Skip to main content

Home/ Dr. Goodyear/ Group items matching "N" in title, tags, annotations or url

Group items matching
in title, tags, annotations or url

Sort By: Relevance | Date Filter: All | Bookmarks | Topics Simple Middle
Nathan Goodyear

N-AcetylcysteiNe Improves Liver FuNctioN iN PatieNts with NoN-Alcoholic Fatty Liver Disease - 0 views

www.ncbi.nlm.nih.gov/...PMC3270338

NAC N-acetylcysteine NAFLD non-alcoholic fatty liver fatty liver liver enzymes

shared by Nathan Goodyear on 17 Jul 18 - No Cached
  • Nathan Goodyear on 17 Jul 18
     
    Oral NAC useful for elevated liver eNzymes iN NAFLD
Nathan Goodyear

Immunotherapy for Prostate Cancer with Gc Protein-Derived Macrophage-Activating Factor, GcMAF - Europe PMC Article - Europe PMC - 0 views

europepmc.org/...PMC2510818

GC-MAF Nagalase cancer prostate cancer immunotherapy PSA

shared by Nathan Goodyear on 08 May 18 - No Cached
  • the MAF precursor activity of prostate cancer patient Gc protein is lost or reduced, because their serum Gc protein is deglycosylated by serum α-n-acetylgalactosaminidase (nagalase) secreted from cancerous cells
  • Administration of 100 ng of GcMAF
  • 100 ng of GcMAF was administered intramuscularly once a week
  • ...11 more annotations...
  • As GcMAF therapy progressed the MAF precursor activity of all five patients increased and their serum nagalase activity decreased inversely
  • As GcMAF therapy progressed, the MAF precursor activity increased with a concomitant decrease in serum nagalase activity
  • serum Nagalase is proportioNal to tumor burdeN
  • as GcMAF therapy progressed, serum Nagalase activity decreased aNd, coNcomitaNtly, tumor burdeN decreased
  • the serum Nagalase activities of all 16 patieNts decreased as GcMAF therapy progressed
  • annual computed tomographic scans of these patients confirmed them being tumor recurrence-free for the 7 years
  • undifferentiated cells were killed rapidly during the first few weeks, and the differentiated cells were killed slowly in the remaining GcMAF therapeutic period
  • PSA levels of prostatectomized patients decreased as serum nagalase decreased during GcMAF therapy
  • In patients without tumor resection, however, although serum nagalase activity decreased as GcMAF therapy progressed, their PSA values remained unchanged. The result suggests that the PSA derived from tumor-bearing prostate did not change while tumor burden decreased. Because tumor-induced inflammation in the noncancerous prostate tissues causes secretion of PSA [38], the PSA produced from these inflamed noncancerous prostate tissues cannot be changed by the decrease in tumor burden
  • Advanced cancer patients have high serum nagalase activities, resulting in no macrophage activation and severe immunosuppression that explain why cancer patients die with overwhelming infection
  • Prognostic utility of serum α-n-acetylgalactosaminidase and immunosuppression resulted from deglycosylation of serum Gc protein in oral cancer patients
  • Nathan Goodyear on 08 May 18
     
    GC-MAF levels exist in inverse relationship to nagalase.  In this study of men with prostate cancer, weekly GCMAF injections reduced nagalase activity to levels found in healthy controls suggesting tumor free. The dose was 100 ng/week. nagalase is a protein that suppresses GC-MAF production and thus is immunosuppressive.
Nathan Goodyear

http://cancerres.aacrjournals.org/content/canres/56/12/2827.full.pdf - 0 views

cancerres.aacrjournals.org/...2827.full.pdf

Nagalase immune system cancer

shared by Nathan Goodyear on 25 Jul 18 - No Cached
  • Nathan Goodyear on 25 Jul 18
     
    Older study reviews nagalase as a component in the immunosuppression state in cancer.  alpha-n-acetylgalactosaminidase, nagalase for short, inactivates teh MAF precursor activity of the Gc protein which leads to macrophage inactivation.
Nathan Goodyear

Glucocorticoids plus N-AcetylcysteiNe iN Severe Alcoholic Hepatitis | NEJM - 0 views

www.nejm.org/...NEJMoa1101214

NAC N-acetylcysteine bilirubin liver hepatitis alcoholic hepatitis

shared by Nathan Goodyear on 20 Aug 18 - No Cached
  • Nathan Goodyear on 20 Aug 18
     
