#TNF-alpha
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https://bundas24.com/read-blog/118482_tumor-necrosis-factor-tnf-alpha-inhibitors-market-size-overview-share-and-foreca.html
The Tumor Necrosis Factor (TNF) Alpha Inhibitors Market in 2023 is US$ 41.88 billion, and is expected to reach US$ 44.35 billion by 2031 at a CAGR of 0.7%.
#Tumor Necrosis Factor (TNF) Alpha Inhibitors Market#Tumor Necrosis Factor (TNF) Alpha Inhibitors Market Analysis#Tumor Necrosis Factor (TNF) Alpha Inhibitors Market Overview
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Give me strength to call a rheumatologist please
#I’ve been suffering for 5 years and I’m so T I R E D#physically and emotionally#this disease is so draining#I want tnf alpha blockers already#or something besides ibuprofen#dmard#whatever really
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Cytokines are so cute, you know those weird numbers you see in medical text? The one you'll likely see around is Interleukin, shortned to IL. The name literally means 'Cell communication', they're chemicals that cells release to speak to one another, depending what interleukin you find in a test, you can deduce what these little guys are planning and doing at the moment
The most common ones are TNF-a (tumor necrosis alpha) and IL-6, both stimulate inflammation in damaged area. Inflammation is just the cells setting up the battlefield, the redness is due to bloodflow in the area bringing more immune cells in, the pain is that sometimes the area increases, pressing onto nerves. It's your body telling you that you need to stop using that part.
IL-6 and TNF-a are the cytokines that the cells use to call one another, kind of a "I need backup here" signal. Some of these cytokines are pyrogenic, which is what we call the ones that go to the brain and tell it to raise body temperature!
You also have interferons (shortned to IFN), those are what cells produce to warn others in a "I'm infected with something, stay away" kind of way, this tells the other cells that they need to protect themselves, it also calls some cells responsible to kill infected cells to do their jobs
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Progress in the Study of the Protective Effect and Mechanism of C-phycocyanin on Liver Injury
Abstract: C-phycocyanin (C-phycocyanin) is a pigment-containing protein from marine algae that has shown promising results in the treatment of many inflammatory diseases and tumors. C-alpha-cyanobilin is a pigment-containing protein from marine algae that has been shown to be effective in the treatment of various inflammatory diseases and tumors. C-alpha-cyanobilin has a protective effect on various liver diseases, such as drug-induced or toxic substance-induced liver damage, non-alcoholic fatty liver disease, hepatic fibrosis, and hepatic ischemia-reperfusion injury. The protective effect of C-alginin on liver injury is mainly realized through the regulation of signaling pathways such as nuclear factor (NF)-κB, phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) and AMP-dependent protein kinase (AMPK), and the inhibition of oxidative stress, etc., and is not toxic to normal cells. Therefore, C-alginin has a broad application prospect as a potential natural hepatoprotective marine active substance. In recent years, the research progress of the protective effect of C-alginin on liver injury and its mechanism is summarized.
C-phycocyanin (C-phycocyanin) is a complex protein of cyanobacteria and a natural food protein pigment with pharmacological effects such as antioxidant, anti-inflammatory and anti-tumor effects, as well as fast-acting and low-toxicity, it can be used as a functional food [1-2]. C-Alginin can also enhance immunity and is safe, without causing acute and subacute toxic reactions [3]. Selenium-enriched PC has been shown to have stronger pharmacological effects [4]. Therefore, C-alginate has important research value both as a drug and a functional food, and has become a hot spot in the field of pharmaceutical research [5]. In this paper, we summarize the progress of research on the application and mechanism of C-alginin in liver diseases.
1 Ameliorative effect of C-phycocyanin on liver injury caused by drugs and toxic substances
The liver is the metabolic center of drugs and exogenous toxic substances, and metabolites are prone to liver injury. C-PC can inhibit the synthesis and release of inflammatory factors such as tumor necrosis factor (TNF)-α and interferon-γ, and increase the activities of catalase and superoxide dismutase (SOD), which can inhibit hepatic inflammation and alleviate hepatic injury [3]. It has been found that C-PC can significantly prevent thioacetamide-induced liver injury, significantly reduce the levels of alanine aminotransferase (ALT) and aliquot aminotransferase (AST), shorten the prothrombin time and reduce the hepatic histopathological damage, and improve the survival rate of rats with fulminant hepatic failure [6]. C-alginin also has a good effect on thioacetamide-induced hepatic encephalopathy, which can be seen in the reduction of tryptophan and lipid peroxidation indexes in different regions of the brain, and the enhancement of catalase and glutathione peroxidase activities in rats with fulminant hepatic failure [6].
Another study found that C-alginin not only attenuates the oxidative stress induced by 2-acetylaminofluorene and reduces the generation of reactive oxygen species (ROS) radicals, but also inhibits the phosphorylation of protein kinase B (Akt) and the nuclear translocation of nuclear factor (NF)-κB induced by 2-acetylaminofluorene, thus inhibiting the expression of multidrug resistance genes [7]. Osman et al. [8] also showed that C-alginin could normalize the levels of ALT, AST, catalase, urea, creatinine, SOD and glutathione-s-transferase in the livers of rats poisoned with carbon tetrachloride (CCl4). This result was also verified in human liver cell line (L02) [9]. C-phycocyanin can effectively scavenge ROS and inhibit CCl4-induced lipid peroxidation in rat liver [10], and C-PC can improve the antioxidant defense system and restore the structure of hepatocytes and hepatic enzymes in the liver of gibberellic acid-poisoned albino rats [11]. As a PC chromophore, phycocyanin can also significantly inhibit ROS generation and improve liver injury induced by a variety of drugs and toxic substances [10]. Liu et al. [12] found that phycocyanin showed strong anti-inflammatory effects in a CCl4-induced hepatic injury model in mice, which could significantly reduce the levels of ALT, AST, the expression of TNF-α and cytochrome C, increase the levels of albumin and SOD, and proliferate cytosolic nuclei. It can significantly reduce ALT and AST levels and the expression of TNF-α and cytochrome C, increase albumin levels and the expression of SOD and proliferating cell nuclear antigen, promote hepatocyte regeneration and improve the survival rate of mice with acute liver failure.
