Glycogen Synthesis
•Download as PPT, PDF•
0 likes•3,043 views
This document discusses experiments related to glycogen synthesis and Lafora disease. Experiment I aims to prove that downregulating glycogen synthase stops and prevents adult polyglucosan body disease by crossing PTG-/- and GBE1-/- mice. Experiment II aims to prove that introducing amylase into neurons can clear polyglucosans and cure the disease by crossing GBE1-/- and amylase +/+ mice. Experiment III proposes introducing amylase or other molecules across the blood brain barrier to actually apply the previous experiments and eliminate polyglucosan bodies.
Report
Share
Report
Share
Recommended
Therapeutic Interventions Tested in APBD Models
Researchers have developed a neuronal model of APBD that recapitulates glycogen accumulation and increased apoptosis seen in patients. Treating the model with rapamycin reversed adverse phenotypes by possibly stimulating autophagosome formation and exosome release, or inhibiting glycogen synthase. Researchers are now testing rapamycin and other therapies like iron chelators in the neuronal model, mouse model, and patient cells to identify effective treatments for APBD.
Advances in APBD Research: High Content Screening, Antisense Oligonucleotides...
This document summarizes research on Adult Polyglucosan Body Disease (APBD) presented at an annual meeting. There are three main strategies discussed to treat APBD:
1) Reducing the ratio of Glycogen Synthase to Glycogen Branching Enzyme activity through antisense oligonucleotides, candidate compound testing, or high content screening.
2) Candidate compound testing of inhibitors that reduce Glycogen Synthase or stabilize Glycogen Branching Enzyme.
3) High content screening to find compounds that clear polyglucosan bodies through autophagy induction or other mechanisms. Early results show rapamycin may decrease polyglucosan formation but not clear pre
Molecular Characterization of Polyglucosan Body, Cause or Consequence in the ...
This document describes research into polyglucosan body disease (PGBD), caused by glycogen branching enzyme (GBE) deficiency. Researchers generated two mouse models of PGBD - one with complete GBE loss and one with 20% residual activity. Both models accumulated polyglucosan (insoluble glucose polymer) in tissues like liver, heart and muscle, similar to human PGBD. The models showed physical impairment and altered glucose metabolism. The findings support that these mouse models can help study polyglucosan accumulation and determine if it is a cause or consequence of PGBD.
Structural Studies of Human GBE1 and Relevance to APBD
The document summarizes Wyatt Yue's work studying the structure of human GBE1 and its relevance to Adult Polyglucosan Body Disease (APBD). Key points:
1. Wyatt determined the crystal structures of human GBE1 in its apo form and bound to acarbose and Glc7, to understand its shape and function.
2. Mutations in GBE1 cause APBD. Wyatt purified several GBE1 mutants to characterize, including Y329S, and determined the Y329 site is disrupted in the mutant structure.
3. Wyatt collaborates with APBD patient groups like APBDRF to translate structural findings into potential pharmacological chaperone treatments for
Zack Brittingham Poster draft 121014 Updated-2
GBA activity was assessed in cell lines with and without GBA knockout. Activity decreased in a dose-dependent manner with CBE treatment but not ambroxol or isofagomine after short incubation. Mutant B lymphocytes and fibroblasts generally had lower GBA levels and activity than controls, with some donor variability. Treatment of A53T transgenic mouse neurons with ambroxol and isofagomine decreased α-synuclein levels, indicating potential as chaperones to increase GBA activity and reduce α-synuclein aggregates.
2015_SummerScholarsProgramPresentation- Daniel Donchev
This document summarizes a student's research project on the role of survivin in gastric wound healing. Survivin inhibits apoptosis and cell division and may also be involved in angiogenesis and cell migration during wound healing. The student aims to prove survivin's critical role in these processes. Their methods involve cloning promoters for genes related to blood vessels and the stomach into lentiviral vectors. They successfully cloned the promoters for VE-cadherin and EGFR and will next insert these into CRISPR/Cas9 and other vectors. The overall research aims to further understanding of gastric wound healing and could translate to new treatment strategies.
Abhishek Mogili USRTP Poster
1) The protein SAMP1 localizes to both the endoplasmic reticulum (ER) and microtubules, suggesting it may associate the ER with microtubules.
2) RNAi treatments to stop SAMP1 synthesis in HeLa cells resulted in changes to cell morphology, including the presence of stress fibers and abnormal mitotic cell shapes.
3) This indicates SAMP1 likely plays a role in cell adhesion and cytoplasmic structure.
NIH Poster Brian A. Smith
1) The study investigated the effects of dopamine (DA), dihydroxyphenylacetaldehyde (DOPAL), and dihydroxyphenylacetic acid (DOPAC) on oligomerization of wild-type α-synuclein and mutated forms (A53T, A30P).
2) DOPAL was found to potently oligomerize α-synuclein, around 10 times more than DA. DOPAC had little effect.
3) DOPAL also oligomerized the mutated forms of α-synuclein and appeared to aggregate the A53T form to the point that it did not migrate in gels.
Recommended
Therapeutic Interventions Tested in APBD Models
Researchers have developed a neuronal model of APBD that recapitulates glycogen accumulation and increased apoptosis seen in patients. Treating the model with rapamycin reversed adverse phenotypes by possibly stimulating autophagosome formation and exosome release, or inhibiting glycogen synthase. Researchers are now testing rapamycin and other therapies like iron chelators in the neuronal model, mouse model, and patient cells to identify effective treatments for APBD.
Advances in APBD Research: High Content Screening, Antisense Oligonucleotides...
This document summarizes research on Adult Polyglucosan Body Disease (APBD) presented at an annual meeting. There are three main strategies discussed to treat APBD:
1) Reducing the ratio of Glycogen Synthase to Glycogen Branching Enzyme activity through antisense oligonucleotides, candidate compound testing, or high content screening.
2) Candidate compound testing of inhibitors that reduce Glycogen Synthase or stabilize Glycogen Branching Enzyme.
3) High content screening to find compounds that clear polyglucosan bodies through autophagy induction or other mechanisms. Early results show rapamycin may decrease polyglucosan formation but not clear pre
Molecular Characterization of Polyglucosan Body, Cause or Consequence in the ...
This document describes research into polyglucosan body disease (PGBD), caused by glycogen branching enzyme (GBE) deficiency. Researchers generated two mouse models of PGBD - one with complete GBE loss and one with 20% residual activity. Both models accumulated polyglucosan (insoluble glucose polymer) in tissues like liver, heart and muscle, similar to human PGBD. The models showed physical impairment and altered glucose metabolism. The findings support that these mouse models can help study polyglucosan accumulation and determine if it is a cause or consequence of PGBD.
Structural Studies of Human GBE1 and Relevance to APBD
The document summarizes Wyatt Yue's work studying the structure of human GBE1 and its relevance to Adult Polyglucosan Body Disease (APBD). Key points:
1. Wyatt determined the crystal structures of human GBE1 in its apo form and bound to acarbose and Glc7, to understand its shape and function.
