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Background: Mucinous adenocarcinoma (MC) has attracted much attention as a distinct histologic subtype of colorectal cancer in recent years. However, data about its epidemiologic and prognostic characteristics are limited. Therefore, patient data extracted from the National Cancer Institute's Surveillance, Epidemiology, and End Results Program were collected to analyze the epidemiologic and clinicopathological characteristics of MC., Aim: To determine the epidemiologic and clinicopathological characteristics of MC., Methods: The incidence trend of MC was calculated through the Joinpoint Regression Program. Cox regression analyses were performed to identify prognostic factors associated with overall survival (OS). A nomogram was established to predict the survival probability of individual patients with MC., Results: We found that rates of MC decreased from 4.50/100000 in 2000 to 1.54/100000 in 2018. Rates of MCs in patients aged ≤ 50 years decreased 2.27%/year during 2000-2018. The incidence of appendiceal MCs increased from 0.14/100000 in 2000 to 0.24/100000 in 2018, while the incidence in other anatomic subsites continued to decrease. On multivariable Cox analyses, age, race, tumor site, T stage, N stage, M stage, surgery, and chemotherapy were associated with OS. A nomogram was developed based on these factors, and the area under the curve for 1-year, 3-year, and 5-year OS in the training cohort was 0.778, 0.778, and 0.768, respectively., Conclusion: Our results demonstrated that MC incidence decreased in almost all anatomic subgroups except for the appendix. A nomogram predicting the survival probability of patients with MCs showed good performance., Competing Interests: Conflict-of-interest statement: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (©The Author(s) 2023. Published by Baishideng Publishing Group Inc. All rights reserved.)

Bimodal imaging probes that combine magnetic resonance imaging (MRI) and photoluminescence imaging are quite appealing since they can supply both anatomical and molecular information to effectively ameliorate the accuracy of detection. In this study, an activatable nanoprobe, [Eu(BTD) 3 (DPBT)]@MnO 2 , for bimodal time-gated luminescence imaging (TGLI) and MRI has been constructed by anchoring visible-light-excitable Eu 3+ complexes on lamellar MnO 2 nanosheets. Due to the luminescence quenching effect and non-magnetic resonance (MR) activity of MnO 2 nanosheets, the developed nanoprobe presents quite weak TGL and MR signals. After exposure to H 2 O 2 or GSH, accompanied by the transformation from MnO 2 to Mn 2+ , the nanoprobe exhibits rapid, sensitive, and selective "turn-on" responses towards GSH and H 2 O 2 in TGL and MR detection modes. Furthermore, the nanoprobe displays high stability, low cytotoxicity, good biocompatibility and water dispersion. Given the high contents of GSH and H 2 O 2 in cancer cells, the nanoprobe was used for the identification of cancer cells by TGLI of intracellular GSH and H 2 O 2 , as well as for the tracing of tumor cells in tumor-bearing mice by tumor-targeting in vivo MRI and TGLI of tumor tissues. The research outcomes proved the potential of [Eu(BTD) 3 (DPBT)]@MnO 2 as a useful nanoprobe for the tracing and accurate detection of cancer cells in vitro and in vivo via bimodal TGLI and MRI.

The synergy of magnetic resonance imaging (MRI) and time-gated luminescence imaging (TGLI) provides a robust platform with extensive spatial resolution (from submicrometer to hundred-micron) and unlimited penetration depth for visual detection of lesion tissues and target biomolecules. In this work, highly stable lanthanide (Eu 3+ and Gd 3+ ) complexes with a terpyridine polyacid ligand, CNSTTA-Ln 3+ , were chosen as signal reporters for TGLI (Ln 3+ = Eu 3+ ) and MRI (Ln 3+ = Gd 3+ ), respectively. After conjugating CNSTTA-Ln 3+ with a tumor-targetable glycoprotein, transferrin (Tf), the obtained bioconjugate, showed low cytotoxicity and high stability and exhibited strong long-lived luminescence (Tf-CNSTTA-Eu 3+ , ϕ = 10.8%, τ = 1.27 ms), high magnetic resonance relaxivity (Tf-CNSTTA-Gd 3+ , r 1 = 8.70 mM -1 s -1 , r 2 = 10.90 mM -1 s -1 ), and high binding affinity toward Tf receptor-overexpressed cancerous cells. On the basis of these features, a tumor-targetable probe was constructed by simply mixing Tf-CNSTTA-Eu 3+ and Tf-CNSTTA-Gd 3+ , and successfully used for the bimodal TGLI and MRI of tumor cells in tumor-bearing mice. The bimodal imaging simultaneously provided the anatomical and molecular information of the tumor, which enabled the accuracy for tumor diagnosis to be mutually verified, and revealed the potential of Tf-CNSTTA-Gd 3+ /Eu 3+ for the monitoring of cancer cells in vivo .

Microbiota succession in spontaneous fermentation of Cabernet Sauvignon cultivated under the rain-shelter was characterized, with open-field cultivation as the control. For both cultivation modes, Saccharomyces , Starmerella , and Mycosphearella were the principal fungi, and Tatumella , Gluconobacter , and Acinetobacter were the prevailing bacteria. Rain-shelter reduced the abundance of Hanseniaspora , Candida , Starmerella , Gluconobacter , and Lactococcus . During fermentation, fungal microbiota diversity in samples from the rain-shelter cultivation decreased more drastically than the control ( p  < 0.05). In terms of the correlation between microbiota and volatile compounds production, the abundance of Hanseniaspora uvarum , Candida apicola , Starmerella bacillaris , Gluconobacter oxydans , and Lactococcus lactis were positively correlated with the production of esters and higher alcohols. Instead of bacterial microbiota, fungal community succession exhibited a positive correlation with the final wine volatiles under the rain-shelter cultivation. These findings demonstrated rain-shelter cultivation influences the succession pattern of microbial communities and in turn impacts the wine aromas and flavors., Competing Interests: The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (© 2023 The Author(s).)