Gammoudi et al [13] used response surface method to optimize the extraction process of C-phycocyanin, and obtained high extraction recovery. C-phycocyanin extracted by the optimized method has the ability of scavenging hydroxyl, superoxide anion and nitric oxide radicals as well as the ability of metal chelating, and it has stronger antioxidant effect; C-PC significantly increased the activity of SOD and inhibited the increase of ALT, AST, and bilirubin in cadmium-poisoned rats. C-PC significantly increased the activity of SOD and inhibited the increase of ALT, AST and bilirubin in rats with cadmium poisoning. The above studies show that C-phycocyanin can effectively protect liver injury caused by drugs and toxic substances, and has the efficacy as the basis for drug development.
2 Preventive effect of C-alginin on hepatic fibrosis
Liver fibrosis is an inevitable process in the development of various chronic liver diseases and may be reversed with early and timely treatment. The key to liver fibrosis is the activation of hepatic stellate cells. Previous studies have found that low-dose C-alginin combined with soy isoflavones can inhibit hepatic stellate cell activation by inhibiting the activity of reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase[14], but it is not clear whether C-alginin alone can inhibit the activity of NADPH oxidase. Therefore, the combination of C-algin and soy isoflavones at appropriate doses may have a preventive effect on liver fibrosis in high-risk groups. C-alginin may inhibit the progression of NADPH by suppressing oxidative damage, thereby inhibiting the development of hepatic fibrosis [15].
Epithelial mesenchymal transition (EMT) is one of the key mechanisms contributing to the development of fibrotic diseases. C-alginin inhibits transforming growth factor β1 (TGF-β1)-induced human EMT [16]. Although the effect of C-alginin on EMT in hepatic fibrosis has not been reported, it has been found that C-alginin can reduce pulmonary fibrosis by inhibiting epithelial mesenchymal transition [17]. Another study found that C-alginin could reduce the expression of α-smooth muscle actin (α-SMA) and connective tissue growth factor (CTGF) mRNA in human dermal fibroblasts and alleviate fibrous contracture [18]. The results of these studies also have significance for the inhibition of hepatic fibrosis, and provide a theoretical basis for the further study of C-PC as a potential antifibrotic drug.
3 Protective effect of C-alginin on hepatic ischemia-reperfusion injury
Liver ischemia/reperfusion injury is an important clinicopathophysiological phenomenon. It was found that the addition of two different doses (0.1 g/L and 0.2 g/L) of C-alginin to the Krebs Henseleit preservation solution significantly decreased hepatic ALT, AST and alkaline phosphatase activities, and reduced the rate of lipid peroxidation and malondialdehyde content in an isolated perfused rat liver model, and increased the activities of hepatic glutathione-s-transferase and glutathione peroxidase, as well as sulfhydryl groups in hepatic tissue. On the other hand, it can increase the activities of hepatic glutathione-s-transferase and glutathione peroxidase and the content of sulfhydryl groups in liver tissues, therefore, C-alginin can significantly reduce hepatic ischemia/reperfusion injury as an antioxidant [19]. In isolated perfused mouse livers, it was found that C-alginin significantly reduced the phagocytosis and respiratory burst activity of hepatic macrophages (Kupffer cells), attenuated cytotoxicity and inflammation induced by highly active Kupffer cells, and dose-dependently inhibited carbon phagocytosis and carbon-induced oxygen uptake by perfused livers, and then inhibited the increase of hepatic nitric oxide synthase activity induced by gonadotropins [20]. and thus inhibit the thyroid hormone-induced elevation of hepatic nitric oxide synthase activity [20].
However, C-alginin has a very short half-life in vivo, which limits its application in vivo. It was found that the use of polyethylene glycol-b-(polyglutamic acid-g-polyethyleneimine), a macromolecular material with good drug-carrying capacity and slow-release properties, as a nanocarrier of C-alginin could solve this problem, and the release of C-alginin could be delayed by subcutaneous injection into the abdominal region of rats, which could attenuate islet damage caused by hepatic ischemia/reperfusion and enhance the function of the islets [21]. This study broadens the scope of application of C-alginin in vivo and improves the therapeutic effect of C-alginin.
4 Inhibitory effect of C-alginin on hepatocellular carcinoma
It was found that C-alginin significantly reduced the expression of matrix metalloproteinase (MMP)-2 and MMP-9 and the expression of tissue inhibitor of metalloproteinase 2 (TIMP2) mRNA in human hepatocellular carcinoma cells (HepG2 cells) [22]. C-alginin is a natural photosensitizer, and photodynamic therapy (PDT) mediated by alginin microcystin induced a large accumulation of ROS in HepG2 cells, which promoted mitochondrial damage and cytochrome C release, and led to apoptosis of hepatocellular carcinoma cells [23].
Liu et al. [24] used nanoscale C-alginate particles prepared by lactobionic acid grafting and adriamycin loading to enhance the growth inhibition of HepG2 cells when combined with chemo-PDT, and the C-alginate particles could effectively accumulate and diffuse in tumor multicellular spheres. In vitro and in vivo studies on the effects of selenium-enriched PCs on PDT in hepatocellular carcinoma showed that selenium-enriched PCs could migrate from lysosomes to mitochondria in a time-dependent manner, and that selenium-enriched PCs could induce the death of tumor cells through the generation of free radicals in vivo, increase the activities of antioxidant enzymes in vivo, induce mitochondria-mediated apoptosis, and inhibit autophagy, thus offering a relatively safe pathway to tumor treatment and showing new development perspectives [4]. It can provide a relatively safe way to treat tumors and shows a new development prospect [4].
Lin et al. [25] combined C-phycocyanin with single-walled carbon nanohorns and prepared phycocyanin-functionalized single-walled carbon nanohorn hybrids, which enhanced the photostability of C-phycocyanin and protected the single-walled carbon nanohorns from adsorption of plasma proteins, and synergistically used with PDT and photothermal therapy (PTT) to treat tumors. C-phycocyanin covalently coupled with biosilica and PDT or non-covalently coupled with indocyanine green and PTT on tumor-associated macrophages can also increase the apoptosis rate of tumor cells [26-27]. The development of PDT and PTT synergistic methods for the treatment of cancer has broadened the application of C-PC and enhanced its value in the treatment of hepatocellular carcinoma.