2. Mutations in GBE1 cause APBD. Wyatt purified several GBE1 mutants to characterize, including Y329S, and determined the Y329 site is disrupted in the mutant structure.
3. Wyatt collaborates with APBD patient groups like APBDRF to translate structural findings into potential pharmacological chaperone treatments for
Zack Brittingham Poster draft 121014 Updated-2
GBA activity was assessed in cell lines with and without GBA knockout. Activity decreased in a dose-dependent manner with CBE treatment but not ambroxol or isofagomine after short incubation. Mutant B lymphocytes and fibroblasts generally had lower GBA levels and activity than controls, with some donor variability. Treatment of A53T transgenic mouse neurons with ambroxol and isofagomine decreased α-synuclein levels, indicating potential as chaperones to increase GBA activity and reduce α-synuclein aggregates.
2015_SummerScholarsProgramPresentation- Daniel Donchev
This document summarizes a student's research project on the role of survivin in gastric wound healing. Survivin inhibits apoptosis and cell division and may also be involved in angiogenesis and cell migration during wound healing. The student aims to prove survivin's critical role in these processes. Their methods involve cloning promoters for genes related to blood vessels and the stomach into lentiviral vectors. They successfully cloned the promoters for VE-cadherin and EGFR and will next insert these into CRISPR/Cas9 and other vectors. The overall research aims to further understanding of gastric wound healing and could translate to new treatment strategies.
Abhishek Mogili USRTP Poster
1) The protein SAMP1 localizes to both the endoplasmic reticulum (ER) and microtubules, suggesting it may associate the ER with microtubules.
2) RNAi treatments to stop SAMP1 synthesis in HeLa cells resulted in changes to cell morphology, including the presence of stress fibers and abnormal mitotic cell shapes.
3) This indicates SAMP1 likely plays a role in cell adhesion and cytoplasmic structure.
NIH Poster Brian A. Smith
1) The study investigated the effects of dopamine (DA), dihydroxyphenylacetaldehyde (DOPAL), and dihydroxyphenylacetic acid (DOPAC) on oligomerization of wild-type α-synuclein and mutated forms (A53T, A30P).
2) DOPAL was found to potently oligomerize α-synuclein, around 10 times more than DA. DOPAC had little effect.
3) DOPAL also oligomerized the mutated forms of α-synuclein and appeared to aggregate the A53T form to the point that it did not migrate in gels.
A systems biology approach for understanding skeletal muscle abnormalities in...
A systems biology approach for understanding skeletal muscle abnormalities in...European Institute for Systems Biology & Medicine.
This document summarizes a study that used a systems biology approach to analyze skeletal muscle abnormalities in COPD patients. The study integrated multi-level measurements including transcriptomics, physiological measurements, and serum protein levels from COPD patients and healthy individuals before and after exercise training. Networks were constructed from the data to identify relationships between molecular and physiological variables. The networks showed an uncoupling between tissue remodeling and bioenergetics pathways specific to COPD muscles. Additionally, IL-1 was found to promote tissue remodeling and mimic the training response in healthy individuals. Overall, the study provided new insights into the failure of COPD muscles to respond to exercise training.PDE AND IT'S INHIBITORS
Phosphodiesterases (PDEs) are enzymes that break down cyclic nucleotides and regulate various cellular functions. There are 11 families of PDEs with over 60 isoforms that are specifically expressed in different tissues. PDE inhibitors are used to treat conditions like erectile dysfunction, heart failure, and thrombosis. For example, PDE5 inhibitors like sildenafil and tadalafil are used for erectile dysfunction by relaxing smooth muscles. PDE3 inhibitors increase cardiac contractility and output for heart failure while also causing vasodilation. The specificity of PDE isoforms is derived from their active site structures, allowing them to selectively target cyclic AMP or cyclic GMP.
BMES poster 2016
This study investigated the effects of lyophilized platelet-rich plasma (PRGF) on osteoblast-like MG-63 cells. The results showed that PRGF significantly increased cell proliferation, as measured by total protein content, and alkaline phosphatase (ALP) activity, a marker of osteoblast function. Specifically, cells treated with PRGF for 6 days in low-serum or serum-free medium had higher ALP activity and protein levels compared to controls. This suggests PRGF supports osteoblast proliferation and differentiation.
Timothy Sveeggen Capstone Final Paper
1) Timothy Sveeggen conducted mutagenesis experiments on the Mms6 protein, which is involved in iron manipulation in magnetotactic bacteria. He generated two double mutants, S119A/S122A and S119A/E124A, predicted to inhibit the protein's reductase activity.
2) Assays found that the S119A/S122A mutant completely lacked reductase activity, while the S119A/E124A mutant showed mixed results, possibly due to sample precipitation.
3) The study provides insight into Mms6's mechanism of iron reduction and how mutations affect this activity, furthering understanding of biological iron manipulation at the molecular level.
Seminario biologia molecular
This document summarizes a medical student's research on the differential effects of the protein kinase C-eta (PKCη) on apoptosis versus senescence. The student conducted experiments using cell culture, transfection, and Western blot analysis to determine that depletion of PKCη induces senescence and upregulates the protein p27, leading to resistance to chemotherapy, while depletion of p27 can restore apoptosis. The research contributes to understanding PKCη's controversial roles in tumor promotion and suppression and could help develop more targeted chemotherapy treatments.
Biotech 2012 spring_8_post-trans
This document discusses post-translational modifications and quality control mechanisms. It covers several topics: 1) Purposes of post-translational modifications like quality control, protein function, and localization. 2) Quality control mechanisms in the cytoplasm and endoplasmic reticulum, including molecular chaperones. 3) Selective post-translational proteolysis via ubiquitination and the proteasome system for degradation of misfolded proteins. The document provides details on these various post-translational modification processes.
(1)Complete project report - Gremlin exhibits bindng specificity with heparin...
This document summarizes research investigating the binding specificity between the BMP-7 antagonist Gremlin and heparan sulfate glycosaminoglycans (GAGs). Competitive binding assays were performed using wild type Gremlin and two mutated variants along with naturally occurring GAGs (heparan sulfate, heparan sulfate A, and kidney heparan sulfate). The results indicate that Gremlin associates with GAGs in a specific manner influenced by Gremlin's structural elements and the sulfation patterns of different GAGs. Mutagenesis of Gremlin altered its binding profile for each GAG, demonstrating that protein surface structures impact GAG interactions. This specificity could influence Gremlin's roles in processes like tissue fibrosis and angiogenesis.
AGEP:SRI research project
1) The study examines the role of tissue plasminogen activator (tPA) and plasmin in promoting axonal regrowth after spinal cord injury (SCI) via degradation of chondroitin sulfate proteoglycans (CSPGs).
2) It finds that tPA and plasmin are upregulated after SCI and can degrade CSPG core proteins. Mice lacking tPA show attenuated neurite outgrowth and recovery after SCI, even with chondroitinase ABC (ChABC) treatment to degrade CSPG sugar chains.
