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Blogs

Domestic Flat Screen Printer

April 19, 2019

Author: flat printer

  Flat Screen Printer is widely used in cotton, chemical fiber and its blended fabrics, printing in silk, knitted fabrics, bed sheets, decorative fabrics and so on with wide adaptability, large flower return size, high pattern fineness, low netting cost, and matching plate-making equipment, etc. , adopted by the majority of customers. In recent years, the demand for flat screen printing machines by domestic customers has been maintained at a high level, but the regional development is not balanced, mainly concentrated in Jiangsu, Zhejiang, Shandong, Guangdong, especially in Shaoxing, Zhejiang. Domestically used imported flat screen printing machines mainly include Swiss company Beruser; Japan's TOSIN company; Taiwan's Qizheng company; Italy's REGGIANI company, South Korea's DEAWOO company, and other products. Among them, BUSER and TOSIN have a high reputation, but the models from the Gulf and South Korea have also attracted many users with low-cost payment methods. Among these companies, Buser uses the form of a hydraulic floating roller. Other companies are in the form of AC servo motor drag. Each company's frame promotion system is different, each with its own advantages and disadvantages. For example, in Italy, each printing unit is separately lifted. Although the rack is simple, the printing unit is complicated and difficult to wipe the net. The machines in Taiwan Province were lifted twice to solve the problem of difficulty in wiping the net. Because of the floating roller structure, Buser has a long guide belt and a complicated mechanism. Therefore, the cost is high. However, it also has the following advantages: continuous feeding and cleaning of the guide tape can be achieved. Sizing. Therefore, the tension of the cloth is reduced, the cleaning effect of the conduction belt is good, with the uniform size. At the same time, when the guide belt is pushed, only the 1/2 guide belt is deformed small, and the flower return accuracy is easily ensured. The main advantage of the servo motor form of other companies is that the vehicle speed is higher and the mechanism is simple, but the weakness is that the electrical control is complicated, and the flower return accuracy is not easy to maintain. LiCheng as a professional manufacturer of Flat Screen Printing Machine and hot air stenter machine, we are so glad that you pay a visit, more information, please click https://www.hotairstenter.com/  

Some professional terms about protein

April 19, 2019

Author: chen shanshan

Protein is not new to us, but most of us don't know much about it. We don't even know how much impact opal has on our lives. Today I will introduce some professional terms about protein. Protein engineering applications It is important for protein development. Based on the structural rules of protein molecules and the relationship between their biological functions, the existing proteins can be modified or synthesized by means of chemical, physical and molecular biology, or a new protein can be made to meet the needs of human production and life. You can get some information from creative biostructure. Native protein purification Protein purification should make use of the internal similarity and difference between different proteins, use the similarity between various proteins to remove the pollution of non-protein substances, and use the difference of each protein to purify the target protein from other proteins. The size, shape, charge, hydrophobicity, solubility, and biological activity of each protein vary, and these differences can be used to extract the proteins from mixtures such as e. coli lysates to produce recombinant proteins. Protein purification can be roughly divided into two stages: coarse separation stage and fine purification stage. The common method of protein purification is resin method. In the crude separation stage, the target protein is mainly separated from other cellular components, such as DNA and RNA, etc. Due to the large sample size and miscellaneous components, high volume, high flow rate, large particles and wide particle size distribution of the resin are required. The protein can be quickly separated from the pollutants, if necessary, can be added to the corresponding protective agents (such as protease inhibitors), to prevent the degradation of the target protein. In this stage, the target protein should be distinguished from those proteins with similar molecular weight and physical and chemical properties. Smaller resin particles should be used to improve the resolution. Ion exchange column and hydrophobic column are commonly used. Selectivity refers to the specificity of the binding of the resin to the target protein, while column efficiency refers to the ability of each protein component to elution from the resin one by one. The narrower the elution peak, the better the column efficiency. Only with good selectivity, the elution peak was too wide and the protein could not be separated effectively. Protein dialysis Dialysis membrane is a semi-permeable membrane, and protein is a macromolecular substance. It cannot pass through the dialysis membrane, while small molecules (inorganic salts, monosaccharides, etc.) can freely exchange solutes with the surrounding buffer solution through the dialysis membrane and enter the dialysis fluid. Dialysis is often used to remove small molecules from protein solutions during protein purification in the laboratory. Protein denaturation It means that the electrons outside the nucleus of acyl oxygen atom in the protein molecule move towards the proton under the influence of the proton, and the electrons outside the adjacent carbon nucleus move towards the oxygen. The relatively bare carbon nucleus is added by nucleophilic, making the molecule larger and less fluidity. Protein salting out It is to point to the phenomenon that protein precipitates out with the increase of salt concentration when neutral salt is added to protein aqueous solution. Neutral salt is a strong electrolyte with high solubility. In the protein solution, on the one hand, it competes with proteins for water molecules and destroys the water film on the surface of protein colloidal particles. On the other hand, it can neutralize the electric charge on the protein particles in large quantities, so that the protein particles in the water can accumulate and precipitate out. So much for the introduction of protein in this article. Protein has a great influence on our life. We can further study protein to improve our life. We should use our minds to explore proteins. Hopefully one day we can do more with protein.

