A new method to analysis synthetic acetic acid to vinegar: Hydrogen isotope ratio at the methyl site of acetic acid in vinegar by GC-IRMS.

Acetic acid is the key organic substance used to verify the authenticity of vinegar. A new method for precisely determining acetic acid δDCH3 in vinegar via gas chromatography -pyrolytic-stable isotope ratio mass spectrometry (GC-P-IRMS) was established. The δDCH3 values were obtained via calibration with a series of standards. The optimised method demonstrated a repeatability standard deviation within 3 ‰. The standard deviation of accuracy of the new method compared with that of the SNIF-NMR method was within 2.6 ‰. The synthetic acetic acid δDCH3 values was -136.7 ‰ ± 29.6 ‰, and the δDCH3 value of acetic acid in vinegar was -414.9 ‰ ± 40.5 ‰, with significant isotopic distribution characteristics. This methodology serves as a supplementary method for measuring the δDCH3 value of acetic acid in vinegar. It has advantages over other methods in terms of time, sensitivity and operability. And provides a new idea for solving the problem of analyzing substances in the presence of exchangeable groups.

A rapid method for the determination of stable hydrogen isotope ratios of acetic acid in vinegar.

RATIONALE: Vinegar is an everyday condiment made from fermented grains or fruits. It contains acetic acid which is the main organic material produced by fermentation. Vinegar suffers from the authenticity problem of exogenous adulteration due to the indistinguishability of low-cost chemical sources of synthetic acetic acid from acetic acid produced by fermentation. It is necessary to establish a simple and rapid measurement technique. METHODS: Determination was according to the total acid content of vinegar diluted with acetone to a certain concentration. Online separation and determination of acetic acid δD in vinegar were carried out using gas chromatography-pyrolysis-isotope ratio mass spectrometry. RESULTS: An HP-Plot/U column was selected for online separation of acetic acid and water with molecular sieve characteristics. At the same time, combined with the instrument blowback function to remove water. Dilute solvent acetone was treated with a molecular sieve to remove trace water. The reproducibility of this method is less than 3‰. The long-term stability is within a reasonable error range. The accuracy correlation coefficient is greater than 0.99. The δD values of acetic acid in vinegar (-264.5 ± 20.3‰) and from chemical sources (-30.5 ± 90.8‰) were obtained. CONCLUSIONS: A rapid method was developed for identification of different sources of acetic acid. These different sources of acetic acid exhibited significant hydrogen isotope distribution characteristics. Additionally, it was observed that the carboxyl hydrogen of acetic acid exhibited facile exchange with water. In future investigations, we aim to mitigate this interference.

Natural diterpenoid EKO activates deubiqutinase ATXN3 to preserve vascular endothelial integrity and alleviate diabetic retinopathy through c-fos/focal adhesion axis.

Diabetic retinopathy (DR) is one of the most prevalent severe diabetic microvascular complications caused by hyperglycemia. Deciphering the underlying mechanism of vascular injury and finding ways to alleviate hyperglycemia induced microvascular complications is of great necessity. In this study, we identified that a compound ent-9α-hydroxy-15-oxo-16-kauren-19-oic acid (EKO), the diterpenoid isolated and purified from Pteris semipinnata L., exhibited good protective roles against vascular endothelial injury associated with diabetic retinopathy in vitro and in vivo. To further uncover the underlying mechanism, we used unbiased transcriptome sequencing analysis and showed substantial impairment in the focal adhesion pathway upon high glucose and IL-1ß stimulation. EKO could effectively improve endothelial focal adhesion pathway by enhancing the expression of two focal adhesion proteins Vinculin and ITGA11. We found that c-fos protein was involved in regulating the expression of Vinculin and ITGA11, a transcription factor component that was downregulated by high glucose and IL-1ß stimulation and recovered by EKO. Mechanically, EKO facilitated the binding of deubiquitylation enzyme ATXN3 to c-fos protein and promoted its deubiquitylation, thereby elevating its protein level to enhance the expression of Vinculin and ITGA11. Besides, EKO effectively suppressed ROS production and restored mitochondrial function. In vivo studies, we confirmed EKO could alleviate some of the indicators of diabetic mice. In addition, protein levels of ATXN3 and focal adhesion Vinculin molecule were also verified in vivo. Collectively, our findings addressed the endothelial protective role of natural diterpenoid EKO, with emphasize of mechanism on ATXN3/c-fos/focal adhesion signaling pathway as well as oxygen stress suppression, implicating its therapeutic potential in alleviating vascular endothelium injury and diabetic retinopathy.