3) Coadministration of ChABC and plasmin enhanced recovery in tPA-deficient mice and further supported recovery in wild-type mice with S
Heat shock proteins
Heat shock proteins (HSPs) help maintain protein structure and prevent aggregation. They are classified by molecular weight and function. HSP100, HSP90, HSP70, HSP60 and small HSPs aid in protein folding, transport, and solubilization. When stressed, proteins can unfold but HSPs bind to prevent aggregation and allow refolding. HSPs are more stable due to strong hydrogen bonds and packing that maintain their structure even in stressful conditions.
Prp Presentation
The document discusses prion diseases and the protein-only hypothesis of pathogenesis. It summarizes the structures of cellular and scrapie prion protein and describes techniques used to study prion protein aggregates, including EPR spectroscopy. The document outlines research showing recombinant prion protein forms amyloid fibrils with a parallel in-register beta-sheet structure between residues 160-220. Both denaturing and native conditions produce similar amyloid fibrils, but buffer conditions can lead to structurally distinct fibrils. Substitution of single residues is also shown to produce different amyloid structures.
Auxin and Cytokinin Cross-talk at the Level of Gene Expression in Arabidopsis...
This study examines the interaction between the plant hormones auxin and cytokinin in Arabidopsis thaliana. The researchers used mutant plant lines with decreased cytokinin signaling ability due to knockout mutations in cytokinin response genes. They analyzed the expression of auxin reporter genes DR5:GFP and DR5:GUS in the mutant lines. They found that decreased cytokinin signaling results in redistribution of auxin activity, particularly in vascular tissue and epidermal regions. Their results indicate that cytokinin plays an important role in regulating auxin activity in root meristems, and that the DR5 reporter element, which was designed to respond to auxin, is also activated by cytokinin.
Gabibov Alexander mechanisms of antigen degradation
The document discusses catalytic antibodies and their potential applications. It describes how catalytic antibodies can be obtained through various methods like immunization or phage display. It presents examples of catalytic antibodies that can degrade organophosphates and discusses their structure-function relationships. It also proposes approaches for generating artificial biocatalysts in vivo and targeting the immunoproteasome to treat multiple sclerosis.
Presentation Seminar in Novara University Italy
The document discusses the role of citrullination in multiple sclerosis and describes research synthesizing altered peptide ligands of myelin basic protein to modulate the immune response. Studies showed that citrullinated peptides induced cytokine secretion from MS patient immune cells. Additional experiments conjugating myelin peptide analogs to mannan were able to divert the immune response from a Th1 to a Th2 profile, demonstrating the immunomodulatory potential of altered peptide ligands.
Jack Tuszynski
This document discusses the possibility of using computational drug design for neurological disorders. It summarizes research showing that microtubules in neurons may function as quantum computers capable of vast information processing and storage comparable to the human brain. Various neurological diseases like Alzheimer's, Parkinson's, and ALS involve disruption of microtubule structure and function. The document proposes that stabilizing microtubules through drug design could help treat and prevent neurodegeneration in these diseases. It reviews evidence that general anesthetics may interact with and alter microtubules, influencing memory formation and consciousness. Overall, the document argues microtubules are promising targets for computational drug design approaches to neurological disorders.
To spore or not to spore
This document summarizes a research paper that investigated the relationship between sporulation gene expression and DNA replication in bacteria. The paper found that:
1. There is a single pulse of the master sporulation regulator Spo0A activity each cell cycle that peaks after DNA replication is complete.
2. A hidden negative feedback loop in the phosphorelay system, where Spo0F inhibits KinA, leads to an ultrasensitive response that causes the pulsing behavior.
3. The chromosomal arrangement of the phosphorelay genes spo0F and kinA, which are involved in this feedback loop, provides a perturbation that couples the pulsing of Spo0A activity to DNA replication.
Determining the Interaction between ssSPTa Associated Proteins and Human ORM1...
The interaction between human ORM1-3 proteins and BCAP31, PLP2, and VAMP2 proteins was tested using a split ubiquitin yeast two-hybrid system to better understand how ORM proteins regulate sphingolipid synthesis and their link to asthma. Strong interactions were found between the ORM proteins and the three candidate proteins when the Cub tag was on the C-terminus of the ORM proteins. Western blot and protein spotting showed ORM1 had the strongest interaction while ORM2 had the weakest. This suggests the candidate proteins interact with ORM proteins and may play a role in regulating sphingolipid synthesis and asthma.
GaborSRPPoster JM edits
- Male rats self-administered cocaine for 14 days and then underwent extinction training with saline instead of cocaine.
- Rats were given stress-potentiated reinstatement tests with intermittent footshock stress or corticosterone injection before a low-dose of cocaine.
- The study aims to examine activation of the cortico-accumbens pathway, which connects the prelimbic cortex to the nucleus accumbens core and is important for reinstatement, by measuring expression of c-Fos protein in neurons projecting from the prelimbic cortex to the nucleus accumbens core following reinstatement tests.
Discovery Day 2014 Final Poster - JP
KM409 and KM456 are allosteric modulators of the serotonin transporter hSERT that were investigated. KM456 is a partial, non-competitive inhibitor of hSERT, suggesting it binds to an allosteric site. KM409 has a biphasic effect on hSERT, activating it at low concentrations but inhibiting at higher concentrations. A mutation at residue E493D disrupted KM456's inhibitory effect, indicating its importance for allosteric binding. A biotinylation assay was developed to study the interaction of KM409 and KM456 with hSERT residues, which could provide insight into their therapeutic potential for mental health disorders.
Tautomers
Tautomers are alternate forms of DNA bases that are produced through rearrangements of electrons and protons. When bases tautomerize, they can incorrectly pair with each other during DNA replication, causing mutations known as transitions. Mutations can be classified by their impact on protein function, such as loss of function (null), reduced function (hypomorphic), increased function (hypermorphic), or acquisition of a new function (neomorphic). They can also be dominant or recessive. Examples of different mutation types and their effects are provided.
APBDRF Webinar: Mary Wallace on Patient Nutrition
The document provides dietary guidance for patients with Adult Polyglucosan Body Disease (APBD). It summarizes the results of studies on 19 APBD patients, finding no nutrition deficiencies. Key concerns addressed are maintaining a healthy weight, hydration to prevent urinary tract infections, and minimizing gastrointestinal issues like reflux and constipation. Dietary recommendations focus on meeting calorie needs, sufficient fiber intake, limiting reflux triggers, and getting 50-100g of carbs per day.
APBDRF Scientific Advisory Board Meeting December 2013: Research Update
1) Researchers generated a mouse model of Adult Polyglucosan Body Disease (APBD) with a Y329S mutation to further study the disease and test potential treatments.
2) Initial results found that mice with the Y329S mutation developed polyglucosan bodies in the liver, brain, and muscle and lived longer than a related knockout mouse model.