In addition, C-phycocyanin can inhibit the expression of multidrug-resistant genes in HepG2 cells through NF-κB and activated protein-1 (AP-1)-mediated pathways, and C-phycocyanin increases the accumulation of adriamycin in HepG2 cells in a dose-dependent manner, which results in a 5-fold increase in the susceptibility of cells to adriamycin [28]. Even in adriamycin-resistant HepG2 cells, C-PC induced the activation of apoptotic pathways such as cytochrome C and caspase-3 [29], and the results of Prabakaran et al. [30] also confirmed the inhibitory effect of C-PC on the proliferation of HepG2 cells, mediated by the inactivation of BCR-ABL signaling and the downstream PI3K/Akt pathway. mediated by BCR-ABL signaling and inactivation of downstream PI3K/Akt pathway. In addition, C-phycocyanin modifies the mitochondrial membrane potential and promotes apoptosis in cancer cells [30]. Currently, C-phycocyanin is a synergistic molecule with other drugs that have been widely used in the treatment of cancer [31]. The above studies demonstrate that C-phycocyanin has good therapeutic potential in the field of hepatocellular carcinoma.
5 Amelioration of metabolic syndrome and non-alcoholic fatty liver disease by C-phycocyanin
It has been found that C-alginin can reduce ALT and AST levels, decrease ROS production and NF-κB activation, and attenuate hepatic fibrosis in rats induced by high-fat choline-deficient diets, and thus C-alginin has a protective effect on NAFLD rats through anti-inflammatory and antioxidant mechanisms [15].
Another study on the effects of aqueous extract of Spirulina (mainly C-alginin) on NAFLD induced by a high-calorie/high-fat Western diet in C57Bl/6J mice showed that aqueous extract of Spirulina significantly improved glucose tolerance, lowered plasma cholesterol, and increased ursodeoxycholic acid in bile in mice [32]. Kaspi-Chadli et al. Kasbi-Chadli et al. [33] showed that aqueous extract of Spirulina could reduce cholesterol and sphingolipid levels in the liver and aortic cholesterol levels in hamsters fed a high-fat diet by significantly decreasing the expression of hydroxy-3-methylglutaryl-coenzyme A reductase (HMG CoA) gene, a limiting enzyme for cholesterol synthesis, and TGF-β1 gene, and that ursodeoxycholic acid levels in the feces of hamsters fed high-fat diets were increased in the high Spirulina aqueous extract treatment group.
A daily dose of C-alginin-enriched Spirulina can reduce the harmful effects of oxidative stress induced by a diet rich in lipid peroxides [34]. Ma et al. [35] found that C-alginin promoted the phosphorylation of hepatocyte AMP-dependent protein kinase (AMPK) in vivo and ex vivo, and increased the phosphorylation of acetyl coenzyme A carboxylase. In the treatment of NAFLD in mice, C-alginin can improve liver inflammation by up-regulating the expression of phosphorylated AMPK and AMPK-regulated transcription factor peroxisome proliferator-activated receptor α (PPAR-α) and its target gene, CPT1, and by down-regulating the expression of pro-inflammatory factors such as TNF-α and CD36 [35]. This suggests that C-phycocyanin can also improve lipid deposition in the liver through the AMPK pathway.
Endothelial dysfunction is associated with hypertension, atherosclerosis and metabolic syndrome. Studies in animal models of spontaneous hypertension have shown that long-term administration of C-alginin may improve systemic blood pressure in rats by increasing aortic endothelial nitric oxide synthase levels, with a dose-dependent decrease in blood pressure, and thus C-alginin may be useful in preventing endothelial dysfunction-related diseases in the metabolic syndrome [36]. In the offspring of ApoE-deficient mice fed C-alginate during gestation and lactation, male littermates had an elevated hepatic reduced/oxidized glutathione ratio and significantly lower hepatic SOD and glutathione peroxidase gene expression.
C-PC is effective in preventing atherosclerosis in adult hereditary hypercholesterolemic mice [37]. In vitro, C-phycocyanin also improved glucose production and expression of phosphoenolpyruvate carboxykinase (PEPCK) and glucose-6-phosphatase (G-6-Pase) in high-glucose-induced insulin-resistant HepG2 cells [38]. C-alginin also increases glucose uptake in high glucose-induced insulin-resistant HepG2 cells through the insulin receptor substrate (IRS)/PI3K/Akt and Sirtuin-1 (SIRT1)/liver kinase B1 (LKB1)/AMPK signaling pathways, activates glycogen synthase, and increases the amount of glycogen [38]. C-phycocyanin can improve blood glucose and fasting serum insulin levels in tetracycline-induced diabetic mice [39]. Therefore, C-phycocyanin can maintain cellular glucose homeostasis by improving insulin resistance in hepatocytes.
6 Hepatoprotective role of C-phycocyanin in other liver diseases
Studies have shown that C-alginin can inhibit total serum cholesterol, triacylglycerol, LDL, ALT, AST, and malondialdehyde levels in mice modeled with alcoholic liver injury, significantly increase SOD levels in the liver, and promote the activation and proliferation of CD4+ T cells, which can have an ameliorative effect on alcoholic liver injury [40]. In addition, C-phycocyanin may enhance the intestinal barrier function, regulate the intestinal flora, reduce the translocation of bacteria and metabolites to the liver, and inhibit the activity of the Toll-like receptor 4 (TLR4)/NF-κB pathway, which may reduce the inflammation of the liver and prevent the occurrence of hepatic fibrosis in mice [41]. In mice with X-ray radiation-induced liver injury, C-phycocyanin can reduce radiation-induced DNA damage and oxidative stress injury by up-regulating the expression of nuclear factor (NF)-E2-related factor 2 (Nrf2) and downstream genes, such as HO-1, and play a hepatoprotective role by enhancing the activities of SOD and glutathione peroxidase [42].
7 Outlook
Liver fibrosis is the common final process of chronic liver diseases, and there is no effective therapeutic drug at present. Although some research progress has been made in the field of traditional Chinese medicine (TCM) on the reversal of liver fibrosis [43], its toxicological effects have not yet been clarified. Although the incidence of viral hepatitis has gradually decreased with the development and popularization of vaccines and antiviral drugs, the incidence of drug-induced liver injury (DILI) and liver diseases such as NAFLD has been increasing year by year with the improvement of people's living conditions [44]. Therefore, there is an urgent need to find drugs or nutrients that can help maintain normal hepatocyte function and effectively inhibit liver inflammation and fibrosis. C-alginin, with its anti-inflammatory, antioxidant, and antitumor effects, as well as good food coloring, has a wide range of applications in both the pharmaceutical and food industries.