Early Progression of Abdominal Aortic Aneurysm is Decelerated by Improved Endothelial Barrier Function via ALDH2-LIN28B-ELK3 Signaling.

The involvement of endothelial barrier function in abdominal aortic aneurysm (AAA) and its upstream regulators remains unknown. Single-cell RNA sequencing shows that disrupted endothelial focal junction is an early (3 days) and persistent (28 days) event during Angiotensin II (Ang II)-induced AAA progression. Consistently, mRNA sequencing on human aortic dissection tissues confirmed downregulated expression of endothelial barrier-related genes. Aldehyde dehydrogenase 2 (ALDH2), a negative regulator of AAA, is found to be upregulated in the intimal media of AAA samples, leading to testing its role in early-stage AAA. ALDH2 knockdown/knockout specifically in endothelial cells (ECs) significantly increases expression of EC barrier markers related to focal adhesion and tight junction, restores endothelial barrier integrity, and suppresses early aortic dilation of AAA (7 and 14 days post-Ang II). Mechanically, ELK3 acts as an ALDH2 downstream regulator for endothelial barrier function preservation. At the molecular level, ALDH2 directly binds to LIN28B, a regulator of ELK3 mRNA stability, hindering LIN28B binding to ELK3 mRNA, thereby depressing ELK3 expression and impairing endothelial barrier function. Therefore, preserving vascular endothelial barrier integrity via ALDH2-specific knockdown in ECs holds therapeutic potential in the early management of AAAs.

Coaggregation of polyglutamine (polyQ) proteins is mediated by polyQ-tract interactions and impairs cellular proteostasis.

Nine polyglutamine (polyQ) proteins have already been identified that are considered to be associated with the pathologies of neurodegenerative disorders called polyQ diseases, but whether these polyQ proteins mutually interact and synergize in proteinopathies remains to be elucidated. In this study, 4 polyQ-containing proteins, androgen receptor (AR), ataxin-7 (Atx7), huntingtin (Htt) and ataxin-3 (Atx3), are used as model molecules to investigate their heterologous coaggregation and consequent impact on cellular proteostasis. Our data indicate that the N-terminal fragment of polyQ-expanded (PQE) Atx7 or Htt can coaggregate with and sequester AR and Atx3 into insoluble aggregates or inclusions through their respective polyQ tracts. In vitro coprecipitation and NMR titration experiments suggest that this specific coaggregation depends on polyQ lengths and is probably mediated by polyQ-tract interactions. Luciferase reporter assay shows that these coaggregation and sequestration effects can deplete the cellular availability of AR and consequently impair its transactivation function. This study provides valid evidence supporting the viewpoint that coaggregation of polyQ proteins is mediated by polyQ-tract interactions and benefits our understanding of the molecular mechanism underlying the accumulation of different polyQ proteins in inclusions and their copathological causes of polyQ diseases.

Comparative Study of Unilateral Biportal Endoscopic and Traditional Open Surgery in the Treatment of Lumbar Disc Herniation.

Objective: We aimed to compare the efficacy of unilateral biportal endoscopic (UBE) surgery and traditional open surgery in the treatment of lumbar disc herniation (LDH). The complications and learning curve of UBE surgery are also discussed. Methods: Clinical data from 66 patients with single-level LDH admitted to Dezhou Hospital, Qilu Hospital of Shandong University in China from May 2020 to December 2021 were retrospectively analyzed. The patients were divided into the UBE surgery group and the traditional open surgery group according to patient choice. Intraoperative bleeding; surgery duration; length of hospital stay; preoperative visual analogue scale (VAS); VAS score 1 week after surgery, 1 month after surgery, 3 months after surgery and 6 months after surgery; early complications; chronic low back pain 1 year after surgery; Oswestry Disability Index (ODI) before surgery and 6 months after surgery were compared between the 2 groups. Results: Postoperative VAS and ODI scores in the 2 groups were significantly lower than before surgery (P < .05). There were significant differences in intraoperative bleeding, duration of surgery, length of hospital stay, VAS score 1 week after operation and 1 month after operation, postoperative white blood cells (WBCs), early complications and long-term chronic low back pain in the 2 groups (P < .05). There was no significant difference in VAS score 3 or 6 months after surgery or ODI score 6 months after surgery between the 2 groups (P > .05). Conclusion: Both UBE and traditional open surgery are effective in the treatment of LDH. Early pain relief was significantly better in the UBE surgery group than the traditional open surgery group, and the UBE group had a lower incidence of long-term chronic low back pain than the traditional open surgery group. However, but the number of early complications in the UBE group was higher than in the traditional open surgery group.

