicated that males who underwent MVL with higher TMC and lower FSH preoperatively have higher possibility of pregnancy postoperatively.

Rationale: Gitelman syndrome (GS) is a rare autosomal recessive hereditary salt-losing tubulopathy caused by loss-of-function mutations in the SLC12A3 gene. It is usually characterized by hypokalemia, metabolic alkalosis, hypomagnesemia, and hypocalciuria. There are only a few reports on GS combined with growth hormone deficiency (GHD). Patient concerns: Three patients presented with weakness, spasm, and growth retardation, respectively. Diagnoses: GS was diagnosed based on the clinical symptoms, laboratory test results, and genetic analysis. GH stimulation tests were performed when the magnesium level returned to normal under magnesium oxide (MgO) therapy. Interventions: Initially, all patients received oral replacement of MgO and potassium chloride, and 2 of them received simultaneous spironolactone therapy. Recombinant human growth hormone (rhGH) therapy was initiated after they were diagnosed with GHD. Outcomes: All 3 patients exhibited satisfactory growth velocity and normal serum magnesium level, although the potassium level was still slightly lower than normal. Lessons: We suggest that all GS patients should undergo genetic evaluation, especially regarding SLC12A3 gene mutation. GHD should be considered if these patients have short stature. rhGH therapy is useful for stimulating the patients’ growth, and it may increase the serum magnesium level.

There is conflicting evidence regarding the effectiveness of remote ischemic preconditioning (RIPC) in patients undergoing elective percutaneous coronary intervention (PCI). Therefore, we prospectively enrolled elderly patients with coronary heart disease (CHD) with diabetes mellitus (DM) undergoing elective drug-eluting stent (DES) implantation. They were randomized to receive RIPC within 2 hours before PCI (n = 102) or not (controls, n = 98). Baseline clinical characteristics were similar between the 2 groups. Despite a trend toward decline, the median high-sensitivity cardiac troponin I (hscTnI) level ( P = .256) and the incidence of myocardial infarction (MI) type 4a ( P = .106) in the RIPC group 16 hours after PCI procedure was not significantly different from the control group. The RIPC could attenuate the release of a myocardial biomarker but failed to show a significant effect on hscTnI level or MI type 4a incidence after PCI procedure in elderly patients with CHD having DM undergoing elective DES implantation.

Liver cancer stem cells (LCSCs) can drive and maintain hepatocellular carcinoma (HCC) growth, metastasis, and recurrence. Therefore, they are potentially responsible for the poor prognosis of HCC. Oxygen and nutrient deficiencies are common characteristics of the tumor microenvironment. However, how LCSCs adapt to oxygen- and nutrient-deprived conditions is unclear. Here, we used immunofluorescent staining and flow cytometry analysis to show that CD133+ cells were significantly enriched after hypoxia and nutrient starvation (H/S) in the human HCC cell line Huh7. Sorted CD133+ cells showed higher survival, less apoptosis, and possess higher clonogenic ability under H/S compared to the CD133- population. Under H/S, electron microscopy revealed more advanced autophagic vesicles in CD133+ cells. Additionally, CD133+ cells had higher autophagy levels as measured by both RT-qPCR and Western blotting. CD133+ cells had more accumulated GFP-LC3 puncta, which can be detected by fluorescence microscopy. The autophagic inhibitor chloroquine (CQ) significantly increased apoptosis and decreased the clonogenic capacity of CD133+ cells under H/S. Pre-culturing in H/S enhanced the sphere-forming capacity of CD133+ cells. However, CQ significantly impaired this process. Therefore, autophagy is essential for LCSCs maintenance. CD133+ cells were also found to have a higher tumor-forming ability in vivo, which could be inhibited by CQ administration. Collectively, our results indicate that the involvement of autophagy in maintenance of CD133+ LCSCs under the oxygen- and nutrient-deprived conditions that are typical of the tumor microenvironment in HCC. Therefore, autophagy inhibitors may make LCSCs more sensitive to the tumor microenvironment and be useful in improving anti-cancer treatments.

