A new strategy for an improved detection of residual heparin and excess protamine – A first in-vitro approach

2021 ◽  
Author(s):  
Philipp Groene ◽  
Susana da Silva Gaspar Jung ◽  
Alice-Christin Acevedo ◽  
Barbara Lenhart ◽  
Simon Thomas Schäfer
Keyword(s):  
New Strategy

scholarly journals The in vitro manipulation of carbohydrate metabolism: a new strategy for deciphering the cellular defence mechanisms against nitric oxide attack

1999 ◽  
Vol 344 (3) ◽  
pp. 643 ◽  
Author(s):  
Claire LE GOFFE ◽  
Geneviève VALLETTE ◽  
Anne JARRY ◽  
Chantal BOU-HANNA ◽  
Christian L. LABOISSE
Keyword(s):  
Nitric Oxide ◽  
Carbohydrate Metabolism ◽  
Defence Mechanisms ◽  
New Strategy ◽  
Cellular Defence

scholarly journals Berberine-Coated Biomimetic Composite Microspheres for Simultaneously Hemostatic and Antibacterial Performance

Polymers ◽  
2021 ◽  
Vol 13 (3) ◽  
pp. 360
Author(s):  
Xiaojian Zhang ◽  
Kaili Dai ◽  
Chenyu Liu ◽  
Haofeng Hu ◽  
Fulin Luo ◽  
...  
Keyword(s):  
In Vitro Test ◽  
Water Emulsion ◽  
Biomedical Material ◽  
Composite Microspheres ◽  
Antibacterial Performance ◽  
New Strategy ◽  
Oil In Water Emulsion ◽  
Hemostatic Powder

Biomimetic microspheres containing alginate/carboxymethylcellulose/gelatin and coated with 0%, 1%, 3%, and 6% berberine (BACG, BACG-1B, BACG-3B, BACG-6B) were prepared by the oil-in-water emulsion method combined with spray drying. Through a series of physicochemical parameters and determination of hemostatic properties in vitro and in vivo, the results indicated that BACG and BACG-Bs were effective in inducing platelet adhesion/aggregation and promoting the hemostatic potential due to their biomimetic structure and rough surface. In addition, BACG-6B with high berberine proportion presented better hemostatic performance compared with the commercial hemostatic agent compound microporous polysaccharide hemostatic powder (CMPHP). BACG-6B also showed strong antibacterial activity in the in vitro test. The hemolysis test and cytotoxicity evaluation further revealed that the novel composite biomaterials have good hemocompatibility and biocompatibility. Thus, BACG-6B provides a new strategy for developing a due-functional (hemostat/antibacterial) biomedical material, which may have broad and promising applications in the future.

scholarly journals Targeting the Variable Surface of African Trypanosomes with Variant Surface Glycoprotein-Specific, Serum-Stable RNA Aptamers

2003 ◽  
Vol 2 (1) ◽  
pp. 84-94 ◽  
Author(s):  
Mihaela Lorger ◽  
Markus Engstler ◽  
Matthias Homann ◽  
H. Ulrich Göringer
Keyword(s):  
Antigenic Variation ◽  
Sleeping Sickness ◽  
Rna Aptamers ◽  
Surface Glycoprotein ◽  
Variant Surface Glycoprotein ◽  
Parasite Protein ◽  
African Trypanosomes ◽  
Variable Surface ◽  
New Strategy

ABSTRACT African trypanosomes cause sleeping sickness in humans and Nagana in cattle. The parasites multiply in the blood and escape the immune response of the infected host by antigenic variation. Antigenic variation is characterized by a periodic change of the parasite protein surface, which consists of a variant glycoprotein known as variant surface glycoprotein (VSG). Using a SELEX (systematic evolution of ligands by exponential enrichment) approach, we report the selection of small, serum-stable RNAs, so-called aptamers, that bind to VSGs with subnanomolar affinity. The RNAs are able to recognize different VSG variants and bind to the surface of live trypanosomes. Aptamers tethered to an antigenic side group are capable of directing antibodies to the surface of the parasite in vitro. In this manner, the RNAs might provide a new strategy for a therapeutic intervention to fight sleeping sickness.