Background: The global rising prevalence and incidence of multiple sclerosis (MS) has been reported during the past decades. However, details regarding the evolution of MS burden have not been fully studied. This study aimed to investigate the global, regional, and national burden and temporal trends in MS incidence, deaths, and disability-adjusted life years (DALYs) from 1990 to 2019 using the age-period-cohort analysis., Methods: We performed a secondary comprehensive analysis of incidence, deaths, and DALYs of MS by calculating the estimated annual percentage change from 1990 to 2019 obtained from the Global Burden of Disease (GBD) 2019 study. The independent age, period, and birth cohort effects were evaluated by an age-period-cohort model., Results: In 2019, there were 59,345 incident MS cases and 22,439 MS deaths worldwide. The global number of incidences, deaths, and DALYs of MS followed an upward trend, whereas the age-standardized rates (ASR) slightly declined from 1990 to 2019. High socio-demographic index (SDI) regions had the highest ASR of incidences, deaths, and DALYs in 2019, while the rate of deaths and DALYs in medium SDI regions are the lowest. Six regions which include high-income North America, Western Europe, Australasia, Central Europe, and Eastern Europe had higher ASR of incidences, deaths, and DALYs than other regions in 2019. The age effect showed that the relative risks (RRs) of incidence and DALYs reached the peak at ages 30-39 and 50-59, respectively. The period effect showed that the RRs of deaths and DALYs increased with the period. The cohort effect showed that the later cohort has lower RRs of deaths and DALYs than the early cohort., Conclusion: The global cases of incidence, deaths, and DALYs of MS have all increased, whereas ASR has declined, with different trends in different regions. High SDI regions such as European countries have a substantial burden of MS. There are significant age effects for incidence, deaths, and DALYs of MS globally, and period effects and cohort effects for deaths and DALYs., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Qian, Li, Guan, Guo, Zheng, Du, Yin, Chen, Wang, Jiang, Qiu and Zhang.)

Objective: To investigate the effect of different treatment methods on the vertebral stability of osteoporotic vertebral compression fracture (OVCF) by finite element analysis., Methods: Ten patients with thoracolumbar OVCF admitted between January 2020 and June 2021 were selected, 5 of whom underwent operation (operation group), 5 underwent conservative treatment (conservative treatment group). Another 5 healthy volunteers were selected as the control group. There was no significant difference in gender and age between groups ( P >0.05). The operation group and the conservative treatment group received CT examination of the fractured vertebral body and adjacent segments before and after treatments, while the control group received CT examination of T 12 -L 2 . By importing CT data into Mimics 10.01 software, the finite element model was constructed. After comparing the finite element model of control group with the previous relevant literature measurement results to verify the validity, the spinal structural stress and range of motion (ROM) in each group under different conditions were measured., Results: The three-dimensional finite element model was verified to be valid. There were significant differences in spinal structural stress after treatment between groups under different conditions ( P <0.05). Before treatment, the ROMs of operation group and conservative treatment group under difference conditions were significantly lower than those of control group ( P <0.05), and there was no difference between conservative treatment group and operation group ( P >0.05). After treatment, the ROMs of the control group and the operation group were significantly higher than those of the conservative treatment group ( P <0.05), and there was no significant difference between the operation group and the control group ( P >0.05)., Conclusion: For patients with OVCF, the minimally invasive operation can achieve better results. Compared with conservative treatment, it can reduce the effect on spinal stability, and can be as a preferred treatment method, which is helpful to improve the prognosis of patients.

Competing Interests: The authors declare no conflict of interest.

Objective: To estimate the burden of potential productivity losses due to uncorrected and under-corrected presbyopia in LMICs among the working-age population in both the cross-sectional and longitudinal manner., Methods: We extracted data for the prevalence of presbyopia from the Global Burden of Diseases (GBD), Injuries, and Risk Factors Study 2019. Data for the gross domestic product (GDP) per capita were extracted from the World Bank database and Central Intelligence Agency's World Factbook. We introduced life table models to construct age cohorts (in 5-year age groups) of the working-age population (aged from 40 to 64 years old) in LMICs, with simulated follow-up until 65 years old in people with and without uncorrected presbyopia. The differences in productivity-adjusted life years (PALYs) lived and productivity between these two cohorts were calculated. The potential productivity loss was estimated based on GDP per capita. The WHO standard 3% annual discount rate was applied to all years of life and PALYs lived., Results: In 2019, there were 238.40 million (95% confidence interval [CI]: 150.92-346.78 million) uncorrected and under-corrected presbyopia cases in LMICs, resulting in 54.13 billion (current US dollars) (95% confidence interval [CI]: 34.34-79.02 billion) potential productivity losses. With simulated follow-up until retirement, those with uncorrected and under-corrected presbyopia were predicted to experience an additional loss of 155 million PALYs (an average loss of 0.7 PALYs per case), which was equivalent to a total loss of US$ 315 billion (an average loss of US$ 1453.72 per person)., Conclusions: Our findings highlight the considerable productivity losses due to uncorrected and under-corrected presbyopia in LMICs, especially in a longitudinal manner. There is a great need for the development of enabling eye care policies and programs to create access to eye care services, and more healthcare investment in the correction of presbyopia in the working-age population in LMICs. This study could provide evidences for some potential health-related strategies for socio-economic development., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Ma, Chen, Li, Zhou, Du, Yin, Chen, Wang, Jiang, Guan and Qiu.)

Objectives: Clinical studies are important in informing evidence-based practice for patients with acute pancreatitis (AP). To determine whether registered studies adequately meet this need, we leveraged the ClinicalTrials.gov database to provide an overview of studies pertaining to AP., Methods: ClinicalTrials.gov was searched and the search term used was AP. Analysis was restricted to studies registered before January 12, 2021., Results: Of 363,632 trials overall, 234 (0.06%) were eventually included for analysis. Interventional studies and observational studies comprised 67.5% and 32.5% of these studies respectively. Most studies were initiated 2007 or later. Endoscopic retrograde cholangiopancreatography was the single most frequent cause of AP specified in these studies (16.7%). Nearly 72% of these studies had a sample size greater than 50. With respect to study design, 87.3% of interventional studies were randomized, 53.5% were blinded. The top 3 countries with the largest number of registered studies were China (n = 59), followed by the United States (n = 53) and India (n = 12)., Conclusions: Our results indicate that the research activity falls short of what is needed in terms of the burden of AP. The distribution of these AP-related studies by global regions indicates that there exists regional disparities., Competing Interests: The authors declare no conflict of interest., (Copyright © 2022 Wolters Kluwer Health, Inc. All rights reserved.)

Seedlessness is a valuable agronomic trait in watermelon (Citrullus lanatus) breeding. Conventional less seed watermelons are mainly triploid, which has many disadvantages due to unbalanced genome content. Less seed watermelon can be achieved at the diploid level when certain reproductive genes are mutated or by chromosome translocation, which leads to defects during meiosis. However, the formation mechanism of diploid less seed watermelons remains largely unknown. Here, we identified a spontaneous mutant line, watermelon line "148", which can set seeds normally when self-pollinated. A total of 148 × JM F 1 hybrid plants exhibited seed number reductions to 50.3% and 47.3% of those of the two parental lines, respectively, which are considered to be less seed. Examination of pollen viability and hybridization experiments revealed that F 1 hybrids produce semisterile pollen and ovules. Further cytological observations indicated that semisterility was a result of a reciprocal translocation of chromosomes, which exhibited one quadrivalent ring of four chromosomes at prometaphase I during meiosis. RT-qPCR analysis indirectly confirmed that the semisterile phenotype is caused by chromosome translocation rather than disruption of specific meiotic gene expression. F 2 population genetic analysis indicated that the "148" watermelon line is a homozygous translocation and that the less seed phenotype of the F 1 hybrid is prompted by one chromosome fragment translocation. The translocated fragment was further fine mapped to a 2.09 Mb region on chromosome 6 by whole-genome resequencing and genetic map cloning procedures. Our work revealed that a 2.09 Mb chromosome fragment translocation on chromosome 6, causing meiotic defects at metaphase I during meiosis, leads to diploid less seed watermelon. Our findings provide a new promising method for less seed watermelon breeding at the diploid level, as well as a fragment size reference for breeding less seed watermelon through artificially induced chromosome translocation., (© 2021. The Author(s).)