Stress hyperglycemia (SH) in a setting of acute myocardial infarction increases the risk of in-hospital mortality. The relationship between SH and in-hospital stent thrombosis (ST) is rare. The aim of our study was to assess the impact of SH on in-hospital ST and prognosis in nondiabetic patients with ST-segment elevation myocardial infarction (STEMI) undergoing a primary percutaneous coronary intervention (p-PCI).This study included 853 patients without diabetes mellitus with STEMI. All patients were treated with p-PCI. Blood glucose (BG) was measured on admission. The patients were divided into two groups on the basis of admission BG (SH, BG≥180 mg/dl; non-SH, BG180 mg/dl). The two groups were compared with respect to baseline characteristics and primary endpoints.During hospitalization, all-cause mortality was 2.9%. The total incidence of ST was 1.9%. Patients with SH experienced a significantly higher incidence of mortality (P=0.045), ST (P=0.038), and composite major adverse cardiac events (MACE) (P=0.008) than patients without SH. Patients with SH extended hospital days (P0.001). After multivariate analysis, SH was associated independently with in-hospital mortality, incidence of ST, and composite MACE.In nondiabetic patients with STEMI undergoing p-PCI, the patients with SH experienced a significantly higher incidence of mortality, ST, and composite MACE.

Supplemental Digital Content is available in the text., Background Pancreatic cancer is a rapidly fatal disease with gemcitabine remaining the first-line therapy. We performed a genotype–phenotype association study to identify biomarkers for predicting gemcitabine treatment outcome. Materials and methods We selected the top 200 single nucleotide polymorphisms (SNPs) identified from our previous genome-wide association study to associate with overall survival using 400 patients treated with/or without gemcitabine, followed by imputation analysis for regions around the identified SNPs and a replication study using an additional 537 patients by the TaqMan genotyping assay. Functional validation was performed using quantitative reverse transcription-PCR for gemcitabine-induced expression in genotyped lymphoblastoid cell lines and siRNA knockdown for candidate genes in pancreatic cancer cell lines. Results Four SNPs in chromosome 1, 3, 9, and 20 showed an interaction with gemcitabine from the discovery cohort of 400 patients (P

Background: Breast cancer is characterized by a distinct metastatic pattern involving the regional lymph nodes, bone marrow, lung and liver. This study is aimed to investigate the effects of silencing the HAS-2 gene on the proliferation and apoptosis of human breast cancer cells. Methods: MCF-7 cells were collected and assigned into control, scrambled siRNA and HAS-2- siRNA groups. After transfection, the morphological changes in the MCF-7 cells were observed using phase contrast microscopy. qRT-PCR and Western blot assays were used to detect the mRNA and protein expression of apoptosis-related proteins. CCK-8 and flow cytometry were performed to evaluate cell proliferation, the cell cycle and apoptosis. Results: In the control and the scrambled siRNA groups, cells grew adhered to the wall and mainly showed a spindle shape with a clear nucleolus. Compared with the control and scrambled siRNA groups, increases in the number of cells in early apoptosis and metaphase cells in apoptosis were observed in the HAS-2-siRNA group. The HAS-2-siRNA group showed decreased expression of HAS-2 relative to that in the control and scrambled siRNA groups. No significant differences in cell proliferation, cell cycle distribution or apoptosis were noted between the control and scrambled siRNA groups. In the HAS-2-siRNA group, the cell proliferation ability decreased significantly, but the number of cells in the G0/G1 stage, the number of apoptotic cells and the expression of caspase-3 and caspase-9 increased significantly. Conclusion: Our findings indicate that HAS-2 gene silencing may inhibit proliferation and promote apoptosis in the MCF-7 human breast cancer cell line.