Detailed introduction about Toll-like receptors

April 18, 2019

Author: chen shanshan

Recent studies have found that TLRs can bind to some endogenous molecules (ie, endogenous ligands) produced by the body itself. Immunological adjuvants enhance anti-tumor immunity, and their molecular and cellular mechanisms further clarify that TLRs also play an important role. Since tumors can produce endogenous ligands that can be recognized by TLRs during their development, TLRs may play a role in tumor immune surveillance.     Molecular overview   Toll-like receptors (TLRs) are an important class of protein molecules involved in non-specific immunity (innate immunity) and a bridge between non-specific immunity and specific immunity. TLR is a single transmembrane non-catalytic protein that recognizes molecules with conserved structures derived from microorganisms. When microorganisms break through the physical barriers of the body, such as skin, mucous membranes, etc., TLRs can recognize them and activate the body to produce immune cell responses.   Discovery history As early as the 19th century, when people learned about the concept of microbial pathogenesis, they thought that there should be such molecules in multicellular organisms that recognize microbial-specific molecules and thus identify invading microorganisms. As early as more than 100 years ago, people began to look for such molecules. Richard Pfeiffe, a disciple of the famous German bacteriologist Koch, coined the term "endotoxin" to refer to a component of Gram-negative bacteria that causes fever and shock in animals. It was later discovered that this substance is a lipopolysaccharide (LPS) produced by most Gram-negative bacteria. It has also been found that other molecules, such as bacterial lipopeptides, flagellin, unmethylated DNA, etc., can elicit a protective response from the host, but if such a response persists for too long or is too strong, it can cause harm. Therefore, people logically assume that there must be receptors for such molecules in the body, and they can give the body an alarm of infection. However, people have not found such receptors after many years.   In 1980, Nusslein-Volhard et al. discovered a gene in the development of Drosophila embryos that determines the dorsal ventral differentiation of Drosophila, and named it the Toll gene. In 1988, Hashimoto et al. found that the Toll gene encodes a transmembrane protein and clarifies the structure of the Toll protein. In 1991, Gay et al. found that Toll protein is structurally homologous to the interleukin-1 receptor (IL-1R), a natural immune function molecule in mammals: the cytoplasmic parts of the two are similar. This first reminded people that Toll may be related to immunity. In 1994, Nomura et al first reported Toll-like receptors in humans. However, Toll's immunological function was not elucidated at the time, so it is still believed that Toll-like receptors are involved in mammalian development. However, two years later, in 1996, Jules A. Hoffmann and his colleagues discovered that Toll plays an important role in the immunity of Drosophila to fungal infections, thus establishing the immunological significance of Toll.In the second year, Charles Janeway and Ruslan Medzhitov demonstrated that a Toll-like receptor (later named TLR4) can activate genes involved in adaptive immunity. Bruce A. Beutle later discovered that TLR4 was able to detect the presence of LPS. Later, they found that mice did not respond to LPS if they lost their function by mutating TLR4 in mice. Later, scientists used gene targeting to study the loss of function of various other TLRs. As a result, it is believed that each TLR can recognize a different class of molecules.   