Irrational use of antimicrobial agents for preventing postoperative SSIs is a common phenomenon in China, which results in more bacterial resistance, higher hospital infection rates, extra costs of antimicrobial agents. The aim of the study is to evaluate the effect of Drug Rational Usage Guidelines System (DRUGS) on the surgeon's prescription behavior of antimicrobial agents.
We present a structural comparison of monolayers on a SiO2 substrate of two asymmetrically substituted sexithiophenes (6T). Molecule 1 consists of 6T with a branched alkyl chain at one end only and shows a crystalline structure. In molecule 2, the bifunctional 6T has in addition at the other end a linear alkyl chain. It displays thermotropic liquid crystalline (LC) behavior. Both compounds form readily single molecular layers from solution. Remarkably, full monolayer coverage can be achieved before multilayer growth starts. LC properties promote preordering near the interface as well as exchange of molecules between the growing domains, thus regulating the domain sizes. As a result, the LC compound 2 forms single-molecule islands with larger domain sizes compared to compound 1. Surface X-ray investigations indicate that the 6T cores are tilted relative to the layer normal. The tilt angle is as large as 54° for compound 2 compared to 28° for compound 1. For molecule 2, interfacial constraints and packing requirements because of the asymmetric substitution cause a rather loosely organized core structure.
We intended to identify risk factors that affect brain metastases (BM) in patients with locally advanced non-small cell lung cancer (LA-NSCLC) receiving definitive radiation therapy, which may guide the choice of selective prevention strategies.
The balance between bone formation and resorption is compromised in diabetes, which may contribute to the high risk of fractures in diabetic patients. However, the mechanism by which high glucose affects bone turnover remains to be elucidated. The present study demonstrated that high glucose inhibited receptor activator of nuclear factor??B ligand (RANKL)?induced osteoclastogenesis. In order to examine the mechanism involved in the inhibition of osteoclastogenesis, the present study examined several key molecules involved in osteoclast differentiation, including v?ATPase V0 subunit d2 (Atp6V0d2), dendritic cell?specific transmembrane protein (DC-STAMP), c?fos and nuclear factor of activated T cells c1 (NFATc1). The expression levels of Atp6V0d2 and DC?STAMP are regulated by NFATc1 and c?fos, and are required for osteoclast fusion, which is important for osteoclast maturation. To the best of our knowledge, the present study demonstrated for the first time that high glucose decreased the gene expression of ATP6v0d2 and DC?STAMP in RAW264.7 cells mediated by RANKL. Therefore, the suppression of pre?osteoclast or osteoclast fusion may be essential for the inhibition of osteoclast differentiation.
Radiation is the foundation of treatment for locally advanced non-small cell lung cancer (NSCLC), and as such, optimal radiation dose is essential for successful treatment. This article will briefly review biological considerations of radiation dose and their effect in the context of three-dimensional conformal radiation therapy (3D-CRT) including intensity modulated radiation therapy (IMRT) and stereotactic body radiation therapy (SBRT) for NSCLC. It will focus on literature review and discussions regarding radiation dose effect in locally advanced NSCLC including potential severe and lethal toxicities of high dose radiation given with concurrent chemotherapy. Potential new approaches for delivering safe and effective doses by individualizing treatment based on functional imaging are being applied in studies such as the PET boost trial and RTOG1106. The RTOG concept of delivering high dose radiation to the more resistant tumors with the use of isotoxic dose prescription and adaptive planning will also be discussed in detail.
5-Fluorouracil (5-FU) and its pro-drug Capecitabine have been widely used in treating colorectal cancer. However, not all patients will respond to the drug, hence there is a need to develop reliable early predictive biomarkers for 5-FU response. Here, we report a novel potentially functional Single Nucleotide Polymorphism (pfSNP) approach to identify SNPs that may serve as predictive biomarkers of response to 5-FU in Chinese metastatic colorectal cancer (CRC) patients. 1547 pfSNPs and one variable number tandem repeat (VNTR) in 139 genes in 5-FU drug (both PK and PD pathway) and colorectal cancer disease pathways were examined in 2 groups of CRC patients. Shrinkage of liver metastasis measured by RECIST criteria was used as the clinical end point. Four non-responder-specific pfSNPs were found to account for 37.5% of all non-responders (P<0.0003). Five additional pfSNPs were identified from a multivariate model (AUC under ROC?=?0.875) that was applied for all other pfSNPs, excluding the non-responder-specific pfSNPs. These pfSNPs, which can differentiate the other non-responders from responders, mainly reside in tumor suppressor genes or genes implicated in colorectal cancer risk. Hence, a total of 9 novel SNPs with potential functional significance may be able to distinguish non-responders from responders to 5-FU. These pfSNPs may be useful biomarkers for predicting response to 5-FU.