Background Some studies have shown that hypoglycemic episodes in diabetic patients might be associated with increased cardiovascular events. It is not clear whether episodes of silent hypoglycemia had greater prognostic value on cardiac events compared with normoglycemia or hyperglycemia in non-diabetic patients, so the aim of this study was to investigate the association of silent hypoglycemia and cardiac events in non-diabetic patients with acute ST-segment elevation myocardial infarction (STEMI) who underwent primary percutaneous coronary intervention (p-PCI). Methods We enrolled non-diabetic patients with STEMI who underwent p-PCI and whose clinical and laboratory data were collected. Interstitial glucose values were recorded using a continuous glucose monitoring system (CGMS), and Holter monitoring was recorded for 3 days in parallel. Cardiac ischemia and ventricular arrhythmia was evaluated. Results Based on the inclusion and exclusion criteria, we enrolled 164 STEMI patients undergoing p-PCI for final analysis. A total of 280 episodes of silent hypoglycemia (CGMS glucose

Martentoxin as a 37-residue peptide was capable of blocking large-conductance Ca(2+)-activated K(+) (BK) channels in adrenal medulla chromaffin cells. This study investigated the pharmacological discrimination of martentoxin on BK channel subtypes. The results showed that the iberiotoxin-insensitive neuronal BK channels (alpha+beta4) could be potently blocked by martentoxin (IC(50) = approximately 80 nM). In contrast, the iberiotoxin-sensitive BK channel consisting of only alpha-subunit was less sensitive to martentoxin. Distinctively, martentoxin inhibited neuronal BK channels (alpha+beta4) with a novel interaction mode. Two possible interaction sites of neuronal BK channels (alpha+beta4) might be responsible for the binding with martentoxin: one for trapping and the other located at the pore region for blocking. In addition, the inhibition of martentoxin on neuronal BK channels (alpha+beta4) depended on cytoplasmic Ca(2+) concentration. On the other hand, in vivo experiments from EEG recordings suggested that neuronal BK channels (alpha+beta4) were the primary target of martentoxin. Therefore, this research not only sheds light on a unique ligand for neuronal BK channels (alpha+beta4), but also highlights a novel model approach for the interaction between K(+) channels and specific-ligands.

There is no radical cure for all cancer types. The most frequently used therapies are surgical treatment, radiotherapy and chemotherapy. However, recrudescence, radiation resistance and chemotherapy resistance are the most challenging issues in clinical practice. To address these issues, they should be further studied at the molecular level, and the signaling pathways involved represent a promising avenue for this research. In the present review, we mainly discuss the components and mechanisms of activation of the Notch and Wnt signaling pathways, and we summarize the recent research efforts on these two pathways in different cancers. We also evaluate the ideal drugs that could target these two signaling pathways for cancer therapy, summarize alterations in the Notch and Wnt signaling pathways in cancer, and discuss potential signaling inhibitors as effective drugs for cancer therapy.

DNA is the prime target of anticancer treatments. DNA damage triggers a series of signaling cascades promoting cellular survival, including DNA repair, cell cycle arrest, and autophagy. The elevated basal and/or stressful levels of both DNA repair and autophagy observed in tumor cells, in contrast to normal cells, have been identified as the most important drug-responsive programs that impact the outcome of anticancer therapy. The exact relationship between DNA repair and autophagy in cancer cells remains unclear. On one hand, autophagy has been shown to regulate some of the DNA repair proteins after DNA damage by maintaining the balance between their synthesis, stabilization, and degradation. One the other hand, some evidence has demonstrated that some DNA repair molecular have a crucial role in the initiation of autophagy. In this review, we mainly discuss the interplay between DNA repair and autophagy in anticancer therapy and expect to enlighten some effective strategies for cancer treatment.

In humans, telomerase reverse transcriptase (hTERT) determines the activity of telomerase. hTERT is an ideal anticancer target because it is universally expressed in cancer cells and plays a crucial role in carcinogenesis. In this study, we report the miR-1182-mediated post-transcriptional regulation of hTERT. Over-expression of miR-1182 in different gastric cancer cells decreased hTERT protein levels. Bioinformation and dual-luciferase assays revealed that miR-1182 modulated hTERT by binding to its open reading frame (ORF), and this miRNA recognizes elements in the nucleotide region between 2695 and 2719 of hTERT mRNA. Over-expression of hTERT by transfecting pIRES2-hTERT into U2OS cells was abolished by miR-1182, while pIRES2-hTERT-MT, in which miR-1182 target site was synonymously mutated, failed to respond to miR-1182. Further investigation revealed that miR-1182 inhibited gastric cancer proliferation and migration by targeting the ORF1 of hTERT. We also found that miR-1182 could attenuate the proliferative and metastatic potential of SGC-7901 cell in vivo. Moreover, we found a statistically significant inverse correlation between miR-1182 and hTERT protein levels in tissues from 42 gastric cancer patients. These data indicate that miR-1182 suppresses TERT, and thus it could be an effective target for the treatment of gastric cancer.