Gliosarcoma (GSM) is a rare central nervous system tumor. Clinical management of it is similar to glioblastoma (GBM). However, due to a few comparative studies exist, uncertainty and disagreements remain in the literatures. To assess the available evidence on the value of different treatments and to carry out an up-to-date evaluation to summarize the evidence for the optimal treatment in GSM patients. Free words were used to search for the relevant studies without language limitations in electronic databases including PubMed, Ovid EMBASE, Cochrane Central Register of Controlled Trials from inception to September 15, 2019. Pooled hazard ratio (HR) with 95% confidence interval (CI) were calculated using a random-effects model. The main endpoint was all-cause mortality. Overall, 10 studies published between 2008 and 2018 including 803 patients were selected for the meta-analysis. Temozolomide (TMZ)-dominated chemotherapy was associated with a reduced risk of overall survival (OS), with HR 0.49 (95% CI 0.37-0.66). The pooled HR of OS was 0.40 (95% CI 0.29-0.56) between radiotherapy and without radiotherapy. The pooled HR (0.52, 95% CI 0.32-0.85) indicated gross total resection (GTR) had a positive impact on OS in GSM. In patients with GSM, survival benefits as currently performed are associated with TMZ-dominated chemotherapy and high-dose radiotherapy. Our systematic review and meta-analysis also demonstrate GTR is associated with a reduction in all-cause mortality in patients with primary GSM., (© 2020. Belgian Neurological Society.)

Background: Kinesin (KIN) as a motor protein is a versatile nano-machine and involved in diverse essential processes in plant growth and development. However, the kinesin gene family has not been identified in watermelon, a valued and nutritious fruit, and yet their functions have not been characterized. Especially, their involvement in early fruit development, which directly determines the size, shape, yield and quality of the watermelon fruit, remains unclear., Results: In this study, we performed a whole-genome investigation and comprehensive analysis of kinesin genes in C. lanatus. In total, 48 kinesins were identified and categorized into 10 kinesin subfamilies groups based on phylogenetic analysis. Their uneven distribution on 11 chromosomes was revealed by distribution analysis. Conserved motif analysis showed that the ATP-binding motif of kinesins was conserved within all subfamilies, but not the microtubule-binding motif. 10 segmental duplication pairs genes were detected by the syntenic and phylogenetic approaches, which showed the expansion of the kinesin gene family in C. lanatus genome during evolution. Moreover, 5 ClKINs genes are specifically and abundantly expressed in early fruit developmental stages according to comprehensive expression profile analysis, implying their critical regulatory roles during early fruit development. Our data also demonstrated that the majority of kinesin genes were responsive to plant hormones, revealing their potential involvement in the signaling pathways of plant hormones., Conclusions: Kinesin gene family in watermelon was comprehensively analyzed in this study, which establishes a foundation for further functional investigation of C. lanatus kinesin genes and provides novel insights into their biological functions. In addition, these results also provide useful information for understanding the relationship between plant hormone and kinesin genes in C. lanatus.

Complex composition is one of the most important features of the immune system, involving many types of organs, tissues, cells, and molecules that perform immune functions. The normal function of each component of the immune system is the guarantee for maintaining the relatively stable immune function of the body. When the self-immune tolerance mechanism of the body is unregulated or destroyed, the immune system reacts to autoantigens, resulting in damage to self-tissues and organs or an immunopathological state with abnormal functions. Autoimmune diseases are diverse, and their pathogenesis is complicated. Various immune cells and their interactions play significant roles in the occurrence and development of diseases. The solution to heterogeneity of immune cells is the basic science and translational understanding of how genes and the environment interact to induce disease so that we can develop personalized medicine, a goal that has to this point eluded scientists. Single-cell RNA sequencing (scRNA-Seq) refers to a new technique allowing high-throughput sequencing analysis of the whole transcriptome to reveal the gene expression status of individual cells. It has emerged as an indispensable tool in the field of life science research, and can help identify the complex mechanism of cell heterogeneity, discover new cell subsets, and help uncover the molecular mechanisms of pathogenesis, the evolution of disorders, and drug resistance. This information can provide us with new strategies for diagnosis and prognostic evaluation, as well as monitoring treatment responses. In this review, we summarize the crucial experimental procedures used for single-cell RNA sequencing, and the current applications of this technique to study autoimmune diseases are described in detail. This technique will be widely used in more in-depth studies of autoimmune diseases and will contribute to the diagnosis and therapies of these disorders.

Type I interferons (IFN-Is) are a very important group of cytokines that are produced by innate immune cells but also act on adaptive immune cells. IFN-Is possess antiviral, antitumor, and anti-proliferative effects, as well are associated with the initiation and maintenance of autoimmune disorders. Studies have shown that aberrantly expressed IFN-Is and/or type I IFN-inducible gene signatures in the serum or tissues of patients with autoimmune disorders are linked to their pathogenesis, clinical manifestations, and disease activity. Type I interferonopathies with mutations in genes impacting the type I IFN signaling pathway have shown symptoms and characteristics similar to those of systemic lupus erythematosus (SLE). Furthermore, both interventions in animal models and clinical trials of therapies targeting the type I IFN signaling pathway have shown efficacy in the treatment of autoimmune diseases. Our review aims to summarize the functions and targeted therapies (as well as clinical trials) of IFN-Is in both adult and pediatric autoimmune diseases, such as SLE, pediatric SLE (pSLE), rheumatoid arthritis (RA), juvenile idiopathic arthritis (JIA), juvenile dermatomyositis (JDM), Sjögren syndrome (SjS), and systemic sclerosis (SSc), discussing the potential abnormal regulation of transcription factors and epigenetic modifications and providing a potential mechanism for pathogenesis and therapeutic strategies for future clinical use.