PolyQ-expanded proteins impair cellular proteostasis of ataxin-3 through sequestering the co-chaperone HSJ1 into aggregates.

Polyglutamine (polyQ) expansion of proteins can trigger protein misfolding and amyloid-like aggregation, which thus lead to severe cytotoxicities and even the respective neurodegenerative diseases. However, why polyQ aggregation is toxic to cells is not fully elucidated. Here, we took the fragments of polyQ-expanded (PQE) ataxin-7 (Atx7) and huntingtin (Htt) as models to investigate the effect of polyQ aggregates on the cellular proteostasis of endogenous ataxin-3 (Atx3), a protein that frequently appears in diverse inclusion bodies. We found that PQE Atx7 and Htt impair the cellular proteostasis of Atx3 by reducing its soluble as well as total Atx3 level but enhancing formation of the aggregates. Expression of these polyQ proteins promotes proteasomal degradation of endogenous Atx3 and accumulation of its aggregated form. Then we verified that the co-chaperone HSJ1 is an essential factor that orchestrates the balance of cellular proteostasis of Atx3; and further discovered that the polyQ proteins can sequester HSJ1 into aggregates or inclusions in a UIM domain-dependent manner. Thereby, the impairment of Atx3 proteostasis may be attributed to the sequestration and functional loss of cellular HSJ1. This study deciphers a potential mechanism underlying how PQE protein triggers proteinopathies, and also provides additional evidence in supporting the hijacking hypothesis that sequestration of cellular interacting partners by protein aggregates leads to cytotoxicity or neurodegeneration.

Self-assembly of carbon nanotube/graphitic-like flake/BiOBr nanocomposite with 1D/2D/3D heterojunctions for enhanced photocatalytic activity.

A self-assembled nanocomposite of lamellar BiOBr covalently bonded with conductive network of dispersive one-dimensional carbon nanotubes (1D CNT) and two-dimensional reduced graphitic-like flakes (2D GF) had been in situ constructed using one-pot facile solvothermal technique. Through self-assembly, BiOBr/CNT/GF (BiOBr/CG) displayed three-dimensional architectures in which a strong interfacial contact interaction and covalent banding between BiOBr nanostructures and CNT/GF network appeared. Furthermore, visible-light-driven catalytic activity of BiOBr/CG for RhB dye degradation was superior to that of pure BiOBr or BiOBr/C. Interestingly, the photodegradation activity of the BiOBr/CG nanocomposite could be improved further by subsequent facile annealing treatment, in which the annealed BiOBr/CG-DS had degraded almost 97.9% of RhB dye within only 100 min of visible-light irradiation. Moreover, analysis of the photodegradation mechanism revealed that the repression of electron-hole recombination in the nanocomposites, with sufficient covalent interfacial contact with CNT/GF as effective electron collecting and transferring system, were responsible for the outstanding photocatalytic performance. This effect, in turn, led to the continuous generation of O2- and OH reactive oxygen species for the degradation of RhB dye, which was verified by active species trapping and ESR spectra.

Combined use of tranexamic acid and rivaroxaban in posterior lumbar interbody fusion safely reduces blood loss and transfusion rates without increasing the risk of thrombosis-a prospective, stratified, randomized, controlled trial.

PURPOSE: This prospective, stratified, randomized, single-blind, placebo-controlled multicentre study investigated the safety and effectiveness of reducing blood loss and preventing venous thromboembolism (VTE) during posterior lumbar interbody fusion (PLIF) in patients with stenosis or spondylolisthesis using the combination of tranexamic acid (TXA) and rivaroxaban. METHODS: The Autar score was evaluated in patients after admission. Patients with an Autar score ≤ 10 were randomized to group A or B. Group A was the placebo-controlled group. Patients in group B were treated with 1 g TXA via intravenous injection and 1 g TXA for external use. Patients with an Autar score > 10 were randomized to group C or D. Patients in group C were treated with 10-mg rivaroxaban qd for 35 days after surgery. Patients in group D received the same treatment as those in group B intra-operatively and as those in group C post-operatively. RESULTS: A total of 599 patients from eight hospitals participated in this clinical trial. The total blood loss, intra-operative blood loss, and drainage volume were reduced by the administration of TXA (group A vs group B, P < 0.01; group C vs group D, P < 0.01), and the blood transfusion rate was also decreased (group A vs group B, P < 0.01; group C vs group D, P < 0.01). There were no significant differences (P > 0.05) in the VTE incidence rates among group A and group B. In patients with high-risk thrombosis, the number of patients with VTE was only three and seven after the application of rivaroxaban. Epidural haematoma was not discovered in any patients in our trial. CONCLUSION: The combined application of tranexamic acid and rivaroxaban significantly reduced the amount of blood loss and the transfusion rate during PLIF surgery and avoided an increase in the probability of thrombosis and the occurrence of epidural haematoma. TRIAL REGISTRATION NUMBER AND DATE OF REGISTRATION: ChiCTR-1800016430 2018-06-01.