Recently, several studies indicated that senescent tumor cells are resistant to apoptosis in chemotherapy. They may return to cell cycle, thus act as stumbling blocks in anticancer treatments. In the present study, we found that, in human colorectal cancer cells, low-dose camptothecin (CPT) simultaneously induced autophagy and premature senescence through AMPK-TSC2-mTOR pathway and ATM-Chk2-p53-p21 pathway respectively. What's important is the suppression of autophagy substantially increased apoptosis and greatly attenuated senescence possibly by blocking p53/p21 pathway, which suggests that autophagy plays an indispensable role in sustaining cell senescence caused by low-dose CPT. The combination of low-dose CPT and autophagy inhibitor, a way to lead senescent cells to die, would be potentially valuable in cancer therapy.

Trimetazidine has been shown to improve angina pectoris and left ventricular (LV) function in diabetic patients with ischaemic cardiomyopathy. The objective of this study was to evaluate the effects of trimetazidine on recurrent angina pectoris and LV structure after drug-eluting stent (DES) implantation in elderly multivessel coronary heart disease (CHD) patients with diabetes mellitus (DM) and a left ventricular ejection fraction (LVEF) of ≥50 %. This was a single-centre, prospective, randomized, double-blind evaluation study. Between January 2010 and September 2010, 700 CHD patients with DM who were aged ≥65 years and undergoing coronary angiography at An Zhen Hospital (Beijing, China) were recruited and prospectively randomized to receive trimetazidine (20 mg three times daily) or placebo after DES implantation as an addition to conventional CHD treatment. The primary end points were the incidence of recurrent angina pectoris and measures of various echocardiographic parameters, which included LVEF. At 2-year follow-up, patients in the trimetazidine group (n = 255) showed significant improvements in the incidence (P = 0.024) and severity of angina pectoris, compared with the control group, as well as silent myocardial ischaemia (P = 0.009) and angina pectoris-free survival (P = 0.011). LV function and structure in trimetazidine-treated patients were relatively stable at 2-year follow-up, while they deteriorated in the control group (n = 255) with a significant difference between groups (all P

The objective of this paper was to investigate the characteristics and general rules of domestic safflower injection causing allergic shock, to retrieve the medical journals published domestically, and to make statistical analysis on the cases of allergic shock caused by safflower injection. Results showed that the incidence of allergic shock caused by safflower injection in patients above 40 years old was high: females were more than males. It occurred within 30min after medication, and no patient died after emergency treatment. The study concluded that allergic shock caused by safflower injection is related to many factors, and clinical care personnel should pay more attention to it.Keywords: safflower injection; allergic shock; literature analysis

To probe the effects of dexamethasone (DEX) combined with histone deacetylase (HDAC) inhibitor vorinostat on inhibiting proliferation and inducing differentiation and apoptosis in Kasumi-1 leukemia cells, and its possible mechanisms in order to provide a theoretical basis for the treatment of AML1-ETO positive AML.The cell survival, differentiation and apoptosis rates were tested by MTT or flow cytometry analysis after Kasumi-1 cells were treated by DMSO, DEX (20 nmol/L), vorinostat (1 μmol/L) or DEX (20 nmol/L) in combination with vorinostat (1 μmol/L). WB and IP-WB were performed to detect AML1-ETO and its ubiquitination.Treatment with the combination of DEX and vorinostat for 48 h led to statistically significant differences of inhibited proliferation [(42.06±8.20)%], increased differentiation [(52.83±8.97)%] and apoptosis [(52.92±2.53)%] of Kasumi-1 cells when compared with vorinostat [(33.82±9.41)%, (43.93±9.04)% and (42.98±3.01)%, respectively], DEX [(17.30±3.49)%, (22.53±4.51)% and (19.57±2.17)%, respectively] or control [(6.96±0.39)%, (21.73±2.03)% and (6.96±0.39)%, respectively]. Also significant ubiquitination and decreased AML1-ETO protein in Kasumi-1 cells after the combination treatment over single agent or control were observed.The results indicated that DEX and vorinostat could synergistically inhibit the Kasumi-1 cells proliferation, induce Kasumi-1 cells differentiation and apoptosis through ubiquitination and degradation of AML1-ETO.