    NAC beNefits short-term survival iN alcoholic hepatitis, iNcludiNg a drop iN bilirubiN.
Nathan Goodyear

[A clinical study of n-acetylcysteine treatment in chronic hepatitis B patients]. - PubMed - nCBI - 0 views

www.ncbi.nlm.nih.gov/...18647523

NAC N-acetylcysteine hepatitis liver bilirubin glutathione

shared by Nathan Goodyear on 20 Aug 18 - No Cached
  • Nathan Goodyear on 20 Aug 18
     
    NAC more beNeficial iN loweriNg Total bilirubiN compared to glutathioNe iN patieNts with chroNic hepatitis B.
Nathan Goodyear

Survey of n-3 and n-6 polyunsaturated fatty acids in fish and fish products - 0 views

www.ncbi.nlm.nih.gov/...PMC3543232

omega 3 omega-6 omega-3 fish EPA DHA ALA diet nutrition

shared by Nathan Goodyear on 14 Sep 17 - No Cached
  • Nathan Goodyear on 14 Sep 17
     
    Good read on the omega 3 versus omega 6 content of different fish.
Nathan Goodyear

Omega-3 Fatty Acids and Inflammatory Processes - 0 views

www.ncbi.nlm.nih.gov/...PMC3257651

fats nutrition diet omega 3 inflammation NF-kappaB TNF-alpha omega-3 fish oil DHA EPA docosahexaenoic acid eicosapentaenoic acid

shared by Nathan Goodyear on 15 Sep 17 - No Cached
  • marine n-3 PUFAs have also been shown to alter the production of inflammatory proteins including chemokines, cytokines, growth factors and matrix proteases
  • Two transcription factors that are likely to play a role in inflammation are nuclear factor κ B (nFκB) and PPAR-γ
  • NFκB is the priNcipal traNscriptioN factor iNvolved iN upregulatioN of iNflammatory cytokiNe, adhesioN molecule aNd cyclooxygeNase-2 geNes
  • ...3 more annotations...
  • PPAR-γ, is believed to act in an anti-inflammatory manner
  • PPAR-γ directly regulates inflammatory gene expression, it also interferes with the activation of nFκB creating an intriguing interaction between these two transcription factors
  • Both NFκB aNd PPAR-γ may be regulated by N-3 PUFAs.
  • Nathan Goodyear on 15 Sep 17
     
    great review of the anti-inflammatory effects of omega 3 DHA and EPA.  EPA inhibits COX and 5-LOX and their downstream prostaglandin and leukotrienes.  EPA/DHA inhibited endotoxin-stimulated IL-6, IL-8,TnF-alpha, and nFkappaB.
Nathan Goodyear

Role of maximum standardized uptake value in fluorodeoxyglucose positron emission tomography/computed tomography predicts malignancy grade and prognosis of operable breast cancer: a multi-institute study - 0 views