Author Correction: Structural and dynamic studies reveal that the Ala-rich region of ataxin-7 initiates α-helix formation of the polyQ tract but suppresses its aggregation.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Galvanic replacement mediated 3D porous PtCu nano-frames for enhanced ethylene glycol oxidation.

Three dimensional (3D) porous PtCu nano-frames with a unique hollow structure were obtained after a galvanic replacement reaction, exhibiting a high normalized mass activity of 23.1 A m-2 µg-1 towards ethylene glycol oxidation with excellent stability. The morphological evolution and catalytic mechanism were detailed.

Structural and dynamic studies reveal that the Ala-rich region of ataxin-7 initiates α-helix formation of the polyQ tract but suppresses its aggregation.

Ataxin-7 (Atx7) is a disease-related protein associated with the pathogenesis of spinocerebellar ataxia 7, while its polyglutamine (polyQ) tract in N-terminus is the causative source of aggregation and proteinopathy. We investigated the structure, dynamics and aggregation properties of the N-terminal 62-residue fragment of Atx7 (Atx7-N) by biochemical and biophysical approaches. The results showed that the normal Atx7-N with a tract of 10 glutamines (10Q) overall adopts a flexible and disordered structure, but it may contain a short or small population of helical structure in solution. PolyQ expansion increases the α-helical propensity of the polyQ tract and consequently enhances its transformation into ß-sheet structures during amyloid aggregation. An alanine-rich region (ARR) just ahead of the polyQ tract forms a local and relatively stable α-helix. The ARR α-helix can initiate and stabilize helical formation of the following polyQ tract, but it may suppress aggregation of the polyQ-expanded Atx7-N both in vitro and in cell. Thus, the preceding ARR segment in Atx7-N may influence the dynamic structure and aggregation property of the polyQ tract and even determine the threshold of the pathogenic polyQ lengths. This study may gain structural and dynamic insights into amyloid aggregation of Atx7 and help us further understand the Atx7 proteinopathy based on polyQ expansion.

Emerging roles of sphingosylphosphorylcholine in modulating cardiovascular functions and diseases.

Sphingosylphosphorylcholine (SPC) is a bioactive sphingolipid in blood plasma that is metabolized from the hydrolysis of the membrane sphingolipid. SPC maintains low levels in the circulation under normal conditions, which makes studying its origin and action difficult. In recent years, however, it has been revealed that SPC may act as a first messenger through G protein-coupled receptors (S1P1-5, GPR12) or membrane lipid rafts, or as a second messenger mediating intracellular Ca2+ release in diverse human organ systems. SPC is a constituent of lipoproteins, and the activation of platelets promotes the release of SPC into blood, both implying a certain effect of SPC in modulating the pathological process of the heart and vessels. A line of evidence indeed confirms that SPC exerts a pronounced influence on the cardiovascular system through modulation of the functions of myocytes, vein endothelial cells, as well as vascular smooth muscle cells. In this review we summarize the current knowledge of the potential roles of SPC in the development of cardiovascular diseases and discuss the possible underlying mechanisms.

PolyQ-expanded huntingtin and ataxin-3 sequester ubiquitin adaptors hHR23B and UBQLN2 into aggregates via conjugated ubiquitin.