A growing amount of evidence indicates that miRNAs are important regulators of multiple cellular processes and, when expressed aberrantly in different types of cancer such as hepatocellular carcinoma (HCC), play significant roles in tumorigenesis and progression. Aberrant expression of miR-199a-5p (also called miR-199a) was found to contribute to carcinogenesis in different types of cancer, including HCC. However, the precise molecular mechanism is not yet fully understood. The present study showed that miR-199a is frequently down-regulated in HCC tissues and cells. Importantly, lower expression of miR-199a was significantly correlated with the malignant potential and poor prognosis of HCC, and restoration of miR-199a in HCC cells led to inhibition of the cell proliferation and cell cycle in vitro and in vivo. Furthermore, Frizzled type 7 receptor (FZD7), the most important Wnt receptor involved in cancer development and progression, was identified as a functional target of miR-199a. In addition, these findings were further strengthened by results showing that expression of FZD7 was inversely correlated with miR-199a in both HCC tissues and cells and that over-expression of miR-199a could significantly down-regulate the expression of genes downstream of FZD7, including ?-catenin, Jun, Cyclin D1 and Myc. In conclusion, these findings not only help us to better elucidate the molecular mechanisms of hepatocarcinogenesis from a fresh perspective but also provide a new theoretical basis to further investigate miR-199a as a potential biomarker and a promising approach for HCC treatment.
In 2012, the cumulative mortality of farmed sturgeons in Beijing was almost 60% with various symptoms, including the reddening of the anus with yellow exudation, ascities in the peritoneal cavity, petechial haemorrhages in liver and internal muscle wall, and the swollen spleen.
An anaerobic/aerobic/anoxic-type sequencing batch reactor was started up during a summer rainy season to obtain enhanced biological phosphorus removal (EBPR), and its sludge microbial community was also monitored in the hope of observing the microbial community evolution of polyphosphate-accumulating organisms (PAOs). During the start-up process, a total of 17 bands of highest species richness were detected in the sludge microbial community, including Alpha-, Beta-, and Gamma- Proteobacteria, as well as Actinobacteria and Planctomycetes. Major microbial community structural change was observed in Rhodocyclus-related and Acinetobacter-related PAOs, glycogen-accumulating organisms (GAOs), and Actinobacteria. In contrast to the current belief that enrichment of PAOs is essential for the establishment of EBPR, PAOs were not favourably enriched in this study. Instead, Actinobacteria and GAOs overwhelmingly flourished. The overall conclusion of this study challenges the conventional view that EBPR cannot live without traditional PAOs. However, it suggests an non-negligible role of denitrifying phosphorus-accumulating bacteria in EBPR systems, as well as other uncultured bacteria.
This paper concentrates on the separation of three conjugated linoleic acid (CLA) isomers (trans-9,trans-11 CLA, trans-10,cis-12 CLA and cis-9,trans-11 CLA) by ?-cyclodextrin (?-CD) encapsulation using countercurrent chromatography from Camellia oleifera Abel cake fermented by lactic acid bacteria Lactobacillus sp. LL-ZSDS001. The elution sequence of the CLA isomers, the mixing zones and mechanism of separation are discussed. The separation of 305.9mg of the crude sample yielded three isomeric compounds: 91.3mg of trans-9,trans-11 CLA, 84.1mg of trans-10,cis-12 CLA and 79.7mg of cis-9,trans-11 CLA at high purities of 98%, 94% and 96%, respectively.