www.ncbi.nlm.nih.gov/...PMC3785187

PET scan PET_CT scan maxSUV cancer breast

shared by Nathan Goodyear on 19 Mar 18 - No Cached
  • 18F-fluorodeoxyglucose positron emission tomography/computed tomography (FDG-PET/CT) is an effective and popular technique for evaluating patients before and after breast cancer surgery.
  • Quantitative FDG-PET/CT imaging is becoming prevalent in cancer treatment as it measures glucose metabolism that reflects the growth potential and metabolic activity of malignant tumors
  • The FDG-PET/CT findings of primary lesions in colorectal and lung cancers correlate with metastasis and prognosis because FDG reflects tumor viability
  • ...15 more annotations...
  • The technique is valuable for predicting the prognosis of patients with recurrent breast cancer and for determining and predicting the outcomes of neoadjuvant chemotherapy
  • FDG-PET/CT is useful not only for evaluating metastasis but also for predicting the prognosis of recurrent breast cancer and measuring treatment effects
  • reports remain limited to small-scale clinical trials of about 100 patients.
  • MaxSUV, which is the most popular FDG-PET/CT value, can vary up to 30 % because of differences among PET/CT devices and among the operators who create the images
  • the degree of malignancy would increase with an increase in maxSUV when ER or HER-2 signaling is involved.
  • Factors that determine the rate of cancer progression include T-factor (tumor diameter) and n-factor (presence or absence/number of lymph node metastasis)
  • The prognostic factors applied in breast cancer can be broadly divided into those that determine staging and those that determine biological tumor characteristics
  • Prognosis was previously predicted based on T, n, and M staging, which indicates the degree of progression. However, prognosis is now predicted and treatment regimes are presently selected by also considering ER and HER-2 levels, which determine the nature of the tumor
  • maxSUV presently serves as an indicator of metabolic activity during cancer therapy. For instance, the maxSUV of primary lung and hematological cancer lesions correlates with metastasis and prognosis, whereas maxSUV also seems useful for predicting the prognosis of recurrent breast cancer and in determining and predicting the outcome of neoadjuvant chemotherapy
  • The maxSUV cut-off calculated from ROC curves for recurrence was 3.0
  • Factors that determine the nature of tumors also include ER, HER-2, Ki-67 labeling index, and nuclear grade
  • both ER status and maxSUV as independent prognostic factors
  • maxSUV has a closer correlation with prognosis
  • maxSUV, clinical T-factor and ER were significant prognostic factors
  • Our results showed that maxSUV has the potential to be a novel prognostic factor and that it can be used to determine future therapies
  • Nathan Goodyear on 19 Mar 18
     
    Retrospective, multi-facility finds maxSUV can be used in prognosis in cancer.  Others have shown benefit in recurrence risk.  MaxSUV was found to be an independent factor.
Nathan Goodyear

Estimates of optimal vitamin D status. - PubMed - nCBI - 0 views

www.ncbi.nlm.nih.gov/...15776217

vitamin d fracture injury

shared by Nathan Goodyear on 19 Oct 16 - No Cached
  • Nathan Goodyear on 19 Oct 16
     
    Optimal fracture prevention is between 50 and 80 n/mol/l per the opinions of these authors.
herbnclay

Calcium Bentonite Clay Benefits - Internal and External Uses - 0 views

www.herbnclay.com/fits-of-calcium-bentonite-clay

best clay mask for oily skin green powder uses natural healing

shared by herbnclay on 23 Jan 18 - No Cached
  • herbnclay on 23 Jan 18
     
    HERB n' CLAY provides you with 100 percent all natural Calcium Bentonite Clay. Bentonite clay has microscopic layers through which it absorbs the toxins in our bowels. It contains silica with high traces of Calcium. In addition there are more than 50 trace elements in Calcium Bentonite Clay.
Nathan Goodyear

Effect of Lorazepam in Reducing Psychological Distress and Anticipatory nausea and Vomiting in Patients Undergoing Chemotherapy - 0 views

www.ncbi.nlm.nih.gov/...PMC5642123

nausea chemotherapy Ativan vomiting

shared by Nathan Goodyear on 11 Jul 19 - No Cached
  • Nathan Goodyear on 11 Jul 19
     
    Nice review of ativaN's aNti-emetic properties which is useful iN those with chemo iNduced N/V.
Nathan Goodyear

N-acetylcysteiNe improves aNtitumoural respoNse of INterferoN alpha by NF-kB dowNregulatioN iN liver caNcer cells - 0 views

www.ncbi.nlm.nih.gov/...PMC3539937

IFN-alpha N-acetylcysteine hepatocellular cancer liver cancer NAC hepatocellular carcinoma

shared by Nathan Goodyear on 03 Mar 21 - No Cached
  • Nathan Goodyear on 03 Mar 21
     