To analyze the clinical data and prognosis of gastric small cell carcinoma (GSCC), summarize recent progress in diagnosis and therapy of this disease reported in the literature, and to provide the theoretical basis for its appropriate treatment.Clinicopathological data of 17 patients with pathologically confirmed GSCC, treated in our hospital between 1999 to 2012, were retrospectively reviewed.There were 16 males and 1 female, ranged from 46 to 75 years (mean 64.6 years). The tumor was located in the gastric cardia in 13 cases, three in the gastric fundus, and one in the gastric body. All the 17 patients received surgery and 10 of them received postoperative adjuvant chemotherapy, one received preoperative adjuvant chemotherapy. Thirteen patients were followed up. Among them, two 1ived for 40 months all along, the other 3 cases died of recurrence and extensive metastasis in 6 month after operation. The median survival was 13.0 months. The median survival of the patients with and without lymph node metastasis were 42 months and 13 months, respectively. The median survival time of stage II and III patients were 24 months and 14 months, respectively.It is difficult to make a definite diagnosis before or during the operation for GSCC. Radical operation could be done according to other gastric cancers and lymph node dissection could be simplified. Postoperative chemotherapy with the same scheme as lung small cell carcinoma may help to improve the outcome and prolong the survival of the patients.

Objective To date, no study in the published literature has investigated the role of various serum uric acid (SUA) concentrations in the development of angiographically-proven coronary artery disease (CAD) in premenopausal women. Therefore, the aim of this study was to investigate the role SUA levels may play in the prevalence, severity, and prognosis of CAD in premenopausal women. Methods This cross-sectional retrospective study included 607 premenopausal women who had undergone coronary angiography. The CAD diagnosis was based upon stenosis affecting ≥50% of the luminal diameter. Association of the SUA levels with CAD prevalence, severity, and clinical outcomes were assessed by statistical analysis. Results In total, 369 (60.8%) of the patients were diagnosed with CAD. The CAD patients had significantly higher SUA levels than those without CAD (5.3±1.9 vs. 4.8±1.7 mg/dL, P = 0.001). The SUA levels were found to be significantly associated with CAD prevalence (P = 0.013). Patients with higher levels of SUA also showed increased rates of multivessel disease and composite end-points, such as major adverse cardiac events. Furthermore, multivariate analysis identified abnormally high levels of uric acid (hyperuricemia) as an independent risk factor for CAD (OR 1.51 (1.11–2.53), P

To investigate the role of repairing tissue defects by infrahyoid myocutaneous flap after oral cancer surgery in elder patients.From December 2005 to November 2010, we used infrahyoid myocutaneous flaps to reconstruct soft tissue defects in 19 elder patients after radical operation of oral cancer. There were 11 males and 8 females with the age range of 65 to 89 years (average: 72.8) .The lesions included 10 tongue cancers, 2 buccal cancers, 6 mouth floor cancers and 1 gingival cancer.All wound healed uneventfully, and all the 19 infrahyoid myocutaneous flaps survived without total or partial necrosis. The results were satisfactory both in appearance and functions. The patients were followed up for 6 months to 5 years, no tumour relapse and metastasis occurred.The procedure of preparing the infrahyoid myocutaneous flap is simple and the result is reliable. The flap is useful for reconstruction of soft tissue defects in elder patients.