Primary biliary cirrhosis (PBC) is a chronic cholestatic liver disease of unknown etiology and abnormality of hepatobiliary transport might contribute to its pathogenesis. In this study, we aimed to isolate and identify new molecules associated with PBC. With hepatocyte canalicular membrane vesicles (CMVs) of PBC patients as immunogens, we screened the monoclonal antibody 1F9 (mAb1F9), whose antigen dominantly recognized the subapical domains in hepatocytes in normal livers. Immunohistochemistry revealed that the expression of mAb1F9 antigen (mAb1F9-Ag) significantly increased in PBC livers compared with control groups including normal livers, cirrhosis or cholestasis other than PBC. Interestingly, the augmented expression of mAb1F9-Ag was correlated with the severity of PBC, and ursodeoxycholic acid treatment may significantly improve the recovery of mAb1F9-Ag. In addition, redistribution of mAb1F9-Ag was found in 46% of PBC. mAb1F9-Ag was isolated and analyzed with mass spectrometry, which indicated lysosome-associated membrane protein 2 (LAMP-2) as the candidate. Further studies showed that mAb1F9 recognized LAMP-2 immunoprecipitates and vice verse, mAb1F9 reacted with recombinant LAMP-2. mAb1F9 and LAMP-2 antibody exhibited similar staining pattern and displayed similar subcellular localization. Together, the identity of mAb1F9-Ag is LAMP-2, suggesting that LAMP-2 may assist in the differentiation of PBC and predict a poor outcome in patients with PBC.
Diagnostic and therapeutic biomarkers useful for esophageal squamous cell carcinoma (ESCC) have the ability to increase the long term survival of cancer patients. A metabolomics study, using plasma from four groups including ESCC patients before, during, and after chemoradiotherapy (CRT) and healthy controls, was originally carried out by LC-MS to determine global alterations in the metabolic profiles and find biomarkers potentially applicable to diagnosis and monitoring treatment effects. It is worth pointing out that a clear clustering and separation of metabolic data from the four groups was observed, which indicated that disease status and treatment intervention resulted in specific metabolic perturbations in the patients. A series of metabolites were found to be significantly altered in ESCC patients versus healthy controls and in pre- versus post-treatment patients based on multivariate statistical data analysis (MVDA). To further validate the reliability of these potential biomarkers, an independent validation was performed by using the selected reaction monitoring (SRM) based targeted approach. Finally, 18 most significantly altered plasma metabolites in ESCC patients, relative to healthy controls, were tentatively identified as lysophosphatidylcholines (lysoPCs), fatty acids, l-carnitine, acylcarnitines, organic acids, and a sterol metabolite. The classification performance of these metabolites were analyzed by receiver operating characteristic (ROC)(1) analysis and a biomarker panel was generated. Together, biological significance of these metabolites was discussed. Comparison between pre- and post-treatment patients generated 11 metabolites as potential therapeutic biomarkers that were tentatively identified as amino acids, acylcarnitines, and lysoPCs. Levels of three of these (octanoylcarnitine, lysoPC(16:1), and decanoylcarnitine) were closely correlated with treatment effect. Moreover, variation of these three potential biomarkers was investigated over the treatment course. The results suggest that these biomarkers may be useful in diagnosis, as well as in monitoring therapeutic responses and predicting outcomes of the ESCC.
The catalytic steam gasification of pig compost (PC) for hydrogen-rich gas production was experimentally investigated in a fixed bed reactor using the developed NiO on modified dolomite (NiO/MD) catalyst. A series of experiments have been performed to explore the effects of catalyst, catalytic temperature, steam to PC ratio and PC particle size on the gas quality and yield. The results indicate that the NiO/MD catalyst could significantly eliminate the tar in the gas production and increase the hydrogen yield, and the catalyst lives a long lifetime in the PC steam gasification. Moreover, the higher catalytic temperature and smaller PC particle size can contribute to more hydrogen production and gas yield. Meanwhile, the optimal ratio of steam to PC (S/P) is found to be 1.24.
In this in vivo study, degradable Mg-3Zn-0.8Zr cylinders were coated with a calcium phosphorus compound (Ca-P) layer or a magnesium fluoride (MgF2) layer; uncoated Mg-3Zn-0.8Zr alloy was used as a control. These were then implanted intramedullary into the femora of nine Japanese big-ear white rabbits for implantation periods of 1, 2 and 3 months. During the postoperative observation period with radiographic examination, the results showed that the MgF2-coated implants were tolerated well compared to the Ca-P-coated implants and uncoated implants. Moreover, large amounts of cells, rich fibrillar collagen and calcium and phosphorus products were found on the surface of the MgF2-coated implants using scanning electron microscopy. Micro-computed tomography further showed a slight decrease in volume (23.85%) and a greater increase in new bone mass (new bone volume fraction=11.56%, tissue mineral density=248.81 mg/cm(3)) for the MgF2-coated implants in comparison to uncoated and Ca-P compound-coated implants after 3 months of implantation.