Since then, people have not only revealed the immunological significance of Toll-like receptors, but also the mystery that people searched for more than 100 years ago.   Receptor structure   All Toll-like receptor homologous molecules are type I transmembrane proteins, which can be divided into three parts: extracellular region, cytoplasmic region and transmembrane region. The extracellular domain of the Toll-like receptor mainly functions to recognize the receptor and bind to other co-receptors to form a receptor complex. The cytoplasmic domain of the Toll-like receptor is highly homologous to the cytoplasmic domain of IL-1R family members (IL-1R-mediated signaling systems and mechanisms similar to Drosophila), a region known as the Toll-IL-1 receptor structure. Domain (Toll-IL-1 receptor domain, TIR domain). TIR has a homophilic interaction whereby a downstream TIR-containing signaling molecule is recruited to form a signal complex. However, the extracellular portions of the two are not related. The TLR extracellular domain has 17 to 31 leucine-rich repeats (LRRs), and both contain three extracellular domain accessory proteins, MD- 1. MD-2 and RP105 are involved in the recognition of disease-associated molecular patterns (PAMP); while IL-1R is an Ig-like structure. In mammals, some cytoplasmic proteins also have TIR domains, such as two signaling proteins. , MyD88 and TIR domain-containing adaptor protein (TIRAP), both play a role in TIR signaling.   Receptor classification   Currently, there are 11 members of the human TLRs family that have been found in mammals and humans. Among them, TLR2, TLR4, TLR5 and TLR9 are well understood. The human TLRs family gene localization is set (TLR1, 2, 3, 6, 10) chromosome 4, chromosome 9 (TLR4), chromosome 1 (TLR5), chromosome 3 (TLR9), chromosome x (TLR7) ,8). According to the distribution characteristics of TLRs, they can be divided into ubiquitous (TLR1), restricted (TLR2, TLR4, TLR5) and specific (TLR3). Human TLRs receptors can be divided into five subfamilies, namely TLR2, TLR3, TLR4, TLR5 and TLR9, depending on the location, gene structure and amino acid sequence of the chromosome. TLR2 subfamily has TLR1, TLR2, TLR6 and TLR10; TLR9 subfamily has TLR7, TLR8 and TLR9; TLR3, TLR4 and TLR5 each form a subfamily.   Receptor distribution editing There are more than 20 kinds of cells distributed by TLRs. Muzio M et al. found that TLR1 can be expressed in human leukocytes, including TLR1, polymorphonuclear cells, T, B lymphocytes and NK cells. In cells, TLR2, TLR4, and TLR5 are expressed only on myeloid cells (such as monocyte macrophages), while TLR3 is specifically expressed in dendritic cells (DC).     About us We provide a wide range of high quality normal human and animal cells, cell culture medium and reagents, FISH probes, tissue arrays, microorganisms and equipment. In addition, we also offer series of related services including cell services, biosample services and histology services for the researcher to make their project better and faster. Here are some products:CAV1,CCNB1,CD180,CD46,etc.

Progress for Autoimmune Disease Vaccine (Part One)