References:
[ 1 ] LIU Q, HUANG Y, ZHANG R, et al. Medical aapplication of spirulina platensis derived C-phycocyanin [J]. Evid Based Complement Alternat Med, 2016, 2016: 7803846. doi: 10. 1155/ 2016/7803846.
[2] BRAUNE S , KRÜGER-GENGE A , KAMMERER S , et al. Phycocyanin from Arthrospira platensis as potential anti-cancer drug: review of in vitro and in vivo studies[J]. studies[J]. Life (Basel), 2021, 11 (2): 91. doi:10.3390/life11020091.
[3] GROVER P, BHATNAGAR A, KUMARI N, et al. C-phycocyanin- a novel protein from spirulina platensis- in vivo toxicity, antioxidant and immunomodulatory studies[J]. Saudi J Biol Sci, 2021, 28(3):1853-1859. doi: 10. 1016/j.sjbs.2020.12.037.
[4] LIU Z, FU X, HUANG W, et al. Photodynamic effect and mechanism study of selenium-enriched phycocyanin from spirulina platensis against liver tumours. [J Photochem Photobiol B] J Photochem Photobiol B, 2018, 180: 89-97. doi: 10. 1016/j.jphotobiol.2017.12.020.
[5] JIANG L, WANG Y, YIN Q, et al. Phycocyanin: a potential drug for cancer treatment[J]. J Cancer, 2017, 8 (17): 3416-3429. doi: 10.7150/jca.21058.
[6] SATHYASAIKUMAR K V, SWAPNA I, REDDY P V, et al. Co- administration of C-phycocyanin ameliorates thioacetamide- induced hepatic encephalopathy in Wistar rats[J]. J Neurol Sci, 2007, 252(1):67-75. doi: 10. 1016/j.jns.2006.10.014.
[7] ROY K R , NISHANTH R P , SREKANTH D , et al. C- phycocyanin ameliorates 2-acetylaminofluorene induced oxidative stress and MDR1 expression in the liver of albino mice [J]. of albino mice[J]. Hepatol Res, 2008, 38(5): 511-520. doi: 10.1111/j. 1872-034X. 2007. 00290.x.
[8] OSMAN A, SALAMA A, EMAM MAHMOUD K, et al. Alleviation of carbon tetrachloride-induced hepatocellular damage and oxidative stress in rats by anabaena oryzae phycocyanin[J]. J Food Biochem, 2021, 45(1):e13562. doi:10.1111/jfbc.13562.
[9] OU Y, ZHENG S, LIN L, et al. Protective effect of C-phycocyanin against carbon tetrachloride-induced hepatocyte damage in vitro and in vivo[J]. Chem Biol Interact, 2010, 185(2): 94-100. doi: 10. 1016/j.cbi.2010.03.013.
[10] BHAT V B, MADYASTHA K M. C-phycocyanin: a potent peroxyl radical scavenger in vivo and in vitro [J]. Biochem Biophys Res Commun, 2000, 275(1): 20-25. doi: 10. 1006/bbrc.2000.3270.
[ 11] HUSSEIN M M, ALI H A, AHMED M M. Ameliorative effects of phycocyanin against gibberellic acid induced hepatotoxicity[J]. Pestic Biochem Physiol, 2015, 119: 28-32. doi: 10. 1016/j. pestbp. 2015.02.010.
[ 12]LIU J, ZHANG Q Y, YU L M, et al. Phycocyanobilin accelerates liver regeneration and reduces mortality rate in carbon tetrachloride-induced liver injury mice[J]. World J Gastroenterol, 2015, 21(18):5465-5472. doi:10.3748/wjg.v21.i18.5465.
[13] GAMMOUDI S, ATHMOUNI K, NASRI A, et al. Optimization, isolation, characterization and hepatoprotective effect of a novel pigment-protein complex (phycocyanin) producing microalga: phormidium versicolorNCC-466 using response surface methodology [J]. versicolorNCC-466 using response surface methodology [J]. Int J Biol Macromol, 2019, 137: 647-656. doi: 10. 1016/j. ijbiomac.2019.06.237.
[14] MCCARTY M F , BARROSO-ARANDA J , CONTRERAS F. Genistein and phycocyanobilin may prevent hepatic fibrosis by suppressing proliferation and activation of hepatic stellate cells[J]. Med Hypotheses, 2009, 72(3):330-332. doi: 10. 1016/j.mehy.2008. 07.045.
[15]PAK W, TAKAYAMA F, MINE M, et al. Anti-oxidative and anti- inflammatory effects of spirulina on rat model of non-alcoholic steatohepatitis[J]. J Clin Biochem Nutr, 2012, 51(3):227-234. doi:10.3164/jcbn.12-18.
[16] PATTARAYAN D, RAJARAJAN D, SIVANANTHAM A, et al. C- phycocyanin suppresses transforming growth factor- β 1-induced epithelial mesenchymal transition in human epithelial cells [J]. Pharmacol Rep, 2017, 69(3): 426-431. doi: 10. 1016/j. pharep. 2016.12.013.
[ 17]LI C, YU Y, LI W, et al. Phycocyanin attenuates pulmonary fibrosis via the TLR2-MyD88-NF- κB signaling pathway[J]. Sci Rep, 2017, 7 (1): 5843. doi: 10. 1038/s41598-017-06021-5.
[18] AN E, PARK H, LEE A C. Inhibition of fibrotic contraction by C- phycocyanin through modulation of connective tissue growth factor and α-smooth muscle actin expression[J]. Tissue Eng Regen Med, 2016, 13(4):388-395. doi: 10. 1007/s13770-015-0104-5.
[19] GDARA N B, BELGACEM A, KHEMIRI I, et al. Protective effects of phycocyanin on ischemia/reperfusion liver injuries [J]. Biomed Pharmacother, 2018, 102: 196-202. doi: 10. 1016/j. biopha. 2018. 03.025.
