#TNF-alpha

[medicomunicare]

Depression "under pressure": the better we know mechanisms, the better come out managements

Deporession ad public health emergency Depression is a growing mental health concern and is associated with significant levels of disability across the world. Depressive symptoms, such as persistent low mood, fatigue, cognitive impairments, anhedonia, or a lack of interest or pleasure in the activities of life, are categorized as interest-activity symptoms. These symptoms contribute substantially…

[unibiotech]

BLUelf Prestained Protein Ladder

Explore a range of high-quality protein ladders at unibiotech.in, including BLUeye and BLUelf Prestained Protein Ladders. Perfect for molecular biology applications, our protein ladders ensure accurate molecular weight determination in your experiments. As your trusted protein ladder supplier, we offer reliable products to streamline your research process. Browse our selection today to find the ideal protein ladder for your molecular biology experiments.

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[mitalipingale]

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%.

[kiwitheft]

Give me strength to call a rheumatologist please

[mleprae]

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

[helen0086]

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.

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[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

[fivehundredwords]

Alzheimer's Disease: biomarkers and neuroimaging markers cheatsheet for research articles

As Alzheimer's Disease (AD) research skews toward understanding the brain than the pathogenic proteins, studies exploring biomarkers and neuroimaging are hopeful toward developing a method for successful prevention of AD. A biomarker is a molecule, whose presence indicates abnormality or disease, and thus, is crucial in diagnostic procedures. Levels of certain molecules is notably altered in cerebrospinal fluid and in blood plasma, which helps in diagnosing the occurrence of AD. Neuroimaging involves the use of techniques such as magnetic resonance imaging and computed tomography to observe neuronal activity in the brain. This is good news, especially for AD, as the asymptomatic stage of the disease can be identified early enough.

Although the exact function and involvement in clinical practice is not profuse, altered concentrations of these biomarkers in plasma or cerebrospinal fluid encourage further research:

Amyloid and tau serve as the unsurprising biomarkers of AD pathology.

Neurofilament-light chain (NF-L) and visinin-like protein-1 (VILIP-1) are the most promising biomarkers of neuronal injury.

Post-synaptic protein neurogranin (Ng) and pre-synaptic proteins synaptosome-associated protein-25 (SNAP-25) and synaptotagmin-1 (Syt-1) are considered major biomarkers of synaptic injury.

Brain and CSF levels of tumor necrosis factor alpha (TNF-α) and increased levels of interleukin group of proteins (ILs) indicate intensified microglial response to neuroinflammation.

TREM2 receptor and YKL-40 glycoprotein are also reliable indicators of inflammation and impaired clearance of amyloid beta.

Heart-type fatty acid-binding protein (hFABP) could be a marker for pathology in blood vessels supplying the brain. Some vascular markers also show potential as markers of vascular injury in AD: von Willebrand factor (vWF) and monokine induced by γ-interferon (MIG, also known as CXCL-9).

Concentrations of TAR-DNA binding protein (TDP-43) in the brain and plasma and serum indicate, even contribute to, inflammation, mitochondrial dysfunction, and neuronal/synaptic injury in AD.

Neuroimaging techniques reveal structural, functional, and diffusion-related activities of the neurons. To identify them, markers are tracked in images obtained. Each marker is determined with the activity and biochemistry of the group of/individual neurons being studied.

Structural MRI will show location and severity of atrophy which can be identified in grey scale images by applying programs that create analogous color grading.

Functional MRI relies on blood oxygenation level dependent (BOLD) signal which reflects changes in blood oxygenation levels in response to neural activity.

Diffusion weighted imaging (DWI) focuses on diffusion of water molecules. A tensor model is applied to images obtained from DWI. The diffusion tensor imaging (DTI) metrics thus obtained help in studying connectivity through structural integrity of white matter tracts.

Tractography involves 3-D reconstruction of white matter as observed in DWI, which provides a more detailed look into a patient’s neural networks.

In positron emission tomography (PET), markers are identified and labelled so their features or functions can be traced during this procedure to obtain a resulting PET scan. The imaging procedure is named according to its marker: amyloid-PET, tau-PET, FDG-PET, inflammation-PET, receptor-PET.