Objective: To study the changes in pulmonary function in infants and young children with Mycoplasma pneumoniae pneumonia (MPP)., Methods: A total of 196 hospitalized children (at age of 0-36 months) who were diagnosed with MPP from January 2014 to June 2018 were enrolled as study subjects. A total of 208 children (at age of 0-36 months) with pneumonia not caused by Mycoplasma pneumoniae infection during the same period of time were enrolled as controls (non-MPP group). A retrospective analysis was performed for their clinical data. The two groups were compared in the pulmonary function on the next day after admission and on the day of discharge. The children with MPP were followed up to observe pulmonary function at weeks 2 and 4 after discharge., Results: Compared with the non-MPP group, the MPP group had significant reductions in the ratio of time to peak tidal expiratory flow to total expiratory time (TPTEF/TE), ratio of volume to peak tidal expiratory flow to total expiratory volume (VPTEF/VE), inspiratory-to-expiratory time ratio, and tidal expiratory flow at 25% remaining expiration on the next day after admission and on the day of discharge (P<0.05). In addition there were significant increases in the ratio of peak tidal expiratory flow to tidal expiratory flow at 25% remaining expiration, respiratory rate, effective airway resistance, and plethysmographic functional residual capacity per kilogram (P<0.05). Compared with the normal reference values of pulmonary function parameters, both groups had reductions in VPTEF/VE and TPTEF/TE on the next day after admission; on the day of discharge, the MPP group still had reductions in VPTEF/VE and TPTEF/TE, while the non-MPP group had normal values. The MPP group had increases in VPTEF/VE and TPTEF/TE from the day of discharge to weeks 2 and 4 after discharge (P<0.05), but TPTEF/TE still did not reach the normal value at week 4 after discharge., Conclusions: Airway obstruction is observed in infants and young children with acute MPP or non-MPP, and the children with MPP have a higher severity of airway obstruction and a longer time for improvement, with a certain degree of airway limitation in the recovery stage.

Status epilepticus (SE) is defined as continuous seizure activity lasting more than 5 minutes. It results in neuronal cell death, mediated by endoplasmic reticulum (ER) stress response. Previously, metformin demonstrated neuroprotective effects in primary cortical neurons. In this study, we analyzed the effect of metformin on ER stress via the pro-apoptotic protein kinase RNA-like endoplasmic reticulum kinase (PERK)-eukaryotic initiation factor 2α (eIF2α)-C/EBP homologous protein (CHOP) pathway. SE was induced in rats by pentylenetetrazole. Following SE, the rats were treated with salubrinal, GSK2656157, or metformin. In a control group (normal saline) SE was not induced. CHOP, eIF2α, and PERK expression was determined by Western blot; apoptosis was analyzed by TUNEL assay. CHOP expression was significantly increased at 6 and 24 hours following SE. At both time points, eIF2α and PERK levels were also increased. At 6 hours, CHOP expression was significantly reduced in salubrinal, GSK2656157 and metformin groups versus SE group. eIF2α and PERK levels were decreased in metformin compared to SE group. eIF2α expression was markedly decreased in salubrinal versus SE group, while PERK expression was markedly reduced in GSK2656157 versus SE group. At 6 and 24 hours, the apoptosis rate was significantly increased in SE versus control group, while it was significantly reduced in salubrinal, GSK2656157, and metformin groups compared to SE group. The apoptosis rate also decreased in salubrinal group at 24 hours, although not to the extent observed in metformin group. Overall, CHOP expression and apoptosis induced by SE in rats were reduced with metformin. Further studies are required to evaluate the clinical relevance of metformin for patients with SE.

DREAM (downstream regulatory element antagonist modulator), Calsenilin and KChIP3 (potassium channel interacting protein 3) belong to the neuronal calcium sensor (NCS) superfamily, which transduces the intracellular calcium signaling into a variety of activities. They are encoded by the same gene locus, but have distinct subcellular locations. DREAM was first found to interact with DRE (downstream regulatory element) site in the vicinity of the promoter of prodynorphin gene to suppress gene transcription. Calcium can disassemble this interaction by binding reversibly to DREAM protein on its four EF-hand motifs. Apart from having calcium dependent DRE site binding, DREAM can also interact with other transcription factors, such as cAMP responsive element binding protein (CREB), CREB-binding protein (CBP) and cAMP responsive element modulator (CREM), by this concerted actions, DREAM extends the gene pool under its control. DREAM is predominantly expressed in central nervous system with its highest level in cerebellum, and accumulating evidence demonstrated that DREAM might play important roles in pain sensitivity. Novel findings have shown that DREAM is also involved in learning and memory processes, Alzheimer's disease and stroke. This mini-review provides a brief introduction of its discovery history and protein structure properties, focusing on the mechanism of DREAM nuclear translocation and gene transcription regulation functions.

Uranium is one of the important nuclear materials to nuclear industry. Because of the direct disposal of spent fuel, there is still a huge possibility that uranium migrates into the groundwater, causing water contamination. It is of great importance to understand the concentration and their species distribution in aqueous solutions. Surface-Enhanced Raman Scattering (SERS) technique has been widely used for the detection of uranium (Ⅵ). However, the interactions between uranium (Ⅵ) and SERS substrate cause the symmetric stretching vibration peak of uranium (Ⅵ) shift to low wave number direction, which is unfavorable for confirming the species of uranium (Ⅵ) in aqueous solution. For instance, the normal Raman bands of uranyl in nitric acid solution are 871 cm-1, which belongs to the symmetric stretching mode of UO2+2. However, it moves to 710 cm-1 on the surface of silver nanorods SERS substrtate. What’s more, different SERS substrate causes different number of shift. Graphene has advantages of inertness and integrity as well as 2-dimensional thickness. In this paper, graphene-isolated SERS substrate which is silver nanoparticles (AgNPs)/graphene complex substrate, was designed to prevent the interaction between SERS substrate and it was analyzed by using the inert graphene layer. First of all, according to our previous work, AgNPs SERS substrate was fabricated on silicon wafer by using an ascorbic acid-actived self-assembly method. Then, AgNPs/graphene complex substrate was prepared by transfering monolayer graphene onto the self-assembly AgNPs substrate. The morphology of complex substrate was obtained by SEM. Some AgNPs link together closely to form nanochain structures. Nanochain structures were distributed evenly on the surface of silicon wafer. The 2-dimensional thickness of graphene did not affect the morphology of AgNPs. When using the complex substrate to detect uranyl nitrate (5×10-4 mol·L-1)，the Raman peak that appeared around 771 cm-1 is considered to be the symmetric stretching mode of UO2+2, shifting back about 52 cm-1 to high wave number direction when compared with AgNPs substrate, which was about ~719 cm-1. The result indicates that graphene layer isolates the interaction between AgNPs substrate and uranyl in some degree.