    NAC for treatmeNt of hepatocellular caNcer.
Nathan Goodyear

Induction of metastasis, cancer stem cell phenotype, and oncogenic metabolism in cancer cells by ionizing radiation - 0 views

www.ncbi.nlm.nih.gov/...PMC5282724

EMT TME metastasis cancer stem cells cancer MMP2 Notch MMP-9 MMP-2 radioresistance Hedgehog CSC MMP9 Snail HIF-1alpha tumor microenvironment epithelial to mesenchymal transition TGF-beta radiation

shared by Nathan Goodyear on 09 Feb 21 - No Cached
  • More than half of cancer patients are treated with IR at some point during their treatment
  • fractionation schedule is the delivery of 1.8–2.0 Gy per day, five days per week
  • Nuclear DNA is the primary target of IR; it causes DNA damage (geNotoxic stress) by direct DNA ioNizatioN
  • ...121 more annotations...
  • IR also indirectly induces DnA damage by stimulating reactive oxygen species (ROS) production
  • IR is known to induce EMT in vitro
  • p53 is activated in response to IR-induced DnA damage
  • IR paradoxically also promotes tumour recurrence and metastasis
  • DNA double-straNd breaks (DSBs)
  • cancer cells undergoing EMT acquire invasive and metastatic properties
  • changes in the tumour microenvironment (TME)
  • IR seems to induce EMT and CSC phenotypes by regulating cellular metabolism
  • EMT, stemness, and oncogenic metabolism are known to be associated with resistance to radiotherapy and chemotherapy
  • Hanahan and Weinberg proposed ten hallmarks of cancer that alter cell physiology to enhance malignant growth: 1) sustained proliferation, 2) evasion of growth suppression, 3) cell death resistance, 4) replicative immortality, 5) evasion of immune destruction, 6) tumour-promoting inflammation, 7) activation of invasion and metastasis, 8) induction of angiogenesis, 9) genome instability, and 10) alteration of metabolism
  • EMT is a developmental process that plays critical roles in embryogenesis, wound healing, and organ fibrosis
  • IR is known to induce stemness and metabolic alterations in cancer cells
  • transforming growth factor-β [TGF-β], epidermal growth factor [EGF]) and their associated signalling proteins (Wnt, notch, Hedgehog, nuclear-factor kappa B [nF-κB], extracellular signal-regulated kinase [ERK], and phosphatidylinositol 3-kinase [PI3K]/Akt
  • activate EMT-inducing transcription factors, including Snail/Slug, ZEB1/δEF1, ZEB2/SIP1, Twist1/2, and E12/E47
  • Loss of E-cadherin is considered a hallmark of EMT
  • IR has been shown to induce EMT to enhance the motility and invasiveness of several cancer cells, including those of breast, lung, and liver cancer, and glioma cells
  • IR may increase metastasis in both the primary tumour site and in normal tissues under some circumstance
  • sublethal doses of IR have been shown to enhance the migratory and invasive behaviours of glioma cells
  • ROS are known to play an important role in IR-induced EMT
  • High levels of ROS trigger cell death by causing irreversible damage to cellular components such as proteins, nucleic acids, and lipids, whereas low levels of ROS have been shown to promote tumour progression—including tumour growth, invasion, and metastasis
  • hypoxia-inducible factor-1 (HIF-1) is involved in IR-induced EMT
  • Treatment with the n-acetylcysteine (nAC), a general ROS scavenger, prevents IR-induced EMT, adhesive affinity, and invasion of breast cancer cells
    • Nathan Goodyear
      Nathan Goodyear on 09 Feb 21
       