Our previous study revealed that human ribosomal protein L6 (RPL6) was up-regulated in multidrug-resistant gastric cancer cells and over-expression of RPL6 could protect gastric cancer from drug-induced apoptosis. It was further demonstrated that up-regulation of RPL6 accelerated growth and enhanced in vitro colony forming ability of GES cells while down-regulation of RPL6 exhibited the opposite results. The present study was designed to investigate the potential role of RPL6 in therapy of gastric cancer for clinic. The expression of RPL6 and cyclin E in gastric cancer tissues and normal gastric mucosa was evaluated by immunohistochemisty. It was found that RPL6 and cyclin E were expressed at a higher level in gastric cancer tissues than that in normal gastric mucosa and the two were correlative in gastric cancer. Survival time of postoperative patients was analyzed by Kaplan- Meier analysis and it was found that patients with RPL6 positive expression showed shorter survival time than patients that with RPL6 negative expression. RPL6 was then genetically down-regulated in gastric cancer SGC7901 and AGS cell lines by siRNA. It was demonstrated that down-regulation of RPL6 reduced colony forming ability of gastric cancer cells in vitro and reduced cell growth in vivo. Moreover, down-regulation of RPL6 could suppress G1 to S phase transition in these cells. Further, we evidenced that RPL6 siRNA down-regulated cyclin E expression in SGC7901 and AGS cells. Taken together, these data suggested that RPL6 was over-expressed in human gastric tissues and caused poor prognosis. Down-regulation of RPL6 could suppress cell growth and cell cycle progression at least through down-regulating cyclin E and which might be used as a novel approach to gastric cancer therapy.
Survivin is involved in multiple signaling mechanisms in tumor maintenance, and accumulated studies elucidate that knockdown of survivin in endothelial cells could inhibit angiogenesis; however, the role of survivin in tumor cells to regulate tumor-derived angiogenesis remains largely unclear. In the present study 80 cases of brain glioma were chosen and protein expressions of survivin, vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), and platelet-derived growth factor (PDGF) in glioma cells were investigated by immunohistochemistry (IHC). Human umbilical vein endothelial cells (HUVEC) were cocultured with human glioma U251 wild-type cells, U251 cells survivin silenced, SHG44 wild-type cells, and SHG44 survivin-overexpressing cells, respectively. The proliferation and migration of HUVEC were evaluated by MTT assay and transwell chamber assay. The microvessels density (MVD) marked by CD31 expression in vascular endothelial cells in glioma xenografts in nude mice was detected by IHC. VEGF, bFGF, and PDGF in the aforementioned cells were detected by quantitive PCR (qPCR), Western blot, ELISA, and IHC in vitro and in vivo. The results showed that VEGF immunoreactivity score (IRS), bFGF IRS, and PDGF IRS were all positively correlated with survivin IRS in gliomas, respectively (P < 0.01). Survivin in human glioma cells could significantly promote the proliferation and migration of HUVEC and increase MVD, which could be contributed to survivin-dependent burst of VEGF and bFGF expression, followed by increase of tumor growth and proliferation. In summary, survivin, through upregulation of VEGF and bFGF, plays an essential role during glioma angiogenesis.
Recent studies proved that inflammatory bowel disease (IBD) patients had a higher risk of thromboembolism and a Factor V Leiden mutation that prevents the efficient inactivation of factor V, which leads to thromboembolism and thus contributes to a high potential risk of IBD. However, the relationship between Factor V Leiden mutation and IBD remains controversial.
Nodal staging of non-small-cell lung cancer (NSCLC) is crucial in evaluation of prognosis and determination of therapeutic strategy. This study aimed to determine the negative predictive value (NPV) of combined positron emission tomography and computed tomography (PET-CT) in patients with stage I (T1-2N0) NSCLC and to investigate the possible risk factors for occult nodal disease.
Myocardial microvascular endothelial cells (MMECs) play a vital role in modulating cardiomyocyte development, survival, and contraction during embryonic cardiogenesis and mature myocardium. However, specific molecular composition of MMECs is still not well known, with no special MMEC marker to distinguish microvascular endothelial cells (ECs) from macrovascular ECs. In the present study, we immunized BALB/c mice with membrane proteins of MMECs. Through screening by enzyme linked immunosorbent assay and immunohistochemistry, a new monoclonal antibody that specifically recognizes MMECs was yielded. Immunohistochemistry of tissue arrays showed that MAb B7 also selectively recognized microvascular ECs but not macrovascular ECs in other tissues. Immunofluorescence and immuno-electron microscope assay indicated that B7 antigen was a plasma membrane molecule. Interestingly, we also found that B7 antigen was dramatically decreased in diabetic rat compared with that in normal rat. In conclusion, MAb B7 not only provides a new biomarker to help us understand the molecular composition of microvascular ECs, but also indicates that B7 antigen might play an important role in the dysfunction of microvascular ECs.