Transmembrane p24 Trafficking Protein 2 Regulates Inflammation Through the TLR4/NF-κB Signaling Pathway in Lung Adenocarcinoma

2021 ◽  
Author(s):  
Longhua Feng ◽  
Pengjiang Cheng ◽  
Zhengyun Feng ◽  
Xiaoyu Zhang
Keyword(s):  
Lung Adenocarcinoma ◽  
Signaling Pathway ◽  
Enrichment Analysis ◽  
Gene Set Enrichment Analysis ◽  
Inflammatory Factors ◽  
Normal Tissues ◽  
Kaplan Meier ◽  
New Strategy

Abstract Background: To investigate the role of transmembrane p24 trafficking protein 2 (TMED2) in lung adenocarcinoma (LUAD) and determine whether TMED2 knockdown could inhibit LUAD in vitro and in vivo.Methods: TIMER2.0, Kaplan-Meier plotter, gene set enrichment analysis (GSEA), Target Gene, and pan-cancer systems were used to predict the potential function of TMED2. Western blotting and immunohistochemistry were performed to analyze TMED2 expression in different tissues or cell lines. The proliferation, development, and apoptosis of LUAD were observed using a lentivirus-mediated TMED2 knockdown. Bioinformatics and western blot analysis of TMED2 against inflammation via the TLR4/NF-κB signaling pathway were conducted. Results: TMED2 expression in LUAD tumor tissues was higher than that in normal tissues and positively correlated with poor survival in lung cancer and negatively correlated with apoptosis in LUAD. The expression of TMED2 was higher in tumors or HCC827 cells. TMED2 knockdown inhibited LUAD development in vitro and in vivo and increased the levels of inflammatory factors via the TLR4/NF-κB signaling pathway. TMED2 was correlated with TME, immune score, TME-associated immune cells, their target markers, and some mechanisms and pathways, as determined using the TIMER2.0, GO, and KEGG assays.Conclusions: TMED2 may regulate inflammation in LUAD through the TLR4/NF-κB signaling pathway, and enhance the proliferation, development, and prognosis of LUAD by regulating inflammation, which provide a new strategy for treating LUAD by regulating inflammation.

X-Ray responsive nanoparticles with triggered release of nitrite, a precursor of reactive nitrogen species, for enhanced cancer radiosensitization

Nanoscale ◽  
2017 ◽  
Vol 9 (38) ◽  
pp. 14627-14634 ◽  
Author(s):  
Fang Liu ◽  
Junzhe Lou ◽  
Dimitre Hristov
Keyword(s):  
Cancer Cells ◽  
Cell Nucleus ◽  
Reactive Nitrogen Species ◽  
Nitrogen Species ◽  
Triggered Release ◽  
X Ray ◽  
Enhanced Sensitivity ◽  
New Strategy ◽  
Targeting Peptide

New strategy to enhance cancer radiotherapy: A novel gold nanosystem with surface-grafted nitroimidazole and cell nucleus-targeting peptide achieves the release of a RNS precursor, nitrite, by ionizing radiation. In vitro radiotherapy shows enhanced sensitivity of hypoxic cancer cells to X-ray radiation, presumably due to the generation of both reactive oxygen and nitrogen species.

scholarly journals The SARS CoV-2 spike domain, RGD and integrin binding effect-relationship for vaccine design strategy

2021 ◽  
Vol 5 (1) ◽  
pp. 027-041
Author(s):  
M Luisetto ◽  
G Tarro ◽  
Edbey Khaled ◽  
N Almukthar ◽  
L Cabianca ◽  
...  
Keyword(s):  
Vaccine Design ◽  
Design Strategy ◽  
Spike Protein ◽  
Pathological Effect ◽  
Technical Data ◽  
Binding Effect ◽  
New Strategy ◽  
Rare Side Effect ◽  
New Generation

Related the need to search new strategy in vaccine design in order to reduce also some rare effect like trombosys for some registered products it is interesting the role played by the SPIKE RGD domain. The binding with molecules like Fibronectin is a process that must to be deeply investigated. A better understanding in this process can be used to improve safety of the new generation of COVID vaccine. The rare effect like thrombosis recognized by regulatory agency produced a modification of technical data sheet of some vaccine so the phenomena Is interesting to be more investigated. Spike protein and its domains are involved in producing pathological effect of the COVID-19 disease. What it is interesting is that some pathological effect of this pathology are similar to some rare side effect produced by some COVID-19 vaccine classes. After a review of interesting literature related this topics is submitted an experimental projects able to verify in vitro the spike procoaugulant property.