Bioleaching combined with Fenton-like oxidation was used to condition sewage sludge. The results showed that it took approximately 1 d to decrease pH from 6.9 to 2.5 by bioleaching, with fixed sulfur power and FeSO4 x 7H2O dosages of 3 g x L(-1) and 8 g x L(-1), respectively. After bioleaching, the volatile solids(VS) reduction was 13.4%, and the specific resistance to filtration(SRF) dropped from 3.1 x 10(9)s2 x g(-1) to 1.5 x 10(9)s2 x g(-1) with a reduction of 51.6%, but the bioleached sludge was still difficult to be dewatered. The bioleached sludge was further oxidized by Fenton-like oxidation. The results indicated that the optimal H2O2 dosage and reaction time were 3.3 g x L(-1) and 60 min, respectively. Under the optimal conditions, VS reduction was 30.8%, SRF was declined to 1.9 x 10(8) s2 x g(-1) with a reduction of 93.9%, and the moisture of sludge cake was 76.9%. After treated by bioleaching combined with Fenton-like oxidation, the dewaterability and stability of sewage sludge were significantly improved. Besides, the combined technology was more efficient in conditioning sewage sludge than single Fenton-like oxidation.

Water movement plays vital roles in both physiological and pathological conditions in the brain. Astrocytes are responsible for regulating this water movement and are the major contributors to brain edema in pathological conditions. Aquaporins (AQPs) in astrocytes play critical roles in the regulation of water movement in the brain. AQP1, 3, 4, 5, 8, and 9 have been reported in the brain. Compared with AQP1, 4, and 9, AQP3, 5, and 8 are less studied. Among the lesser known AQPs, AQP5, which has multiple functions identified outside the central nervous system, is also indicated to be involved in hypoxia injury in astrocytes. In our study, AQP5 expression could be detected both in primary cultures of astrocytes and neurons, and AQP5 expression in astrocytes was confirmed in 1- to 4-week old primary cultures of astrocytes. AQP5 was localized on the cytoplasmic membrane and in the cytoplasm of astrocytes. AQP5 expression was downregulated during ischemia treatment and upregulated after scratch-wound injury, which was also confirmed in a middle cerebral artery occlusion model and a stab-wound injury model in vivo. The AQP5 increased after scratch injury was polarized to the migrating processes and cytoplasmic membrane of astrocytes in the leading edge of the scratch-wound, and AQP5 over-expression facilitated astrocyte process elongation after scratch injury. Taken together, these results indicate that AQP5 might be an important water channel in astrocytes that is differentially expressed during various brain injuries., (Copyright © 2013 Wiley Periodicals, Inc.)

When a distal common bile duct neoplasm is at the stage of carcinoma in situ or high-grade dysplasia, it is difficult for the surgeon to decide whether to perform pancreaticoduodenectomy. Here we describe a patient with a progressive dysplastic lesion in the common bile duct, which developed from moderate-high to high-grade dysplasia in approximately 2 mo. The patient refused major surgery. Therefore, endoscopic-assisted photodynamic therapy was performed. The result at follow-up using a trans-T-tube choledochoscope showed that the lesion was completely necrotic. This report is the first to describe the successful treatment of high-grade dysplasia of the distal bile duct using photodynamic therapy via a choledochoscope.

Objective: To construct and characterize EGFP reporter gene labeled Sindbis virus (SINV)., Methods: The reporter gene EGFP was inserted into the genome of infectious clone pBR-XJ160 by using multi-fusion long fragment PCR method. Then apply reverse genetic manipulation technique to rescue and obtain EGFP labeled SINV., Results: We successively obtained labeled SINV, which has good fluorescent expression characteristics and genetic stability., Conclusion: The labeled virus can be seen in living cells and living body, and this serves as a good tool for cell and tissue tropism and biological function study of viruses. This study laid a foundation for further studying the cell tropism, biological functions and infection mechanism of SINV.

Objective: To investigate retrospectively the relationship between clinicopathological factors and lymph node matastasis of pancreatic adenocarcinoma., Methods: 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., Results: Among the 71 cases, there were 49 males (69.0%) and 22 females (31.0%). Forty-eight were ≥ 60 (67.6%) and 23 were < 60 (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%), and > 5 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 (P < 0.05). Multivariate logistic regression analysis also showed that differentiation and range of local infiltration were significantly associated with lymph node meatstasis (P < 0.05)., Conclusions: 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.

Watermelon, Citrullus lanatus, is an important cucurbit crop grown throughout the world. Here we report a high-quality draft genome sequence of the east Asia watermelon cultivar 97103 (2n = 2× = 22) containing 23,440 predicted protein-coding genes. Comparative genomics analysis provided an evolutionary scenario for the origin of the 11 watermelon chromosomes derived from a 7-chromosome paleohexaploid eudicot ancestor. Resequencing of 20 watermelon accessions representing three different C. lanatus subspecies produced numerous haplotypes and identified the extent of genetic diversity and population structure of watermelon germplasm. Genomic regions that were preferentially selected during domestication were identified. Many disease-resistance genes were also found to be lost during domestication. In addition, integrative genomic and transcriptomic analyses yielded important insights into aspects of phloem-based vascular signaling in common between watermelon and cucumber and identified genes crucial to valuable fruit-quality traits, including sugar accumulation and citrulline metabolism.

An isolated parenchymal gastric metastasis from ovarian carcinoma without any other sites of recurrence is extremely rare. Only two cases have been reported, both of which were symptomatic. We herein report such a case without any symptoms. A 61-year-old woman presented with a high cancer antigen-125 level without any other clinical manifestation. A subsequent ¹⁸F-fluorodeoxyglucose (¹⁸F-FDG) positron emission tomography/computed tomography scan revealed a submucosal mass with hypermetabolism of ¹⁸F-FDG (standardized uptake value: 5.36) in the gastric antrum. The final pathology after gastric antrectomy showed a metastatic gastric tumor from a primary ovarian carcinoma. We also performed an extensive literature review about gastric metastasis from ovarian carcinoma published until recently, and this is the first case of an isolated parenchymal gastric metastasis from ovarian carcinoma without any symptoms.

Objective: To construct the recombinant virus-like particles containing HCV envelope glycoprotein E1E2 based on sindbis virus vector., Methods: The gene encoding HCV envelope glycoprotein E1E2 was cloned into sindbis virus vector to construct recombinant plasmids pBR-XJE1E2 and pVA-XJE1E2, and transfect them into BHK-21 cells to obtain recombinant virus-like particles. The expression of E1 and E2 protein were verified by Western Blot and indirect immunofluorescent assay (IFA)., Results: The results of restriction enzyme digestion, PCR and sequencing analysis showed that the recombinant plasmids were constructed successfully. And the results of RT-PCR, Western blotting and IFA detection showed that the transfect cells could package HCV-like particles of expressing structural proteins E1E2., Conclusion: The recombinant expression plasmids pBR-XJE1E2 and pVA-XJE1E2 based on sindbis virus vector could package HCV-like particles in eukaryotic cell, which provides a foundation for further study of its in vivo animal immune response.