April 16, 2019

Author: chen shanshan

Autoimmune diseases are disordered caused by an immune response of the body's immune system to its own components, and are the result of abnormal regulation in the basic process of immune tolerance recognized by itself or non-self. According to the target antigen distribution to which the autoimmune response is directed, it can be classified into an organ-specific or organ-non-specific autoimmune disease. The former includes multiple sclerosis, myasthenia gravis and insulin-dependent diabetes mellitus, the latter including systemic lupus erythematosus and rheumatoid arthritis. Autoimmune diseases can be controlled by pathogen infection, using immunosuppressive agents, anti-inflammatory drugs, cytokines, specific antibodies and oral autoantigens. The most common treatment is to use immunosuppressive agents before cell differentiation. Block antigen specific cell activation and amplification. These treatments are effective in reducing clonal expansion and altering early signaling pathways. However, once an autoimmune response is established, immunological interference to the differentiated cell subset or at the site of the inflammatory response to eliminate the target tissue immune response becomes less effective. Moreover, current immunosuppressive therapies require continuous use because the immune system is not in a long-term tolerant state, and continuous use of immunosuppressive agents can lead to long-term toxicity and protective immune responses to viruses, bacteria and other pathogens. Significant inhibition, and non-specific inhibition of these immunosuppressive agents may cause serious complications during treatment. Each pathogen has an analogue whose chemical composition is very similar and can lead to an immune cross-reactivity. Moreover, since the latter has knocked out the harmful substances in the original virus or the toxins of the bacteria, it is biologically harmless. Pathogenic analogs can be used in vaccine research, and therapeutic vaccines for a variety of autoreactive diseases can be developed based on similarities to autoantigens. Current advances in the development of vaccines for autoimmune diseases. Autoimmune diseases vaccines are primarily based on DNA, altered peptide ligands, T cells, and T cells receptors. 1.1. DNA Based Vaccines DNA vaccines have high priority because they usually have lower immunogenicity compared to other conventional vaccine types. DNA vaccine encoding autoantigen of autoimmune disease is not only safe and well tolerated but also stable, inexpensive and easy to scale up. More importantly, DNA vaccination can be easily improved. A DNA vaccine consisting of some cytokine genes and genes encoding self-peptide proteins can significantly enhance the immune effect. This indicates that the DNA vaccine plays an important role in regulating the immune system and may have clinical application value in the treatment of autoimmune diseases. 1.2. Peptide-based Vaccines One of the most accurate selections of vaccine components exists in epitope-based peptide vaccines, where the peptide can mimic naturally processed epitopes to act as tolerogens in autoimmune diseases. Altered peptide ligands (APLs) are analogs of immunogenic epitopes that are modified by the introduction of one to several amino acid substitutions while retaining MHC binding properties. APLs induce antigen-specific Th2 T cell responses that may inhibit disease activity, therefore, have been designed as a vaccine for the prevention of autoimmune diseases. 1.3. T Cell Vaccines The T cell vaccines for the treatment of autoimmune diseases is to generate an immune response against the pathogenic autoreactive T cells by isolating autoantigen-specific T cell clones from the intended recipients and after attenuation / inactivation, re-injecting the isolated cells as a vaccine to stimulate endogenous regulatory circuits. T cell vaccines are safe, effective, well-tolerated, have no side effects and could be applied despite the autoantigens are unknown. 1.4. T Cell Receptor Peptide Vaccines The synthetic T cell receptor (TCR) peptide vaccines are typically derived from the hypervariable region of the TCR molecule or idiotypic determinants of CDR3 / CDR2. They could induce specific regulatory immunity and modulate the activity of autoreactive T cells in several autoimmune diseases, leading to clinical benefit. Currently developed autoimmune diseases and vaccines 2.1 Multiple sclerosis (MS) Multiple sclerosis is a self-reactive, CD4+ T lymphocyte-mediated, autoimmune disease of the nervous system characterized by perivascular mononuclear cell infiltration and white matter demyelination in the central nervous system. It is a myelin basic protein (MBP). Experimental autoimmune encephalomyelitis is an ideal animal model of multiple sclerosis, and has the same