FDA approved drugs Galantamine, Rivastigmine, and Donepezil alleviate symptoms such as memory loss and confusion in mild to moderate AD, although their effects seem to be negligible. They also cause nausea and vomiting as side effects and are not suitable for every patient. Recently approved drugs, Aducanumab and Lecanemab focus on removing accumulated amyloid. Their effectiveness is still doubted on the basis of studies finding that targeting amyloid has little to do with curbing the actual progression of the disease.

bibliography -

Tarawneh R. Biomarkers: our path towards a cure for Alzheimer disease. Biomarker insights. 2020 Nov;15:1177271920976367.

Cavedo E, Lista S, Khachaturian Z, Aisen P, Amouyel P, Herholz K, Jack Jr CR, Sperling R, Cummings J, Blennow K, O’Bryant S. The road ahead to cure Alzheimer’s disease: development of biological markers and neuroimaging methods for prevention trials across all stages and target populations. The journal of prevention of Alzheimer's disease. 2014 Dec;1(3):181.

Medications for Alzheimer's Disease Stanford Healthcare. Accessed 21-04-2023.

[senselessalchemist]

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

🙃

[baddieladdie]

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

[oaresearchpaper]

Interrelationship of anti-oxidative status and circulating biochemical markers in patients with cancer experience tumor lysis syndrome (TLS)

[quirksphere]

Understanding Inflammatory Biomarkers: What They Are and Why They Matter

Inflammation is a natural process by which the body responds to injury, infection, or harmful stimuli. While it plays a crucial role in healing and defense, chronic or excessive inflammation can contribute to various diseases, such as cardiovascular disorders, diabetes, autoimmune conditions, and even cancer. To better understand and manage inflammation-related health conditions, researchers and healthcare providers rely on inflammatory biomarkers.

What Are Inflammatory Biomarkers?

Inflammatory biomarkers are measurable molecules in the blood, tissues, or other bodily fluids that indicate the presence or extent of inflammation in the body. These biomarkers are typically proteins, enzymes, or metabolites produced by the immune system or damaged tissues during an inflammatory response. By measuring their levels, healthcare providers can gain insights into a patient’s health status, track disease progression, or assess the effectiveness of treatments.

Types of Inflammatory Biomarkers

Inflammatory biomarkers can be broadly classified based on their origin or function. Some of the most commonly studied biomarkers include:

C-Reactive Protein (CRP): CRP is produced by the liver in response to inflammation. Elevated CRP levels are often associated with acute inflammation, infections, or chronic conditions like rheumatoid arthritis and cardiovascular disease.

Erythrocyte Sedimentation Rate (ESR): ESR measures how quickly red blood cells settle at the bottom of a test tube. A higher sedimentation rate can indicate inflammation or infection.

Cytokines: Cytokines are signaling proteins that regulate immune and inflammatory responses. Common pro-inflammatory cytokines include interleukin-6 (IL-6), interleukin-1β (IL-1β), and tumor necrosis factor-alpha (TNF-α).

Fibrinogen: A protein involved in blood clotting, fibrinogen levels often rise during systemic inflammation and are linked to cardiovascular risk.

Serum Amyloid A (SAA): This acute-phase protein is produced in response to inflammatory signals and can serve as an indicator of infection or chronic inflammation.

Prostaglandins and Leukotrienes: These lipid molecules mediate inflammatory processes and are often studied in relation to asthma, arthritis, and other inflammatory conditions.

How Are Inflammatory Biomarkers Measured?

Inflammatory biomarkers are typically measured using blood tests, though some can be detected in saliva, urine, or tissue samples. Advanced laboratory techniques such as enzyme-linked immunosorbent assay (ELISA), mass spectrometry, and multiplex immunoassays are used to quantify these molecules with precision.

Clinical Applications of Inflammatory Biomarkers

Inflammatory biomarkers have a wide range of applications in medicine and research:

Disease Diagnosis and Monitoring: Elevated levels of certain biomarkers can help identify inflammatory or autoimmune conditions, such as lupus, rheumatoid arthritis, or inflammatory bowel disease. They are also used to monitor disease progression.

Cardiovascular Risk Assessment: High levels of CRP and fibrinogen are associated with an increased risk of heart attacks and strokes, making them valuable in assessing cardiovascular health.

Therapeutic Guidance: Biomarkers can help evaluate the effectiveness of anti-inflammatory medications, allowing for personalized treatment strategies.

Predicting Outcomes: In conditions like sepsis or COVID-19, elevated biomarkers such as IL-6 and CRP can predict disease severity and guide critical care interventions.