3) A high-throughput drug screen identified 15 FDA-approved compounds that decreased polyglucosan content in cell cultures, and further testing is being done to validate these potential drug candidates.
4) Improved diagnostic techniques for APBD are also being developed, including GBE enzyme assays and RNA sequencing to identify genetic changes underlying the condition.
GBE1 Interactions with Membrane Implications in APBD
This document summarizes a presentation on interactions between GBE1 and membranes and their implications for adult polyglucosan body disease (APBD). It discusses how GBE1 binding to membranes may be altered by mutations and age-related lipid changes, linking lipids to APBD pathology. Studies showed GBE1 localizes to cell membranes and binds model membranes. Supplementation with triheptanoin or hydroxylated triglyceride drugs lowered the membrane phase transition temperature, suggesting these lipids and drugs could be used to treat APBD by modulating membrane structure. Future research plans include further investigating wild type and mutant GBE1 interactions with membranes and the effects of triglyceride molecules on these interactions.
More Related Content
What's hot
A systems biology approach for understanding skeletal muscle abnormalities in...
A systems biology approach for understanding skeletal muscle abnormalities in...European Institute for Systems Biology & Medicine.
This document summarizes a study that used a systems biology approach to analyze skeletal muscle abnormalities in COPD patients. The study integrated multi-level measurements including transcriptomics, physiological measurements, and serum protein levels from COPD patients and healthy individuals before and after exercise training. Networks were constructed from the data to identify relationships between molecular and physiological variables. The networks showed an uncoupling between tissue remodeling and bioenergetics pathways specific to COPD muscles. Additionally, IL-1 was found to promote tissue remodeling and mimic the training response in healthy individuals. Overall, the study provided new insights into the failure of COPD muscles to respond to exercise training.PDE AND IT'S INHIBITORS
Phosphodiesterases (PDEs) are enzymes that break down cyclic nucleotides and regulate various cellular functions. There are 11 families of PDEs with over 60 isoforms that are specifically expressed in different tissues. PDE inhibitors are used to treat conditions like erectile dysfunction, heart failure, and thrombosis. For example, PDE5 inhibitors like sildenafil and tadalafil are used for erectile dysfunction by relaxing smooth muscles. PDE3 inhibitors increase cardiac contractility and output for heart failure while also causing vasodilation. The specificity of PDE isoforms is derived from their active site structures, allowing them to selectively target cyclic AMP or cyclic GMP.
BMES poster 2016
This study investigated the effects of lyophilized platelet-rich plasma (PRGF) on osteoblast-like MG-63 cells. The results showed that PRGF significantly increased cell proliferation, as measured by total protein content, and alkaline phosphatase (ALP) activity, a marker of osteoblast function. Specifically, cells treated with PRGF for 6 days in low-serum or serum-free medium had higher ALP activity and protein levels compared to controls. This suggests PRGF supports osteoblast proliferation and differentiation.
Timothy Sveeggen Capstone Final Paper
1) Timothy Sveeggen conducted mutagenesis experiments on the Mms6 protein, which is involved in iron manipulation in magnetotactic bacteria. He generated two double mutants, S119A/S122A and S119A/E124A, predicted to inhibit the protein's reductase activity.
2) Assays found that the S119A/S122A mutant completely lacked reductase activity, while the S119A/E124A mutant showed mixed results, possibly due to sample precipitation.
3) The study provides insight into Mms6's mechanism of iron reduction and how mutations affect this activity, furthering understanding of biological iron manipulation at the molecular level.
Seminario biologia molecular
This document summarizes a medical student's research on the differential effects of the protein kinase C-eta (PKCη) on apoptosis versus senescence. The student conducted experiments using cell culture, transfection, and Western blot analysis to determine that depletion of PKCη induces senescence and upregulates the protein p27, leading to resistance to chemotherapy, while depletion of p27 can restore apoptosis. The research contributes to understanding PKCη's controversial roles in tumor promotion and suppression and could help develop more targeted chemotherapy treatments.
Biotech 2012 spring_8_post-trans
This document discusses post-translational modifications and quality control mechanisms. It covers several topics: 1) Purposes of post-translational modifications like quality control, protein function, and localization. 2) Quality control mechanisms in the cytoplasm and endoplasmic reticulum, including molecular chaperones. 3) Selective post-translational proteolysis via ubiquitination and the proteasome system for degradation of misfolded proteins. The document provides details on these various post-translational modification processes.
(1)Complete project report - Gremlin exhibits bindng specificity with heparin...
This document summarizes research investigating the binding specificity between the BMP-7 antagonist Gremlin and heparan sulfate glycosaminoglycans (GAGs). Competitive binding assays were performed using wild type Gremlin and two mutated variants along with naturally occurring GAGs (heparan sulfate, heparan sulfate A, and kidney heparan sulfate). The results indicate that Gremlin associates with GAGs in a specific manner influenced by Gremlin's structural elements and the sulfation patterns of different GAGs. Mutagenesis of Gremlin altered its binding profile for each GAG, demonstrating that protein surface structures impact GAG interactions. This specificity could influence Gremlin's roles in processes like tissue fibrosis and angiogenesis.
AGEP:SRI research project
1) The study examines the role of tissue plasminogen activator (tPA) and plasmin in promoting axonal regrowth after spinal cord injury (SCI) via degradation of chondroitin sulfate proteoglycans (CSPGs).
2) It finds that tPA and plasmin are upregulated after SCI and can degrade CSPG core proteins. Mice lacking tPA show attenuated neurite outgrowth and recovery after SCI, even with chondroitinase ABC (ChABC) treatment to degrade CSPG sugar chains.
3) Coadministration of ChABC and plasmin enhanced recovery in tPA-deficient mice and further supported recovery in wild-type mice with S
Heat shock proteins
Heat shock proteins (HSPs) help maintain protein structure and prevent aggregation. They are classified by molecular weight and function. HSP100, HSP90, HSP70, HSP60 and small HSPs aid in protein folding, transport, and solubilization. When stressed, proteins can unfold but HSPs bind to prevent aggregation and allow refolding. HSPs are more stable due to strong hydrogen bonds and packing that maintain their structure even in stressful conditions.
Prp Presentation
The document discusses prion diseases and the protein-only hypothesis of pathogenesis. It summarizes the structures of cellular and scrapie prion protein and describes techniques used to study prion protein aggregates, including EPR spectroscopy. The document outlines research showing recombinant prion protein forms amyloid fibrils with a parallel in-register beta-sheet structure between residues 160-220. Both denaturing and native conditions produce similar amyloid fibrils, but buffer conditions can lead to structurally distinct fibrils. Substitution of single residues is also shown to produce different amyloid structures.
Auxin and Cytokinin Cross-talk at the Level of Gene Expression in Arabidopsis...