Herein, we describe the synthesis of a low-symmetry monodendron, 3,4-bis(dodecyloxy)-5-[3,4,5-tris(dodecyloxy)benzyloxy]benzoic acid, following a simple route which starts from gallic acid ethyl ester and does not require any protecting groups. The self-assembled structures formed by the compound in 3D and 2D were investigated by synchrotron X-ray scattering and scanning force microscopy (SFM). In 3D, the compound forms a stable crystalline phase with an orthorhombic lattice in which the alkyl chains connected to different benzene rings form crystalline and amorphous domains. Upon cooling from the isotropic melt the compound exhibits a monotropic smectic mesophase. In 100-nm-thick films on a neutral substrate the structure loses its biaxiality, adopting a hexagonal columnar structure with the columns oriented parallel to the substrate. By contrast, in ultrathin films on graphite the SFM likely reveals two crystal orientations, which can develop due to the epitaxial adsorption on the substrate of the alkyl chains pertinent to different benzene rings.
Circulating monocytes have been exploited as an important progenitor cell resource for hepatocytes in vitro and are instrumental in the removal of fibrosis. We investigated the significance of monocytes in peripheral blood stem cells (PBSC) for the treatment of liver cirrhosis.
Our previous study revealed that human ribosomal protein L6 (RPL6) was upregulated in multidrug-resistant gastric cancer cells and over-expression of RPL6 could protect gastric cancer cells from drug-induced apoptosis. The present study was designed to explore the role of RPL6 in tumorigenesis and development of gastric cancer. The expression of RPL6 in gastric cancer tissues and normal gastric mucosa was evaluated by immunohistochemical staining. It was found RPL6 was expressed at a higher level in gastric cancer tissues than that in normal gastric mucosa. RPL6 was then genetically overexpressed or knocked down in human immortalized gastric mucosa epithelial GES cells. It was demonstrated that upregulation of RPL6 accelerated the growth and enhanced in vitro colony forming ability of GES cells whereas downregulation of RPL6 showed adverse effects. Moreover, over-expression of RPL6 could promote G1 to S phase transition of GES cells. It was further evidenced that upregulation of RPL6 resulted in elevated cyclin E expression while downregulation of RPL6 caused decreased cyclin E expression in GES cells. Taken together, these data indicated that RPL6 was overexpressed in human gastric cancer and its over-expression could promote cell growth and cell cycle progression at least through upregulating cyclin E expression.
Opioid drug response and pain perception differs greatly amongst different individuals. The micro-opioid receptor (MOR) is the main receptor target for important opioid analgesics. As SNPs may contribute to interindividual differences in drug response, in silico signatures of recent positive selection (RPS) were utilized to seek out potentially functional SNPs in the MOR gene in order to facilitate the prioritization of SNPs for evaluation in genetic association studies. Out of over 1000 SNPs at the MOR locus, 184 high-frequency SNPs were interrogated for signatures of RPS. A total of five SNPs (four noncoding and one nonsynonymous coding) demonstrated in silico evidence of RPS. Significantly, the nonsynonymous E1/A118G SNP, which was previously reported to be functionally important, showed in silico evidence of RPS. This reaffirms the feasibility of utilizing in silico signatures of RPS to identify potentially functionally significant SNPs for association studies. Interestingly, the positively selected G allele of this RPS SNP was also predicted to create a novel exon splice enhancer as well as p53 binding sites.
SNPs are known to contribute to variations in drug response and there are more than 14 million polymorphisms spanning the human genome. However, not all of these SNPs are functional. It would be impractical and costly to evaluate every individual SNP for functionality experimentally. Consequently, one of the major challenges for researchers has been to seek out functional SNPs from all the SNPs in the human genome. In silico or bioinformatic methods are economical, less labor intensive, yet powerful approaches to filter out potentially functional SNPs in drug-response genes for further study. This allows researchers to prioritize which SNPs to subsequently evaluate experimentally for drug-response studies, as well as potentially providing insights into possible mechanisms underlying how SNPs may affect drug-response genes.