      NAC for all patieNts receiviNg radiatioN therapy
  • Snail has been shown to play a crucial role in IR-induced EMT, migration, and invasion
  • IR activates the p38 MAPK pathway, which contributes to the induction of Snail expression to promote EMT and invasion
  • NF-κB sigNalliNg that promotes cell migratioN
  • ROS promote EMT to allow cancer cells to avoid hostile environments
  • HIF-1 is a heterodimer composed of an oxygen-sensitive α subunit and a constitutively expressed β subunit.
  • Under normoxia, HIF-1α is rapidly degraded, whereas hypoxia induces stabilisation and accumulation of HIF-1α
  • levels of HIF-1α mRNA are eNhaNced by activatioN of the PI3K/Akt/mammaliaN target of rapamyciN (mTOR)
  • IR is known to increase stabilisation and nuclear accumulation of HIF-1α, since hypoxia is a major condition for HIF-1 activation
  • IR induces vascular damage that causes hypoxia
  • ROS is implicated in IR-induced HIF-1 activation
  • IR causes the reoxygenation of hypoxic cancer cells to increase ROS production, which leads to the stabilisation and nuclear accumulation of HIF-1
  • IR increases glucose availability under reoxygenated conditions that promote HIF-1α translation by activating the Akt/mTOR pathway
  • The stabilised HIF-1α then translocates to the nucleus, dimerizes with HIF-1β, and increases gene expression— including the expression of essential EMT regulators such as Snail—to induce EMT, migration, and invasion
  • TGF-β signalling has been shown to play a crucial role in IR-induced EMT
  • AP-1 transcription factor is involved in IR-induced TGF-β1 expression
  • Wnt/β-catenin signalling is also implicated in IR-induced EMT
  • Notch sigNalliNg is kNowN to be iNvolved iN IR-iNduced EMT
  • IR also increases notch-1 expression [99]. notch-1 is known to induce EMT by upregulating Snail
  • PAI-1 signalling is also implicated in IR-induced Akt activation that increases Snail levels to induce EMT
  • EGFR activation is known to be associated with IR-induced EMT, cell migration, and invasion by activating two downstream pathways: PI3K/Akt and Raf/MEK/ERK
  • ROS and RnS are also implicated in IR-induced EGFR activation
  • IR has also been shown to activate Hedgehog (Hh) signalling to induce EMT
  • IR has been shown to induce Akt activation through several signalling pathways (EGFR, C-X-C chemokine receptor type 4 [CXCR4]/C-X-C motif chemokine 12 [CXCL12], plasminogen activator inhibitor 1 [PAI-1]) and upstream regulators (Bmi1, PTEn) that promote EMT and invasion
  • CSCs possess a capacity for self-renewal, and they can persistently proliferate to initiate tumours upon serial transplantation, thus enabling them to maintain the whole tumour
  • Conventional cancer treatments kill most cancer cells, but CSCs survive due to their resistance to therapy, eventually leading to tumour relapse and metastasis
  • identification of CSCs, three types of markers are utilised: cell surface molecules, transcription factors, and signalling pathway molecules
  • CSCs express distinct and specific surface markers; commonly used ones are CD24, CD34, CD38, CD44, CD90, CD133, and ALDH
  • Transcription factors, including Oct4, Sox2, nanog, c-Myc, and Klf4,
  • signalling pathways, including those of TGF-β, Wnt, Hedgehog, notch, platelet-derived growth factor receptor (PDGFR), and JAK/STAT
  • microRNAs (miRNAs), iNcludiNg let-7, miR-22, miR-34a, miR-128, the miR-200 family, aNd miR-451
  • NoN-CSCs caN be reprogrammed to become CSCs by epigeNetic aNd geNetic chaNges
  • EMT-inducing transcription factors, such as Snail, ZEB1, and Twist1, are known to confer CSC properties
  • Signalling pathways involved in EMT, including those of TGF-β, Wnt, and notch, have been shown to play important roles in inducing the CSC phenotype
  • TGF-β1 not only increases EMT markers (Slug, Twist1, β-catenin, n-cadherin), but also upregulates CSC markers (Oct4, Sox2, nanog, Klf4) in breast and lung cancer cells
  • some CSC subpopulations arise independently of EMT
  • IR has been shown to induce the CSC phenotype in many cancers, including breast, lung, and prostate cancers, as well as melanoma
  • Genotoxic stress due to IR or chemotherapy promotes a CSC-like phenotype by increasing ROS production
  • IR has been shown to induce reprogramming of differentiated cancer cells into CSCs
  • In prostate cancer patients, radiotherapy increases the CD44+ cell population that exhibit CSC properties
  • IR also induces the re-expression of stem cell regulators, such as Sox2, Oct4, nanog, and Klf4, to promote stemness in cancer cells
  • EMT-inducing transcription factors and signalling pathways, including Snail, STAT3, notch signalling, the PI3K/Akt pathway, and the MAPK cascade, have been shown to play important roles in IR-induced CSC properties
  • STAT3 directly binds to the Snail promoter and increases Snail transcription, which induces the EMT and CSC phenotypes, in cisplatin-selected resistant cells
  • Other oncogenic metabolic pathways, including glutamine metabolism, the pentose phosphate pathway (PPP), and synthesis of fatty acids and cholesterol, are also enhanced in many cancers
  • metabolic reprogramming
  • HIF-1α, p53, and c-Myc, are known to contribute to oncogenic metabolism
  • metabolic reprogramming
  • tumour cells exhibit high mitochondrial metabolism as well as aerobic glycolysis
  • occurring within the same tumour