[20] REMIREZ D, FERNÁNDEZ V, TAPIA G, et al. Influence of C- phycocyanin on hepatocellular parameters related to liver oxidative stress and kupffer cell functioning[J]. Inflamm Res, 2002, 51(7): 351-356. doi: 10. 1007/pl00000314.
[21] TONG F, TANG X, LIU D. Phycocyanin/PEG-b-(PG-g-PEI) attenuated hepatic ischemia/reperfusion-induced pancreatic islet injury and enlarged islet functionality [J]. Int J Nanomedicine, 2019, 14: 339-351. doi: 10.2147/IJN.S190938.
[22]KUNTE M, DESAI K. The inhibitory effect of C-phycocyanin containing protein extract on human matrix metalloproteinases (MMP-2) and MMP-9 in hepatocellular cancer cell line (HepG2)[J]. and MMP-9) in hepatocellular cancer cell line (HepG2) [J]. Protein J, 2017, 36(3): 186-195. doi: 10. 1007/s10930-017-9707-0.
[23]WANG C Y, WANG X, WANG Y, et al. Photosensitization of phycocyanin extracted from microcystis in human hepatocellular carcinoma cells: implication of mitochondria-dependent apoptosis [J]. J Photochem Photobiol B, 2012, 117: 70-79. doi: 10. 1016/j. jphotobiol.2012.09.001.
[24]LIU X, DU J, XIE Z, et al. Lactobionic acid-modified phycocyanin nanoparticles loaded with doxorubicin for synergistic chemo- photodynamic therapy[J]. therapy[J]. Int J Biol Macromol, 2021, 186: 206- 217. doi: 10. 1016/j.ijbiomac.2021.07.047.
[25]LIN Z, JIANG B P, LIANG J, et al. Phycocyanin functionalized single-walled carbon nanohorns hybrid for near-infrared light- mediated cancer phototheranostics [J]. Carbon, 2019, 143: 814- 827. doi: 10. 1016/j.carbon.2018.12.011.
[26] PU Y, WEI M, WITKOWSKI A, et al. A hybrid biomaterial of biosilica and C-phycocyanin for enhanced photodynamic effect towards tumor cells[J]. Biochem Biophys Res Commun, 2020, 533 (3): 573-579. doi: 10. 1016/j.bbrc.2020.09.049.
[27] WAN D H, MA X Y, LIN C, et al. Noncovalent indocyanine green conjugate of C-phycocyanin: preparation and tumor-associated macrophages-targeted photothermal therapeutics[J]. Bioconjug Chem, 2020, 31(5): 1438-1448. doi: 10. 1021/acs. bioconjchem. 0c00139.
[28]NISHANTH R P, RAMAKRISHNA B S, JYOTSNA R G, et al. C- phycocyanin inhibits MDR1 through reactive oxygen species and cyclooxygenase-2 mediated pathways in human hepatocellular carcinoma cell line[J]. Eur J Pharmacol, 2010, 649(1/3):74-83. doi: 10. 1016/j.ejphar.2010.09.011.
[29] ROY K R, ARUNASREE K M, REDDY N P, et al. Alteration of mitochondrial membrane potential by spirulina platensis C- phycocyanin induces apoptosis in the doxorubicinresistant human hepatocellular-carcinoma cell line HepG2[J]. Biotechnol Appl Biochem, 2007, 47 (Pt 3): 159-167. doi: 10. 1042/BA20060206.
[30] PRABAKARAN G, SAMPATHKUMAR P, KAVISRI M, et al. Extraction and characterization of phycocyanin from spirulina platensis and evaluation of its anticancer , antidiabetic and antiinflammatory effect[J]. Int J Biol Macromol, 2020, 153: 256- 263. doi: 10. 1016/j.ijbiomac.2020.03.009.
[31] SILVA M R O B D, M DA SILVA G, SILVA A L F D, et al. Bioactive compounds of Arthrospira spp. (spirulina) with potential anticancer activities: a systematic review[J]. ACS Chem Biol, 2021, 16 (11): 2057-2067. doi: 10. 1021/acschembio.1c00568.
[32] COUÉ M, TESSE A, FALEWÉE J, et al. Spirulina liquid extract protects against fibrosis related to non-alcoholic steatohepatitis and increases ursodeoxycholic acid [J]. Nutrients, 2019, 11 (1): 194. doi:10.3390/nu11010194.
[33] KASBI-CHADLI F, COUÉ M, AGUESSE A, et al. Spirulina liquid extract prevents metabolic disturbances and improves liver sphingolipids profile in hamster fed a high-fat diet[J]. Eur J Nutr, 2021, 60(8):4483-4494. doi: 10. 1007/s00394-021-02589-x.
[34] OULD AMARA-LEFFAD L, RAMDANE H, NEKHOUL K, et al. Spirulina effect on modulation of toxins provided by food, impact on hepatic and renal functions [J] . . Arch Physiol Biochem, 2019, 125 (2): 184-194. doi: 10. 1080/13813455.2018.1444059.
[35] MA P, HUANG R, JIANG J, et al. Potential use of C-phycocyanin in non-alcoholic fatty liver disease [J]. Biochem Biophys Res Commun, 2020, 526(4):906-912. doi: 10. 1016/j.bbrc.2020.04.001.
[36]ICHIMURA M, KATO S, TSUNEYAMA K, et al. Phycocyanin prevents hypertension and low serum adiponectin level in a rat model of metabolic syndrome[J]. Nutr Res, 2013, 33(5): 397-405. doi: 10. 1016/j.nutres.2013.03.006.
[37] COUÉ M, CROYAL M, HABIB M, et al. Perinatal administration of C-phycocyanin protects against atherosclerosis in apoE-deficient mice by modulating cholesterol and trimethylamine-N-oxide metabolisms[J]. Arterioscler Thromb Vasc Biol, 2021, 41(12): e512-e523. doi: 10. 1161/ATVBAHA.121.316848.
[38]REN Z, XIE Z, CAO D, et al. C-phycocyanin inhibits hepatic gluconeogenesis and increases glycogen synthesis via activating Akt and AMPK in insulin resistant hepatocytes [J]. Food Funct, 2018, 9(5): 2829-2839. doi: 10. 1039/c8fo00257f.