Approximately 10-15% of the human prion disease is inherited and one of the important genetic mutations occurs in the octapeptide repeat region of prion protein gene. One of the variants, one octapeptide repeat deletion (1-OPRD), existed in several gastric cancer cell lines and its mutation frequency was higher in gastric cancer cases. However, the biological functions of it remain unknown. Wild-type and mutation forms of PrP(C) were cloned and transfected into gastric cancer cells. Cell apoptosis, adhesion, invasion, multidrug resistance (MDR) and proliferation were, respectively, investigated. Different expressed genes were screened by gene array and proved by PT-PCR. Further, luciferase report assay was used to explore the transcriptional activation of target genes. Forced overexpression PrP(C) (1-OPRD) could promote the gastric cancer cells SGC7901 growth through facilitating G1- to S-phase transition in the cell cycle. PrP(C) (1-OPRD) could also inhibit apoptosis, and promote adhesion, invasion and MDR in SGC7901. However, it exhibited no significant difference between wild-type PrP(C) (1-OPRD) and PrP(C) on apoptosis, invasion or MDR effects. Further experiments indicated that PrP(C) (1-OPRD) could trigger the transactivation of cyclinD3 besides cyclinD1 to promote cell transition and proliferation. Overexpression of PrP(C) (1-OPRD) might promote the proliferation of gastric cancer cells at least partially through transcriptional activation of cyclinD3 to accelerate the G1-/S-phase transition. The promoting proliferation effect of PrP(C) (1-OPRD) was more than that of wild-type PrP(C). However, they showed no difference on apoptosis, adhesion, invasion or MDR effects of gastric cancer cells.
Chronic hepatitis B virus (HBV) infection is epidemiologically associated with hepatocellular carcinoma (HCC), but its role in HCC remains poorly understood due to technological limitations. In this study, we systematically characterize HBV in HCC patients. HBV sequences were enriched from 48 HCC patients using an oligo-bead-based strategy, pooled together and sequenced using the FLX-Genome-Sequencer. In the tumors, preferential integration of HBV into promoters of genes (P < 0.001) and significant enrichment of integration into chromosome 10 (P < 0.01) were observed. Integration into chromosome 10 was significantly associated with poorly differentiated tumors (P < 0.05). Notably, in the tumors, recurrent integration into the promoter of the human telomerase reverse transcriptase (TERT) gene was found to correlate with increased TERT expression. The preferred region within the HBV genome involved in integration and viral structural alteration is at the 3-end of hepatitis B virus X protein (HBx), where viral replication/transcription initiates. Upon integration, the 3-end of the HBx is often deleted. HBx-human chimeric transcripts, the most common type of chimeric transcripts, can be expressed as chimeric proteins. Sequence variation resulting in non-conservative amino acid substitutions are commonly observed in HBV genome. This study highlights HBV as highly mutable in HCC patients with preferential regions within the host and virus genome for HBV integration/structural alterations.
Different techniques for a relatively fast self-assembled monolayer film formation such as Langmuir-Blodgett (LB), spin-coating, and dip-coating methods have been compared using chloro[11-(5-ethyl-2,2:5,2?:5,2:5,2-quinquethiophene-5-yl)undecyl]dimethylsilane as a reactive precursor. It was shown that both spin-coating and LB techniques are very promising methods for preparation of highly ordered monolayer films of organosilicon-functionalized quinquethiophene with vertical orientation of oligothiophene fragments, while dip-coating gives only partial coverage. Optimal conditions for complete filling out the substrate surface by the quinquethiophene-containing monolayer by spin-coating and LB methods have been found. Grazing incidence X-ray diffraction measurements confirmed formation of in-plane crystalline order within the monolayer film. Changes in the layer structure were established by X-ray reflectivity and grazing incidence X-ray diffraction methods.
The purpose of this study was to investigate the effects of yeast polysaccharide (YPS) on growth and flavonoid accumulation in sprout cultures of Fagopyrum tataricum (tartary buckwheat). Without obvious change in the appearance of the sprouts, the exogenous YPS notably stimulated the production of functional metabolites in F. tataricum sprouts, and the stimulation effect was concentration-dependent. With 400 mg/L of YPS applied to the sprout cultures on day 6, the total rutin and quercentin content was effectively increased to 42.8 mg/gdw, or about 1.4-fold in comparison with the control of 31.2 mg/gdw. Feeding with 800 mg/L of YPS on day 9, the sprouts biomass was increased by about 8% compared to the control culture (0.99 gdw/100 sprouts versus 0.92 gdw/100 sprouts). Moreover, the present study revealed that the accumulation of these bioactive metabolites resulted from the stimulation of the phenylpropanoid pathway by YPS treatment. It could be an effective strategy for improving the functional quality of the F. tataricum sprouts provided with YPS.