  • CSCs can be highly glycolytic-dependent or oxidative phosphorylation (OXPHOS)-dependen
  • mitochondrial function is crucial for maintaining CSC functionality
  • cancer cells depend on mitochondrial metabolism and increase mitochondrial production of ROS that cause pseudo-hypoxia
  • HIF-1 then enhances glycolysis
  • CAFs have defective mitochondria that lead to the cells exhibiting the Warburg effect; the cells take up glucose, and then secrete lactate to 'feed' adjacent cancer cells
  • lactate transporter, monocarboxylate transporter (MCT)
  • nutrient microenvironment
  • Epithelial cancer cells express MCT1, while CAFs express MCT4. MCT4-positive, hypoxic CAFs secrete lactate by aerobic glycolysis, and MCT1-expressing epithelial cancer cells then uptake and use that lactate as a substrate for the tricarboxylic acid (TCA) cycle
  • MCT4-positive cancer cells depend on glycolysis and then efflux lactate, while MCT1-positive cells uptake lactate and rely on OXPHOS
  • metabolic heterogeneity induces a lactate shuttle between hypoxic/glycolytic cells and oxidative/aerobic tumour cells
  • bulk tumour cells exhibit a glycolytic phenotype, with increased conversion of glucose to lactate (and enhanced lactate efflux through MCT4), CSC subsets depend on oxidative phosphorylation; most of the glucose entering the cells is converted to pyruvate to fuel the TCA cycle and the electron transport chain (ETC), thereby increasing mitochondrial ROS production
  • the major fraction of glucose is directed into the pentose phosphate pathway, to produce redox power through the generation of nADPH and ROS scavengers
  • HIF-1α, p53, and c-Myc, are known to contribute to oncogenic metabolism
  • regulatory molecules involved in EMT and CSCs, including Snail, Dlx-2, HIF-1, STAT3, TGF-β, Wnt, and Akt, are implicated in the metabolic reprogramming of cancer cells
  • HIF-1 induces the expression of glycolytic enzymes, including the glucose transporter GLUT, hexokinase, lactate dehydrogenase (LDH), and MCT, resulting in the glycolytic switch
  • HIF-1 represses the expression of pyruvate dehydrogenase kinase (PDK), which inhibits pyruvate dehydrogenase (PDH), thereby inhibiting mitochondrial activity
  • STAT3 has been implicated in EMT-induced metabolic changes as well
  • TGF-β and Wnt play important roles in the metabolic alteration of cancer cells
  • Akt is also implicated in the glycolytic switch and in promoting cancer cell invasiveness
  • EMT, invasion, metastasis, and stemness
  • pyruvate kinase M2 (PKM2), LDH, and pyruvate carboxylase (PC), are implicated in the induction of the EMT and CSC phenotypes
  • decreased activity of PKM2 is known to promote an overall shift in metabolism to aerobic glycolysis
  • LDH catalyses the bidirectional conversion of lactate to pyruvate
  • High levels of LDHA are positively correlated with the expression of EMT and CSC markers
  • IR has been shown to induce metabolic changes in cancer cells
  • IR enhances glycolysis by upregulating GAPDH (a glycolysis enzyme), and it increases lactate production by activating LDHA, which converts pyruvate to lactate
  • IR enhances glycolysis by upregulating GAPDH (a glycolysis enzyme), and it increases lactate production by activating LDHA, which converts pyruvate to lactate
  • IR also elevates MCT1 expression that exports lactate into the extracellular environment, leading to acidification of the tumour microenvironment
  • IR increases intracellular glucose, glucose 6-phosphate, fructose, and products of pyruvate (lactate and alanine), suggesting a role for IR in the upregulation of cytosolic aerobic glycolysis
  • Lactate can activate latent TGF-
  • lactate stimulates cell migration and enhances secretion of hyaluronan from CAF that promote tumour metastasis
  • promote tumour survival, growth, invasion, and metastasis; enhance the stiffness of the ECM; contribute to angiogenesis; and induce inflammation by releasing several growth factors and cytokines (TGF-β, VEGF, hepatocyte growth factor [HGF], PDGF, and stromal cell-derived factor 1 [SDF1]), as well as MMP
  • tumours recruit the host tissue’s blood vessel network to perform four mechanisms: angiogenesis (formation of new vessels), vasculogenesis (de novo formation of blood vessels from endothelial precursor cells), co-option, and modification of existing vessels within tissues.
  • immunosuppressive cells such as tumour-associated macrophages (TAM), MDSCs, and regulatory T cells, and the immunosuppressive cytokines, TGF-β and interleukin-10 (IL-10)
  • immunosuppressive cells such as tumour-associated macrophages (TAM), MDSCs, and regulatory T cells, and the immunosuppressive cytokines, TGF-β and interleukin-10 (IL-10)
  • intrinsic immunogenicity or induce tolerance
  • cancer immunoediting’
  • three phases: 1) elimination, 2) equilibrium, and 3) escape.
  • The third phase, tumour escape, is mediated by antigen loss, immunosuppressive cells (TAM, MDSCs, and regulatory T cells), and immunosuppressive cytokines (TGF-β and IL-10).
  • IR can elicit various changes in the TME, such as CAF activity-mediated ECM remodelling and fibrosis, cycling hypoxia, and an inflammatory response
  • IR activates CAFs to promote the release of growth factors and ECM modulators, including TGF-β and MMP
  • TGF-β directly influences tumour cells and CAFs, promotes tumour immune escape, and activates HIF-1 signalling
    • Nathan Goodyear
      Nathan Goodyear on 09 Feb 21
       