The Future of Inflammatory Biomarkers

Advances in genomics, proteomics, and bioinformatics are driving the discovery of novel inflammatory biomarkers. Researchers are exploring multi-biomarker panels that provide a more comprehensive picture of inflammation. Additionally, wearable technologies capable of monitoring biomarkers in real-time are on the horizon, promising to revolutionize how inflammation is tracked and managed.

Conclusion

Inflammatory biomarkers are powerful tools for understanding the body’s response to injury and disease. They offer invaluable insights into diagnosing, monitoring, and treating a wide range of conditions. As research progresses, these biomarkers will likely play an even greater role in precision medicine, helping to improve outcomes for patients worldwide. By staying informed about these advancements, both healthcare providers and patients can better navigate the complexities of inflammation-related health issues.

[mitalipingale]

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%.

[many-to-mention10001]

What are inflammatory biomarkers?

What are inflammatory biomarkers? Inflammatory biomarkers are molecules found in blood or other body fluids that indicate the presence and intensity of inflammation in the body.

What are the common inflammatory biomarkers? Common biomarkers include C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), interleukins (e.g., IL-6), tumor necrosis factor-alpha (TNF-α), and procalcitonin.

What conditions can inflammatory biomarkers detect? They can indicate infections, autoimmune diseases (e.g., rheumatoid arthritis), cardiovascular diseases, and some cancers.

What does a high CRP level indicate? High CRP levels suggest acute or chronic inflammation, often due to infection, autoimmune diseases, or tissue injury.

What is ESR, and what does it measure? ESR measures the rate at which red blood cells settle in a test tube, with faster rates indicating inflammation.

[dhakshin-ayurveda]

Curcuma Longa Powder: The Golden Spice for Health and Healing

Introduction

Curcuma longa also commonly referred to as turmeric is a herbaceous perennial plant originated from the Zingiberacae family. Grown in SouthEast Asia, the dried and powdered form of its rootstock has been used as a spice, colorant and medicine for millennia. It reaches its vibrant yellow hue as well as reveals its medicinal effects largely because of curcuminoids; curcumin has received the most focus. In this blog, you will learn about the background, the content of Curcuma longa powder, and its related health values with scientific introductions.

1. Historical and Traditional Use of Turmeric

Gurpur, a natural yellow dye extracted from the root of turmeric, has been in use as medicine in Ayurveda, Chinese and Unani systems for thousands of years. 

Ayurveda: Haridra or Indian Saffron is characterised as ‘cleanser’ and ‘vitalizer’. It helps in pacifying the three dosha and is utilized in illnesses of skin, inflammatory and digestive disorders. 

Traditional Chinese Medicine (TCM): To a traditional Chinese medicine practitioner, turmeric is beneficial in circulation, liver complaint, and arthritis.

Cultural and Ritual Use: In many traditions, the yellow pigment obtained from the root was employed as dye in rituals, while in other traditions it was used as a sort of natural preservative for food

2.Chemical Composition of Curcuma Longa Powder

The medicinal properties of turmeric are attributed to its bioactive compounds, including:

Curcuminoids (2–5%): o Curcumin (C₂₁H₂₀O₆): The major curcuminoid contributing to nearly all the health benefits of turmeric including excellent anti-inflammatory as well as antioxidant activity.  o Demethoxycurcumin and Bisdemethoxycurcumin: Other individuals related with curcuminoids with similar pharmacological effect.

Volatile Oils (4–14%): oTurmerone, Zingiberene, and Ar-turmerone: Well documented for possession of antimicrobial and anti-inflammatory characteristics.

Other Components: oPolysaccharides: Help contribute to modifying the effect of the immune system. oProteins and Resins: In order to serve this goal, it should be noted how turmeric can improve its therapeutic attributes.

3. Health Benefits of Curcuma Longa Powder

a) Anti-inflammatory and Antioxidant Properties 

Actually, inflammation and oxidative stress are the most advertised properties of turmeric among all others.

Inhibition of Inflammatory Pathways: Curcumin suppresses certain cytokines stimulating inflammation such as TNF-alpha, IL-1 beta, and IL-6 with interference with NF-kappa B a signaling pathway.

Antioxidant Mechanism: Besides, curcumin physically chelates with metal ions to remove free radicals and modulates the cellular antioxidant system, including SOD and catalase .

b) Joint Health and Pain Relief 

Some of the most common uses of Curcuma longa powder include relief in arthritis and other diseases of the joints. 

Osteoarthritis Relief: Recent studies have shown that curcumin works on patients with osteoarthritis, alleviates pain, and enhances joint mobility on par with NSAIDs without side effects . 