[39]OU Y, REN Z, WANG J, et al. Phycocyanin ameliorates alloxan- induced diabetes mellitus in mice :involved in insulin signaling pathway and GK expression [J]. Chem Biol Interact, 2016, 247: 49- 54. doi: 10. 1016/j.cbi.2016.01.018.
[40] XIA D, LIU B, XIN W, et al. Protective effects of C-phycocyanin on alcohol-induced subacute liver injury in mice [J]. Journal of Applied Phycology, 2015, 28(2):765-772. doi: 10. 1007/s10811- 015-0677-3.
[41] XIE Y, LI W, ZHU L, et al. Effects of phycocyanin in modulating the intestinal microbiota of mice [J]. Microbiologyopen, 2019, 8 (9): e00825. doi: 10. 1002/mbo3.825.
[42]LIU Q, LI W, QIN S. Therapeutic effect of phycocyanin on acute liver oxidative damage caused by X-ray[J]. Biomed Pharmacother, 2020, 130: 110553. doi: 10. 1016/j.biopha.2020.110553.
[43]SONG Y N, CHEN J, CAI F F, et al. A metabolic mechanism analysis of fuzheng-huayu formula for improving liver cirrhosis with traditional chinese medicine syndromes [J]. Acta Pharmacol Sin, 2018, 39(6): 942-951. doi: 10. 1038/aps.2017.101.
[44]XIAO J, WANG F, WONG N K, et al. Global liver disease burdens and research trends : analysis from a chinese perspective[J]. J Hepatol, 2019, 71(1):212-221. doi: 10. 1016/j.jhep.2019.03.004.
#phycocyanin #cphycocyanin #phycocyaninspirulina
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Some personal nonsense, medical tw
tfw you cant fucking remember what leg you did your anti tnf alpha shot in two weeks ago and have to just make a blind guess and hope you choose the opposite one
🙃
#medical tw#injection tw#needles tw#i love having a chronic disease its a constant adventure in stupidity#its been like 6 years of this you would think i would have learned to remember where i did my injection#but tbf now i do my other injections in my abdomen so it makes it much harder to do a rotation#incredible how used to injecting medications i have become#standard routine#an annoying weekly occurence
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This would absolutely happen!
Storytime: I was working on my independent research thesis. It had me reading a few articles published from the 1940s-1960s. Specifically, I wanted to know if scar tissue could ever become cancerous or how it could be similar given TNF-alpha pathways. And the way these peofessional researchers would use the N-word? Oh goooood lord. I never could get myself to actually take their findings seriously.
Hey remember how Noir is an anti-fascist from 1933
#biochemistry#research study#it was a different time#into the spider verse#spiderman noir#itsv#spiderverse
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Remicade Infusion Treatment: What You Need to Know for Autoimmune Diseases
Even though it is a difficult condition, it is worth noting that these days, modern therapies can effectively help many individuals enjoy fuller lives and healthier living. One very powerful treatment patients are increasingly enthusiastic about is Remicade Infusion Treatment. Among many other therapies,, we ogy pride ourselves pride ourselves on offering this interesting new therapy combined with with compassionate, expert,, individualized care. Whether you are newly diagnosed or looking for a new treatment option, learning really what this particular treatment is all about helps one make the right decisions about their health.
Understanding Remicade Infusion Treatment
Commercially known as Remicade and commonly referred to as infliximab, it is a biologic therapy administered primarily to neutralize the selective protein TNF-alpha. This protein is said to be the major instigator of inflammation in autoimmune disorders. Autoimmune disorders involving an overactive immune system that attacks healthy tissues, including rheumatoid arthritis, psoriatic arthritis, Crohn's disease, ulcerative colitis, and ankylosing spondylitis, are treated with infusions of Remicade that work by blocking TNF-alpha. Thus, treatment works to control inflammation, reduce symptoms, and prevent future joint damage.
At VIP Rheumatology, the infusion therapy treatment is custom designed to best suit your needs, which guarantees that our patients receive the optimal care and the best outcome possible.
What to Expect During Remicade Infusion Treatment
At VIP Rheumatology, you can trust that your Remicade Infusion Treatment will be smooth and will make you feel supported—the treatment is delivered through intravenous infusion, meaning the medicine gets pumped right into your bloodstream for effectiveness. The first time you receive your infusion, it usually takes a little longer, between two and three hours, because everyone has to carefully feel the pulse of your reaction. Future infusions might be shorter, depending on how well your body tolerates the medication.
You will be in a safe and cozy area, and specialized infusion staff members will stay close to monitor your health and answer questions or concerns. Many people come with books to read, just watch a show, or simply sleep through the entire procedure. Most importantly, it will be a low-stress, welcoming environment where you feel very safe and cared for through your treatment process.
How Often Do You Need Remicade Infusions?
Usually, given at the intervals of 0, 2, and 6 weeks after those initial three loading doses, maintenance infusions will generally take place every eight weeks. However, this interval could vary according to your condition and how you respond to treatment. Here at VIP Rheumatology, we will follow up on the progress and tailor the treatment schedule upon achieving appropriate control of your autoimmune disease.
Regularity assumes paramount importance where Remicade Infusion Treatment is concerned. Your infusion schedule is maintained so that the drug is kept at therapeutic levels and further relieves symptoms and lowers chances of eruptions in the disease.
Benefits of Remicade Infusion Treatment
Patients at VIP Rheumatology typically enjoy dramatic improvements after starting on Remicade Infusion Treatment. Decrease in joint pain, mobility improvement, decline in intestinal symptoms, and, in general, improved quality of life are just among the many outcomes we have seen from this treatment. The majority of the time, patients will reduce their consumption of steroids and other orally ingested medications that have serious long-term effects on the body.
Moreover, another major advantage is that Remicade could actually slow or completely stop the joint damage and tissue destruction and preserve your health for a longer time. Good management now means that most can keep on working, traveling, or enjoying daily living without being limited by conditions.
Potential Side Effects to Be Aware Of
Like any medical therapy, infusion therapy with Remicade has some probable side effects. Common side effects include minor reactions such as headache, nausea, and rash at the infusion site. Rarer side effects could include severe infections because the medication alters immune function.
At VIP Rheumatology, patient safety is our highest priority. A complete workup is done before starting the treatment and monitoring during and after each infusion. If you have any queries regarding side effects, our expert team is always available for counseling and support.