      And now the receipts
  • MMPs degrade ECM that facilitates angiogenesis, tumour cell invasion, and metastasis
    • Nathan Goodyear
      Nathan Goodyear on 09 Feb 21
       
      Receipts and mechanisms
  • IR also promotes MMP-2/9 activation in cancer cells to promote EMT, invasion, and metastasis
  • IR-induced Snail increases MMP-2 expression to promote EMT
  • Radiotherapy has the paradoxical side-effect of increasing tumour aggressiveness
  • IR promotes ROS production in cancer cells, which may induce the activation of oncogenes and the inactivation of tumour suppressors, which further promote oncogenic metabolism
  • Metabolic alterations
  • oncogenic metabolism
  • elicit various changes in the TME
  • Although IR activates an antitumour immune response, this signalling is frequently suppressed by tumour escape mechanisms
  • Nathan Goodyear on 09 Feb 21
     
    Important review article.
snfilms

Check out the Fresh Magnificent White Rose - 0 views

#snfilms #productionHouseHooghly #filmInstituteHooghly #flowersPhotography #rosePhotography #whiteRose

shared by snfilms on 30 Jul 20 - No Cached
  • snfilms on 30 Jul 20
     
    Look at this magnificent White Rose. It symbolises innocence, eternal loyalty, purity and young love. nothing to do with the symbolisation. However, it's eternal fun to be young and loyal in love. Click: Sanjib nath Courtesy: #canondslr https://youtu.be/n-EY1LUqbSc Contact Sn FILMS for online #acting #singing #spokenEnglish classes at #SnFPA head office at Chandannagar, Hooghly.
spineneuro

French to India Medical Travel: Sentez-vous mieux avec des soins fiables dispensés par le meilleur neurochirurgien de l'hôpital Fortis de Delhi, le Dr Sandeep Vaishya - 0 views

frenchtoindiamedicaltravel.blogspot.com/...le-care-best-neurosurgeon.html

Meilleur neurochirurgien du Fortis Hospital Delhi Dr Sandeep Vaishya Dr Sandeep Vaishya Meilleur neurochirurgien Gamma Knife en Inde Radiochirurgie au couteau gamma Hôpitaux à bas prix pour la chirurgie radio-gamma Knife

shared by spineneuro on 17 Nov 21 - No Cached
  • spineneuro on 17 Nov 21
     
    Aujourd'hui, le meilleur neurochirurgien de l'hôpital Fortis de Delhi, le Dr Sandeep Vaishya, est le premier fournisseur national de procédures au couteau gamma aux personnes du monde entier. Pour une réponse rapide aux requêtes Adresse e-mail : dr.sandeepvaishya@neurospinehospital.com n° de téléphone : +91-9325887033
« First ‹ Previous 41 - 60 of 167 Next › Last »
Showing 20▼ items per page