To investigate retrospectively the relationship between clinicopathological factors and lymph node matastasis of pancreatic adenocarcinoma.The clinicopathological factors, including gender, age, preoperative CA-19-9 level etc. of 71 patients with pancreatic adenocarcinoma were summarized to analyze the relationship between those factors and lymph node matastasis.Among the 71 cases, there were 49 males (69.0%) and 22 females (31.0%). Forty-eight were ≥ 60 (67.6%) and 23 were60 (32.4%) years old. Twenty patients had normal preoperative CA-19-9 level (28.2%) and 51 had elevated level (71.8%). The tumor in 43 (60.6%) cases located in the pancreatic head and neck, and 28 (39.4%) in the body and tail. The tumors in 8 patients were well-differentiated (11.3%), 27 were moderately differentiated (38.0%), and 36 were poorly differentiated (50.7%). The maximum diameter of the tumor was ≤ 2 cm in 11 cases (15.5%), 2 - 5 cm in 45 cases (63.4%), and5 cm in 15 cases (21.1%). Ten patients had tumor confined to the pancreas (14.1%), and 61 invaded peripancreatic tissues (85.9%). Vascular tumor thrombus was found in 48 cases (67.6%), and 23 cases were absent (32.4%). Thirty-six cases had lymph node matastasis (50.7%). Univariate chi-square test revealed that differentiation and range of local infiltration were significantly associated with lymph node meatstasis (P0.05). Multivariate logistic regression analysis also showed that differentiation and range of local infiltration were significantly associated with lymph node meatstasis (P0.05).The differentiation of tumor and range of local infiltration of pancreatic adenocarcinoma are significantly associated with lymph node metastasis. There is no significant relationship of location of the tumor, maximum diameter, presence or absence of vascular tumor thrombus with lymph node metastasis. Therefore, special attention should be paid to lymph node dissection in cases with a poorly differentiated pancreatic adenocarcinoma invading into peripancreatic tissues.

To develop a novel rapid protocol for the detection of occult disseminated tumor cells by a recombinant herpes simplex virus expressing GFP (HSV(GFP)).Tumor cells of seven cell lines were exposed to HSV(GFP) and then examined for GFP expression by fluorescence microscopy. Various numbers of tumor cells (10, 100, 1000, 10 000) were mixed into 2 ml human whole blood, separated with lymphocytes separation medium, exposed to HSV(GFP), incubated at 37°C for 6 - 24 h and then counted for the number of green cells under the fluorescence microscope. Some clinical samples including peripheral blood, pleural effusion, ascites, spinal fluid from tumor-bearing patients were screened using this protocol in parallel with routine cytological examination.HSV(GFP) was able to infect all 7 tumor cell lines indicating that the HSV(GFP) can be used to detect different types of tumor cells. The detection sensitivity was 10 cancer cells in 2 ml whole blood. In the clinical samples, there were 4/15 positive by routine cytological examination but 11/15 positive by HSV(GFP), indicating a higher sensitivity of this new protocol.Recombinant herpes simplex virus-mediated green fluorescence is a simple and sensitive technique for the identification of occult disseminated cancer cells including circulating tumor cells (CTCs).

To assess the effects of acupuncture combined Chinese materia medica for tonifying shen and soothing gan (CMMTSSG) on the anxiety and depression of patients with in vitro fertilization and embryo transplantation (IVF-ET), and to observe the treatment outcomes.Totally 97 IVF-ET patients were randomly assigned to two groups, the acupuncture combined CMMTSSG (group A, 51 cases) and the Western medicine treatment group (group B, 46 cases). The long protocol of IVF-ET in a mid luteal phase was performed in all patients. Patients in group A received acupuncture and CMMTSSG (erzhi tiangui granule and xiaoyao granule) during the process of ovarian hyperstimulation, while those in group B only received the routines of IVF-ET. The improvement of Shen deficiency Gan depression syndrome (SDGDS) between after and before treatment were observed in the two groups. The changes of self-rating anxiety scale (SAS) and Beck depression inventory (BDI) score were observed. The endometrial thickness, typing, and endometrial blood flow resistance index (RI) on the day of injecting HCG, the number of retrieved oocytes, the rate of high quality oocytes, the fertilization rate, the rate of high quality embryos, and the clinical pregnancy rate were respectively compared between the two groups.The scores of SDGDS, SAS, and BDI were improved more obviously in group A than in group B, showing statistical difference (P0.01). There was no statistical difference in the endometrial thickness on the day of injecting HCG between the two groups (P0.05). The proportion of type A endometrium was 74.5% (38/51 cases) in group A and 45.7% (21/46 cases) in group B, showing statistical difference between the two groups (P0.01). The RI was significantly lower in group A (0.48 +/- 0.03) than in group B on the day of injecting HCG (0.52 +/- 0.06, P0.01). There was no statistical difference in the number of retrieved oocytes and the fertilization rate between the two groups (P0.05). The rate of high quality oocyte, the rate of high quality embryos, and the clinical pregnancy rate were all improved more significantly in group A than in group B, showing statistical difference between the two groups (P0.05).Acupuncture combined CM-MTSSG could obviously alleviate unfavorable emotions as anxiety and depression in patients with IVF-ET, effectively improve the treatment outcomes. Its effects might be correlated with lowering the excitability of the sympathetic nervous system, elevating the quality of oocytes, and improving the endometrial receptivity.