Is Remicade Right for You?
Autoimmune diseases are not synonymous with the use of biologics; however, for people who have not been helped by standard treatment, Remicade Infusion Treatment presents an attractive option. If you are suffering from intractable symptoms or if your disease has shown resistance to other medications, you should at least consider this important therapy.
At your consultation at VIP Rheumatology, we will evaluate your medical history, review your symptoms, and undertake any necessary testing to determine if Remicade is appropriate for you. We value a more personalized approach to health care, with you and your preferences as the principal actors in the decision-making process.
Why Choose VIP Rheumatology for Your Remicade Infusion Treatment?
Choosing the best provider for infusion therapy is a crucial decision. At VIP Rheumatology, we have specialists that have focused on targeting autoimmune disease with the latest, evidence-based treatments for many years. Our state-of-the-art infusion center is designed for comfort and safety, while our dedicated team works to provide a warm atmosphere to make every patient feel welcome.
From the first visit until the last follow-up, you will be treated as a true VIP. Our goal is to empower you to live your best life possible while carrying as few burdens of autoimmune disease as possible. If you want to know more about Remicade Infusion Treatment or schedule a consultation, contact VIP Rheumatology today. Let's take that next step to a healthier tomorrow!
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Interrelationship of anti-oxidative status and circulating biochemical markers in patients with cancer experience tumor lysis syndrome (TLS)
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Adalimumab: A Medication for Autoimmune Diseases
Adalimumab: A Medication for Autoimmune Diseases Adalimumab is a medication used to treat autoimmune diseases. It belongs to a class of drugs called TNF-alpha inhibitors. These diseases include rheumatoid arthritis, psoriatic arthritis, and Crohn’s disease. How Adalimumab Works Adalimumab blocks a protein called tumor necrosis factor-alpha (TNF-alpha). TNF-alpha causes inflammation and damage…
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Probiotics For Liver Health
The human gut is home to trillions of microorganisms that not only assist in digestion but also play a critical role in maintaining overall health. Probiotics For Liver Health Among these beneficial microbes, probiotics live bacteria and yeasts that confer health benefits to the host have garnered attention for their wide-ranging effects, from boosting immune function to improving mental health. More recently, science has begun to uncover the significant influence of probiotics on liver health, highlighting the importance of the gut-liver axis in managing and even preventing liver disease.

The Gut-Liver Axis: A Two-Way Street
The liver and the gut are intricately connected via the portal vein, which carries blood from the digestive tract directly to the liver. This means that whatever enters the gut including food, toxins, microbes, and microbial byproducts has a direct impact on the liver. Conversely, liver function influences the gut environment through bile acids and immune signalling. This bidirectional communication, known as the gut-liver axis, underlies the close relationship between gastrointestinal health and liver function.
When the gut microbiome is disrupted, a condition known as dysbiosis it can lead to increased intestinal permeability or "leaky gut." This allows bacterial endotoxins, such as lipopolysaccharides (LPS), to translocate into the bloodstream, triggering systemic inflammation and placing a heavy burden on the liver. Chronic exposure to these endotoxins is associated with a range of liver conditions, including non-alcoholic fatty liver disease (NAFLD), alcoholic liver disease (ALD), and cirrhosis.
How Probiotics Support Liver Health
Probiotics help restore balance to the gut microbiome and offer several mechanisms that benefit liver health:
1. Reducing Intestinal Permeability
Probiotic Strains Such as Lactobacillus RhamnosesGg and Bifidobacterium Longum Have Been Shown to Strengthen Tight Junctions in the Intestinal Wall, Reducing Gut Permeability and Preventing the Translocation of Harmful Bacterial Byproducts to the Liver.
2. Lowering Endotoxin Levels
By modulating the composition of gut flora, probiotics reduce the population of pathogenic bacteria that produce endotoxins. This in turn decreases the inflammatory load on the liver.
3. Modulating Inflammation
Chronic liver diseases are often driven by low-grade inflammation. Probiotics can help regulate the immune response by promoting anti-inflammatory cytokines (such as IL-10) and reducing pro-inflammatory markers like TNF-alpha. This helps attenuate liver inflammation and slow disease progression.
4. Improving Lipid Metabolism
NAFLD is characterized by fat accumulation in liver cells. Certain probiotic strains improve lipid metabolism by decreasing intestinal absorption of fats and modulating bile acid composition. This may help reduce hepatic steatosis and improve liver enzyme profiles.
5. Enhancing Insulin Sensitivity
Metabolic syndrome, insulin resistance, and type 2 diabetes are key risk factors for liver disease. Probiotics have been found to enhance insulin sensitivity, likely due to their ability to modulate gut-derived short-chain fatty acids (SCFAs) and reduce systemic inflammation.
Clinical Evidence and Applications
Multiple studies have examined the impact of probiotics on various liver conditions:
Non-Alcoholic Fatty Liver Disease (NAFLD): Randomized controlled trials have demonstrated that probiotic supplementation can reduce liver enzymes (ALT, AST), improve lipid profiles, and decrease hepatic fat content. A 2020 meta-analysis concluded that probiotics are effective in improving liver function in patients with NAFLD, particularly when combined with lifestyle changes.
Alcoholic Liver Disease (ALD): In individuals with chronic alcohol consumption, probiotics may help restore gut barrier integrity and reduce systemic endotoxin levels. Animal studies have shown that Lactobacillus strains can reduce liver inflammation and fat accumulation in alcohol-induced liver injury.
Hepatic Encephalopathy (HE): In advanced liver disease, the buildup of toxins like ammonia can impair brain function. Probiotics have been used to reduce blood ammonia levels and improve cognitive outcomes in patients with HE, offering a non-pharmacologic adjunct to standard therapy.
Cirrhosis: Though more research is needed, some studies suggest that probiotics can improve immune function and reduce the risk of spontaneous bacterial peritonitis (SBP) in cirrhotic patients by modulating gut flora and intestinal permeability.