Muscle Recovery: The recorded benefits of curcumin include an ability to minimise muscle soreness caused by exercises, hence enhancing muscle recovery.

c) Digestive Health 

Turmeric also has benefits to the digestive system, which can cure some stomach problems. 

Bile Secretion Stimulation: You see turmeric helps in the production of bile that in turn promotes digestion of fats and absorption of nutrients. 

Gut Microbiome Support: Curcumin acts as a prebiotic which generates favorable bacteria in the gut such as Lactobacillus and Bifidobacterium .

d) Cardiovascular Benefits

Turmeric is also good for the heart by regulating lipid factors and lowering inflammation in the body.

Anti-thrombotic Effects: Curcumin suppresses the platelet coagglutination ability and decreases the formation of thrombin, thus enhancing the blood circulation .

Cholesterol Regulation: According to research, curcumin is effective at reducing levels of LDL cholesterol and triglycerides, and increasing levels of HDL cholesterol .

e) Immune System Support 

Turmeric in the present study may stimulate the immune system by its anti-inflammatory and antibacterial properties. 

Modulation of Immune Responses: It has been found that curcumin has an effect in regulating cell volumetric activity and thereby lifts the activity of macrophages, T cells and natural killer NK cells that is so important in combating illnesses. 

Antiviral Properties: It is found that curcumin has the possibility to prevent the viral proliferation in infections such as flu and hepatitis.

f) Anti-cancer Potential

There has been increasing interest in curcumin for cancer prevention and therapy. 

Induction of Apoptosis: Curcumin is seen to bring about apoptosis in California cells while not affecting normal cells. 

Angiogenesis Inhibition: Curcumin reduces the production by tumor cells of vascular endothelial growth factor (VEGF), which is active in constructing new blood vessels necessary for tumor growth .

Synergistic Effects: Curcumin can also works synergistically with chemotherapy and radiation therapy to increase the cancer cells sensitivity to treatment.

4. Mechanisms of Action

Inhibition of Enzymes: Curcumin even suppresses such enzymes as cyclooxygenase (COX) and lipoxygenase (LOX), thereby decreasing manufacturing of inflammatory mediators . 

Regulation of Gene Expression: Through evaluating the molecular targets present in curcumin for its anti-inflammatory effects, the NF-κB and MAPK signaling pathways alongside alterations in inflammation-modulating genes are influenced by curcumin . 

Antioxidant Activity: Through its antioxidant property curcumin scavenge the free radicals and enhances antioxidant enzymes to reduce oxidative stress and cell damage

5. Modern Applications of Curcuma Longa Powder

The versatility of turmeric makes it a key ingredient in various health and wellness products: 

Nutraceuticals: Turmeric supplements have gained popularity in the market regarding joint health, digestion, and immune system support. 

Functional Foods: Turmeric is mixed with beverages, foods and golden milk due to its health implications. 

Cosmetics: In skin care, turmeric is incorporated in skin care products owing to it’s ability to reduce inflammation and lighten skin color. 

Pharmaceuticals: Technological advancement in the formulation for using turmeric extract for the treatment of inflammation and metabolism disease .

6. Safety and Side Effects

Turmeric powder is not toxic in most cases when taken as a dietary product in the correct proportions. However: 

Potential Side Effects: At higher doses there may be minor side effects of gastrointestinal irritation. 

Drug Interactions: These include anticoagulants, among others, although curcumin interacts with certain types of medication. Seek the  attention of a doctor if you are taking any form of medication. 

Recommended Dosage: The daily dose of curcumin in standardized turmeric extracts is between 500 mg and 1,500 mg.

Conclusion

Curcuma longa powder which contains bio-active compounds and health benefits of this spice has been discovered through clinical research and has traditional remedies too. Whether for anti-inflammatory properties, as an aid for digestion or its many other uses, turmeric remains a key component in natural health care. Being incorporated into advanced nutraceutical and pharmaceutical products, it has its place in both preventive and curative medicine.

[credenceresearchdotblog]

The Psoriasis Treatment Market is projected to grow from USD 25,671.82 million in 2023 to an estimated USD 52,179.75 million by 2032, with a compound annual growth rate (CAGR) of 8.20% from 2024 to 2032. Psoriasis, a chronic autoimmune skin disorder characterized by red, scaly patches, impacts millions of people globally. Its multifaceted nature, affecting both physical and psychological well-being, has driven continuous innovation in its treatment landscape. The psoriasis treatment market is witnessing significant growth due to increasing awareness, advancements in therapies, and rising prevalence rates. This article explores the current trends, key drivers, and challenges shaping the psoriasis treatment market.