The components of ubiquitin (Ub)-proteasome system, such as Ub, Ub adaptors, or proteasome subunits, are commonly accumulated with the aggregated proteins in inclusions, but how protein aggregates sequester Ub-related proteins remains elusive. Using N-terminal huntingtin (Htt-N552) and ataxin (Atx)-3 as model proteins, we investigated the molecular mechanism underlying sequestration of Ub adaptors by polyQ-expanded proteins. We found that polyQ-expanded Htt-N552 and Atx-3 sequester endogenous Ub adaptors, human RAD23 homolog B (hHR23B) and ubiquilin (UBQLN)-2, into inclusions. This sequestration effect is dependent on the UBA domains of Ub adaptors and the conjugated Ub of the aggregated proteins. Moreover, polyQ-expanded Htt-N552 and Atx-3 reduce the protein level of xeroderma pigmentosum group C (XPC) by sequestration of hHR23B, suggesting that this process may cut down the available quantity of hHR23B and thus affect its normal function in stabilizing XPC. Our findings demonstrate that polyQ-expanded proteins sequester Ub adaptors or other Ub-related proteins into aggregates or inclusions through ubiquitination of the pathogenic proteins. This study may also provide a common mechanism for the formation of Ub-positive inclusions in cells.-Yang, H., Yue, H.-W., He, W.-T., Hong, J.-Y., Jiang, L.-L., Hu, H.-Y. PolyQ-expanded huntingtin and ataxin-3 sequester ubiquitin adaptors hHR23B and UBQLN2 into aggregates via conjugated ubiquitin.

HSP90 recognizes the N-terminus of huntingtin involved in regulation of huntingtin aggregation by USP19.

Huntington's disease (HD) is caused by aberrant expansion of polyglutamine (polyQ) in the N-terminus of huntingtin (Htt). Our previous study has demonstrated that HSP90 is involved in the triage decision of Htt, but how HSP90 recognizes and regulates Htt remains elusive. We investigated the interaction between HSP90 and the N-terminal fragments of Htt (Htt-N), such as the N-terminal 90-residue fragment (Htt-N90). Our results showed that HSP90 binds to the N-terminal extreme of Htt-N in a sequence just ahead of the polyQ tract. Structural integration of the middle and C-terminal domains of HSP90 is essential for interacting with Htt-N90, and the dimerization mediated by the C-terminal domain facilitates this interaction. Moreover, ubiquitin-specific protease 19 (USP19), a deubiquitinating enzyme interacting with HSP90, up-regulates the protein level of Htt-N90 and consequently promotes its aggregation, whereas disruption of the interaction between Htt-N90 and HSP90 attenuates the effect of USP19 on Htt-N90. Thus, HSP90 interacts with Htt-N90 on the N-terminal amphipathic α-helix, and then recruits USP19 to modulate the protein level and aggregation of Htt-N90. This study provides mechanistic insights into the recognition between HSP90 and the N-terminus of Htt, and the triage decision for the Htt protein by the HSP90 chaperone system.

Dynamic updating atlas for heart segmentation with a nonlinear field-based model.

BACKGROUND: Segmentation of cardiac computed tomography (CT) images is an effective method for assessing the dynamic function of the heart and lungs. In the atlas-based heart segmentation approach, the quality of segmentation usually relies upon atlas images, and the selection of those reference images is a key step. The optimal goal in this selection process is to have the reference images as close to the target image as possible. METHODS: This study proposes an atlas dynamic update algorithm using a scheme of nonlinear deformation field. The proposed method is based on the features among double-source CT (DSCT) slices. The extraction of these features will form a base to construct an average model and the created reference atlas image is updated during the registration process. A nonlinear field-based model was used to effectively implement a 4D cardiac segmentation. RESULTS: The proposed segmentation framework was validated with 14 4D cardiac CT sequences. The algorithm achieved an acceptable accuracy (1.0-2.8 mm). CONCLUSION: Our proposed method that combines a nonlinear field-based model and dynamic updating atlas strategies can provide an effective and accurate way for whole heart segmentation. The success of the proposed method largely relies on the effective use of the prior knowledge of the atlas and the similarity explored among the to-be-segmented DSCT sequences.

Simulation of multi-probe radiofrequency ablation guided by optical surgery navigation system under different active modes.

Radiofrequency ablation (RFA) is a crucial alternative treatment for liver cancer with the advantages of minimal invasion and a fast prognosis. However, two problems limit its further application: the orientation of the puncture point and the ablation of large tumors. The optical surgery navigation system in the RFA presents a promising approach for solving the localization problem in the puncturing process, which greatly increases puncture accuracy and has overcome the disadvantages of traditional RFA surgery. In addition, the use of multiple electrodes in the RFA (multi-probe RFA) is proposed and is applied clinically to deal with large tumors. In this study, we present a multi-probe RFA model using the finite element method (FEM) combined with a self-developed optical surgical navigation system. A real 3D liver model was adopted as an effective reference. Based on this model, two-probe RFA simulations were performed under different active modes. An analysis was conducted from the perspective of the temperature and electric potential fields and cell necrosis. The simulation results showed that different active modes had separate advantages and were suitable for different situations. Understanding their advantages can not only help doctors make surgical plans that fit the patients' conditions, but also the understanding can offer a virtual surgery platform for further development in the preoperative planning of RFA incorporated with the surgery navigation system.