This study examines the interaction between the plant hormones auxin and cytokinin in Arabidopsis thaliana. The researchers used mutant plant lines with decreased cytokinin signaling ability due to knockout mutations in cytokinin response genes. They analyzed the expression of auxin reporter genes DR5:GFP and DR5:GUS in the mutant lines. They found that decreased cytokinin signaling results in redistribution of auxin activity, particularly in vascular tissue and epidermal regions. Their results indicate that cytokinin plays an important role in regulating auxin activity in root meristems, and that the DR5 reporter element, which was designed to respond to auxin, is also activated by cytokinin.
Gabibov Alexander mechanisms of antigen degradation
The document discusses catalytic antibodies and their potential applications. It describes how catalytic antibodies can be obtained through various methods like immunization or phage display. It presents examples of catalytic antibodies that can degrade organophosphates and discusses their structure-function relationships. It also proposes approaches for generating artificial biocatalysts in vivo and targeting the immunoproteasome to treat multiple sclerosis.
Presentation Seminar in Novara University Italy
The document discusses the role of citrullination in multiple sclerosis and describes research synthesizing altered peptide ligands of myelin basic protein to modulate the immune response. Studies showed that citrullinated peptides induced cytokine secretion from MS patient immune cells. Additional experiments conjugating myelin peptide analogs to mannan were able to divert the immune response from a Th1 to a Th2 profile, demonstrating the immunomodulatory potential of altered peptide ligands.
Jack Tuszynski
This document discusses the possibility of using computational drug design for neurological disorders. It summarizes research showing that microtubules in neurons may function as quantum computers capable of vast information processing and storage comparable to the human brain. Various neurological diseases like Alzheimer's, Parkinson's, and ALS involve disruption of microtubule structure and function. The document proposes that stabilizing microtubules through drug design could help treat and prevent neurodegeneration in these diseases. It reviews evidence that general anesthetics may interact with and alter microtubules, influencing memory formation and consciousness. Overall, the document argues microtubules are promising targets for computational drug design approaches to neurological disorders.
To spore or not to spore
This document summarizes a research paper that investigated the relationship between sporulation gene expression and DNA replication in bacteria. The paper found that:
1. There is a single pulse of the master sporulation regulator Spo0A activity each cell cycle that peaks after DNA replication is complete.
2. A hidden negative feedback loop in the phosphorelay system, where Spo0F inhibits KinA, leads to an ultrasensitive response that causes the pulsing behavior.
3. The chromosomal arrangement of the phosphorelay genes spo0F and kinA, which are involved in this feedback loop, provides a perturbation that couples the pulsing of Spo0A activity to DNA replication.
Determining the Interaction between ssSPTa Associated Proteins and Human ORM1...
The interaction between human ORM1-3 proteins and BCAP31, PLP2, and VAMP2 proteins was tested using a split ubiquitin yeast two-hybrid system to better understand how ORM proteins regulate sphingolipid synthesis and their link to asthma. Strong interactions were found between the ORM proteins and the three candidate proteins when the Cub tag was on the C-terminus of the ORM proteins. Western blot and protein spotting showed ORM1 had the strongest interaction while ORM2 had the weakest. This suggests the candidate proteins interact with ORM proteins and may play a role in regulating sphingolipid synthesis and asthma.
GaborSRPPoster JM edits
- Male rats self-administered cocaine for 14 days and then underwent extinction training with saline instead of cocaine.
- Rats were given stress-potentiated reinstatement tests with intermittent footshock stress or corticosterone injection before a low-dose of cocaine.
- The study aims to examine activation of the cortico-accumbens pathway, which connects the prelimbic cortex to the nucleus accumbens core and is important for reinstatement, by measuring expression of c-Fos protein in neurons projecting from the prelimbic cortex to the nucleus accumbens core following reinstatement tests.
Discovery Day 2014 Final Poster - JP
KM409 and KM456 are allosteric modulators of the serotonin transporter hSERT that were investigated. KM456 is a partial, non-competitive inhibitor of hSERT, suggesting it binds to an allosteric site. KM409 has a biphasic effect on hSERT, activating it at low concentrations but inhibiting at higher concentrations. A mutation at residue E493D disrupted KM456's inhibitory effect, indicating its importance for allosteric binding. A biotinylation assay was developed to study the interaction of KM409 and KM456 with hSERT residues, which could provide insight into their therapeutic potential for mental health disorders.
Tautomers
Tautomers are alternate forms of DNA bases that are produced through rearrangements of electrons and protons. When bases tautomerize, they can incorrectly pair with each other during DNA replication, causing mutations known as transitions. Mutations can be classified by their impact on protein function, such as loss of function (null), reduced function (hypomorphic), increased function (hypermorphic), or acquisition of a new function (neomorphic). They can also be dominant or recessive. Examples of different mutation types and their effects are provided.
What's hot (19)
A systems biology approach for understanding skeletal muscle abnormalities in...
A systems biology approach for understanding skeletal muscle abnormalities in...
(1)Complete project report - Gremlin exhibits bindng specificity with heparin...
(1)Complete project report - Gremlin exhibits bindng specificity with heparin...
Auxin and Cytokinin Cross-talk at the Level of Gene Expression in Arabidopsis...
Auxin and Cytokinin Cross-talk at the Level of Gene Expression in Arabidopsis...
Gabibov Alexander mechanisms of antigen degradation
Gabibov Alexander mechanisms of antigen degradation
Determining the Interaction between ssSPTa Associated Proteins and Human ORM1...
Determining the Interaction between ssSPTa Associated Proteins and Human ORM1...
Viewers also liked
APBDRF Webinar: Mary Wallace on Patient Nutrition
The document provides dietary guidance for patients with Adult Polyglucosan Body Disease (APBD). It summarizes the results of studies on 19 APBD patients, finding no nutrition deficiencies. Key concerns addressed are maintaining a healthy weight, hydration to prevent urinary tract infections, and minimizing gastrointestinal issues like reflux and constipation. Dietary recommendations focus on meeting calorie needs, sufficient fiber intake, limiting reflux triggers, and getting 50-100g of carbs per day.
APBDRF Scientific Advisory Board Meeting December 2013: Research Update
1) Researchers generated a mouse model of Adult Polyglucosan Body Disease (APBD) with a Y329S mutation to further study the disease and test potential treatments.
2) Initial results found that mice with the Y329S mutation developed polyglucosan bodies in the liver, brain, and muscle and lived longer than a related knockout mouse model.
3) A high-throughput drug screen identified 15 FDA-approved compounds that decreased polyglucosan content in cell cultures, and further testing is being done to validate these potential drug candidates.
4) Improved diagnostic techniques for APBD are also being developed, including GBE enzyme assays and RNA sequencing to identify genetic changes underlying the condition.
GBE1 Interactions with Membrane Implications in APBD
This document summarizes a presentation on interactions between GBE1 and membranes and their implications for adult polyglucosan body disease (APBD). It discusses how GBE1 binding to membranes may be altered by mutations and age-related lipid changes, linking lipids to APBD pathology. Studies showed GBE1 localizes to cell membranes and binds model membranes. Supplementation with triheptanoin or hydroxylated triglyceride drugs lowered the membrane phase transition temperature, suggesting these lipids and drugs could be used to treat APBD by modulating membrane structure. Future research plans include further investigating wild type and mutant GBE1 interactions with membranes and the effects of triglyceride molecules on these interactions.