scholarly journals tRNA Modification by GidA/MnmE Is Necessary for Streptococcus pyogenes Virulence: a New Strategy To Make Live Attenuated Strains

2008 ◽  
Vol 76 (7) ◽  
pp. 3176-3186 ◽  
Author(s):  
Kyu Hong Cho ◽  
Michael G. Caparon
Keyword(s):  
Virulence Factors ◽  
Streptococcus Pyogenes ◽  
Vaccine Development ◽  
Translation Efficiency ◽  
Trna Modification ◽  
Necrosis Factor Alpha ◽  
New Strategy ◽  
In The Wild ◽  
Interleukin 23

ABSTRACT Studies directed at vaccine development and mucosal immunity against Streptococcus pyogenes would benefit from the availability of live attenuated strains. Our approach for production of candidate live attenuated strains was to identify mutations that did not alter growth in vitro and did not alter the overall complement of virulence factors produced but did result in reduced levels of expression of multiple secreted virulence factors. A global reduction but not elimination of expression would likely lead to attenuation while maximizing the number of antigenic targets available for stimulation of immunity. Adaptation of Tn5-based transposome mutagenesis to S. pyogenes with initial screening for reduced expression of the SpeB protease resulted in identification of mutations in gidA, which encodes an enzyme involved in tRNA modification. Reduced SpeB expression was due to delayed onset of speB transcription resulting from reduced translation efficiency of the message for RopB, a transcriptional activator. Overall, GidA− mutants had a nearly normal global transcription profile but expressed significantly reduced levels of multiple virulence factors due to impaired translation efficiencies. A translation defect was supported by the observation that mutants lacking MnmE, which functions in the same tRNA modification pathway as GidA, phenocopied GidA deficiency. The mutants stimulated a cytokine response in cultured macrophages identical to that in the wild type, with the exception of reduced levels of tumor necrosis factor alpha and interleukin-23. Significantly, GidA− mutants were highly attenuated in the murine ulcer model of soft tissue infection. These characteristics suggest that GidA pathway tRNA modification mutants are attractive candidates for further evaluation as live attenuated strains.

scholarly journals Tetracycline Analogs Inhibit Osteoclast Differentiation by Suppressing MMP-9-Mediated Histone H3 Cleavage

2019 ◽  
Vol 20 (16) ◽  
pp. 4038 ◽  
Author(s):  
Yeojin Kim ◽  
Jinman Kim ◽  
Hyerim Lee ◽  
Woo-Ri Shin ◽  
Sheunghun Lee ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Osteoclast Differentiation ◽  
Histone H3 ◽  
Inhibitory Effect ◽  
Osteoclast Formation ◽  
Receptor Activator ◽  
New Strategy ◽  
Docking Approach ◽  
Metalloproteinase 9

Osteoporosis is a common disorder of bone remodeling, caused by the imbalance between bone resorption by osteoclasts and bone formation by osteoblasts. Recently, we reported that matrix metalloproteinase-9 (MMP-9)-dependent histone H3 proteolysis is a key event for proficient osteoclast formation. Although it has been reported that several MMP-9 inhibitors, such as tetracycline and its derivatives, show an inhibitory effect on osteoclastogenesis, the molecular mechanisms for this are not fully understood. Here we show that tetracycline analogs, especially tigecycline and minocycline, inhibit osteoclast formation by blocking MMP-9-mediated histone H3 tail cleavage. Our molecular docking approach found that tigecycline and minocycline are the most potent inhibitors of MMP-9. We also observed that both inhibitors significantly inhibited H3 tail cleavage by MMP-9 in vitro. These compounds inhibited receptor activator of nuclear factor kappaB ligand (RANKL)-induced osteoclast formation by blocking the NFATc1 signaling pathway. Furthermore, MMP-9-mediated H3 tail cleavage during osteoclast differentiation was selectively blocked by these compounds. Treatment with both tigecycline and minocycline rescued the osteoporotic phenotype induced by prednisolone in a zebrafish osteoporosis model. Our findings demonstrate that the tetracycline analogs suppress osteoclastogenesis via MMP-9-mediated H3 tail cleavage, and suggest that MMP-9 inhibition could offer a new strategy for the treatment of glucocorticoid-induced osteoporosis.

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