Choosing the Right Probiotic
Not all probiotics are created equal. Their effects are strain-specific and disease-specific, which means that one size does not fit all. For liver health, some of the most studied strains include:
Lactobacillus rhamnosus GG
Bifidobacterium longum
Lactobacillus plantarum
Lactobacillus casei
Multi-strain formulations including prebiotics (synbiotics)
Formulation, dosage, and duration of use are also important considerations. Clinical studies typically use dosages in the range of 10⁸ to 10¹¹ colony-forming units (CFU) per day over a period of 8–12 weeks. It's advisable to consult a healthcare professional for personalized recommendations.
Dietary Sources and Lifestyle Integration
While supplements provide a convenient and concentrated source of probiotics, fermented foods can also support gut and liver health. Examples include:
Yogurt with live cultures
Kefir
Sauerkraut
Kimchi
Miso
Tempeh
These foods not only deliver probiotics but also contain other beneficial compounds such as enzymes, fiber, and antioxidants. Pairing these with a fiber-rich, anti-inflammatory diet supports a healthy gut-liver axis. Avoiding excessive alcohol, refined sugars, and trans fats is also essential in preventing liver damage.
Conclusion
The emerging science on probiotics and liver health is both promising and exciting. By modulating the gut microbiota, reducing inflammation, and improving metabolic function, probiotics offer a supportive approach to managing liver conditions especially in the early stages of disease. While they are not a replacement for medical treatment or lifestyle change, they represent a powerful adjunct in a comprehensive liver health strategy.
As research continues to evolve, the future may hold more targeted probiotic therapies tailored to individual microbiome profiles and specific liver conditions. Until then, incorporating probiotics through supplements and diet under the guidance of a healthcare professional can be a proactive step toward preserving liver health and overall well-being. Read Also : https://draswinkrishna.com/best-endoscopy-doctor-in-chennai/
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The Tumor Necrosis Factor (TNF) Alpha Inhibitors Market in 2023 is US$ 41.88 billion, and is expected to reach US$ 44.35 billion by 2031 at a CAGR of 0.7%.
#Tumor Necrosis Factor (TNF) Alpha Inhibitors Market#Tumor Necrosis Factor (TNF) Alpha Inhibitors Market Forecast#Tumor Necrosis Factor (TNF) Alpha Inhibitors Market Overview
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Infliximab solution
Infliximab solution Catalog number: B2022442 Lot number: Batch Dependent Expiration Date: Batch dependent Amount: 0.25 mL Molecular Weight or Concentration: N/A Supplied as: Solution Applications: a molecular tool for various biochemical applications Storage: -20°C Keywords: Remicade, Infliximab injection, Infliximab infusion, monoclonal antibody therapy, TNF-alpha inhibitor Grade: Biotechnology…
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Research Antibodies Market Trends and Forecast 2024-2032
The Research Antibodies Market was valued at USD 1.4 billion in 2023 and is projected to reach USD 2.3 billion by 2032, growing at a compound annual growth rate (CAGR) of 5.5% over the forecast period from 2024 to 2032. This growth is primarily driven by increased governmental investments in biotechnology and healthcare research aimed at developing novel antibodies. Rising demand for high-quality antibodies in diagnostic, therapeutic, and pharmaceutical applications is further propelling the market forward.
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Regional Analysis
North America: Dominates the market due to substantial government funding and a strong presence of pharmaceutical companies and research organizations. The region’s focus on life sciences research continues to create business opportunities.
Europe: Research and development initiatives supported by large-scale funding are driving market expansion. The growing emphasis on antibody development for cancer and immunology is a key factor in this region’s market growth.
Asia-Pacific: Rapidly increasing research activities and investment in biotechnology are creating new opportunities. The demand for research antibodies is on the rise due to expanding biopharmaceutical industries and technological advancements.
Market Segmentation
By Product:
Antibodies
Reagents
By Technology:
Western Blotting
Flow Cytometry
Enzyme-linked Immunosorbent Assay (ELISA)
Immunoprecipitation
Immunohistochemistry
Immunofluorescence
Other Technologies
By Application:
Proteomics
Drug Development
Genomics
By End User:
Academic & Research Institutes
Pharmaceutical & Biotechnological Companies
Contract Research Organizations
Key Players
Key Service Providers/Manufacturers
Abcam Plc (Anti-GAPDH Antibody, Anti-CD3 Antibody)
Thermo Fisher Scientific, Inc. (Anti-Histone H3 Antibody, Alexa Fluor 488 Secondary Antibody)
Merck KGaA (Anti-β-Actin Antibody, Anti-IL-6 Antibody)
Cell Signaling Technology, Inc. (Phospho-Akt Antibody, Anti-p53 Antibody)
Bio-Rad Laboratories, Inc. (Anti-GFP Antibody, Anti-Flag M2 Antibody)
R&D Systems, Inc. (a Bio-Techne brand) (Anti-TNF-alpha Antibody, Anti-BDNF Antibody)
GenScript Biotech Corporation (Anti-His Tag Antibody, Anti-Mouse IgG Antibody)
Rockland Immunochemicals, Inc. (Anti-VEGF Antibody, Anti-Human IgG Antibody)
PerkinElmer, Inc. (LanthaScreen Antibodies, AlphaLISA Detection Antibodies)
Santa Cruz Biotechnology, Inc. (Anti-CXCR4 Antibody, Anti-Bcl-2 Antibody)
Key Points
Academic-biotech partnerships are fostering innovation in antibody research.
Next-generation sequencing and high-throughput screening technologies are enhancing antibody research efficiency.
Asia-Pacific presents significant growth opportunities due to increased research activities and a booming biotech sector.
Future Scope
The research antibodies market is set for substantial expansion, driven by advancements in antibody engineering and production technologies that improve specificity and efficacy. Increased investments in biomedical research and personalized medicine will further accelerate market growth. As precision therapies gain prominence, research antibodies will play an essential role in scientific innovation, disease diagnostics, and targeted drug development.
Conclusion
The research antibodies market is witnessing significant growth due to increasing global research activities, government investments, and technological advancements. As the demand for targeted therapies and personalized medicine rises, research antibodies will remain a critical component in advancing healthcare and biotechnology research.
Contact Us: Jagney Dave - Vice President of Client Engagement Phone: +1-315 636 4242 (US) | +44- 20 3290 5010 (UK)
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#Research Antibodies Market#Research Antibodies Market Share#Research Antibodies Market Trends#Research Antibodies Market Size#Research Antibodies Market Growth
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