High Throughput Screening for Glycogen and Polyglucosan
This document discusses high throughput screening (HTS) for identifying compounds that modulate glycogen and polyglucosan. HTS uses robotics, liquid handling devices, and detectors to quickly test thousands of compounds. The researcher has prepared an assay to observe changes in glycogen quality and quantity using limited digestion and staining. Mouse fibroblasts with genetic defects resulting in low glycogen branching enzyme activity and no polyglucosan are being used. Currently, 1700 FDA-approved compounds are being tested in triplicates using an automated assay to identify potential modulators of glycogen and polyglucosan pathways.
Glycogen metabolism
Examville is an online learning platform that provides free and premium educational resources such as practice tests, live classes, tutoring, study guides, Q&A sessions, and more to help students prepare for exams. Users can access basic functions for free or subscribe to premium content and features. The website aims to help test-takers succeed through comprehensive learning tools and support.
Evolution of man
Our species evolved over 250,000 years ago in Africa, where early humans learned to hunt and gather food. Agricultural developments in the Fertile Crescent revolutionized farming and domestication of animals. This led to the rise of civilizations like Mesopotamia, where societies flourished with laws, culture, literacy and economies. Successful agriculture also resulted in social hierarchies and the use of slave labor. The spread of civilization into Eurasia and the Americas influenced cultures like Greece, Rome, China and India, establishing influential religions such as Christianity, Confucianism, Daoism and Buddhism.
Glycogen metabolism
Glycogen is broken down through the sequential removal of glucose residues by glycogen phosphorylase. Near branch points, a two-step process involving a debranching enzyme is required to release the final glucose residues. Glycogen synthesis involves the conversion of glucose-6-phosphate to UDP-glucose by phosphoglucomutase and UDP-glucose pyrophosphorylase. This UDP-glucose then donates glucose residues to form glycogen chains and branches, with the glycogen-branching enzyme forming new branch points. Glycogenin primes initial glycogen synthesis by both providing the primer chain and catalyzing the assembly of new chains.
glycogen metabolism
This document summarizes the process of gluconeogenesis. It begins by defining gluconeogenesis as the production of glucose from non-carbohydrate precursors when sufficient carbohydrates are not available from diet or glycogen reserves. The major sites are the liver and kidney. The key substrates that enter gluconeogenesis after conversion to pyruvate or later intermediates are listed as lactate, glucogenic amino acids, glycerol, and propionyl CoA. The document then describes the individual pathways for each substrate and explains how gluconeogenesis bypasses the irreversible steps of glycolysis through specific enzymes. It concludes by discussing the regulation and significance of maintaining glucose production through gluconeogenesis.
Glycogen Metabolism
Glycogen Metabolism , synthesis , degradation ....
References : " Lippincott's Biochemistry " book. and of curse "Wikipedia, the free encyclopedia"
Glycogen Metabolism
Glycogen is the storage from of glucose. The metabolism of glycogen both as glycogenolysis, breakdown of glycogen, and glycogenesis, formation of glycogen along with their regulation is briefed in the slides.
Glycogenesis and Glycogenolysis (BIOCHEMISTRY)
Glycogenesis is the formation of glycogen from glucose, which occurs when glucose and ATP levels are high. Glycogenolysis is the breakdown of glycogen into glucose, which is stimulated by glucagon and epinephrine when blood glucose levels drop. Together, glycogenesis and glycogenolysis regulate glucose concentrations by converting excess glucose to glycogen for storage and releasing glucose from glycogen as needed.
GLYCOGENESIS
The synthesis of glycogen from glucose (glycogenesis) involves multiple enzymatic steps that takes place in the cytosol. Glucose is first converted to glucose-6-phosphate by hexokinase or glucokinase in muscle and liver respectively. It is then converted to UDP-glucose which acts as the donor of glucose units. A glycogen primer, initiated by the enzyme glycogen synthase, is required to begin glycogen synthesis. Glycogen is then elongated through alpha-1,4 glycosidic linkages by glycogen synthase and branched through alpha-1,6 linkages by the branching enzyme glucosyltransferase. This leads to the formation of the branched glyc
Gluconeogenesis - The Pathway and Regulation
Gluconeogenesis is the process by which glucose is synthesized from non-carbohydrate precursors in the liver and kidneys. It occurs mainly during periods of fasting and involves converting substrates like lactate, glycerol, and certain amino acids into glucose. The pathway overcomes three thermodynamic barriers of glycolysis through smaller successive steps. Regulation occurs through allosteric control of enzymes, hormonal control of fructose 2,6-bisphosphate levels, and transcriptional control of key genes like PEPCK and FOXO1. Together these mechanisms help direct carbon fluxes towards gluconeogenesis or glycolysis based on energy demands.
Metabolism of glycogen
Glycogen is the major storage form of glucose found mainly in the liver and skeletal muscles. It is formed from glucose through glycogenesis and broken down into glucose through glycogenolysis. These pathways are regulated by enzymes like glycogen synthase and glycogen phosphorylase in response to hormones like insulin and glucagon to maintain blood glucose levels. Deficiencies in enzymes of glycogen metabolism can result in glycogen storage diseases characterized by hypoglycemia, hepatomegaly and other symptoms.
Evolution of man
Neanderthals were the first human species identified by scientists in 1856. They evolved to be adapted to cold environments with short, stocky bodies. Neanderthals cared for sick and injured members of their group, and evidence suggests they had basic medical knowledge and engaged in cultural practices like painting. Cro-Magnons, found in France in 1868, were early modern humans who made burial art, fire-based hunting techniques, and ceremonial practices. Homo sapiens, emerging around 300,000 years ago, had larger brains and more sophisticated culture and technology, including advanced stone tools, musical instruments, shelters, and burial rituals, representing more complex cognition and symbolism.
Research project - human evolution
The document summarizes research on human evolution from early hominids like Australopithecus to modern Homo sapiens. It discusses topics like the incomplete fossil record, disagreements around hominid species numbers and timelines, and key species like Australopithecus afarensis, Homo erectus, and Homo sapiens. Comparisons are made between skeletal structures, brain sizes, and pelvises of different hominids to illustrate anatomical changes over time.
Human evolution
Some slides of our presentations about hominins.
4º ESO students
IES Claudio Sánchez Albornoz, León, Spain
Evolution of Man
This document summarizes the evolution of man from early primate ancestors like Propliopithecus through different hominin species like Homo erectus, Neanderthals, and Cro-Magnon man. Key transitional species discussed include Australopithecus, which had characteristics of both apes and humans, and Homo erectus, considered the first true humans. Neanderthals were an advanced primitive species that lived in Europe and West Asia until around 25,000 years ago, while Cro-Magnon man was a extinct modern human that originated around 3 million years ago.