As part of our ongoing efforts to sequence and map the watermelon (Citrullus spp.) genome, we have constructed a high density genetic linkage map. The map positioned 234 watermelon genome sequence scaffolds (an average size of 1.41 Mb) that cover about 330 Mb and account for 93.5% of the 353 Mb of the assembled genomic sequences of the elite Chinese watermelon line 97103 (Citrullus lanatus var. lanatus). The genetic map was constructed using an F(8) population of 103 recombinant inbred lines (RILs). The RILs are derived from a cross between the line 97103 and the United States Plant Introduction (PI) 296341-FR (C. lanatus var. citroides) that contains resistance to fusarium wilt (races 0, 1, and 2). The genetic map consists of eleven linkage groups that include 698 simple sequence repeat (SSR), 219 insertion-deletion (InDel) and 36 structure variation (SV) markers and spans ∼800 cM with a mean marker interval of 0.8 cM. Using fluorescent in situ hybridization (FISH) with 11 BACs that produced chromosome-specifc signals, we have depicted watermelon chromosomes that correspond to the eleven linkage groups constructed in this study. The high resolution genetic map developed here should be a useful platform for the assembly of the watermelon genome, for the development of sequence-based markers used in breeding programs, and for the identification of genes associated with important agricultural traits.

Objective: To determine the effects of interleukin (IL)-17A inhibition on experimental atherosclerosis., Methods and Results: ApoE(-/-) mice were treated with either rat anti-mouse IL-17A, mouse anti-mouse IL-17A or isotype-matched control antibodies for 12 weeks (n=8-10 per group). Ldlr(-/-) mice were transplanted with IL-17A-deficient or wild type bone marrow (n=8 per group). Rat anti-mouse IL-17A treatment obviously reduced plaque size by 43% (p<0.01) without evidence of reduced IL-17A signaling. In contrast, mouse anti-mouse IL-17A treatment and IL-17A deficiency in bone marrow cells did not alter lesion size despite significant reduction of IL-17A production., Conclusions: Inhibition of IL-17A signaling does not alter lesion development in Th1-biased C57BL/6 ApoE(-/-) and Ldlr(-/-) mice with already low levels of IL-17A production. Alteration of lesion development after repeated injections of rat anti-mouse IL-17A antibody in ApoE(-/-) mice could not be attributed to blockade of IL-17A signaling., (Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.)

Objective: Animal studies suggest that regulatory T (T(reg)) cells play a beneficial role in ventricular remodeling and our previous data have demonstrated defects of T(reg) cells in patients with chronic heart failure (CHF). However, the mechanisms behind T(reg-)cell defects remained unknown. We here sought to elucidate the mechanism of T(reg-)cell defects in CHF patients., Methods and Results: We performed flow cytometry analysis and demonstrated reduced numbers of peripheral blood CD4(+)CD25(+)FOXP3(+)CD45RO(-)CD45RA(+) naïve T(reg) (nT(reg)) cells and CD4(+)CD25(+)FOXP3(+)CD45RO(+)CD45RA(-) memory T(reg) (mT(reg)) cells in CHF patients as compared with non-CHF controls. Moreover, the nT(reg)/mT(reg) ratio (p<0.01), CD4(+)CD25(+)FOXP3(+)CD45RO(-) CD45RA(+)CD31(+) recent thymic emigrant T(reg) cell (RTE-T(reg)) frequency (p<0.01), and T-cell receptor excision circle levels in T(reg) cells (p<0.01) were lower in CHF patients than in non-CHF controls. Combined annexin-V and 7-AAD staining showed that peripheral T(reg) cells from CHF patients exhibited increased spontaneous apoptosis and were more prone to interleukin (IL)-2 deprivation- and CD95 ligand-mediated apoptosis than those from non-CHF individuals. Furthermore, analyses by both flow cytometry and real-time polymerase chain reaction showed that T(reg)-cell frequency in the mediastinal lymph nodes or Foxp3 expression in hearts of CHF patients was no higher than that of the non-CHF controls., Conclusion: Our data suggested that the T(reg)-cell defects of CHF patients were likely caused by decreased thymic output of nascent T(reg) cells and increased susceptibility to apoptosis in the periphery.

Objective: Atherosclerosis is a chronic inflammatory disease in which the renin-angiotensin-aldosterone system plays an important role. Evidence indicate that the angiotensin type 1 receptor blockers can suppress atherogenesis, but the exact mechanisms have not been fully elucidated. The study was undertaken to investigate the potential effects and molecular mechanisms of an angiotensin type 1 receptor blocker irbesartan on atherogenesis in high cholesterol-diet apolipoprotein E knock-out mice., Methods and Results: Adult male apolipoprotein E knock-out mice were given normal diet or high cholesterol-diet and randomized to receive no treatment or irbesartan 10 mg kg(-1) d(-1) for 12 weeks. The apolipoprotein E knock-out mice with high cholesterol-diet were associated with a marked increase in atherosclerotic lesion area, plasma lipid and angiotensin II levels, as well as the expressions of angiotensin type 1 receptor in the aorta. High cholesterol-diet feeding increases the activity of NADPH oxidase subunits (p47(phox) and Rac), extracellular signal-regulated kinase 1/2, janus kinase 2, signal transducer and activator of transcription 3, nuclear factor-kappaB and the expression of tumor necrosis factor-alpha, interleukin 6, monocyte chemoattactant protein-1 and vascular cell adhesion molecule-1 in the aortas. These changes were suppressed in mice that were treated with irbesartan 10 mg kg(-1) d(-1), with no significant change in systolic blood pressure and plasma lipid levels., Conclusions: The results suggest that irbesartan can attenuate atherosclerosis, and this effect is partly related to the inhibition of oxidative stress and inflammatory signal transduction pathways which eventually leads to the decrease in the expression of inflammatory cytokines., (Copyright 2008 Elsevier Ireland Ltd. All rights reserved.)

Objective: Atherosclerosis is a chronic inflammatory disease regulated by T lymphocyte subsets. Recently, CD4(+) CD25(+) Foxp3(+) regulatory T (Treg) cells and Th17 cells have been described as two distinct subsets and have the opposite effects on autoimmunity. Clinical observation has revealed that the Th17/Treg imbalance exists in patients with acute coronary syndrome. We investigated whether the Th17/Treg functional imbalance existed during atherogenesis in ApoE(-/-) mice., Methods and Results: Th17/Treg functions at different levels including cell frequencies, related cytokine secretion and key transcription factors were investigated comparatively between ApoE(-/-) mice and their age-matched C57BL/6J mice. The results demonstrated that ApoE(-/-) mice revealed significantly increased secretion of Th17 related cytokines (IL-17 and IL-6) and expression of transcription factor (RORgammat) levels and obviously decreased number in Treg cells, secretion of Treg related cytokines (TGF-beta(1)) and expression of transcription factor (Foxp3) levels as compared with age-matched C57BL/6J mice. Th17 related mediators reached their maximum expression values at the early stage (8-16weeks of age) in ApoE(-/-) mice, and then followed by continuous depression of their expression levels. Meanwhile, the expression of Treg related mediators was much lower in ApoE(-/-) mice than in their age-matched wild-type littermates., Conclusions: Th17/Treg functional imbalance exists during atherogenesis in ApoE(-/-) mice, suggesting a potential role of Th17/Treg imbalance in the formation and progression of atherosclerosis., (Copyright 2009 Elsevier Ltd. All rights reserved.)