GSK-3ß promotes PA-induced apoptosis through changing ß-arrestin 2 nucleus location in H9c2 cardiomyocytes.

Palmitic acid (PA), a type of saturated fatty acids, induces cardiovascular diseases by causing cardiomyocyte apoptosis with unclear mechanisms. Akt participates in PA-induced cardiomyocyte apoptosis. GSK-3ß is a substrate of Akt, we investigated its role in PA-induced apoptosis. We reveal that PA inhibits GSK-3ß phosphorylation accompanied by inactivation of Akt in H9c2 cardiomyocytes. We also reveal that inhibition the activity of GSK-3ß by its inhibitor LiCl or knockdown by siRNA significantly attenuates PA-induced cardiomyocyte apoptosis, this suggesting that GSK-3ß plays a pro-apoptotic role. To detect its downstream factors, we analyzed the roles of JNK, p38 MAPK and ß-arrestin 2 (ß-Arr2). Here, we report that GSK-3ß regulate PA-induced cardiomyocyte apoptosis by affecting the distribution of ß-Arr2. PA diminishes the protein level of ß-Arr2 and changes its distribution from nucleus to cytoplasm. Either inhibition of ß-Arr2 by its siRNA or overexpression of its protein level by transfection of ß-Arr2 full-length plasmid promotes PA-induced cardiomyocyte apoptosis, which remind us to focus on the changes of its location. ß-Arr2 siRNA decreased the background level of ß-Arr2 in nucleus in normal H9c2 cells. Overexpression of ß-Arr2 increased cytoplasm level of ß-Arr2 as PA did. While LiCl, the inhibitor of GSK-3ß decreased PA-induced apoptosis, accompany with increased nucleus level of ß-Arr2. Then we concluded that GSK-3ß is closely associated with cardiomyocyte apoptosis induced by PA, it performs its pro-apoptotic function by affecting the location of ß-Arr2. LiCl inhibits PA-induced cardiomyocyte apoptosis, which might provide novel therapeutic for cardiovascular diseases induced by metabolic syndrome.

Construction of a linker library with widely controllable flexibility for fusion protein design.

Flexibility or rigidity of the linker between two fused proteins is an important parameter that affects the function of fusion proteins. In this study, we constructed a linker library with five elementary units based on the combination of the flexible (GGGGS) and the rigid (EAAAK) units. Molecular dynamics (MD) simulation showed that more rigid units in the linkers lead to more helical conformation and hydrogen bonds, and less distance fluctuation between the N- and C-termini of the linker. The diversity of linker flexibility of the linker library was then studied by fluorescence resonance energy transfer (FRET) of cyan fluorescent protein (CFP)-yellow fluorescent protein (YFP) fusion proteins, which showed that there is a wide range of distribution of the FRET efficiency. Dissipative particle dynamics (DPD) simulation of CFP-YFP with different linkers also gave identical results with that of FRET efficiency analysis, and we further found that the combination manner of the linker peptide had a remarkable effect on the orientation of CFP and YFP domains. Our studies demonstrated that the construction of the linker library with the widely controllable flexibility could provide appropriate linkers with the desirable characteristics to engineer the fusion proteins with the expected functions.

Sphingosylphosphorylcholine in cancer progress.

Sphingosylphosphorylcholine (SPC) is a naturally occurring bioactive sphingolipid in blood plasma, metabolizing from the hydrolysis of the membrane sphingolipid. It has been shown to exert multifunctional role in cell physiological regulation either as an intracellular second messenger or as an extracellular agent through G protein coupled receptors (GPCRs). Because of elevated levels of SPC in malicious ascites of patients with cancer, the role of SPC in tumor progression has prompted wide interest. The factor was reported to affect the proliferation and/or migration of many cancer cells, including pancreatic cancer cells, epithelial ovarian carcinoma cells, rat C6 glioma cells, neuroblastoma cells, melanoma cells, and human leukemia cells. This review covers current knowledge of the role of SPC in tumor.