Glycogen metabolism
Glycogen is a branched polymer of glucose residues that serves as a storage form of glucose. It is composed mainly of α-1,4 glycosidic linkages with branches every tenth residue by α-1,6 linkages. Glycogen is found primarily in liver and muscle cells bound in granules and provides a readily available source of glucose through breakdown. Glycogen synthesis utilizes UDP-glucose and glycogenin to initiate polymer formation, while breakdown is catalyzed by phosphorylase releasing glucose-1-phosphate and other enzymes are needed to further process the glucose for energy production.
Glycogen metabolism- revision
Glycogen is a readily available storage form of glucose found mainly in the liver and muscle. It is synthesized through glycogenesis, which involves four steps - activation of glucose to UDP-glucose, initiation using the primer glycogenin, elongation by glycogen synthase adding glucose units via alpha-1,4 glycosidic bonds, and branching every 7-10 units via alpha-1,6 bonds by branching enzyme. Glycogen synthesis requires two enzymes - glycogen synthase which elongates the chain and branching enzyme which introduces branches, and continues till sufficient glycogen is synthesized or glucose is no longer available.
Viewers also liked (20)
APBDRF Scientific Advisory Board Meeting December 2013: Research Update
APBDRF Scientific Advisory Board Meeting December 2013: Research Update
GBE1 Interactions with Membrane Implications in APBD
GBE1 Interactions with Membrane Implications in APBD
High Throughput Screening for Glycogen and Polyglucosan
High Throughput Screening for Glycogen and Polyglucosan
Similar to Glycogen Synthesis
Prostaglandins
The document discusses prostaglandins, including their classification, biosynthesis, physiological effects, and inhibitors. It summarizes a 1971 study that discovered the mechanism of action of aspirin and other NSAIDs. The study found that incubating guinea pig lung tissue with arachidonic acid leads to increased production of prostaglandins PGE2 and PGF2α over time. Aspirin, indomethacin, and sodium salicylate were shown to inhibit this prostaglandin production in a dose-dependent manner. This established that aspirin-like drugs work by inhibiting the enzyme that synthesizes prostaglandins from arachidonic acid.
Prostaglandins
Prostaglandins are locally-acting lipid mediators derived from arachidonic acid through the cyclooxygenase pathway. They have diverse hormone-like effects and are produced throughout the body, acting on nearby cells through G-protein coupled receptors. Prostaglandins have many functions including regulating inflammation, sensitizing neurons to pain, inducing labor, and vasodilation. They are different from true hormones as they act locally rather than at a distance and are synthesized as needed rather than being stored.
MBBS AIMC prostaglandins and uses and pharma.pptx
Prostaglandins are lipid mediators derived from arachidonic acid through the cyclooxygenase pathway. They have diverse hormone-like effects and are involved in processes like inflammation and gastric acid secretion. The two main cyclooxygenase enzymes, COX-1 and COX-2, convert arachidonic acid into prostaglandin H2, which is then converted to other prostaglandins. Prostaglandins act locally through G-protein coupled receptors to regulate various physiological functions. They are different from true hormones as they act locally rather than at a distance and are synthesized on demand rather than being stored.
Prostaglandins-Introduction and Biological Importance
Contains introduction to prostaglandins and their biological importance, occurrence and general structure
ABSTRACT of thesis
Monosodium glutamate (MSG) is commonly used as a food flavor enhancer but can be neurotoxic in excess amounts. MSG was administered to mice in varying daily doses for 12 days. Higher MSG doses significantly decreased body weight. Behavioral tests showed MSG impaired the mice's memory and ability to navigate mazes. Examination of the brain found damage to cells in the hippocampus, which is associated with memory. Biochemical analysis revealed MSG disrupted liver and kidney function and decreased cholesterol and brain phospholipids, suggesting negative effects on brain structure and function.
Prostaglandins and leucotrienes mani
Autacoids are locally acting hormones that are synthesized and act in the tissues where they are produced. They differ from hormones in that they do not circulate in the bloodstream and have short durations of action. Major classes of autacoids include amines, lipid derivatives, and peptides. Lipid derivatives include prostaglandins, thromboxanes, leukotrienes, and platelet activating factor, which are derived from arachidonic acid. These eicosanoids have various physiological and pathophysiological roles such as platelet aggregation, bronchioconstriction, and inflammation. Nonsteroidal anti-inflammatory drugs inhibit their synthesis.
Arachidonic acid metabolism
1. Arachidonic acid is released from cell membranes and metabolized via either the cyclooxygenase pathway or lipoxygenase pathway to produce prostaglandins, thromboxanes, leukotrienes, and lipoxins.
2. These metabolites are involved in various physiological and pathological processes such as inflammation, hemostasis, smooth muscle contraction, and pain sensation.
3. Nonsteroidal anti-inflammatory drugs function by inhibiting cyclooxygenase, thereby blocking prostaglandin production and reducing inflammation.
Prostaglandins pharmacology
This document discusses prostaglandins, which are locally acting hormone-like lipid mediators derived from arachidonic acid. Prostaglandins have diverse roles in processes like inflammation, fever regulation, and reproduction. They act by binding G protein-coupled receptors on target cells. Nonsteroidal anti-inflammatory drugs inhibit prostaglandin production by blocking the enzyme prostaglandin-H synthase. Aspirin irreversibly inhibits this enzyme through acetylation, reducing thromboxane formation in platelets and thus having an anti-clotting effect.
Similar to Glycogen Synthesis (8)
Prostaglandins-Introduction and Biological Importance
Prostaglandins-Introduction and Biological Importance
Recently uploaded
TEST BANK For Community and Public Health Nursing: Evidence for Practice, 3rd...