To assess the diagnostic value of magnetic resonance imaging (MRI) in the follow-up of patients with hepatocellular carcinomas treated with radiofrequency ablation (RFA) and to compare it with that of computed tomography (CT).From December 2009 to September 2011, 40 patients (47 hepatocellular carcinomas) were treated with RFA after transcatheter arterial chemoembolization and underwent MRI and CT for follow-up. RFA margins were assessed on a five-point scale with receiver operating characteristic curve analysis. Sensitivity, specificity, positive predictive value, negative predictive value, and accuracy were evaluated.The interobserver agreement rate for MRI was significantly higher (Kappa=0.935) than for CT (Kappa=0.714; P0.05). The scores of 1 and 5 points for MRI, which confirms the presence or absence of residual tumor, accounted for 89.4% (84/94), while for CT accounting for only 31.9% (30/94). The area under the receiver operating characteristic curve of MRI was significantly higher than that of CT (P0.05), as were the sensitivity, specificity, positive predictive value, negative predictive value, and accuracy of detection rate (mean, 100%, 96.4%, 76.9%, 100%, and 96.8% for MRI, respectively, vs. 30.0%, 57.1%, 10.3%, 87.7%, and 63.8% for CT).MRI is superior to CT in assessing the RFA margins in terms of the diagnostic accuracy and detection rate .

Chronic obstructive pulmonary disease (COPD) is common in patients undergoing percutaneous coronary intervention (PCI), but the impact of COPD on outcomes after PCI has received limited attention. Consecutive patients with coronary heart disease (n = 5155) undergoing PCI were enrolled in this study; 645 patients (73% men) aged 68.4 ± 13.2 years had COPD and 4510 patients (71% men) aged 64.7 ± 12.1 years did not. During the in-hospital period after PCI, the patients with COPD experienced a significantly higher incidence of angina ( P < .001), arrhythmias ( P < .001), and composite major adverse cardiac events (MACEs; P < .001) and longer hospital stay ( P < .001) than those without COPD. Additionally, severity of COPD (measured by pulmonary function tests) was associated with increased composite MACE ( P < .001) and hospital stay ( P < .001) after PCI. In conclusion, COPD is associated with significantly increased composite MACE and hospital stay in patients after PCI. Increasing severity of COPD is associated with increased composite MACE and hospital stay after PCI.

To investigate the clinical efficacy of Shengjing prescription for oligoasthenozoospermia and its action mechanism.We equally assigned 120 patients with oligoasthenozoospermia to receive Shengjing prescription (treatment group) and vitamin E (control group), respectively, for 12 weeks. Before and after the treatment, were obtained sperm concentration, sperm motility, the percentage of morphologically normal sperm, the levels of serum follicle-stimulating hormone (FSH), testosterone (T) and luteinizing hormone (LH), sperm DNA fragmentation index (DFI), the percentage of hypotonic swelling sperm, and the levels of seminal plasma elastase, x-glucosidase, fructose, zinc and acrosin.Compared with vitamin E, Shengling prescription significantly improved sperm concentration, motility and morphology (P0.01), decreased the serum FSH level, elevated the serum T level (P0. 01) , reduced DFI and seminal plasma elastase, and increased the percentage of hypotonic swelling sperm as well as the levels of seminal plasma cx-glucosidase, fructose, zinc and acrosin.Shengjing prescription improves semen parameters of patients with oligoasthenozoospermia at multiple levels and through multiple channels.