Aims: Increasing evidences confirm the role of immune activation in the pathogenesis of chronic heart failure (CHF). Regulatory T cells appear central to the control of immune homeostasis. We assessed the hypothesis that the circulating frequency and function of CD4+CD25+ Foxp3+CD127(low) T regulatory cells (Tregs) would be deranged in patients with CHF., Methods: Ninety-nine CHF patients due to non-ischemic (NIHF) or ischemic etiology (IHF) and 24 control donors were enrolled in the study. Frequency of circulating Tregs was evaluated by flow cytometry. Foxp3 in peripheral blood mononuclear cells (PBMCs) was assayed at the mRNA level by real-time PCR. Functional properties of Tregs to suppress proliferation and pro-inflammatory cytokines secretion of activated CD4+CD25(-) T cells were measured by proliferation assay and ELISA., Results: The results demonstrated that CHF patients had significantly lower frequency of circulating Tregs and reduced Foxp3 expression in PBMCs compared with control donors. Moreover, Tregs from CHF patients showed compromised function to suppress CD4+CD25(-) T cells proliferation and pro-inflammatory cytokines secretion. A similar pattern with reduced Tregs frequency and compromised function was found in both NIHF and IHF patients. Correlation analysis suggested that Tregs frequency and function positively correlated with LVEF, whereas negatively correlated with LVEDD and NT-proBNP in patients with CHF., Conclusions: Our data are the first to demonstrate that frequencies of circulating Tregs in patients with CHF are reduced and their suppressive function compromised independently of the etiology. Defective Tregs may be an underlying mechanism of immune activation in CHF patients., (2010 S. Karger AG, Basel.)

Aim: Hyperhomocysteinemia (Hhcy) is an important and independent risk factor for atherosclerosis. Recent studies have shown that Poly (ADP-ribose) polymerase (PARP) activation may be associated with Hhcy-induced endothelial dysfunction, which is an important mechanism for Hhcy to affect atherosclerotic progress. Thus, we investigated whether PARP inhibitors may attenuate atheroscle-rotic plaque development in an Hhcy-induced experimental animal model with atherosclerosis., Methods: Six-week-old homozygous apolipoprotein E-deficient (ApoE-/-) male mice fed a normal diet or high methionine diet randomly received intraperitoneal injections of 10 mg/kg 3-aminoben-zamide (3-AB, a PARP inhibitor) dissolved in phosphate-buffered saline (PBS), or physiological saline every other day for 12 weeks. Atherosclerotic lesion sizes and PARP activity were measured. Related inflammatory factors in atherogenesis were investigated by real-time quantitative PCR and Western blot analysis., Results: Our data demonstrated that ApoE-/- mice fed a high methionine diet generated Hhcy, which subsequently increased the atherosclerotic lesion size significantly, promoted oxidative stress-associated DNA damage and PARP activation, then increased the expression of proinflammatory fac-tors within atherosclerotic plaques. Although PARP inhibition by 3-AB did not markedly inhibit plaque development in ApoE-/- mice with spontaneous hyperlipidemia by feeding a normal diet, it significantly reduced the atherosclerotic lesion size by 40% in Hhcy-induced atherosclerosis without affecting plasma homocysteine levels and lipid contents, effectively suppressed PARP activation, and inhibited nuclear translocation of nuclear factor-(kappa)B (NF-(kappa)B) and subsequent production of inflam-matory factors, such as vascular cell adhesion molecule-1 (VCAM-1) and monocyte chemoattactant protein-1 (MCP-1)., Conclusion: Our results suggest that PARP inhibition attenuates atherosclerotic plaque development under hyperhomocysteinemic conditions, through the inhibition of PARP activation, nuclear NF-kappaB translocation and subsequent expression of inflammatory factors.

Introduction: We investigated the possible protective effect of poly (ADP-ribose) polymerase (PARP) inhibition in preventing endothelial dysfunction induced by hyperhomocysteinemia (Hhcy)., Methods: Sprague-Dawley rats were divided into Hhcy group, Hhcy + 3-aminobenzamide(3-AB) group, control group and control + 3-AB group. A high-methionine diet was given to induce hyperhomocysteinemia. In Hhcy + 3-AB and control + 3-AB groups, rats were injected intraperitoneally with 3-AB (inhibitor of PARP). After 45 days, ultrastructural changes of aortas were observed by transmission electron microscope. Vascular reactivity of thoracic aortic rings was measured in organ chambers. PARP activity was detected. The levels of plasma total homocysteine, nitrite/nitrate, endothelin (ET)-1 and malondialdehyde were assayed., Results: Rats in Hhcy group developed severe hyperhomocysteinemia and significant loss of endothelial function as measured by both vascular rings and levels of nitrite/nitrate and ET-1. Malondialdehyde levels increased significantly in Hhcy rats compared with control rats. 3-AB improved Ach-induced, NO-mediated vascular relaxation and stabilized the level of nitrite/nitrate and ET-1. Obvious improvement of ultrastructure can be observed in Hhcy + 3-AB group., Conclusions: These results suggest that pharmacological inhibition of PARP prevents the development of endothelial dysfunction in rats with hyperhomocysteinemia which may represent a novel approach to improve vascular dysfunction associated with hyperhomocysteinemia.

Rab family proteins play a crucial role in regulating vesicular traffic in eukaryotic cells. EoRab43 is an atypical Rab gene identified in Euplotes octocarinatus. In order to understand the function of EoRab43, the 153bp fragment of the 3'-end of EoRab43 gene was subcloned into expression vector pGEX-6P-1, and the recombinant plasmid pGEX-EoRab43(153bp) was transfered into E.coli BL21 (DE3) to express the fusion protein. The fusion protein GST-EoRab43C was expressed and purified by affinity chromatography. BALB/c mice were immunolized by purified GST-EoRab43C. The titer of anti-EoRab43C polyclonal antibody was detected by indirect ELISA assay and the specificity of the antibody was detected by Western blot. Immunofluorescence experiments were performed using anti-EoRab43C antibody in the cells of Euplotes. The results showed that EoRab43 displayed a punctuate pattern in the cytoplasm around the macronuclear chromosome of Euplotes.