TEST BANK For Community and Public Health Nursing: Evidence for Practice, 3rd Edition by DeMarco, Walsh, Verified Chapters 1 - 25, Complete Newest Version TEST BANK For Community and Public Health Nursing: Evidence for Practice, 3rd Edition by DeMarco, Walsh, Verified Chapters 1 - 25, Complete Newest Version TEST BANK For Community and Public Health Nursing: Evidence for Practice, 3rd Edition by DeMarco, Walsh, Verified Chapters 1 - 25, Complete Newest Version Test Bank For Community and Public Health Nursing: Evidence for Practice 3rd Edition Pdf Chapters Download Test Bank For Community and Public Health Nursing: Evidence for Practice 3rd Edition Pdf Download Stuvia Test Bank For Community and Public Health Nursing: Evidence for Practice 3rd Edition Study Guide Test Bank For Community and Public Health Nursing: Evidence for Practice 3rd Edition Ebook Download Stuvia Test Bank For Community and Public Health Nursing: Evidence for Practice 3rd Edition Questions and Answers Quizlet Test Bank For Community and Public Health Nursing: Evidence for Practice 3rd Edition Studocu Test Bank For Community and Public Health Nursing: Evidence for Practice 3rd Edition Quizlet Test Bank For Community and Public Health Nursing: Evidence for Practice 3rd Edition Stuvia Community and Public Health Nursing: Evidence for Practice 3rd Edition Pdf Chapters Download Community and Public Health Nursing: Evidence for Practice 3rd Edition Pdf Download Course Hero Community and Public Health Nursing: Evidence for Practice 3rd Edition Answers Quizlet Community and Public Health Nursing: Evidence for Practice 3rd Edition Ebook Download Course hero Community and Public Health Nursing: Evidence for Practice 3rd Edition Questions and Answers Community and Public Health Nursing: Evidence for Practice 3rd Edition Studocu Community and Public Health Nursing: Evidence for Practice 3rd Edition Quizlet Community and Public Health Nursing: Evidence for Practice 3rd Edition Stuvia Community and Public Health Nursing: Evidence for Practice 3rd Edition Test Bank Pdf Chapters Download Community and Public Health Nursing: Evidence for Practice 3rd Edition Test Bank Pdf Download Stuvia Community and Public Health Nursing: Evidence for Practice 3rd Edition Test Bank Study Guide Questions and Answers Community and Public Health Nursing: Evidence for Practice 3rd Edition Test Bank Ebook Download Stuvia Community and Public Health Nursing: Evidence for Practice 3rd Edition Test Bank Questions Quizlet Community and Public Health Nursing: Evidence for Practice 3rd Edition Test Bank Studocu Community and Public Health Nursing: Evidence for Practice 3rd Edition Test Bank Quizlet Community and Public Health Nursing: Evidence for Practice 3rd Edition Test Bank Stuvia
Top Effective Soaps for Fungal Skin Infections in India
Swisschem Dermacare has mentioned the List of The Best Antifungal Soap In India 2022. All of these soaps are trusted by various Dermatology Experts.
Hemodialysis: Chapter 4, Dialysate Circuit - Dr.Gawad
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
REGULATION FOR COMBINATION PRODUCTS AND MEDICAL DEVICES.pptx
It includes regulation of combination products and medical devices. FDA and industry liaisons.
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
Clinic ^%[+27633867063*Abortion Pills For Sale In Tembisa Central
Clinic ^%[+27633867063*Abortion Pills For Sale In Tembisa Central Clinic ^%[+27633867063*Abortion Pills For Sale In Tembisa CentralClinic ^%[+27633867063*Abortion Pills For Sale In Tembisa CentralClinic ^%[+27633867063*Abortion Pills For Sale In Tembisa CentralClinic ^%[+27633867063*Abortion Pills For Sale In Tembisa Central
Osteoporosis - Definition , Evaluation and Management .pdf
Osteoporosis is an increasing cause of morbidity among the elderly.
In this document , a brief outline of osteoporosis is given , including the risk factors of osteoporosis fractures , the indications for testing bone mineral density and the management of osteoporosis
Artificial Intelligence Symposium (THAIS)
Artificial Intelligence Symposium (THAIS). Parc Taulí. Sabadell
Ketone bodies and metabolism-biochemistry
This slide consists of all the topics of ketone . This can be used for exam purpose for writing about Diabetic keto acidosis etc . Thank you
Part II - Body Grief: Losing parts of ourselves and our identity before, duri...
Learn about body grief and ways to cope with it. We will also explore methods to heal from this challenging experience.
Histopathology of Rheumatoid Arthritis: Visual treat
Histopathology of Rheumatoid Arthritis: Visual treat
Recently uploaded (20)
Ear and its clinical correlations By Dr. Rabia Inam Gandapore.pptx
Ear and its clinical correlations By Dr. Rabia Inam Gandapore.pptx
CHEMOTHERAPY_RDP_CHAPTER 6_Anti Malarial Drugs.pdf
CHEMOTHERAPY_RDP_CHAPTER 6_Anti Malarial Drugs.pdf
TEST BANK For Community and Public Health Nursing: Evidence for Practice, 3rd...
TEST BANK For Community and Public Health Nursing: Evidence for Practice, 3rd...
Top Effective Soaps for Fungal Skin Infections in India
Top Effective Soaps for Fungal Skin Infections in India
Hemodialysis: Chapter 4, Dialysate Circuit - Dr.Gawad
Hemodialysis: Chapter 4, Dialysate Circuit - Dr.Gawad
REGULATION FOR COMBINATION PRODUCTS AND MEDICAL DEVICES.pptx
REGULATION FOR COMBINATION PRODUCTS AND MEDICAL DEVICES.pptx
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...
Clinic ^%[+27633867063*Abortion Pills For Sale In Tembisa Central
Clinic ^%[+27633867063*Abortion Pills For Sale In Tembisa Central
Osteoporosis - Definition , Evaluation and Management .pdf
Osteoporosis - Definition , Evaluation and Management .pdf
Muscles of Mastication by Dr. Rabia Inam Gandapore.pptx
Muscles of Mastication by Dr. Rabia Inam Gandapore.pptx
Part II - Body Grief: Losing parts of ourselves and our identity before, duri...
Part II - Body Grief: Losing parts of ourselves and our identity before, duri...
Histopathology of Rheumatoid Arthritis: Visual treat
Histopathology of Rheumatoid Arthritis: Visual treat
Glycogen Synthesis
- 6. Glycogen Synthesis Glycogen synthase Glycogen branching enzyme
- 8. GS ~ BE
- 10. ↑GS Or ↓BE
- 11. ↑GS Or ↓BE
- 13. Adult Polyglucosan Lafora Disease ↑GS Body Disease ↓BE
- 14. GS ~ BE
- 15. GS ~ BE
- 16. PTG PP1 GS
- 17. PTG -/- Laforin -/- X PTG -/- Laforin -/-
- 18. 0.3 LKO 0.25 DKO 0.2 0.15 0.1 0.05 0 1
- 26. GS ~ BE
- 28. PTG -/- Malin -/- X PTG -/- Malin -/-
- 30. Adult Polyglucosan Lafora Disease Body Disease
- 34. GS ~ BE
- 35. PTG -/- GBE1 -/- X PTG -/- GBE1 -/-
- 36. Small molecule Glycogen synthase siRNA
- 41. Amylase +/+ GBE1 -/- X Amylase +/+ GBE1 -/-
- 45. Summary Experiment I: GBE-/- x Experiment II: GBE-/- x Experiment III: Introducing PTG-/- Amylase +/+ amylase (or other) across the blood brain barrier Will prove whether Will prove whether introducing amylase into This experiment would be downregulating GS neurons clears the way to actually apply STOPS and PREVENTS polyglucosans and cures the previous experiment, APBD. APBD. and introduce amylase into the brain and neurons and eliminate Will focus subsequent Will focus subsequent work polyglucosan bodies. work on finding a small on finding a way to molecule that interferes introduce amylase into the with and slows GS brain, ONLY ONCE. Single introduction should activity. clear polyglucosans accumulated for 50 years and thus allow freedom Polyglucosan from disease for the next 50 accumulation is probably years. a NET accumulation, i.e. the difference between their production and elimination. Potentially, stopping production could result in natural gradual elimination, and cure.