characteristics as multiple sclerosis in clinical, biochemical, immunological and pathological aspects. Cop1 is a therapeutic vaccine against relapsing-remitting multiple sclerosis that has passed clinical trials. It consists of a large amount of L-alanine, a small amount of L-glutamic acid, a slight amount of L-lysine and some L- A positively charged amino acid random copolymer formed by tyrosine mixing, which is similar in structure to positively charged MBP, has significant immunological cross-reactivity at antibody level and T cell level and MBP. Cop1 is not a universal immunosuppressive agent, it only works on MS and EAE. However, the inhibitory effect of Cop1 in EAE is a common phenomenon that is not limited by specific populations, disease types or encephalogenic substances used to induce EAE. The immunosuppressive effects of Cop1 include competitive inhibition of encephalitin and inhibition of specific regulatory T cells (Treg). Cop1 competitively inhibits the binding of MBP or other myelin-related proteins to MHC class II molecules and T cell receptors, and it is effective in replacing myelin-derived peptides from the binding sites of MHC class II molecules. Treg can be isolated from the peripheral immune system of Cop1-treated animals, which are CD4+CD25+Treg subpopulations that secrete immunosuppressive IL4, IL-10 and TGF-β, which inhibits immune responses against MS. Greatly, it can protect EAE in an uninterrupted way. 2.2 Myasthenia gravis(MG)   MG is a chronic progressive autoimmune disease acquired at the neuromuscular junction, and its autoimmune attack is mainly focused on the nicotinic acetylcholine receptor (AchR) located on the postsynaptic muscle terminal plate. Experimental autoimmune myasthenia gravis (EAMG) is a well-recognized animal model of MG. T cells play an important role in the development of MG: 195-212 and 259-271 of the AchRα subunit are immune-dominant T cell epitopes of SJI mice and BALB/C mice that are highly reactive to myogenic ability. The "double-altered peptide ligand" formed by the two "single altered myogenic peptide-free peptides" (Ala207~Lys262) obtained by substituting Ala207 and Lys262 for the corresponding amino acids in 195~212 and 259~271, respectively APL specifically regulates autoimmune responses associated with MG and EAMG in vivo and in vitro without interfering with immune responses against other antigens. Dual APL may also immune-modulate other determinants other than 195-212 and 259-271 in the AchR molecule by epitope extension. The mechanism of dual APL inhibitory effects may be the induction of immunosuppressive effects mediated by regulatory cells and/or immunosuppressive cytokines such as TGF-β. It induces the inhibitory activity of immune-regulatory T cells by up-regulating the expression of CTLA4 on the surface of CD4+CD25+ regulatory T cells and down-regulating the expression of CD28, and also down-regulating the secretion and up-regulation of Th1 type cytokines (IL-1, IFN-γ). Secretion of IL-10 and TGF-β leads to apoptotic lymph node cells. Dual APL also down-regulates the adhesion of T-cells in their own reactive T cells, interfering with signaling and migration-related events. The ultimate efficacy of dual APL is to improve the established EAMG symptoms. Dual APL can activate the inhibition of EAMG-related reactions, alleviate the EAMG symptoms of BALB/C mice and female Lewis rats induced by 259-271 specific T cell lines, and significantly down-regulate the clinical symptoms of C57BL/6 mice sensitive to AchR. Clinical studies have also shown that dual APL down-regulates the autoimmune response of MG patients, which specifically inhibits the proliferative response of peripheral blood lymphocytes of MG patients to eight myogenic dystrophic peptides, and immune-modulates MG-related responses. Dual APL has the specific therapeutic potential we desire and can be used as a therapeutic vaccine for new MG-specific therapies. To be continued in Part Two…   Reference [1] Jones T B, Basso D M, Sodhi A, et al. Pathological CNS autoimmune disease triggered by traumatic spinal cord injury: implications for autoimmune vaccine therapy[J]. Journal of Neuroscience the Official Journal of the Society for Neuroscience, 2002, 22(7):2690. [2] Saad C G S, Borba E F, Aikawa N E, et al. Immunogenicity and safety of the 2009 non-adjuvanted influenza A/H1N1 vaccine in a large cohort of autoimmune rheumatic diseases[J]. Annals of the Rheumatic Diseases, 2011, 70(6):1068-1073. [3] Zaccone P, Cooke A. Vaccine against autoimmune disease: can helminths or their products provide a therapy?[J]. Current Opinion in Immunology, 2013, 25(3):418-423. [4] Anderson R P, Jabri B. Vaccine against autoimmune disease: antigen-specific immunotherapy.[J]. Current Opinion in Immunology, 2013, 25(3):410-417.

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