Atherosclerosis is a chronic inflammatory disease, which is positively and negatively regulated by T helper (Th) 1 and Th2 lymphocytes, respectively. Recent findings indicate that suppressive oligodeoxynucleotides (ODNs) expressing TTAGGG motifs selectively reduce Th1 cytokine production and have been proven effective at blocking the development of organ-specific autoimmune diseases. In the current research, we hypothesized that suppressive ODNs may alter the development of atherosclerosis. Eight-week-old homozygous ApoE(-/-) male mice were injected with 300 mug ODNs A151 (TTAGGG) or nonspecific ODNs 1612. Atherosclerotic lesion sizes were dramatically reduced by ODNs A151, but not by nonspecific ODNs. MCP-1 and VCAM-1, which are the key inflammatory factors in atherogenesis, were significantly attenuated by the suppressive ODNs A151. In the splenic lymphocytes, FACS analysis showed ODNs A151 reduced the percentage of IFN-gamma-producing Th1 cells and slightly increased the percentage of IL-4-producing Th2 cells, indicating that suppressive ODNs skewed the Th1/Th2 balance toward Th2 inflammation in vivo. Furthermore, ODNs A151 down-regulated the phosphorylation of STAT1 and STAT4 and suppressed up-regulation of T-bet, a signal modulator for Th1, and didn't impact GATA-3 and STAT6, which are associated with a Th2 phenotype. Consistent with this in vivo observation, ELISA analysis demonstrated that ODNs A151 suppressed Th1 cytokines IFN-gamma and TNF-alpha, and augmented Th2 cytokines IL-4 and IL-10 in vitro. This study provides the first experimental evidence that suppressive ODNs inhibit the development of atherosclerosis through inhibition of the STAT1/4 and T-bet pathways, which further modulate the Th1/Th2 balance in vivo.

Atherosclerosis is a chronic inflammatory disease regulated by T lymphocyte subsets. Recently, CD4+CD25+Foxp3+ regulatory T (Treg) cells and Th17 cells have been described as two distinct subsets from Th1 and Th2 cells and have the opposite effects on autoimmunity. Th17/Treg balance controls inflammation and may be important in the pathogenesis of plaque destabilization and the onset of acute coronary syndrome [ACS, including unstable angina (UA) and acute myocardial infarction (AMI)]. To assess whether this balance was broken in patients with coronary heart disease, we detected Th17/Treg functions on different levels including cell frequencies, related cytokine secretion and key transcription factors in patients with AMI, UA, stable angina (SA) and controls. The results demonstrated that patients with ACS revealed significant increase in peripheral Th17 number, Th17 related cytokines (IL-17, IL-6 and IL-23) and transcription factor (RORgammat) levels and obvious decrease in Treg number, Treg related cytokines (IL-10 and TGF-beta1) and transcription factor (Foxp3) levels as compared with patients with SA and controls. Results indicate that Th17/Treg functional imbalance exists in patients with ACS, suggesting a potential role for Th17/Treg imbalance in plaque destabilization and the onset of ACS.

Objective: To explore the relation between changes in expression of aquaporin-4(AQP4) protein and acute radiation-induced cerebral edema after Gamma knife radiation., Methods: The experimental model was established in rats by radiating 2 mm right to median line in cerebral hemisphere with 50 Gy Gamma knife (the center located at the line of auditory canal). The changes of brain water content were measured by the wet and dry weight method. Immunohistochemistry was used to determine the change of expression of AQP4 protein at different periods after Gamma knife radiation., Results: The brain water content and the expression of AQP4 in the target area and the peripheral zone obviously increased at 12 h after Gamma knife radiation, and achieved the peak after 2 d. It was still higher than normal after 14 d. The gray value of expression of aquaporin-4 was negatively related to brain water content (r=-0.9857, P<0.05)., Conclusion: AQP4 has a close relationship with acute radiation-induced cerebral edema.

Oxidative stress and inflammation processes are key components of atherosclerosis, from fatty streak formation to plaque rupture and thrombosis. Evidence has revealed that calcium-channel blockers (CCB) could retard atherogenesis, but the exact mechanisms have not been fully elucidated. The present study was undertaken to investigate the potential effects and molecular mechanisms of the CCB felodipine on the process of atherosclerosis in high-cholesterol-diet (HCD) apolipoprotein E-knockout (ApoE KO) mice. Adult male ApoE KO mice were given a normal diet (ND) or HCD and were randomized to no treatment or felodipine (5 mg / kg per day for 12 weeks). The ApoE KO mice with HCD were associated with a marked increase in plasma lipid levels, atherosclerotic lesion area, and the expressions of NADPH oxidase subunits (p47 and Rac-1), nuclear factor-kappaB (NF-kappaB) in nucleus, phosphor-inhibitors of kappaB (p-IkappaB), tumor necrosis-alpha (TNF-alpha), monocyte chemoattractant protein-1 (MCP-1), and vascular cell-adhesion molecule-1 (VCAM-1). These changes were suppressed in mice that were treated with felodipine (5 mg/kg per day for 12 weeks) concomitant with HCD administration, with no significant change in systolic blood pressure and plasma lipid levels. The results suggest that felodipine can attenuate atherosclerosis, and this effect is partly related to inhibition of oxidative stress and inflammatory signal-transduction pathways, which lead to decreases in the expression of inflammatory cytokines.

Objective: To explore the levels of sex hormones in female patients with systemic lupus erythematosus (SLE) and its role in the genesis of SLE., Methods: The serum levels of estradiol, estriol, testosterone, progesterone, and prolactin were determined by electro-chemiluminescence immunoassay in 98 female patients with SLE and compared with those of 38 healthy women., Results: The serum levels of estradiol, estriol, progesterone, and prolactin were significantly higher than those in the healthy women (P <0.05). The serum levels of estradiol, progesterone, and prolactin in patients with SLE in 25 to 34 year old group were higher than the other age groups and the control group (P < 0.05), and the serum levels of estradiol and prolactin in patients with active phase of SLE were significantly higher than those in patients with stable phase of SLE (P <0.05)., Conclusion: The levels of sex hormones have a close corretation with the genesis and development of SLE.

Objective: To evaluation the clinical effect of combination of traditional Chinese medicine and western medicine on Bell's palsy., Methods: 83 patients with Bell's palsy were randomly divided into two groups (trail group 54 cases and control group 29 cases). Patients in two groups were treated with medicine, acupuncture, physiotherapy, while patients in the trail group were treated with massage and functional exercise as the same time. The results of both groups were evaluated according to Portmann's Simple Scale., Results: The score before treatment of trail group was 2.907 +/- 1.794, while control group was 2.931 +/- 2.034. And the score after treatment of trail group was 18.593 +/- 1.743, while control group was 9.862 +/- 3.091. Score of the function of facial muscles obtained from trail group was distinctly higher than that was from the control group (P < 0.01), as well as the improvement index (P < 0.01, trail group: 0.844 +/- 0.095, control group: 0.712 +/- 0.129)., Conclusion: There is significant curative effect and suitability in the treatment of Bell's palsy with combination of traditional Chinese medicine and western medicine. The improvement of facial muscles' motive function pre- and post-treatment and quantitative evaluation of curative effect can be objectively obtained by evaluation of facial muscles' function.