Browse the full report https://www.credenceresearch.com/report/psoriasis-treatment-market

Market Overview

The psoriasis treatment market is poised for robust growth, fueled by a surge in cases worldwide. According to the World Health Organization (WHO), psoriasis affects approximately 2-3% of the global population. While genetic predisposition is a major risk factor, environmental triggers such as stress, infections, and lifestyle choices exacerbate its incidence. The increasing burden of this disease has heightened the demand for effective and long-lasting treatments.

The market is segmented based on treatment type, including topicals, systemic therapies, and biologics. Among these, biologics have revolutionized psoriasis management, offering targeted solutions with fewer side effects compared to traditional treatments. Additionally, the growing adoption of combination therapies has broadened the scope of effective treatment regimens.

Key Drivers of Growth

Technological Advancements The advent of biologics and biosimilars has transformed the psoriasis treatment landscape. Biologics, such as TNF-alpha inhibitors and IL-17 inhibitors, specifically target immune pathways responsible for inflammation, providing significant relief for moderate-to-severe cases. Ongoing research into gene and cell-based therapies is expected to further expand treatment options.

Rising Prevalence and Awareness Psoriasis prevalence is increasing, especially in urban populations, due to lifestyle changes and environmental stressors. Campaigns and initiatives by organizations such as the International Federation of Psoriasis Associations (IFPA) have amplified awareness, reducing stigma and encouraging individuals to seek treatment.

Investment in R&D Pharmaceutical companies are investing heavily in developing innovative drugs. Clinical trials for next-generation biologics, oral therapies, and topical treatments are addressing unmet needs in the market. For instance, drugs targeting novel pathways like IL-23 and JAK inhibitors are gaining traction.

Personalized Medicine Advances in precision medicine are enabling tailored treatment approaches based on genetic, environmental, and lifestyle factors. This paradigm shift promises more effective management of psoriasis with minimized side effects.

Challenges in the Market

High Costs of Treatment Despite the efficacy of biologics, their high cost limits accessibility, especially in developing regions. Affordability remains a major challenge for healthcare systems and patients alike.

Side Effects and Non-Compliance Many systemic treatments come with adverse side effects, including immunosuppression, which can deter long-term adherence. Ensuring patient compliance remains a hurdle in achieving optimal outcomes.

Regulatory Hurdles Regulatory approvals for novel therapies can be time-consuming and expensive, delaying the entry of new drugs into the market. Stringent requirements often prolong the commercialization process.

Future Outlook

The psoriasis treatment market is on an upward trajectory, propelled by advancements in medical science and growing awareness. The focus on biologics, biosimilars, and personalized medicine is expected to redefine the therapeutic landscape. Moreover, the integration of digital health tools, such as mobile apps and telemedicine, is enhancing patient engagement and monitoring.

As pharmaceutical companies continue to innovate and governments address affordability and accessibility concerns, the future looks promising for the psoriasis treatment market. The shift towards holistic care, encompassing physical, mental, and social aspects, will likely play a pivotal role in improving the quality of life for individuals with psoriasis.

Key players

AbbVie Inc.

Novartis AG

Pfizer Inc.

LEO Pharma A/S

Merck & Co., Inc.

Amgen Inc.

Eli Lilly and Company

Evelo Biosciences, Inc.

UCB S.A.

Sun Pharmaceutical Industries Ltd.

Segments

Based on type

Plaque Psoriasis

Psoriatic Arthritis

Others

Based on Drug

TNF Inhibitors

Interleukins Inhibitors

Others

Based on Product

Biologics

Non-Biologics

Based on route of administration

Oral

Parenteral/Systemic

Topical

Based on Distribution channel

Hospital Pharmacies

Retail Pharmacies

Online Pharmacie

Based on region

North America

U.S.

Canada

Mexico

Europe

Germany

France

U.K.

Italy

Spain

Rest of Europe

Asia Pacific

China

Japan

India

South Korea

South-east Asia

Rest of Asia Pacific

Latin America

Brazil

Argentina

Rest of Latin America

Middle East & Africa

GCC Countries

South Africa

Rest of the Middle East and Africa

Browse the full report https://www.credenceresearch.com/report/psoriasis-treatment-market

Contact:

Credence Research

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