Despite the extensive hepatic differentiation potential of human umbilical cord lining-derived mesenchymal stem cells (hUC-MSC), little is known about the molecular mechanisms of hUC-MSC differentiation. At the post-transcriptional level, microRNAs are key players in the control of cell fate determination during differentiation. In this study, we aimed to identify microRNAs involved in the hepatic differentiation of hUC-MSCs. After successfully isolating hUC- MSCs, we induced hepatocyte formation in vitro with growth factors. After 26 days of induction, hUC-MSCs could express hepatocyte-specific genes, synthesize urea and glycogen and uptake low-density lipoprotein. Cellular total RNA from hUC-MSCs and hepatic differentiated hUC-MSCs was collected at 7 time points, including 2 days, 6 days, 10 days, 14 days, 22 days and 26 days, for microRNA microarray analysis. Dynamic microRNA profiles were identified that did not overlap or only partially overlapped with microRNAs reported to be involved in human liver development, hepatocyte regeneration or hepatic differentiation of liver-derived progenitor cells. A total of 61 microRNAs among 1205 human and 144 human viral microRNAs displayed consistent changes and were altered at least 2-fold between hUC-MSCs and hepatic differentiated hUC-MSCs. Among these microRNAs, 25 were over-expressed; this over-expression occurred either gradually or increased sharply and was maintained at a high level. A total of 36 microRNAs were under-expressed, with an expression pattern similar to that of the over-expressed microRNAs. The expression of the altered expressed microRNAs was also confirmed by quantitative reverse-transcription polymerase chain reaction. We also found that microRNAs involved in hepatic differentiation were not enriched in hepatocyte or hepatocellular carcinoma cells and can potentially target liver-enriched transcription factors and genes. The elucidation of the microRNA profile during the hepatic differentiation of hUC-MSCs provides the basis for clarifying the role of microRNAs in hUC-MSC hepatic differentiation and specific microRNA selection for the conversion of hUC-MSCs to hepatocytes.
The aims of this study were to: (1) estimate the volumetric and metabolic growth rate of non-small cell lung cancer (NSCLC), (2) evaluate disease progression prior to treatment, and (3) explore the effects of tumor growth rate and time to treatment (TTT) on survival outcome.
Poor pulmonary function (PF) is often considered a contraindication to definitive radiation therapy for lung cancer. This study investigated whether baseline PF was associated with radiation-induced lung toxicity (RILT) in patients with non-small cell lung cancer (NSCLC) receiving conformal radiation therapy (CRT).
Single nucleotide polymorphisms (SNPs) are the commonest genetic variant in the human genome and have been associated with inter-individual differences in drug response. Finding the causative SNPs underlying variations in drug response has been a cornerstone of personalized medicine. However, as there are over 19 million SNPs, the task of finding causative SNPs underlying differences in drug response using in vitro and in vivo methods can be intimidating. SNP related web resources can be invaluable in the search for SNPs relevant to drug response phenotypes as they represent relatively cheaper yet efficient ways of prioritizing relevant SNPs for further study. These resources serve as repositories of SNP information or contain in silico tools that can predict the functionality of a SNP. More sophisticated resources integrate the information repository function with the predictive function to create a one stop SNP resource for researchers. SNP related web resources can also aid researchers in planning and analyzing different types of genetic association studies by aiding in selecting SNPs for genotyping in these studies. The focus of this mini review is to outline the SNP related web resources that are available to researchers and how these resources may aid researchers studying SNP-drug response phenotype associations. Through efficient utilization of SNP related web resources, researchers will hopefully be able accelerate the pace of SNP related research in pharmacogenomics by identifying high risk SNP variants contributing to drug response as well as developing novel therapeutic targets based on understanding how SNPs alter drug response pathways.
Septithiophene with endgroups designed to form liquid crystalline phases and allows controlled deposition of an electrically connected monolayer. Field effect mobilies mobilities of charge carriers and spectroscopic properties of the monolayer provide evidence of sustainable transport and delocalization of the excitation through intermolecular interactions within the layer.
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